Journal of the American Heart Association

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Association Between Social Vulnerability Index and Cardiovascular Disease: A Behavioral Risk Factor Surveillance System Study
Journal of the American Heart Association - Tập 11 Số 15 - 2022
Vardhmaan Jain, Mahmoud Al Rifai, Safi U. Khan, Ankur Kalra, Fátima Rodríguez, Zainab Samad, Yashashwi Pokharel, Arunima Misra, Laurence S. Sperling, Jamal S. Rana, Waqas Ullah, Ankit Medhekar, Salim S. Virani
Background Social and environmental factors play an important role in the rising health care burden of cardiovascular disease. The Centers for Disease Control and Prevention developed the Social Vulnerability Index (SVI) from US census data as a tool for public health officials to identify communities in need of support in the setting of a hazardous event. SVI (ranging from a least vulnerable score of 0 to a most vulnerable score of 1) ranks communities on 15 social factors including unemployment, minoritized groups status, and disability, and groups them under 4 broad themes: socioeconomic status, housing and transportation, minoritized groups, and household composition. We sought to assess the association of SVI with self‐reported prevalent cardiovascular comorbidities and atherosclerotic cardiovascular disease (ASCVD).

Methods and Results We performed a retrospective cohort analysis of adults (≥18 years) in the Behavioral Risk Factor Surveillance System 2016 to 2019. Data regarding self‐reported prevalent cardiovascular comorbidities (including diabetes, hypertension, hyperlipidemia, smoking, substance use), and ASCVD was captured using participants' response to a structured telephonic interview. We divided states on the basis of the tertile of SVI (first—participant lives in the least vulnerable group of states, 0–0.32; to third—participant lives in the most vulnerable group of states, 0.54–1.0). Multivariable logistic regression models adjusting for age, race and ethnicity, sex, employment, income, health care coverage, and association with federal poverty line were constructed to assess the association of SVI with cardiovascular comorbidities. Our study sample consisted of 1 745 999 participants ≥18 years of age. States in the highest (third) tertile of social vulnerability had predominantly Black and Hispanic adults, lower levels of education, lower income, higher rates of unemployment, and higher rates of prevalent comorbidities including hypertension, diabetes, chronic kidney disease, hyperlipidemia, substance use, and ASCVD. In multivariable logistic regression models, individuals living in states in the third tertile of SVI had higher odds of having hypertension (odds ratio (OR), 1.14 [95% CI, 1.11–1.17]), diabetes (OR, 1.12 [95% CI, 1.09–1.15]), hyperlipidemia (OR, 1.09 [95% CI, 1.06–1.12]), chronic kidney disease (OR, 1.17 [95% CI, 1.12–1.23]), smoking (OR, 1.05 [95% CI, 1.03–1.07]), and ASCVD (OR, 1.15 [95% CI, 1.12–1.19]), compared with those living in the first tertile of SVI.

Conclusions SVI varies across the US states and is associated with prevalent cardiovascular comorbidities and ASCVD, independent of age, race and ethnicity, sex, employment, income, and health care coverage. SVI may be a useful assessment tool for health policy makers and health systems researchers examining multilevel influences on cardiovascular‐related health behaviors and identifying communities for targeted interventions pertaining to social determinants of health.

Nuclear Activation Function 2 Estrogen Receptor α Attenuates Arterial and Renal Alterations Due to Aging and Hypertension in Female Mice
Journal of the American Heart Association - Tập 9 Số 5 - 2020
E. Guivarch, Julie Favre, Anne‐Laure Guihot, Emilie Vessières, Linda Grimaud, C Proux, J Rivron, Agnès Barbelivien, Céline Fassot, Marie Briet, Françoise Lenfant, Coralie Fontaine, Laurent Loufrani, Jean‐François Arnal, Daniel Henrion
Background The cardiovascular protective effects of estrogens in premenopausal women depend mainly on estrogen receptor α (ERα). ERα activates nuclear gene transcription regulation and membrane‐initiated signaling. The latter plays a key role in estrogen‐dependent activation of endothelial NO synthase. The goal of the present work was to determine the respective roles of the 2 ERα activities in endothelial function and cardiac and kidney damage in young and old female mice with hypertension, which is a major risk factor in postmenopausal women.

