Adalet Gürlek

Effect of losartan on circulating Tnfα levels and left ventricular systolic performance in patients with heart failure

Background Tumor necrosis factor alpha (TNFα) plays an important role in the pathophysiology of heart failure. Recent studies have shown a beneficial effect of losartan in these patients. However, the effect of losartan on TNFα levels in heart failure has not yet been studied. We evaluated the effect of losartan on circulating TNFα levels and ejection fraction (EF) in patients with congestive heart failure. Methods Forty patients with heart failure and EF ≤ 40% were enrolled into the study. All of the patients have been given diuretic and digitalis therapy. Twenty patients were given losartan (50 mg/d) (Group I, 10 women, 10 men, 12 dilated cardiomyopathy, 8 ischemic heart disease, mean age 64.9 ± 8.9), and another 20 patients were not given losartan because of hypotension or renal dysfunction (Group II, 13 men, 7 women, 10 dilated cardiomyopathy, 10 ischemic heart disease, mean age 61.2 ±10.5). EF was measured at the initial evaluation and on the fifteenth day of the therapy by echocardiographic examination using an acoustic quantification method. Circulating TNFα levels were also measured at the initial evaluation and on the fifteenth day of therapy by the ELISA method. Results Losartan significantly increased EF and decreased TNFα (EF increased from 29.4 ± 7.3% to 36.0 ± 8.5%, P < 0.001, and TNFα decreased from 39.2 ± 37.4 pg/ml to 27.0 ± 30.0 pg/ml, P < 0.05). Changes in TNFα levels and EF were not found to be correlated (r=−0.28, P=0.24). However, in the control group, EF and TNFα levels were similar at baseline and at the fifteenth day (EF 31.4 ± 8.1% vs 31.7 ± 7.8%, P=0.1, and TNFα 91.5 ± 86.0 pg/ml vs 110.0 ± 80.7 pg/ml, P=0.1, respectively). Conclusions Losartan improves left ventricular systolic function and decreases TNFα level. The decreased TNFα level seems to be independent of EF.

Restenosis after Transluminal Coronary Angioplasty: A Risk Factor Analysis

Background: Restenosis after percutaneous transluminal coronary angioplasty (PTCA) is a major problem limiting the long-term efficacy of the procedure. The purpose of this study was to determine whether risk factors such as cigarette smoking, diabetes mellitus, hypertension or hypercholesterolaemia correlate with restenosis after PTCA. We also studied the relationship between a history of previous myocardial infarction and the extent of coronary artery disease (single-, two- or three-vessel) with restenosis after coronary angioplasty. Methods: A total of 360 patients underwent successful PTCA. Follow-up coronary angiograms were performed in 181 patients after a mean ± SD period of 6 ± 4 months. Results: The restenosis rate was 49%. We divided the patients into two groups: 89 patients with restenosis (8 women and 81 men) and 92 patients with no restenosis (14 women and 78 men). Age, sex, a history of cigarette smoking, diabetes mellitus and a history of previous myocardial infarction were not associated with restenosis. Serum levels of triglyceride were also unrelated to the restenosis rate. Restenosis was associated with hypertension, low levels of high-density-lipoprotein cholesterol, high levels of low-density-lipoprotein cholesterol and high total cholesterol levels (P < 0.001). Patients with two-vessel or multivessel disease had significantly higher restenosis rates than patients with single-vessel disease (P < 0.001). Conclusion: Patients with hyperlipidaemia, hypertension and multi-vessel disease appear to be at higher risk of recurrent restnosis.

Antiarrhytmic effect of converting enzyme inhibitors in congestive heart failure

Abstract In this study 24-h Holter electrocardiographic recordings were used to measure the effects of an angiotensin converting enzyme inhibitor, enalapril given for 4 weeks, on the frequency of cardiac arrhythmias in 24 patients (14 patients had enalapril, 30 patients had placebo) with congestive heart failure (New York Heart Association Functional Class 3) receiving maintenance therapy with digoxin and furosemide. Although the placebo group had no change in the frequence of arrhythmias, enalapril-treated patients showed significant decrease in the frequency of premature ventricular complexes couplet, bigemine VPS and ventricular tachycardia. Moreover, it was observed that six cases of atrial fibrillation returned to sinus rhythm. During enalapril treatment, some, patients experienced increased serum potassium levels, but there was no change in serum digoxin levels. We also observed echocardiographic improvement in left ventricular function as well as clinical symptoms of congestive heart failure. Finally we observed that there was an antiarrhythmic effect of enalapril in congestive heart failure. We thought that the antiarrhythmic effect of enalapril in congestive heart failure was probably due to hemodynamic improvement.

