Cardiology in Review最新文献

Atrial fibrillation (AF) stands as a prevalent and escalating cardiac arrhythmia in the United States, with obesity emerging as a prominent modifiable risk factor. This article explores the intricate relationship between obesity and AF, delving into the multifaceted pathophysiological mechanisms linking the 2 conditions. Various factors, such as autonomic dysfunction, left atrial stretch, inflammation, and hormonal imbalances, contribute to the initiation and perpetuation of AF in obese individuals. The Atrial Fibrillation Better Care pathway, emphasizing lifestyle modifications and weight loss strategies, emerges as a practical guideline for managing AF in obesity. This comprehensive review underscores the critical role of obesity as a significant modifiable risk factor for AF, urging a proactive approach to its management. Implementing the Atrial Fibrillation Better Care approach, focusing on encouraging physical activity, promoting healthy dietary habits, and raising awareness about the risks associated with obesity prove essential in preventing and mitigating the burden of AF in the obese population.

Cardiovascular disease (CVD) refers to a wide array of conditions that damage the heart muscle and impede its ability to effectively circulate blood throughout the body. In damaged or pathological states, the heart muscle might not function as effectively as it would have had there been no insult to it. Understanding this, certain CVDs can put the heart in a "metabolic disadvantage"-a state in which it cannot synthesize energy stores, in the form of adenosine triphosphate (ATP), as efficiently as it was once able to do. While the heart typically uses fatty acids for its ATP synthesis, the metabolic processes required to do so consume more oxygen per mole than the processes required to convert glucose (or carbohydrates) to ATP. In conditions when oxygen demand outweighs supply-such as angina, heart failure, and certain inherited CVDs-the myocardium can more efficiently run via glucose oxidation. Despite this knowledge, there are no currently approved therapeutics or interventions that encourage this "metabolic shift" in the myocardial cells. Currently in phase II clinical trials, however, is a novel medication called ninerafaxstat. This novel drug is a partial inhibitor of fatty acid oxidation and thus pushes the heart to convert glucose (instead of fatty acids) to ATP-ultimately cutting down on oxygen supply. While still completing clinical trials, ninerafaxstat must undergo further safety and efficacy evaluation before it can be used as a standard of care. If, however, the drug makes it to market, it might offer a unique way to improve both the symptoms and quality of life of the millions of Americans who suffer from CVDs.

Long coronavirus disease (COVID) is the development or persistence of symptoms after an acute SARS-CoV-2 (COVID-19) infection. Fewer patients are developing acute COVID-19 infections, but patients with long COVID continue to have alarming long-term sequelae. Many cardiac magnetic resonance imaging studies show significant changes in cardiac structure after a COVID-19 infection, suggestive of an increased burden of many cardiovascular diseases, notably myocarditis. The pathophysiology of COVID-19 requires viral binding to angiotensin-converting enzyme 2 protein receptors throughout the body, which are upregulated by inflammation. Consequently, the numerous preexisting conditions that worsen or prolong inflammation enhance this binding and have differing effects on patients based on their unique immune systems. These pathophysiological changes drive long COVID cardiac sequelae such as inappropriate sinus tachycardia, postural orthostatic tachycardia, and other types of orthostatic intolerance. Increased screening for long COVID and low-risk interventions such as exercise regimens could alleviate the suffering endured by patients with long COVID. Many studies such as the Researching COVID to Enhance Recovery Initiative (RECOVER) trials at the National Institutes of Health are exploring potential treatments for long COVID patients.

Cardiac amyloidosis (CA) represents an emerging challenge in cardiovascular medicine, with notable clinical overlaps and diagnostic complexities when coexisting with coronary artery disease (CAD). This integrative review navigates the intricate terrain of CA and CAD, elucidating epidemiology, clinical presentations, and diagnostic considerations. Examining both immunoglobulin light chain amyloidosis (AL) and transthyretin amyloidosis, we underscore their shared demographic associations, diagnostic intricacies, and potential diagnostic confounders with CAD. Notably, we emphasize the impact of CA on epicardial coronary arteries and the consequential implications for coronary microcirculation. Further exploration reveals the connection between CA and acute myocardial infarction, emphasizing early recognition as pivotal. In terms of differential diagnosis, we underscore the significance of clinical symptoms, electrocardiography, echocardiography, cardiac magnetic resonance, and bone scintigraphy. Additionally, we scrutinize the intricate realm of treatment, encompassing medication selection, antithrombotic strategies, and revascularization modalities. Our review addresses the distinctive challenges posed by CA patients' limited tolerance for conventional therapies. This comprehensive synthesis serves as an invaluable resource for clinicians confronting the intricate intersection of CA and CAD. By offering insights into diagnostic refinement and innovative therapeutic avenues, we aim to enhance patient outcomes and quality of life within this complex clinical landscape.

