Wearable devices are increasingly used to detect arrhythmias, including life-threatening ventricular tachycardia (VT). This case highlights their role in clinical settings. A patient with prior surgical aortic valve replacement because of a bicuspid valve experienced symptomatic palpitations, and his smartwatch recorded a wide complex tachycardia at 165 beats/min. His presentation led to intensive care admission and later to a diagnosis of VT successfully treated with an implantable defibrillator and ultimately requiring radiofrequency ablation. Smartwatches provide a noninvasive tool for detecting arrhythmias like VT, using photoplethysmography and single-lead ECG. Limitations include validation gaps, false positives, and user activation. Integration into clinical practice requires updated guidelines, structured reimbursement, and legal clarity. This case demonstrates the critical role of smartwatch data in VT detection and management.

Hypertrophic cardiomyopathy (HCM) is a common contemporary, treatable, genetic disorder that can be compatible with normal longevity. While current medical therapies are ubiquitous, they are limited by a lack of solid evidence, are often inadequate, poorly tolerated, and do not alter the natural disease course. As such, there has long been a need for effective, evidence-based, and targeted disease-modifying therapies for HCM. In this review, we redefine HCM as a treatable condition, evaluate current strategies for therapeutic intervention, and discuss novel myosin inhibitors. The majority of patients with HCM have elevated left ventricular outflow tract gradients, which predicts worse symptoms and adverse outcomes. Conventional pharmacological therapies for symptomatic HCM can help improve symptoms but are often inadequate and poorly tolerated. Septal reduction therapies (surgical myectomy and alcohol septal ablation) can safely and effectively reduce refractory symptoms and improve outcomes in patients with obstructive HCM. However, they require expertise that is not universally available and are not without risks. Currently, available therapies do not alter the disease course or the progressive cardiac remodeling that ensues, nor subsequent heart failure and arrhythmias. This has been regarded as an unmet need in the care of HCM patients. Novel targeted pharmacotherapies, namely cardiac myosin inhibitors, have emerged to reverse key pathophysiological changes and alter disease course. Their favorable outcomes led to the early Food and Drug Administration approval of mavacamten, a first-in-class myosin modulator, changing the paradigm for the pharmacological treatment of HCM.

The metabolic syndrome (MetS) is a constellation of comorbid derangements that increase the risk for both type 2 diabetes mellitus (DM) and cardiovascular disease (CVD). Diabetes may be preventable in many individuals with the MetS through the implementation of lifestyle and behavioral preventive strategies including dietary approaches. Several dietary patterns demonstrate efficacy in those living with the MetS to prevent progression to diabetes and reduce the risk of CVD. In this chapter, we review the Mediterranean dietary approach, plant-based diet, dietary approaches to stop hypertension (DASH), and intermittent fasting (IF) focusing on their impact on the MetS and the prevention of DM.

Objective: The underlying pathobiology of the paradoxical relationship between obesity and adverse outcomes in coronary artery disease (CAD) is unclear. Our objective was to determine the association between obesity and circulating progenitor cell (CPC) counts-a measure of intrinsic regenerative capacity-in asymptomatic individuals and patients with CAD and its impact on the obesity paradox. Approach and Results: CPCs were enumerated by flow cytometry as CD45(med+) cells expressing CD34+, CD133+, and CXCR4+ epitopes in 672 asymptomatic individuals (50 years of age; 28% obese) and 1277 patients with CAD (66 years of age; 39% obese). The association between obesity and CPCs was analyzed using linear regression models. The association of obesity and CPCs with cardiovascular death/myocardial infarction events over 3.5-year follow-up in patients with CAD was studied using Cox models. Obesity was independently associated with 16% to 34% higher CPC counts (CD34+, CD34+/CD133+, and CD34+/CXCR4+) in asymptomatic individuals. This association was not attenuated by systemic inflammation, insulin resistance, or secretion but partly attenuated by cardiorespiratory fitness and body composition. In patients with CAD, obesity was associated with 8% to 12% higher CPC counts and 30% lower risk of adverse outcomes. Compared with nonobese patients, only obese patients with high CPC counts (CD34+ cells >= median, 1806 cells/mL) were at a lower risk (hazard ratio, 0.52 [95% CI, 0.31-0.88]), whereas those with low counts (<median) were at a similar risk (hazard ratio, 0.75 [95% CI, 0.48-1.15]). Conclusions: Obesity is associated with higher CPC counts. The obesity paradox of improved outcomes with obesity in CAD is limited to patients with intact regenerative capacity who have high CPC counts.

