Atrial fibrillation recurrence after cardioversion: is there a simple electrocardiographic parameter to predict it?
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Biomedical subjects
Publications and source records attributed to Ertan Yetkin.
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It has been reported that deep breathing at 6 breaths/min is associated with reduction of premature ventricular complexes. The beneficial effect of deep breathing is supposed to be due to vagal modulation of sinoatrial and atrioventricular node. Beside the modulating effects of deep breathing, we believe that deep breathing, which is also used in yoga training, might have additional effects via decreasing QT dispersion.
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The association between metabolic syndrome and coronary artery disease, either clinical or subclinical, has been well established. There is also a consensus regarding the higher prevalence of metabolic syndrome in females compared with males with coronary artery disease. However, the impact of gender on the coronary artery disease severity has not been investigated in patients with metabolic syndrome. The available data have suggested no significant association between gender and the extent and severity of coronary artery disease.
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Accessory mitral valve tissue is an extremely rare congenital cardiac anomaly. Most of the cases reported in the literature were associated with left ventricular outflow tract obstruction. In this report, a second cerebrovascular event is presented in the same patient two years after an operation in which septal myectomy was performed but accessory mitral valve tissue was not excised.
OBJECTIVE: Hyperhomocysteinemia is recognized as an independent risk factor for arterial disease including coronary artery disease, cerebrovascular disease and peripheral vascular disease. Previously, an association between increased plasma homocysteine level and peripheral arterial aneurysms has been reported. However, the relationship between coronary artery ectasia (CAE) and plasma homocysteine level has not been investigated. Accordingly, this study was designed to investigate plasma homocysteine level in patients with isolated CAE. METHODS: Thirty-two patients with isolated CAE without significant stenosis and 30 control subjects with angiographically normal coronary arteries were included in this study. Fasting plasma homocysteine concentrations were measured by Fluorescence Polarization Immunoassay method using homocysteine kids. Hyperhomocysteinemia is defined as plasma homocysteine levels above the 95th percentile of the control subjects (13.6 mumol/l). RESULTS: According to the definition of hyperhomocysteinemia, 19 (59%) of patients with isolated CAE had elevated levels of plasma homocysteine compared to 2 (7%) in the control subjects with angiographically normal coronary arteries (p<0.001). In addition, patients with isolated CAE had significantly higher levels of plasma homocysteine compared to control subjects (14.9+/-4.5 micromol/l vs. 8.6+/-1.9 micromol/l respectively, p<0.001). Besides, we detected a significant positive correlation between the number of ectasic segment and plasma homocysteine level (r=0.537, p=0.002). CONCLUSION: We have shown for the first time an association between elevated plasma homocysteine level and isolated CAE. Larger prospective studies are needed to confirm the role of hyperhomocysteinemia in CAE and to evaluate the usefulness of homocysteine-lowering therapies.
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BACKGROUND: Elevated plasma levels of homocysteine are currently considered a major, independent risk factor for cardiovascular diseases. Recently, several investigators have suggested that even mild elevation in plasma homocysteine level can severely disturb vascular endothelial function and subsequently impair coronary blood flow. Accordingly, we investigated plasma homocysteine level in patients with slow coronary flow. METHOD: Study population included 53 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (group I, 21 females, 32 males, mean age=48+/-9 years), and 50 subjects with angiographically proven normal coronary arteries without associated slow coronary flow (group II, 22 females, 28 males, mean age=50+/-8 years). Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction frame count (TIMI frame count). All patients in group I had TIMI frame counts greater than two standard deviations above those of control subjects (group II) and, therefore, were accepted as exhibiting slow coronary flow. The mean TIMI frame count for each patient and control subject was calculated by adding the TIMI frame counts for each major epicardial coronary artery and then dividing the obtained value into 3. Plasma homocysteine level was measured in all patients and control subjects using commercially available homocysteine kits. RESULTS: There was no statistically significant difference between two groups in respect to age, gender, hypertension, diabetes mellitus, hyperlipidemia and cigarette smoking (p>0.05). Plasma homocysteine level of patients with slow coronary flow were found to be significantly higher than those of control subjects (15.5+/-5.7 vs. 8.7+/-4.2 microM/l, respectively, p<0.001). Moreover, we found a significant positive correlation between plasma homocysteine level and mean TIMI frame count (r=0.660, p<0.001). CONCLUSION: We have shown that patients with slow coronary flow have raised level of plasma homocysteine compared to control subjects with normal coronary flow. This data suggests that elevated level of plasma homocysteine may play a role in the pathogenesis of slow coronary flow.
