Hypertension is a multifactorial disease, in which genetic factors play an important role. This study was carried out to determine angiotensin-converting enzyme levels and angiotensin-converting enzyme gene polymorphism in Turkish hypertensive patients, and to establish whether there is an association of angiotensin-converting enzyme gene polymorphism with clinical and echocardiographic parameters. We have investigated the association among the allelic distribution of the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme gene identified by polymerase chain reaction, angiotensin-converting enzyme activity determined spectrophotometrically, cardiac morphology and function assessed by means of echocardiography. Distribution of angiotensin-converting enzyme gene I/D polymorphism and allele frequencies in hypertensive patients was not significantly different from controls. D allele frequency was 51.7% in hypertensives vs. 51.9% in controls and I allele 48.3 vs. 48.1%, respectively. The level of angiotensin-converting enzyme activity was significantly higher in the patients homozygotes for D allele (DD = 59.93 U/l) than in heterozygotes (ID = 39.49) and in homozygotes for I allele (II = 40.28 U/l). In addition to these, the level of angiotensin-converting enzyme activity was significantly lower in the ID and especially II patients receiving ACE inhibitors than the others. Also, it was determined that left atrium diameter was larger in the patients homozygotes for I allele than the others.

Noncompaction of the ventricular myocardium is a rare, unclassified cardiomyopathy due to an arrest of myocardial morphogenesis. The characteristic echocardiographic findings consist of multiple, prominent myocardial trabeculations and deep intertrabecular spaces communicating with the left ventricular (LV) cavity. The disease typically involves the LV myocardium, but right ventricular (RV) involvement is not uncommon. The clinical manifestations include heart failure (HF) signs, ventricular arrhythmias and cardioembolic events. Noncompacted myocardium may occur as an isolated cardiac lesion, as well as it can be in association with congenital anomalies. We describe two illustrative cases of noncompaction of the ventricular myocardium, a 19-year-old male with bicuspid aortic valve and progressive worsening of HF, and a 61-year-old male with marked RV involvement in addition to LV apical involvement, both with the typical clinical and echocardiographic features of the 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.

The stored ICEGs demonstrate that PVT is most often preceded by ventricular ectopy. To be reverted, nonsudden onset episodes require higher levels of shock energy and more frequently multiple shock achievements than sudden onset episodes.

As a result, the incidence of IR of AF after IC was higher in the patients with shorter P wave amplitude (for lead II P<0.01, for V1 P<0.01) and larger P wave duration (for lead II P<0.01, for V1 P<0.05).