We evaluated both the effect of 5 mg single-dose oral amlodipine during the peak effect time and at the end of a short-term period of 4 weeks on left ventricular diastolic function measured by transmitral and pulmonary venous flow velocities and the antihypertensive efficacy and tolerability in 25 patients with mild to moderate essential hypertension. Pulse and blood pressure measurements and echocardiographic assessment by standard techniques were performed at baseline, peak effect time and at the end of the 4-week short-term period. Amlodipine affecting the small and large arteries reduced both the total peripheral vascular resistance and pulse pressure/stroke volume rate (p<0.001, p<0.01, respectively) during the peak effect time and at the end of the 4-week short-term period. Thus, it increased the arterial distensibility while causing significant decrease in systolic, diastolic and mean blood pressure (p<0.001, p<0.001 and p<0.01 respectively). It had no effect on heart rate, stroke volume and cardiac output. It was observed that amlodipine did not affect diastolic filling parameters which had been assessed by transmitral flow velocities during the peak effect time and at the end of the 4-week short-term period. No change on systolic and diastolic pulmonary venous flow was observed. However, significant decrease in reverse pulmonary flow was recorded. In conclusion, the acute and short-term effects of amlodipine in moderate to mild hypertension caused significant increase in arterial distensibility and signifiant decrease in blood presure. However, it had no effect on heart rate, stroke volume and cardiac output. It affected only the reverse pulmonary flow.

It this study we aimed to assess left ventricular enddiastolic pressure by detecting pulmonary venous flow with transthoracic echocardiogrphy. The study group consisted of 47 patients, who underwent hemodynamic study, because of various reasons in the Cardiology Department of Gülhane Military Medical Academy and Medical Faculty. Of these 47 patients, 38 (80%) were men and 9 (20%) were women with a mean age of 51.9±7.8 years. Pulmonary venous flow patterns of patients were recorded by transthoracic echocardiography immediately before the hemodynamic study. The relation between pulmonary venous flow pattern variables and left ventricular enddiastolic pressure was analysed. Left ventricular enddiastolic pressure was best correlated with atrial reversed flow velocity (the correlation coefficient was 0.74). The sensitivity and specificity of predicting high left ventricular enddiastolic pressure (>15 mmHg) of high atrial reversed flow velocity (> 30 cm/sec) was 95%, and 85%, respectively. Positive predictive value was 84%, and negative predictive value was 95%. In conclusion, pulmonary venous flow can be detected by transthoracic approach. Left ventricular enddiastolic pressure is accurately assessed by analysing atrial reversed flow velocity in pulmonary venous flow pattern, in patients with a left atrium diameter in normal ranges, in sinus rhythm, and without cardiac valve pathology.

We studied at the cardiology out-patient clinic of Erciyes University Medical Faculty, the relation between left ventricular diastolic function and plasma atrial natriuretic peptide (ANP) levels in patients with moderate essential hypertension. Sixteen patients who had an initial diagnosis of moderate essential hypertension were included in the study; twelve healthy subjects served as a control group. Left ventricular diastolic dysfunction existed in seven patients by continuous Doppler echocardiography. The ANP levels were significantly higher in all hypertensives and in hypertensive patients with diastolic dysfunction than in the control group (241.3±216.3 pg/ml, 410.6±209.5 pg/ml and 79.3±15.8 pg/ml, p<0.01, p<0.001, respectively). ANP levels were significantly (p<0.01) higher in patients with diastolic dysfunction than in those with normal diastolic function (410.6±209.5 pg/ml and 103.6±37.1 pg/ml). There was no significant difference between hypertensive patients with normal diastolic function and the control group although the ANP levels were higher in hypertensive patients with normal diastolic function (p>0.05). There were statistically significant differences of left atrial, left ventricular systolic and diastolic diameters, interventricular septal thickness between patients and the control group (p<0.01, p<0.001, p<0.001, p<0.05, respectively). As a conclusion, diastolic dysfunction in hypertensive patients results in high ANP levels.

