Heart最新文献

Background: 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.

Methods: 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.

Results: 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).

Conclusions: 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.

Background: Although the prognostic implications of severe mitral regurgitation (MR) are well recognised, they are less clear in moderate MR. We therefore explored the prognostic impact of both moderate and severe MR within the large National Echocardiography Database Australia cohort.

Methods: Echocardiography reports from 608 570 individuals were examined using natural language processing to identify MR severity and leaflet pathology. Atrial (aFMR) or ventricular (vFMR) functional MR was assessed in those without reported leaflet pathology. Using individual data linkage over median 1541 (IQR 820 to 2629) days, we examined the association between MR severity and all-cause (153 612/25.2% events) and cardiovascular-related mortality (47 840/7.9% events).

Results: There were 319 808 men and 288 762 women aged 62.1±18.5 years, of whom 456 989 (75.1%), 102 950 (16.9%), 38 504 (6.3%) and 10 127 (1.7%) individuals had no/trivial, mild, moderate and severe MR, respectively, reported on their last echo. Compared with those with no/trivial MR (26.5% had leaflet pathology, 19.2% died), leaflet pathology (51.8% and 78.9%, respectively) and actual 5-year all-cause mortality (54.6% and 67.5%, respectively) increased with MR severity. On an adjusted basis (age, sex and leaflet pathology), long-term mortality was 1.67-fold (95% CI 1.65 to 1.70) and 2.36-fold (95% CI 2.30 to 2.42) higher in moderate and severe MR cases (p<0.001) compared with no/trivial MR. The prognostic pattern for moderate and severe MR persisted for cardiovascular-related mortality and within prespecified subgroups (leaflet pathology, vFMR or aFMR, and age<65 years).

Conclusions: Within a large real-world clinical cohort, we confirm that conservatively managed severe MR is associated with a poor prognosis. We further reveal that moderate MR is associated with increased mortality, irrespective of underlying aetiology.

Trial registration: Australian New Zealand Clinical Trials Registry (ACTRN12617001387314).

Exercise offers a plethora of health benefits. However, certain genetic and acquired diseases such as cardiomyopathies and channelopathies are associated with sudden cardiac death during exercise. Several factors complicate exercise prescription in individuals living with these conditions. The lack of high-quality evidence supporting exercise recommendations, variation in the clinical phenotypes within the same condition and sparse physician education around exercise prescription all leads to a reluctance to provide specific guidance on how to engage in physical activity.This article aims to summarise the latest evidence underpinning risk stratification and current guideline recommendations for physical activity in individuals with cardiomyopathies and channelopathies wishing to engage in exercise. It also aims to provide a basic practical approach to exercise prescription for health professionals involved in the care of these patients. This approach may then serve as a foundation that can be easily personalised. Since risk can never be completely eliminated, all decisions regarding exercise participation should be taken following shared dialogue between the physician, patient and wider stake holders where appropriate.

Patients with acute pulmonary embolism (PE) have a wide spectrum of clinical presentations, from incidental findings to sudden cardiac death. Management and treatment recommendations in currently available guidelines vary according to patient risk and haemodynamic profile. A clot-in-transit (CiT) in the right heart chambers may be occasionally identified and is, therefore, an under-recognised but challenging condition, often preceding an abrupt clinical deterioration, and associated with increased mortality. Data on the detection of a CiT are sparse but consistent in attributing negative prognostic relevance, and therefore the presence of CiT should be systematically investigated and recorded in the setting of PE.In this review, the challenges related to the identification of a CiT are highlighted. Here, we propose an algorithm where the role of the Pulmonary Embolism Response Team (PERT) is reinforced. The PERT should convene once the CiT is suspected, to define the timeline for the diagnostic steps and subsequent management on a case-by-case basis. A patient with PE and CiT requires close bedside monitoring and rapid escalation therapy in case of clinical deterioration. Beyond anticoagulation alone, more aggressive strategies can be considered, including systemic thrombolysis, surgical pulmonary embolectomy and the currently emerging catheter-directed therapies. PROSPERO registration number: CRD42024493303.

Background: Subclinical leaflet thrombosis (SLT) is a common complication after transcatheter aortic valve replacement (TAVR). Multidimensional CT (MDCT) is the main imaging mortality for the diagnosis of SLT but it enhances the risk of contrast-induced nephropathy. Our study aimed to use an innovative wearable acoustic cardiography (ACG) device to diagnose SLT as an alternative option.

