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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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SCIE","scie",[936,813],"SCIE","https:\u002F\u002Fmjl.clarivate.com\u002Fsearch-results?issn=0929-5305",[939,940,941],"4f363738-bd8a-4ecf-bff7-e3fa60978c08","0ddd214e-2317-43ae-8737-4f5747adc536","22fd6c38-3ec0-41e0-8ae8-a4290171207e","https:\u002F\u002Flink.springer.com\u002Fjournal\u002F11239",{"impactFactor":32,"impactFactorByYear":944,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":358,"totalPublicationByYear":945,"totalCitation":32,"totalCitationByYear":946,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":947,"hindexLast5Year":32,"hindex":32},{},{"1997":205,"1998":323,"1999":47,"2000":357,"2001":46,"2002":145,"2003":42,"2007":42,"2011":40,"2013":123,"2015":40,"2016":123,"2017":42,"2018":40,"2019":40,"2020":46,"2021":123,"2022":45},{},{},{"meta":949,"data":951},{"total":950},"2589",[952,1113,1189,1343,1575,1785,1857,1942,2122,2287],{"id":953,"createTime":954,"updateTime":955,"relativeEntities":956,"slug":957,"properties":958,"entityType":967,"verifyStatus":26,"verifyTime":955,"verifyNote":968,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":969,"fullTextUrl":28,"authors":970,"publicationType":1056,"publisherRelationship":1057,"citationCount":28,"citationInfo":28,"publishDate":1109,"publishYear":1110,"citationAnalyzeStatus":880,"lastCitationAnalyze":28,"indexDatabases":1111,"openAccess":28,"references":28,"isForceReanalyzing":1112},"00526d9f-4eda-4851-a927-a32f740f9976","2024-01-20T09:27:20.837+00:00","2025-02-06T21:02:36.960+00:00",[],"High-prevalence-of-heparin-induced-thrombocytopenia-with-thrombosis-among-patients-with-essential-thrombocytemia-carrying-V617F-mutation",{"abstract":959,"title":961,"references":963,"doi":965},{"EN":960},"Arterial and venous complications are major causes of morbidity and mortality in myeloproliferative neoplasms (MPNs). MPNs patients, frequently receive heparin. Heparin-induced thrombocytopenia (HIT) is a rare but potentially life-threatening complication resulting in a severe acquired thrombophilic condition. We carried out a retrospective analysis to evaluate occurrence of new thrombotic events during heparin therapy in essential thrombocythemia (ET) patients. We studied 108 ET patients on heparin for treatment of previous thrombotic events or in thromboprophilaxis. Fifty-eight of them carried JAK 2 V617F mutation while 50 patients were without V617F mutation. Ten patients, among those with JAK 2 V617F mutation after a median of 10 days from heparin treatment presented a platelet drop, new thrombotic events and in 10\u002F10 cases heparin-related antibodies were found. In the other group, two patients (4%) presented a platelet drop, thrombotic manifestations and heparin related antibodies. Our data show that HIT is more frequent, during heparin treatment, in patients with ET carrying V617F mutation, as compared with patients without mutations (P = 0.029). ET with V617F mutation seems to be associated with higher risk of thrombotic complications during heparin treatment. Monitoring platelet counts very closely during the course of heparin is essential especially in ET patients in which platelet drop may be hidden by constitutional thrombocytosis.",{"EN":962},"High prevalence of heparin induced thrombocytopenia with thrombosis among patients with essential thrombocytemia carrying V617F mutation",{"VOID":964},"Marchioli R (2005) Vascular and neoplastic risk in a large cohort of patients with polycythemia vera. J Clin Oncol 23:2224–2232. doi:10.1200\u002FJCO.2005.07.062\nGianelli U, Iurlo A, Cattaneo D et al (2015) Discrepancies between bone marrow histopathology and clinical phenotype in BCR-ABL1-negative myeloproliferative neoplasms associated with splanchnic vein thrombosis. Leuk Res 39:525–529. doi:10.1016\u002Fj.leukres.2015.03.009\nKaifie A, Kirschner M, Wolf D et al (2016) Bleeding, thrombosis, and anticoagulation in myeloproliferative neoplasms (MPN): analysis from the German SAL-MPN-registry. J Hematol Oncol 9:18. doi:10.1186\u002Fs13045-016-0242-9\nGisslinger H, Gotic M, Holowiecki J et al (2013) Anagrelide compared with hydroxyurea in WHO-classified essential thrombocythemia: the ANAHYDRET Study, a randomized controlled trial. Blood 121:1720–1728. doi:10.1182\u002Fblood-2012-07-443770\nMarchioli R, Finazzi G, Landolfi R et al (2005) Vascular and neoplastic risk in a large cohort of patients with polycythemia vera. J Clin Oncol 23:2224–2232. doi:10.1200\u002FJCO.2005.07.062\nCarobbio A, Thiele J, Passamonti F et al (2011) Risk factors for arterial and venous thrombosis in WHO-defined essential thrombocythemia: an international study of 891 patients. Blood 117:5857–5859. doi:10.1182\u002Fblood-2011-02-339002\nSpanoudakis E, Tsatalas C (2009) Hemopoiesis in Ph-negative chronic myeloproliferative disorders. Curr Stem Cell Res Ther 4:154–160\nHu G-Y, Deng M-Y, Zhang G-S et al (2009) The frequency of JAK2 V617F mutation, expression level of phosphorylated JAK\u002FSTATs proteins and their clinical significance in myeloproliferative disorders patients. Zhonghua Xue Ye Xue Za Zhi 30:394–398\nLange T, Edelmann A, Siebolts U et al (2013) JAK2 p.V617F allele burden in myeloproliferative neoplasms one month after allogeneic stem cell transplantation significantly predicts outcome and risk of relapse. Haematologica 98:722–728. doi:10.3324\u002Fhaematol.2012.076901\nPassamonti F, Rumi E (2009) Clinical relevance of JAK2 (V617F) mutant allele burden. Haematologica 94:7–10. doi:10.3324\u002Fhaematol.2008.001271\nAntonioli E, Guglielmelli P, Poli G et al (2008) Influence of JAK2V617F allele burden on phenotype in essential thrombocythemia. Haematologica 93:41–48. doi:10.3324\u002Fhaematol.11653\nVannucchi AM (2010) JAK2 mutation and thrombosis in the myeloproliferative neoplasms. Curr Hematol Malig Rep 5:22–28. doi:10.1007\u002Fs11899-009-0038-x\nScully M, Gates C, Neave L (2016) How we manage patients with heparin induced thrombocytopenia. Br J Haematol. doi:10.1111\u002Fbjh.14102\nRumi E, Pietra D, Pascutto C et al (2014) Clinical effect of driver mutations of JAK2, CALR, or MPL in primary myelofibrosis. Blood 124:1062–1069. doi:10.1182\u002Fblood-2014-05-578435\nBertozzi I, Bogoni G, Biagetti G et al (2017) Thromboses and hemorrhages are common in MPN patients with high JAK2V617F allele burden. Ann Hematol 96:1297–1302. doi:10.1007\u002Fs00277-017-3040-8\nTefferi A, Barbui T (2017) Polycythemia vera and essential thrombocythemia: 2017 update on diagnosis, risk-stratification, and management. Am J Hematol 92:94–108. doi:10.1002\u002Fajh.24607\nPassamonti F, Rumi E, Pietra D et al (2010) A prospective study of 338 patients with polycythemia vera: the impact of JAK2 (V617F) allele burden and leukocytosis on fibrotic or leukemic disease transformation and vascular complications. Leukemia 24:1574–1579. doi:10.1038\u002Fleu.2010.148\nBeer PA, Campbell PJ, Scott LM et al (2008) MPL mutations in myeloproliferative disorders: analysis of the PT-1 cohort. Blood 112:141–149. doi:10.1182\u002Fblood-2008-01-131664\nKlampfl T, Gisslinger H, Harutyunyan AS et al (2013) Somatic mutations of calreticulin in myeloproliferative neoplasms. N Engl J Med 369:2379–2390. doi:10.1056\u002FNEJMoa1311347\nRumi E, Pietra D, Ferretti V et al (2014) JAK2 or CALR mutation status defines subtypes of essential thrombocythemia with substantially different clinical course and outcomes. Blood. doi:10.1182\u002Fblood-2013-11-539098\nWarkentin TE (2011) How I diagnose and manage HIT. Hematology Am Soc Hematol Educ Progr 2011:143–149. doi:10.1182\u002Fasheducation-2011.1.143\nWarkentin TE, Aird WC, Rand JH (2003) Platelet-endothelial interactions: sepsis, HIT, and antiphospholipid syndrome. Hematology Am Soc Hematol Educ Progr 497–519. doi:10.1182\u002Fasheducation-2003.1.497\nCastelli R, Cassinerio E, Cappellini MD et al (2007) Heparin induced thrombocytopenia: pathogenetic, clinical, diagnostic and therapeutic aspects. Cardiovasc Hematol Disord Drug Targets 7:153–162\nBarbui T (2011) How to manage thrombosis in myeloproliferative neoplasms. Curr Opin Oncol 23:654–658. doi:10.1097\u002FCCO.0b013e32834bb867\nBovet J, De Maistre E, Bejot Y, Girodon F (2015) Are Myeloproliferative neoplasms a risk factor for Heparin-Induced Thrombocytopenia? Br