Methods and Results Five‐ and 18‐month‐old female mice lacking either ERα (ERα −/− ), the nuclear activating function AF2 of ERα (AF2°), or membrane‐located ERα (C451A) were treated with angiotensin II (0.5 mg/kg per day) for 1 month. Systolic blood pressure, left ventricle weight, vascular reactivity, and kidney function were then assessed. Angiotensin II increased systolic blood pressure, ventricle weight, and vascular contractility in ERα −/− and AF2° mice more than in wild‐type and C451A mice, independent of age. In both the aorta and mesenteric resistance arteries, angiotensin II and aging reduced endothelium‐dependent relaxation in all groups, but this effect was more pronounced in ERα −/− and AF2° than in the wild‐type and C451A mice. Kidney inflammation and oxidative stress, as well as blood urea and creatinine levels, were also more pronounced in old hypertensive ERα −/− and AF2° than in old hypertensive wild‐type and C451A mice.

Conclusions The nuclear ERα‐AF2 dependent function attenuates angiotensin II–dependent hypertension and protects target organs in aging mice, whereas membrane ERα signaling does not seem to play a role.

Sustained Captopril‐Induced Reduction in Blood Pressure Is Associated With Alterations in Gut‐Brain Axis in the Spontaneously Hypertensive Rat
Journal of the American Heart Association - Tập 8 Số 4 - 2019
Tao Yang, Victor Aquino, Gilberto O. Lobaton, Hong‐Bao Li, Luis M. Colon‐Perez, Ruby Goel, Yanfei Qi, Jasenka Zubcevic, Marcelo Febo, Elaine M. Richards, Carl J. Pepine, Mohan K. Raizada
Background We have demonstrated that the antihypertensive effect of the angiotensin‐converting enzyme inhibitor, captopril ( CAP ), is associated with beneficial effects on gut pathology. Coupled with the evidence that CAP exerts prolonged reduction in blood pressure ( BP ) after discontinuation of treatment, we investigate whether persistent beneficial actions of CAP are linked to alterations of gut microbiota and improvement of hypertension‐induced gut pathology.

Methods and Results Spontaneously hypertensive rats ( SHR ) and Wistar Kyoto rats were treated with CAP (250 mg/kg/day) for 4 weeks followed by withdrawal for 16 weeks. Gut microbiota, gut pathology, BP, and brain neuronal activity were assessed. CAP resulted in a ≈60 mm Hg decrease in systolic BP after 3 weeks of treatment in SHR , and the decrease remained significant at least 5 weeks after CAP withdrawal. In contrast, CAP caused modest decrease in systolic BP in Wistar Kyoto. 16S rRNA gene‐sequencing–based gut microbial analyses in SHR showed sustained alteration of gut microbiota and increase in Allobaculum after CAP withdrawal. Phylogenetic investigation of communities by reconstruction of unobserved states analysis revealed significant increase in bacterial sporulation upon CAP treatment in SHR . These were associated with persistent improvement in gut pathology and permeability. Furthermore, manganese‐enhanced magnetic resonance imaging showed significantly decreased neuronal activity in the posterior pituitary of SHR 4 weeks after withdrawal.

Conclusions Decreased BP , altered gut microbiota, improved gut pathology and permeability, and dampened posterior pituitary neuronal activity were maintained after CAP withdrawal in the SHR . They suggest that CAP influences the brain‐gut axis to maintain the sustained antihypertensive effect of CAP after withdrawal.

Risk Profiles for Aortic Dissection and Ruptured or Surgically Treated Aneurysms: A Prospective Cohort Study
Journal of the American Heart Association - Tập 4 Số 1 - 2015
Maya Landenhed, Gunnar Engström, Anders Gottsäter, Michael P. Caulfield, Bo Hedblad, Christopher Newton‐Cheh, Olle Melander, J. G. Smith
Background Community screening to guide preventive interventions for acute aortic disease has been recommended in high‐risk individuals. We sought to prospectively assess risk factors in the general population for aortic dissection ( AD ) and severe aneurysmal disease in the thoracic and abdominal aorta.