The effect of antihypertensive therapy with amlodipine on left ventricular mass and diastolic function was examined. After a wash-out period of 2 weeks and a single-blind placebo period of 4 weeks, patients found to have mild to moderate systemic heypertension, left ventricular hypertrophy (LVH) and diastolic dysfunction (DD) with echo-Doppler were included in the study. LVH was described as left ventricular mass index (LVMI) > 134 g/m2 in men and > 110 g/m2 in women and DD as mitral inflow E/A < 1. Amlodipine was given 5 mg daily and if neccessary was increased to 10 mg in the 4th week and continued for 6 months. 30 patients in the sixth month with controlled hypertension were reevaluated. Blood pressure decreased from 164±13/104±6 to 134±10/84±5 in the 3rd month (p<0.01) and to 131±10/85±5 mmHg in the 6th month. LVMI decreased from 157.7±30 to 135.7±27.2 in the 3rd month (p<0.01) and to 131.8±24.9 g/m2 in the 6th month (p<0.01). The regression of LVH was seen to be due mainly on the regression of septal thickness (12.8±0.2 baseline, 11.7±1.8 in 3 months p<0.05, and 11.2±1.8 p<0.01, in 6 months). Although a small improvement in E/A ratio was observed in 6 months, the change was not significant. In conclusion; 1) amlodipine was found to be effective in reducing LVH in patients with mild to moderate hypertension, 2) the regression in LVH was persistent in 6 months, 3) the regression in LVH was mainly due to regression in septal thickness and 4) despite blood pressure control and regression in left ventricular mass, a significant improvement in diastolic function was not achieved.

Baroleflex sensitivity (BRS) is predictor of lethal arrhythmias and cardiac sudden death after acute myocardial infarction (AMI). Despite the fact that angiotensin convertign enzyme inhibitors (ACEI) were shown to increase the vagal activity, their effects on BRS after AMI are yet to determined. Hence, we aimed to assess the effects of ACEI on BRS values after AMI. 15 cases with anterior AMI, who were given early thrombolytic therapy, were enrolled into the study. After phenylephrine test was performed on the third of fourt in-hospital days to obtain BRS values, 10 randomized cases were given enalpril 5 mg bid orally, and the remaining 5 were included in the control group. The phenylephrine test was repeated three days later. While the mean BRS value rose from 5.6±3.6 msec/mmHg to 8±4.5 msec/mmHg (p<0.001) after enalapril administration, it decreased from 9±7.5 msec/mmHg to 7.4±5.2 msec/mmHg in the control group. BRS increase of about 2.4±1.6 msec/mmHg induced by enalapril was significantly different from the BRS decrease of about 1.6±3.6 msec/mmHg that was determined as control value, although the difference between the corresponding first and second mean BRS values among the two groups were not statistically significant (p>0.2, p>0.3). Thus, enalapril significantly improves reflex vagal activity in uncomplicated AMI cases during in-hospital days.

Anterior myocardial infarction (MI) generaly is due to occlusion of the left anterior descending (LAD) coronary artery. The more proximal culprit lesion will cause extended myocardial involvement. Although coronary angiography is the gold standard to determine the site of the culprit lesion, it is not practical in the acute period. To predict the site of the culprit lesion, we used electrocardiography. Thirty-nine patients (five women, 34 men) with an average age of 53±9 years who were admitted to GATA Coronary Care Unit with acute anterior MI between January 1992 and December 1994 and in whom we were subsequently able to detect the culprit lesion by coronary angiography, were included in this study. Patients were divided into 2 groups (proximal and distal) according to the site of culprit narrowing in relation to the origin of the first diagonal branch. Electrocardiograms of the groups were evaluated in regard to ST-segment changes. ST depressions in leads II, III and aVF in the proximal group were more significantly pronounced than in the distal group (P values for leads II, III, and aVF were 0.003, 0.025 and 0.037, respectively). Logistic regression analysis of the ST depression =0.5 mm in leads II, III, aVF and V6 revealed a predictive accuracy of 92% and 50% (overall accuracy 79%) in estimation of the culprit lesion proximal and distal to the first diagonal artery, respectively. In conclusion, the culprit lesion in patients with acute anterior MI with an ECG showing ST depressions in leads II, III and aVF will generally be located proximal to the first diagonal artery.