J Haematol. doi:10.1111\u002Fbjh.13874\nLapecorella M, Lucchesi A, Di Ianni M et al (2010) Unusual onset of venous thromboembolism and heparin-induced thrombocytopenia in a patient with essential thrombocythemia. Blood Coagul Fibrinolysis 21:85–90. doi:10.1097\u002FMBC.0b013e32832f2b08\nRandi ML, Tezza F, Scapin M et al (2010) Heparin-induced thrombocytopenia in patients with philadelphia-negative myeloproliferative disorders and unusual splanchnic or cerebral vein thrombosis. Acta Haematol 123:140–145. doi:10.1159\u002F000280466\nTefferi A, Vardiman JW (2008) Classification and diagnosis of myeloproliferative neoplasms: the 2008 World Health Organization criteria and point-of-care diagnostic algorithms. Leukemia 22:14–22. doi:10.1038\u002Fsj.leu.2404955\nCampbell PJ, Baxter EJ, Beer PA et al (2006) Mutation of JAK2 in the myeloproliferative disorders: timing, clonality studies, cytogenetic associations, and role in leukemic transformation. Blood 108:3548–3555. doi:10.1182\u002Fblood-2005-12-013748\nPancrazzi A, Guglielmelli P, Ponziani V et al (2008) A sensitive detection method for MPLW515L or MPLW515K mutation in chronic myeloproliferative disorders with locked nucleic acid-modified probes and real-time polymerase chain reaction. J Mol Diagn 10:435–441. http:\u002F\u002Fwww.ncbi.nlm.nih.gov\u002Fpubmed\u002F18669880\nLo GK, Juhl D, Warkentin TE et al (2006) Evaluation of pretest clinical score (4 T’s) for the diagnosis of heparin-induced thrombocytopenia in two clinical settings. J Thromb Haemost 4:759–765. doi:10.1111\u002Fj.1538-7836.2006.01787.x\nPrandoni P, Siragusa S, Girolami B, Fabris F The incidence of heparin-induced thrombocytopenia in medical patients treated with low-molecular-weight heparin: a prospective cohort study. doi:10.1182\u002Fblood-2005-03-0912\nEichler P, Budde U, Haas S et al (1999) First workshop for detection of heparin-induced antibodies: validation of the heparin-induced platelet-activation test (HIPA) in comparison with a PF4\u002Fheparin ELISA. Thromb Haemost 81:625–629\nNiccolai CS, Hicks RW, Oertel L et al (2004) Unfractionated heparin: focus on a high-alert drug. Pharmacotherapy 24:146S–155S\nWarkentin TE, Greinacher A (2004) Heparin-induced thrombocytopenia: recognition, treatment, and prevention. Chest 126:311S–337S. doi:10.1378\u002Fchest.126.3_suppl.311S\nMartel N, Lee J, Wells PS (2005) Risk for heparin-induced thrombocytopenia with unfractionated and low-molecular-weight heparin thromboprophylaxis: a meta-analysis. Blood 106:2710–2715. http:\u002F\u002Fwww.ncbi.nlm.nih.gov\u002Fpubmed\u002F15985543\nSpectre G, Kalish Y, Schliamser L, Varon D (2008) Heparin-induced thrombocytopenia in myeloproliferative disorders: a rare or under-diagnosed complication? Am J Hematol 83:420–423. doi:10.1002\u002Fajh.21128\nGreinacher A (2015) Heparin-Induced Thrombocytopenia. N Engl J Med 373:252–261. doi:10.1056\u002FNEJMcp1411910\nDunn FW, Soria C, Thomaidis A et al (1984) Interactions of platelets with standard heparin and low molecular weight fractions. Nouv Rev Fr d’hématologie 26:249–253\nCampbell PJ, Scott LM, Buck G et al (2005) Definition of subtypes of essential thrombocythaemia and relation to polycythaemia vera based on JAK2 V617F mutation status: a prospective study. 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Including Thrombosis",{"VOID":1123},"10.1023\u002FA:1018633828318","Author affiliation is blank","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1023\u002FA:1018633828318",[1127],{"id":1128,"sortIndex":32,"researcher":28,"roles":1129,"affiliations":1130,"properties":1131,"displayName":1133,"givenName":28,"familyName":28},"31a50d57-b418-44f4-b282-c3826594864e",[974],[],{"title":1132},{"VI":1133},"Oscar E. Starobin",{"url":1125,"publisher":1135,"properties":1181},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1136,"slug":872,"properties":1137,"entityType":25,"verifyStatus":880,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1141,"manageAffiliations":1150,"indexDatabases":1161,"url":942,"thumbnailPath":28,"statistic":1176,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1138,"title":1139,"eissn":1140},{"VOID":875},{"EN":877},{"VOID":879},[1142,1146],{"id":883,"createTime":28,"updateTime":28,"relativeEntities":1143,"label":1144,"description":1145,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":886},{},{"id":889,"createTime":28,"updateTime":28,"relativeEntities":1147,"label":1148,"description":1149,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":892},{},[1151,1156],{"id":896,"createTime":28,"updateTime":28,"relativeEntities":1152,"slug":28,"properties":1153,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1155,"statistic":28},[],{"title":1154},{"EN":900},[],{"id":903,"createTime":28,"updateTime":28,"relativeEntities":1157,"slug":28,"properties":1158,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1160,"statistic":28},[],{"title":1159},{"EN":907},[909],[1162,1169],{"id":912,"indexDatabase":1163,"url":918,"indexYears":919,"academicFieldIds":1168,"indexDatabaseRanking":923},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1164,"label":1165,"description":1166,"key":781,"publicationTags":1167,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[921,922],{"id":925,"indexDatabase":1170,"url":937,"indexYears":28,"academicFieldIds":1175,"indexDatabaseRanking":28},{"id":927,"createTime":28,"updateTime":28,"relativeEntities":1171,"label":1172,"description":1173,"key":934,"publicationTags":1174,"standard":28},[],{"EN":930,"VI":930},{"EN":932,"VI":933},[936,813],[939,940,941],{"impactFactor":32,"impactFactorByYear":1177,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":358,"totalPublicationByYear":1178,"totalCitation":32,"totalCitationByYear":1179,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":1180,"hindexLast5Year":32,"hindex":32},{},{"1997":205,"1998":323,"1999":47,"2000":357,"2001":46,"2002":145,"2003":42,"2007":42,"2011":40,"2013":123,"2015":40,"2016":123,"2017":42,"2018":40,"2019":40,"2020":46,"2021":123,"2022":45},{},{},{"pages":1182,"volume":1184},{"VOID":1183},"105-106",{"VOID":1185},"9","2000-01-01",2000,[936,923],{"id":1190,"createTime":1191,"updateTime":1192,"relativeEntities":1193,"slug":1194,"properties":1195,"entityType":967,"verifyStatus":26,"verifyTime":1192,"verifyNote":968,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1204,"fullTextUrl":28,"authors":1205,"publicationType":1056,"publisherRelationship":1290,"citationCount":28,"citationInfo":28,"publishDate":1341,"publishYear":1187,"citationAnalyzeStatus":880,"lastCitationAnalyze":28,"indexDatabases":1342,"openAccess":28,"references":28,"isForceReanalyzing":1112},"00ac5df6-dfd5-4624-ad7f-347387122c6a","2024-01-20T01:23:15.804+00:00","2025-02-14T00:32:22.545+00:00",[],"Time-to-Treatment-and-Cost-of-Thrombolysis-A-Multicenter-Comparison-of-tPA-and-rPA",{"abstract":1196,"title":1198,"references":1200,"doi":1202},{"EN":1197},"Study Objective: This study reports a comparison of the time to treatment and cost of administration of alteplase (tPA) and reteplase (rPA) in patients with acute myocardial infarction (MI). Design: Retrospective chart review.). Setting: Hospital emergency department.). Interventions: A retrospective chart review of 500 MI patients who received alteplase or reteplase was performed. A comparison of time from presentation in the emergency department to start of treatment was performed, and the cost of administration of drugs, including cost of supplies, monitoring time, and IV line complications, was calculated for each drug.). Results: The time from presentation to start of treatment was significantly shorter for reteplase than alteplase (51 vs 34 min). This difference resulted from a shorter decision to treat to start of treatment time for reteplase (11 min) compared to alteplase (31 min). The cost of administration of alteplase ranged from $136 to $184 per patient, while the cost of administration of reteplase ranged from $87 to $120 per patient.). Discussion: Given the similar safety and efficacy profiles of these thrombolytic agents, the advantages of reteplase in speed of administration and the reduction in cost should be considered when making formulary and drug product selection decisions.). Abbreviated Abstract. Alteplase (tPA) and reteplase (rPA) were compared in a retrospective review of 500 patients. rPA was associated with 17 minute time savings from presentation-to-treatment compared to tPA. rPA was also associated with a per patient cost savings $49 to $64 compared to tPA. The time and cost advantages of rPA should be considered when making drug product selection decisions.).",{"EN":1199},"Time to Treatment and Cost of Thrombolysis: A Multicenter Comparison of tPA and rPA",{"VOID":1201},"White H, Van deWerf F. Thrombolysis for acute myocardial infarction. Circulation 1998;97:1632–1646.