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Journal of Medicine and Pharmacy","Tạp chí Y Dược học Cần Thơ",{"EN":487,"VI":488},"\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">04\u002F10\u002F2015 Ministry of Information and Communications allowed Can Tho journal of medicine and pharmacy to operate (102 \u002FGP-BTTTT)\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">07\u002F16\u002F2015 Can Tho journal of medicine and pharmacy is internationally recognized: ISSN 2354-1210\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">In 2016, The journal has been included in the list of medical science journals by The State Council for professorship which is awarded a work score of 0-0.5 points for a published article.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Can Tho Journal of Medicine and Pharmacy welcome original works that haven’t been submitted or published in other medical journals. Posts must contain content related to one of the journal’s categories.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The content published\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The journal is divided into 3 categories:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Scientific research article: are valuable scientific works, which have been researched and accepted.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Overview of medicine, biology and pharmacy: serving the objective of continuing training in the fields of medicine, biology and pharmacy; to systematize classical and modern knowledge.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Update information on new knowledge about medicine, biology, pharmacy in the country and in the world.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Scope\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Publication and introduction of scientific research in the fields:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Medicine (internal medicine, surgery, pediatrics, obstetrics and gynecology, odonto-stomatology, laboratory, oncology, traditional medicine, nursing).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Biology (genetics, biotechnology).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Pharmacology (pharmaceutics, drug quality analysis-control, synthetic pharmaceutical chemistry, biochemistry, pharmacognosy, botany, clinical pharmacy).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- To enhance the quality of undergraduate, postgraduate education, scientifically researching and meet the necessary treatment in hospital.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Introducing the updated domestic and oversea information about science technology to promote scientific research and exchanging technology in local, other universities.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Exchanging pharmaceutical and medical information for social health developing in the Mekong Delta and Vietnam.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The object\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Postgraduate students, student of Can Tho University of Medicine and Pharmacy, scientists from schools, research institutes, hospitals, health centers, pharmaceutical companies of the Mekong Delta; other provinces and regions in Vietnam and other country.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Address\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Headquarters of Can Tho Journal of Medicine and Pharmacy, located Scientific Research and International Cooperation Office: 179 Nguyen Van Cu Street, An Khanh Ward, Ninh Kieu District, Can Tho City, Vietnam.\u003C\u002Fspan>\u003C\u002Fp>","\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Ngày 16\u002F7\u002F2015, Tạp chí Y Dược học Cần Thơ được cấp chỉ số quốc tế: ISSN 2354-1210.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 4\u002F2016, Tạp chí đã được Hội đồng Giáo sư ngành Y đưa vào danh sách các tạp chí khoa học Y học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Năm 2020 Tạp chí Y Dược học Cần Thơ đã được phê duyệt vào danh mục của các Hội đồng Giáo sư ngành Dược học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ ra 12 số\u002Fnăm, 180-200 trang\u002Fsố.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 12\u002F2022 Tạp chí Y Dược học Cần Thơ là thành viên của hệ thống Crossref và từ tháng 01\u002F2023 tạp chí thực hiện bình duyệt online kín 2 chiều nhằm tăng tính minh bạch, tin cậy của các công trình nghiên cứu khoa học và đảm bảo tốt nhất chất lượng khoa học của bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ, mục đích và phạm vi của tạp chí\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ và mục đích hoạt động của tạp chí: xuất bản nhằm mục đích phổ biến kết quả từ các đề tài nghiên cứu khoa học; giao lưu trao đổi khoa học, chia sẻ kinh nghiệm, học tập, đồng thời cập nhật thông tin khoa học mới trong các lĩnh vực y, sinh, dược học trong và ngoài nước.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phạm vi của tạp chí: Tạp chí xuất bản được chia thành 3 chuyên mục: (i) Bài báo nghiên cứu khoa học là kết quả công trình nghiên cứu khoa học có giá trị đã được triển khai nghiên cứu, (ii) Bài tổng quan y, sinh, dược học: phục vụ mục tiêu đào tạo liên tục trong lĩnh vực y, sinh, dược học; nhằm hệ thống hóa những kiến thức kinh điển và hiện đại; (iii) Thông tin cập nhật kiến thức mới về y, sinh, dược học trong nước và trên thế giới.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Chính sách truy cập mở\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ áp dụng chính sách truy cập mở đối với các bài báo đã xuất bản đến với độc giả, nhằm mở rộng cơ hội tiếp cận các kết quả nghiên cứu chất lượng cao và tăng cường trao đổi kiến thức. Tạp chí đăng tải trực tuyến (miễn phí) toàn văn các bài báo được công bố trên website của Tạp chí (https:\u002F\u002Ftapchi.ctump.edu.vn).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đạo đức xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ cam kết tuân thủ đạo đức xuất bản phù hợp với các hướng dẫn và tiêu chuẩn của the Committee on Publication Ethics (COPE), tuân thủ các nguyên tắc của COPE’s Core Practices, Best Practices Guidelines for Journal Editors và Guidelines on Good Publication Practices.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Bản thảo bài báo chỉ được chấp nhận khi được tác giả chịu trách nhiệm chính cam kết các nội dung sau: Các nội dung của bản thảo chưa được đăng tải toàn bộ hoặc một phần ở các tạp chí khác; Tất cả các tác giả đều có đóng góp một cách đáng kể vào quá trình nghiên cứu hoặc chuẩn bị bản thảo và cùng chịu trách nhiệm về các nội dung của bản thảo; Tuân thủ các biện pháp đảm bảo đạo đức nghiên cứu (ví dụ thỏa thuận đồng ý tham gia nghiên cứu).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Cam kết bảo mật\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí cam kết thực hiện và tuân thủ các quy định của luật và các văn bản hướng dẫn liên quan đến bảo mật thông tin cá nhân trên không gian mạng. Các thông tin mà người dùng (tác giả, độc giả, biên tập viên, người phản biện) nhập vào các biểu mẫu trên Hệ thống Quản lý xuất bản trực tuyến của tạp chí chỉ được sử dụng vào các mục đích đã được tuyên bố rõ ràng và sẽ không được cung cấp cho bất kỳ bên thứ ba nào khác, hay dùng vào bất kỳ mục đích nào khác.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phí gửi bài\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng bài: 1.000.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng nhanh: 1.500.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với tác giả là cán bộ viên chức thuộc Trường Đại học Y Dược Cần Thơ thì được hỗ trợ 50% lệ phí gửi đăng bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với sinh viên thực hiện đề tài nghiên cứu khoa học cấp trường được hỗ trợ 100% lệ phí đăng bài ( Tác giả gửi đính kèm “ Quyết định về việc giao tổ chức thực hiện đề tài nghiên cứu khoa học cấp Trường của sinh viên”).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Hình thức nộp lệ phí:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Tiền mặt:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Nộp trực tiếp tại Phòng Tài chính - Kế toán, Trường Đại học Y Dược Cần Thơ, số 179 Nguyễn Văn Cừ, P. An Khánh, Q. Ninh Kiều, thành phố Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Chuyển khoản:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tên Tài khoản: Trường ĐHYD Cần Thơ, Số TK: 0111000115668, tại ngân hàng Vietcombank chi nhánh Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Thời gian: Áp dụng từ ngày 01\u002F02\u002F2023.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">* Phí gửi bài không được hoàn trả khi bài viết bị từ chối hoặc tác giả xin rút bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Quy trình phản biện bài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ thực hiện quy trình phản biện kín hai chiều nghiêm ngặt. Danh tính của những người phản biện không được tiết lộ cho các tác giả và ngược lại. Quy trình thẩm định bài báo đăng gồm các bước sau:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tiếp nhận bản thảo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tác giả liên hệ gửi bản thảo đến Tạp chí qua hệ thống trực tuyến tại website: https:\u002F\u002Ftapchi.ctump.edu.vn. Hướng dẫn về cách đăng ký, gửi bài và chuẩn bị bản thảo được cung cấp trên website của Tạp chí.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sàng lọc sơ bộ\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sau khi Tòa soạn nhận được bài báo của tác giả, Ban Thư ký sẽ tiến hành kiểm tra sơ bộ bài báo (các yêu cầu về nội dung và hình thức). Những bài báo không đúng quy cách hoặc có nội dung không phù hợp hoặc vi phạm bản quyền sẽ bị từ chối (Ban Thư ký thông báo phản hồi đến tác giả trong vòng 1 tuần). Những bài báo đủ điều kiện, được Ban Thư ký tòa soạn chuyển đến Ban Biên tập có cùng chuyên môn với nội dung bài báo để đề xuất người phản biện. Thời gian kể từ khi Ban Biên tập nhận bài báo đến khi đề xuất người phản biện bài báo chậm nhất là 5 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Vòng phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký gửi bài và yêu cầu phản biện đến 02 phản biện độc lập.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Các phản biện gởi nhận xét cho Ban Thư ký. Thời gian từ khi gửi bài cho phản biện đến khi nhận ý kiến của phản biện tối đa là 20 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xử ký kết quả phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Nếu ý kiến đồng ý cho đăng và không cần chỉnh sửa, Ban Thư ký tiếp tục đăng bài theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Nếu ý kiến đồng ý đăng và cần chỉnh sửa, Ban Thư ký sẽ thông tin đến tác giả chỉnh sửa theo yêu cầu của người phản biện. Thời gian chỉnh sửa và gửi lại kéo dài không quá 2 tuần, từ khi tác giả bài báo nhận được thông tin (Quá trình này có thể lặp lại tối đa 2 lần\u002F1 bài báo). Khi có sự thống nhất, đồng ý của người phản biện; bài báo được tiếp tục đăng theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Những bài báo có chất lượng không đạt yêu cầu, cả 2 phản biện không đồng ý cho đăng sẽ bị Tòa soạn từ chối đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký tổng hợp các bản thảo đã được tác giả hoàn thiện sau thẩm định trình Ban Biên tập xem xét, Tổng Biên tập phê duyệt, quyết định bài đăng theo các tiêu chí: sự phù hợp nội dung với tôn chỉ và mục đích, thể loại bài viết (ưu tiên các bài có bài có nghiên cứu chuyên sâu, hàm lượng khoa học cao), đóng góp mới bài báo, bài báo được ưu tiên đăng trong số gần nhất của Tạp chí theo thứ tự: tính thời sự, chất lượng bài báo và thời gian gửi bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Ban Biên tập và Ban Thư ký biên tập bản thảo, chế bản, đọc rà soát lỗi. Thời gian hoàn thành từ 10-15 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Ban Thư ký có trách nhiệm thông báo cho tác giả bài báo (bằng e-mail) về tình hình phê duyệt bài báo, thời gian, số kỳ, tập xuất bản bài báo theo qui định.