While the diagnosis of aortic stenosis (AS) is relatively straightforward on physical examination and echocardiographic imaging, the determination of severity is often challenging. Assessment of severity assumes the greatest importance when aortic valve replacement is under consideration. In addition to a number of well-known technical frustrations in the Doppler diagnosis, a puzzling and persistent discrepancy between aortic valve gradients obtained by Doppler and those measured at catheterization emerged, further clouding the issue. This discordance led several investigators to the discovery of pressure recovery (PR) of varying degrees in the ascending aorta in AS patients distal to the stenotic valve. PR is often a significant factor in assessing the physiologic burden of AS. The impact of PR must be considered in the comprehensive assessment of AS severity.

Hyperlipidemia is a major risk factor for myocardial infarction (MI), yet trends and disparities in MI-related mortality among older adults in the United States are poorly understood. This study aimed to examine temporal trends and demographic disparities in MI-related mortality among adults aged ≥65 years. Death certificate data from the CDC WONDER database (1999-2020) were analyzed using ICD-10 codes for MI (I21-I22) and hyperlipidemia (E78.0-E78.9). Age-adjusted mortality rates (AAMR) per 100,000 were calculated, and temporal trends were evaluated using Joinpoint regression. Among 90,568 MI-HL deaths, men comprised 55%. AAMR increased from 6.4 in 1999 to 11.9 in 2020, with the steepest rise between 1999-2005 (APC 7.40%). Men consistently had higher AAMRs than women (2020: 16 vs 8.8). Whites had the highest overall AAMR (10.0), followed by Blacks (9.4) and Hispanics (7.8). Age-stratified mortality was highest in those ≥85 (21.4), followed by 75-84 (11.6) and 65-74 (6.0). Significant geographic variation existed, with states in the top 90th percentile (Vermont, Rhode Island, South Dakota, Ohio) showing nearly fourfold higher AAMRs than those in the lowest 10th percentile (Nevada, Alabama, Connecticut, Georgia). MI-related mortality with hyperlipidemia shows marked demographic and geographic disparities among older U.S. adults. Men, Whites, the oldest age groups, and residents of certain states and non-metropolitan areas are at greatest risk. Enhanced screening, preventive strategies, and equitable access to care are essential to reduce disparities and improve cardiovascular outcomes.

Chronic kidney disease (CKD) significantly increases the risk of acute myocardial infarction (AMI)-related mortality by accelerating atherosclerosis and impairing cardiovascular outcomes. This study analyzes long-term trends in AMI mortality among patients with CKD in the United States from 1999 to 2024. We used the Centers for Disease Control and Prevention's Wide-ranging Online Data for Epidemiologic Research database to identify death certificates of individuals aged ≥45 years from 1999 to 2024, listing AMI as the underlying and CKD as a contributing cause of death. Age-adjusted mortality rates (AAMRs) per 100,000 population were calculated, and annual percent changes were determined using Joinpoint regression analysis. A total of 81,465 deaths were attributed to AMI in patients with CKD. The overall AAMR declined from 4.5 in 1999 to 1.5 in 2024, with a temporary increase between 2009 and 2012 (annual percent change: 18.03; P < 0.05). Males had consistently higher AAMRs (3.8) than females (2.0), and non-Hispanic African Americans (5.2) experienced nearly double the rates of other racial/ethnic groups. Older adults (≥65 years) had an AAMR of 6.2, 9 times higher than that of middle-aged adults (0.7). The highest rates were observed in the Western US and in nonmetropolitan areas (3.0 each). Despite an overall decline in AMI-related mortality among CKD patients over the past 2 decades, persistent disparities by age, sex, race/ethnicity, and geography remain, calling for the development of targeted and equitable approaches to reduce mortality burden across high-risk groups such as males and nonmetropolitan residents.