Methods and Results We studied the incidence of AD and ruptured or surgically treated aneurysms in the abdominal ( AAA ) or thoracic aorta ( TAA ) in 30 412 individuals without diagnosis of aortic disease at baseline from a contemporary, prospective cohort of middle‐aged individuals, the Malmö Diet and Cancer study. During up to 20 years of follow‐up (median 16 years), the incidence rate per 100 000 patient‐years at risk was 15 (95% CI 11.7 to 18.9) for AD , 27 (95% CI 22.5 to 32.1) for AAA , and 9 (95% CI 6.8 to 12.6) for TAA . The acute and in‐hospital mortality was 39% for AD , 34% for ruptured AAA , and 41% for ruptured TAA . Hypertension was present in 86% of individuals who subsequently developed AD , was strongly associated with incident AD (hazard ratio [ HR ] 2.64, 95% CI 1.33 to 5.25), and conferred a population‐attributable risk of 54%. Hypertension was also a risk factor for AAA with a smaller effect. Smoking ( HR 5.07, 95% CI 3.52 to 7.29) and high apolipoprotein B/A1 ratio ( HR 2.48, 95% CI 1.73 to 3.54) were strongly associated with AAA and conferred a population‐attributable risk of 47% and 25%, respectively. Smoking was also a risk factor for AD and TAA with smaller effects.

Conclusions This large prospective study identified distinct risk factor profiles for different aortic diseases in the general population. Hypertension accounted for more than half of the population risk for AD , and smoking for half of the population risk of  AAA .

Reduced Long‐Term Risk of Aortic Aneurysm and Aortic Dissection Among Individuals With Type 2 Diabetes Mellitus: A Nationwide Observational Study
Journal of the American Heart Association - Tập 7 Số 3 - 2018
Tarik Avdic, Stefan Franzén, Moncef Zarrouk, Stefan Acosta, Peter M. Nilsson, Anders Gottsäter, Ann‐Marie Svensson, Soffia Guðbjörnsdóttir, Björn Eliasson
Background No studies have examined long‐term risks for aortic aneurysm ( AA ) and aortic dissection ( AD ) or mortality after AA or AD hospitalization among patients with type 2 diabetes mellitus (T2 DM ).

Methods and Results In this observational cohort study, we linked data for patients with T2 DM in the Swedish National Diabetes Register, and 5 individually matched population‐based control subjects ( CSs ) without diabetes mellitus (on the basis of sex, age, and county), to other national databases to capture hospitalizations and death. We examined the risk of hospitalization for AA and AD , as well as mortality risk after AA and AD using Kaplan‐Meier curves and Cox regression hazards models. Data on 448 319 patients with T2DM and 2 251 015 CSs were obtained between 1998 and 2015. Mean follow‐up time was 7.0 years for the T2 DM group and 7.2 years for the CS group. Patients with T2 DM had a relative risk reduction of 28% (hazard ratio, 0.72; 95% confidence interval, 0.68–0.76; P <0.0001) for AA and a 47% relative risk reduction (hazard ratio, 0.53; 95% confidence interval, 0.42–0.65; P <0.0001) for AD compared with CSs . Patients with T2DM had a relative risk reduction of 12% (hazard ratio, 0.88; 95% confidence interval, 0.82–0.94; P <0.0001) for mortality after hospitalization for AA , and unaltered risk (hazard ratio, 1.07; 95% confidence interval, 0.85–1.34; P =0.5859) for mortality after AD , up to 2 years compared with CSs .

Conclusions Patients with T2DM had significantly reduced risks of AA and AD as well as reduced risk of mortality after hospitalization for AA, compared to CS . Data suggest that glycated cross‐links in aortic tissue may play a protective role in the progression of aortic diseases among patients with T2DM.