\nSmalling R. A fresh look at the molecular pharmacology of plasminogen activators: From theory to test tube to clinical outcomes. Am J Health Syst Pharm 1997;54:517–522.\nGonzalez E, Jones L, Ornato J. Hospital days and problems with thrombolytic administration in patients receiving thrombolytic therapy: A multicenter prospective assessment. Am Emerg Med 1992;21:1215–1221.\nThe GUSTO-III Investigators. A comparison of reteplase with alteplase for acute myocardial infarction. N Engl J Med 1997;337:1118–1123.\nFTT Collaborative Group. Indications for fibrinolytic therapy in suspected acute myocardial infarction: Collaborative overview of early mortality and major morbidity results from all randomized trials of more than 1000 patients. Lancet 1994;343:311–322.\nKline E, Smith O, Martin J. In-hospital treatment delays in patients treated with thrombolytic therapy: A report of the GUSTO time-to-treat substudy. Circulation 1992;86:702.\nRyan T, Anderson J, Antman L. ACC\u002FAHA guidelines for the management of patients with acute myocardial infarction: A report of the American College of Cardiology\u002F American Heart Association Task Force on Proactive Guidelines (Committee on Management of Acute Myocardial Infarction). J Am Coll Cardiol 1996;27:737–750.\nRogers W, Bowlby L, Nisha C. Treatment of myocardial infarction in the United States (1990–1995). Circulation 1994;90:2103–2114.\nSharkey S, Brunette D, Ruiz E. An analysis of time delays preceding thrombolysis for acute myocardial infarction. JAMA 1989;262:3171–3174.\nTiefenbrunn AJ, Chandra NC, French WJ, et al. Clinical experience with primary percutaneous transluminal coronary angioplasty compared with alteplase (recombinant tissue-type plasminogen activator) in patients with acute myocardial infarction. JACC 1998;31(6):1240–1245.\nKirchbaum DW, Grabavoy O, Finley RC, Harnid I. Use of alteplase for myocardial infarction in two community hospitals. Am J Hosp Pharm 1990;47:1535–1540.\nNewby KL, Rutsch WR, Califf RM, et al. Time from symptom onset to treatment and outcomes after thrombolytic therapy. J Am Coll Cardiol 1996;27:1645–1646.\nKereiakes DJ, Weaver DW, Anderson JL, et al. Time delays in the diagnosis and treatment of acute myocardial infarction: A tale of eight cities. Am Heart J 1990;120: 773–780.\nLambrew CT, Bowlby LJ, Rogers WJ, Chandra NC, Weaver WD, for the Time to Thrombolysis substudy of the National Registry of Myocardial Infarction-1. Factors influencing the time to thrombolysis in acute myocardial infarction. Arch Intern Med 1997;157:2577–2582.",{"VOID":1203},"10.1023\u002FA:1018797411812","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1023\u002FA:1018797411812",[1206,1221,1236,1249,1262,1277],{"id":1207,"sortIndex":32,"researcher":28,"roles":1208,"affiliations":1209,"properties":1218,"displayName":1220,"givenName":28,"familyName":28},"901de44c-5e4c-4439-91a8-e5cf79a2e8f7",[974],[1210],{"id":1211,"sortIndex":32,"affiliation":1212,"properties":28},"001e8e28-d6e6-4d02-9086-399df41dcd24",{"id":1211,"createTime":28,"updateTime":28,"relativeEntities":1213,"slug":28,"properties":1214,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1217,"statistic":28},[],{"title":1215},{"VI":1216},"Creighton University Schools of Medicine and Pharmacy & Allied Health Professions, Omaha",[],{"title":1219},{"VI":1220},"Ali Seyedroudbari",{"id":1222,"sortIndex":40,"researcher":28,"roles":1223,"affiliations":1224,"properties":1233,"displayName":1235,"givenName":28,"familyName":28},"88894300-5234-491d-aa19-3e7e5c2bcf62",[974],[1225],{"id":1226,"sortIndex":32,"affiliation":1227,"properties":28},"41b9e640-be29-413c-9ead-985334577cfd",{"id":1226,"createTime":28,"updateTime":28,"relativeEntities":1228,"slug":28,"properties":1229,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1232,"statistic":28},[],{"title":1230},{"VI":1231},"Bowling Green Medical Center, Bowling Green",[],{"title":1234},{"VI":1235},"E. 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Observational, case–control study including 2535 consecutive patients undergoing percutaneous coronary intervention (PCI) in two reference hospitals in Brazil, from October 2013 to December 2015. ST patients were matched to controls in a 1:3 ratio for gender, age, procedure indication, and performing hospital. From the total sample, 65 (2.5%) ST occurred and were matched with 195 controls (age 64.9 ± 11.8 years; hypertension, 78.8%; diabetes, 30%). Clopidogrel and aspirin early withdrawal (OR 19.25; 95% CI 1.66–23.52; p \u003C 0.01 and OR 4.36; 95% CI 1.81–10.50; p = 0.001, respectively), hypertension (OR 3.64; 95% CI 1.38–9.61; p = 0.006), dyslipidemia (OR 2.84; 95% CI 1.48–5.45; p = 0.002), smoking (OR 3.09; 95% CI 1.28–7.43; p = 0.02), body mass index ≥ 30 kg\u002Fm2 (OR 2.10; 95% CI 1.02–4.49; p = 0.012), previous myocardial infarction (OR 2.98; 95% CI 1.14–7.47; p \u003C 0.001), bifurcation lesion (OR 2.44; 95% CI 1.05–5.67; p = 0.03), and ≥ 3 stents (OR 3.90; 95% CI 1.78–8.52; p = 0.002) were associated with ST. Stent type, diameter or length, severity of coronary artery disease, calcified lesions, and thrombus were not associated with ST. We found a similar frequency of ST from developed countries and identified strong predictors (clopidogrel and aspirin withdrawal, hypertension, dyslipidemia, smoking, obesity, previous myocardial infarction, bifurcation lesion, number of stents), which are in line with reports from developed countries.",{"EN":1352},"Predictors of coronary stent thrombosis: a case–control study",{"VOID":1354},"Byrne RA, Joner M, Kastrati A (2015) Stent thrombosis and restenosis: what have we learned and where are we going? The Andreas Grüntzig Lecture ESC 2014. Eur Heart J 36:3320–3331\nMauri L, Hsieh WH, Massaro JM, Ho KK, D’Agostino R, Cutlip DE (2007) Stent thrombosis in randomized clinical trials of drug-eluting stents. N Engl J Med 356:1020–1029\nSommer P, Armstrong EJ (2015) Stent thrombosis: current management and outcomes. Curr Treat Options Cardiovasc Med 17:7\nHolmes DR, Kereiakes DJ, Garg S et al (2010) Stent thrombosis. J Am Coll Cardiol 56:1357–1365\nKumar DR, Hanlin E, Glurich I, Mazza JJ, Yale SH (2010) Virchow’s contribution to the understanding of thrombosis and cellular biology. Clin Med Res 8:168–172\nLuscher TF, Steffel J, Eberli FR et al (2007) Drug-eluting stent and coronary thrombosis: biological mechanisms and clinical implications. Circulation 115:1051–1058\nChesnutt JKW, Han HC (2015) Simulation of the microscopic process during initiation of stent thrombosis. Comput Biol Med 56:182–191\nCutlip DE, Windecker S, Mehran R et al (2007) Clinical end points in coronary stent trials: a case for standardized definitions. Circulation 115:2344–2351\nClaessen BE, Henriques JPS, Jaffer FA, Mehran R, Piek JJ, Dangas GD (2014) Stent thrombosis. JACC: Cardiovasc Interv 7:1081–1092\nvan Werkum JW, Heestermans AA, Zomer AC et al (2009) Predictors of coronary stent thrombosis. J Am Coll Cardiol 53:1399–1409\nD’Ascenzo F, Bollati M, Clementi F et al (2013) Incidence and predictors of coronary stent thrombosis: evidence from an international collaborative meta-analysis including 30 studies, 221,066 patients, and 4276 thromboses. Int J Cardiol 167:575–584\nvan Werkum JW, Heestermans AACM., de Korte FI et al (2009) Long-term clinical outcome after a first angiographically confirmed coronary stent thrombosis: an analysis of 431 cases. Circulation 119:828–834\nLevine GN, Bates ER, Blankenship JC, Bailey SR, Bittl JA, Cercek B, Chambers CE, Ellis SG, Guyton RA, Hollenberg SM, Khot UN, Lange RA, Mauri L, Mehran R, Moussa ID, Mukherjee D, Nallamothu BK, Ting HH (2011) 2011 ACCF\u002FAHA\u002FSCAI guideline for percutaneous coronary intervention: a report of the American College of Cardiology Foundation\u002FAmerican Heart Association Task Force on Practice Guide-lines and the Society for