Cardiology in Review最新文献

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.

Albuminuria, once viewed solely as a renal biomarker, has emerged as an integrative indicator of endothelial dysfunction, vascular injury, and systemic congestion in heart failure (HF). Evidence now suggests it not only reflects disease severity but also contributes to the cardiorenal mechanisms that drive progression. Hemodynamic stress, glomerular glycocalyx disruption, and renin-angiotensin-aldosterone system activation promote albumin leakage through oxidative and inflammatory injury. Large studies such as BIOlogy Study to TAilored Treatment in Chronic Heart Failure and FINerenone trial to investigate Efficacy and sAfety supeRioR to placebo in paTientS with Heart Failure show that 40-50% of patients with HF exhibit albuminuria, which correlates with markers of congestion and independently predicts hospitalization and mortality in both reduced and preserved ejection fraction phenotypes. Even low-grade albuminuria is associated with increased cardiovascular risk, and changes in urinary albumin-to-creatinine ratio (uACR) over time track with outcomes. Therapies including mineralocorticoid receptor antagonists, sodium-glucose cotransporter 2 inhibitors, and renin-angiotensin-aldosterone system blockade can reduce albuminuria, though whether lowering uACR itself improves outcomes remains uncertain. Albuminuria bridges renal, vascular, and hemodynamic risk and may serve as both a biomarker and modifiable target in HF. Incorporating routine uACR measurement into clinical care could refine risk stratification and therapeutic monitoring, while future studies should clarify whether targeted albuminuria reduction yields meaningful improvements in HF outcomes.

Assessment of the optimal management in patients requiring reintervention after transcatheter aortic valve replacement (TAVR). Since its inception in 2002, TAVR has significantly transformed the management of aortic stenosis. The treatment for TAVR procedural and device failures varies depending on the specific cause of failure. As the number of TAVR procedures increases, particularly in individuals aged 70 or younger, it is likely that we will see a rise in the number of patients needing further treatment due to degeneration of the transcatheter heart valve. Although TAVR has proved to be safe and effective, structural valve deterioration is inevitable. Even though TAVR has shown promising data of low structural valve deterioration rates up to 6 years from various clinical trials and up to 10 years in isolated series, the majority of these patients were older. But, reintervention after TAVR seems unavoidable. It may need reintervention with a second TAVR valve, or it may require surgical TAVR-explant and subsequent surgical aortic valve replacement. Also, a third option in the form of a hybrid technique, is available now. Thus, the selection of patients is crucial in choosing the appropriate initial management as it can have long-term repercussions.

Acute myocardial infarction (AMI) remains a leading cause of hospitalization and mortality in the United States. Percutaneous coronary intervention (PCI) improves outcomes, but contemporary research on nationwide PCI access is scarce. This study investigates geographic, demographic, and socioeconomic determinants of PCI usage and inpatient outcomes among AMI hospitalizations. A retrospective cross-sectional analysis of the National Inpatient Sample (October 2015-December 2021) identified US hospitalizations for AMI. Outcomes including PCI utilization, in-hospital mortality, routine discharge, and postacute transfer, were stratified by region, urban-rural status, and income quartile. Multivariable logistic regression assessed factors associated with PCI use, adjusting for demographics, comorbidities, and hospital characteristics. Among 5,752,863 AMI hospitalizations, 20.2% occurred in rural and 79.8% in urban counties; 36.8% involved PCI (20.1% rural, 79.9% urban). After adjustment, urban hospitals had higher odds of PCI [adjusted odds ratio: 1.15; 95% confidence interval (1.13-1.18); P < 0.001), routine discharge [1.06 (1.04-1.08), P < 0.001], and transfer [1.09 (1.07-1.11), P < 0.001], with lower mortality [0.962 (0.941-0.983), P < 0.001]. Higher-income patients were more likely to undergo PCI [1.10 (1.08-1.12), P < 0.001] and routine discharge [1.06 (1.04-1.08), P < 0.001], and had lower odds of mortality [0.963 (0.941-0.986), P = 0.002] and postacute care transfer [0.957 (0.938-0.976), P < 0.001]. PCI was significantly associated with age, sex, race, insurance status, comorbidity burden, hospital location, and bed size. Notable PCI disparities persist between urban and rural populations, with lower mortality in urban regions. Socioeconomic and demographic factors continue to influence PCI, underscoring inequities in AMI care. These findings highlight the need for quality initiatives to ensure equitable treatment nationwide.