BACKGROUND: Inflammation has been reported to be a major contributing factor to many cardiovascular events. In the present study, we aimed to evaluate plasma soluble adhesion molecules; intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin as possible indicators of endothelial activation or inflammation in patients with slow coronary flow. METHOD: Study population included 17 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (group I, 11 male, 6 female, mean age=48+/-9 years), and 20 subjects with angiographically proven normal coronary arteries without associated slow coronary flow (group II, 11 male, 9 female, mean age=50+/-8 years). Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction frame count (TIMI frame count). All patients in group I had TIMI frame counts greater than two standard deviation above those of control subjects (group II) and, therefore, were accepted as exhibiting slow coronary flow. Serum levels of ICAM-1, VCAM-1, and E-selectin were measured in all patients and control subjects using commercially available ELISA kits. RESULTS: Serum ICAM-1, VCAM-1, and E-selectin levels of patients with slow coronary flow were found to be significantly higher than those of control subjects with normal coronary flow (ICAM-1: 545+/-198 ng/ml vs. 242+/-113 ng/ml respectively, p<0.001, VCAM-1: 2040+/-634 ng/ml vs. 918+/-336 ng/ml respectively, p<0.001, E-selectin: 67+/-9 ng/ml vs. 52+/-8 ng/ml respectively, p<0.001). Average TIMI frame count was detected to be significantly correlated with plasma soluble ICAM-1 (r=0.550, p<0.001), VCAM-1 (r=0.569, p<0.001) and E-selectin (r=0.443, p=0.006). CONCLUSION: Increased levels of soluble adhesion molecules in patients with slow coronary flow may be an indicator of endothelial activation and inflammation and are likely to be in the causal pathway leading to slow coronary flow.
BACKGROUND: P-wave dispersion (PWD), has been defined as the difference between maximum and minimum P-wave duration. Prolonged P-wave duration and increased PWD have been reported to be related with increased risk for atrial fibrillation (AF). AF is the most common sustained arrhythmia encountered in patients with rheumatic mitral stenosis (MS). Beta-blockers are the mainstay of therapy in patients with rheumatic MS to control ventricular rate both during sinus rhythm and AF. In the present study, we aimed to evaluate the effect of long-term beta-blocker therapy on P-wave duration and PWD in patients with rheumatic MS. METHOD: Study population includes 46 patients (group I, 8 men, 38 women, mean age = 34+/-8 years) with newly diagnosed moderate-to-severe rheumatic MS who have not taken any medication before and prescribed oral beta-blocker therapy and 46 healthy control subjects without any cardiovascular disease (group II, 8 men, 38 women, mean age = 35+/-7 years). Mitral valve area, maximum and mean diastolic mitral gradients, left atrial diameter, and systolic pulmonary artery pressure were evaluated by transthoracic echocardiography before initiation of beta blocker therapy and repeated at the end of the first month. Baseline maximum and minimum P-wave duration and PWD were determined on 12-lead electrocardiogram recorded for each patient and control subject and repeated at the end of the first month after initiation of beta-blocker therapy in patient group. RESULTS: Maximum P-wave duration and PWD were found to be significantly higher in patients with MS than those in control subjects (Maximum P-wave duration: 128+/-7 ms vs. 104+/-4 ms and PWD: 52+/-6 ms vs. 27+/-3 ms, p < 0.001 for both). Both groups had comparable minimum P-wave duration (75+/-4 ms vs. 76+/-4 ms, p = 0.093). Maximum P-wave duration and PWD were found to be significantly decreased by long-term beta blocker therapy (Maximum P-wave duration; 128+/-7 ms vs. 122+/-6 ms, p < 0.001, PWD; 52+/-6 ms vs. 47+/-5 ms, p < 0.001). However, there was no significant difference between the values of minimum P wave duration measured before and at the end of the first month of beta-blocker therapy (75+/-4 ms vs. 75+/-3 ms, p = 0.678). Statistically significant decrease were detected on maximum and mean mitral gradient and systolic pulmonary artery pressure and resting heart rate at the end of the first month of beta-blocker therapy. However, only the change in resting heart rate was found to be significantly correlated with the decrease in maximum P-wave duration and PWD (Maximum P-wave duration: r = 0.327, p = 0.026, PWD: r = 0.378, p = 0.01). CONCLUSION: We have shown for the first time that long-term beta-blocker therapy causes a significant decrease in maximum P-wave duration and PWD in patients with rheumatic MS.
