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Öğe Antianginal and anti-ischemic effects of nisoldipine and ramipril in patients with syndrome X(Clinical Cardiology Publ Co, 1999) Özçelik, F; Altun, A; Özbay, GBackground: Syndrome X is defined as typical angina pectoris, positive treadmill exercise test, negative intravenous ergonovine test, and angiographically normal coronary arteries. Hypothesis: In the present study, we investigated the antiischemic and antianginal effects of nisoldipine and ramipril in patients with syndrome X. Methods: After 2 weeks of the first wash-out period, 18 patients (7 men, 11 women, age 46 +/- 10 years) were given nisoldipine (NIS) 5 mg twice daily for 4 weeks, and after 2 weeks of the second wash-out period, the same patients were given ramipril (RAM) 2.5 mg once daily for 4 weeks. A treadmill exercise test with modified Bruce protocol was performed at the end of each period. Results: The time to angina in exercise (607 +/- 115 s-650 +/- 117 s, p = 0.006, vs. 630 +/- 114 s-660 +/- 123 s, p = 0.02), total exercise time (612 +/- 110 s-656 +/- 114 s, p = 0.0008, vs. 630 +/- 114 s-660 +/- 123 s, p = 0.02), and maximum MET value (11.09 +/- 2.08-11.86 2.04, p = 0.0016, vs. 11.42 +/- 2.09-12.2 +/- 2.26, p = 0.01) were increased significantly with both therapy modalities. The time to 1 mm ST-segment depression(123 +/- 93 s - 220 +/- 172 s, p = 0.002) was increased significantly with NIS therapy. The time to ST-segment recovery (434 +/- 268 s-330 +/- 233 s, p = 0.016 vs. 443 +/- 259 s-370 +/- 278 s, p = 0.012), the frequency of anginal attacks per week (1.27 +/- 1.4-0 +/- 0.38, p = 0.005, vs. 1 +/- 1.32-0.33 +/- 0.59, p = 0.028), and the need for sublingual nitroglycerin (1.16 +/- 1.29-0.11 +/- 0.32, p = 0.005, vs. 0.94 +/- 1.16-0.27 +/- 0.57, p = 0.012) were decreased significantly with both drugs. Conclusion: We observed that 10 mg daily NIS and 2.5 mg daily RAM have similar anti-ischemic and antianginal effects in patients with syndrome X.Öğe Automatic backscatter analysis of regional right ventricular systolic function using color kinesis in patients with inferior wall acute myocardial infarction(Medimond S R L, 1999) Kürüm, T; Korucu, C; Özçelik, F; Eker, H; Öztekin, E; Özbay, G[Abstract Not Available]Öğe Early and late advanced atrioventricular black in acute inferior myocardial infarction(Lippincott Williams & Wilkins, 1998) Altun, A; Özkan, B; Gürçagan, A; Kadi, H; Özçelik, F; Özbay, GBackground Advanced atrioventricular block is a frequent complication in patients with inferior acute myocardial infarction (AMI); in patients in hospital, it often occurs concurrently with other complications and is associated with high mortality, Very little information is available about early and late advanced atrioventricular block in inferior AMI, We hypothesized that the time of appearance of advanced atrioventricular block characterized by poor response to atropine requiring temporary pacemaker therapy may affect the prognosis of patients with inferior AMI. Methods We studied 51 patients with inferior AMI and advanced atrioventricular block characterized by poor response to atropine requiring temporary pacemaker therapy. According to pre-established electrocardiographic criteria and the time of appearance of the advanced atrioventricular block, patients were divided into two groups: an early block group consisting of 30 patients who developed advanced atrioventricular block during the first 24 h of inferior AMI, and a late block group consisting of 21 patients who developed advanced atrioventricular block after the first 24 h of chest pain. Results The groups were similar regarding age, coronary risk factors, frequency of right ventricular infarction, QRS score, atrial and ventricular rates, the time of return to first-degree atrioventricular block, cardiac arrhythmias, heart failure and mortality. The early advanced atrioventricular block group included a greater number of men than did the late group (P = 0.017). Conclusion These data suggest that the time of appearance of advanced atrioventricular block does not affect the prognosis of hospital patients with inferior AMI. (C) 1998 Lippincott-Raven Publishers.Öğe Effect of obesity on coronary collateral vessel development in patients with coronary artery disease(Sage Publications Inc, 2005) Tath, E; Yildiz, M; Gül, E; Birsin, A; Karahasanoglu, E; Özçelik, F; Özbay, GThe purpose of this study was to compare coronary collateral circulation and with other risk factors in patients with coronary artery disease and different body mass index. Between January 1999 and December 2001, of 867 patients who underwent angiography for the first time, 90 patients (24 women and 66 men), with occlusion in only I coronary artery participated in the study. Information regarding age, body mass index, sex, smoking, hypertension, diabetes mellitus, hyperlipidemia, preinfarction angina, and use of oral beta blockers and nitrates were recorded for all patients. The patients were separated into 2 groups in accordance with development of their coronary collateral circulation; those with insufficient (Rentrop 0, 1, and 2) and those with sufficient coronary collateral circulation. They were also divided into 3 groups on the basis of body mass index as follows: (1) 18.0-24.9 kg/m(2), (11) 25.0-29.9 kg/m(2), and (111) more than 30 kg/ml. In the obesity and overweight groups, hyperlipidemia, diabetes mellitus, and nitrate use were identified more frequently than in the other groups (p < 0.05). Use of oral nitrates more than 6 months before the myocardial infarction and existence of preinfarction angina affected collateral coronary vessel development in the positive direction (p=0.01, p = 0.03, respectively). There was no correlation between coronary artery disease and coronary collateral vessel development in the obese patients (p = 0.6). Although it has been shown that coronary collateral vessel development was affected negatively in obese patients with coronary artery disease, no statistical significance was identified.