Methods: This prospective cohort study consecutively enrolled patients with severe symptomatic aortic stenosis who underwent successful TAVR. We collected and analysed clinical data including ACG measurements and imaging results. Discrimination capability analysis (ie, area under the curve (AUC), sensitivity, specificity) of a composite feature from ACG readings in predicting SLT during follow-up was performed. Based on the severity of SLT, patients were categorised into three groups: Group 1 (no SLT), Group 2 (mild SLT) and Group 3 (moderate-to-severe SLT).

Results: 116 patients consented and enrolled in the study. At the 1-month follow-up, MDCT revealed a 25% prevalence of SLT with 11.2% classified as moderate-to-severe. ACG analysis revealed distinctive patterns of early systolic, baseless and high-energy murmurs exclusively in patients in Group 3 but not in group 2. The diagnostic performance of ACG for moderate-to-severe SLT showed a sensitivity of 84.62%, specificity of 91.26% and AUC of 0.920 (95% CI: 0.855 to 0.962, p<0.001). At 6 months, both MDCT and ACG indicated that nine (70%) patients in Group 3 who received anticoagulant therapy achieved complete resolution of SLT.

Conclusion: ACG can be considered as an effective tool to assist in the diagnosis of SLT based on deterioration of transvalvular haemodynamics post-TAVR. Further studies are required to confirm its utility as a valuable non-invasive diagnostic and monitoring tool.

Trial registration number: ChiCTR2300072300.

Background: The SCN5A gene polymorphism histidine-558-to-arginine (H558R) has been associated with atrial fibrillation (AF) and may affect the therapeutic effects of flecainide. This study aimed to assess the prevalence of the H558R polymorphism in a European cohort of patients with AF and examine its association with flecainide's effects on AF recurrence and toxicity.

Methods: This cohort study included patients diagnosed with AF and prescribed flecainide between 2017 and 2021 in a regional health area. Patients without the polymorphism (H558R-/-) were compared with heterozygous patients (H558R+/-) for a primary outcome of combined 6-month AF recurrence or toxicity. Secondary analyses evaluated the long-term outcomes and compared the prevalence of H558R in the AF cohort to a general population sample (n=3401).

Results: A total of 104 patients were enrolled, with 57% H558R-/-, 37% H558R+/- and 6% H558R+/+. The prevalence of the H558R polymorphism was significantly higher in the AF cohort than in the general population (43.27% vs 24.37%, prevalence ratio 1.78, 95% CI 1.41 to 2.23, p<0.01). H558R+/- patients had a significantly lower risk of 6-month AF recurrence or toxicity (p=0.023, risk ratio 0.423, 95% CI 0.189 to 0.947), corresponding to an absolute risk difference of 21.5%. These findings were similar in the multivariable analysis. In long-term follow-up, H558R+/- patients continued to demonstrate a lower risk of AF recurrence or toxicity (p=0.039, HR 0.53, 95% CI 0.276 to 0.999).

Conclusions: The H558R polymorphism is more prevalent in patients with AF compared with the general population and its presence is associated with a more favourable response to flecainide treatment.

Background: We evaluated the potential of circulating bone morphogenetic protein 10 (BMP10) as a biomarker for atrial stress and remodelling in patients with heart failure (HF), in comparison to N-terminal pro-B-type natriuretic peptide (NT-proBNP). We also assessed the predictive value of BMP10 for adverse clinical outcomes.

Methods: BMP10 levels were quantified in 2085 chronic HF patients from the European BIOlogy Study to TAilored Treatment in Chronic Heart Failure (BIOSTAT-CHF) cohort and in 1487 patients from the Scottish validation cohort. Multivariable linear regression identified independent associates of BMP10. Proteomic analysis of 6369 proteins with subsequent gene set enrichment analysis was used to explore biological pathways associated with elevated BMP10. Cox proportional hazards models adjusting for established risk factors were used to associate BMP10 levels with clinical outcomes, including all-cause mortality and HF hospitalisation.