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">4. Danh sách bài báo theo số Tạp chí được in ấn và phát hành trong năm định kỳ được công bố chính thức trên website: https:\u002F\u002Ftapchi.ctump.edu.vn\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>",{"VOID":490},"wcQ1uqwAAAAJ","2023-05-30T08:17:21.868+00:00",[],[494],{"id":495,"createTime":28,"updateTime":28,"relativeEntities":496,"slug":28,"properties":497,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":507,"parentIds":508,"statistic":28},"6413896b-eca9-442b-a73f-182a58a0ce40",[],{"title":498,"address":501,"country":504,"abbreviation":505},{"EN":499,"VI":500},"Can Tho University of Medicine and Pharmacy","Trường Đại học Y Dược Cần Thơ",{"EN":502,"VI":503},"No 179, Nguyen Van Cu street, An Khanh ward, Ninh Kieu district, Can Tho city, Vietnam","Số 179, đường Nguyễn Văn Cừ, phường An Khánh, quận Ninh Kiều, thành phố Cần Thơ, Việt Nam",{"VOID":15},{"VOID":506},"ctump","http:\u002F\u002Fwww.ctump.edu.vn\u002F",[],[],"https:\u002F\u002Ftapchi.ctump.edu.vn\u002Findex.php\u002Fctump",{"impactFactor":32,"impactFactorByYear":512,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":514,"totalPublicationByYear":515,"totalCitation":520,"totalCitationByYear":521,"totalCitationPerPublication":108,"totalCitationPerPublicationByYear":523,"hindexLast5Year":45,"hindex":45},{"2022":513,"2023":111,"2024":106},0.01,1556,{"2020":47,"2021":516,"2022":517,"2023":518,"2024":519,"2025":122},57,306,801,358,161,{"2021":146,"2022":280,"2023":522},99,{"2021":524,"2022":318,"2023":104},0.23,{"impactFactor":28,"impactFactorByYear":28,"i10Index":123,"i10IndexLast5Year":123,"totalPublication":526,"totalPublicationByYear":527,"totalCitation":526,"totalCitationByYear":528,"totalCitationPerPublication":40,"totalCitationPerPublicationByYear":531,"hindexLast5Year":49,"hindex":49},476,{"0":205,"2019":123,"2021":139,"2022":459,"2023":451,"2024":357,"2025":49,"2026":48},{"2021":42,"2022":123,"2023":161,"2024":529,"2025":360,"2026":530},136,83,{"2021":105,"2022":513,"2023":532,"2024":127,"2025":533,"2026":534},0.62,25.43,13.83,{"id":536,"createTime":537,"updateTime":382,"relativeEntities":538,"slug":539,"properties":540,"entityType":25,"verifyStatus":26,"verifyTime":28,"verifyNote":28,"languages":552,"translateLanguages":28,"viewCount":133,"subjectFields":553,"manageAffiliations":554,"indexDatabases":555,"url":556,"thumbnailPath":557,"statistic":558,"gsStatistic":594,"type":55,"analyzePriority":28},"6984a56a-db70-403b-9cc4-4013e1ceaffa","2023-05-09T06:47:40.346+00:00",[],"T%E1%BA%A1p%20ch%C3%AD%20Nghi%C3%AAn%20c%E1%BB%A9u%20n%C6%B0%E1%BB%9Bc%20ngo%C3%A0i",{"country":541,"issn":542,"title":544,"introduce":547,"gsId":550},{"VOID":15},{"VOID":543},"25252445",{"EN":545,"VI":546},"VNU Journal of Foreign Studies","Tạp chí Nghiên cứu nước ngoài",{"EN":548,"VI":549},"{\"ops\":[{\"insert\":\"\\n\\nThe \\n\"},{\"attributes\":{\"italic\":true},\"insert\":\"VNU Journal of Science\"},{\"insert\":\"\\n was established in 1985 for the publication of national and international research papers in all fields of natural sciences and technology, social sciences and humanities. 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anticoagulant therapy, such as vitamin K antagonists (VKAs), is prominent for the prevention of cerebral ischemic stroke or systemic embolism and all-cause mortality in patients with atrial fibrillation, venous thromboembolism, and mechanical or biological valve. VKA treatment requires monitoring of the international normalized ratio (INR) in order to maintain it in a therapeutic range, avoiding side effects, the main and most significant of which is bleeding. The aim of the present study was to evaluate the event rates of several clinical composite outcomes, such as bleeding, thromboembolic events, and all-cause death. We compared three organizational models distinguished by a total (from 1 January to 31 December 2015 in which PT\u002FINR analysis with the relative internal and external quality controls was performed by the surveillance center) or partial (from 15 January to 15 July 2016 and from 15 August to 15 November 2016, in which the surveillance center had the ability to view only the PT\u002FINR results or all patients analyses, including blood count, creatinine, liver enzymes, etc., respectively) analytical patient management. The present longitudinal follow-up study included 1225 patients, recruited from 1 January 2015 to 15 November 2016 at a surveillance center for the prevention of cerebral ischemic stroke and systemic embolism in Chieti (Italy). The results show a significant rise of the incidence rate ratio in patients undergoing VKA treatment during the period 15 January to 15 July 2016 compared to the previous one regarding total bleeding, especially for minor bleeding and digestive bleeding; thromboembolic events; and all-death cause. These findings show that analytical and clinical data and information should be under the direct supervision and responsibility of the surveillance center. In fact, this approach seems to highlight the best results in terms of safety and therapeutic effectiveness.",{"EN":946},"Analytical Management of Patients Undergoing Oral Anticoagulant Therapy Could Have a Strong Impact on Clinical Outcomes: A Follow-up Study",{"VOID":948},"Connolly SJ, Ezekowitz MD, Yusuf S, et al. Dabigatran versus warfarin in patients with atrial fibrillation. N Engl J Med. 2009;361:1139–51.\nPatel MR, Mahaffey KW, Garg J, et al. Rivaroxaban versus warfarin in nonvalvular atrial fibrillation. N Engl J Med. 2011;365:883–91.\nGranger CB, Alexander JH, McMurray JJ, et al. Apixaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2011;365:981–92.\nGiugliano RP, Ruff CT, Braunwald E, et al. Edoxaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2013;369:2093–104.\nAlTurki A, Proietti R, Birnie DH, Essebag V. Management of antithrombotic therapy during cardiac implantable device surgery. J Arrhythm. 2016;32(3):163–9.\nFalk RH. Atrial fibrillation. N Engl J Med. 2001;344:1067–78.\nKasperska-Zajac A, Grzanka A, Kowalczyk J, et al. Refractory chronic spontaneous urticaria and permanent atrial fibrillation associated with dental infection: mere coincidence or something more to it? Int J Immunopathol Pharmacol. 2016;29(1):112–20.\nWipf JE, Lipsky BA. Atrial fibrillation. Thromboembolic risk and indications for anticoagulation. Arch Int Med. 1990;150:1598–1603.\nMenke J, Luthje L, Kastrup A. Thromboembolism in atrial fibrillation. Am J Cardiol. 2010;105:502–10.\nSteinberg BA, Piccini JP. Anticoagulation in atrial fibrillation. Br Med J. 2014;348:g2116.\nReynolds MW, Fahrbach K, Hauch O. Warfarin anticoagulation and outcomes in patients with atrial fibrillation: a systematic review and metaanalysis. Chest. 2004;126:1938–45.\nTidjane N, Hachem A, Zaid Y, et al. A primary role for kinin B1 receptor in inflammation, organ damage, and lethal thrombosis in a rat model of septic shock in diabetes. Euro J Inflamm. 2015;13:40–52.\nSchneider DJ, Sobel BE. Conundrums in the combined use of anticoagulants and antiplatelet drugs. Circulation. 2007;116:305–15.\nJia XF, Hong Z, Fan JH, Zhang YM. Clinical effect of mechanical fragmentation combined with recombinant tissue plasminogen activator artery thrombolysis on acute cerebral infarction. J Biol Regul Homeost Agents. 2016;30(3):821–6.\nFang Y, Zong HL, Zhang L, Wang ZH, Sun LM, Zhang RF. Vena-venous hemofiltration in treating severe injury-induced multiple organ dysfunction syndrome. J Biol Regul Homeost Agents. 2016;30(2):477–84.\nMallouppas M, Vassiliou V. Anticoagulation for atrial fibrillation: is this the end of warfarin? Not just yet. J Angiol. 2013. doi:10.1155\u002F2013\u002F874827\nJanuary CT, Wann LS, Alpert JS. AHA\u002FACC\u002FHRS guideline for the management of patients with atrial fibrillation: executive summary. J Am Coll Cardiol. 2014;64:2246–80.\nCAST (Chinese Acute Stroke Trial) Collaborative Group. CAST: randomized placebo-controlled trial of early aspirin use in 20,000 patients with acute ischaemic stroke. Lancet. 1997;349(9066):1641–9.\nMascali A, Franzese O, Nisticò S, et al. Obesity and kidney disease: beyond the hyperfiltration. Int J Immunopathol Pharmacol. 2016;29(3):354–63.\nPiotrowska Ż, Janiuk I, Lewandowska A, Kasacka I. Decreased immunoreactivity of visfatin in the pancreas and liver of rats with renovascular hypertension. J Biol Regul Homeost Agents. 2016;30(4):1073–8.\nCrincoli V, Ballini A, Fatone L, Di Bisceglie MB, Nardi GM, Grassi FR. Cytokine genotype distribution in patients with periodontal disease and rheumatoid arthritis or diabetes mellitus. J Biol Regul Homeost Agents. 2016;30(3):863–6.\nMahmoud MH, Badr G, El Shinnawy NA. Camel whey protein improves lymphocyte function and protects against diabetes in the offspring of diabetic mouse dams. Int J Immunopathol Pharmacol. 2016;29(4):632–46.\nBianchi E, Ripandelli G, Taurone S, et al. Age and diabetes related changes of the retinal capillaries: an ultrastructural and immunohistochemical study. Int J Immunopathol Pharmacol. 2016;29(1):40–53.\nAdar T, Edden Y, Shteingart S, et al. Portal hypertension is associated with modulation of regulatory T cells. Eur J Inflamm. 2016;14:40–47.\nRietbrock S, Heeley E, Plumb J. Chronic atrial fibrillation: incidence, prevalence, and prediction of stroke using the congestive heart failure, hypertension, age >75, diabetes mellitus, and prior stroke or transient ischemic attack (CHADS2) risk stratification scheme. Am Heart J. 2008;156:57–64.\nLip GY, Nieuwlaat R, Pisters R. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation. Chest. 2010;137:263–72.\nOlesen JB, Lip GY, Hansen ML. Validation of risk stratification schemes for predicting stroke and thromboembolism in patients with atrial fibrillation: nationwide cohort study. Br Med J. 2011;342:d124.\nMant J, Hobbs FD, Fletcher K. Warfarin versus aspirin for stroke prevention in an elderly community population with atrial fibrillation (the Birmingham Atrial Fibrillation Treatment of the Aged Study, BAFTA): a randomised controlled trial. Lancet. 2007;370:493–503.\nArbring K, Uppugunduri S, Lindhal TL. Comparison of prothrombin time (INR) results and main characteristics of patients on warfarin treatment in primary health care centers and anticoagulation clinics. BMC Health Serv Res. 2013;7(13):85.\nWieloch M, Själander A, Frykman V, Rosenqvist M, Eriksson N, Svensson PJ. Anticoagulation control in Sweden: reports of time in therapeutic range, major bleeding, and thrombo-embolic complications from the national quality registry AuriculA. Eur Heart J. 2011;32(18):2282–9.\nWysowski DK, Nourjah P. Bleeding complications with warfarin use: a prevalent adverse effect resulting in regulatory action. Arch Int Med. 2007;167:1414–9.\nMolteni M, Cimminiello C. Warfarin and atrial fibrillation: from ideal to real the warfarin affaire. Thromb J. 2014;12:5.\nChow S, Shao J, Wang H. Sample size calculations in clinical research, 2nd ed. Boca Raton: Chapman & Hall\u002FCRC Biostatistic Series.\nSchulman S, Kearon C, Subcommittee on Control of Anticoagulation of the Scientific Standardization Committee of the International Society on Thrombosis and Haemostasis. Definition of major bleeding in clinical investigations of antihemostatic medicinal products in non-surgical patients. J Thromb Haemost. 2005;3:692–4.\nAtarashi H, Inoue H, Okumura K, Yamashita T, Origasa H. Investigation of optimal anticoagulation strategy for stroke prevention in Japanese patients with atrial fibrillation: the J-RHYTHM Registry study design. J Cardiol. 2011;57:95–9.\nChuai JB, Shi L, Ma XY, Wu D, Kang K, Jiang SL. Curative effect of mechanical heart valve replacement and anticoagulant therapy after surgery. J Biol Regul Homeost Agents. 2016;30(1):141–6.\nYang F, Xiang ML, Liu YM. Thrombin in combination with intensive nursing in treating upper gastrointestinal bleeding in children. 