Öğe Heart failure during first inferior acute myocardial infarction(Lippincott Williams & Wilkins, 1999) Altun, A; Özçelik, F; Özkan, B; Özbay, GBackground Inferior acute myocardial infarctions (AMI) have better in-hospital prognosis than do anterior AMI. Authors of several studies reported that patients with inferior AMI complicated by atrioventricular block, concomitant precordial ST-segment depression and involvement of right ventricle have larger infarctions and a worse prognoses than do patients without these features. Objective To analyse the incidence, clinical course and in-hospital prognosis of patients with heart failure and first inferior AMI. Methods We analysed in 257 consecutive patients with first inferior AMI who had been admitted to the coronary care unit during January 1991 and March 1995. The clinical and electrocardiographic characteristics, as well as the morbidities and in-hospital mortalities, of groups of patients with and without heart failure during inferior AMI were compared. Results Symptoms and signs of heart failure were noted for 49 patients (19%). We found that patients who had suffered heart failure during inferior AMI were older (61.1 +/- 9.86 versus 58.78 +/- 1 0.58 years, P<0.05) than those who had not suffered heart failure. There was no significant difference between patients' sex, history of diabetes mellitus, hypertension, smoking status, thrombolytic therapy, involvement of right ventricle and QRS score for these two groups. We found a greater prevalence of ST-segment depression (ST-segment depression greater than or equal to 1 mV in more than one precordial lead with maximal ST-segment depression in leads V4-V6) of V4-V6 precordial leads (57 versus 26%, P=0.00002) and a lesser prevalence of no ST-segment depression (ST-segment depression <0.1 mV in each precordial lead; 14 versus 38%, P=0.001) among patients who had suffered heart failure. We found greater incidences of serious ventricular arrhythmias (53 versus 26, P=0.0002) and ventricular tachycardia-fibrillation (16 versus 7%, P=0.03) among patients who had suffered heart failure than we did among those who had not. Third-degree atrioventricular block was more often found in patients who had suffered heart failure (23 versus 12%, P=0.07) but this difference was not statistically significant. We found that the in-hospital mortality among patients who had suffered heart failure was much higher than that among those who had not (24.5 versus 3.8%, P=0.000001). Conclusion We found that heart failure occurs primarily in old patients, and in those with precordial ST-segment depression, especially in leads V4-V6. The patients who suffer heart failure have worse in-hospital prognosis due to serious ventricular arrhythmias and cardiogenic shock. Coronary Artery Dis 10:455-458 (C) 1999 Lippincott Williams & Wilkins.Öğe Predictive value of admission electrocardiogram for multivessel disease in acute anterior and anterior-inferior myocardial infarction(Futura Publ Co, 2002) Kürüm, T; Öztekin, E; Özçelik, F; Eker, H; Türe, M; Özbay, GBackground: Our aim was to investigate the correlation between admission ECG and coronary angiography findings in terms of predicting the culprit vessel responsible for the infarct or multivessel disease in acute anterior or anterior-inferior myocardial infarction (AMI). Methods: We investigated 101 patients with a diagnosis of anterior AMI with or without ST-segment elevation or ST-segment depression in at least two leads in DII, III, aVF. The patients were classified as those with vessel involvement in the left anterior descending (LAD) coronary artery and patients with multivessel disease. Vessel involvement in LAD + circumflex artery (Cx) or LAD + right coronary artery (RCA) or LAD + Cx + RCA were considered as multivessel disease. Thus, (a) anterior AMI patients with reciprocal changes in inferior leads, (b) anterior AMI patients with inferior elevations, (c) all anterior AMI patients according to the ST-segment changes in the inferior region were analyzed according to the presence of LAD or multivesssel involvement. Results: Presence of ST-segment depression in aVL and V6 was significantly correlated with the presence of multivessel disease in anterior AMI patients with reciprocal changes in the inferior leads (P = 0.005 and P = 0.003, respectively). No statistically significant difference between the leads were detected in terms of ST-segment elevation in predicting vessel involvement in the two groups of anterior AMI patients with inferior elevations, When all the patients with anterior AMI were analyzed, the presence of ST-segment depression in leads aVL, V4, V5 and V6 were significantly associated with the presence of multivessel disease (P = 0.035, P = 0.010, P = 0.011, P = 0.001, respectively). Conclusions: The presence of ST-segmert depression in anterolateral leads in the admission ECG of anterior AMI patients with reciprocal changes in inferior leads was associated with multivessel disease.