HeartPub Date : 2025-03-26DOI: 10.1136/heartjnl-2024-324171
Philippe Charron, Julie Proukhnitzky
{"title":"Modern clinical genetics in cardiology.","authors":"Philippe Charron, Julie Proukhnitzky","doi":"10.1136/heartjnl-2024-324171","DOIUrl":"10.1136/heartjnl-2024-324171","url":null,"abstract":"<p><p>Advances in molecular genetics during the past decades led to seminal discoveries in the genetic basis of cardiovascular diseases, resulting in a new understanding of their pathogenesis, determinants of natural history and more recently paved the way for innovative therapies. A significant gap, however, exists between the rapidly increasing knowledge, especially of cardiovascular Mendelian disorders, and the medical applications in daily practice. This paper will focus on the practical issues the cardiologist may be faced with when suspecting a Mendelian disorder. The objective is to review the general issues related to genetic counselling and genetic testing, and to provide key messages for their integration into the medical management of the patients and relatives, according to a precision medicine approach.</p>","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":"378-386"},"PeriodicalIF":5.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142969798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HeartPub Date : 2025-03-26DOI: 10.1136/heartjnl-2024-325565
Massimo Imazio
{"title":"Prevention of pericardial complications after cardiac surgery: myth or reality?","authors":"Massimo Imazio","doi":"10.1136/heartjnl-2024-325565","DOIUrl":"10.1136/heartjnl-2024-325565","url":null,"abstract":"","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":"337-338"},"PeriodicalIF":5.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143364493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Synergistic effects of female-specific conditions and genetic risk on cardiometabolic disease: a cohort study.","authors":"Jiayu Yin, Tingting Li, Zongliang Yu, Lingchan Yu, Liyan Bian, Boyang Xiang, Xiaosong Gu","doi":"10.1136/heartjnl-2024-325355","DOIUrl":"https://doi.org/10.1136/heartjnl-2024-325355","url":null,"abstract":"<p><strong>Background: </strong>The role of female-specific factors in the occurrence and progression of cardiometabolic disease (CMD) across different genetic risks remains incompletely clear. This study aimed to comprehensively assess the association of female-specific factors with the occurrence and progression of CMD.</p><p><strong>Methods: </strong>This was a prospective cohort study of 150 413 female individuals from the UK Biobank. The female-specific factors in this study included premature menopause, adverse pregnancy outcomes, early or late menarche, multiparity, infertility, use of oral contraceptive or hormone therapy and autoimmune diseases, and a weighted female-specific risk score (FSRS, ranging from 0 to 6) was constructed. We analysed the association of female-specific factors with the occurrence and progression of CMD across genetic risks.</p><p><strong>Results: </strong>A total of 16 636 CMD events were documented after a median follow-up of 13.7 years. A one-point increase in FSRS was associated with a 24% higher risk of incident CMD, with persistent association with progression to first CMD, cardiometabolic multimorbidity and mortality. Female-specific factors and genetic susceptibility were synergistically associated with a higher risk of CMD (p<sub>Interaction</sub><0.001). Compared with the group with low female-specific and genetic risks, the group with high female-specific and genetic risk had a 243% increased risk of CMD. FSRS had a relatively high predictive value for CMD, especially in the group with higher genetic risks, and modestly improved the performance of two recommended cardiovascular algorithms. Phenotypic ageing, inflammation, metabolic factors, renal function and oestradiol collectively explained 21.6% of the association between FSRS and CMD.</p><p><strong>Conclusions: </strong>Female-specific health factors significantly contribute to CMD risk and interact with genetic susceptibility. Incorporating these factors into risk assessment models could enhance predictive accuracy, particularly for women with high genetic risk.</p>","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HeartPub Date : 2025-03-26DOI: 10.1136/heartjnl-2024-324805