Electromechanical uncoupling is increasingly recognized as a key mechanism underlying arrhythmias in patients supported with extracorporeal membrane oxygenation (ECMO) and ventricular assist devices. This review summarizes current evidence on how mechanical unloading, altered preload and afterload conditions, myocardial stretch, inflammation, hypothermia, and electrolyte disturbances contribute to electrical instability during mechanical circulatory support. We describe device-specific arrhythmia patterns, including atrial fibrillation in venovenous ECMO, ventricular tachyarrhythmias and electrical storm in venoarterial ECMO, and suction- or remodeling-related arrhythmias in continuous-flow left ventricular assist devices. We also review findings from electrophysiologic mapping, strain imaging, and cardiac magnetic resonance imaging that characterize the evolving arrhythmic substrate during support. Emerging technologies such as artificial intelligence prediction models, computational mechanoelectric simulations, and sensor-based device analytics offer promising tools for early detection and individualized management. Despite these advances, current data remain limited by small sample sizes, heterogeneous populations, and a lack of standardized definitions or prospective validation. A deeper understanding of dynamic electromechanical interactions, combined with integrated monitoring and refined device management strategies, will be essential to improve rhythm stability, myocardial recovery, and overall survival.

Hyperlipidemia in children is an increasingly recognized public health concern. Both primary genetic disorders-notably familial hypercholesterolemia, which affects roughly 1 in 250 children-and secondary factors like obesity, diabetes, hypothyroidism, and nephrotic syndrome contribute to pediatric dyslipidemia. Unmanaged childhood hyperlipidemia can track into adulthood and drive premature atherosclerosis and cardiovascular disease. The American Academy of Pediatrics and National Heart, Lung, and Blood Institute recommend universal lipid screening at ages 9-11 years and again in late adolescence, with earlier targeted screening for high-risk children. Lifestyle modification is first-line therapy. When lifestyle measures are insufficient, pharmacologic treatment is considered from around 10 years of age for those with markedly elevated low-density lipoprotein or additional risk factors. Statins are the cornerstone, achieving 20-50% reductions in low-density lipoprotein levels with a favorable safety profile in children. Other agents, including ezetimibe, bile acid sequestrants, fibrates, omega-3 fish oils, and newer monoclonal antibodies to proprotein convertase subtilisin/kexin type 9, are used in select cases such as familial hypercholesterolemia or severe hypertriglyceridemia. Managing pediatric hyperlipidemia also entails overcoming challenges. Recent advances include the approval of proprotein convertase subtilisin/kexin type 9 inhibitors for pediatric use.

The prevalence of cardiovascular disease increases with age, driven by processes of inflammation, oxidative stress, and mitochondrial dysfunction. Delaying the cascade caused by these risk factors will be essential to reducing cardiovascular morbidity and mortality in our aging population. Sirtuins are nicotinamide adenine dinucleotide-dependent deacetylase enzymes involved in metabolic regulation that show promise in attenuating these disease processes and increasing longevity. This review will examine the role of sirtuins at the cellular level in relation to cardiovascular health and discuss their potential as novel therapeutic targets for atherosclerosis, heart failure, and metabolic syndrome.

