Relationship between TIMI frame count and admission glucose values in acute ST elevation myocardial infarction patients who underwent successful primary percutaneous intervention.

OBJECTIVE: Admission hyperglycemia is associated with poor prognosis in patients with acute myocardial infarction. Final Thrombolysis in Myocardial Infarction (TIMI) frame counts of culprit coronary arteries may show significant variability despite successful coronary reperfusion after primary percutaneous coronary intervention (PCI). In this prospective observational study, relationship between final TIMI frame counts of the culprit coronary artery and admission glucose values was investigated in patients who underwent successful primary PCI due to acute ST-elevation myocardial infarction (STEMI). METHODS: During a 6- month period of time, 73 non-diabetic patients presented with acute STEMI who have undergone primary PCI with final TIMI 3 flow were consecutively included in the study. Patients were divided into two groups according to final TIMI frame counts. Group 1 (n=53) consisted of patients with final TIMI frame counts of the culprit coronary artery within the two standard deviation of predefined values and Group 2 (n=20) consisted of those with higher TIMI frame counts. Statistical analysis was performed using Chi-square, Mann-Whitney U tests and multiple linear regression analysis. RESULTS: Despite similar fasting glucose values, admission glucose levels were significantly higher in Group 2 as compared to Group 1 (138 [114-165] vs. 123 [97-143] mg/dl, p=0.03). In whole group, admission glucose values were significantly correlated with corrected TIMI frame counts of culprit coronary arteries (r=0.30, p=0.01). In addition, there were significant association between admission glucose values and peak creatine kinase-MB (r=0.36, p=0.007) values as well as left ventricular ejection fraction (r=-0.43, p=0.009). In multiple linear regression analysis, only admission glucose value was found to be significantly related to the final TIMI frame count of the culprit artery (ß=0.04, 95%CI: 0.02-0.085, p=0.04). CONCLUSION: High admission glucose values were significantly associated with impaired coronary flow even after successful primary PCI in non-diabetic patients with STEMI.

Impact of metabolic syndrome on future cardiovascular events in patients with first acute myocardial infarction.

The prevalence of metabolic syndrome (MetS) is increasing worldwide and patients with MetS have increased risk of cardiovascular events. Recent studies in different populations showed higher prevalences of MetS in patients with acute myocardial infarction (MI) and identified MetS as an independent predictor of future cardiac events. This study sought to determine the prevalence of MetS in patients with acute MI and investigate the impact of MetS on adverse cardiovascular events after acute MI. One hundred and eighty-eight patients (155 men, 33 women) admitted with first acute MI were enrolled into the study. Of the total patients, 80 (42.6%) patients were diagnosed with MetS according to the National Cholesterol Education Program Adult Treatment Panel III criteria with modifications for high blood pressure and high fasting plasma glucose. Kaplan-Meier curves showed that the cumulative event-free survival rates did not differ between the patients with and without MetS during a median follow-up period of 27.7 (min:14, max:42) months (P>0.05). On multivariate Cox regression analysis controlling for hypertension, diabetes mellitus, glucose, MetS, and waist-to-hip ratio, there was no association between the major adverse coronary events and the presence of MetS (P>0.05), whereas Killip class (relative risk: 2.853, 95% confidence interval: 1.606-5.070; P<0.001) was identified as the only independent predictor of long-term cardiovascular outcomes. This study shows that MetS has no effect on long-term prognosis after MI. However, Killip class was identified as an independent predictor of major cardiac events.

Decreased plasma concentrations of adiponectin in patients with slow coronary flow.

Adiponectin has multiple protective effects on vascular endothelium through anti-inflammatory and anti-atherogenic properties. Recent data suggested that endothelial activation and inflammation may contribute to the pathogenesis of slow coronary flow (SCF). Therefore, we investigated whether adiponectin plasma concentrations were decreased in patients with SCF compared to subjects with normal coronary flow. The study population consisted of 35 patients with angiographically documented SCF in all three coronary arteries and 35 sex- and age-matched cases with normal coronary flow. Coronary flow rates of all participants were determined by Thrombolysis in Myocardial Infarction (TIMI) frame count. Plasma adiponectin concentrations were measured by an enzyme-linked immunosorbent assay method using commercially available adiponectin kits. There were no statistically significant differences between the patients with SCF and the subjects with normal coronary flow in terms of demographic characteristics and cardiovascular risk factors (P>0.05). Plasma adiponectin concentrations of patients with SCF were found to be significantly lower than those with normal coronary flow (4.77+/-3.86 mg/ml vs 10.8+/-6.60 mg/ml, P=0.001, respectively). Plasma adiponectin levels were correlated significantly and inversely with mean TIMI frame count in patients with SCF (r= -0.441, P=0.008). Furthermore, the Receiver Operator Characteristics curve of adiponectin concentrations showed that an adiponectin <4.6 mg/ml is associated with SCF with a sensitivity of 68.6%, specificity of 82.9%, positive predictive value of 80.0%, and negative predictive value of 72.5%. Our findings suggest that endothelial inflammation may play a role in the pathogenesis of SCF phenomenon.