MicroRNA‐33 Deficiency Reduces the Progression of Atherosclerotic Plaque in ApoE −/− Mice
Journal of the American Heart Association - Tập 1 Số 6 - 2012
Takahiro Horie, Osamu Baba, Yasuhide Kuwabara, Yoshimasa Chujo, Shin Watanabe, Minako Kinoshita, Masahito Horiguchi, Tomoyuki Nakamura, Kazuhisa Chonabayashi, Masakatsu Hishizawa, Koji Hasegawa, Noriaki Kume, Masayuki Yokode, Toru Kita, Takeshi Kimura, Koh Ono
Background Cholesterol efflux from cells to apolipoprotein A‐I (apoA‐I) acceptors via the ATP ‐binding cassette transporters ABCA 1 and ABCG 1 is thought to be central in the antiatherogenic mechanism. Micro RNA (miR)‐33 is known to target ABCA 1 and ABCG 1 in vivo.

Methods and Results We assessed the impact of the genetic loss of miR‐33 in a mouse model of atherosclerosis. MiR‐33 and apoE double‐knockout mice (miR‐33 −/− Apoe −/− ) showed an increase in circulating HDL‐C levels with enhanced cholesterol efflux capacity compared with miR‐33 +/+ Apoe −/− mice. Peritoneal macrophages from miR‐33 −/− Apoe −/− mice showed enhanced cholesterol efflux to apoA‐I and HDL‐C compared with miR‐33 +/+ Apoe −/− macrophages. Consistent with these results, miR‐33 −/− Apoe −/− mice showed reductions in plaque size and lipid content. To elucidate the roles of miR‐33 in blood cells, bone marrow transplantation was performed in these mice. Mice transplanted with miR‐33 −/− Apoe −/− bone marrow showed a significant reduction in lipid content in atherosclerotic plaque compared with mice transplanted with miR‐33 +/+ Apoe −/− bone marrow, without an elevation of HDL‐C . Some of the validated targets of miR‐33 such as RIP 140 ( NRIP 1) and CROT were upregulated in miR‐33 −/− Apoe −/− mice compared with miR‐33 +/+ Apoe −/− mice, whereas CPT 1a and AMPK α were not.

Conclusions These data demonstrate that miR‐33 deficiency serves to raise HDL‐C , increase cholesterol efflux from macrophages via ABCA 1 and ABCG 1, and prevent the progression of atherosclerosis. Many genes are altered in miR‐33‐deficient mice, and detailed experiments are required to establish miR‐33 targeting therapy in humans.

Simple Risk Model Predicts Incidence of Atrial Fibrillation in a Racially and Geographically Diverse Population: the CHARGE‐AF Consortium
Journal of the American Heart Association - Tập 2 Số 2 - 2013
Álvaro Alonso, Bouwe P. Krijthe, Thor Aspelund, Katherine A. Stepas, Michael Pencina, Carlee Moser, Moritz F. Sinner, Nona Sotoodehnia, João D. Fontes, A. Cecile J.W. Janssens, Richard A. Kronmal, Jared W. Magnani, Jacqueline C.M. Witteman, Alanna M. Chamberlain, Steven A. Lubitz, Renate B. Schnabel, Sunil Agarwal, David D. McManus, Patrick T. Ellinor, Martin G. Larson, Gregory L. Burke, Lenore J. Launer, Albert Hofman, Daniel Levy, John S. Gottdiener, Stefan Kääb, David Couper, Tamara B. Harris, Elsayed Z. Soliman, Bruno H. Stricker, Vilmundur Guðnason, Susan R. Heckbert, Emelia J. Benjamin
Background Tools for the prediction of atrial fibrillation ( AF ) may identify high‐risk individuals more likely to benefit from preventive interventions and serve as a benchmark to test novel putative risk factors.

Methods and Results Individual‐level data from 3 large cohorts in the U nited S tates (Atherosclerosis Risk in Communities [ ARIC ] study, the Cardiovascular Health Study [ CHS ], and the Framingham Heart Study [ FHS ]), including 18 556 men and women aged 46 to 94 years (19% A frican A mericans, 81% whites) were pooled to derive predictive models for AF using clinical variables. Validation of the derived models was performed in 7672 participants from the Age, Gene and Environment—Reykjavik study ( AGES ) and the Rotterdam Study ( RS ). The analysis included 1186 incident AF cases in the derivation cohorts and 585 in the validation cohorts. A simple 5‐year predictive model including the variables age, race, height, weight, systolic and diastolic blood pressure, current smoking, use of antihypertensive medication, diabetes, and history of myocardial infarction and heart failure had good discrimination (C‐statistic, 0.765; 95% CI , 0.748 to 0.781). Addition of variables from the electrocardiogram did not improve the overall model discrimination (C‐statistic, 0.767; 95% CI , 0.750 to 0.783; categorical net reclassification improvement, −0.0032; 95% CI , −0.0178 to 0.0113). In the validation cohorts, discrimination was acceptable ( AGES C‐statistic, 0.664; 95% CI , 0.632 to 0.697 and RS C‐statistic, 0.705; 95% CI , 0.664 to 0.747) and calibration was adequate.