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apolipoprotein A1 (apoA1) remnant ratio has been identified as an independent cardiovascular (CV) risk factor. Higher apoA1 remnant ratios may predict lower CV risk in some patients. This analysis aimed to evaluate the effects of evolocumab on the change from baseline in the apoA1 remnant ratio compared with placebo. This pooled post hoc analysis included 2464 patients with mixed dyslipidemia treated with evolocumab 140 mg every 2 weeks (Q2W) or 420 mg once monthly (QM) in three phase 3 evolocumab trials. The apoA1 remnant ratio was calculated by dividing apoA1 by the difference between non-high-density lipoprotein cholesterol (non-HDL-C) and low-density lipoprotein cholesterol (LDL-C). ApoA1 remnant ratio strata were generated using previously published tertile (\u003C 4.7, 4.7–6.8, and > 6.8) and partitioning categories (\u003C 3.6, 3.6–6.0, and > 6.0). The baseline apoA1 remnant ratio in evolocumab and placebo treatment arms was 7.1 and 7.3, respectively. At week 12, evolocumab 140 mg Q2W and 420 mg QM increased the apoA1 remnant ratio by 25.0% and 33.6%, respectively, versus placebo (p \u003C 0.0001 for both groups). When patients were categorized by week 12 apoA1 remnant ratio thresholds (\u003C 3.6 vs. > 3.6, and \u003C 4.7 vs. > 4.7), those with higher week 12 apoA1 remnant ratios were significantly more likely to have also achieved a target non-HDL-C level of \u003C 100 mg\u002Fdl. In the subset of women > 50 years of age, the proportion of patients at apoA1 remnant ratio thresholds \u003C 3.6, 3.6–6.0, and > 6.0 at baseline shifted toward or remained at higher thresholds at week 12. This post hoc analysis suggests that evolocumab increases the apoA1 remnant ratio. Amgen Inc. Plain language summary available for this article.",{"EN":1215},"Effects of Evolocumab on the ApoA1 Remnant Ratio: A Pooled Analysis of Phase 3 Studies",{"EN":1217},"",{"VOID":1219},"No authors listed. The Lipid Research Clinics Coronary Primary Prevention Trial results. II. The relationship of reduction in incidence of coronary heart disease to cholesterol lowering. JAMA. 1984;251:365–74.\nNo authors listed. The Lipid Research Clinics Coronary Primary Prevention Trial results. I. Reduction in incidence of coronary heart disease. JAMA. 1984;251:351–64.\nCholesterol Treatment Trialists Collaboration, Baigent C, Blackwell L, et al. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet. 2010;376:1670–81.\nFruchart JC, Davignon J, Hermans MP, et al. Residual macrovascular risk in 2013: what have we learned? Cardiovasc Diabetol. 2014;13:26.\nWong ND. Residual risk after treatment of patients with atherosclerotic cardiovascular disease with proprotein convertase subtilisin-kexin type 9 monoclonal antibody therapy (from the Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk Trial). Am J Cardiol. 2017;120:1220–2.\nMay HT, Nelson JR, Lirette ST, et al. The utility of the apolipoprotein A1 remnant ratio in predicting incidence coronary heart disease in a primary prevention cohort: the Jackson Heart Study. Eur J Prev Cardiol. 2016;23:769–76.\nAverna M, Stroes E, The lipid alterations beyond LDL expert working group. How to assess and manage cardiovascular risk associated with lipid alterations beyond LDL. Atheroscler Suppl. 2017;26:16–24.\nVarbo A, Benn M, Nordestgaard BG. Remnant cholesterol as a cause of ischemic heart disease: evidence, definition, measurement, atherogenicity, high risk patients, and present and future treatment. Pharmacol Ther. 2014;141:358–67.\nVarbo A, Benn M, Tybjaerg-Hansen A, Jorgensen AB, Frikke-Schmidt R, Nordestgaard BG. Remnant cholesterol as a causal risk factor for ischemic heart disease. J Am Coll Cardiol. 2013;61:427–36.\nVarbo A, Benn M, Tybjaerg-Hansen A, Nordestgaard BG. Elevated remnant cholesterol causes both low-grade inflammation and ischemic heart disease, whereas elevated low-density lipoprotein cholesterol causes ischemic heart disease without inflammation. Circulation. 2013;128:1298–309.\nToth PP, Grabner M, Punekar RS, Quimbo RA, Cziraky MJ, Jacobson TA. Cardiovascular risk in patients achieving low-density lipoprotein cholesterol and particle targets. Atherosclerosis. 2014;235:585–91.\nJialal I, Devaraj S. Remnant lipoproteins: measurement and clinical significance. Clin Chem. 2002;48:217–9.\nJoshi PH, Khokhar AA, Massaro JM, et al. Remnant lipoprotein cholesterol and incident coronary heart disease: the Jackson Heart and Framingham Offspring Cohort Studies. J Am Heart Assoc. 2016;5:e002765.\nVallejo-Vaz AJ, Fayyad R, Boekholdt SM, et al. Triglyceride-rich lipoprotein cholesterol and risk of cardiovascular events among patients receiving statin therapy in the Treating to New Targets (TNT) trial. Circulation. 2018;138:770–81.\nCooper AD. Hepatic uptake of chylomicron remnants. J Lipid Res. 1997;38:2173–92.\nChappell DA, Medh JD. Receptor-mediated mechanisms of lipoprotein remnant catabolism. Prog Lipid Res. 1998;37:393–422.\nTakahashi S, Suzuki J, Kohno M, et al. Enhancement of the binding of triglyceride-rich lipoproteins to the very low density lipoprotein receptor by apolipoprotein E and lipoprotein lipase. J Biol Chem. 1995;270:15747–54.\nWalldius G, Jungner I, Holme I, Aastveit AH, Kolar W, Steiner E. High apolipoprotein B, low apolipoprotein A-I, and improvement in the prediction of fatal myocardial infarction (AMORIS study): a prospective study. Lancet. 2001;358:2026–33.\nMay HT, Nelson JR, Kulkarni KR, et al. A new ratio for better predicting future death\u002Fmyocardial infarction than standard lipid measurements in women > 50 years undergoing coronary angiography: the apolipoprotein A1 remnant ratio (Apo A1\u002F[VLDL(3) + IDL]). Lipids Health Dis. 2013;12:55.\nNelson J, He L, Dansinger M. ApoA1 remnant ratio in very high risk patients with LDL-c, 70 mg\u002Fdl and nonHDL-c, 100 mg\u002Fdl: ramifications for residual risk in women > 55 years of age [abstract 186]. J Clin Lipidol. 2018;12 515–6.\nLangslet G, Emery M, Wasserman SM. Evolocumab (AMG 145) for primary hypercholesterolemia. Expert Rev Cardiovasc Ther. 2015;13:477–88.\nAwan Z, Baass A, Genest J. Proprotein convertase subtilisin\u002Fkexin type 9 (PCSK9): lessons learned from patients with hypercholesterolemia. Clin Chem. 2014;60:1380–9.\nChan JC, Piper DE, Cao Q, et al. A proprotein convertase subtilisin\u002Fkexin type 9 neutralizing antibody reduces serum cholesterol in mice and nonhuman primates. Proc Natl Acad Sci USA. 2009;106:9820–5.\nPoirier S, Mayer G, Benjannet S, et al. The proprotein convertase PCSK9 induces the degradation of low density lipoprotein receptor (LDLR) and its closest family members VLDLR and ApoER2. J Biol Chem. 2008;283:2363–72.\nCanuel M, Sun X, Asselin MC, Paramithiotis E, Prat A, Seidah NG. Proprotein convertase subtilisin\u002Fkexin type 9 (PCSK9) can mediate degradation of the low density lipoprotein receptor-related protein 1 (LRP-1). PLoS One. 2013;8:e64145.\nBlom DJ, Hala T, Bolognese M, et al. A 52-week placebo-controlled trial of evolocumab in hyperlipidemia. N Engl J Med. 2014;370:1809–19.\nSabatine MS, Giugliano RP, Keech AC, et al. Evolocumab and clinical outcomes in patients with cardiovascular disease. N Engl J Med. 2017;376:1713–22.\nSabatine MS, Leiter LA, Wiviott SD, et al. Cardiovascular safety and efficacy of the PCSK9 inhibitor evolocumab in patients with and without diabetes and the effect of evolocumab on glycaemia and risk of new-onset diabetes: a prespecified analysis of the FOURIER randomised controlled trial. Lancet Diabetes Endocrinol. 2017;5:941–50.\nBonaca MP, Nault P, Giugliano RP, et al. Low-density lipoprotein cholesterol lowering with evolocumab and outcomes in patients with peripheral artery disease: insights from the FOURIER trial (Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk). Circulation. 2018;137:338–50.\nToth PP, Sattar N, Blom DJ, et al. Effect of evolocumab on lipoprotein particles. Am J Cardiol. 2018;121:308–14.\nKoren MJ, Lundqvist P, Bolognese M, et al. Anti-PCSK9 monotherapy for hypercholesterolemia: the MENDEL-2 randomized, controlled phase III clinical trial of evolocumab. J Am Coll Cardiol. 2014;63:2531–40.\nRaal FJ, Stein EA, Dufour R, et al. PCSK9 inhibition with evolocumab (AMG 145) in heterozygous familial hypercholesterolaemia (RUTHERFORD-2): a randomised, double-blind, placebo-controlled trial. Lancet. 2015;385:331–40.\nRobinson JG, Nedergaard BS, Rogers WJ, et al. Effect of evolocumab or ezetimibe added to moderate- or high-intensity statin therapy on LDL-C lowering in patients with hypercholesterolemia: the LAPLACE-2 randomized clinical trial. JAMA. 2014;311:1870–82.\nStroes E, Robinson JG, Raal FJ, et al. Clinical equivalence of evolocumab among patient subgroups in PROFICIO: a pooled analysis of 3146 patients from phase 3 studies. London: European Society of Cardiology; 2015.\nLawler PR, Akinkuolie AO, Harada P, et al. Residual risk of atherosclerotic cardiovascular events in relation to reductions in very-low-density lipoproteins. J Am Heart Assoc. 2017;6:e007402.",{"VOID":1221},"10.1007\u002Fs40119-019-0133-6","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs40119-019-0133-6",[1224,1239,1260,1275,1288,1301],{"id":1225,"sortIndex":32,"researcher":28,"roles":1226,"affiliations":1227,"properties":1236,"displayName":1238,"givenName":28,"familyName":28},"b99a10a8-112f-45fb-a885-6455136bb66b",[958],[1228],{"id":1229,"sortIndex":32,"affiliation":1230,"properties":28},"4b019866-4525-4ccc-beaa-67266a8869cc",{"id":1229,"createTime":28,"updateTime":28,"relativeEntities":1231,"slug":28,"properties":1232,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1235,"statistic":28},[],{"title":1233},{"VI":1234},"Intermountain Heart Institute, Intermountain Medical Center, Murray, USA",[],{"title":1237},{"VI":1238},"Heidi T. May",{"id":1240,"sortIndex":40,"researcher":28,"roles":1241,"affiliations":1242,"properties":1257,"displayName":1259,"givenName":28,"familyName":28},"bfd402f9-8d36-4f54-8784-07deaed49fac",[958],[1243,1249],{"id":1229,"sortIndex":32,"affiliation":1244,"properties":28},{"id":1229,"createTime":28,"updateTime":28,"relativeEntities":1245,"slug":28,"properties":1246,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1248,"statistic":28},[],{"title":1247},{"VI":1234},[],{"id":1250,"sortIndex":32,"affiliation":1251,"properties":28},"c01b7eea-8709-40a2-90a6-e27b6b8c4c9b",{"id":1250,"createTime":28,"updateTime":28,"relativeEntities":1252,"slug":28,"properties":1253,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1256,"statistic":28},[],{"title":1254},{"VI":1255},"Department of Medicine, University of Utah, Salt Lake City, USA",[],{"title":1258},{"VI":1259},"Joseph B. 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Many patients with ATTR present with cardiac involvement; recent studies indicate that ATTR prevalence is higher than expected in patients with certain heart conditions. Although long delays to diagnosis are common, recent treatment advances have made timely diagnosis critical to ensure appropriate patient management. Despite clinical guideline updates, it remains unclear how these are being implemented in routine patient care. We performed a survey of practicing cardiologists in Switzerland to assess their knowledge of ATTR and current clinical practice. Overall, 72 cardiologists completed the questionnaire in a face-to-face interview (n = 16) or online (n = 56). Key findings highlighted wide variation in cardiologists’ knowledge about the diagnostic tests required for a differential diagnosis of ATTR. In particular, many cardiologists lacked familiarity with radiolabeled bone scintigraphy, an important non-invasive test that is part of the diagnostic algorithm for ATTR. Another challenge in diagnosing amyloidosis appears to be general awareness of ATTR among cardiologists. Survey results highlight that cardiologists in Switzerland would benefit from information on the latest advances in ATTR to support them in screening heart failure patients and ensure that patients benefit from treatment advances.",{"EN":1372},"Diagnosis of Amyloidosis: A Survey of Current Awareness and Clinical Challenges Among Cardiologists in Switzerland",{"VOID":1374},"Gonzalez-Lopez E, Lopez-Sainz A, Garcia-Pavia P. Diagnosis and treatment of transthyretin cardiac amyloidosis. Progress Hope. 2017;70(11):991–1004.