The COVID-19 pandemic disrupted health services, particularly affecting individuals with cardiometabolic diseases. This study compared health care use and mortality trends in adults with cardiometabolic diseases during the first pandemic year. It also examined associations between changes in outpatient visits and diagnostic tests with acute health care utilization and mortality.

PYGM (muscle glycogen phosphorylase), the rate-limiting enzyme in glycogenolysis, plays an indispensable role in maintaining cardiac energy metabolism. However, the role of PYGM in the pathogenesis of myocardial infarction (MI) remains unclear.

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.