{"title":"Coronary microvascular dysfunction, arrythmias, and sudden cardiac death: A literature review","authors":"Razan Dankar, Jad Wehbi, Mohamad Montaser Atasi, Samir Alam, Marwan M. Refaat","doi":"10.1016/j.ahjo.2024.100389","DOIUrl":"https://doi.org/10.1016/j.ahjo.2024.100389","url":null,"abstract":"<div><p>The coronary vascular system has a unique structure and function that is adaptive to myocardial demand. It is composed of a continuous network of vessels receding in size from epicardial arteries to the microvascular circulation. Failure to meet myocardial demand results in ischemia, angina, and adverse myocardial outcomes. It is evident that 50 % of patients with angina have a non-obstructive coronary disease and 66 % of these patients have coronary microvascular dysfunction (CMD). The impact of CMD on the atria and ventricles is exhibited through its association with atrial fibrillation and distortion of ventricular repolarization. Ultimately, this influence increases the risk of mortality, morbidity, and sudden cardiac arrest. CMD serves as an independent risk for atrial fibrillation, increases ventricular electrical inhomogeneity, and contributes to the progression of cardiac disease. The underlying pathogenesis may be attributed to oxidative stress evident through reactive oxygen species, impaired vasoactive function, and structural disorders such as fibrotic changes. Myocardial ischemia, brought about by a demand-supply mismatch in CMD, may create a milieu for ventricular arrythmia and sudden cardiac arrest through distortion of ventricular repolarization parameters such as QT dispersion and corrected QT dispersion.</p></div>","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"41 ","pages":"Article 100389"},"PeriodicalIF":0.0,"publicationDate":"2024-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666602224000326/pdfft?md5=91f030183b75bbf5d9b7c4a45878ed69&pid=1-s2.0-S2666602224000326-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140321308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Arun J. Sanyal , Mansoor Husain , Crystel Diab , Kamal Kant Mangla , Ahsan Shoeb , Ildiko Lingvay , Elliot B. Tapper
{"title":"Cardiovascular disease in patients with metabolic dysfunction-associated steatohepatitis compared with metabolic dysfunction-associated steatotic liver disease and other liver diseases: A systematic review","authors":"Arun J. Sanyal , Mansoor Husain , Crystel Diab , Kamal Kant Mangla , Ahsan Shoeb , Ildiko Lingvay , Elliot B. Tapper","doi":"10.1016/j.ahjo.2024.100386","DOIUrl":"https://doi.org/10.1016/j.ahjo.2024.100386","url":null,"abstract":"<div><p>The burden of cardiovascular disease (CVD) in patients with metabolic dysfunction-associated steatohepatitis (MASH) is poorly characterized, particularly <em>vs</em> other liver diseases including metabolic dysfunction-associated steatotic liver disease (MASLD). To identify available evidence, Embase, MEDLINE, and Cochrane database searches (main search: 2011–September 6, 2021; additional <em>ad hoc</em> search [MEDLINE only]: September 7, 2021–February 15, 2023), plus manual searches (2019–September 2021), were performed. Studies reporting CVD outcomes (angina, coronary artery disease [CAD], heart failure, myocardial infarction, peripheral artery disease, stroke, venous thromboembolic disease, and CV mortality) in adults with histologically confirmed MASH and MASLD or other liver diseases were identified, with studies of MASLD without confirmed MASH excluded. Of 8732 studies, 21 were included. An increased incidence or prevalence of CVD in patients with MASH <em>vs</em> other conditions was reported in 12 studies; odds ratios (OR), where reported, ranged from 3.12 (95 % CI: 1.33–5.32) to 4.12 (95 % CI: 1.91–8.90). The risk of CAD was increased in people with MASH in 6 of 7 studies, while the risk of stroke was increased in 6 of 6 studies, and heart failure in 2 of 4 studies. Three of 6 studies provided evidence of increased CVD-related mortality in patients with MASH <em>vs</em> those without. In conclusion, this literature review suggests that CVD is prevalent in patients with MASH and may contribute to increased mortality. Accordingly, cardiovascular risk factors should be aggressively managed in this population. Whether the CVD burden in patients with MASH is a direct consequence of MASH itself requires further study.</p></div>","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"41 ","pages":"Article 100386"},"PeriodicalIF":0.0,"publicationDate":"2024-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666602224000296/pdfft?md5=d8a245456afa25a08a909904194f11ce&pid=1-s2.0-S2666602224000296-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140543335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
George R. Abraham , Colin Berry , Qing Fu , Stephen P. Hoole , Jonathan R. Weir-McCall