\nTanskanen M, Peuralinna T, Polvikoski T, Notkola IL, Sulkava R, Hardy J, et al. Senile systemic amyloidosis affects 25% of the very aged and associates with genetic variation in alpha2-macroglobulin and tau: a population-based autopsy study. Ann Med. 2008;40(3):232–9.\nGonzalez-Lopez E, Gallego-Delgado M, Guzzo-Merello G, de Haro-Del Moral FJ, Cobo-Marcos M, Robles C, et al. Wild-type transthyretin amyloidosis as a cause of heart failure with preserved ejection fraction. Eur Heart J. 2015;36(38):2585–94.\nCastano A, Narotsky DL, Hamid N, Khalique OK, Morgenstern R, DeLuca A, et al. Unveiling transthyretin cardiac amyloidosis and its predictors among elderly patients with severe aortic stenosis undergoing transcatheter aortic valve replacement. Eur Heart J. 2017;38(38):2879–87.\nScully PR, Treibel TA, Fontana M, Lloyd G, Mullen M, Pugliese F, et al. Prevalence of cardiac amyloidosis in patients referred for transcatheter aortic valve replacement. J Am Coll Cardiol. 2018;71(4):463–4.\nCavalcante JL, Rijal S, Abdelkarim I, Althouse AD, Sharbaugh MS, Fridman Y, et al. Cardiac amyloidosis is prevalent in older patients with aortic stenosis and carries worse prognosis. J Cardiovasc Magn Reson. 2017;19(1):98.\nBrunjes DL, Castano A, Clemons A, Rubin J, Maurer MS. Transthyretin cardiac amyloidosis in older Americans. J Card Fail. 2016;22(12):996–1003.\nRapezzi C, Lorenzini M, Longhi S, Milandri A, Gagliardi C, Bartolomei I, et al. Cardiac amyloidosis: the great pretender. Heart Fail Rev. 2015;20(2):117–24.\nLane T, Fontana M, Martinez-Naharro A, Quarta CC, Whelan CJ, Petrie A, et al. Natural history, quality of life, and outcome in cardiac transthyretin amyloidosis. Circulation. 2019;140(1):16–26.\nBishop E, Brown EE, Fajardo J, Barouch LA, Judge DP, Halushka MK. Seven factors predict a delayed diagnosis of cardiac amyloidosis. Amyloid. 2018;25(3):174–9.\nGonzalez-Lopez E, Gagliardi C, Dominguez F, Quarta CC, de Haro-Del Moral FJ, Milandri A, et al. Clinical characteristics of wild-type transthyretin cardiac amyloidosis: disproving myths. Eur Heart J. 2017;38(24):1895–904.\nTreglia G, Glaudemans A, Bertagna F, Hazenberg BPC, Erba PA, Giubbini R, et al. Diagnostic accuracy of bone scintigraphy in the assessment of cardiac transthyretin-related amyloidosis: a bivariate meta-analysis. Eur J Nucl Med Mol Imaging. 2018;45(11):1945–55.\nPonikowski P, Voors AA, Anker SD, Bueno H, Cleland JGF, Coats AJS, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur Heart J. 2016;37(27):2129–200.\nSeferovic PM, Ponikowski P, Anker SD, Bauersachs J, Chioncel O, Cleland JGF, et al. Clinical practice update on heart failure 2019: pharmacotherapy, procedures, devices and patient management. An expert consensus meeting report of The Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2019;21:1169–86.\nGillmore JD, Maurer MS, Falk RH, Merlini G, Damy T, Dispenzieri A, et al. Nonbiopsy diagnosis of cardiac transthyretin amyloidosis. Circulation. 2016;133(24):2404–12.\nDorbala S, Ando Y, Bokhari S, Dispenzieri A, Falk RH, Ferrari VA, et al. ASNC\u002FAHA\u002FASE\u002FEANM\u002FHFSA\u002FISA\u002FSCMR\u002FSNMMI expert consensus recommendations for multimodality imaging in cardiac amyloidosis: Part 2 of 2-Diagnostic criteria and appropriate utilization. J Nucl Cardiol. 2019;. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs12350-019-01761-5.\nKyriakou P, Mouselimis D, Tsarouchas A, Rigopoulos A, Bakogiannis C, Noutsias M, et al. Diagnosis of cardiac amyloidosis: a systematic review on the role of imaging and biomarkers. BMC Cardiovasc Disord. 2018;18(1):221.\nDamy T, Kristen AV, Suhr OB, Maurer MS, Plante-Bordeneuve V, Yu CR, et al. Transthyretin cardiac amyloidosis in continental Western Europe: an insight through the Transthyretin Amyloidosis Outcomes Survey (THAOS). Eur Heart J. 2019;. https:\u002F\u002Fdoi.org\u002F10.1093\u002Feurheartj\u002Fehz173.\nCzobor P, Hung YY, Baer D, McGlothlin D, Weisshaar D, Zaroff J. Amyloid cardiomyopathy in a large integrated health care system. Am Heart J. 2019;216:42–52.\nAus Dem Seipen F, Hein S, Prestel S, Baumgartner C, Schonland S, Hegenbart U, et al. Carpal tunnel syndrome and spinal canal stenosis: harbingers of transthyretin amyloid cardiomyopathy? Clin Res Cardiol. 2019;108:1324–30.\nFosbol EL, Rorth R, Leicht BP, Schou M, Maurer MS, Kristensen SL, et al. Association of carpal tunnel syndrome with amyloidosis, heart failure, and adverse cardiovascular outcomes. J Am Coll Cardiol. 2019;74(1):15–23.\nWitteles RM, Bokhari S, Damy T, Elliott PM, Falk RH, Fine NM, et al. Screening for transthyretin amyloid cardiomyopathy in everyday practice. JACC Heart Fail. 2019;7(8):709–16.",{"VOID":1376},"10.1007\u002Fs40119-019-00160-8","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs40119-019-00160-8",[1379],{"id":1380,"sortIndex":32,"researcher":28,"roles":1381,"affiliations":1382,"properties":1391,"displayName":1393,"givenName":28,"familyName":28},"31812808-4cbd-42ac-8527-db31818e1daf",[958],[1383],{"id":1384,"sortIndex":32,"affiliation":1385,"properties":28},"d4e89d14-ca48-4a40-8709-98f2cc839eb7",{"id":1384,"createTime":28,"updateTime":28,"relativeEntities":1386,"slug":28,"properties":1387,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1390,"statistic":28},[],{"title":1388},{"VI":1389},"Pfizer AG, Zurich, Switzerland",[],{"title":1392},{"VI":1393},"Dennis Mircsof",{"url":1377,"publisher":1395,"properties":1437},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1396,"slug":872,"properties":1397,"entityType":25,"verifyStatus":880,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1401,"manageAffiliations":1406,"indexDatabases":1417,"url":926,"thumbnailPath":28,"statistic":1432,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1398,"title":1399,"eissn":1400},{"VOID":875},{"EN":877},{"VOID":879},[1402],{"id":883,"createTime":28,"updateTime":28,"relativeEntities":1403,"label":1404,"description":1405,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":886},{},[1407,1412],{"id":890,"createTime":28,"updateTime":28,"relativeEntities":1408,"slug":28,"properties":1409,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1411,"statistic":28},[],{"title":1410},{"EN":894},[896],{"id":898,"createTime":28,"updateTime":28,"relativeEntities":1413,"slug":28,"properties":1414,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1416,"statistic":28},[],{"title":1415},{"EN":902},[],[1418,1425],{"id":906,"indexDatabase":1419,"url":912,"indexYears":28,"academicFieldIds":1424,"indexDatabaseRanking":28},{"id":803,"createTime":28,"updateTime":28,"relativeEntities":1420,"label":1421,"description":1422,"key":810,"publicationTags":1423,"standard":28},[],{"EN":806,"VI":806},{"EN":808,"VI":809},[812,813],[914],{"id":916,"indexDatabase":1426,"url":922,"indexYears":923,"academicFieldIds":1431,"indexDatabaseRanking":788},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1427,"label":1428,"description":1429,"key":781,"publicationTags":1430,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[925],{"impactFactor":32,"impactFactorByYear":1433,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":42,"totalPublicationByYear":1434,"totalCitation":32,"totalCitationByYear":1435,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":1436,"hindexLast5Year":32,"hindex":32},{},{"2019":40,"2020":123},{},{},{"pages":1438,"volume":1440},{"VOID":1439},"127-138",{"VOID":1441},"9","2020-01-20",2020,[812,783],{"id":1446,"createTime":1447,"updateTime":1447,"relativeEntities":1448,"slug":1449,"properties":1450,"entityType":951,"verifyStatus":880,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1460,"fullTextUrl":28,"authors":1461,"publicationType":1152,"publisherRelationship":1477,"citationCount":28,"citationInfo":28,"publishDate":1520,"publishYear":1521,"citationAnalyzeStatus":880,"lastCitationAnalyze":28,"indexDatabases":1522,"openAccess":28,"references":28,"isForceReanalyzing":1204},"070d53e0-eca9-4443-b5c0-40157ce99898","2024-04-06T13:27:54.198+00:00",[],"Effect-of-Thermal-Therapy-Using-Hot-Water-Bottles-on-Brain-Natriuretic-Peptide-in-Chronic-Hemodialysis-Patients",{"abstract":1451,"title":1453,"keywords":1455,"references":1456,"doi":1458},{"EN":1452},"The use of repeated thermal therapy for improving the symptoms of chronic heart failure (CHF) has been recently demonstrated. Usually, thermal therapy requires an infrared dry sauna. However, it is difficult for small clinics to acquire such an expensive and extensive system. The present study assessed the efficacy of its substitution with hot water bottles. Moreover, there are no prior studies demonstrating the efficacy of thermal therapy in hemodialysis patients with CHF. Plasma brain natriuretic peptide (BNP) levels were evaluated in 98 hemodialysis patients in a clinic. Nine patients whose BNP levels were >500 pg\u002FmL agreed to be enrolled in the study and received thermal therapy using hot water bottles. Plasma BNP levels, a potential marker for CHF, tended to decrease (891 ± 448 to 680 ± 339 pg\u002FmL), but the difference was not significant (P = 0.0845). The oral temperature changed from 36.44 ± 0.45°C to 37.04 ± 0.48°C (+0.597°C, P \u003C 0.0001). No side effects were experienced during the therapy. Moreover, most patients had an improvement in their symptoms and the ability to perform activities of daily living. Thermal therapy using hot water bottles is very safe and tends to reduce plasma BNP levels in hemodialysis patients with CHF.",{"EN":1454},"Effect of Thermal Therapy Using Hot Water Bottles on Brain Natriuretic Peptide in Chronic Hemodialysis Patients",{"EN":1217},{"VOID":1457},"Parfery PS, Foley RN. The clinical epidemiology of cardiac disease in chronic heart failure. J Am Soc Nephrol. 1999;10:1606–15.\nHamett JD, Foley RN, Kent GM, et al. Congestive heart failure in dialysis patients: prevalence, incidence, prognosis and risk factors. Kidney Int. 1995;47:884–90.\nRonco C, Happio M, House AA, et al. Cardio-renal syndrome. J Am Coll Cardiol. 2008;52:1527–39.\nKihara T, Miyata M, Fukudome T, et al. Waon therapy improves the prognosis of patients with chronic heart failure. J Cardiol. 2009;53:214–8.\nMiyata M, Kihara T, Kubozono T, et al. Beneficial effects of Waon therapy on patients with chronic heart failure: results of a prospective multicenter study. J Cardiol. 2008;52:79–85.\nKihara T, Biro S, Ikeda Y, et al. Effects of repeated sauna treatment on ventricular arrhythmia inpatients with chronic heart failure. Circ J. 2004;68:1146–51.\nWilkins MR, Redondo J, Brown LA. The natriuretic-peptide family. Lancet. 1997;349:1307–10.\nHunt SA, Baker DW, Chin MH, et al.; American College of Cardiology\u002FAmerican Heart Association. ACC\u002FAHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary. A report of the American College of Cardiology\u002FAmerican Heart Association Task Force on Practice Guidelines (Committee to revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol. 2001;38:2101–13.\nTei C, Prihara K, Fukudome T. Remarkable efficacy of thermal therapy for Sjogren syndrome. J Cardiol. 2007;49:217–9.\nBiro S, Masuda A, Kihara T, et al. Clinical implications of thermal therapy in lifestyle-related diseases. Exp Biol Med. 2003;228:1245–9.\nMadarame H, Kawashima A. Use of hot water bottles can improve lymphocytopenia. Biomed Res. 2006;27:45–8.\nToyabe S, IIai T, Fukuda M, et al. Identification of nicotinic acetylcholine receptors on lymphocytes in the periphery as well as thymus in mice. Immunology. 1997;92:201–5.