Type 2 myocardial infarction (MI) is common among older adults and is associated with adverse outcomes in single-center studies. We aimed to examine temporal trends and compare outcomes between type 1 and type 2 MI in Medicare beneficiaries.

Some, but not all, patients with heart failure (HF) develop pulmonary vascular disease (PVD), which contributes to poor prognosis. Mechanisms leading to PVD in HF are poorly understood. We aimed to analyze transpulmonary gradients of proteins consumed or elaborated across the lungs to identify mediators of PVD by unbiased proteomics.

Platelet reactivity (PR) and clinical risk factors are known to have impact on outcomes in patients receiving percutaneous coronary intervention (PCI). We aimed to assess the interaction of PR and clinical risk assessment using the Thrombolysis in Myocardial Infarction Risk Score for Secondary Prevention (TRS2P) on adverse clinical outcomes following PCI.

The importance of psychological distress in patients with cardiovascular disease is increasingly recognized as both a contributing factor to the development and progression of cardiovascular disease and a consequence of the development of cardiovascular disease. Patients with acute myocardial infarction have increased risks for depression, anxiety, psychosocial stress, or posttraumatic stress disorder. Together, these negative psychological factors when occurring after myocardial infarction have been referred to as postmyocardial psychological distress. Up to half of patients after myocardial infarction may experience some form of psychological distress, and this postmyocardial psychological distress has been associated with an increased risk of future cardiac events. Biologically plausible mechanisms by which postmyocardial psychological distress may lead to increased future cardiac risk include lesser physical activity, smoking (and failure to stop smoking), excess alcohol consumption, poor diet, obesity, inadequate sleep, inadequate social support, decreased medication adherence, and poor attendance at cardiac rehabilitation. The data on whether treatment of postmyocardial psychological distress improves cardiac prognosis are mixed and of variable quality, and further studies, particularly in patients with anxiety, stress, and posttraumatic stress disorder, would be helpful. Regardless, multiple interventions can reduce psychological distress and thus lead to improved psychological health, a greater sense of emotional well-being, and a better quality of life. A goal of health care professionals should be to treat not only the disease but also the person as a whole in front of us.

In patients surviving myocardial infarction, adipose tissue infiltration within the scar is a common pathological finding and has been suggested to contribute to dysfunction and arrhythmogenesis. However, the cellular mechanisms for lipomatous metaplasia after infarction remain enigmatic. Our study reveals a novel molecular mechanism that mediates fibroblast-to-adipocyte conversion and causes fatty infiltration in the infarcted heart.

Pathological cardiomyocyte (CM) hypertrophy is a hallmark of dilated cardiomyopathy and heart failure, driven by mechanical or neurohumoral stress. Although we previously demonstrated PDE10A (phosphodiesterase 10A) as a critical contributor and potential therapeutic target in pathological cardiac remodeling and dysfunction, the underlying mechanisms remain unclear. Here, we investigated the specific signaling pathways and sources of cyclic nucleotides modulated by PDE10A in CM hypertrophy.

Hereditary hemorrhagic telangiectasia (HHT) is a near-fully penetrant autosomal dominant disorder characterized by nosebleeds, anemia, and arteriovenous malformations. The great majority of HHT cases are caused by heterozygous loss-of-function mutations in ACVRL1 or ENG, which encode proteins that function in bone morphogenetic protein signaling. HHT prevalence is estimated at 1 in 5000 and is accordingly classified as rare. However, HHT is suspected to be underdiagnosed.

Mechanical thrombectomy offers a promising alternative to thrombolytic-based approaches for reducing thrombus burden and right heart strain in acute pulmonary embolism. This pivotal Food and Drug Administration-approval trial evaluated the safety and efficacy of the Symphony Thrombectomy System (Imperative Care, Inc, Campbell, CA) in acute intermediate-risk pulmonary embolism.

Self-expanding transcatheter pulmonary valves (TPV) offer a promising alternative to surgical pulmonary valve replacement in patients with a large patched or native right ventricular outflow tract. Little is known about remodeling of the implanted valve or valve-anatomy interactions.

In the randomized EBC MAIN trial (European Bifurcation Club Left Main Coronary Stent), target lesion revascularization at 3 years poststenting of left main (LM) bifurcations was more frequent with upfront dual-stenting compared with the stepwise provisional approach. Restenosis location and its relation to stent technique are poorly characterized. The aim of this study was to investigate restenosis location after LM bifurcation stenting, and the impact of stent implantation technique.

Right ventricular functional adaptation to afterload is a major determinant of outcome in pulmonary arterial hypertension (PAH). We aimed to investigate if right ventricular-pulmonary artery (PA) coupling evaluated by the ratio of tricuspid annular plane systolic excursion (TAPSE) to systolic pulmonary artery pressure (sPAP) improves risk assessment scores for survival prediction.

Neointimal hyperplasia is the major cause of significant vascular complications after arterial interventions. Despite the advancements in strategies such as drug-eluting stents to minimize neointimal hyperplasia, achieving consistently effective long-term outcomes remains a challenge. Protein-protein interactions mediated by PDZ (PSD-95, Discs-large, and ZO-1) domains are essential for numerous biological processes. However, little is known about the role of PDZ proteins in neointima formation. This study aims to explore the role of TAX1BP3 (Tax1 binding protein 3), a singular PDZ protein, in phenotypic switching of vascular smooth muscle cells (VSMCs) and its implication in neointimal hyperplasia.

