Necla Ozer

P Wave Dispersion on 12-Lead Electrocardiography in Patients with Paroxysmal Atrial Fibrillation

The prolongation of intraatrial and interatrial conduction time and the inhomogeneous propagation of sinus impulses have been shown in patients with atrial fibrillation. Recently P wave dispersion (PWD), which is believed to reflect inhomogeneous atrial conduction, has been proposed as being useful for the prediction of paroxysmal atrial fibrillation (PAF). Ninety consecutive patients (46 men, 44 women; aged 55 ± 13 years) with a history of idiopathic PAF and 70 healthy subjects (42 men, 28 women; mean age, 53 ± 14 years) were studied. The P wave duration was calculated in all 12 leads of the surface ECC. The difference between the maximum and minimum P wave duration was calculated and this difference was defined as P wave dispersion (PWD = Pmax ‐ Pmin). All patients and controls were also evaluated by echocardiography to measure the left atrial diameter and left ventricular ejection fraction (LVEF). There was no difference between patients and controls in gender (P = 0.26), age (P = 0.12), LVEF (66 ± 4% vs 67 ± 5%, P = 0.8) and left atrial diameter (36 ± 4 mm vs 34 ± 6 mm, P = 0.13). P maximum duration was found to be significantly higher in patients with a history of PAF (116 ± 17 ms) than controls (101 ±11 ms. P < 0.001). P wave dispersion was also significantly higher in patients than in controls (44 ± 15 ms vs 27 ± 10 ms, P < 0.001). There was a weak correlation between age and P wave dispersion (r = 0.27, P < 0.001). A P maximum value of 106 ms separated patients with PAF from control subjects with a sensitivity of 83%, a specificity of 72%, and a positive predictive accuracy of 79%. A P wave dispersion value of 36 ms separated patients from control subjects with a sensitivity of 77%, a specificity of 82%, and a positive predictive accuracy of 85%. In conclusion, P maximum duration and P wave dispersion calculated on a standard surface ECG are simple ECG markers that could be used to identify the patients with idiopathic paroxysmal atrial fibrillation.

Methylene tetrahydrofolate reductase genotype and the risk and extent of coronary artery disease in a population with low plasma folate

OBJECTIVE To determine the effects of the thermolabile methylene tetrahydrofolate reductase (MTHFR) mutation on the presence and extent of coronary atherosclerosis in a population with low plasma folate. METHODS 242 consecutive patients undergoing coronary angiography were prospectively evaluated for conventional risk factors, plasma homocysteine, vitamin B-12, and folate, and MTHFR genotype. The severity of coronary atherosclerosis was determined by the Leaman score. RESULTS Mean (SD) plasma homocysteine was 15.6 (10) μmol/l in controls and 18.5 (11) μmol/l in patients with coronary artery disease (p > 0.05). Plasma homocysteine concentrations above 15 μmol/l were a risk factor for coronary artery disease (p = 0.03, risk ratio 2.1, 95% confidence interval (CI) 1.07 to 4.4). Homocysteine remained an independent risk factor on multivariate analysis when conventional risk factors were taken into account (p = 0.04). Homocysteine concentrations above 15 μmol/l were correlated with the extent of atherosclerosis (p = 0.04, risk ratio 3.2, 95% CI 1.3 to 8.2). Homocysteine had no effect on other lipid variables (p > 0.05). Plasma folate was 15.8 (7.2) nmol/l in controls and 11.5 (2.9) nmol/l in patients with coronary artery disease. Plasma folate concentrations below 12.9 nmol/l (5.7 ng/ml) conferred a risk for coronary artery disease (p = 0.03, risk ratio 2.42, 95% CI 1.05 to 5.59). When the MTHFR genotype was determined, the TT genotype was present in 7.4% of patients and 5.2% of controls (p > 0.05). The prevalence of alleles was within the Hardy–Weinberg equilibrium (TT 7, CT 40, CC 53, χ2 = 2.3, p = 0.3). The highest homocysteine concentrations were found in patients with the TT genotype and folate below the median of the population (p = 0.01). The extent of coronary atherosclerosis judged by the Leaman score was significantly higher in patients with the TT genotype (p = 0.03). CONCLUSIONS Plasma homocysteine over 15 μmol/l was a significant risk factor for the presence and extent of coronary artery disease. The mean plasma folate of the population was low and correlated negatively with homocysteine. Although TT genotype was not an independent predictor of coronary artery disease, it was an important predictor of the extent of coronary atherosclerosis and plasma homocysteine, especially in the presence of plasma folate values below the median of the population. These findings may have important implications for folate replacement in patients with the TT genotype.