\nWatanabe M, Tomiyama-Miyaji C, Kainuma E, et al. Role of alpha-adrenergic stimulus in stress-induced modulation of body temperature, blood glucose and innate immunity. Immunol Lett. 2008;15:43–9.\nNishikimi T, Futoo Y, Tamano K, et al. Plasma brain natriuretic peptide levels in chronic hemodialysis patients: influence of coronary artery disease. Am J Kidney Dis. 2001;37:1201–8.\nAustin WJ, Bhalla V, Hernandez-Arce I, et al. Correlation and prognostic utility of B-type natriuretic peptide and its amino-terminal fragment in patients with chronic kidney disease. Am J Clin Pathol. 2006;126:506–12.\nMcCullough PA, Duc P, Omland T, Breathing Not Properly Multinational Study Investigators, et al. B-type natriuretic peptide and renal function in the diagnosis of heart failure: an analysis from the Breathing Not Properly Multinational Study. Am J Kidney Dis. 2003;41:571–9.\nNaganuma T, Sugimura K, Wada S, et al. The prognostic role of brain natriuretic peptides in hemodialysis patients. Am J Nephrol. 2002;22:437–44.\nPark S, Cho GY, Kim SG, et al. Brain natriuretic peptide levels have diagnostic and prognostic capability for cardio-renal syndrome type 4 in intensive care unit patients. Crit Care. 2009;13:R70.\nAkiba T, Tachibana K, Togashi M, et al. Plasma human brain natriuretic peptide in chronic renal disease. Clin Nephrol. 1995;44:S61–4.\nZoccali C, Mallamaci F, Benedetto FA, et al. Cardiac natriuretic peptides are related to left ventricular mass and function and predict mortality in dialysis patients. J Am Soc Nephrol. 2001;12:1508–15.\nTakami Y, Horio T, Iwashima Y, et al. Diagnostic and prognostic value of plasma brain natriuretic peptide in non-dialysis-dependent CRF. Am J Kidney Dis. 2004;44:420–8.\nGoto T, Takase H, Toriyama T, et al. Increased circulating levels of natriuretic peptides predict future cardiac event in patients with chronic hemodialysis. Nephron. 2002;92:610–5.\nGardin JM, Leifer ES, Fleg JL, HF-ACTION Investigators, et al. Relationship of Doppler-echocardiographic left ventricular diastolic function to exercise performance in systolic heart failure: the HF-ACTION study. Am Heart J. 2009;158:S45–52.\nde Filippi CR, Fink JC, Nass CM, et al. N-terminal pro-B-type natriuretic peptide for predicting coronary disease and left ventricular hypertrophy in asymptomatic CKD not requiring dialysis. Am J Kid Dis. 2005;46:35–44.\nMark PB, Stewart GA, Gansevoort RT, et al. Diagnostic potential of circulating natriuretic peptides in chronic kidney disease. Nephrol Dial Transplant. 2006;21:402–10.",{"VOID":1459},"10.1007\u002Fs40119-012-0002-z","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs40119-012-0002-z",[1462],{"id":1463,"sortIndex":32,"researcher":28,"roles":1464,"affiliations":1465,"properties":1474,"displayName":1476,"givenName":28,"familyName":28},"c25b5474-ac1f-481a-b61e-d66ade32540b",[958],[1466],{"id":1467,"sortIndex":32,"affiliation":1468,"properties":28},"c8389e66-f49d-496a-a286-2af3d32700a7",{"id":1467,"createTime":28,"updateTime":28,"relativeEntities":1469,"slug":28,"properties":1470,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1473,"statistic":28},[],{"title":1471},{"VI":1472},"Yoko Clinic, Kitakyushu, Japan",[],{"title":1475},{"VI":1476},"Yoko Uchiyama-Tanaka",{"url":28,"publisher":1478,"properties":28},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1479,"slug":872,"properties":1480,"entityType":25,"verifyStatus":880,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1484,"manageAffiliations":1489,"indexDatabases":1500,"url":926,"thumbnailPath":28,"statistic":1515,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1481,"title":1482,"eissn":1483},{"VOID":875},{"EN":877},{"VOID":879},[1485],{"id":883,"createTime":28,"updateTime":28,"relativeEntities":1486,"label":1487,"description":1488,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":886},{},[1490,1495],{"id":890,"createTime":28,"updateTime":28,"relativeEntities":1491,"slug":28,"properties":1492,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1494,"statistic":28},[],{"title":1493},{"EN":894},[896],{"id":898,"createTime":28,"updateTime":28,"relativeEntities":1496,"slug":28,"properties":1497,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1499,"statistic":28},[],{"title":1498},{"EN":902},[],[1501,1508],{"id":906,"indexDatabase":1502,"url":912,"indexYears":28,"academicFieldIds":1507,"indexDatabaseRanking":28},{"id":803,"createTime":28,"updateTime":28,"relativeEntities":1503,"label":1504,"description":1505,"key":810,"publicationTags":1506,"standard":28},[],{"EN":806,"VI":806},{"EN":808,"VI":809},[812,813],[914],{"id":916,"indexDatabase":1509,"url":922,"indexYears":923,"academicFieldIds":1514,"indexDatabaseRanking":788},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1510,"label":1511,"description":1512,"key":781,"publicationTags":1513,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[925],{"impactFactor":32,"impactFactorByYear":1516,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":42,"totalPublicationByYear":1517,"totalCitation":32,"totalCitationByYear":1518,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":1519,"hindexLast5Year":32,"hindex":32},{},{"2019":40,"2020":123},{},{},"2012-08-01",2012,[812,783],{"id":1524,"createTime":1525,"updateTime":1526,"relativeEntities":1527,"slug":1528,"properties":1529,"entityType":951,"verifyStatus":26,"verifyTime":1526,"verifyNote":952,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1539,"fullTextUrl":28,"authors":1540,"publicationType":1152,"publisherRelationship":1584,"citationCount":28,"citationInfo":28,"publishDate":1627,"publishYear":1202,"citationAnalyzeStatus":880,"lastCitationAnalyze":28,"indexDatabases":1628,"openAccess":28,"references":28,"isForceReanalyzing":1204},"080a18da-bcb0-40b3-9b88-f4c3830dbd31","2024-04-08T02:29:26.931+00:00","2025-01-14T21:45:33.575+00:00",[],"The-Rise-and-Fall-of-Anticoagulation-with-Bivalirudin-During-Percutaneous-Coronary-Interventions-A-Review-Article",{"abstract":1530,"title":1532,"keywords":1534,"references":1535,"doi":1537},{"EN":1531},"Bivalirudin is a direct thrombin inhibitor used during percutaneous coronary intervention (PCI). Treatment with bivalirudin compared to heparin plus glycoprotein IIb\u002FIIIa inhibitors (GPI) reduced bleeding complications, but resulted in higher rates of ischemic events, including acute stent thrombosis in ST segment elevation myocardial infarction (STEMI) patients. Thus, it may be considered a reasonable alternative antithrombotic agent in patients at high risk of bleeding undergoing PCI. However its superiority over heparin alone is questioned particularly in the era of novel antiplatelet agents and transradial PCI.",{"EN":1533},"The Rise and Fall of Anticoagulation with Bivalirudin During Percutaneous Coronary Interventions: A Review Article",{"EN":1217},{"VOID":1536},"Libby P. Mechanisms of acute coronary syndromes and their implications for therapy. N Engl J Med. 2013;368(21):2004–13.\nStone GW, McLaurin BT, Cox DA, et al. Bivalirudin for patients with acute coronary syndromes. N Engl J Med. 2006;355(21):2203–16.\nStone GW, Witzenbichler B, Guagliumi G, et al. Bivalirudin during primary PCI in acute myocardial infarction. N Engl J Med. 2008;358(21):2218–30.\nWarkentin TE, Greinacher A, Koster A. Bivalirudin. Thromb Haemost. 2008;99(5):830–9.\nDi Nisio M, Middeldorp S, Buller HR. Direct thrombin inhibitors. N Engl J Med. 2005;353(10):1028–40.\nKastrati A, Mehilli J, Schuhlen H, et al. A clinical trial of abciximab in elective percutaneous coronary intervention after pretreatment with clopidogrel. N Engl J Med. 2004;350(3):232–8.\nBittl JA, Strony J, Brinker JA, et al. Treatment with bivalirudin (Hirulog) as compared with heparin during coronary angioplasty for unstable or postinfarction angina. Hirulog Angioplasty Study Investigators. N Engl J Med. 1995;333(12):764–9.\nLincoff AM, Kleiman NS, Kottke-Marchant K, et al. Bivalirudin with planned or provisional abciximab versus low-dose heparin and abciximab during percutaneous coronary revascularization: results of the Comparison of Abciximab Complications with Hirulog for Ischemic Events Trial (CACHET). Am Heart J. 2002;143(5):847–53.\nLincoff AM, Bittl JA, Kleiman NS, et al. Comparison of bivalirudin versus heparin during percutaneous coronary intervention (the Randomized Evaluation of PCI Linking Angiomax to Reduced Clinical Events [REPLACE]-1 trial). Am J Cardiol. 2004;93(9):1092–6.\nLincoff AM, Bittl JA, Harrington RA, et al. Bivalirudin and provisional glycoprotein IIb\u002FIIIa blockade compared with heparin and planned glycoprotein IIb\u002FIIIa blockade during percutaneous coronary intervention: REPLACE-2 randomized trial. JAMA. 2003;289(7):853–63.\nLincoff AM, Kleiman NS, Kereiakes DJ, et al. Long-term efficacy of bivalirudin and provisional glycoprotein IIb\u002FIIIa blockade vs heparin and planned glycoprotein IIb\u002FIIIa blockade during percutaneous coronary revascularization: REPLACE-2 randomized trial. JAMA. 2004;292(6):696–703.\nKastrati A, Neumann FJ, Mehilli J, et al. Bivalirudin versus unfractionated heparin during percutaneous coronary intervention. N Engl J Med. 2008;359(7):688–96.\nSchulz S, Mehilli J, Ndrepepa G, et al. Bivalirudin vs. unfractionated heparin during percutaneous coronary interventions in patients with stable and unstable angina pectoris: 1-year results of the ISAR-REACT 3 trial. Eur Heart J. 2010;31(5):582–7.\nParodi G, Migliorini A, Valenti R, et al. Comparison of bivalirudin and unfractionated heparin plus protamine in patients with coronary heart disease undergoing percutaneous coronary intervention (from the Antithrombotic Regimens aNd Outcome [ARNO] trial). Am J Cardiol. 2010;105(8):1053–9.\nBriguori C, Visconti G, Focaccio A, et al. Novel approaches for preventing or limiting events (Naples) III trial: randomized comparison of bivalirudin versus unfractionated heparin in patients at increased risk of bleeding undergoing transfemoral elective coronary stenting. JACC Cardiovasc Interv. 2015;8(3):414–23.\nKolh P, Windecker S, Alfonso F, et al. 2014 ESC\u002FEACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur Heart J. 2014;35(37):2541–2619.\nGibson CM, Morrow DA, Murphy SA, et al. A randomized trial to evaluate the relative protection against post-percutaneous coronary intervention microvascular dysfunction, ischemia, and inflammation among antiplatelet and antithrombotic agents: the PROTECT-TIMI-30 trial. J Am Coll Cardiol. 2006;47(12):2364–73.\nRoffi M, Patrono C, Collet JP, et al. 2015 ESC guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). Eur Heart J. 2016;37(3):267–315.\nHamm CW, Bassand JP, Agewall S, et al. ESC guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. The Task Force for the management of acute coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC). G Ital Cardiol (Rome). 2012;13(3):171–228.\nKastrati A, Neumann FJ, Schulz S, et al. Abciximab and heparin versus bivalirudin for non-ST-elevation myocardial infarction. N Engl J Med. 2011;365(21):1980–9.\nSchulz S, Kastrati A, Ferenc M, et al. One-year outcomes with abciximab and unfractionated heparin versus bivalirudin during percutaneous coronary interventions in patients with non-ST-segment elevation myocardial infarction: updated results from the ISAR-REACT 4 trial. EuroIntervention. 2013;9(4):430–6.\nWaksman R, Bertrand O, Driesman M, et al. Bivalirudin versus unfractionated heparin during percutaneous coronary intervention in patients with non-ST-segment elevation acute coronary syndrome initially treated with fondaparinux: results from an international, multicenter, randomized pilot study (SWITCH III). J Interv Cardiol. 2013;26(2):107–13.\nHamon M, Rao SV, Steg G, et al. Bivalirudin versus unfractionated heparin in percutaneous coronary interventions of patients having received initial fondaparinux treatment: a propensity matched study. EuroIntervention. 2012;8(4):486–92.\nAngeras O, Koul S, Albertsson P, et al. 