Background: Black patients have higher rates of hospitalization for acute heart failure than other race/ethnic groups. We sought to determine whether diuretic efficiency is associated with racial differences in risk for rehospitalization after acute heart failure. Methods: A post hoc analysis was performed on 721 subjects (age, 68±13 years; 22% black) enrolled in 3 acute heart failure clinical trials: ROSE-AHF (Renal Optimization Strategies Evaluation in Acute Heart Failure), DOSE-AHF (Diuretic Optimization Strategy Evaluation in Acute Decompensated Heart Failure), and CARRESS-HF (Cardiorenal Rescue Study in Acute Decompensated Heart Failure). Repeated-measures ANOVA was used to test for a race×time effect on measures of decongestion. Diuretic efficiency was calculated as net fluid balance per total furosemide equivalents. In a subset of subjects, Cox regression was used to examine the association between race and rehospitalization according to plasma renin activity (PRA). Results: Compared with nonblack patients, black patients were younger and more likely to have nonischemic heart failure. During the first 72 to 96 hours, there was greater fluid loss ( P =0.001), decrease in NT-proBNP (N-terminal pro-B-type natriuretic peptide; P =0.002), and lower levels of PRA ( P <0.0001) in black patients. Diuretic efficiency was higher in black than in nonblack patients (403 [interquartile range, 221–795] versus 325 [interquartile range, 154–698]; P =0.014). However, adjustment for baseline PRA attenuated the association between black race and diuretic efficiency. Over a median follow-up of 68 (interquartile range, 56–177) days, there was an increased risk of all-cause and heart failure–specific rehospitalization in nonblack patients with increasing levels of PRA, while the risk of rehospitalization was relatively constant across levels of PRA in black patients. Conclusions: Higher diuretic efficiency in black patients with acute heart failure may be related to racial differences in activity of the renin-angiotensin-aldosterone system.

Effusive-constrictive pericarditis is typically caused by tuberculosis or other severe inflammatory conditions that affect the pericardium. We report a case of effusive-constrictive pericarditis consequent to a motor vehicle accident. A 32-year-old man with gastroesophageal reflux disease presented with severe substernal chest pain of a month's duration and dyspnea on exertion for one week. Echocardiograms revealed a moderate pericardial effusion, and the diagnosis was subacute effusive-constrictive pericarditis. After thorough tests revealed nothing definitive, we learned that the patient had been in a motor vehicle accident weeks before symptom onset, which made blunt trauma the most likely cause of pericardial injury and effusion. Medical management resolved the effusion and improved his symptoms. To our knowledge, this is the first report of effusion from posttraumatic constrictive pericarditis associated with a motor vehicle accident. We encourage providers to consider recent trauma as a possible cause of otherwise idiopathic pericarditis.

Patients without obstructive coronary artery disease (CAD) may have epicardial or microvascular dysfunction. The purpose of this study was to characterize patterns of epicardial and microvascular dysfunction in men and women with stable and unstable angina undergoing functional coronary angiography to inform medical therapy.

