Fatih Özçelik

Serum total and lipid-bound sialic acid levels following acute myocardial infarction

Abstract Although serum total sialic acid has been shown to be a cardiovascular risk factor, with elevated levels 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 levels 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.

Relationship between serum sialic acids, sialic acid-rich inflammation-sensitive proteins and cell damage in patients with acute myocardial infarction

Abstract The 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 α1-antitrypsin, α2-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 α1-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.

Early and late advanced atrioventricular block in acute inferior myocardial infarction.

BackgroundAdvanced 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. MethodsWe 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. ResultsThe 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). ConclusionThese data suggest that the time of appearance of advanced atrioventricular block does not affect the prognosis of hospital patients with inferior AMI. Coronary Artery Dis 9:1–4

Evaluation of early cardiac dysfunction in patients with systemic lupus erythematosus with or without anticardiolipin antibodies

The aim of this study was to use transthoracic Doppler echocardiographic (TTE) imaging methods to identify cardiac dysfunction, an indicator of subclinical atherosclerosis in asymptomatic systemic lupus erythematosus (SLE) patients in terms of cardiac effects. This study involved 80 patients: a study group (n = 50) and control group (n = 30). They were categorized into four subgroups: anticardiolipin antibodies (aCL) (+) (n = 14) and aCL (−) (n = 36); systemic lupus erythematosus disease activity index (SLEDAI) ≥ 6 (n = 15) and SLEDAI < 6 (n = 35); disease period ≥ 5 years (n = 21) and disease period < 5 years (n = 29); major organ involvement (+) (n = 19), major organ involvement (−) (n = 31). The ratio of mitral peak velocity of early filling to early diastolic mitral annular velocity (E/E′) for the study group was found to be higher than the control (p < 0.01). Systolic septal motion velocity (Ssm) was lower in the study group compared with the control (p < 0.01). Left atrium (LA) dimension was greater in the study group than the control (p < 0.01). Ssm was found to be lower in the aCL (+) patients compared with the control and aCL (−) groups (p < 0.01, p < 0.05, respectively). LA dimension was greater in the aCL (+) and (−) groups compared with the control, (p < 0.01, p < 0.05, respectively) and aCL groups compared with each other (p < 0.05). The E/E′ ratio for the aCL (+) and (−) groups was found to be greater than the control (p < 0.05). In the study, both the Ssm and the late diastolic septal velocity (sA′) was found to be lower in the SLEDAI ≥6 group compared with SLEDAI<6 group, (p < 0.001, p < 0.05, respectively). LA dimension was statistically greater in the SLEDAI ≥6 group compared with the SLEDAI <6 group (p < 0.001). E′ and early diastolic septal velocity (sE′) were statistically lower in the disease period >5 years group compared with the disease period <5 years group (p < 0.01, p < 0.05, respectively). Carrying out regular scans with TTE image of SLE patients is important in order to identify early cardiac involvement during monitoring and treatment. Identifying early cardiac involvement in SLE may lead to a reduction in mortality and morbidity rates.

The relation between the levels of osteoprotegerin and the degree of coronary artery disease in patients with acute coronary syndrome and stable angina pectoris

BACKGROUND Osteoprotegerin (OPG), an inhibitor of osteoclastogenesis, has recently been under the spotlight in studies regarding the pathophysiology of atherosclerosis. AIM To evaluate the value of serum OPG in the diagnosis and severity in patients with stable angina pectoris (SA) and unstable angina pectoris/non ST elevation myocardial infarction. METHODS This study involved 160 patients, SA (n = 65), acute coronary syndrome (NSTE-ACS; n = 65), and a control group (n = 30). Blood samples were collected in the first hour, after 24 hours and on the fifth day. The prevalence of coronary artery atherosclerotic lesions was determined using the Gensini scoring system. RESULTS A statistically significant difference was observed in the first hour OPG levels between the control group and both the SA and NSTE-ACS group (p < 0.001). When the cut-off value was determined as 247.71 pg/mL, the sensitivity and specificity of the first hour OPG levels indicating coronary artery disease were 91.54% and 46.67%, respectively, while the positive predictive value was 88.1% and the negative predictive value was 56%. No correlations were observed between the first, 24th hour and the fifth day OPG levels and the Gensini scores. No relation was denoted between the OPG levels and number of diseased coronary arteries. CONCLUSIONS In our study, serum OPG level seemed to be unrelated to the severity or the degree of coronary artery disease in patients with SA and unstable angina pectoris/non ST elevation myocardial infarction. OPG may only be accepted as an indicator of coronary atherosclerosis.

