Chike C. Nwabuo

Primary malignant cardiac tumors (PMCTs) are rare but lethal neoplasms. There are limited evidence-based treatment guidelines for PMCTs. We evaluated the relation of chemotherapy with mortality outcomes in patients with PMCTs in the United States. Data were from patients aged ≥ 20 years from the Surveillance, Epidemiology, and End Results program who were diagnosed with PMCTs from 2000 to 2020. Cox regression, competing risk, and propensity score analyses were performed to estimate hazard ratios (HR) and confidence intervals (CI). About 53% of the 563 patients with PMCTs received chemotherapy as the first course of treatment. During a mean follow-up of 24.7 months (median: 10), 458 deaths occurred with 81.7% and 9.4% due to cancer and cardiovascular disease (CVD), respectively. In models adjusted for sociodemographic and clinico-pathophysiological factors including histology, receipt of chemotherapy was associated with low risk for all-cause (HR: 0.56, 95%CI: 0.45–0.69), cancer (HR: 0.63, 95%CI: 0.50–0.80) and CVD mortality (HR: 0.27, 95%CI: 0.12–0.58). Patients who had both chemotherapy and surgery had the lowest risk for all-cause and cancer mortality. This study suggests that the subpopulations of patients with PMCTs who receive chemotherapy may have better prognosis than those who do not receive this therapy regardless of histology.

Objective Established preclinical imaging assessments of heart failure (HF) risk are based on macrostructural cardiac remodelling. Given that microstructural alterations may also influence HF risk, particularly in women, we examined associations between microstructural alterations and incident HF. Methods We studied N=2511 adult participants (mean age 65.7±8.8 years, 56% women) of the Framingham Offspring Study who were free of cardiovascular disease at baseline. We employed texture analysis of echocardiography to quantify microstructural alteration, based on the high spectrum signal intensity coefficient (HS-SIC). We examined its relations to incident HF in sex-pooled and sex-specific Cox models accounting for traditional HF risk factors and macrostructural alterations. Results We observed 94 new HF events over 7.4±1.7 years. Individuals with higher HS-SIC had increased risk for incident HF (HR 1.67 per 1-SD in HS-SIC, 95% CI 1.31 to 2.13; pConclusions Cardiac microstructural alterations are associated with elevated risk for HF, particularly in women. Microstructural alteration may identify sex-specific pathways by which individuals progress from risk factors to clinical HF.

Aims: Atherosclerotic cardiovascular disease (ASCVD) risk prediction equations apply to older adults. For this study, the Pathobiologic Determinants of Atherosclerosis in Youth (PDAY) risk score, based on post-mortem measurements of atherosclerosis in 15–34-year olds dying accidentally, was used to predict ASCVD events, specifically myocardial infarction and revascularization, in middle age, from risk measured at ≤40 years of age. Methods and results: The Coronary Artery Risk Development in Young Adults Study (CARDIA) collected longitudinal cardiovascular risk data, coronary artery calcium (CAC) scores, and ASCVD data beginning at age 18 and 30 years with 30-year follow-up. Predictive accuracy for ASCVD of the PDAY risk score, calculated at baseline (mean age 24) and at all six CARDIA examinations up until year 15, was examined. We also examined whether the presence of CAC improved model discrimination. The cohort for this study comprised 5004 Black and White men and women, at baseline and 3558 with data at year 15. Each standard deviation increase in PDAY score, at each examination, was significantly associated with future ASCVD. Hazard ratios (per standard deviation) increased from 1.74 to 2.04 from year 0 to year 15. C-statistics ranged from 0.771 to 0.794. Coronary artery calcium measurement at age 33–45 years improved risk prediction only if the score was 0. Cumulative risk exposure over the first 15 years of the CARDIA study also had high-predictive value (c-statistic 0.798, 95% confidence interval 0.762–0.835). Conclusion: The PDAY risk score may be used in young adults, prior to age 40 years to predict ASCVD events.