Alireza Malektojari, Rosa Tahmasebipour, Maedeh Fadaeihosein, Sara Ghazizadeh, Fatemeh Ardali, Bahareh Haghighat, Fatemeh Keshavarz, Yalda Yousefi Azari, Fatemeh Javdan, Elahe Shahsavari, Mohammad Hamed Ersi, Shahin Abbaszadeh, Rami Al-Jafar, Abbas Dehghan, Tyler Pitre
{"title":"Pharmacological preventions and treatments for pericardial complications after open heart surgeries.","authors":"Alireza Malektojari, Rosa Tahmasebipour, Maedeh Fadaeihosein, Sara Ghazizadeh, Fatemeh Ardali, Bahareh Haghighat, Fatemeh Keshavarz, Yalda Yousefi Azari, Fatemeh Javdan, Elahe Shahsavari, Mohammad Hamed Ersi, Shahin Abbaszadeh, Rami Al-Jafar, Abbas Dehghan, Tyler Pitre","doi":"10.1136/heartjnl-2024-324805","DOIUrl":"10.1136/heartjnl-2024-324805","url":null,"abstract":"<p><strong>Background: </strong>Pericardial complications following cardiac surgery are common and debilitating, significantly impacting patients' survival. We performed this network meta-analysis to identify the most effective and safest preventions and treatments for pericardial complications following cardiac surgery.</p><p><strong>Methods: </strong>We systematically searched PubMed/MEDLINE, EMBASE and Cochrane CENTRAL from inception to 22 January 2024. Pairs of reviewers screened eligible studies. They included randomised controlled trials that enrolled adults undergoing major cardiac surgeries and reported postpericardiotomy syndrome, pericardial effusion and pericarditis as primary or secondary outcomes. We summarised the effects of interventions using relative risks and corresponding 95% CIs. We performed a frequentist random-effects network meta-analysis using the restricted maximum likelihood estimator.</p><p><strong>Results: </strong>We included 39 trials that enrolled a total of 6419 participants. Our network meta-analysis demonstrates colchicine reduces the risk of postpericardiotomy syndrome (RR 0.53, 95% CI 0.38 to 0.73). Beta-blockers probably prevent atrial fibrillation with a large magnitude of effect (RR 0.4, 95% CI 0.20 to 0.81) and may prevent postoperative pericarditis (RR 0.66, 95% CI 0.45 to 0.97) compared with control. Fish oil (RR 0.28, 95% CI 0.09 to 0.90), non-steroidal anti-inflammatory drugs (RR 0.37, 95% CI 0.23 to 0.59) and colchicine (RR 0.37, 95% CI 0.23 to 0.59) may reduce the risk of postoperative atrial fibrillation. We found no evidence of a difference in the risk of pleural effusion, all-cause mortality, serious adverse events or postoperative ICU stay.</p><p><strong>Conclusions: </strong>The results of our study highly recommend colchicine use to reduce the risk of the postpericardiotomy syndrome and beta-blocker use to reduce postoperative atrial fibrillation. Additionally, our study suggests that further research is needed to investigate other interventions and to evaluate newly proposed interventions in large, high-quality trials, as the current evidence for some interventions is relatively weak.</p>","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":"353-361"},"PeriodicalIF":5.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HeartPub Date : 2025-03-26DOI: 10.1136/heartjnl-2024-324761
Zainab Abdali, Karina V Bunting, Samir Mehta, John Camm, Kazem Rahimi, Mary Stanbury, Sandra Haynes, Dipak Kotecha, Sue Jowett
{"title":"Cost-effectiveness of digoxin versus beta blockers in permanent atrial fibrillation: the Rate Control Therapy Evaluation in Permanent Atrial Fibrillation (RATE-AF) randomised trial.","authors":"Zainab Abdali, Karina V Bunting, Samir Mehta, John Camm, Kazem Rahimi, Mary Stanbury, Sandra Haynes, Dipak Kotecha, Sue Jowett","doi":"10.1136/heartjnl-2024-324761","DOIUrl":"10.1136/heartjnl-2024-324761","url":null,"abstract":"<p><strong>Background: </strong>Atrial fibrillation (AF) is a major and increasing burden on health services. This study aimed to evaluate the cost-effectiveness of digoxin versus beta-blockers for heart rate control in patients with permanent AF and symptoms of heart failure.