Introduction Men have worse mortality in heart failure with reduced ejection fraction (HFrEF), even after accounting for traditional risk factors. Hypothesis A metabolomics risk score, capturing the end-effect of sex-dependent karyotypic, genetic, hormonal and environmental influences, will attenuate the increased residual risk of mortality observed in males. Methods Metabolome-wide association study was performed in 187 HFrEF (EF <50%) patients in the Metabolomics, Oxidative Stress and Vascular Function in HF (MOV) study (Discovery Cohort (DC), mean age 54.0 ± 13.0 yrs, 49.2% male, 62.0% black) to determine unique endogenous metabolites associated with all-cause mortality (n=19). Metabolites that were significantly different between sexes, or had a significant metabolite*sex interaction (n=11) were further selected. Of these metabolites, those that attenuated the association of male sex with mortality were included in the metabolomics risk score (MS) (n=7). Association of male sex with mortality was determined in Cox proportional hazards models with and without inclusion of MS. Results were validated in an external validation cohort of 240 HFrEF patients in the The Atlanta Cardiomyopathy Consortium (TACC) study (Validation Cohort (VC), mean age 56.6 ± 12.0 yrs, 66.3% male, 45.4% black). Results There were 24 deaths (12.8%) during a median follow up of 782 [IQR 453, 1069] days in the DC. Males had a higher risk of mortality than females (adjusted HR: 3.84, 95% CI: 1.43-10.27; p=0.01). Metabolites that met aforementioned criteria for inclusion in the MS were: Bilirubin, Uric Acid, Hypoxanthine, L-Tyrosine, Phenylpyruvate, Oleoylcarnitine and Linoelaidyl carnitine (Table 1A). MS was higher in men than in women (0.90 ± 4.76 vs -0.66 ± 4.97, p=0.03) and associated with mortality in men (adjusted HR: 1.73, 95% CI: 1.20-2.29, p<0.001) but not in women (p=0.32) (p<0.001 for MS*sex interaction). Addition of MS to Cox models attenuated the association of male sex with mortality by 22.16%. The VC confirmed these findings: MS attenuated the association of male sex with mortality by 33.59% (Table 1B). The MS remained significantly associated with mortality (p≤0.01) in all models. Conclusions A metabolomics risk score representing the cardio-hepatic axis, purine metabolism, phenylalanine metabolism and the carnitine shuttle contributes to the increased residual risk of mortality in males with HFrEF.

Cardiovascular disease remains one of the most prevalent and preventable chronic conditions worldwide. Diet modification is the foundation of cardiovascular disease prevention. Several dietary approaches have emerged to promote better cardiovascular health. The rapid dissemination of anecdotal and observational data through the internet and social media has caused confusion amongst providers and patients. The aim of this comprehensive review is to present objective insights into 2 of today's most popular fad diets: ketogenic diet and intermittent fasting. We will evaluate the performance of these diets based on their impact on cardiovascular risk factors.

Introduction: Obese patients (BMI≥30 kg/m 2 ) with CAD have better outcomes as compared with non-obese patients, but the underlying pathobiology is unclear. Hypothesis: Obesity is directly associated with vascular regenerative capacity, measured as circulating progenitor cell (CPC) count, and this association provides insight into obesity paradox pathobiology. Methods: CPCs were enumerated by flow cytometry as CD45 med+ cells expressing CD34+, CD133+, and CXCR4+ epitopes in 672 asymptomatic individuals (50 y, 66% women, 23% Black, 28% obese) and 1,277 patients with CAD (66 y, 39% women, 22% Black, 39% obese). Association of obesity with CPC counts was analyzed using multivariable-adjusted linear regression models. Association of obesity and CPCs with cardiovascular death/myocardial infarction events over 3.5-y follow-up was studied using Kaplan-Meir survival curves and Cox models. Results: Obesity was independently associated with 16-34% higher CPC count (CD34+, CD34+/CD133+, and CD34+/CXCR4+) in asymptomatic individuals. This association was not attenuated after adjusting for measures of systemic inflammation, insulin resistance, or insulin secretion. Cardiorespiratory fitness and android fat only partly attenuated the obesity-CPC relationship. In patients with CAD, obesity was independently associated with 8-12% higher CPC counts, and with 30% lower outcome risk. Lower CPC counts were associated with outcome risk in obese patients. Obese patients with high CD34+ count (≥median) were at a lower risk, while obese participants with low counts (<median) were at a similar risk as compared with non-obese patients with high counts. The highest risk was observed in non-obese patients with low counts. Similar results were observed with CD34+/CD133+ and CD34+/CXCR4+ cells. Conclusions: Obesity is directly associated with vascular regenerative capacity, and the obesity paradox in CAD is observed in obese patients with high, but not low, CPC counts.

Solid-cystic papillary tumor (SCPT) of the pancreas is a rare neoplasm mainly affecting young women. The clinical presentation is usually nonspecific. A common problem encountered is misdiagnosis of the tumor on imaging. We report two patients with SCPT of the pancreas diagnosed incorrectly on preoperative imaging. Any cystic lesion of the pancreas with solid elements on radiology should raise the suspicion of this diagnosis. Considered to be a tumor of low malignant potential, surgical resection is associated with excellent prognosis. Surgery may be conservative in localized tumors and aggressive if nonlocalized.