Ventricular Arrhythmia Risk in Noncardiac Diseases

Abstract

diseases, to mention the main methods used to assess arrhythmia risk, as well as to elucidate their relation to long-term outcome. Dyslipidemia, obesity, diabetes mellitus, liver, hematologic, neurologic and psychiatric disorders, are discussed. Dyslipidaemia and ventricular arrhythmia riskElevated LDL cholesterol was associated with all manifestations of coronary artery disease including sudden cardiac death [7]. Hypercholesterolemia is not only atherogenic, but is also associated with autonomic imbalance, alteration of the contractile properties of the myocardium, increased oxidative stress and ventricular electrophysiological remodeling [8,9]. Myocardial electrical remodeling due to hypercholesterolemia caused prolonged action potential durations, longer QTc (heart rate corrected QT interval durations), conduction slowing and increased repolarization dispersion [9,10].Several clinical and autopsy studies demonstrated an association between elevated cholesterol levels and sudden cardiac death [11,12]. Gualdiero et al. reported a positive correlation between cholesterol level, QT dispersion and premature ventricular contractions in patients with isolated hypercholesterolemia, and normalization of serum cholesterol and QT dispersion and improvement of ventricular ectopic activity, with simvastatin [13]. Szabo et al. found significant correlations of QT interval duration and QT dispersion with total and LDL cholesterol, triglycerides and apoplipoprotein B, respectively, in patients with type IIb hyperlipoproteinemia, without myocardial ischemia, suggesting a direct effect of hyperlipidemia on ventricular repolarization [14]. LDL increases the cholesterol to phospholipid ratio in the cell membrane, enhancing membrane rigidity and impairing functionality of the ion channels and ventricular repolarization [14,15]. Ventricular repolarization is reflected by the QT interval on the ECG, which is regulated mainly by potassium channels. On the other hand, type II hyperlipoproteinemia is characterized by accelerated atherosclerosis, related to small dense LDL synthesis.It was also hypothesized that hypercholesterolemia causes repolarization abnormalities, probably, by beta or IK channel phosphorylation mediated mechanisms [9]. Hypercholesterolemia causes also endothelial dysfunction, with impaired microvascular vasodilatation, facilitating vasoconstriction, and electrical heterogeneity and extrasystolic activity [13]. The increase in the QT interval duration in cholesterol fed rabbits was lesser if L-Arginine was supplemented, suggesting a beneficial role of L-Arginine (a nitric acid precusror) in hypercholesterolemia induced repolarization characteristics [9]. L-Arginine increases endogenous nitric oxide, which may activate ATP dependent K channels, shortening the action potential [9].Late ventricular potentials were detected in patients with high and moderately elevated serum cholesterol [5,16].Cardiac Arrhythmias -Mechanisms, Pathophysiology, and Treatment 90

Long-Term Outcome of Non-Sustained Ventricular Tachycardia in Structurally Normal Hearts

“…Ventricular arrhythmia could be related to many reported non-cardiac systemic diseases, including metabolic, liver disease, electrolyte imbalance…etc. [ 22 ] NSVT in patients with apparent structural normal heart may have subclinical noncardiac disorder. Intensified follow-up and cardiac evaluation might be warranted for patients with NSVT, and future prospective trials may address this strategy.…”

Early Detection of Iron Overload Cardiomyopathy in Transfusion Dependent Thalassemia Patients in Sulaimaniyah City, Iraq

“…ECG changes such as P-wave abnormalities, P-wave dispersion, QT interval prolongation and dispersion, QRS widening and T-wave abnormality; were found to proceed with echocardiographic abnormalities. 20 Patients with iron-overload cardiomyopathy (IOC) can be asymptomatic, have diastolic dysfunction, systolic dysfunction, congestive heart failure, pulmonary hypertension and arrhythmia, which may lead to sudden death. 21 , 22 …”

Signal-Averaged ECG: Basics to Current Issues

“…Several factors enable ventricular arrhythmias in patients with epilepsy, such as sympathovagal imbalance, impaired cardiac repolarization, mutations of ionic channels afecting both the brain and the heart, dysfunctional cortical networks, ictal hypoxemia and hypercapnia, stress hormones, therapy, cardiorespiratory interactions, and associated cardiovascular diseases [24,30]. Epilepsy patients more frequently displayed abnormal SAECGs with LVPs compared to healthy controls, correlated with disease duration, uncontrolled seizures, and polytherapy [23].…”

“…The association between LVPs and rejection of heart transplant is explained by occurrence of areas of myocardial ibrosis, due to cell changes caused by alloreactive T lymphocytes against graft antigens and ischemia-reperfusion injuries as soon as the blood low is reestablished [22]. 20 young heart transplant patients SAECG is not efective in detecting heart transplant rejection in young patients Horenstein et al [21] Extracardiac disorders were also associated with LVPs, especially hypertension, metabolic syndrome, obesity, eating disorders, diabetes mellitus, renal failure, chronic obstructive pulmonary disease (COPD), acromegaly, thalassemia, connective tissue diseases, epilepsy, and schizophrenia [6,[23][24][25][26][27]. Antiarrhythmic therapy, thrombolytic drugs, statins, steroids, and coronary interventions may inluence LVPs [6].…”