P Wave Dispersion in Hypertensive Patients with Paroxysmal Atrial Fibrillation

It is important to assess the risk of developing paroxysmal atrial fibrillation (PAF) in hypertensive patients since hypertension is a common disorder predisposing to PAF. We sought to determine if patients with hypertension at risk of PAF can be identified while in sinus rhythm by measurements of P wave dispersion. Twelve‐lead surface electrocardiograms were recorded in 44 hypertensive patients with history of PAF (group I, mean age = 60) and in 50 hypertensive patients without history of AF (group II, mean age = 57). The maximum P wave duration, the minimum P wave duration, and P wave dispersion (Pd = Pmax ‐Pmin) were calculated from 12‐lead surface ECGs. Left atrial dimension (LAD) and left ventricular ejection fraction (LVEF) were measured by echocardiography. P wave dispersion was significantly greater in group I than group II (50 ± 12 vs 38 ± 8 ms, P = 0.001). P minimum (75 ± 13 vs 87 ± 11 ms, P = 0.001) and LVEF (0.63 ± 0.05 vs 0.67 ± 0.04, P = 0.03) were significantly lower in group I than group II. However P maximum and LAD were not significantly different in group I than group II (P > 0.05). In univariate analysis, P minimum, P wave dispersion, and LVEF were significant predictors of PAF, whereas only P wave dispersion remained a significant independent predictor of PAF in a multivariate analysis. Measurement of P wave dispersion in sinus rhythm may be a useful noninvasive clinical tool to identify patients with hypertension at risk of developing atrial electrical instability and atrial fibrillation.

Prediction of atrial fibrillation recurrence after cardioversion by P wave signal-averaged electrocardiography

The purpose of this report was to determine prospectively whether P wave signal-averaged electrocardiography (ECG) is useful for the prediction of recurrences of atrial fibrillation after cardioversion. The P wave signal-averaged ECG was recorded in 73 patients after successful cardioversion. Duration of the filtered P wave and the root mean square voltages for the last 20 ms of the P wave were calculated. In addition to signal-averaged ECG P wave analysis, all patients were evaluated by echocardiography. During 6 months follow-up period recurrence of atrial fibrillation was observed in 31 (42.5%) patients and in 42 (57.5%) patients sinus rhythm was maintained. There was no difference in gender, age, presence of organic heart disease, left atrial diameter, left ventricular ejection fraction, use of antiarrhythmic drug, and duration of atrial fibrillation (P>0.05). The filtered P-wave duration was longer and the root mean square voltages for the last 20 ms of the P wave was lower in patients with recurrence of atrial fibrillation than in patients who maintained sinus rhythm (138.3+/-12.5 ms vs. 112.4+/-11.8 ms, P = 0.001; 1.9+/-0.7 microV vs. 2.5+/-0.6 microV, P = 0.001). A filtered P-wave duration > or =128 ms associated with a root mean square voltage for the last 20 ms of the P wave < or =2.1 microV had a sensitivity of 70% and specificity of 76% for the detection of patients with recurrence of atrial fibrillation after successful cardioversion of atrial fibrillation. We found that the likelihood of recurrence of atrial fibrillation after cardioversion was increased 4.31-fold (95% confidence interval 2.08-9.83) if these parameters were used. These results suggest that P wave signal-averaged ECG could be useful to identify patients at risk for recurrence of atrial fibrillation after cardioversion.

Atrial fibrillation after coronary artery bypass surgery: P wave signal averaged ECG, clinical and angiographic variables in risk assessment.