</p><p><strong>Methods: </strong>RAte control Therapy Evaluation in permanent Atrial Fibrillation (RATE-AF) was a randomised, open-label, blinded, endpoint trial embedded in the UK National Health Service (NHS) to directly compare low-dose digoxin with beta-blockers (ClinicalTrials.gov: NCT02391337). A trial-based cost-utility analysis was performed from a healthcare perspective over 12 months. Resource use in primary and secondary healthcare services, medications and patient-reported quality of life were prospectively collected to estimate differences in costs and quality-adjusted life years (QALYs).</p><p><strong>Results: </strong>RATE-AF randomised 160 patients with mean age of 76 (SD 8) years and 46% women, of which 149 patients (n=73 digoxin, n=76 beta blockers) had complete data and survived to 12-month follow-up. Treatment with digoxin was significantly less costly, with a mean saving of £530.41 per patient per year (95% CI -£848.06 to -£249.38, p=0.001). This was principally due to substantially lower rates of adverse events, with less primary and secondary healthcare utilisation compared with beta-blocker therapy. There was no significant difference in QALYs (0.013; 95% CI -0.033 to 0.052, p=0.56). At the £20 000 per-QALY willingness to pay threshold, the probability of digoxin being cost-effective compared with beta-blockers was 94%, with potential annual savings to the NHS of £102 million/year (95% CI £48 million to £164 million saving, p=0.001).</p><p><strong>Conclusions: </strong>Digoxin is a less costly option when compared with beta-blockers for control of heart rate in suitable patients with permanent AF, with larger cost-effectiveness studies warranted to advise on national and global policy-making.</p><p><strong>Trial registration number: </strong>NCT02391337, EudraCT 2015-005043-13.</p>","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":"362-369"},"PeriodicalIF":5.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Heart failure in low-income and middle-income countries.","authors":"Irina Mbanze, Timothy F Spracklen, Neusa Jessen, Albertino Damasceno, Karen Sliwa","doi":"10.1136/heartjnl-2024-324176","DOIUrl":"10.1136/heartjnl-2024-324176","url":null,"abstract":"<p><p>Heart failure (HF) is a complex syndrome which leads to significant morbidity and mortality, poor quality of life and extremely high costs to healthcare systems worldwide. Although progress in the management of HF in high-income countries is leading to an overall reduction in the incidence and mortality of HF, there is a starkly different scenario in low- and middle-income countries (LMICs). There is a substantial lack of data on HF in LMICs, as well as a scarcity of diagnostic tools, limited availability and affordability of healthcare and high burdens of cardiovascular risk factors and communicable diseases. Patients in this setting present with more advanced HF at much younger ages and are, more often, women. In this review, we aim to comprehensively describe the burden of HF from an LMIC perspective, based on the more recent available data. We summarise the major causes of HF that are endemic in these regions, including hypertension, cardiomyopathy, rheumatic heart disease, HIV-associated heart disease and endomyocardial fibrosis. Finally, we discuss the challenges faced by the least developed health systems and highlight interventions that may prove to be more efficient in changing the paradigm of HF of the more vulnerable populations.</p>","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":"341-351"},"PeriodicalIF":5.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143515418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Pulse pressure and aortic valve peak velocity and incident heart failure after myocardial infarction: a cohort study.","authors":"Yuzhong Wu, Jingjing Zhao, Chen Chen, Jiale Huang, Weihao Liang, Jiayong Li, Yugang Dong, Chen Liu, Ruicong Xue","doi":"10.1136/heartjnl-2024-324517","DOIUrl":"10.1136/heartjnl-2024-324517","url":null,"abstract":"<p><strong>Background: </strong>Heart failure with preserved ejection fraction is a recognised outcome in patients with myocardial infarction, although heart failure with reduced ejection fraction is more common. Identifying early indicators specific to heart failure with preserved ejection fraction in patients with myocardial infarction could support targeted preventive strategies. This study aimed to determine if pulse pressure and aortic valve peak velocity could serve as early predictors of heart failure with preserved ejection fraction in patients with myocardial infarction.