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Bivalirudin versus heparin monotherapy and glycoprotein IIb\u002FIIIa plus heparin for patients with AMI undergoing coronary stenting (BRIGHT). China Interventional Therapeutics (CIT 2014). Shanghai, China, March 21, 2014.\nLeonardi S, Frigoli E, Rothenbuhler M, et al. Bivalirudin or unfractionated heparin in patients with acute coronary syndromes managed invasively with and without ST elevation (MATRIX): randomised controlled trial. BMJ. 2016;354:i4935.\nCavender MA, Sabatine MS. Bivalirudin versus heparin in patients planned for percutaneous coronary intervention: a meta-analysis of randomised controlled trials. Lancet. 2014;384(9943):599–606.\nBangalore S, Toklu B, Kotwal A, et al. Anticoagulant therapy during primary percutaneous coronary intervention for acute myocardial infarction: a meta-analysis of randomized trials in the era of stents and P2Y12 inhibitors. BMJ. 2014;349:g6419.\nCapodanno D, De Caterina R. Bivalirudin for acute coronary syndromes: premises, promises and doubts. Thromb Haemost. 2015;113(4):698–707.\nNavarese EP, Schulze V, Andreotti F, et al. Comprehensive meta-analysis of safety and efficacy of bivalirudin versus heparin with or without routine glycoprotein IIb\u002FIIIa inhibitors in patients with acute coronary syndrome. JACC Cardiovasc Interv 8(1 Pt B):201–13.\nStone GW, Mehran R, Goldstein P, et al. Bivalirudin versus heparin with or without glycoprotein IIb\u002FIIIa inhibitors in patients with STEMI undergoing primary percutaneous coronary intervention: pooled patient-level analysis from the HORIZONS-AMI and EUROMAX trials. J Am Coll Cardiol. 2015;65(1):27–38.\nFahrni G, Wolfrum M, De Maria GL, Banning AP, Benedetto U, Kharbanda RK. Prolonged high-dose bivalirudin infusion reduces major bleeding without increasing stent thrombosis in patients undergoing primary percutaneous coronary intervention: novel insights from an updated meta-analysis. 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Am Heart J. 2016;175:36–46.",{"VOID":1538},"10.1007\u002Fs40119-017-0082-x","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs40119-017-0082-x",[1541,1556,1571],{"id":1542,"sortIndex":32,"researcher":28,"roles":1543,"affiliations":1544,"properties":1553,"displayName":1555,"givenName":28,"familyName":28},"f0934f57-4d19-4d85-a154-773f64694592",[958],[1545],{"id":1546,"sortIndex":32,"affiliation":1547,"properties":28},"eca673b5-89cf-47f1-b460-ea88a40f3a65",{"id":1546,"createTime":28,"updateTime":28,"relativeEntities":1548,"slug":28,"properties":1549,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1552,"statistic":28},[],{"title":1550},{"VI":1551},"Cardiology Department, Leiden University Medical Center, Leiden, The Netherlands",[],{"title":1554},{"VI":1555},"Constantinos Andreou",{"id":1557,"sortIndex":40,"researcher":28,"roles":1558,"affiliations":1559,"properties":1568,"displayName":1570,"givenName":28,"familyName":28},"a16613e3-04e4-4913-ad3b-de333d20dbb0",[958],[1560],{"id":1561,"sortIndex":32,"affiliation":1562,"properties":28},"b89ef1ea-05b0-4a49-9d1c-e86f4bef4fef",{"id":1561,"createTime":28,"updateTime":28,"relativeEntities":1563,"slug":28,"properties":1564,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1567,"statistic":28},[],{"title":1565},{"VI":1566},"2nd Cardiology Department, Hellenic Red Cross General Hospital, Athens, Greece",[],{"title":1569},{"VI":1570},"Christos Maniotis",{"id":1572,"sortIndex":123,"researcher":28,"roles":1573,"affiliations":1574,"properties":1581,"displayName":1583,"givenName":28,"familyName":28},"39b4f568-bae4-45e6-896e-252522742ad5",[958],[1575],{"id":1561,"sortIndex":32,"affiliation":1576,"properties":28},{"id":1561,"createTime":28,"updateTime":28,"relativeEntities":1577,"slug":28,"properties":1578,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1580,"statistic":28},[],{"title":1579},{"VI":1566},[],{"title":1582},{"VI":1583},"Michael Koutouzis",{"url":28,"publisher":1585,"properties":28},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1586,"slug":872,"properties":1587,"entityType":25,"verifyStatus":880,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1591,"manageAffiliations":1596,"indexDatabases":1607,"url":926,"thumbnailPath":28,"statistic":1622,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1588,"title":1589,"eissn":1590},{"VOID":875},{"EN":877},{"VOID":879},[1592],{"id":883,"createTime":28,"updateTime":28,"relativeEntities":1593,"label":1594,"description":1595,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":886},{},[1597,1602],{"id":890,"createTime":28,"updateTime":28,"relativeEntities":1598,"slug":28,"properties":1599,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1601,"statistic":28},[],{"title":1600},{"EN":894},[896],{"id":898,"createTime":28,"updateTime":28,"relativeEntities":1603,"slug":28,"properties":1604,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1606,"statistic":28},[],{"title":1605},{"EN":902},[],[1608,1615],{"id":906,"indexDatabase":1609,"url":912,"indexYears":28,"academicFieldIds":1614,"indexDatabaseRanking":28},{"id":803,"createTime":28,"updateTime":28,"relativeEntities":1610,"label":1611,"description":1612,"key":810,"publicationTags":1613,"standard":28},[],{"EN":806,"VI":806},{"EN":808,"VI":809},[812,813],[914],{"id":916,"indexDatabase":1616,"url":922,"indexYears":923,"academicFieldIds":1621,"indexDatabaseRanking":788},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1617,"label":1618,"description":1619,"key":781,"publicationTags":1620,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[925],{"impactFactor":32,"impactFactorByYear":1623,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":42,"totalPublicationByYear":1624,"totalCitation":32,"totalCitationByYear":1625,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":1626,"hindexLast5Year":32,"hindex":32},{},{"2019":40,"2020":123},{},{},"2017-01-19",[812,783],{"id":1630,"createTime":1631,"updateTime":1632,"relativeEntities":1633,"slug":1634,"properties":1635,"entityType":951,"verifyStatus":26,"verifyTime":1632,"verifyNote":952,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1644,"fullTextUrl":28,"authors":1645,"publicationType":1152,"publisherRelationship":1674,"citationCount":28,"citationInfo":28,"publishDate":1721,"publishYear":1443,"citationAnalyzeStatus":880,"lastCitationAnalyze":28,"indexDatabases":1722,"openAccess":28,"references":28,"isForceReanalyzing":1204},"08bcc432-6614-433e-a422-31b27aade137","2024-02-13T22:22:43.537+00:00","2025-01-29T08:30:34.606+00:00",[],"Lipoprotein-a-and-Cardiovascular-Disease-Prevention-across-Diverse-Populations",{"abstract":1636,"title":1638,"references":1640,"doi":1642},{"EN":1637},"Lipoprotein(a) (Lp(a)) is a highly proatherogenic lipid fraction that is genetically determined and minimally responsive to lifestyle or behavior changes. 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Accessed 8 Apr 2020.\nSchettler VJJ, Ringel J, Jacob S, Julius U, Klingel R, Heigl F, et al. Current insights into the German lipoprotein apheresis standard: PCSK9-inhibitors, lipoprotein apheresis or both? Atheroscler Suppl. 2017;1(30):44–9.\nThe HPS2-THRIVE Collaborative Group. Effects of extended-release niacin with laropiprant in high-risk patients. N Engl J Med. 2014;371(3):203–12.\nParish S, Hopewell JC, Hill MR, Marcovina S, Valdes-Marquez E, Haynes R, et al. Impact of apolipoprotein(a) isoform size on lipoprotein(a) lowering in the HPS2-THRIVE study. Circ Genom Precis Med. 2018;11(2):e001696.\nAIM-HIGH Investigators, Boden WE, Probstfield JL, Anderson T, Chaitman BR, Desvignes-Nickens P, et al. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med. 2011;365(24):2255–67.\nAnderson TJ, Boden WE, Desvigne-Nickens P, Fleg JL, Kashyap ML, McBride R, et al. Safety profile of extended-release niacin in the AIM-HIGH trial. N Engl J Med. 2014;371(3):288–90.\nBittner VA, Szarek M, Aylward PE, Bhatt DL, Diaz R, Edelberg JM, et al. Effect of Alirocumab on lipoprotein(a) and cardiovascular risk after acute coronary syndrome. J Am Coll Cardiol. 2020;75(2):133–44.\nO’Donoghue ML, Fazio S, Giugliano RP, Stroes ESG, Kanevsky E, Gouni-Berthold I, et al. Lipoprotein(a), PCSK9 inhibition, and cardiovascular risk: insights from the FOURIER trial. Circulation. 2019;139(12):1483–92.\nSantos RD, Raal FJ, Catapano AL, Witztum JL, Steinhagen-Thiessen E, Tsimikas S. Mipomersen, an antisense oligonucleotide to apolipoprotein B-100, reduces lipoprotein(a) in various populations with hypercholesterolemia. Arterioscler Thromb Vasc Biol. 2015;35(3):689–99.\nAntisense therapy targeting apolipoprotein(a): a randomised, double-blind, placebo-controlled phase 1 study| Elsevier Enhanced Reader [Internet]. [cited 2020 Mar 22]. https:\u002F\u002Freader.elsevier.com\u002Freader\u002Fsd\u002Fpii\u002FS0140673615612521?token=7F42DDEE825CFFF47784525B56C8D3D15F019936124FA0A2E1055BC650E91D805A71583F82498D3635D72B0F98860AB5. Accessed 20 Mar 2020.",{"VOID":1643},"10.1007\u002Fs40119-020-00177-4","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs40119-020-00177-4",[1646,1661],{"id":1647,"sortIndex":32,"researcher":28,"roles":1648,"affiliations":1649,"properties":1658,"displayName":1660,"givenName":28,"familyName":28},"5fcdbf19-f9b0-4ec9-afd1-0d9f989293b5",[958],[1650],{"id":1651,"sortIndex":32,"affiliation":1652,"properties":28},"8610cf6d-f1ee-4180-a631-74e91b9cf443",{"id":1651,"createTime":28,"updateTime":28,"relativeEntities":1653,"slug":28,"properties":1654,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1657,"statistic":28},[],{"title":1655},{"VI":1656},"Division of Cardiovascular Medicine and the Cardiovascular Institute, Stanford University, Stanford, USA",[],{"title":1659},{"VI":1660},"Keon Pearson",{"id":1662,"sortIndex":40,"researcher":28,"roles":1663,"affiliations":1664,"properties":1671,"displayName":1673,"givenName":28,"familyName":28},"6293b52a-5524-4916-bb57-fb2188e0e9da",[958],[1665],{"id":1651,"sortIndex":32,"affiliation":1666,"properties":28},{"id":1651,"createTime":28,"updateTime":28,"relativeEntities":1667,"slug":28,"properties":1668,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1670,"statistic":28},[],{"title":1669},{"VI":1656},[],{"title":1672},{"VI":1673},"Fatima Rodriguez",{"url":1644,"publisher":1675,"properties":1717},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1676,"slug":872,"properties":1677,"entityType":25,"verifyStatus":880,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1681,"manageAffiliations":1686,"indexDatabases":1697,"url":926,"thumbnailPath":28,"statistic":1712,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1678,"title":1679,"eissn":1680},{"VOID":875},{"EN":877},{"VOID":879},[1682],{"id":883,"createTime":28,"updateTime":28,"relativeEntities":1683,"label":1684,"description":1685,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":886},{},[1687,1692],{"id":890,"createTime":28,"updateTime":28,"relativeEntities":1688,"slug":28,"properties":1689,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1691,"statistic":28},[],{"title":1690},{"EN":894},[896],{"id":898,"createTime":28,"updateTime":28,"relativeEntities":1693,"slug":28,"properties":1694,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1696,"statistic":28},[],{"title":1695},{"EN":902},[],[1698,1705],{"id":906,"indexDatabase":1699,"url":912,"indexYears":28,"academicFieldIds":1704,"indexDatabaseRanking":28},{"id":803,"createTime":28,"updateTime":28,"relativeEntities":1700,"label":1701,"description":1702,"key":810,"publicationTags":1703,"standard":28},[],{"EN":806,"VI":806},{"EN":808,"VI":809},[812,813],[914],{"id":916,"indexDatabase":1706,"url":922,"indexYears":923,"academicFieldIds":1711,"indexDatabaseRanking":788},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1707,"label":1708,"description":1709,"key":781,"publicationTags":1710,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[925],{"impactFactor":32,"impactFactorByYear":1713,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":42,"totalPublicationByYear":1714,"totalCitation":32,"totalCitationByYear":1715,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":1716,"hindexLast5Year":32,"hindex":32},{},{"2019":40,"2020":123},{},{},{"pages":1718,"volume":1720},{"VOID":1719},"275-292",{"VOID":1441},"2020-05-25",[812,783],{"id":1724,"createTime":1725,"updateTime":1726,"relativeEntities":1727,"slug":1728,"properties":1729,"entityType":951,"verifyStatus":26,"verifyTime":1726,"verifyNote":952,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1738,"fullTextUrl":28,"authors":1739,"publicationType":1152,"publisherRelationship":1798,"citationCount":28,"citationInfo":28,"publishDate":1846,"publishYear":1847,"citationAnalyzeStatus":880,"lastCitationAnalyze":28,"indexDatabases":1848,"openAccess":28,"references":28,"isForceReanalyzing":1204},"09242c2d-2a81-4afc-b358-f127a6d00f66","2023-12-07T13:33:02.275+00:00","2025-02-23T19:42:25.785+00:00",[],"Drug-Coated-Balloon-Only-Percutaneous-Coronary-Intervention-for-the-Treatment-of-De-Novo-Coronary-Artery-Disease-A-Systematic-Review",{"abstract":1730,"title":1732,"references":1734,"doi":1736},{"EN":1731},"Percutaneous