{"title":"Differences in quantitative myocardial perfusion mapping by CMR at 1.5 T and 3 T","authors":"George R. Abraham , Colin Berry , Qing Fu , Stephen P. Hoole , Jonathan R. Weir-McCall","doi":"10.1016/j.ahjo.2024.100388","DOIUrl":"https://doi.org/10.1016/j.ahjo.2024.100388","url":null,"abstract":"","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"41 ","pages":"Article 100388"},"PeriodicalIF":0.0,"publicationDate":"2024-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666602224000314/pdfft?md5=a7de17e0b16527cff232d07f4029f0c6&pid=1-s2.0-S2666602224000314-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140191762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The role of coronary microvascular dysfunction in the pathogenesis of heart failure with preserved ejection fraction","authors":"Becker Al-Khayatt, Divaka Perera, Haseeb Rahman","doi":"10.1016/j.ahjo.2024.100387","DOIUrl":"https://doi.org/10.1016/j.ahjo.2024.100387","url":null,"abstract":"<div><p>Heart failure with preserved ejection fraction (HFpEF) is a common condition with few effective therapies and hence represents a major healthcare burden. The clinical syndrome of HFpEF can be caused by varying pathophysiological processes, with coronary microvascular dysfunction (CMD) proposed as one of the aetiologies, although confirming causality has been challenging. CMD is characterised by the inability of the coronary vasculature to augment blood flow in response to a physiological stressor and has been established as the driver of angina in patients with non-obstructed coronaries (ANOCA), and this has subsequently led to efficacious endotype-directed therapies. CMD is also highly prevalent among sufferers of HFpEF and may represent a novel treatment target for this particular endotype of this condition. This review aims to discuss the role of the microcirculation in the healthy heart how it's dysfunction may precipitate HFpEF and explore the current diagnostic tools available. We also discuss the gaps in evidence and where we believe future research should be focussed.</p></div>","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"41 ","pages":"Article 100387"},"PeriodicalIF":0.0,"publicationDate":"2024-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666602224000302/pdfft?md5=44186507383977326ebbe176f17cb967&pid=1-s2.0-S2666602224000302-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140296530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Corrigendum to “Oncostatin M mediates cardioprotection via angiogenesis in ischemic heart disease” [Am. Heart J. Plus Cardiol. Res. Pract. vol. 35, 2023, 100331]","authors":"Shohei Ikeda, Koichi Sato, Morihiko Takeda, Mariko Shinozaki, Keita Miki, Michinori Hirano, Koji Fukuda, Nobuyuki Shiba","doi":"10.1016/j.ahjo.2024.100385","DOIUrl":"https://doi.org/10.1016/j.ahjo.2024.100385","url":null,"abstract":"","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"40 ","pages":"Article 100385"},"PeriodicalIF":0.0,"publicationDate":"2024-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666602224000284/pdfft?md5=1f779dc9a0b6a15791191e5c7e5db6c7&pid=1-s2.0-S2666602224000284-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140295878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Impact of ABO blood type on the risk of atrial fibrillation recurrence after catheter ablation","authors":"Michitaka Amioka , Hiroki Kinoshita , Akinori Sairaku , Tomoki Shokawa , Yukiko Nakano","doi":"10.1016/j.ahjo.2024.100384","DOIUrl":"https://doi.org/10.1016/j.ahjo.2024.100384","url":null,"abstract":"<div><h3>Background</h3><p>Blood types are classified based on the specific antigenic characteristics they possess. Despite documented associations between antigens and inflammation, a scarcity of data exists concerning the impact of antigens on atrial fibrillation (AF).</p></div><div><h3>Methods</h3><p>OSHOH-rhythm study is a multi-center, prospective observational study of 601 patients who underwent catheter ablation for AF. We examined the correlation between blood type groups and both the incidence and recurrence of AF. Additionally, we analyzed the recurrence of AF across antigenic profiles.</p></div><div><h3>Results</h3><p>The frequencies of individual blood types were 239 (39.8 %), 190 (31.6 %), 122 (20.3 %), and 50 (8.3 %) for A, O, B, and AB, respectively, aligning closely with the prevalent blood type distribution among the Japanese populace. During follow-up period (18.8 months, median), AF recurrence occurred in 96 patients (22.4 %) lacking the B antigen (A and O), and 26 patients (15.1 %) possessing B antigen (B and AB), respectively (Log-rank test: <em>P</em> = 0.034). A multivariate analysis demonstrated that blood types lacking the B antigen (hazard ratio [HR], 1.55; 95 % CI, 1.01 to 2.42; <em>P</em> = 0.037), hypertension (HR, 1.51; 95 % CI, 1.05 to 2.17; <em>P</em> = 0.026) and non-paroxysmal AF (HR, 1.70; 95 % CI, 1.17 to 2.47; <em>P</em> = 0.005) were independently associated with the recurrence of AF.</p></div><div><h3>Conclusions</h3><p>This study elucidates that, despite the absence of direct correlation between blood types and the occurrence of AF, blood types devoid of the B antigen exhibit an enhanced predisposition to AF recurrence. Nonetheless, the intricate mechanism linking blood type to recurrence remains elusive, warranting further comprehensive foundational research on blood types.</p></div>","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"40 ","pages":"Article 100384"},"PeriodicalIF":0.0,"publicationDate":"2024-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666602224000272/pdfft?md5=9ec61cace98b39dbdc9ae103e63e90f9&pid=1-s2.0-S2666602224000272-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140138598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The potential contribution of aromatase inhibitors to frailty in breast cancer patients with cardiovascular events","authors":"Yu Hiasa, Akinori Higaki, Osamu Yamaguchi","doi":"10.1016/j.ahjo.2024.100383","DOIUrl":"https://doi.org/10.1016/j.ahjo.2024.100383","url":null,"abstract":"","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"40 ","pages":"Article 100383"},"PeriodicalIF":0.0,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666602224000260/pdfft?md5=470f864a0b41a5efd710a98ae80e7481&pid=1-s2.0-S2666602224000260-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140113728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Omar M. Makram , Harikrishnan Hyma Kunhiraman , Ryan A. Harris , Catherine C. Hedrick , Khurram Nasir , Neal L. Weintraub , Xiaoling Wang , Avirup Guha