Conclusion A risk model including variables readily available in primary care settings adequately predicted AF in diverse populations from the U nited S tates and E urope.

Impact of Complications During Transfemoral Transcatheter Aortic Valve Replacement: How Can They Be Avoided and Managed?
Journal of the American Heart Association - Tập 8 Số 18 - 2019
Roberto Scarsini, Giovanni Luigi De Maria, Jubin Joseph, Lampson M. Fan, Thomas J. Cahill, Rafail A. Kotronias, Francesco Burzotta, James D. Newton, Rajesh Kharbanda, Bernard Prendergast, Flavio Ribichini, Adrian Banning
Heart Rhythm Monitoring Strategies for Cryptogenic Stroke: 2015 Diagnostics and Monitoring Stroke Focus Group Report
Journal of the American Heart Association - Tập 5 Số 3 - 2016
Gregory W. Albers, Richard A. Bernstein, Johannes Brachmann, A. John Camm, J. Donald Easton, Peter Fromm, Shinya Goto, Christopher B. Granger, Stefan H. Hohnloser, Elaine M. Hylek, Amir K. Jaffer, Derk Krieger, Rod Passman, Jesse M. Pines, Shelby D. Reed, Peter M. Rothwell, Peter R. Kowey
Fibroblast Growth Factor‐23 and Incident Coronary Heart Disease, Heart Failure, and Cardiovascular Mortality: The Atherosclerosis Risk In Communities Study
Journal of the American Heart Association - Tập 3 Số 3 - 2014
Pamela L. Lutsey, Álvaro Alonso, Elizabeth Selvin, James S. Pankow, Erin D. Michos, Sunil Agarwal, Laura R. Loehr, John H. Eckfeldt, Josef Coresh
Background Fibroblast growth factor‐23 ( FGF ‐23) is a hormone involved in phosphorous regulation and vitamin D metabolism that may be associated with cardiovascular risk, and it is a potential target for intervention. We tested whether elevated FGF ‐23 is associated with incident coronary heart disease, heart failure, and cardiovascular mortality, even at normal kidney function.

Methods and Results A total of 11 638 Atherosclerosis Risk In Communities study participants, median age 57 at baseline (1990–1992), were followed through 2010. Cox regression was used to evaluate the independent association of baseline serum active FGF‐23 with incident outcomes. Models were adjusted for traditional cardiovascular risk factors and estimated glomerular filtration rate. During a median follow‐up of 18.6 years, 1125 participants developed coronary heart disease, 1515 developed heart failure, and 802 died of cardiovascular causes. For all 3 outcomes, there was a threshold, whereby FGF‐23 was not associated with risk at <40 pg/mL but was positively associated with risk at >40 pg/mL. Compared with those with FGF‐23 <40 pg/mL, those in the highest FGF‐23 category (≥58.8 pg/mL) had a higher risk of incident coronary heart disease (adjusted hazard ratio, 95% CIs: 1.65, 1.40 to 1.94), heart failure (1.75, 1.52 to 2.01), and cardiovascular mortality (1.65, 1.36 to 2.01). Associations were modestly attenuated but remained statistically significant after further adjustment for estimated glomerular filtration rate. In stratified analyses, similar results were observed in African Americans and among persons with normal kidney function.

Conclusions High levels of serum FGF ‐23 were associated with increased risk of coronary heart disease, heart failure, and cardiovascular mortality in this large, biracial, population‐based cohort. This association was independent of traditional cardiovascular risk factors and kidney function.

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