Obstructive sleep apnea (OSA) is a common sleep-related breathing disorder defined by repeated upper airway collapse, intermittent hypoxia, and sleep disruption. Continuous positive airway pressure (CPAP) is the gold-standard treatment of moderate-to-severe OSA but is limited by long-term discomfort and inconvenience. Lifestyle changes, such as weight loss, are highly effective, especially for patients with obesity, where decreases in upper airway adiposity are highly correlated with decreases in apnea-hypopnea index. Recent developments of oral drug treatments have introduced the use of glucagon-like peptide-1 receptor agonists, tirzepatide and liraglutide, as new treatments of OSA for patients with obesity. Clinical trials, such as SURMOUNT-OSA and SCALE Sleep Apnea, demonstrate that glucagon-like peptide-1 receptor agonist--induced weight loss significantly reduces apnea-hypopnea index, suggesting that weight loss is the primary mechanism of improvement in OSA. Other mechanisms of action, such as reduction of inflammation, may contribute to the therapeutic effect. Other new oral treatments, such as atomoxetine and aroxybutynin (AD109), are promising treatments that can work within a few hours and are independent of weight loss and may offer new treatment profiles of nonobese patients or CPAP-intolerant patients. Incorporating these new treatments within practice has the possibility of improving adherence and reducing cardiometabolic complications and may overcome limitations of the treatment with CPAP. Further research will establish longer-term outcomes, optimal patient selection, and possible combinations with other treatments.

Nephrolithiasis is a crystal concretion formed within the kidneys; it affects ~10-12% of the world population and confers an increased risk of end-stage renal failure. Its global burden comprised 106 million incident cases in 2021 (67% men); incident cases, deaths, and disability-adjusted life-years increased by ~27%, 60%, and 35%, respectively, between 2000 and 2021. Environmental factors play a crucial role in renal stone development, in addition to an underlying genetic background. Nephrolithiasis raises cardiovascular (CV) risk, including the risk for coronary artery disease (CAD) or stroke. Endothelial dysfunction is strongly linked with nephrolithiasis, and it may be an intermediate and modifiable feature between nephrolithiasis and CV diseases. Nutrition is closely linked with the risk of nephrolithiasis; diets high in animal protein, low in alkali, magnesium, and citrate, and high in oxalate- and calcium-containing foods lead to negative calcium balance, low urine pH, and low urinary excretion of citrate, potassium, and magnesium, all favoring stone formation. Raising fluid intake prevents the development of a first kidney stone (primary prevention) and also decreases the risk of stone recurrence (secondary prevention). Kidney stone formers exhibit 25% higher risk of CAD, 17% higher risk of stroke, and 39% higher risk of arterial disease, albeit with high heterogeneity. Lifestyle modifications, dietary interventions, and pharmacological therapies may prevent recurrences and manage residual stone fragments. The use of sodium-glucose cotransporter-2 inhibitors may inhibit nephrolithiasis by restoring impaired autophagic flux; however, adding an autophagy inhibitor (eg, hydroxychloroquine) should be avoided as it compromises the protection provided by a sodium-glucose cotransporter-2 inhibitor. Nephrolithiasis confers a long-term risk of a future CV event. An increased risk of CAD and/or hypertension has also been linked with a prior history of kidney stones. Hence, one should view nephrolithiasis as a systemic disorder, linked with hypertension, chronic kidney disease, bone, and CV damage.

Recent evidence suggests that Glucagon-Like Peptide-1 receptor agonists (GLP-1RAs) can assist in alcohol and related substance use disorders (ASUD). GLP-1RAs act on the same receptor targets as native GLP-1, but last from several hours to a week, compared to the 1.5-5 minutes for naturally occurring GLP-1. These receptor targets are the GLP-1 G-protein coupled receptors. They are part of a large family of 800-1000 receptors that are present throughout the human body, but higher in concentration in the hypothalamus, brainstem, and the gastrointestinal tract. Four hundred sixty of the G-protein coupled receptors are in the olfactory system, mediating smell and taste. Mechanistically, GLP-1RAs reduce activity in the dopamine reward system. The observational literature demonstrates that GLP-1RAs mitigate the risk of hospitalizations associated with alcohol use disorder and other substance use disorders. Semaglutide and liraglutide reduced ASUD-related hospitalizations compared to other GLP-1RAs and standard previously prescribed ASUD pharmacotherapy. This review will detail the evidence supporting this.