Myocardial noncompaction presenting with Brucella endocarditis.

Noncompaction of ventricular myocardium is a unique congenital cardiomyopathy with its own clinical presentation and course. It is more frequently associated with complications of congestive heart failure, thromboembolism and malignant ventricular arrhythmias; however, concomitance of valvular pathologies or infective endocarditis with noncompaction of ventricular myocardium has seldom been reported. We describe herein the first case of left ventricular myocardial noncompaction presenting with Brucella endocarditis with aortic and mitral valve involvements, whom subsequently underwent successful medical and surgical treatment.

[The effect of plasma asymmetric dimethylarginine (ADMA) level and L-arginine/ADMA ratio on the development of coronary collaterals]. / Plazma asimetrik dimetilarginin (ADMA) düzeyi ve L-arginin/ADMA oraninin koroner kollateral gelisimi üzerine etkisi.

OBJECTIVES: It has been shown that asymmetric dimethylarginine (ADMA), an endogenous competitive antagonist of nitric oxide (NO) synthase, inhibits angiogenesis by reducing the production and bioavailability of NO. We investigated the effect of plasma ADMA level and L-arginine/ADMA ratio on the development of coronary collateral arteries. STUDY DESIGN: The study consisted of 94 patients (66 males, 28 females; mean age 59+/-11 years) who underwent coronary angiography for suspected coronary artery disease and were found to have severe stenosis (>95%) in at least one major coronary artery. The patients were evaluated in two groups with poor (Rentrop score 0-1, n=44) and good (score 2-3, n=50) coronary collateral circulation according to the Rentrop collateral scoring system. Plasma levels of ADMA and L-arginine were measured by high-performance liquid chromatography. RESULTS: The two groups were similar with regard to basal characteristics and cardiovascular risk factors (p>0.05) except for stable angina, which was more common in patients with Rentrop score 2-3 collateral circulation (p<0.001). Despite similar L-arginine levels (p>0.05), patients with Rentrop score 0-1 had a significantly higher ADMA level (p=0.003) and lower L-arginine/ADMA ratio (p=0.019). Multivariate logistic regression analysis showed that plasma ADMA concentration was an independent predictor of coronary collateral development (odds ratio=0.674; 95% confidence interval=0.508-0.894; p=0.006). CONCLUSION: Elevated plasma ADMA concentrations are associated with a poorly developed coronary collateral circulation, suggesting that dysregulation of the NO synthase pathway may result in impaired collateral development.

Impact of plasma adiponectin levels to the presence and severity of coronary artery disease in patients with metabolic syndrome.

OBJECTIVES: Adiponectin is thought to serve a protective function for the coronary endothelium by inhibiting many of the crucial steps in atherosclerotic process. Previous research has indicated an increased risk of coronary artery disease (CAD) in patients with metabolic syndrome (MetS). The objective of this study was to investigate whether plasma adiponectin concentrations were associated with the presence and severity of CAD in patients with MetS undergoing coronary angiography. METHODS: We measured plasma adiponectin levels in 167 consecutive patients with MetS undergoing coronary angiography. The severity of coronary atherosclerosis was defined by using Gensini score system. RESULTS: CAD was found in 70.1% of the patients. Patients with significant CAD had lower plasma adiponectin concentrations than those without CAD (4.14+/-3.83 vs. 8.94+/-6.63 microg/ml, P<0.001). Multiple regression analysis demonstrated that plasma adiponectin level was independently associated with CAD (odds ratio: 0.86; 95% confidence interval: 0.78-0.94; P=0.001). Plasma adiponectin levels were inversely related to the Gensini score (rho: -0.480, P<0.001) and predicted the severity of coronary atherosclerosis independent of other risk factors (beta: -0.054; 95% confidence interval: -0.074--0.034; P<0.001). CONCLUSIONS: These findings suggest that hypoadiponectinemia may play a role in the development of coronary atherosclerosis and the observation of adiponectin levels may be indicative of the presence of significant CAD in patients with MetS.