BACKGROUND: Hyperthyroidism is a major cause of paroxysmal atrial fibrillation (AF). The purpose of this study was to evaluate the predictors of AF in the patients with clinical and subclinical hyperthyroidism. METHODS AND RESULTS: The study population consisted of four groups: group I (57 euthyroid healthy persons), group II (33 patients with subclinical hyperthyroidism), group III (69 patients with overt hyperthyroidism) and group IV (31 patients with overt hyperthyroidism and documented paroxysmal AF). The maximum P wave duration (P maximum) in group IV (114 +/- 8 ms) was significantly higher than group I (102 +/- 7 ms, p < 0.001), group II (106 +/- 7 ms, p < 0.001) and group III (108 +/- 9 ms, p0.005). The P wave dispersion (PWD) was measured as 46 +/- 9 ms in group IV and this was significantly higher than group I (29 +/- 8 ms, p < 0.001), group II (36 +/- 9 ms, p < 0.001) and grup III (38 +/- 8 ms, p = 0.001). The P maximum and PWD were higher in the patients with subclinical hyperthyroidism compared to healthy individuals. Univariate regression analysis revealed that age, P maximum and PWD, multivariate analysis showed that P maximum and PWD were significant predictors of paroxysmal AF. A PWD value of 37.5 ms separated group IV from others with a sensitivity of 90%, specificity of 85%, and positive predictive accuracy of 77%. CONCLUSION: Simply measuring P maximum and PWD values, we could identify the patients with high risk for the development of AF and these simple ECG parameters may help in clinical judgement to determine the requirement for treatment in the patients with subclinical hyperthyroidism.
BACKGROUND: Thrombolysis in myocardial infarction (TIMI) frame count is a simple clinical tool for assessing quantitative indexes of coronary blood flow. This technique counts the number of cineangiographic frames from initial contrast opacification of the proximal coronary artery to opacification of distal arterial landmarks. We hypothesized that patients with normal coronary artery (NCA) and myocardial infarction (MI) might have impaired coronary flow. Accordingly, we assessed the TIMI frame counts of patients with NCA and MI and compared to patients with NCA and without MI. MATERIALS AND METHOD: This retrospective study included consecutive patients with MI and who were found to have normal coronary angiograms performed between 1999 and 2003. Fifty patients (group I) with NCA and MI were enrolled in the study. Fifty consecutive patients with NCA and without MI were also enrolled in the study as control group (group II). Mean time interval between MI and coronary angiography was 6 +/- 2 days. RESULTS: There were statistically significant differences between groups I and II in respect to gender (11 females (22%) versus 22 females (44%), p = 0.003, respectively) and smoking status (62% (31/50) versus 38% (19/50), p = 0.02). Comparison of TIMI frame counts between two groups revealed that group I patients had significantly higher TIMI frame counts than group two patients for all three coronary arteries (LAD: 40 +/- 12 versus 23 +/- 7, Cx: 47 +/- 14 versus 27 +/- 7, RCA: 36 +/- 10 versus 26 +/- 10, respectively, p < 0.001 for all). Smokers were significantly younger when compared to non-smokers (44 +/- 5 years versus 51 +/- 9 years, p = 0.008, respectively). TIMI frame counts of smokers did not significantly differ from those of non-smokers in group I patients. There were statistically significant differences between smokers and non-smokers in group II patients regarding TIMI frame counts for all three coronary arteries (LAD: 29 +/- 7 versus 18 +/- 3, LCX: 34 +/- 10 versus 22 +/- 4, RCA: 34+ /- 13 versus 20 +/- 4, respectively, p < 0.001 for all). CONCLUSION: We have shown that patients with MI and NCA have higher TIMI frame counts for all coronary arteries when compared to patients without MI and NCA. Absence of difference between smokers and non-smoker in the myocardial infarction group in respect to TIMI frame count, has suggested that smoking does not lead to further increase of TIMI frame counts. On the other hand, in patients without MI and with NCA, smokers have higher TIMI frame counts than non-smokers have.