Results: In a multivariable model including clinical and echocardiographic parameters, log-transformed and standardised BMP10 levels were significantly associated with a history of atrial fibrillation (Sβ=0.419; p<0.001), and with echocardiographic features reflecting atrial stress, such as increased left atrial diameter (Sβ=0.075; p=0.048). By contrast, these were not among the strongest associates of NT-proBNP levels. Gene set enrichment analysis showed significant overrepresentation in pathways of muscle contraction and extracellular matrix organisation. Higher log-transformed and standardised BMP10 levels predicted a combined outcome of 2-year all-cause mortality and HF rehospitalisation (HR=1.10, 95% CI=1.02-1.19), with the validation cohort yielding comparable results.

Conclusion: BMP10 emerges as a novel biomarker reflecting atrial stress and remodelling in chronic HF patients. Its additional predictive value for adverse outcomes underscores its potential utility in enhancing risk stratification and guiding therapeutic interventions in HF management.

Objectives: Although financial interactions between physicians and pharmaceutical and medical device companies could be potential conflicts of interest, in certain instances, industry promotion targeted at physicians may facilitate the early adoption of effective, novel care for patients such as sacubitril/valsartan in the USA. This study aims to evaluate associations between industry-sponsored meal payments to physicians and their prescribing patterns for sacubitril/valsartan in the USA.

Methods: Using the publicly accessible Centers for Medicare and Medicaid Services Medicare Part D database and the Open Payments Database, this study assessed associations between industry-sponsored meal payments to physician prescribers and total amounts of Medicare claims and spending for sacubitril/valsartan between 2015 and 2021.

Results: Among 220 147 eligible physician prescribers, 60 568 (27.5%) received at least one meal payment related to sacubitril/valsartan from the manufacturer, totaling US$13.9 million. The receipt of meal payments was significantly associated with a higher proportion of sacubitril/valsartan prescriptions to all sacubitril/valsartan, angiotensin receptor blocker and angiotensin-converting enzyme inhibitor prescriptions, with an OR of 2.04 (95% CI: 1.98 to 2.10, p<0.001). Moreover, a 10% increase in the annual number of meal payments was associated with a 2.6% (95% CI: 2.5% to 2.6%, p<0.001) increase in the annual number of Medicare claims and a 7.3% (95% CI: 7.1% to 7.5%, p<0.001) increase in annual Medicare spending per physician.

Conclusions: Given the underprescription of sacubitril/valsartan in the USA, the positive associations between meal payments and physicians' prescribing patterns suggest that industry-sponsored meals may contribute to the early adoption of this cost-effective, novel heart failure drug among US Medicare beneficiaries.

Background: Cardiovascular disease (CVD) preventive medications are recommended for patients at high short-term CVD risk. As most younger people with multiple raised CVD risk factors levels have low short-term risk, they could be falsely reassured to take no action. Heart age-the chronological age of a hypothetical person with the same short-term absolute CVD risk as the patient being assessed, but with an 'ideal' risk profile-is a complementary relative CVD risk metric developed to encourage these younger patients to make long-term lifestyle changes. However, clinicians sometimes use heart age to inform medication decisions. We assessed the appropriateness of this practice by comparing heart age and short-term CVD risk.

Methods: New Zealand primary care patients are recruited to the PREDICT cohort when their CVD risk is assessed. PREDICT is an ongoing prospective study in one-third of New Zealand general practices, designed to derive CVD risk prediction algorithms. Five-year CVD risk was calculated for 35-74-year-old PREDICT participants using published equations. Heart age was calculated using non-smoking, systolic blood pressure of 120 mm Hg and total cholesterol/high-density lipoprotein ratio of 3.5, as the 'ideal' risk profile. CVD risk and heart age gaps (difference between chronological age and heart age) were compared.

Results: Among 371 676 PREDICT participants, 5-year CVD risk increased with age, approximately doubling every 10 years, whereas heart age gaps decreased with increasing age, approximately halving between 35 and 44-year olds and 65-74-year olds. There were 5-40-year heart age gap differences between groups with similar 5-year CVD risks, but different ages.

Conclusion: Short-term CVD risk and heart age are not interchangeable risk metrics. Short-term risk increases with increasing age whereas heart age gaps generally decline, with major differences between younger and older people with similar short-term risk. If heart age is used to inform medication decisions rather than encourage long-term lifestyle changes, older people at high short-term risk could be undertreated and younger people at low short-term risk could be unnecessarily medicated.