Circulating CD4+CD25+ T cells in rheumatic mitral stenosis.

BACKGROUND AND AIM OF THE STUDY: Autoimmunity plays an essential role in the pathogenesis of rheumatic heart disease. Although the ongoing rheumatic process has been demonstrated with high levels of inflammatory markers, the cellular mechanism(s) of autoimmunity have not yet been investigated. The study aim was to examine levels of circulating CD4+CD25+ T cells in patients with rheumatic mitral stenosis, and to evaluate the relationship between regulatory CD4+CD25+ T-cell count and clinical and echocardiographic measures. METHODS: A total of 42 patients with mitral stenosis was enrolled into the study, and 27 normal age- and gender-matched healthy subjects served as controls. All patients and controls underwent clinical, electrocardiographic, echocardiographic and laboratory evaluation. T-cell levels were determined with flow cytometry using monoclonal fluorescein isothiocyanate-labeled anti-CD4 and phycoerythrin-labeled anti-CD25 antibodies. RESULTS: The circulating CD4+CD25+ T-cell count was significantly lower in patients with mitral stenosis than in controls (231 +/- 120 versus 372 +/- 180 per mm3; p = 0.001). The percentage ratio of CD4+CD25+ T cells to total leukocytes and lymphocytes was significantly lower in patients with mitral stenosis than in controls (2.9 +/- 1.5 versus 5.2 +/- 2.1; p < 0.001, and 11.2 +/- 5.6 versus 14.8 +/- 5.6; p = 0.011, respectively). In addition, a significant negative correlation was identified between the erythrocyte sedimentation rate and circulating CD4+CD25+ T-cell count (Spearman rho = -0.414; p = 0.006). No correlation was found between CD4+CD25+ T-cell count and clinical and echocardiographic parameters in patients with mitral stenosis. CONCLUSION: A decrease in CD4+CD25+ T cell numbers in mitral stenosis patients might suggest a role for cellular autoimmunity in a smoldering rheumatic process.

Relationship between inflammation and atrial fibrillation in patients with isolated rheumatic mitral stenosis.

BACKGROUND AND AIM OF THE STUDY: Atrial fibrillation (AF) is the most common arrhythmia in patients with rheumatic mitral stenosis (MS), with an increased risk of mortality and morbidity. Although recent data have suggested that the inflammatory process is associated with non-valvular AF, the relationship between inflammation and AF occurrence in MS patients remains unknown. The study aim was to determine whether plasma levels of high-sensitivity C-reactive protein (hs-CRP), as a marker of inflammation, are elevated in patients with isolated rheumatic MS and AF compared to patients with MS but without AF. METHODS: The study population comprised 89 patients with isolated rheumatic MS (57 patients in sinus rhythm and 32 in AF) and 35 healthy controls. Patients with MS were categorized into subgroups in terms of their mitral valve area (MVA). Mean transmitral diastolic gradients and pulmonary artery pressure were monitored, and morphologic features of the mitral valve classified using an echocardiographic scoring system. Plasma levels of hs-CRP were monitored in all patients and control subjects, using a commercially available analytical kit. RESULTS: Patients with AF were shown to have significantly higher plasma levels of hs-CRP compared to those in sinus rhythm and controls (p < 0.001). In general, patients with AF were older (p < 0.001) and had a larger left atrial diameter (LAD) (p < 0.001). Plasma levels of hs-CRP were associated with LAD only in the AF group (rho = 0.437; p = 0.012). Multivariate logistic regression analysis revealed a significant independent relationship between AF and hs-CRP plasma level (odds ratio (OR) 3.57; 95% confidence interval (CI) 1.2-10.5; p = 0.021), age (OR 1.08; 95% CI 1.03-1.14; p = 0.003), and LAD (OR 1.2; 95% CI 1.02-1.4; p = 0.023). CONCLUSION: The study results indicated that hs-CRP plasma levels are associated with the presence of AF in patients with MS. This finding may have important implications for the development of new therapeutic and preventive approaches of AF in the setting of MS.