Öğe Relationship between serum sialic acids, sialic acid-rich inflammation-sensitive proteins and cell damage in patients with acute myocardial infarction(Walter De Gruyter Gmbh, 2006) Gökmen, SS; Kazezoglu, C; Sunar, B; Özçelik, F; Güngör, Ö; Yorulmaz, F; Gülen, SThe role of sialic acid ( SA) in the pathogenesis of atherosclerosis and as a predictor of cardiovascular events has attracted much attention in recent years. However, most studies investigating the role of total and lipid-bound sialic acids ( TSA and LSA) in the pathogenesis of atherosclerosis lack information on the reason for the elevated SA concentrations in coronary heart disease and myocardial infarction. Since the inflammation-sensitive proteins are glycoproteins with SA residues, an increase in their levels due to some type of acute-phase reaction or inflammation could be responsible for the elevated TSA levels in acute myocardial infarction ( AMI). Elevated serum SA levels might also be due to either shedding or secretion of free SA from the cell or cell membrane surface if neuraminidase levels are increased, or to the release of cellular SA-containing glycolipids and/ or glycoproteins into plasma from myocardial cells after AMI. The aim of the present study was to investigate both the possible role of SA-rich inflammation-sensitive proteins and the cell damage due to elevated serum TSA levels in AMI. A possible role of serum LSA as an indicator of the shedding or secretion of SA from the cell or cell membrane surface in AMI was also evaluated. The study included 38 subjects with AMI and 32 healthy volunteers. Serum TSA and LSA were determined using the methods of Warren and Katopodis, respectively. The concentrations of serum SA-rich inflammation-sensitive proteins, namely alpha(1)-antitrypsin, alpha(2)-macroglobulin and ceruloplasmin were determined immunoturbidimetrically. Our data showed that: a) mean levels of serum TSA and LSA and SA-rich inflammation-sensitive proteins in patients with AMI were significantly increased; and b) there was a significant positive correlation between TSA and LSA and alpha(1)-antitrypsin in patients with AMI. Since the transfer of free SA to lipoproteins is required for an increase in serum LSA levels, and free SA for this transfer can be provided by the secretion of SA from the cell, it is obvious that the shedding or secretion of SA from the cell membrane surface or release of cellular SA from cells into the bloodstream due to cell damage after AMI also occur after AMI. As a result, we can report that either the shedding or secretion of SA from the cell or cell membrane surface and the increased output of SA-rich inflammation-sensitive proteins may together be responsible for the elevated TSA levels in AMI.Öğe Serum total and lipid-bound sialic acid levels following acute myocardial infarction(Walter De Gruyter Gmbh, 2000) Gökmen, SS; Kiliçli, G; Özçelik, F; Gülen, SAlthough serum total sialic acid has been shown to be a cardiovascular risk factor, with elevated levers associated with increased cardiovascular mortality and also with cerebrovascular disease, the reason for the elevation in serum sialic acid content remains obscure. It has been shown that an increased output of serum proteins by the liver due to some type of acute phase reaction may be one of the possible sources of an increased serum sialic acid concentration in patients with myocardial infarction. An increase in the activity of sialidase, which cleaves the terminal sialic acid residues from oligosaccharides, glycoproteins and gangliosides, may also play an important role in the elevation of serum total sialic acid in myocardial infarction. Elevated serum total sialic acid in the blood might result either from the shedding or secreting of sialic acid from the cell membrane surface, or releasing of cellular sialic acid from the cell into the bloodstream due to cell damage after myocardial infarction. The purpose of the present study is to investigate serum total and lipid-bound sialic acid and the enzymes serum lactate dehydrogenase, creatine kinase and aspartate aminotransferase in patients with acute myocardial infarction, at 24 h post-infarction (day 1), 48 h post-infarction (day 2) and 72 h post-infarction (day 3). A possible role of cell damage in the elevation of serum total and lipid-bound sialic acid levels in these patients was also evaluated. In this study, 40 patients with myocardial infarction ranging in age from 42 to 68 years, and 26 healthy volunteers ranging in age from 45 to 71 years were included. Serum total sialic acid determination was carried out by the thiobarbituric acid method of Warren and lipid-bound sialic acid by the method of Katopodis. Our data shows that a) there is a gradual increase in the levels of serum total sialic acid and lipid-bound sialic acid during the first three days after the acute myocardial infarction and b) the elevation in serum total sialic acid revels correlates with the elevation in lactate dehydrogenase activity only on day 1 following infarction. Therefore, either the shedding or secreting of sialic acid from the cell or cell membrane surface may be partly responsible for an increased serum sialic acid concentration especially on day 1 following myocardial infarction.