Cardiovascular Angiography and Interventions. J Am Coll Cardiol 58:e000-00\nde la Torre-Hernández JM, Alfonso F, Hernández F et al (2008) Drug-eluting stent thrombosis: results from the multicenter Spanish registry ESTROFA (Estudio ESpañol sobre TROmbosis de stents FArmacoactivos). J Am Coll Cardiol 51:986–990\nLagerqvist B, Carlsson J, Fröbert O et al (2009) Stent thrombosis in Sweden: a report from the Swedish Coronary Angiography and Angioplasty Registry. Circ: Cardiovasc Interv 2:401–408\nWenaweser P, Daemen J, Zwahlen M et al (2008) Incidence and correlates of drug-eluting stent thrombosis in routine clinical practice: 4-year results from a large 2-institutional cohort study. J Am Coll Cardiol 52:1134–1140\nThe TIMI Study Group (1984) The Thrombolysis in Myocardial Infarction (TIMI) trial: phase I findings. N Engl J Med 33:523–530\nHeestermans AA, vanWerkum JW, Zwart B et al (2010) Acute and subacute stent thrombosis after primary percutaneous coronary intervention for ST-segment elevation myocardial infarction: incidence, predictors and clinical outcome. J Thromb Haemost 8:2385–2393\nPalmerini T, Biondi-Zoccai G, Riva DD et al (2012) Stent thrombosis with drug-eluting and bare-metal stents: evidence from a comprehensive network meta-analysis. Lancet 379:1393–1402\nWHO (2003) Adherence to long term therapies: evidence for action. 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Timing of D-Dimer evaluation in relation to the onset of the disease might have a diagnostic impact. We have presently performed a retrospective analysis of diagnostic procedures performed in individuals who presented to the Emergency department and evaluated for acute venous thromboembolism (VTE) following a single quantitative D-Dimer testing. Individuals who had a negative objective test served as controls to those who had a positive one (Doppler ultrasonography, high probability lung scan or a CT angiography). Seven hundred thirty-four individuals presented to the Emergency department, performed a single D-Dimer test as well as an objective test during their evaluation for an eventual event of acute VTE. One hundred ninety-seven patients had a positive objective test for either deep vein thrombosis (DVT) or pulmonary embolus. They were divided into seven tiles of times from symptoms onset. Highly significant differences between patients and controls regarding D-Dimer concentrations were noted mainly during the early days from symptom onset and turned less significant thereafter. Taking into consideration the time from symptoms onset in patients with acute VTE might have an effect on the diagnostic yield of quantitative D-Dimer in the Emergency department. We suggest not to exclude the eventual presence of acute VTE if quantitative D-Dimer is obtained later than 1 week following the onset of symptoms.",{"EN":1585},"The diagnostic yield of D-Dimer in relation to time from symptom onset in patients evaluated for venous thromboembolism in the emergency medicine department",{"VOID":1587},"Mager JJ, Schutgens RE, Haas FJ, Westermann CJ, Biesma DH (2001) The early course of D-dimer concentration following pulmonary artery embolisation. Thromb Haemost 86(6):1578–1579\nSpeiser W, Mallek R, Koppensteiner R, Stumpflen A, Kapiotis S, Minar E, Ehringer H, Lechner K (1990) D-dimer and TAT measurement in patients with deep venous thrombosis: utility in diagnosis and judgement of anticoagulant treatment effectiveness. Thromb Haemost 64(2):196–201\nHeit JA, Minor TA, Andrews JC, Larson DR, Li H, Nichols WL (1999) Determinants of plasma fibrin D-dimer sensitivity for acute pulmonary embolism as defined by pulmonary angiography. Arch Pathol Lab Med 123(3):235–240\nTorbicki A, Perrier A, Konstantinides S, Agnelli G, Galie N, Pruszczyk P, Bengel F, Brady AJ, Ferreira D, Janssens U et al (2008) Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). Eur Heart J 29(18):2276–2315\nWada H, Kobayashi T, Abe Y, Hatada T, Yamada N, Sudo A, Uchida A, Nobori T (2006) Elevated levels of soluble fibrin or D-dimer indicate high risk of thrombosis. J Thromb Haemost 4(6):1253–1258\nThe DVTENOX Study Group (1993) Markers of hemostatic system activation in acute deep venous thrombosis-evolution during the first days of heparin treatment. Thromb Haemost 70(6):909–914\nCosmi B, Legnani C, Cini M, Guazzaloca G, Palareti G (2005) D-dimer levels in combination with residual venous obstruction and the risk of recurrence after anticoagulation withdrawal for a first idiopathic deep vein thrombosis. Thromb Haemost 94(5):969–974\nJanssen MC, Verbruggen H, Wollersheim H, Hoogkamer B, van Langen H, Novakova IR (1997) D-dimer determination to assess regression of deep venous thrombosis. Thromb Haemost 78(2):799–802\nShrivastava S, Ridker PM, Glynn RJ, Goldhaber SZ, Moll S, Bounameaux H, Bauer KA, Kessler CM, Cushman M (2006) D-dimer, factor VIII coagulant activity, low-intensity warfarin and the risk of recurrent venous thromboembolism. J Thromb Haemost 4(6):1208–1214\nTen Cate-Hoek AJ, Prins MH (2005) Management studies using a combination of D-dimer test result and clinical probability to rule out venous thromboembolism: a systematic review. 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Low molecular weight heparin. Blood 1992;79:1–17.\nWarkentin TE, Levine MN, Hirsh J, et al. Heparin-induced thrombocytopenia in patients treated with low-molecularweight heparin or unfractionated heparin. New Engl J Med 1995;332:1330–1335.\nHirsh J. Heparin. New Engl J Med 1991;324:1565–1574.\nPrandoni P, Lensing AWA, Buller HR, et al. Comparison of subcutaneous low-molecular-weight heparin with intravenous standard heparin in proximal deep-vein thrombosis. Lancet 1992;339:441–445.\nLopaciuk S, Meissner AJ, Filipecki S, et al. Subcutaneous LMWH vs. subcutaneous unfractionated heparin in the treatment of deep vein thrombosis: A Polish Multicenter Trial. Thromb Haemost 1992;68:14–18.\nKoopman MMW, Prandoni P, Piovella F, et al. for the TASMAN Study Group. Treatment of venous thrombosis with intravenous unfractionated heparin administered in the hospital as compared to subcutaneous low-molecular-weight heparin administered at home. New Engl J Med 1996;334: 682–687.\nHull RD, Raskob GE, Pineo GF, et al. Subcutaneous low-molecular-weight heparin compared with continuous intravenous heparin in the treatment of proximal-vein thrombosis. New Engl J Med 1992;326:975–982.\nSimonneau G, Charbonnier B, Decousus H, et al. Subcutaneous low-molecular-weight heparin compared with continuous intravenous unfractionated heparin in the treatment of proximal deep vein thrombosis. Arch Intern Med 1993;153: 1541–1546.\nLevine MN, Gent M, Hirsh J, et al. A comparison of low-molecular-weight heparin administered primarily at home with unfractionated heparin administered in the hospital for proximal deep-vein thrombosis. New Engl J Med 1996;334: 677–681.\nLindmarker P, Holmstrom M, Granqvist S, Johnsson H, Lockner D. Comparison of once-daily subcutaneous Fragmin with continuous intravenous unfractionated heparin in the treatment of deep venous thrombosis. Thromb Haemost 1994;72:186–190.\nFiessinger JN, Fernandez ML, Gatterer E, Ohlsson CG. Fragmin once daily versus continuous infusion heparin in the treatment of DVT: A European Multicentre Trial. Haemost 1994;24(Suppl 1): abstr 44.\nLuomanmaki K and the Finnish Multicentre Group, Hallert C, Kim H. LMWH (Fragmin) once daily vs continuous infusion of standard heparin in the treatment of DVT. Haemost 1994;24(Suppl 1): abstr 248.\nDuroux P. A collaborative European Multicentre Study: A randomised trial of subcutaneous LMWH (CY216) compared with intravenous unfractionated heparin in the treatment of deep vein thrombosis. Thromb Haemost 1991;65: 251–256.\nBratt G, Tornebohm E, Granqvist S, Aberg W, Lockner D. A comparison between LMWH (KAB12165) and standard heparin in the intravenous treatment of Deep Venous Thrombosis. Thromb Haemost 1985;54:813–817.\nFRISC study group. Low-molecular-weight heparin during instability in coronary artery disease: Fragmin during instability in coronary artery disease. Lancet 1996;347:561–568.