Nutrient surplus sensing through PI3K (phosphoinositide-3-kinase) and mTOR (mechanistic target of rapamycin) stimulates anabolism to expand cellular mass, whereas nutrient and energy deprivation sensing through SIRT1 (sirtuin-1) and AMPK (adenosine monophosphate-activated protein kinase) promotes catabolism to support cytoprotective quiescence. By signaling through downstream effectors (PGC-1α [peroxisome proliferator-activated receptor gamma coactivator 1-alpha], PPARα/PPARγ, FoxO1 [forkhead box protein family O1], NRF2 [nuclear factor erythroid-derived factor 2], HIF-1α [hypoxia-inducible factor-1α], and HO-1 [heme oxygenase-1]), environmental nutrients, growth factors, and cellular stress influence mitochondrial biogenesis, autophagic flux, cardiac hypertrophy, and cardiomyocyte senescence and apoptosis. Despite these canonical descriptions, the actual response to each effector is determined by the intensity and duration of signaling. Typically, transient and measured signaling produces adaptive effects, whereas continuous heightened activity yields maladaptive responses. The effects of signaling are also influenced by context; ie, the nature and intermittency of the external stress and the characteristics of the underlying substrate (eg, cardiomyopathy, obesity, or aging). PI3K signaling promotes physiological hypertrophy and is cardioprotective during abrupt cardiac stress, but its sustained activation accelerates pathological hypertrophy related to obesity and aging. Signaling through SIRT1/AMPK (and upregulation of autophagic flux) exerts favorable effects during exercise training and in chronic cardiomyopathy, obesity, and aging, but it undermines the cardiac response to abrupt stress. Intermittent FoxO1 upregulation may promote physiological hypertrophy while antagonizing pathological hypertrophy, but prolonged activation leads to cardiomyocyte apoptosis. NRF2 exerts antioxidant effects when background autophagic flux is vigorous but aggravates cellular stress when autophagy is suppressed (as in pathological hypertrophy). Sustained activation of PPARγ, NRF2, and HIF-1α in nutrient surplus states can lead to maladaptive ventricular remodeling, thus explaining the results of clinical trials with thiazolidinediones, bardoxolone, and prolyl hydroxylase inhibitors. The influence of duration, intensity, and context may be mediated (in part) by the activation or suppression of counterregulatory mechanisms, by the selective recruitment of corepressors, and by posttranslational protein modifications. These observations, considered collectively, suggest that no protein or cellular process viewed in isolation can be regarded as cardioprotective or maladaptive. Cell signals operate usefully if they are delivered as part of an orchestrated program of compartmentalized nuanced bursts, acting as elements of multifaceted oscillating systems whose periodicity is determined by the need to achieve homeostasis.

Ischemic heart disease is the leading cause of heart failure with reduced ejection fraction in the developed world. An evolution of background medical therapy over the past decade has spurred improvement in symptoms and a reduction in morbidity and mortality with ischemic cardiomyopathy. However, there is still ongoing debate about the role and impact of revascularization. Much of the societal guidance regarding revascularization with coronary artery bypass grafting in ischemic cardiomyopathy comes from the STICH trial (Surgical Treatment for Ischemic Heart Failure) which predates improvements in medical therapy. More recently, the REVIVED-BCIS2 trial (Revascularization for Ischemic Ventricular Dysfunction-British Cardiovascular Intervention Society) failed to show a benefit of percutaneous coronary intervention on heart failure hospitalization and mortality in ischemic cardiomyopathy over contemporary medical therapy alone. Yet, there are outstanding questions regarding the role and modality of revascularization required to improve outcomes. We review current data and future directions in the management of ischemic cardiomyopathy and the potential role of revascularization.

The incidence of permanent pacemaker implantation (PPMI) due to high-grade atrioventricular block after transcatheter aortic valve implantation (TAVI) is 10% to 15% at 1-year, and current prediction algorithms remain unreliable.

Stress perfusion cardiovascular magnetic resonance (CMR) is widely used to detect myocardial ischemia, mostly through visual assessment. Recent studies suggest that strain imaging at rest and during stress can also help in prognostic stratification. However, the additional prognostic value of combining both rest and stress strain imaging has not been fully established. This study examined the incremental benefit of combining these strain measures with traditional risk prognosticators and CMR findings to predict major adverse clinical events (MACE) in a cohort of consecutive patients referred for stress CMR.

Previous studies have suggested that the associations between ambient air pollution and atherosclerotic cardiovascular diseases (ASCVD) differ by genotype. A genome-wide approach provides a more comprehensive understanding of this relationship on a genomic scale.

Cardio-kidney-metabolic (CKM) disease represents a significant public health challenge. While proteomics-based risk scores (ProtRS) enhance cardiovascular risk prediction, their utility in improving risk prediction for a composite CKM outcome beyond traditional risk factors remains unknown.

Evidence informing clinical guidelines assumes that all transcatheter aortic valve implantation (TAVI) devices have similar effectiveness, in other words, displaying a class effect across TAVI valves. We aimed to assess the comparative effectiveness of different TAVI platforms relative to other TAVI counterparts or surgical aortic valve replacement (SAVR).

Fetal tachycardias can cause adverse fetal outcomes including ventricular dysfunction, hydrops, and fetal demise. Postnatally, ECG is the gold standard, but, in fetal practice, echocardiography is used most frequently to diagnose and monitor fetal arrhythmias. Noninvasive extraction of the fetal ECG (fECG) may provide additional information about the electrophysiological mechanism and monitoring of intermittent arrhythmias. Signal processing advances could provide improved data quality impacting clinical translation. The aim of this study was to assess the fetus with known or suspected tachycardia using noninvasive abdominal fECG and correlate results with fetal echocardiography and postnatal ECG.