Postmyocardial infarction syndrome (Dressler syndrome) developed in 6 patients among 100 cases hospitalized with a diagnosis of acute myocardial infarction. In 100 patients studied prospectively, blood samples drawn on the 14th, 21st and 33rd days of myocardial infarction were examined for autoantibodies against their own cardiac muscle antigens with indirect fluorescence antibody technique. For evaluating cardiac muscle antibody (CMA) positiveness, monkey heart tissue was placed as an antigenic substrate in the solid phase and intermyofibrillar and sarcolemmal-subsarcolemmal fluorescence dying were taken as base. CMA was present mostly on samples of the 14th and 21st days with respect to elevated antibody titres and the number of CMA positive patients. In 8 of 100 acute myocardial infarction patients, CMA were detected. Dressler's syndrome was diagnosed in 6 of 8 patients while the syndrome did not manifest in two of these patients. In agreement with a number of other studies which showed immunologically a valid relation between CMA and the pathogenesis of Dressler's syndrome, we also found a positive relation between the presence of CMA and Dressler's syndrome.

The incidence and course of acute renal failure (ARF) following open heart surgery was retrospectively analyzed. Nine cases of severe ARF were identified in a total of 730 patients who underwent cardiac operations. Hemodialysis was initiated in all patients, and the mortality rate was 55%. Although hemodialysis was instituted at an early stage in severe ARF, the mortality rate was high. Deaths were caused by sepsis, heart failure, multiorgan failure, and gastrointestinal bleeding. Moderate ARF was found in 65 patients. This incidence of 8.9% is lower than previously reported. This was attributed to pulsalite perfusion during operation. Early postoperative hypotension, low haematocrit value during cardiopulmonary bypass (CBP), longer CPB duration and aortic cross-clamping time increase the incidence of severe ARF in the postoperative course.

This randomized study compared the hemodynamic and metabolic effects of pancuronium, vecuronium and atracurium during treatment of shivering after cardiac surgery with hypothermic cardiopulmonary bypass. 60 patients were evaluated in three groups and were treated with pancuronium (Group I, n=20) 0.08 mg/kg, vecuronium (Group II, n=20) 0.08 mg/kg and atracurium (Group III, n=20) 0.8 mg/kg. Values of heart rate, mean arterial pressure, arterial and venous blood gases, total body oxygen consumption (VO2-I) and pressure-work index (PWI) were measured. Continuous ST segment analysis was used to detect myocardial ischemia. Treatment of shivering with pancuronium decreased VO2-I by 27% and heart rate was increased by 19%. Vecuronium decreased VO2-I by 34% with an increase 5% in heart rate. Atracurium desreased VO2-I41% with no change in heart rate. Myocardial ischemia occurred in 4 patients treated with pancuronium. Ventricular arrhythmias occurred in four patients treated with vecuronium. Only one patient treated with vecuronium had ventricular arrhythmia. Patients treated with pancuronium, vecoronium and atracurium were taking beta-adrenergic blockers preoperatively which was associated with lower PWI at onset of shivering. We concluded that, compared with the other two drugs, atracurium is the best choice during treatment of shivering because of lower hemodynamic and metabolic complications and no increase in PWI.

Between 1985 and 1995, we encountered a left persistent superior vena cava (LPSVC) in 82 (4.7 %) of the patients who underwent open heart surgery because of congenital heart anomalies. LPSVC accompanied most commonly tetralogy of Fallot (20.7 %) and ventricular septal defect (18.2 %). LPSVC drained into the right atrium via coronary sinus in 72 (87.8 %) cases, left atrium directly in 6 (7.3 %) and unroofed coronary sinus in 4 (4.8 %). Twently of these patients needed additional surgical procedure for LPSVC. Ligation of LPSVC was performed on 11 patients. In this group, LPSVC drained into coronary sinus in 6 cases, to left atrium in 2, to unroofed coronary sinus in 3. In 5 patients who underwent total cavapulmonary anastomoses or Fontan procedure, LPSVC was anastomosed to left pulmonary artery as an end-to-side fashion. In 4 patients with LPSVC draining to left atrium. LPSVC was connected to the right atrium via Gore-tex or Hemashield vascular prosthesis. One patient who had ligation of LPSVC and another in whom LPSVC was anastomosed to left pulmonary artery were lost. The patients who had ligation of LPSVC did not show any sign of venous hypertension at their head and upper extremities. In these cases LPSVC was smaller than the right. We observed angiographically that the synthetic grafts were open after 20 months in one of these and after 6 years in another. The patency of the Gore-tex graft was shown echocardiographically in two further patients. We presented surgical strategies for the LPSVC which accompanied congenital heart anomalies.