\nKlein W, Buchwald A, Hillis S, et al. Low molecular weight heparin in the initial and prolonged treatment of unstable coronary artery disease: The Fragmin in Unstable Coronary Heart Disease Study (FRIC) (submitted 1996).",{"VOID":1869},"10.1023\u002FA:1008893231863","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1023\u002FA:1008893231863",[1872],{"id":1873,"sortIndex":32,"researcher":28,"roles":1874,"affiliations":1875,"properties":1884,"displayName":1886,"givenName":28,"familyName":28},"94174598-f5bf-455b-9324-6b0b9e5341c3",[974],[1876],{"id":1877,"sortIndex":32,"affiliation":1878,"properties":28},"8fc397c2-30ab-437f-8183-35e08607af7e",{"id":1877,"createTime":28,"updateTime":28,"relativeEntities":1879,"slug":28,"properties":1880,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1883,"statistic":28},[],{"title":1881},{"VI":1882},"Hamilton Civic Hospitals Research Centre, Hamilton, Ontario, Canada",[],{"title":1885},{"VI":1886},"Jack Hirsh",{"url":1870,"publisher":1888,"properties":1934},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1889,"slug":872,"properties":1890,"entityType":25,"verifyStatus":880,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1894,"manageAffiliations":1903,"indexDatabases":1914,"url":942,"thumbnailPath":28,"statistic":1929,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1891,"title":1892,"eissn":1893},{"VOID":875},{"EN":877},{"VOID":879},[1895,1899],{"id":883,"createTime":28,"updateTime":28,"relativeEntities":1896,"label":1897,"description":1898,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":886},{},{"id":889,"createTime":28,"updateTime":28,"relativeEntities":1900,"label":1901,"description":1902,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":892},{},[1904,1909],{"id":896,"createTime":28,"updateTime":28,"relativeEntities":1905,"slug":28,"properties":1906,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1908,"statistic":28},[],{"title":1907},{"EN":900},[],{"id":903,"createTime":28,"updateTime":28,"relativeEntities":1910,"slug":28,"properties":1911,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1913,"statistic":28},[],{"title":1912},{"EN":907},[909],[1915,1922],{"id":912,"indexDatabase":1916,"url":918,"indexYears":919,"academicFieldIds":1921,"indexDatabaseRanking":923},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1917,"label":1918,"description":1919,"key":781,"publicationTags":1920,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[921,922],{"id":925,"indexDatabase":1923,"url":937,"indexYears":28,"academicFieldIds":1928,"indexDatabaseRanking":28},{"id":927,"createTime":28,"updateTime":28,"relativeEntities":1924,"label":1925,"description":1926,"key":934,"publicationTags":1927,"standard":28},[],{"EN":930,"VI":930},{"EN":932,"VI":933},[936,813],[939,940,941],{"impactFactor":32,"impactFactorByYear":1930,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":358,"totalPublicationByYear":1931,"totalCitation":32,"totalCitationByYear":1932,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":1933,"hindexLast5Year":32,"hindex":32},{},{"1997":205,"1998":323,"1999":47,"2000":357,"2001":46,"2002":145,"2003":42,"2007":42,"2011":40,"2013":123,"2015":40,"2016":123,"2017":42,"2018":40,"2019":40,"2020":46,"2021":123,"2022":45},{},{},{"pages":1935,"volume":1937},{"VOID":1936},"349-351",{"VOID":1938},"4","1997-09-01",1997,[936,923],{"id":1943,"createTime":1944,"updateTime":1945,"relativeEntities":1946,"slug":1947,"properties":1948,"entityType":967,"verifyStatus":26,"verifyTime":1945,"verifyNote":968,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1957,"fullTextUrl":1958,"authors":1959,"publicationType":1056,"publisherRelationship":2065,"citationCount":28,"citationInfo":28,"publishDate":2119,"publishYear":2120,"citationAnalyzeStatus":880,"lastCitationAnalyze":28,"indexDatabases":2121,"openAccess":28,"references":28,"isForceReanalyzing":1112},"01aba0dd-1d1d-4b7b-b15b-b574a2a3f747","2024-01-18T18:10:57.431+00:00","2025-02-20T11:23:43.784+00:00",[],"Plasminogen-activator-inhibitor-1-removal-using-dextran-sulphate-columns-Evidence-of-PAI-1-homeostasis",{"abstract":1949,"title":1951,"references":1953,"doi":1955},{"EN":1950},"Patients with high plasma plasminogen activator inhibitor-1 (PAI-1) antigen levels are prone to develop thrombosis. Lowering PAI-1 levels may offer a therapeutic option and help to better understand PAI-1 metabolism. We examined the effect on plasma PAI-1 levels of LDL-apheresis using dextran sulphate (DS) columns in 12 patients (9 male, 3 female, 49 ± 10 years) with heterozygous familial hypercholesterolaemia and coronary artery disease. One plasma volume equivalent (2.3–4.0 l) was treated during each procedure (at flow rates of 23 ± 2 ml\u002Fmin). Lipids and PAI-1 antigen levels were measured in plasma before and immediately after 19 aphereses (once in 7 patients, twice in 3 patients and three times in 2 patients) and also at 3 and 7 days post apheresis in five of these patients and in the column eluates from 8 of these patients. DS-apheresis reduced plasma cholesterol (50 ± 8%), triglyceride (45 ± 27%), apolipoprotein B (59 ± 10%) and PAI-1 antigen levels from 10.2 ± 5.2 to 6.0 ± 3.1 ng\u002Fml (P = 0.005). The PAI-I changes were independent of circadian variation. PAI-I bound to the DS-columns (3.51 ± 1.03 ng\u002Fml filtered plasma) and the percent of filtered PAI-1 that was bound correlated inversely (r = −0.81, P < 0.02) with basal PAI-1 levels indicating a high affinity saturable binding process. In four patients, plasma PAI-1 levels post-apheresis were higher than expected based on the amount of PAI-removed by the DS columns. The difference between the expected and actual PAI-1 level post apheresis, reflecting PAI-1 secretion or extracellular redistribution, correlated inversely with basal PAI-1 levels (r = −0.83, P = 0.01). PAI-1 levels returned to baseline pre-apheresis values 7 days post apheresis. PAI-1 antigen may be removed from plasma without adverse effect, resulting temporarily in its extracellular redistribution and restoration to baseline levels over one week. PAI-1 redistribution particularly when baseline pre-apheresis values were low may reflect a homeostatic mechanism to maintain sufficient PAI-1 levels. Procedures that could selectively remove PAI-1 from plasma may offer a treatment option for those with very high plasma PAI-1 levels and thrombosis.",{"EN":1952},"Plasminogen activator inhibitor-1 removal using dextran sulphate columns. Evidence of PAI-1 homeostasis",{"VOID":1954},"citation_journal_title=Arterioscler Thromb Vasc Biol; citation_title=Unsaturated fatty acids increase plasminogen activator inhibitor-1 expression in endothelial cells; citation_author=L Nilsson, U Banfi Diczfalusy, E Tremoli, A Hamsten, P Eriksson; citation_volume=18; citation_issue=11; citation_publication_date=1998; citation_pages=1679-1685; citation_id=CR1\ncitation_journal_title=Blood; citation_title=Hepatocyte growth factor stimulates expression of plasminogen activator inhibitor type 1 and tissue factor in HepG2 cells; citation_author=J Wojta, T Nakamura, A Fabry, P Hufnagl, R Beckmann, K Mc Grath; citation_volume=84; citation_issue=1; citation_publication_date=1994; citation_pages=151-157; citation_id=CR2\ncitation_journal_title=Diabetes; citation_title=Glucocorticoids and insulin promote plasminogen activator inhibitor 1 production by human adipose tissue; citation_author=PE Morange, J Aubert, F Peiretti, HR Lijnen, P Vague, M Verdier; citation_volume=48; citation_issue=4; citation_publication_date=1999; citation_pages=890-895; citation_doi=10.2337\u002Fdiabetes.48.4.890; citation_id=CR3\ncitation_journal_title=Blood; citation_title=Plasminogen activator inhibitors; citation_author=ED Sprengers, C Kluft; citation_volume=69; citation_publication_date=1987; citation_pages=381-387; citation_id=CR4\ncitation_journal_title=J Clin Invest; citation_title=Plasmin and plasminogen activator inhibitor type 1 promote cellular motility by regulating the interaction between the urokinase receptor and vitronectin; citation_author=DA Waltz, LR Natkin, RM Fujita, Y Wei, HA Chapman; citation_volume=100; citation_issue=1; citation_publication_date=1997; citation_pages=58-67; citation_doi=10.1172\u002FJCI119521; citation_id=CR5\ncitation_journal_title=Blood; citation_title=Developmental expression of plasminogen activator inhibitor-1 associated with thrombopoietin-dependent megakaryocytic differentiation; citation_author=S Madoiwa, N Komatsu, J Mimuro, K Kimura, M Matsuda, Y