The effects of L-carnitine treatment on left ventricular function and erythrocyte superoxide dismutase activity in patients with ischemic cardiomyopathy

We studied the effects of l‐carnitine on left ventricular systolic function and the erythrocyte superoxide dismutase activity in 51 patients with ischemic cardiomyopathy. They all previously were under the treatment of angiotensin‐converting enzyme inhibitor, digitalis and diuretics. Patients were randomized into two groups. In group I (n = 31), 2 g/day l‐carnitine was added to therapy. l‐Carnitine was not given to the other 20 patients (Group II). In group I (mean age 64.3 ± 7.8 years), 27 of the patients were men, and four were women. In group II (mean age 66.2 ± 8.7 years), 17 of the patients were men, and three were women. Twenty age‐matched healthy subjects (mean age: 60.1 ± 5.3 years) constituted the control group. In each group, left ventricular ejection fraction (LVEF) by echocardiography and red cell superoxide dismutase activity by spectrophotometric method were measured initially and after 1 month of randomisation. Compared with normal healthy subjects (n = 20), patients (n = 51) had significantly higher red cell SOD activity (5633 ± 1225 vs. 3202 ± 373 U/g Hb, P < 0.001). At the end of 1 month of l‐carnitine therapy, red cell SOD activity showed an increase in group I (5918 ± 1448 to 7218 ± 1917 U/g Hb, P < 0.05). In group II, red cell SOD activity showed no significant change after 1 month of randomisation (5190 ± 545 to 5234 ± 487 U/g Hb, P = 0.256). One month after randomisation there was a significant increase in LVEF in both groups I and II (37.8–42.3%, P < 0.001 in group I; 41.5–43.8%, P < 0.001 in group II). The improvement in LVEF was more significant in the l‐carnitine group (4.5% vs. 2.3%, P < 0.01). We conclude that, as a sign of increased free radical production, superoxide dismutase activity was further increased in patients with l‐carnitine treatment. l‐Carnitine treatment in combination with other traditional pharmacological therapy might have an additive effect for the improvement of left ventricular function in ischemic cardiomyopathy.

A case of multiple pericardial hydatid cysts

Pericardial cysts are rare developmental benign intrathoracic lesions and constitute 7% of all mediastinal tumors. As many as 70% of the cysts are found in the right cardiophrenic angle. Unusual locations include the left costophrenic angle, the hilum and the superior mediastinum at the level of the aortic arch. Cysts arising inside the pericardial cavity and attached to the heart are exceedingly rare. We describe a case of multiple pericardial hydatid cysts.

Relation between the insertion/deletion polymorphism of the angiotensin I converting enzyme gene and restenosis after coronary stenting.

Background Observations with intravascular ultrasound demonstrated that neointimal hyperplasia is the predominant factor responsible for in-stent restenosis. Experimental data suggest that angiotensin I converting enzyme (ACE) plays a role in the thickening of neointima after balloon denudation. Insertion/deletion (I/D) polymorphism of the ACE gene is significantly associated with plasma level of ACE and subjects with D/D genotype have significantly higher plasma levels of ACE than normal. Objective To investigate whether this polymorphism influences the risk of restenosis after coronary stenting. Methods We genotyped 158 patients who had undergone single-vessel coronary stenting for the ACE I/D polymorphism. Results Of the 158 patients, 56 (35%) had the D/D genotype, 71 (45%) had the I/D genotype and 31(20%) had the I/I genotype. Prevalences of genotypes were compatible with Hardy-Weinberg equilibrium and distributions of ACE genotype among patients and 132 healthy controls from the same geographic area did not differ. At follow-up (after a median duration of 5.4 months), overall rates of angiographic restenosis and of revascularization of target lesion (RTL) were 32.3 and 22.8%, respectively. Of 51 patients with angiographic restenosis, 31 (60.8%) had focal and 20 (39.2%) had diffuse patterns of restenosis. Diffuse in-stent restenosis was significantly more prevalent among patients with D/D genotype (P= 0.016). Multiple stepwise logistic regression analysis identified ACE I/D polymorphism as the independent predictor of angiographic restenosis and RTL. Relative risk of angiographic restenosis was 6.29 [95% confidence interval (CI), 1.80–22.05, P= 0.0004] for D/D genotype and 3.88 (95% CI 1.11–13.12, P= 0.029) for I/D genotype, whereas relative risk of RTL was 7.44 (95% CI 1.60–34.58, P= 0.01) for D/D genotype and 3.88 (95% CI 0.083–18.15, P= 0.085) for I/D genotype. Conclusions The ACE I/D polymorphism is significantly associated with risk of angiographic and clinical restenosis after coronary stenting. Angiographic pattern of restenosis is also significantly associated with I/D polymorphism, diffuse type being more prevalent among subjects with D/D genotype.