We studied blood endothelin (ET-1) levels during the early phase of myocardial infarction and its relation to the progression of myocardial infarction. We determined serum ET-1 levels in 15 patients (4 females, 11 males) with a mean age of 52±11, with myocardial infarction proved by ECG findings and serum enzyme levels in the first 72 hours from the beginning of pain to find out the effect of ET-1 in the early phase of myocardial infarction. The control group consisted of 15 persons (8 females, 7 males) with a mean age of 42±16. ET-1 levels were studied in the venous sample with radioimmunoassay (Amersham Endothelin 1,2 (125 I) Assay System). ET-1 levels were significantly high in patients with myocardial infarction compared to the control group (p<0.05). The mean ET-1 level in the study group was 3.72±2.16 while it was 1.96±0.72 in the control group. We found a significant correlation with CK-MB, while there was none with lipid fractions, other biochemical values and ECG findings. The level of ET-1 increases in the early phase of myocardial infarction but whether it is the cause or the result should be further investigated.

Tumour necrosis factor (TNF-Å) is a polypeptide (MW 17 kDa) secreted from reticuloendothelial cells in response to a wide variety of inflammatory and infectious stimuli. After bonding with its specific receptor, activation of G protein system and various protein kinases take place and this causes its ubiquitous biological effects in different types of tissues. TNF-Å has important roles in cachexia, endotoxic shock, coagulation, immunity, ischemia and reperfusion. TNF-Å, by causing the activation of important adhesion molecules, leukocytes and platelet activating factor, may aggravate and shapen the ischemic process. The increase of its serum level after acute myocardial infarction and other animal models further supports the notion that TNF-Å has an important role in myocardial ischemia. In this brief review biologic effects of TNF-Å, its possible role in ischemic syndromes. With special reference to myocardial ischemia, are described.

Growth factors were recently held responsible in the pathogenesis of primary hypertrophic cardiomyopathy (PHCM). It appeared that octreotide (OCT), a long-acting somatostatin analog could effectively inhibit growth factors. With this knowledge, OCT treatment was applied to a 34-year-old patient with HCM subcutaneously for four weeks; 50µg three times per day during the first week and 100µg twice per day the following three weeks. Patient's functional capacity was class III, there were P pulmonale (in lead II P wave 0.6 mV) and inverted T waves (inleads I, aVL, V5-6) on the ECG; left ventricular posterior wall thickness was 17 mm, interventricular septum thickness was 24 mm, left ventricular mass (LVM) was 342 g by echocardiography. At the end of four weeks' treatment the functional capacity rose to I, P wave amplitude declined to 0.3 mV and T wave was diphasic on the ECG and the thickness of the posterior wall and of the ventricular septum declined to 14 mm and 16 mm, respectively. LVM was 242 g on echocardiography. No side effect was observed during treatment. In conclusion, the dramatic improvement obtained with OCT treatment in a patient with PHCM seems promising.

A 37-year-old female patient with tricuspid atresia+ventricular septal defect+ventriculo-arterial concordance and pulmonary stenosis was evaluated for her increasing cyanosis and exercise intolerance. The patient had had a left Blalock-Taussig (BT) anastomosis 31 years ago and a Glenn operation 12 years ago. It was determined by echocardiography and hemodynamic study that her left BT anastomosis had extremely stenosed. Because her condition was not amenable to surgical correction, we performed percutaneous balloon dilatation of the stenotic BT anastomosis. To our knowledge, the procedure was the first case in our country, and was successful without complications.

An inferior vena caval filter was percutaneously inserted to a patient due to recurrence of symptoms associated with thromboembolic disease despite effective doses of anticoagulant therapy. The patient had previously been hospitalized in our clinic with the diagnosis of deep venous thrombosis and recurrent pulmonary emboli secondary to the primary hypercoagulable state. Percutaneous vena caval filter placement appears to be an effective, safe and relatively easy and inexpensive method compared to the alternative surgical intervention. Indications and complications of this method were discussed.