Sakata; citation_volume=94; citation_issue=2; citation_publication_date=1999; citation_pages=475-482; citation_id=CR6\ncitation_journal_title=Gastroenterology; citation_title=Imbalance of plasminogen activators and their inhibitors in human colorectal neoplasia. Implications of urokinase in colorectal carcinogenesis; citation_author=CF Sier, HW Verspaget, G Griffioen, JH Verheijen, PH Quax, G Dooijewaard; citation_volume=101; citation_issue=6; citation_publication_date=1991; citation_pages=1522-1528; citation_id=CR7\ncitation_journal_title=Am J Med Sci; citation_title=Overweight\u002Fobesity, smoking, and heavy alcohol consumption are important determinants of plasma PAI-1 levels in healthy men; citation_author=A Sasaki, A Kurisu, M Ohno, Y Ikeda; citation_volume=322; citation_issue=1; citation_publication_date=2001; citation_pages=19-23; citation_doi=10.1097\u002F00000441-200107000-00004; citation_id=CR8\nLyon CJ, Hsueh WA (2003) Effect of plasminogen activator inhibitor-1 in diabetes mellitus and cardiovascular disease. Am J Med 115(Suppl 8A):62S–68S. Review. doi:\n                    10.1016\u002Fj.amjmed.2003.08.014\n                    \n                  \n                        \ncitation_journal_title=Circulation; citation_title=C-reactive protein increases plasminogen activator inhibitor-1 expression and activity in human aortic endothelial cells: implications for the metabolic syndrome and atherothrombosis; citation_author=S Devaraj, DY Xu, I Jialal; citation_volume=107; citation_issue=3; citation_publication_date=2003; citation_pages=398-404; citation_doi=10.1161\u002F01.CIR.0000052617.91920.FD; citation_id=CR10\ncitation_journal_title=Am J Cardiol; citation_title=Correlation of baseline plasminogen activator inhibitor activity with patency of the infarct artery after thrombolytic therapy in acute myocardial infarction; citation_author=GI Barbash, H Hod, A Roth, HI Miller, S Rath, Y Harzahav; citation_volume=64; citation_publication_date=1989; citation_pages=1231-1235; citation_doi=10.1016\u002F0002-9149(89)90559-6; citation_id=CR11\ncitation_journal_title=N Engl J Med; citation_title=Increased plasma levels of a rapid inhibitor of tissue plasminogen activator in young survivors of myocardial infarction; citation_author=A Hamsten, B Wiman, U Faire, M Blomback; citation_volume=313; citation_publication_date=1985; citation_pages=1557-1563; citation_id=CR12\ncitation_journal_title=Lancet; citation_title=Plasminogen activator inhibitor in plasma: risk factor for recurrent myocardial infarction; citation_author=A Hamsten, U Faire, G Walldius, G Dahlen, A Szamosi, C Landon; citation_volume=2; citation_publication_date=1987; citation_pages=3; citation_id=CR13\nNilsson JB, Boman K, Jansson JH, Nilsson T, Naslund U (2007) The influence of acute-phase levels of haemostatic factors on reperfusion and mortality in patients with acute myocardial infarction treated with streptokinase. J Thromb Thrombolysis. doi:\n                    10.1007\u002Fs11239-007-0086-9\n                    \n                  \n                        \ncitation_journal_title=Diabetologia; citation_title=Increased plasma plasminogen activator inhibitor-1 levels. 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G.",{"id":1976,"sortIndex":40,"researcher":28,"roles":1977,"affiliations":1978,"properties":1987,"displayName":1989,"givenName":28,"familyName":28},"aa41bec6-ecc8-4863-9bdd-c2a10918db77",[974],[1979],{"id":1980,"sortIndex":32,"affiliation":1981,"properties":28},"58022bd3-a494-438d-a867-50fa49be0cf0",{"id":1980,"createTime":28,"updateTime":28,"relativeEntities":1982,"slug":28,"properties":1983,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1986,"statistic":28},[],{"title":1984},{"VI":1985},"SUDA Clinic, Tokyo, Japan",[],{"title":1988},{"VI":1989},"Kitano, Yuri",{"id":1991,"sortIndex":123,"researcher":28,"roles":1992,"affiliations":1993,"properties":2002,"displayName":2004,"givenName":28,"familyName":28},"8e7f2dec-262a-4c4c-b8b7-05242afc7018",[974],[1994],{"id":1995,"sortIndex":32,"affiliation":1996,"properties":28},"035e4518-f87f-493f-b6b5-43256c39ae9d",{"id":1995,"createTime":28,"updateTime":28,"relativeEntities":1997,"slug":28,"properties":1998,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2001,"statistic":28},[],{"title":1999},{"VI":2000},"Department of Medicine, Lipid & Cardiovascular Risk Management Clinic, Imperial College, Hammersmith Hospital, London, UK",[],{"title":2003},{"VI":2004},"Neuwirth, Clare",{"id":2006,"sortIndex":42,"researcher":28,"roles":2007,"affiliations":2008,"properties":2017,"displayName":2019,"givenName":28,"familyName":28},"4c6276a1-fb8f-4960-bc6e-b4541ae10a0f",[974],[2009],{"id":2010,"sortIndex":32,"affiliation":2011,"properties":28},"70b38c67-ae51-4450-a839-e2c24bf2ed4e",{"id":2010,"createTime":28,"updateTime":28,"relativeEntities":2012,"slug":28,"properties":2013,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2016,"statistic":28},[],{"title":2014},{"VI":2015},"Department of Cardiology, Hammersmith Hospital London, London, UK",[],{"title":2018},{"VI":2019},"Davies, Graham J.",{"id":2021,"sortIndex":45,"researcher":28,"roles":2022,"affiliations":2023,"properties":2032,"displayName":2034,"givenName":28,"familyName":28},"36a81968-1164-41e6-942e-e164b0454e89",[974],[2024],{"id":2025,"sortIndex":32,"affiliation":2026,"properties":28},"99a1dfd9-71f5-4d27-8fa7-e2eda0e1e9dd",{"id":2025,"createTime":28,"updateTime":28,"relativeEntities":2027,"slug":28,"properties":2028,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2031,"statistic":28},[],{"title":2029},{"VI":2030},"Cardiothoracic & Vascular Department,  Univ. 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Gemelli”, Rome, Italy",[],{"title":2063},{"VI":2064},"Andreotti, Felicita",{"url":1957,"publisher":2066,"properties":2112},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":2067,"slug":872,"properties":2068,"entityType":25,"verifyStatus":880,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":2072,"manageAffiliations":2081,"indexDatabases":2092,"url":942,"thumbnailPath":28,"statistic":2107,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":2069,"title":2070,"eissn":2071},{"VOID":875},{"EN":877},{"VOID":879},[2073,2077],{"id":883,"createTime":28,"updateTime":28,"relativeEntities":2074,"label":2075,"description":2076,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":886},{},{"id":889,"createTime":28,"updateTime":28,"relativeEntities":2078,"label":2079,"description":2080,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":892},{},[2082,2087],{"id":896,"createTime":28,"updateTime":28,"relativeEntities":2083,"slug":28,"properties":2084,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2086,"statistic":28},[],{"title":2085},{"EN":900},[],{"id":903,"createTime":28,"updateTime":28,"relativeEntities":2088,"slug":28,"properties":2089,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2091,"statistic":28},[],{"title":2090},{"EN":907},[909],[2093,2100],{"id":912,"indexDatabase":2094,"url":918,"indexYears":919,"academicFieldIds":2099,"indexDatabaseRanking":923},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":2095,"label":2096,"description":2097,"key":781,"publicationTags":2098,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[921,922],{"id":925,"indexDatabase":2101,"url":937,"indexYears":28,"academicFieldIds":2106,"indexDatabaseRanking":28},{"id":927,"createTime":28,"updateTime":28,"relativeEntities":2102,"label":2103,"description":2104,"key":934,"publicationTags":2105,"standard":28},[],{"EN":930,"VI":930},{"EN":932,"VI":933},[936,813],[939,940,941],{"impactFactor":32,"impactFactorByYear":2108,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":358,"totalPublicationByYear":2109,"totalCitation":32,"totalCitationByYear":2110,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":2111,"hindexLast5Year":32,"hindex":32},{},{"1997":205,"1998":323,"1999":47,"2000":357,"2001":46,"2002":145,"2003":42,"2007":42,"2011":40,"2013":123,"2015":40,"2016":123,"2017":42,"2018":40,"2019":40,"2020":46,"2021":123,"2022":45},{},{},{"issue":2113,"pages":2115,"volume":2117},{"VOID":2114},"2",{"VOID":2116},"166-172",{"VOID":2118},"28","2009-08-01",2009,[936,923],{"id":2123,"createTime":2124,"updateTime":2125,"relativeEntities":2126,"slug":2127,"properties":2128,"entityType":967,"verifyStatus":26,"verifyTime":2125,"verifyNote":968,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":2137,"fullTextUrl":28,"authors":2138,"publicationType":1056,"publisherRelationship":2232,"citationCount":28,"citationInfo":28,"publishDate":2284,"publishYear":2285,"citationAnalyzeStatus":880,"lastCitationAnalyze":28,"indexDatabases":2286,"openAccess":28,"references":28,"isForceReanalyzing":1112},"01dd67be-fa6c-4042-ad1f-553dfaded6e7","2024-02-15T12:59:27.532+00:00","2025-02-13T11:58:23.361+00:00",[],"Effect-of-external-ultrasound-frequency-on-thrombus-disruption-in-vitro",{"abstract":2129,"title":2131,"references":2133,"doi":2135},{"EN":2130},"\nObjectives: This in vitro study assesses the effect of different external ultrasound frequencies on the disruption of human thrombi. Background: Ultrasound energy has been shown to disrupt human thrombi in vitro. However, there have been no previous studies to assess the effect of a range of different ultrasound frequencies on the rate and extent of thrombus disruption. Methods: In vitro, we exposed 56, 1- to 3-hour-old human blood thrombi to continuous wave ultra-sound (2.9 W\u002Fcm2) for 3 minutes. Seven different frequencies, ranging from 243 kHz to 25 kHz, were used. Results: There was a gradual increase in the total reduction of thrombus weight as well as the percent thrombus disruption with the use of lower ultrasound frequencies, reaching 99% at 25 kHz (p \u003C 0.001) and 86% (p \u003C 0.001) at 39 kHz, compared with 25% at 243 kHz. The average particle size of the disrupted thrombi was 3.26 μm (range 2.8–3.8). Conclusions: Our in vitro data with external ultrasound show that for a given power intensity of ultrasound, the extent and magnitude of thrombus disruption is progressively increased as frequencies decrease from 243 to 25 kHz. This might be related to the fact that larger acoustic bubbles are induced by lower frequency ultrasound, which gives rise to greater mechanical energy for thrombus disruption during bubble vibration and their collapse.",{"EN":2132},"Effect of external ultrasound frequency on thrombus disruption in vitro",{"VOID":2134},"Hong AS, Chae JS, Dubin SB, Lee S, Fishbein MC, Siegel RJ. Ultrasonic clot disruption: An in vitro study. Am Heart J 1990;120:418–422.\nAriani M, Fishbein MC, Chae JS, et al. Dissolution of peripheral arterial thrombi by ultrasound. Circulation 1991; 84:1680–1688.\nSteffen W, Fishbein MC, Luo H, et al. High intensity, low frequency catheter-delivered ultrasound dissolution of occlusive coronary artery thrombi: An in vitro and in vivo study. J Am Coll Cardiol 1994;24:1571–1579.\nHamm CW, Reimers J, Koster R, et al. Coronary ultra-sound thrombosis in a patient with acute myocardial infarction. Lancet 1994;343:605–606.\nLuo H, Steffen W, Cercek B, Arunasalam S, Maurer G, Siegel RJ. Enhancement of thrombolysis by external ultrasound. Am Heart J 1993;125:1564–1569.\nSehgal CM, Leveen RF, Shlansky-Goldberg RD. Ultra-sound-assisted thrombolysis.Invest Radiol 1993;28:39–943.\nHarpaz D, Chen X, Francis CW, et al. Ultrasound enhancement of thrombolysis and reperfusion in vitro. J Am Coll Cardiol 1993;21:1507–1511.\nOlsson SB, Johansson B, Nilsson AM, et al. Enhancement of thrombolysis by ultrasound. Ultrasound Med Biol 1994;20:375–382.\nSteffen W, Siegel RJ. Ultrasound angioplasty. J Intervent Cardiol 1993;1:77–88.\nGoldman DE, Lepeschkin WW. Injury to living cells in standing sound waves. J Cell Comp Physiol 1952;40: 255–268.\nAlliger H. Ultrasound disruption. Am Lab 1975;7:75–85.\nKornowski S, Melzer RS, Chernine A, Vered Z, Battler A. Does external ultrasound accelerate thrombolysis? Results from a rabbit model. Circulation 1994;89:3339–3344.\nYoshizawa S. Ultrasound irradiation method for prevention of acute reocclusion after thrombolysis. Tokyo Jikeikai Med J 1992;107:265–274.",{"VOID":2136},"10.1007\u002FBF00226413","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF00226413",[2139,2154,2167,2180,2193,2206,2219],{"id":2140,"sortIndex":32,"researcher":28,"roles":2141,"affiliations":2142,"properties":2151,"displayName":2153,"givenName":28,"familyName":28},"58e0362d-bcf0-44d5-a837-3ab321534d8f",[974],[2143],{"id":2144,"sortIndex":32,"affiliation":2145,"properties":28},"5e0958fc-3bd2-4bd4-b39b-5c8f430b732b",{"id":2144,"createTime":28,"updateTime":28,"relativeEntities":2146,"slug":28,"properties":2147,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2150,"statistic":28},[],{"title":2148},{"VI":2149},"Division of Cardiology, Cedars-Sinai Medical Center, Los Angeles, USA",[],{"title":2152},{"VI":2153},"Huai Luo",{"id":2155,"sortIndex":40,"researcher":28,"roles":2156,"affiliations":2157,"properties":2164,"displayName":2166,"givenName":28,"familyName":28},"98c81a1b-996f-4794-9d67-0b61cefec6b6",[974],[2158],{"id":2144,"sortIndex":32,"affiliation":2159,"properties":28},{"id":2144,"createTime":28,"updateTime":28,"relativeEntities":2160,"slug":28,"properties":2161,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2163,"statistic":28},[],{"title":2162},{"VI":2149},[],{"title":2165},{"VI":2166},"Toshihiko Nishioka",{"id":2168,"sortIndex":123,"researcher":28,"roles":2169,"affiliations":2170,"properties":2177,"displayName":2179,"givenName":28,"familyName":28},"327dca1e-acd9-4426-a9dd-e0bc9bad72ed",[974],[2171],{"id":2144,"sortIndex":32,"affiliation":2172,"properties":28},{"id":2144,"createTime":28,"updateTime":28,"relativeEntities":2173,"slug":28,"properties":2174,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2176,"statistic":28},[],{"title":2175},{"VI":2149},[],{"title":2178},{"VI":2179},"Hans Berglund",{"id":2181,"sortIndex":42,"researcher":28,"roles":2182,"affiliations":2183,"properties":2190,"displayName":2192,"givenName":28,"familyName":28},"a06b26cc-c28b-476c-976e-2d66ddfce1a0",[974],[2184],{"id":2144,"sortIndex":32,"affiliation":2185,"properties":28},{"id":2144,"createTime":28,"updateTime":28,"relativeEntities":2186,"slug":28,"properties":2187,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2189,"statistic":28},[],{"title":2188},{"VI":2149},[],{"title":2191},{"VI":2192},"Chong-Jin Kim",{"id":2194,"sortIndex":45,"researcher":28,"roles":2195,"affiliations":2196,"properties":2203,"displayName":2205,"givenName":28,"familyName":28},"e1e4be0f-841d-4f2f-a82c-fd4f4e10a680",[974],[2197],{"id":2144,"sortIndex":32,"affiliation":2198,"properties":28},{"id":2144,"createTime":28,"updateTime":28,"relativeEntities":2199,"slug":28,"properties":2200,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2202,"statistic":28},[],{"title":2201},{"VI":2149},[],{"title":2204},{"VI":2205},"Michele Carbone",{"id":2207,"sortIndex":46,"researcher":28,"roles":2208,"affiliations":2209,"properties":2216,"displayName":2218,"givenName":28,"familyName":28},"01ef978b-ca03-42d5-bd08-76f54bb1a795",[974],[2210],{"id":2144,"sortIndex":32,"affiliation":2211,"properties":28},{"id":2144,"createTime":28,"updateTime":28,"relativeEntities":2212,"slug":28,"properties":2213,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2215,"statistic":28},[],{"title":2214},{"VI":2149},[],{"title":2217},{"VI":2218},"Bojan Cercek",{"id":2220,"sortIndex":48,"researcher":28,"roles":2221,"affiliations":2222,"properties":2229,"displayName":2231,"givenName":28,"familyName":28},"52d2a7ba-f756-4ceb-959c-8e69f7385fb1",[974],[2223],{"id":2144,"sortIndex":32,"affiliation":2224,"properties":28},{"id":2144,"createTime":28,"updateTime":28,"relativeEntities":2225,"slug":28,"properties":2226,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2228,"statistic":28},[],{"title":2227},{"VI":2149},[],{"title":2230},{"VI":2231},"Robert J. 