Heart最新文献

Background: Determining the most appropriate treatment in patients with cancer with an acute myocardial infarction (MI) can be challenging. Optimal management requires an understanding of bleeding risk which may be different in this population. This study aimed to investigate the bleeding risk among patients with MI with and without cancer, in the first and second year post-MI.

Methods: Patients with MI, with and without cancer were identified from a national cardio-oncology database from England between 2006 and 2019. The outcome was a presentation to hospital for a major bleeding event, with patients followed for a maximum of 24 months. Inverse probability weighting was used to compare cancer and non-cancer cohorts in time-to-event analyses.

Results: 587 279 patients with MI were identified, 9820 (1.7%) had cancer and 577 459 (98.3%) did not. Colorectal, prostate, breast, lung and bladder cancer were the most common types of cancer. The rate of hospital presentation for bleeding in the first year post-MI was higher in patients with cancer than the non-cancer reference population (HR: 1.53, 95% CI 1.45 to 1.62, p<0.001). 506 280 patients with MI were followed up in the second year post-MI. 5666 (1.1%) had cancer and 500 614 (98.9%) did not. The bleeding rate in patients with MI with cancer remained elevated in the second year post-MI (HR: 1.42, 95% CI 1.29 to 1.56, p<0.001). There were marked differences in bleeding between cancer types.

Conclusion: In this real-world observational study, patients with cancer had an increased bleeding risk in the first year post-MI which decreased but persisted in the second year after MI. Bleeding risk in patients with cancer must be carefully assessed post-MI.

Background: Calcific aortic stenosis (CAS) is frequently accompanied by systemic comorbidities, but their causal relationships and shared genetic architecture remain poorly defined. We aimed to map the multisystem comorbidity network of CAS and clarify underlying genetic mechanisms.

Methods: In 467 484 participants from the UK Biobank, observational and polygenic phenome-wide association studies evaluated associations between CAS and 1571 phenotypes, integrating disease-trajectory analyses to visualise temporal patterns. Associations replicated across observational and polygenic analyses were tested using two-sample Mendelian randomisation (MR) based on 22 CAS-related variants from FinnGen. Polygenic risk score (PRS) analyses excluding specific genes assessed their contributions, particularly LPA and plasma lipoprotein(a) (Lp(a)) levels.

Results: CAS was associated with higher risks of 42 cardiovascular and non-cardiovascular conditions, most prominently metabolic, endocrine, haematological and respiratory disorders. Temporal analyses showed that circulatory and metabolic diseases typically precede other comorbidities in CAS trajectories. MR findings were consistent with causal effects of CAS on multiple cardiovascular diseases, iron-deficiency anaemia, mental disorders and pleural effusion. When LPA variants were removed from the CAS PRS or plasma Lp(a) concentration was adjusted for, most associations lost significance, indicating a shared LPA/Lp(a)-mediated genetic pathway.

Conclusions: CAS is embedded within a broad multisystem comorbidity network, driven largely by genetic variation at LPA and elevated Lp(a). These findings highlight pleiotropic mechanisms linking valvular calcification with systemic disease and support LPA-targeted therapies as a promising avenue for reducing the multisystem burden of CAS.

Composite endpoints are widely used in large randomised cardiovascular outcome trials. They are frequently referred to as major adverse cardiovascular event (MACE), although there is no consensus around this definition. In essence, composite endpoints are single measures of effect encompassing multiple individual events, so that if any of them occurs, the patient is considered to present the composite endpoint. Their popularity has grown because of their methodological advantages, such as statistical efficiency and better ability to capture multiple clinically relevant outcomes. However, its use comes at a cost. Many times, composite endpoints are driven by the less meaningful event, or simply dilute a potential treatment effect by including outcomes that are not affected by the intervention. This and other limitations are often overlooked, therefore having a direct impact on the interpretation of clinical practice-changing trials. This review discusses key aspects related to the definition, interpretation, use and misuse of composite endpoints. Alternatives to composite endpoints are also discussed. Essential concepts are illustrated through examples based on key landmark studies, as well as topical trials. This work aims to help future trialists in the design and reporting of cardiovascular trials, and to assist readers in developing a critical understanding of them.

Genetic and epidemiological evidence indicates that triglyceride-rich lipoproteins are causal risk factors for atherosclerotic cardiovascular disease (ASCVD). Elevated levels of plasma triglyceride are common in patients who are diabetic or obese and contribute substantially to residual, ongoing risk of an ASCVD event in individuals on low-density lipoprotein (LDL)-lowering treatment. Hypertriglyceridaemia, therefore, presents a target for further intervention. Clinical trials have demonstrated that high-dose eicosapentaenoic acid (EPA) is effective in reducing ASCVD risk in patients on statin therapy, and it is now being incorporated into strategies using combination lipid-regulating treatment to manage aggressively those at highest risk. This review summarises the concepts underpinning the use of high-dose EPA alongside intensive LDL-lowering therapy, especially in the context of post-acute coronary syndrome. A practical implementation algorithm is presented setting out treatment options for combination therapy, and the place of high-dose EPA in ASCVD prevention in hypertriglyceridaemia.