Relation of vitamin D deficiency and new-onset atrial fibrillation among hypertensive patients.

Vitamin D deficiency is associated with various cardiovascular disorders including hypertension, coronary artery disease, and heart failure. The renin-angiotensin-aldosterone system (RAS) axis is activated in vitamin D deficiency. The RAS axis also plays a role in the pathophysiology of atrial fibrillation (AF). We aimed to investigate whether vitamin D deficiency is a risk factor for the development of new-onset AF in hypertension. A total of 227 hypertensive patients were enrolled, of whom 137 had new-onset AF; 90 patients without AF were included in the control group. The age of the patient, left atrial diameter, and vitamin D deficiency increased the probability of new-onset AF independent from confounding factors (odds ratio [OR], 1.04; 95% confidence interval [CI], 1.01-1.08; P = .03 for age; OR, 1.88; 95% CI, 1.15-3.45; P = .03 for left atrial diameter; OR, 1.68; 95% CI, 1.18-2.64; P = .03 for vitamin D deficiency). Vitamin D deficiency is associated with new-onset AF in hypertension.

The relationship between angiotensin converting enzyme gene I/D polymorphism and qt dispersion in patients with hypertrophic cardiomyopathy

Introduction: Hypertrophic cardiomyopathy (HCM) is characterized by disorganized myocardial architecture, and may cause ventricular arrhythmias and sudden death. The angiotensin-converting enzyme (ACE) with two deletion alleles (DD genotype) has been proposed to be associated with increased myocardial collagen content. We evaluated QT dispersion (QTd), which reflects regional differences in ventricular repolarization, in HCM patient and controls among the three different ACE genotypes. Materials and methods: Sixty-three patients with HCM and 20 healthy subjects were included in the study. QT parameters were measured from 12 lead electrocardiograms. ACE genotypes were determined from the DNA extracted from peripheral blood by a polymerase chain reaction (PCR) method. QT parameters were compared among the three ACE genotypes both in HCM patients and controls. Results: Median ages were similar in HCM and control groups. QTd and corrected QTd (QTcd) were significantly greater in the HCM group compared with the controls. The frequencies of each genotype were similar in both groups. Although QTd and QTcd did not differ among the three genotypes in the control subjects, they were significantly greater in patients with DD genotype compared with other genotypes in the HCM group. Conclusion: QTd and QTcd are increased in patients with HCM, especially in those with the DD genotype.

Significance of resting U wave polarity in patients with atherosclerotic heart disease

The aim of this study was to determine the value of U wave polarity in the electrocardiograms of patients with atherosclerotic heart disease. One hundred twelve consecutive patients with U waves were entered into the study. Forty-eight of them had unstable angina pectoris and 64 had prior myocardial infarction (MI) (20 patients had inferior MI, 35 had anterior MI, and 9 had non Q wave MI). Each of these subgroups was divided into two groups with positive (group 1) and negative (group 2) U waves. All patients in this study underwent routine left ventriculography and coronary angiography. The authors examined coronary arteries and calculated ejection fractions. The authors discovered that patients with unstable angina pectoris or anterior MI (group 2) had three-vessel disease more frequently (P < .05). Also, in these patients, there was more than 90% diameter narrowing in the left anterior descending vessel more frequently (P < .001 in unstable angina pectoris and P < .05 in anterior MI). In patients with unstable angina pectoris, inferior MI, or anterior MI, the authors observed that the ejection fraction was lower in group 2 than in group 1 (P < .001 in unstable angina pectoris, P < .05 in inferior MI, and P < .05 in anterior MI). The authors suggest that negative U waves in patients with unstable angina pectoris or anterior MI may indicate multivessel disease with a severe left anterior descending lesion. Also, in patients with unstable angina pectoris, inferior MI, or anterior MI who had negative U waves, ejection fraction was reduced.

Pheochromocytoma with asymmetric septal hypertrophy and Wolff-Parkinson-White syndrome

A 24-year-old woman with pheochromocytoma associated with asymmetric septal hypertrophy, Wolff-Parkinson-White syndrome and pigmentation was operated on and the tumor was excised. The asymmetric hypertrophy and the pre-excitation disappeared after the operation, but the pigmentation increased. We discuss the relation between excessive catecholamines and these findings.