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Currently used risk score base only on scarce clinical data and do not take into consideration parameters including echocardiographic findings. The aim of this study was to evaluate if left atrium (LA) enlargement is associated with higher thromboembolic risk assessed by CHADS2 and CHA2DS2-VASc scores in a cohort of unselected non-valvular AF patients. Data from 582 AF hospitalizations occurring between November 2012 and January 2014 were analyzed. All patients underwent a standard transthoracic echocardiography and had their thromboembolic risk assessed in both CHADS2 and CHA2DS2-VASc scores. In 494 enrolled patients (48.5 % male; mean age 73.4 ± 11.5 years) AF was classified as paroxysmal in 233 (47.3 %), as persistent in 109 (22.1 %), and as permanent in 151 (30.6 %) patients. LA was enlarged in 426 (86.2 %) patients. Enlargement was classified as mild in 99 (20.0 %) patients, as moderate in 130 (26.3 %) patients, and as severe in 196 (39.7 %) patients. Patients with enlarged LA had higher mean CHADS2 score (2.0 ± 1.5 vs. 2.6 ± 1.3; p = 0.0005) and CHA2DS2-VASc (3.8 ± 2.0 vs. 4.4 ± 1.8; p = 0.02) score than patients with normal LA. The both mean scores rose along with rising LA diameter. LA enlargement is highly prevalent in AF patients. Higher thromboembolic risk assessed by both CHADS2 and CHA2DS2-VASc scores is associated with presence of LA enlargement. Echocardiographically assessed LA size may be an additional parameter useful in thromboembolic risk stratification of AF patients.",{"EN":2297},"Association of the CHADS2 and CHA2DS2-VASc scores with left atrial enlargement: a prospective cohort study of unselected atrial fibrillation patients",{"VOID":2299},"Kirchhof P, Auricchio A, Bax J et al (2005) Outcome parameters for trials in atrial fibrillation: executive summary. Recommendations from a consensus conference organized by the German Atrial Fibrillation Competence NETwork (AFNET) and the European Heart Rhythm Association (EHRA). Eur Heart J 28:2803–2817\nCamm AJ, Kirchhof P, Lip GY, European Heart Rhythm Association, European Association for Cardio-Thoracic Surgery et al (2010) Guidelines for the management of atrial fibrillation: the Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology (ESC). Eur Heart J 31:2369–2429\nCamm AJ, Lip GY, De Caterina R, ESC Committee for Practice Guidelines (CPG) et al (2012) 2012 focused update of the ESC Guidelines for the management of atrial fibrillation: an update of the 2010 ESC Guidelines for the management of atrial fibrillation. Developed with the special contribution of the European Heart Rhythm Association. Eur Heart J 33:2719–2747\nGage BF, Waterman AD, Shannon W et al (2001) Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA 285:2864–2870\nLip GY, Nieuwlaat R, Pisters R et al (2010) 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 137:263–272\nSzymanski FM, Filipiak KJ, Platek AE et al (2014) Assessment of CHADS2 and CHA 2DS 2-VASc scores in obstructive sleep apnea patients with atrial fibrillation. Sleep Breath. doi:10.1007\u002Fs11325-014-1042-5\nThe Stroke Prevention in Atrial Fibrillation Investigators (1992) Predictors of thromboembolism in atrial fibrillation: II. Echocardiographic features of patients at risk. The Stroke Prevention in Atrial Fibrillation Investigators. Ann Intern Med 116:6–12\nLee JM, Shim J, Uhm JS et al (2014) Impact of increased orifice size and decreased flow velocity of left atrial appendage on stroke in nonvalvular atrial fibrillation. Am J Cardiol 113:963–969\nKiliszek M, Miązek N, Peller M et al (2014) Influence of left atrial size on outcome of pulmonary vein isolation in patients with atrial fibrillation. Kardiol Pol 72:1135–1140\nLemola K, Sneider M, Desjardins B et al (2004) Effects of left atrial ablation of atrial fibrillation on size of the left atrium and pulmonary veins. Heart Rhythm 1:576–581\nLang RM, Bierig M, Devereux RB, American Society of Echocardiography’s Nomenclature and Standards Committee, Task Force on Chamber Quantification, American College of Cardiology Echocardiography Committee, American Heart Association, European Association of Echocardiography, European Society of Cardiology et al (2006) Recommendations for chamber quantification. Eur J Echocardiogr 7:79–108\nRudski LG, Lai WW, Afilalo J et al (2010) Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr 23:685–713\nKopeć G, Sobień B, Podolec M et al (2014) The prevalence of abnormal echocardiographic findings in a sample of urban adult population. Kardiol Pol 72:42–49\nLazoura O, Reddy T, Shriharan M et al (2012) Prevalence of left atrial anatomical abnormalities in patients with recurrent atrial fibrillation compared with patients in sinus rhythm using multi-slice CT. J Cardiovasc Comput Tomogr 6:268–273\nAndersen JS, Egeblad H, Abildgaard U et al (1991) Atrial fibrillation and left atrial enlargement: cause or effect? J Intern Med 229:253–256\nParkash R, Green MS, Kerr CR, Canadian Registry of Atrial Fibrillation et al (2004) The association of left atrial size and occurrence of atrial fibrillation: a prospective cohort study from the Canadian Registry of Atrial Fibrillation. Am Heart J 148:649–654\nCasaclang-Verzosa G, Gersh BJ, Tsang TS (2008) Structural and functional remodeling of the left atrium: clinical and therapeutic implications for atrial fibrillation. J Am Coll Cardiol 51:1–11\nDittrich HC, Pearce LA, Asinger RW et al (1999) Left atrial diameter in nonvalvular atrial fibrillation: an echocardiographic study. Stroke Prevention in Atrial Fibrillation Investigators. Am Heart J 137:494–499\nZhuang J, Wang Y, Tang K et al (2012) Association between left atrial size and atrial fibrillation recurrence after single circumferential pulmonary vein isolation: a systematic review and meta-analysis of observational studies. Europace 14:638–645\nKizer JR, Bella JN, Palmieri V et al (2006) Left atrial diameter as an independent predictor of first clinical cardiovascular events in middle-aged and elderly adults: the Strong Heart Study (SHS). Am Heart J 151:412–418\nScherr D, Dalal D, Chilukuri K et al (2009) Incidence and predictors of left atrial thrombus prior to catheter ablation of atrial fibrillation. J Cardiovasc Electrophysiol 20:379–384\nOlshansky B, Heller EN, Mitchell LB et al (2005) Are transthoracic echocardiographic parameters associated with atrial fibrillation recurrence or stroke? Results from the Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) study. J Am Coll Cardiol 45:2026–2033\nShin HY, Jeong IH, Kang CK et al (2013) Relation between left atrial enlargement and stroke subtypes in acute ischemic stroke patients. J Cerebrovasc Endovasc Neurosurg 15:131–136\nLip GY, Frison L, Halperin JL et al (2010) Identifying patients at high risk for stroke despite anticoagulation: a comparison of contemporary stroke risk stratification schemes in an anticoagulated atrial fibrillation cohort. Stroke 41:2731–2738\nSaliba W, Rennert G (2014) CHA2DS2-VASc score is directly associated with the risk of pulmonary embolism in patients with atrial fibrillation. Am J Med 127:45–52\nCetin M, Cakici M, Zencir C et al (2013) Prediction of coronary artery disease severity using CHADS2 and CHA2DS2-VASc scores and a newly defined CHA2DS2-VASc-HS score. Am J Cardiol 113:950–956\nWelles CC, Whooley MA, Na B et al (2011) The CHADS2 score predicts ischemic stroke in the absence of atrial fibrillation among subjects with coronary heart disease: data from the Heart and Soul Study. Am Heart J 162:555–561\nWillens HJ, Gómez-Marín O, Nelson K et al (2013) Correlation of CHADS2 and CHA2DS2-VASc scores with transesophageal echocardiography risk factors for thromboembolism in a multiethnic United States population with nonvalvular atrial fibrillation. J Am Soc Echocardiogr 26:175–184\nPuwanant S, Varr BC, Shrestha K et al (2009) Role of the CHADS2 score in the evaluation of thromboembolic risk in patients with atrial fibrillation undergoing transesophageal echocardiography before pulmonary vein isolation. J Am Coll Cardiol 54:2032–2039\nKleemann T, Becker T, Strauss M et al (2009) Prevalence and clinical impact of left atrial thrombus and dense spontaneous echo contrast in patients with atrial fibrillation and low CHADS2 score. Eur J Echocardiogr 10:383–388\nLip GY, Laroche C, Dan GA et al (2014) A prospective survey in European Society of Cardiology member countries of atrial fibrillation management: baseline results of EURObservational Research Programme Atrial Fibrillation (EORP-AF) Pilot General Registry. Europace 16:308–319\nDerezinski T, Wasikowska B, Strzebonski B et al (2013) Outpatient oral anticoagulation in Poland in 2012: a single centre experience. Kardiol Pol 71:1135–1139\nSimpson E, Stevenson M, Scope A, Poku E, Minton J, Evans P (2013) Echocardiography in newly diagnosed atrial fibrillation patients: a systematic review and economic evaluation. Health Technol Assess 17:1–263\nFaustino A, Providência R, Barra S et al (2014) Which method of left atrium size quantification is the most accurate to recognize thromboembolic risk in patients with non-valvular atrial fibrillation? 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