OBJECTIVES: The electromagnetic field generated by different systems have well-recognized adverse effects on pacemaker functions. The aim of this study is to evaluate the adverse effects of mobile phones on pacemaker functions. METHODS AND RESULTS: A total of 679 patients with permanent pacemakers were enrolled in this study. The study was performed in two steps. Pacemaker lead polarity was unipolar in the first step and bipolar in the second step. Pacemaker sensitivity was first at nominal values, it was then reduced to the minimal value for that pacemaker and tested again. Two mobile phones were symmetrically located on both sides of the pacemaker pocket with the antennas being equidistant at 50, 30, 20 and 10 cm and in close contact with the pocket. The tests were performed when both mobiles were opened, on stand-by, were receiving a call, during the call and were closed. Thirty-seven patients with pacemakers were adversely affected (5.5%) (33 VVI-R pacemakers were converted to asynchronous mode, and 3 were inhibited, 1 DDD-R pacemaker developed ventricular triggering). When the lead polarity was unipolar, the rate of adverse effect was higher when compared to the bipolar state (4.12% and 1.40%, p<0.01). The increase in sensitivity was not an independent factor on the rate of being affected (p>0.05). The rate of observing an adverse effect increased as the pacemaker got older (p<0.05). CONCLUSIONS: Mobile phones might have adverse effects on pacemaker functions under certain conditions. This does not result in any symptoms other than the inhibition of pacemakers, and pacemaker functions return to normal when the mobile phones are removed away from the patient.
BACKGROUND: The metabolic syndrome is more prevalent with the use of the recently defined National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria and is associated with a greater risk of atherosclerotic cardiovascular disease than any of its individual components. This study evaluated the prevalence of metabolic syndrome in female and male patients with newly diagnosed premature coronary artery disease. METHOD: The study population included 582 consecutive patients (496 men, 86 women) with newly diagnosed premature coronary artery disease (aged < or =45 years). Besides classic major coronary risk factors, all patients were evaluated for the presence of metabolic syndrome based on the NCEP ATP III criteria. RESULTS: The majority of patients were male (85% versus 15%). The overall prevalence of metabolic syndrome was 37%. Women with premature coronary artery disease were found to have a higher prevalence of metabolic syndrome than men (73% versus 31% respectively, p < 0.001). Furthermore, the mean number of components of metabolic syndrome was significantly higher in women compared to men (2.81 +/- 1.09 versus 1.85 +/- 1.08 respectively, p < 0.001). In addition, metabolic syndrome was detected to be the most frequent coronary risk factor in women (73%). Besides, cigarette smoking was found to be significantly higher in males compared to females (70% versus 36% respectively, p < 0.001) and it was the most prevalent coronary risk factor in men with premature coronary artery disease. CONCLUSION: We have shown for the first time a higher prevalence of metabolic syndrome in young females compared with young males with premature coronary artery disease. This data may be useful in directing primary and secondary preventive measures.