Globally significant variation in treatment and course of heart valve disease (HVD) exists, and outcome measurement is procedure focused instead of patient focused. This article describes the development of a patient-related (International Consortium for Health Outcomes Measurement) standard set of outcomes and case mix to be measured in patients with HVD.

Chest radiotherapy (XRT) plays a crucial role in the treatment of a multitude of cancers including breast, lung, esophageal, and lymphoma. Although XRT enhances cancer survival rates, it may also expose healthy bystander tissues to radiation, potentially leading to severe complications. Initially considered relatively resistant to radiation damage, the heart has been shown over the past 4 decades to be susceptible to radiation-induced cardiovascular toxicity and despite advances in XRT which can minimize radiation exposure to heart tissue, no cardiac radiation dose is entirely safe. The clinical spectrum of radiation-induced cardiovascular toxicity is broad, encompassing coronary artery disease, myocardial dysfunction, valvular abnormalities, and pericardial disorders. Radiation-induced cardiovascular toxicity may manifest acutely or many years after XRT, with each condition more likely to present at certain time points post-XRT. Cardiac imaging is a crucial tool in both the screening and diagnosis of radiation-induced cardiovascular toxicity with an understanding of its pathophysiology, incidence, and progression required to implement a comprehensive, multimodality imaging approach to detect and manage these complications effectively.

Use of anabolic androgenic steroids (AASs) is associated with increased mortality, and case reports have suggested that some of these deaths are due to cardiovascular disease. However, the epidemiology of cardiovascular disease in AAS users is still relatively unexplored. This study aimed to measure the incidence of cardiovascular disease in male AAS users and to compare these rates with those of a cohort from the general population matched by age and sex.

Critical care cardiology refers to the practice focus of and subspecialty training for the comprehensive management of life-threatening cardiovascular diseases and comorbid conditions that require advanced critical care in an intensive care unit. The development of coronary care units is often credited for a dramatic decline in mortality rates after acute myocardial infarction throughout the 1960s. As the underlying patient population became progressively sicker, changes in organizational structure, staffing, care delivery, and training paradigms lagged. The coronary care unit gradually evolved from a focus on rapid resuscitation from ventricular arrhythmias in acute myocardial infarction into a comprehensive cardiac intensive care unit designed to care for the sickest patients with cardiovascular disease. Over the past decade, the cardiac intensive care unit has continued to transform with an aging population, increased clinical acuity, burgeoning cardiac and noncardiac comorbidities, technologic advances in cardiovascular interventions, and increased use of temporary mechanical circulatory support devices. Herein, we provide an update and contemporary expert perspective on the organizational structure, staffing, and care delivery in the cardiac intensive care unit; examine the challenges and opportunities present in the education and training of the next generation of physicians for critical care cardiology; and explore quality improvement initiatives and scientific investigation, including multicenter registry initiatives and randomized clinical trials, that may change clinical practice, care delivery, and the research landscape in this rapidly evolving discipline.

Although cell therapy has emerged as a promising approach to promote neovascularization, its effects are mostly limited to capillaries. To generate larger or more stable vessels, layering of mural cells such as smooth muscle cells (SMCs) or pericytes is required. Recently, direct reprogramming approaches have been developed for generating SMCs. However, such reprogrammed SMCs lack genuine features of contractile SMCs, a native SMC phenotype; thus, their therapeutic and vessel-forming potential in vivo was not explored. Therefore, we aimed to directly reprogram human dermal fibroblasts toward contractile SMCs (rSMCs) and investigated their role for generating vascular mural cells in vivo and their therapeutic effects on ischemic disease.

It remains challenging to determine which hypertrophic cardiomyopathy (HCM) family members will subsequently develop HCM. Standard 2-dimensional and conventional Doppler echocardiography have been unable to reliably distinguish HCM genotype-positive and phenotype-negative (G+P-) from genotype-negative and phenotype-negative (G-P-) family members. We aimed to determine if advanced echocardiographic modalities can discriminate HCM G+P- from G-P- individuals.

TTN (titin) is the third myofilament type of the cardiac sarcomere and performs important functions that include generating passive tension. Changes in TTN expression are associated with cardiac dysfunction, and TTN is one of the main genes linked to dilated cardiomyopathy (DCM). DCM is frequently associated with changes in the expression of N2BA (compliant cardiac TTN isoform), 1 of the 2 major TTN isoforms found in the heart (the other isoform being the N2B [stiff cardiac TTN isoform]). Whether altered expression of N2BA TTN causes DCM or is a secondary change remains unclear.

Hypertensive disorders of pregnancy (HDP) are a major cause of maternal morbidity and mortality and are associated with acute cardiac events in the peripartum period, as well as cardiovascular disease later in life. Despite the robust association between hypertension and atrial fibrillation (AFib), comparatively little is known about HDP and its subtypes as sex-specific risk factors for AFib.

Atherosclerotic cardiovascular disease is a major health concern worldwide and requires effective preventive measures. Lp(a) (lipoprotein [a]) has recently garnered attention as an independent risk factor for astherosclerotic cardiovascular disease, with proinflammatory and prothrombotic mechanisms contributing to its atherogenicity. On an equimolar basis, Lp(a) is ~5 to 6 times more atherogenic than particles that have been widely associated with adverse cardiovascular outcomes, such as LDL (low-density lipoprotein). Lp(a) can enter the vessel wall, leading to the accumulation of oxidized phospholipids in the arterial intima, which are crucial for initiating plaque inflammation and triggering vascular disease progression. In addition, Lp(a) may cause atherothrombosis through interactions between apoA (apolipoprotein A) and the platelet PAR-1 (protease-activated receptor 1) receptor, as well as competitive inhibition of plasminogen. Because Lp(a) is mostly determined on genetic bases, a 1-time assessment in a lifetime can suffice to identify patients with elevated levels. Mendelian randomization studies and post hoc analyses of randomized trials of LDL cholesterol-lowering drugs showed a causal link between Lp(a) concentrations and cardiovascular outcomes, with therapeutic reduction of Lp(a) expected to contribute to estimated cardiovascular risk mitigation. Many Lp(a)-lowering drugs, including monoclonal antibodies, small interfering ribonucleic acids, antisense oligonucleotides, small molecules, and gene editing compounds, are at different stages of clinical investigation and show promise for clinical use. In particular, increased Lp(a) testing and treatment are expected to have a substantial impact at the population level, enabling the identification of high-risk individuals and the subsequent prevention of a large number of cardiovascular events. Ongoing phase 3 trials will further elucidate the cardiovascular benefits of Lp(a) reduction over the long term, offering potential avenues for targeted interventions and improved cardiovascular outcomes.