{"title":"Examining the interplay between cardiovascular disease and cancer incidence: Data from NHANES III and continuous","authors":"Omar M. Makram , Harikrishnan Hyma Kunhiraman , Ryan A. Harris , Catherine C. Hedrick , Khurram Nasir , Neal L. Weintraub , Xiaoling Wang , Avirup Guha","doi":"10.1016/j.ahjo.2024.100380","DOIUrl":"https://doi.org/10.1016/j.ahjo.2024.100380","url":null,"abstract":"<div><h3>Introduction</h3><p>This study aimed to investigate the relationship between risk factors of cancer among individuals with existing cardiovascular disease (CVD).</p></div><div><h3>Methods</h3><p>The analysis included 438 and 2100 CVD patients aged 65+ from NHANES-III and Continuous datasets, respectively. Competing risk models with subdistribution hazards ratio (aHR) were used to identify risk factors.</p></div><div><h3>Results</h3><p>Females in NHANES-III had lower cancer risk (aHR 0.39, <em>P</em> = 0.001) compared to males. Poor physical activity was associated with increased cancer risk in both datasets (aHR 2.59 in NHANES-III, aHR 1.59 in Continuous). In NHANES-Continuous, age (aHR 1.07, <em>P</em> < 0.001) and current smoking (aHR 2.55, <em>P</em> = 0.001) also showed a significant association with developing cancer. No other factors investigated showed significant associations.</p></div><div><h3>Discussion</h3><p>This study highlights the interplay between traditional risk factors and the elevated risk of cancer in CVD patients. Further research with larger samples and wider age ranges is needed to solidify these findings and inform intervention strategies.</p></div>","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"40 ","pages":"Article 100380"},"PeriodicalIF":0.0,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666602224000235/pdfft?md5=4362480be5e10af10a4978ae58c3c001&pid=1-s2.0-S2666602224000235-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140103551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Renee P. Bullock-Palmer , Panithaya Chareonthaitawee , Ervin Fox , Garth M. Beache
{"title":"Microvascular vasoregulatory dysfunction in African Americans - An enhanced opportunity for early prevention and treatment of atherosclerotic cardiovascular disease","authors":"Renee P. Bullock-Palmer , Panithaya Chareonthaitawee , Ervin Fox , Garth M. Beache","doi":"10.1016/j.ahjo.2024.100382","DOIUrl":"https://doi.org/10.1016/j.ahjo.2024.100382","url":null,"abstract":"<div><p>Atherosclerotic cardiovascular disease and its risk factors and precursors are a major driver of disparities in cardiovascular health. This review examines reported evidence that vascular endothelial dysfunction, and its manifestation as coronary microvascular dysfunction, underlies observed excess morbidity and mortality in African Americans. Advanced imaging insights that reveal patho-mechanisms, along with population evidence from the Jackson Heart Study, and the growing evidence emanating from national and international clinical trials and registries are presented. We examine a physiological framework that recognizes insulin-resistant cardiometabolic underpinnings of the conditions of the American Heart Associations' Life's Essential Eight construct of cardiovascular health as a unifying basis that affords early prevention. Mechanistic-based therapeutic approaches, can subsequently be implemented to interrupt progression to adverse outcomes employing layered, or personalized, treatment strategies of a well-defined set of conditions or diseases. Remaining knowledge gaps are acknowledged.</p></div>","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"40 ","pages":"Article 100382"},"PeriodicalIF":0.0,"publicationDate":"2024-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666602224000259/pdfft?md5=35390b7390c7b288e681691d860c415c&pid=1-s2.0-S2666602224000259-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140163918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Physiology and functional significance of the coronary microcirculation: An overview of its implications in health and disease","authors":"Samir Alam , Carl J. Pepine","doi":"10.1016/j.ahjo.2024.100381","DOIUrl":"https://doi.org/10.1016/j.ahjo.2024.100381","url":null,"abstract":"<div><p>Ischemic, Coronary Heart Disease (CHD) is a leading cause of morbidity and death worldwide.</p></div>","PeriodicalId":72158,"journal":{"name":"American heart journal plus : cardiology research and practice","volume":"40 ","pages":"Article 100381"},"PeriodicalIF":0.0,"publicationDate":"2024-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666602224000247/pdfft?md5=b1906681e51862ee07e11a6eeea98643&pid=1-s2.0-S2666602224000247-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140069667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}