Heart failure management is a rapidly progressing field that has dramatically changed over the past several decades. The development of guideline-directed medical therapy has allowed those with heart failure with reduced ejection fraction to have far better clinical outcomes. Despite these advances, heart failure remains a very prevalent and morbid condition with hundreds of thousands of deaths attributed to heart failure in the United States each year. The need for novel therapeutics remains vital to improve outcomes and help those who continue to have persistent symptoms despite optimal medical therapy. The advent of cell therapy for heart failure has sparked great interest over the years due to its potential to not just temper, but reverse adverse cardiac remodeling. Many preclinical and clinical trials have explored the use of pluripotent stem cells for both ischemic and nonischemic etiologies of heart failure. There have been several pivotal trials in the world of cell therapy that have failed to meet their primary endpoints but have still paved the way to show both the safety of cell therapy and signal towards mortality and quality of life benefits. Although cell therapy has not yet been successful to become a staple of heart failure management, the field continues to be studied and signals potential to have a place in the management of even the sickest heart failure patients.

Spontaneous coronary artery dissection (SCAD) is an emerging cause of acute coronary syndrome, myocardial infarction, and sudden cardiac death, particularly in young women with few established risk factors. We performed a retrospective analysis of 13 consecutive patients diagnosed with SCAD across 3 institutions over 5 years to identify associated cardiovascular risk factors. SCAD accounted for 0.5% of all cardiac catheterizations for chest pain. The average age was 49.3 years, and 84% of them were women. Of those with hyperlipidemia, 61% had it, 46% had hypertension, and 8% had prediabetes. There were no indications of fibromuscular dysplasia or connective tissue disorders in any patients. A mean D-dimer level of 1,578 ng/dL was observed in 38% of individuals, while elevated inflammatory markers were infrequently present. Only 1 patient required percutaneous coronary intervention; the remaining patients were managed conservatively with dual antiplatelet therapy, yielding excellent outcomes. Although historically considered nonatherosclerotic, SCAD in our sample frequently correlated with traditional cardiovascular risk factors, suggesting that endothelial vulnerability associated with these conditions may play a contributory role. Elevated levels of D-dimer may be a sign of disease activity. Most patients respond favorably to conservative treatment; enhanced clinical awareness is essential for prompt diagnosis and management.

Despite widespread use of high-intensity statins, ezetimibe, and proprotein convertase subtilisin/kexin type 9 inhibitors, substantial atherosclerotic cardiovascular disease risk persists, especially in people with heterozygous familial hypercholesterolemia or elevated lipoprotein(a) [Lp(a)] levels. Cholesteryl ester transfer protein (CETP) inhibitors block the transfer of hydrophobic cholesteryl esters from high-density lipoprotein to apolipoprotein B (apoB)-containing particles. This process raises high-density lipoprotein-C and lowers low-density lipoprotein-C, apoB, and Lp(a) levels. The first-generation of CETP inhibitors was limited by toxicity, neutral outcomes, or unfavorable pharmacokinetics. Obicetrapib is a next-generation amphipathic CETP inhibitor that selectively targets both CETP's hydrophobic and hydrophilic tunnels. It reduces low-density lipoprotein-C by about 30-51%, apoB by 20-33%, and Lp(a) by 30-57% without causing tissue accumulation or toxicity. Phase 3 trials (BROOKLYN, BROADWAY, TANDEM) show that obicetrapib is effective when added to maximized therapy, with a safety profile similar to placebo. Its consistent reduction of Lp(a) addresses an important unmet need. In addition to lowering atherogenic lipoproteins, early data suggest potential for neuroprotection, such as reductions in p-tau217 seen among APOE4 carriers. A 2025 pooled analysis offers initial evidence that major adverse cardiovascular events are reduced, as studied in the ongoing PREVAIL outcomes trial. This review covers CETP biology and tunnel mechanics, outcomes from earlier CETP inhibitor studies, obicetrapib's pharmacology, and current efficacy and safety data, and will clarify its potential place in lipid management today.