coronary intervention (PCI) with a drug coated balloon (DCB) is a novel treatment which seeks to acutely dilate a coronary stenosis and deliver an anti-proliferative drug to the vessel wall (reducing the risk of re-stenosis), without implanting a drug eluting stent (DES). In this study, we performed a systematic review of stentless DCB-only angioplasty in de novo coronary artery disease. We identified 41 studies examining the effects of DCB-only PCI in a variety of clinical scenarios including small vessels, bifurcations, calcified lesions, and primary PCI. DCB-only PCI appears to be associated with comparable clinical outcomes to DESs and superior angiographic outcomes to plain-old balloon angioplasty. Although current data are promising, there is still a need for further long-term randomized control trial data comparing a DCB-only approach specifically against a second- or third-generation DES. A 4-week period of dual antiplatelet therapy provides a real advantage for the DCB-only PCI approach, which is not possible with most DESs. Since rates of adverse clinical outcomes are very low for all PCI procedures attention should be turned to the development of robust endpoints with which to compare DCB-only PCI approaches to the standard treatment with a DES.",{"EN":1733},"Drug-Coated Balloon-Only Percutaneous Coronary Intervention for the Treatment of De Novo Coronary Artery Disease: A Systematic Review",{"VOID":1735},"Benjamin EJ, Blaha MJ, Chiuve SE, Cushman M, Das SR, Deo R, et al. Heart disease and stroke statistics-2017. Circulation. 2017;135(10):e146–603.\nNakatani M, Takeyama Y, Shibata M, Yorozuya M, Suzuki H, Koba S, et al. Mechanisms of restenosis after coronary intervention: difference between plain old balloon angioplasty and stenting. Cardiovasc Pathol. 2003;12(1):40–8.\nVenkitachalam L, Kip KE, Selzer F, Wilensky RL, Slater J, Mulukutla SR, et al. 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A multicenter randomized comparison of paclitaxel-coated balloon with plain balloon angioplasty in patients with small vessel disease. Clin Res Cardiol. 2017;106:824–32.\nHer A-Y, Ann SH, Singh GB, Kim YH, Yoo S-Y, Garg S, et al. Comparison of paclitaxel-coated balloon treatment and plain old balloon angioplasty for de novo coronary lesions. Yonsei Med J. 2016;57(2):337.\nKleber FX, Schulz A, Waliszewski M, Hauschild T, Böhm M, Dietz U, et al. Local paclitaxel induces late lumen enlargement in coronary arteries after balloon angioplasty. Clin Res Cardiol. 2015;104(3):217–25.\nCortese B, Silva Orrego P, Agostoni P, Buccheri D, Piraino D, Andolina G, et al. Effect of drug-coated balloons in native coronary artery disease left with a dissection. JACC Cardiovasc Interv. 2015;8(15):2003–9.\nAnn SH, Balbir Singh G, Lim KH, Koo B-K, Shin E-S. Anatomical and physiological changes after paclitaxel-coated balloon for atherosclerotic de novo coronary lesions: serial IVUS-VH and FFR study. PLoS One. 2016;11(1):e0147057.\nAnn SH, Her A-Y, Singh GB, Okamura T, Koo B-K, Shin E-S. Serial morphological and functional assessment of the paclitaxel-coated balloon for de novo lesions. Rev Española Cardiol. 2016;69(11):1026–32.\nPoerner TC, Duderstadt C, Goebel B, Kretzschmar D, Figulla HR, Otto S. Fractional flow reserve-guided coronary angioplasty using paclitaxel-coated balloons without stent implantation: feasibility, safety and 6-month results by angiography and optical coherence tomography. Clin Res Cardiol. 2017;106(1):18–27.\nWöhrle J, Zadura M, Möbius-Winkler S, Leschke M, Opitz C, Ahmed W, et al. SeQuent please world wide registry. J Am Coll Cardiol. 2012;60(18):1733–8.\nZeymer U, Waliszewski M, Spiecker M, Gastmann O, Faurie B, Ferrari M, et al. Prospective ‘real world’ registry for the use of the ‘PCB only’ strategy in small vessel de novo lesions. Heart. 2013;100(4):311–6.\nSinaga D, Ho H, Zeymer U, Waliszewski M, Jafary F, Ooi Y, et al. 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J Interv Cardiol. 2015;28:430–8. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fjoic.12227.\nToelg R, Merkely B, Erglis A, et al. Coronary artery treatment with paclitaxel-coated balloon using a BTHC excipient: clinical results of the international real-world DELUX registry. EuroIntervention. 2014;10:591–9. https:\u002F\u002Fdoi.org\u002F10.4244\u002FEIJV10I5A102.\nCortese B, D’Ascenzo F, Fetiveau R, Balian V, Blengino S, Fineschi M, et al. Treatment of coronary artery disease with a new-generation drug-coated balloon. J Cardiovasc Med. 2018;19(5):247–52.\nGobić D, Tomulić V, Lulić D, Židan D, Brusich S, Jakljević T, et al. Drug-coated balloon versus drug-eluting stent in primary percutaneous coronary intervention: a feasibility study. Am J Med Sci. 2017;354(6):553–60.\nNijhoff F, Agostoni P, Belkacemi A, et al. 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Clin Res Cardiol. 2014;103:451–6. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs00392-014-0671-9.\nSchulz A, Hauschild T, Kleber FX. Treatment of coronary de novo bifurcation lesions with DCB only strategy. Clin Res Cardiol. 2014;103:451–6. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs00392-014-0671-9.\nBruch L, Zadura M, Waliszewski M, Platonic Z, Eränen J, Scheller B, et al. Results from the international drug-coated balloon registry for the treatment of bifurcations. Can a bifurcation be treated without stents? J Interv Cardiol. 2016;29(4):348–56.\nVaquerizo B, Fernández-Nofreiras E, Oategui I, de Suarez Lezo J, Rumoroso J, Martín P, et al. Second-generation drug-eluting balloon for ostial side branch lesions (001-bifurcations): mid-term clinical and angiographic results. J Interv Cardiol. 2016;29(3):285–92.\nHer A, Ann S, Singh G, Kim Y, Okamura T, Garg S, et al. Serial morphological changes of side-branch ostium after paclitaxel-coated balloon treatment of de novo coronary lesions of main vessels. Yonsei Med J. 2016;57(3):606.\nIto R, Ueno K, Yoshida T, Takahashi H, Tatsumi T, Hashimoto Y, et al. Outcomes after drug-coated balloon treatment for patients with calcified coronary lesions. J Interv Cardiol. 2017;31(4):436–41.\nRissanen T, Uskela S, Siljander A, Kärkkäinen J, Mäntylä P, Mustonen J, et al. Percutaneous coronary intervention of complex calcified lesions with drug-coated balloon after rotational atherectomy. J Interv Cardiol. 2017;30(2):139–46.\nKöln P, Scheller B, Liew H, Rissanen T, Ahmad W, Weser R, et al. Treatment of chronic total occlusions in native coronary arteries by drug-coated balloons without stenting—a feasibility and safety study. Int J Cardiol. 2016;225:262–7.\nJeger RV, Farah A, Ohlow M-A, Mangner N, Möbius-Winkler S, Leibundgut G, et al. Drug-coated balloons for small coronary artery disease (BASKET-SMALL 2): an open-label randomised non-inferiority trial. Lancet. 2018;392(10150):849–56.\nVos NS, van der Schaaf RJ, Amoroso G, Herrman J-PR, Patterson MS, Slagboom T, et al. REVascularization with paclitaxEL-coated balloon angioplasty versus drug-eluting stenting in acute myocardial infarcTION—A randomized controlled trial: Rationale and design of the REVELATION trial. Catheter Cardiovasc Interv. 2016;87(7):1213–21.",{"VOID":1737},"10.1007\u002Fs40119-018-0121-2","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs40119-018-0121-2",[1740,1755,1768,1783],{"id":1741,"sortIndex":32,"researcher":28,"roles":1742,"affiliations":1743,"properties":1752,"displayName":1754,"givenName":28,"familyName":28},"cb1ae3bb-024e-4981-8c53-a4d6d139ff9a",[958],[1744],{"id":1745,"sortIndex":32,"affiliation":1746,"properties":28},"1d598b71-5127-488c-8c7e-e001445a9884",{"id":1745,"createTime":28,"updateTime":28,"relativeEntities":1747,"slug":28,"properties":1748,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1751,"statistic":28},[],{"title":1749},{"VI":1750},"Faculty of Medicine, Imperial College London, London, UK",[],{"title":1753},{"VI":1754},"Hasan Mohiaddin",{"id":1756,"sortIndex":40,"researcher":28,"roles":1757,"affiliations":1758,"properties":1765,"displayName":1767,"givenName":28,"familyName":28},"69171619-6554-42b1-a4d5-aa446aa5d670",[958],[1759],{"id":1745,"sortIndex":32,"affiliation":1760,"properties":28},{"id":1745,"createTime":28,"updateTime":28,"relativeEntities":1761,"slug":28,"properties":1762,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1764,"statistic":28},[],{"title":1763},{"VI":1750},[],{"title":1766},{"VI":1767},"Tamar D. F. K. 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This study describes the mixed phenotype cohort in the Transthyretin Amyloidosis Outcomes Survey (THAOS). THAOS is an ongoing, longitudinal, observational survey of patients with ATTR amyloidosis, including both hereditary (ATTRv) and wild-type disease, and asymptomatic carriers of pathogenic transthyretin variants. Baseline characteristics of patients with a mixed phenotype (at enrollment or reclassified during follow-up) are described (data cutoff: January 4, 2022). Approximately one-third of symptomatic patients (n = 1185\u002F3542; 33.5%) were classified at enrollment or follow-up as mixed phenotype (median age, 66.5 years). Of those, 344 (29.0%) were reclassified to mixed phenotype within a median 1–2 years of follow-up. Most patients with mixed phenotype had ATTRv amyloidosis (75.7%). The most frequent genotypes were V30M (38.9%) and wild type (24.3%). These THAOS data represent the largest analysis of a real-world mixed phenotype ATTR amyloidosis population to date and suggest that a mixed phenotype may be more prevalent than previously thought. Patients may also migrate from a primarily neurologic or cardiologic presentation to a mixed phenotype over time. These data reinforce the need for multidisciplinary evaluation at initial assessment and follow-up of all patients with ATTR amyloidosis. ClinicalTrials.gov: NCT00628745.",{"EN":1859},"Clinical and Genotype Characteristics and Symptom Migration in Patients With Mixed Phenotype Transthyretin Amyloidosis from the Transthyretin Amyloidosis Outcomes Survey",{"VOID":1861},"Ando Y, Coelho T, Berk JL, Cruz MW, Ericzon BG, Ikeda S, et al. Guideline of transthyretin-related hereditary amyloidosis for clinicians. Orphanet J Rare Dis. 2013;8:31.\nGertz MA, Benson MD, Dyck PJ, Grogan M, Coelho T, Cruz M, et al. Diagnosis, prognosis, and therapy of transthyretin amyloidosis. J Am Coll Cardiol. 2015;66(21):2451–66.\nAdams D, Ando Y, Beirao JM, Coelho T, Gertz MA, Gillmore JD, et al. Expert consensus recommendations to improve diagnosis of ATTR amyloidosis with polyneuropathy. J Neurol. 2021;268(6):2109–22.\nRowczenio D, Wechalekar A. Mutations in hereditary amyloidosis 2015. Available from: http:\u002F\u002Famyloidosismutations.com\u002Fmut-attr.php Accessed 1 June 2023.\nDispenzieri A, Coelho T, Conceicao I, Waddington-Cruz M, Wixner J, Kristen AV, et al. Clinical and genetic profile of patients enrolled in the Transthyretin Amyloidosis Outcomes Survey (THAOS): 14-year update. Orphanet J Rare Dis. 2022;17(1):236.