Asymmetric dimethylarginine plasma concentrations and L-arginine/asymmetric dimethylarginine ratio in patients with slow coronary flow.

OBJECTIVE: Elevated levels of nitric oxide synthase inhibitor, asymmetric dimethylarginine (ADMA) is considered to be a marker of endothelial dysfunction and increased risk of cardiovascular disease. Recent reports have implicated endothelial dysfunction as an underlying pathophysiological mechanism of slow coronary flow (SCF) phenomenon. Accordingly, we investigated plasma L-arginine, ADMA concentrations and L-arginine/ADMA ratio in patients with SCF in comparison with participants having normal coronary flow. METHODS: We measured plasma levels of L-arginine and ADMA by high-performance liquid chromatography in 31 participants with SCF and 31 age and sex matched control participants with normal coronary flow. Coronary flow was quantified using the thrombolysis in myocardial infarction (TIMI) frame count method. RESULTS: The patients with SCF were detected to have significantly higher concentrations of plasma ADMA (P=0.006) and lower L-arginine/ADMA ratio compared with participants with normal coronary flow (P=0.002). In addition, both ADMA and L-arginine/ADMA ratio were significantly correlated with mean TIMI frame count and TIMI frame count for each coronary artery in patients with SCF and multivariate regression analysis identified plasma ADMA as an independent predictor for SCF. In the receiver operator characteristics curve analysis, patients with SCF were detected by plasma ADMA level with a sensitivity, specificity of 64.5%, 74.2%, at a cut-off of >2.4 micromol/l and L-arginine/ADMA ratio with a sensitivity, specificity of 77.4%, 67.7% at a cut-off of <36.6. CONCLUSION: Our findings provide evidence to support the hypothesis that endothelial dysfunction may be an important factor in the pathogenesis of SCF.

Twenty-two years without anticoagulation with metallic heart valve.

Anticoagulation is essential and vital for mechanical heart valves to prevent lethal complications such as valve thrombosis and systemic embolism. Herein, we reported the third longest survived case with a metallic aortic valve without anticoagulation and reviewed the role of anticoagulation in mechanical heart valves.

Acquired cardiac hypertrophy with outflow tract obstruction in a patient with severe Takayasu arteritis.

Takayasu arteritis with coronary artery involvement is rare and its association with secondary cardiac hypertrophy with severe outflow tract obstruction is not common. We describe a case of Takayasu arteritis, diagnosed 10 years ago, whose coronary artery involvement and obstructive cardiac hypertrophy are ascertained after our investigations.

Do different atrial flutter types carry the same thromboembolic risk?

Thromboembolic risk of atrial flutter (AFl) types has not been elucidated sufficiently in previous reports. The authors classified the patients according to surface electrocardiogram and electrophysiologic characteristics as those with typical AFl (37 patients, 78.4% male, mean age 59.8 +/-9.5 years) and atypical AFl (13 patients, 69.2% male, mean age 60.9 +/-6.9 years) and compared them regarding some clinical, echocardiographic, and hematologic parameters. An age- and gender-matched control group composed of 20 individuals without any organic heart disease in sinus rhythm was chosen (80% male, mean age 60.3 +/-7.9 years). Clinical features such as age, gender, organic heart disease, hypertension, diabetes mellitus, AFl duration, and the prevalence of paroxysmal atrial fibrillation were similar in both AFl groups. Echocardiographic parameters such as left ventricular ejection fraction, left atrial (LA) diameter, LA spontaneous echo contrast, and LA appendage emptying velocities were similar in both AFl groups. Fibrinogen, fibrin D-dimer, and thrombin-antithrombin III levels reflecting coagulation system activity were found to be increased in the patients with atypical AFl when compared with those with typical AFl and the control group (p < 0.001). In Pearson's correlation analysis, significant correlation between these hematologic markers and clinical and echocardiographic parameters were not found (p > 0.05). The coagulation system activity was found to be increased in patients with atypical AFl. Thus, anticoagulation due to the increased thromboembolic risk should be considered in patients with atypical AFl.

The effects of mobile phones on pacemaker function.

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.

Increased P wave dispersion after the radiofrequency catheter ablation in overt pre-excitation patients: the role of atrial vulnerability.