Sodium-glucose co-transporter-2 (SGLT2) inhibitors have evolved over the years based on data from several randomized double-blinded placebo-controlled clinical trials from being used primarily for blood sugar control in patients with diabetes to being used in all patients with heart failure with reduced ejection fraction (HFrEF) to decrease the risk of hospitalization for heart failure (HF) or death from cardiovascular (CV) causes. They have also been shown to slow the progression of renal disease and prevent death related to renal causes in patients with chronic kidney disease (CKD). More recently, they are currently being studied to decrease the risk of HF hospitalization in patients with the preserved ejection fraction subtype of HF and have shown positive results. The transition of SGLT2 from a medication used in diabetes to an established HF medication was a result of the hypothesis generated from the analysis of earlier trials in diabetic patients and further testing of this hypothesis in an HF population. Our distinctive approach in this review is to highlight with greater details in a time-dependent fashion the rationale for the paradigm shift of SGLT2 inhibitors from their use in diabetic patients initially for blood sugar control to their recommendation in all patients with HF regardless of the presence of diabetes by detailing the results of several major clinical trials and a meta-analysis study that led to this discovery and clinical indication. We would also highlight the key properties in detail of seven crucial clinical trials involving SGLT2 inhibitors.

Objective To evaluate the association of cigarette smoking and right ventricular (RV) systolic and diastolic functions in a population-based cohort of individuals at middle age. Methods This cross-sectional study included participants who answered the smoking questionnaire and underwent echocardiography at the Coronary Artery Risk Development in Young Adulthood year 25 examination. RV systolic function was assessed by echocardiographic-derived tricuspid annular plane systolic excursion (TAPSE) and by right ventricular peak systolic velocity (RVS’), while RV diastolic function was evaluated by early right ventricular tissue velocity (RVE’). Multivariable linear regression models assessed the relationship of smoking with RV function, adjusting for age, sex, race, body mass index, systolic blood pressure, total cholesterol, high-density lipoprotein (HDL) cholesterol, diabetes mellitus, alcohol consumption, pulmonary function, left ventricular systolic and diastolic function and coronary artery calcium score. Results A total of 3424 participants were included. The mean age was 50±4 years; 57% were female; and 53% were black. There were 2106 (61%) never smokers, 750 (22%) former smokers and 589 (17%) current smokers. In the multivariable analysis, current smokers had significantly lower TAPSE (β=−0.082, SE=0.031, p=0.008), RVS’ (β=−0.343, SE=0.156, p=0.028) and RVE’ (β=−0.715, SE=0.195, pConclusions In a large multicenter community-based biracial cohort of middle-aged individuals, smoking was independently related to both worse RV systolic and diastolic functions.

Purpose of Review Given that the life expectancy and the burden of hypertension are projected to increase over the next decade, hypertensive heart disease (HHD) may be expected to play an even more central role in the pathophysiology of cardiovascular disease (CVD). A broader understanding of the features and underlying mechanisms that constitute HHD therefore is of paramount importance. Recent Findings HHD is a condition that arises as a result of elevated blood pressure and constitutes a key underlying mechanism for cardiovascular morbidity and mortality. Historically, studies investigating HHD have primarily focused on left ventricular (LV) hypertrophy (LVH), but it is increasingly apparent that HHD encompasses a range of target-organ damage beyond LVH, including other cardiovascular structural and functional adaptations that may occur separately or concomitantly. HHD is characterized by micro- and macroscopic myocardial alterations, structural phenotypic adaptations, and functional changes that include cardiac fibrosis, and the remodeling of the atria and ventricles and the arterial system. In this review, we summarize the structural and functional alterations in the cardiac and vascular system that constitute HHD and underscore their underlying pathophysiology.

To the Editor Green et al performed a cross-sectional analysis of a sample of participants from a prospective cohort of pregnant women to test the association b