Background: Heart auscultation is a widely used and cost-effective clinical tool for detecting valvular heart disease (VHD), particularly in primary care. However, existing evidence on its diagnostic accuracy is limited by small sample sizes, specialist-led studies and high-prevalence settings. Robust population-based data are lacking. This study aimed to assess the prevalence and diagnostic accuracy of heart murmurs for identifying VHD in a general adult population, using echocardiography as the reference standard.

Methods: We conducted a diagnostic accuracy study within the Seventh Tromsø Study (2015-2016), involving 2082 participants aged ≥40 years (mean age 63 years). Heart sounds were recorded at four chest locations and independently classified by general practitioners (GPs) blinded to echocardiographic results. Murmurs were graded and categorised as systolic or diastolic. Clinically significant VHD was defined as ≥mild aortic stenosis (AS) or ≥moderate aortic regurgitation (AR) or mitral regurgitation (MR). We calculated sensitivity, specificity, predictive values and likelihood ratios for murmur detection.

Results: GPs detected heart murmurs in 487 participants (23%). Significant VHD was identified in 392 participants (19%), but only 139 of them (35.5%) had an audible murmur. Systolic murmurs detected all cases of AS (sensitivity 100%, specificity 78%). Sensitivity was lower for AR (43%) and MR (29%), while specificity of distinct murmurs exceeded 94% across all VHD types. Diastolic murmurs were rare (n=9) but highly specific (>99%). Among participants with murmurs, age ≥70 years (OR 2.0, 95% CI 1.2 to 3.4), male sex (OR 3.3, 95% CI 2.0 to 5.3) and previous myocardial infarction (OR 2.3, 95% CI 1.0 to 5.2) were independently associated with VHD.

Conclusion: In this general adult population, heart auscultation by GPs identified murmurs in nearly one in four individuals and showed high specificity but limited sensitivity for diagnosing VHD. Auscultation remains a valuable initial screening tool-especially for AS-but should be complemented by echocardiography in older or high-risk individuals.

Background: The burden of cardiovascular events in Africa is projected to rise significantly in the coming decade, placing additional strain on already overburdened healthcare systems. Mobile health (mHealth) technologies present a promising approach to addressing these challenges. This scoping review mapped the utilisation of mHealth interventions in cardiovascular event care across Africa.

Methods: A systematic search of peer-reviewed and grey literature published between 2013 and 2025 was conducted. Studies were included if they focused on mHealth interventions for cardiovascular event care in Africa. Data were extracted and synthesised, categorising studies by geographical distribution, intervention type and target cardiovascular condition.

Results: A total of 26 studies were identified, comprising small-scale pilots, randomised controlled trials and process evaluations. Geographically, most studies were conducted in Eastern and Western Africa. The majority focused on stroke care (20/26) rather than myocardial infarction (5/26) and predominantly addressed post-event care. The most common technologies used were smartphone applications (11/26) and SMS/phone call interventions (7/26), with one study incorporating artificial intelligence for arrhythmia screening. While positive outcomes were frequently reported, significant challenges included health system constraints, low digital literacy and financial barriers.

Conclusion: mHealth technologies demonstrate potential in improving cardiovascular event care in Africa, particularly for stroke care. However, their widespread adoption is hindered by systemic and contextual challenges. Addressing these barriers through targeted health system strengthening, digital literacy initiatives and the design of mHealth interventions that are cost-effective, user-friendly and aligned with existing workflows is essential to leveraging mHealth in cardiovascular care.

Organ transplantation is the treatment of choice for individuals with kidney failure requiring kidney replacement therapy, as well as for those with end-stage liver disease. Despite the significant reduction in long-term morbidity and mortality with transplantation, kidney and liver allograft recipients remain at high risk for cardiovascular disease (CVD) and premature death from cardiovascular causes. This heightened risk is represented across all phenotypes of CVD, including coronary heart disease, heart failure, arrhythmias, valvulopathies and pulmonary hypertension. Pre-existing vascular risk factors for CVD, coupled with superimposed cardiovascular-kidney-metabolic derangements after transplantation, driven at least in part by post-transplant weight gain, immunosuppressive therapies and de novo risk factors such as dyslipidaemia and diabetes, coalesce to increase total CVD risk. In this review, we summarise pathophysiological considerations for both the short- and long-term increase in CVD risk following kidney/liver transplantation. We review the different phenotypes of CVD, with unique considerations for post-transplant care in this patient population. Finally, we highlight the need for awareness about long-term CVD risk and a multidisciplinary approach to managing organ-specific CVD risk in kidney and liver transplant patients.