The impact of modular cardiac rehabilitation on quality of life and exercise tolerance in patients with myocardial infarction and COVID-19 infection.

Introduction: Acute myocardial infarction (AMI) remains one of the leading causes of death worldwide during cardiovascular diseases. An important step in the secondary prevention of recurrent myocardial infarction is cardiac rehabilitation (CR). However, with the onset of the global COVID-19 pandemic, the CR programs in many clinics were limited due to the quarantine measures. Knowledge about the effects of CR on quality of life and exercise tolerance in AMI patients with COVID is scarce. Aim: To evaluate the use of a modular CR program on quality of life and exercise tolerance among post-AMI patients with COVID-19 recovery, and in those with no history of COVID-19 infection. Material and methods: This study included 118 patients with or recovering from acute myocardial infarction. They were divided into 2 groups: the first group included 86 patients, who had slight "ground-glass opacity" changes on the computed tomography (CT) scans, and the second group comprised 32 patients, who had no history of coronavirus infection or no change on CT scan of the lungs during the pandemic. The CR program was modified due to the pandemic era. Results: Physical tolerance increased in both groups after CR 3.6 months as compared to before the CR program (duration of training in seconds (p < 0.05), a 6-minute walk test (p < 0.05), the maximal oxygen consumption (VO2max) (p < 0.05), and the metabolic equivalent of task (MET) (p < 0.05)). Similarly, quality of life measures improved in both groups. Treatment satisfaction was higher in the first group at the beginning and the end of CR. Conclusions: The modular CR program improves exercise capacity and quality of life with AMI and COVID-19 similar to that of patients without AMI. Patients after COVID-19 should undergo rehabilitation.

Premature ventricular complexes: diagnostic and therapeutic considerations in clinical practice : A state-of-the-art review by the American College of Cardiology Electrophysiology Council.

Premature ventricular complexes (PVCs) are common arrhythmias in the clinical setting. PVCs in the structurally normal heart are usually benign, but in the presence of structural heart disease (SHD), they may indicate increased risk of sudden death. High PVC burden may induce cardiomyopathy and left ventricular (LV) dysfunction or worsen underlying cardiomyopathy. Sometimes PVCs may be a marker of underlying pathophysiologic process such as myocarditis. Identification of PVC burden is important, since cardiomyopathy and LV dysfunction can reverse after catheter ablation or pharmacological suppression. This state-of-the-art review discusses pathophysiology, clinical manifestations, how to differentiate benign and malignant PVCs, PVCs in the structurally normal heart, underlying SHD, diagnostic procedures (physical examination, electrocardiogram, ambulatory monitoring, exercise testing, echocardiography, cardiac magnetic resonance imaging, coronary angiography, electrophysiology study), and treatment (lifestyle modification, electrolyte imbalance, medical, and catheter ablation).

Cigarette smoking increases plasma concentrations of vascular cell adhesion molecule-1 in patients with coronary artery disease.

Cigarette smoking adversely affects endothelial function and increases risk of coronary artery disease (CAD). The pathogenesis of coronary atherosclerosis is currently thought to involve interactions between inflammatory cells and vascular endothelium. Adhesion molecules play a pivotal role in the accumulation of inflammatory cells at the endothelium. Little is known about the role of cigarette smoking in this atherosclerotic inflammatory process. The aim of this study was to evaluate the effects of cigarette smoking on the plasma concentrations of soluble vascular cell adhesion molecule-1 (VCAM-1) in patients with CAD. The soluble VCAM-1 level was quantified in smoking CAD patients (n = 19) in comparison to those from patients with CAD alone (n = 10). Plasma concentrations of soluble VCAM-1 were measured by enzyme-linked immunosorbent assay. The soluble VCAM-1 level was found significantly higher in smokers than in nonsmokers (32.1279 +/- 21.6421 vs 9.4570 +/- 7.8138 ng/mL, p < 0.01), and in patients with previous myocardial infarction (MI) than in those without previous MI, but not significant statistically (27.7279 +/- 22.8813 vs 17.8170 +/- 15.9172 ng/mL, p > 0.05). No significant difference was observed for soluble VCAM-1 levels between hypertensive and nonhypertensive patients, multivessel and one-vessel disease, or anterior and inferior MI localizations. The present study suggests that in patients with CAD, smoking leads to elevated levels of soluble VCAM-1 that may clarify one of the mechanisms of its accelerating effect on the atherosclerotic process.