Effect of Obesity on Coronary Collateral Vessel Development in Patients with Coronary Artery Disease

The 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 1 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: (I) 18.0-24.9 kg/m2, (II) 25.0-29.9 kg/m2, and (III) more than 30 kg/m2. 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.

Non-dipper hypertension is associated with slow coronary flow among hypertensives with normal coronary angiogram.

Summary Aim A person with a drop of more than 10% in nocturnal arterial blood pressure during the circadian rhythm is referred to as a dipper and one with a smaller decrease is referred to as a non-dipper. In our study, we aimed to compare the thrombolysis in myocardial infarction (TIMI) frame count in non-dipper and dipper hypertensive patient groups who had normal coronary artery angiography Methods Patients with normal coronary arteries and with ambulatory blood pressure monitoring follow ups were retrospectively investigated and 60 patients (35%, female) were included in our study. The patients were grouped as dipper (n = 30) and non-dipper (n = 30) hypertensives. Results The TIMI frame counts in all three coronary arteries and the mean TIMI frame count in the dipper hypertensive patient group were significantly lower than those of the non-dipper hypertensives (right coronary artery TIMI frame count: 16.83 ± 3.70; 21.63 ± 3.44, p < 0.001; circumflex artery TIMI frame count: 21.28 ± 3.52; 25.65 ± 3.61, p < 0.001; left anterior descending artery TIMI frame count: 34.20 ± 2.80; 37.05 ± 3.30, p = 0.001; corrected left anterior descending artery TIMI frame count: 20.05 ± 1.63; 21.74 ± 1.95, p = 0.001; mean TIMI frame count: 19.31 ± 2.3; 22.94 ± 2.61, p < 0.001). The body mass index (BMI) was 23.79 ± 2.81 kg/m2 in the dipper patient group, while it was 25.47 ± 2.92 in the non-dippers. BMI was found to be significantly higher in the non-dipper group than in the dipper group (p = 0.027). Conclusions In this study, TIMI frame count, which is a simple, productive, objective and reproducible method for determination of microvascular changes, was found to be higher in non-dipper hypertensive patients than in the dipper patients.

The impact of a single episode of remote ischemic preconditioning on myocardial injury after elective percutaneous coronary intervention

Introduction Myocardial injury after percutaneous coronary intervention (PCI) occurs in approximately 30% of procedures, and is related to worse prognosis. Effects of remote ischemic preconditioning (RIPC) on reperfusion injury have been investigated before, yielding conflicting results. Aim To assess the impact of a single episode of RIPC on myocardial injury after elective PCI. Material and methods One hundred and four patients undergoing elective PCI, with normal baseline cardiac troponin-I (cTn-I) values, were randomized to two groups. Two patients were excluded due to data loss, and 102 patients were analyzed. Five minutes of ischemic preconditioning was delivered just before the intervention to the preconditioning group, by inflating the blood pressure cuff up to 200 mm Hg on the non-dominant arm. Postprocedural 16th hour cTn-I, ΔcTn-I (difference between the 16th h and baseline cTn-I values) and the prevalence of type 4a myocardial infarction were compared between the two groups. Results Median cTn-I values after the procedure were compared. 16th hour cTn-I was insignificantly lower in the preconditioning arm (0.026 μg/l vs. 0.045 μg/l, p = 0.186). The incidence of cTn-I elevation 5-fold above the upper reference limit (URL) (> 0.115 μg/l) was lower in the preconditioning group, but it was also not significant (21.6% vs. 11.8%, p = 0.184). Conclusions A single episode of RIPC before elective PCI demonstrated less troponin elevation but failed to show a significant effect.