</p><p><strong>Methods: </strong>We retrospectively analysed data from 5188 participants in the Atherosclerosis Risk in Communities Study who were free from heart failure at baseline, including 802 individuals with a history of myocardial infarction. Heart failure events were classified as either heart failure with preserved ejection fraction (left ventricular ejection fraction ≥50%) or heart failure with mildly reduced or reduced ejection fraction (left ventricular ejection fraction <50%). Competing risk regression models were used to examine associations of baseline pulse pressure and aortic valve peak velocity with heart failure subtypes.</p><p><strong>Results: </strong>Over 6 years of follow-up, 217 cases of heart failure with preserved ejection fraction (including 50 in patients with myocardial infarction) and 127 cases of heart failure with mildly reduced or reduced ejection fraction (33 in patients with myocardial infarction) were identified. Among patients with myocardial infarction, a 1-SD increase in pulse pressure was associated with a 1.60-fold higher risk of heart failure with preserved ejection fraction (95% CI 1.30 to 1.97), and a similar association was observed for aortic valve peak velocity (HR: 1.37, 95% CI 1.19 to 1.58). Patients with pulse pressure ≥68 mm Hg had a 3.83-fold higher risk of heart failure with preserved ejection fraction compared with those with lower pulse pressure, and those with aortic valve peak velocity ≥1.4 m/s had a 2.10-fold higher risk compared with those with lower values. Patients with myocardial infarction with two or more risk factors among elevated pulse pressure, aortic valve peak velocity, diabetes and atrial fibrillation had over 16 times the risk of developing heart failure with preserved ejection fraction compared with those without these risk factors (p<0.001).</p><p><strong>Conclusions: </strong>Pulse pressure and aortic valve peak velocity are significant predictors of heart failure with preserved ejection fraction in patients with myocardial infarction, suggesting their potential value in early risk stratification. These findings support the use of these markers to guide timely interventions aimed at preventing the progression to heart failure with preserved ejection fraction.</p>","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":"370-377"},"PeriodicalIF":5.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143364501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HeartPub Date : 2025-03-26DOI: 10.1136/heartjnl-2024-325513
Sukrit Trewaree, Alena Shantsila, Gregory Y H Lip
{"title":"Pulse pressure and aortic valve peak velocity as new predictors of heart failure in patients post-myocardial infarction.","authors":"Sukrit Trewaree, Alena Shantsila, Gregory Y H Lip","doi":"10.1136/heartjnl-2024-325513","DOIUrl":"10.1136/heartjnl-2024-325513","url":null,"abstract":"","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":"339-340"},"PeriodicalIF":5.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143364506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HeartPub Date : 2025-03-26DOI: 10.1136/heartjnl-2024-325408
Giovanni Occhipinti, Salvatore Brugaletta, Antonio Abbate, Daniela Pedicino, Marco Giuseppe Del Buono, Ramona Vinci, Giuseppe Biondi Zoccai, Manel Sabate, Dominick Angiolillo, Giovanna Liuzzo