\nRuberg FL, Grogan M, Hanna M, Kelly JW, Maurer MS. Transthyretin amyloid cardiomyopathy: JACC state-of-the-art review. J Am Coll Cardiol. 2019;73(22):2872–91.\nKittleson MM, Ruberg FL, Ambardekar AV, Brannagan TH, Cheng RK, Clarke JO, et al. 2023 ACC expert consensus decision pathway on comprehensive multidisciplinary care for the patient with cardiac amyloidosis: A Report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2023;81(11):1076–126.\nPlante-Bordeneuve V, Suhr OB, Maurer MS, White B, Grogan DR, Coelho T. The Transthyretin Amyloidosis Outcomes Survey (THAOS) registry: design and methodology. Curr Med Res Opin. 2013;29(1):77–84.\nCoelho T, Maurer MS, Suhr OB. THAOS - The Transthyretin Amyloidosis Outcomes Survey: initial report on clinical manifestations in patients with hereditary and wild-type transthyretin amyloidosis. Curr Med Res Opin. 2013;29(1):63–76.\nGonzalez-Moreno J, Losada-Lopez I, Cisneros-Barroso E, Garcia-Pavia P, Gonzalez-Costello J, Munoz-Beamud F, et al. A descriptive analysis of ATTR amyloidosis in Spain from the Transthyretin Amyloidosis Outcomes Survey. Neurol Ther. 2021;10(2):833–45.\nSekijima Y, Mundayat R, Ishii T, Ando Y. The current status of the Transthyretin Amyloidosis Outcomes Survey (THAOS) in Japan. Amyloid. 2019;26(suppl 1):61–2.\nDamy T, Kristen AV, Suhr OB, Maurer MS, Plante-Bordeneuve V, Yu CR, et al. Transthyretin cardiac amyloidosis in continental Western Europe: an insight through the Transthyretin Amyloidosis Outcomes Survey (THAOS). Eur Heart J. 2019;43(5):391–400.\nMaurer MS, Hanna M, Grogan M, Dispenzieri A, Witteles R, Drachman B, et al. Genotype and phenotype of transthyretin cardiac amyloidosis: THAOS (Transthyretin Amyloid Outcome Survey). J Am Coll Cardiol. 2016;68(2):161–72.\nCoelho T, Vinik A, Vinik EJ, Tripp T, Packman J, Grogan DR. Clinical measures in transthyretin familial amyloid polyneuropathy. Muscle Nerve. 2017;55(3):323–32.\nLosada I, Gonzalez-Moreno J, Rodriguez A, Uson M, Ripoll-Vera T, Ferrer-Nadal A, et al. Multidisciplinary approach in the management of hATTR. Eur J Clin Invest. 2020;50(10): e13296.\nPastorelli F, Fabbri G, Rapezzi C, Serenelli M, Plasmati R, Vacchiano V, et al. Neurological involvement in Ile68Leu (p.Ile88Leu) ATTR amyloidosis: not only a cardiogenic mutation. Amyloid. 2021;28(3):173–81.\nKaku MC, Bhadola S, Berk JL, Sanchorawala V, Connors LH, Lau KHV. Neurological manifestations of hereditary transthyretin amyloidosis: a focus on diagnostic delays. Amyloid. 2022;29(3):184–9.\nGentile L, Di Bella G, Minutoli F, Cucinotta F, Obici L, Mussinelli R, et al. Description of a large cohort of Caucasian patients with V122I ATTRv amyloidosis: Neurological and cardiological features. J Peripher Nerv Syst. 2020;25(3):273–8.\nConceicao I, Coelho T, Rapezzi C, Parman Y, Obici L, Galan L, et al. Assessment of patients with hereditary transthyretin amyloidosis - understanding the impact of management and disease progression. Amyloid. 2019;26(3):103–11.\nMaia LF, Magalhaes R, Freitas J, Taipa R, Pires MM, Osorio H, et al. CNS involvement in V30M transthyretin amyloidosis: clinical, neuropathological and biochemical findings. J Neurol Neurosurg Psychiatry. 2015;86(2):159–67.\nFenoglio R, Baldovino S, Barreca A, Bottasso E, Sciascia S, Sbaiz L, et al. Renal involvement in transthyretin amyloidosis: the double presentation of transthyretin amyloidosis deposition disease. Nephron. 2022;146(5):481–8.\nMcColgan P, Viegas S, Gandhi S, Bull K, Tudor R, Sheikh F, et al. Oculoleptomeningeal amyloidosis associated with transthyretin Leu12Pro in an African patient. J Neurol. 2015;262(1):228–34.\nWajnsztajn Yungher F, Kim A, Boehme A, Kleyman I, Weimer LH, Maurer MS, et al. Peripheral neuropathy symptoms in wild type transthyretin amyloidosis. J Peripher Nerv Syst. 2020;25(3):265–72.\nPapagianni A, Ihne S, Zeller D, Morbach C, Uceyler N, Sommer C. Clinical and apparative investigation of large and small nerve fiber impairment in mixed cohort of ATTR-amyloidosis: impact on patient management and new insights in wild-type. Amyloid. 2022;29(1):14–22.\nKleefeld F, Scherret E, Knebel F, Messroghli D, Heidecker B, Wetz C, et al. Same same, but different? The neurological presentation of wildtype transthyretin (ATTRwt) amyloidosis. Amyloid. 2022;29(2):92–101.\nD’Aguanno V, Ralli M, Artico M, Russo FY, Scarpa A, Fiore M, et al. Systemic amyloidosis: a contemporary overview. Clin Rev Allergy Immunol. 2020;59(3):304–22.\nStevens FJ, Kisilevsky R. Immunoglobulin light chains, glycosaminoglycans, and amyloid. Cell Mol Life Sci. 2000;57(3):441–9.\nYan SD, Zhu H, Zhu A, Golabek A, Du H, Roher A, et al. Receptor-dependent cell stress and amyloid accumulation in systemic amyloidosis. Nat Med. 2000;6(6):643–51.\nIhse E, Ybo A, Suhr O, Lindqvist P, Backman C, Westermark P. Amyloid fibril composition is related to the phenotype of hereditary transthyretin V30M amyloidosis. J Pathol. 2008;216(2):253–61.\nKoike H, Nishi R, Ikeda S, Kawagashira Y, Iijima M, Sakurai T, et al. The morphology of amyloid fibrils and their impact on tissue damage in hereditary transthyretin amyloidosis: an ultrastructural study. J Neurol Sci. 2018;394:99–106.\nBergstrom J, Gustavsson A, Hellman U, Sletten K, Murphy CL, Weiss DT, et al. Amyloid deposits in transthyretin-derived amyloidosis: cleaved transthyretin is associated with distinct amyloid morphology. J Pathol. 2005;206(2):224–32.",{"VOID":1863},"10.1007\u002Fs40119-023-00344-3","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs40119-023-00344-3",[1866,1881,1896,1911,1926,1950,1965,1980,2004,2028,2043,2058,2071],{"id":1867,"sortIndex":32,"researcher":28,"roles":1868,"affiliations":1869,"properties":1878,"displayName":1880,"givenName":28,"familyName":28},"db28b2ce-b602-45ef-b7e3-8b1edd0177ce",[958],[1870],{"id":1871,"sortIndex":32,"affiliation":1872,"properties":28},"8498220e-3416-48e5-b1e4-3390f9fa239e",{"id":1871,"createTime":28,"updateTime":28,"relativeEntities":1873,"slug":28,"properties":1874,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1877,"statistic":28},[],{"title":1875},{"VI":1876},"Servicio de Medicina Interna, Hospital Universitario Son Llatzer, Instituto de Investigación Sanitaria Illes Balears, Palma, Spain",[],{"title":1879},{"VI":1880},"Juan 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There are limited human data to establish the safest timing of antiplatelet or anticoagulation therapy following neurosurgical procedures. For patients with malignancy experiencing AMI in the acute postoperative period, staged percutaneous coronary intervention (PCI) with upfront coronary aspiration thrombectomy followed by delayed completion PCI may offer an opportunity for myocardial salvage while minimizing postoperative bleeding risks. CYP2C19 genotyping and platelet aggregation studies can help confirm adequate platelet inhibition once antiplatelet therapy is resumed.",{"EN":2143},"Emergent Coronary Thrombectomy for Acute Myocardial Infarction Immediately Following Craniotomy with Tumor Resection",{"EN":1217},{"VOID":2146},"Puelacher C, Lurati Buse G, Seeberger D, et al. Perioperative myocardial injury after noncardiac surgery: incidence, mortality, and characterization. Circulation. 2018;137:1221–32.\nHan HJ, Kim J, Jang CK, et al. Perioperative low-dose aspirin management for planned clipping surgery: when, how long, and with what precautions? Neurosurgery. 2023. https:\u002F\u002Fdoi.org\u002F10.1227\u002Fneu.0000000000002710.\nSaka E, Canbaz M, Abdullah T, et al. Perioperative myocardial injury after elective neurosurgery: incidence, risk factors, and effects on mortality. Neurosurg Rev. 2022;45:2151–9.\nNavi Babak B, Reiner Anne S, Kamel H, et al. Risk of arterial thromboembolism in patients with cancer. J Am Coll Cardiol. 2017;70:926–38.\nWallentin L, Becker RC, Budaj A, et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2009;361:1045–57.\nMega JL, Close SL, Wiviott SD, et al. Cytochrome P-450 polymorphisms and response to clopidogrel. N Engl J Med. 2009;360:354–62.\nRahman M, Donnangelo LL, Neal D, Mogali K, Decker M, Ahmed MM. Effects of perioperative acetyl salicylic acid on clinical outcomes in patients undergoing craniotomy for brain tumor. World Neurosurgery. 2015;84:41–7.\nLaohaprasit V, Mayberg MR. Risks of anticoagulation therapy after experimental corticectomy in the rat. Neurosurgery. 1993;32:625–9.\nLazio BE, Simard JM. Anticoagulation in neurosurgical patients. Neurosurgery. 1999;45:838.\nBharadwaj A, Potts J, Mohamed MO, et al. Acute myocardial infarction treatments and outcomes in 6.5 million patients with a current or historical diagnosis of cancer in the USA. Eur Heart J. 2020;41:2183–93.\nLandes U, Kornowski R, Bental T, et al. Long-term outcomes after percutaneous coronary interventions in cancer survivors. Coron Artery Dis. 2017;28:5–10.\nNakatsuma K, Shiomi H, Morimoto T, et al. Influence of a history of cancer on long-term cardiovascular outcomes after coronary stent implantation (an Observation from Coronary Revascularization Demonstrating Outcome Study-Kyoto Registry Cohort-2). Eur Heart J Qual Care Clin Outcomes. 2018;4:200–7.\nPotts JE, Iliescu CA, Lopez Mattei JC, et al. Percutaneous coronary intervention in cancer patients: a report of the prevalence and outcomes in the United States. Eur Heart J. 2019;40:1790–800.\nRoule V, Verdier L, Blanchart K, et al. Systematic review and meta-analysis of the prognostic impact of cancer among patients with acute coronary syndrome and\u002For percutaneous coronary intervention. BMC Cardiovasc Disord. 2020;20:38.\nHess CN, Roe MT, Clare RM, et al. Relationship between cancer and cardiovascular outcomes following percutaneous coronary intervention. J Am Heart Assoc. 2015. https:\u002F\u002Fdoi.org\u002F10.1161\u002FJAHA.115.001779.\nUeki Y, Vögeli B, Karagiannis A, et al. Ischemia and bleeding in cancer patients undergoing percutaneous coronary intervention. JACC CardioOncol. 2019;1:145–55.\nKwok CS, Wong CW, Kontopantelis E, et al. Percutaneous coronary intervention in patients with cancer and readmissions within 90 days for acute myocardial infarction and bleeding in the USA. Eur Heart J. 2021;42:1019–34.\nTabata N, Sueta D, Yamamoto E, et al. Outcome of current and history of cancer on the risk of cardiovascular events following percutaneous coronary intervention: a Kumamoto University Malignancy and Atherosclerosis (KUMA) study. Eur Heart J Qual Care Clin Outcomes. 2018;4:290–300.\nGuo W, Fan X, Lewis BR, et al. Cancer patients have a higher risk of thrombotic and ischemic events after percutaneous coronary intervention. JACC Cardiovasc Interv. 2021;14:1094–105.\nIliescu CA, Grines CL, Herrmann J, et al. SCAI expert consensus statement: evaluation, management, and special considerations of cardio-oncology patients in the cardiac catheterization laboratory. 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The clinical presentation is variable and often poses a diagnostic challenge. Here we describe the case of a 52-year-old woman who presented with troponin-positive chest pain, exertional dizziness, and dyspnea as a consequence of a massive left atrial myxoma, which was successfully treated with surgical resection.",{"EN":2295},"Massive Left Atrial Myxoma Presenting With Troponin-Positive Chest Pain",{"VOID":2297},"Cresti A, Chiavarelli M, Glauber M, et al. Incidence rate of primary cardiac tumors: a 14-year population study. J Cardiovasc Med (Hagerstown). 2016;17(1):37–433.\nKarabinis A, Samanidis G, Khoury M, Stavridis G, Perreas K. Clinical presentation and treatment of cardiac myxoma in 153 patients. Medicine (Baltimore). 2018;97(37):e12397.\nLehrman KL, Prozan GB, Ullyot D. Atrial myxoma presenting as acute myocardial infarction. Am Heart J. 1985;110(6):1293–5.\nPanosa A, Kalangosb A, Sztajzela J. Left atrial myxoma presenting with myocardial infarction: Case report and review of the literature. 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