The pathogenesis of paroxysmal atrial fibrillation (PAF) in patients with overt pre-excitation and effect of elimination of accessory pathways on the appearance of AF are still controversial. We demonstrated the increased P max and P wave dispersion (PWD) reflecting more inhomogeneous and prolonged atrial conduction in patients with Wolff-Parkinson-White (WPW) syndrome and PAF attacks. One-hundred and fifty-one patients who underwent radiofrequency (RF) catheter ablation due to paroxysmal tachycardia medicated by accessory pathway were enrolled in this study. The patients were classified into two groups according to the presence of previous PAF attacks. We compared the clinical characteristics, echocardiograhic findings, P max and PWD values measured after normalization of PR intervals and disappearance of pre-excitation after ablation in overt pre-excitation patients. Although the differences in age, left atrial diameter and left ventricular ejection fraction (LVEF) were not significant in both groups, P maximum (130.0+/-8.4 vs. 122.3+/-8.7 ms, p=0.002) and P wave dispersion values measured after ablation (50.3+/-7.2 vs. 35.7+/-6.1 ms, p=0.001) were significantly higher in patients with previous PAF attacks. Accessory pathway (AP) antegrade and retrograde effective refractory period (ERP) values were shorter (276+/-27.3 vs. 321.0+/-48.7, p=0.001; 263.4+/-41.3 vs. 299.7+/-38.2, p=0.002, respectively) in patients with PAF attack when compared to those without PAF attacks. Higher P wave dispersion values in patients with previous PAF attacks suggest the important role of inhomogenous and discontinuous propagation of sinus impulses. Therefore, we concluded that not only the accessory pathway but also inhomogenous propagation of sinus impulses may play an important role in occurrence of AF in patients with pre-excitation.

Evaluation of atrial refractoriness immediately after percutaneous mitral balloon commissurotomy in patients with mitral stenosis and sinus rhythm.

BACKGROUND: Chronic atrial stretch and rheumatic inflammatory activity leads to atrial dilatation and conduction slowing, and this increases the susceptibility to atrial fibrillation (AF). The aim of this study was to examine the effects of changes in the chronic atrial stretch on atrial refractoriness in the early period after percutaneous mitral balloon commissurotomy (PMBC) in patients with mitral stenosis and sinus rhythm. METHODS: Twenty-five patients undergoing PMBC were enrolled in this study. We evaluated the changes in pulmonary arterial pressure (PAP), left atrial (LA) pressure, mean mitral diastolic gradient, and mitral valve area in addition to the changes in atrial effective refractory periods (AERPs), AERP dispersion, and intra-atrial and interatrial conduction times after PMBC. RESULTS: There were significant decreases in mean diastolic gradient, PAP, mean LA pressure, and LA size after PMBC. Accompanying these acute hemodynamic changes after PMBC, AERPs in high right atrium (HRA), distal coronary sinus (DCS), and right posterolateral (RPL) were found to be increased (P <.001), and AERP dispersion, PA(HIS) (an interval between P wave on the surface electrocardiogram and atrial electrogram at the His bundle site), and HRA-DCS intervals were significantly reduced after PMBC (P <.001). It was revealed with linear regression and correlation analysis that only the changes in AERP dispersion were correlated with changes in LA pressure. CONCLUSIONS: Relief of chronic atrial stretch results in an increase in AERPs and decrease in AERP dispersion, suggesting the potential reversibility of the electrophysiological features of chronic atrial dilatation. Our study emphasizes that an acute reduction of chronic atrial stretch in mitral stenosis resulted in favorable effects on atrial electrophysiological characteristics, and our results provide the first detailed insights into the electrophysiological changes after PMBC in patients with sinus rhythm.

[Classification of patients with complete atrioventricular block according to etiological, demographic and clinical features and pacemaker needs]. / Atriyoventriküler Tam Bloklu Hastalarin Etiyolojik, Demografik, Klinik Ozellikleri Ile Pacemaker Ihtiyaçlarina Göre Siniflandirilmalari.