{"title":"Inflammation in coronary atherosclerosis: diagnosis and treatment.","authors":"Giovanni Occhipinti, Salvatore Brugaletta, Antonio Abbate, Daniela Pedicino, Marco Giuseppe Del Buono, Ramona Vinci, Giuseppe Biondi Zoccai, Manel Sabate, Dominick Angiolillo, Giovanna Liuzzo","doi":"10.1136/heartjnl-2024-325408","DOIUrl":"https://doi.org/10.1136/heartjnl-2024-325408","url":null,"abstract":"<p><p>Coronary atherosclerosis is a chronic condition characterised by the development of an atherosclerotic plaque in the inner layer of the coronary artery, mainly associated with cholesterol accumulation and favoured by endothelial dysfunction related to other cardiovascular risk factors, such as smoking, diabetes and hypertension. A key actor in this process is the systemic inflammatory response, which can make plaques either grow slowly over the course of years (like a 'mountain'), obstructing coronary flow, and causing stable coronary artery disease, or make them explode (like a 'volcano') with subsequent abrupt thrombosis causing an acute coronary syndrome. This central role of inflammation in coronary atherosclerosis has led to its consideration as a modifiable cardiovascular risk factor and a therapeutic target. Classic anti-inflammatory drugs have been tested in clinical trials with some encouraging results, and new drugs specifically designed to tackle inflammation are currently being under investigation in ongoing trials. The objectives of this review are to (1) summarise the role of inflammatory biomarkers and imaging techniques to detect inflammation at each stage of plaque progression, and (2) explore currently available and upcoming anti-inflammatory therapies.</p>","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HeartPub Date : 2025-03-26DOI: 10.1136/heartjnl-2024-325104
Peter S Sever, Somayeh Rostamian, William Whiteley, Cono Ariti, Thomas Godec, Ajay Gupta, Judith Mackay, Andrew Whitehouse, Neil R Poulter
{"title":"Long-term benefits of atorvastatin on the incidence of cardiovascular events: the ASCOT-Legacy 20-year follow-up.","authors":"Peter S Sever, Somayeh Rostamian, William Whiteley, Cono Ariti, Thomas Godec, Ajay Gupta, Judith Mackay, Andrew Whitehouse, Neil R Poulter","doi":"10.1136/heartjnl-2024-325104","DOIUrl":"https://doi.org/10.1136/heartjnl-2024-325104","url":null,"abstract":"<p><strong>Aims: </strong>Cardiovascular (CV) deaths were reduced by atorvastatin during a 16-year follow-up of participants in the Anglo-Scandinavian Cardiac Outcomes Trial-lipid-lowering arm. We now extend these observations over 20 years and report both non-fatal and fatal CV outcomes.</p><p><strong>Methods: </strong>A cohort of 4605 UK hypertensive participants with total cholesterol <6.5 mmol/L (2317 atorvastatin vs 2288 placebo) was followed for up to 21 years (IQR 9.1-19.3). Cox proportional hazard models assessed HRs for non-fatal and fatal CV events. At the end of the original trial (3.3 years), all participants were offered atorvastatin. Lipid profiles were obtained from all subjects 2 years later and from subgroups approximately 9 years post-trial.</p><p><strong>Results: </strong>Patients allocated to atorvastatin had a significant reduction in non-fatal myocardial infarction (MI) and fatal coronary heart disease (CHD) events (HR (95% CI) 0.81 (0.69 to 0.94, p=0.006)), total coronary events (0.88 (0.80 to 0.98, p=0.017)) and CV deaths (0.86 (0.74 to 0.99, p=0.048)). No significant reduction in heart failure (HF), strokes, total CV events and all-cause mortality was observed.In participants assigned atorvastatin in the trial, 3-year mean low-density lipoprotein-cholesterol was strongly associated with long-term CV outcomes. The HRs per 1 mmol/L decrease were for non-fatal MI and fatal CHD (0.69 (0.57 to 0.85, p<0.001)), total coronary events (0.70 (0.61 to 0.79, p<0.001)), non-fatal and fatal HF (0.68 (0.57 to 0.81, p<0.001)), non-fatal and fatal stroke (0.74 (0.59 to 0.92, p=0.006)), total CV events and procedures (0.74 (0.66 to 0.81, p<0.001)), CV mortality (0.66 (0.55 to 0.81, p<0.001)) and all-cause mortality (0.81 (0.71 to 0.90, p<0.001)).Two years after the trial, approximately two-thirds of subjects in each arm were taking atorvastatin. At this time point and approximately 9 years post-trial, lipid profiles were similar between those formerly assigned atorvastatin or placebo.</p><p><strong>Conclusions: </strong>These observations provide further evidence for the long-term legacy effects of statins and have implications for the early introduction of statins to prevent CV events and mortality.</p>","PeriodicalId":12835,"journal":{"name":"Heart","volume":" ","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}