OBJECTIVE: Complete atrioventricular (AV) block is a rhythm disorder that can result from various causes. The aim of this study was to define etiological factors, clinical features, pacemaker needs, in-hospital mortality rates and factors affecting these parameters in the patients with complete AV block. METHODS: For this aim, 191 consecutive patients admitted to the hospital with complete AV block or who developed AV block during their hospital course between January 1999-September 2002 were included into the study. RESULTS: The most common underlying cause of AV block was found to be the ischemia, which was followed by unknown etiology and iatrogenic complete AV block. The most common cause of in-hospital mortality was ischemic (especially acute) heart disease. No etiological factor for complete AV block was found in most of symptomatic patients presented with syncope. In patients with ischemic complete AV block, mortality and syncope rates were found to be high, especially in patients with multivessel disease. Permanent pacemaker was implanted in 76 of 191 patients with complete AV block and the significant portion of these patients were those without an etiological cause. CONCLUSION: Thus, it is revealed that factors affecting mortality in patients with complete AV block are acute myocardial infarction and age while other clinical parameters and pacemaker implantation had no effects on mortality.

Determinants of persistent atrial fibrillation in patients with DDD pacemaker implantation.

Occurrence of AF in a pacemaker implanted patient is a significant cause of morbidity and mortality. The aim of this study was to prospectively investigate the clinical, echocardiographic, and electrocardiographic determinants of persistent AF in patients with DDD pacemakers. A 101 consecutive patients were followed for an average of 19.8 +/- 11.8 months. Persistent AF was documented in 21 (20.8%) patients and 80 (79.2%) patients were in sinus or physiologically paced rhythm. In patients with persistent AF, previous AF attacks were observed more frequently (P < 0.03) and left atrial dimension was higher (3.5 +/- 0.6 vs 3.0 +/- 0.5 cm, P < 0.001). Average P maximum and P wave dispersion (PWD) values calculated in a 12-lead surface electrocardiogram were also found to be significantly higher in patients with persistent AF (P < 0.001). Cox regression analysis demonstrated that the presence of previous AF attacks (RR 8.95, P < 0.001), increased left atrial dimension (RR 2.1, P < 0.02), P maximum duration 120 ms (RR 6.1, P < 0.001), and PWD 40 ms (RR 12.2, P < 0.001) were associated with an increased risk of persistent AF. Cut-off points were 120 ms for P maximum and 40 ms for PWD. Sensitivity, specificity, and positive and negative predictive values were calculated as 76.2, 82.5, 53.3, and 92.9 for P maximum and as 85.7, 87.5, 64.3, and 95.9 for PWD, respectively. In patients with DDD pacemakers, previous AF attacks, increased left atrial dimension, P maximum value of 120 ms, and a PWD value of 40 ms were associated with a significantly increased risk of persistent AF. These patients must further be managed with other treatment modalities to prevent the development of persistent AF.

Increased dispersion of refractoriness in patients with atrial fibrillation in the early postoperative period after coronary artery bypass grafting.

INTRODUCTION: Increased atrial effective refractory period (AERP) dispersion is well correlated with vulnerability to atrial fibrillation (AF). However, the preoperative electrophysiologic characteristics of atrial abnormalities that may play an important role in the development of AF postoperatively in patients with coronary artery bypass grafting (CABG) have not been investigated in detail. METHODS AND RESULTS: Fifty-six consecutive patients who underwent CABG were enrolled in this study. Eighteen patients (14 men and 4 women; mean age 57.7 +/- 5.2 years) with AF in the early postoperative period and 38 patients (28 men and 10 women; mean age 56.3 +/- 6.4 years) without AF were compared with regard to preoperative clinical, echocardiographic, angiographic, and electrophysiologic parameters. Preoperative PA interval and AERP dispersion values were higher (P < 0.05) in patients who developed AF in the early postoperative period. PA interval (P < 0.05, odds ratio = 1.64, 95% confidence interval 1.17-2.30), AERP in the high right atrium (AERP(HRA); P < 0.05, odds ratio = 0.94, 95% confidence interval 0.91-0.97), AERP in the right posterolateral atrium (AERP(RPL); P < 0.05, odds ratio = 0.79, 95% confidence interval 0.63-0.98), AERP in the distal coronary sinus (AERP(DCS); P < 0.05, odds ratio = 0.84, 95% confidence interval 0.74-1.02), and AERP dispersion (P < 0.001, odds ratio = 1.29, 95% confidence interval 1.12-1.47) were independently related to post-CABG AF in univariate analysis. Increases in preoperative PA interval and AERP dispersion were found to be associated with a high risk for development of post-CABG AF. CONCLUSION: AERP dispersion is a suitable electrophysiologic indicator for atrial vulnerability. The presence of increased preoperative AERP dispersion and PA interval may indicate patients at high risk for development of AF in the early postoperative period after coronary artery bypass grafting.