BACKGROUND Atrial fibrillation (AF) is a commonly encountered arrhythmia and occurs in up to 40% of patients after coronary artery bypass surgery (CABG). The preoperative signal averaged ECG (SAECG) P wave may be useful indicator of AF after CABG. We prospectively analyzed the predictive value of SAECG P wave compared to clinical variables. METHODS Fifty-three patients with coronary artery disease undergoing first elective CABG were enrolled. All patients had P wave specific SAECG, standard 12 lead ECG, ejection fraction and left atrial posteroanterior diameter from the echocardiogram within the 24 h before surgery. From the SAECG P wave, filtered P wave duration was measured. Lead II P wave duration, left atrial enlargement and left ventricular hypertrophy were determined from standard ECG. Patients were continuously monitored during their postoperative period and serial ECGs were taken. RESULTS During an observation period of up to 16 days, 19 (35.8%) patients developed AF 2.8+/-1.3 days after CABG. Patients with AF more often had left atrial enlargement (LAE) on ECG (P = 0.041) and right coronary artery (RCA) lesion (P = 0.0034). The filtered P wave duration on the SAECG was significantly longer in the AF patients than those without AF (129.7+/-13.2 ms versus 113.9+/-9.0 ms, P = 0.001). Logistic regression analysis identified independent predictors, estimated adjusted relative risk (95% confidence interval) of AF: with LAE, the relative risk was 2.72 (1.13-5.82), RCA lesion, the relative risk was 3.06 (1.45-6.45) and SAECG P wave duration >122.3 ms, the relative risk was 4.58 (2.11-9.97). The occurrence of AF was predicted by electrocardiographically determined left atrial enlargement with a sensitivity of 36%, specificity of 88%, positive predictive accuracy of 63%, negative predictive accuracy of 71%. If presence of right coronary artery lesion was evaluated these values were 63%, 79%, 63%, 79% subsequently. P wave duration >122.3 ms had a sensitivity of 68%, specificity of 88%, positive predictive accuracy of 76%, negative predictive accuracy of 83%. If both P wave >122.3 ms and presence of right coronary artery lesion were combined, these values were 47%, 94%, 81%, 76% subsequently. CONCLUSION The predictors of AF after CABG were left atrial enlargement on standard 12 lead ECG, RCA lesion and SAECG P wave duration. Among these predictors, SAECG P wave duration was the best predictor of AF after CABG.

QT dispersion and autonomic nervous system function in patients with type 1 diabetes

Cardiac arrhythmias and markedly increased mortality rate have been demonstrated in patients with diabetic autonomic neuropathy. Abnormal prolonged QT dispersion interval (QTd) is associated with a higher risk of ventricular arrhythmias. The aim of this study was to evaluate the relationship between autonomic dysfunction, QT and JT interval dispersion parameters and ventricular arrhythmias. Twenty-six patients with type 1 diabetes mellitus and 20 healthy subjects as controls were enrolled in the study. Resting 12-lead electrocardiograms were recorded for measurement of QTd, corrected QTd (QTcd), JT dispersion (JTd) and corrected JT dispersion (JTcd). After taking ECG, all patients underwent autonomic function tests. Patients and control group were also evaluated by 24-h Holter monitoring. Fourteen patients were identified who had autonomic dysfunction. QTd, QTcd, JTd, and JTcd values were significantly higher in patients with autonomic dysfunction than both patients without autonomic dysfunction and the control group (QTd: 78+/-16 vs. 51+/-13 ms, P=0.002; 78+/-16 vs. 48+/-9 ms, P<0.001; QTcd: 91+/-14 vs. 66+/-12 ms, P=0.001; 91+/-14 vs. 61+/-11 ms, P<0.001; JTd: 81+/-12 vs. 58+/-13 ms, P=0.001; 81+/-12 vs. 49+/-7, P<0.001; JTcd: 96+/-15 vs. 73+/-11 ms, P<0.001; 96+/-15 vs. 67+/-8 ms, P=0.001). There was no significant difference between the dispersion parameters in diabetic patients without autonomic dysfunction and the control subjects (P>0.05). Also, patients with autonomic dysfunction had higher Lown classes of ventricular arrhythmias and patients with higher Lown classes of ventricular arrhythmias had more prolonged QTd and QTcd values. The data suggest that diabetic patients with autonomic dysfunction have increased dispersion of ventricular refractoriness, which may be one of the factors contributing to the increased incidence of arrhythmias and sudden death observed in these patients.

Increased plasma levels of soluble selectins in patients with unstable angina

BACKGROUND Inflammation plays an important role in the pathogenesis of unstable angina. Adhesion molecules, such as selectins, mediate the interactions between leukocytes, platelets and endothelial cells during inflammation and thrombogenesis. HYPOTHESIS The purpose of this study was to determine whether soluble E-selectin, P-selectin and L-selectin levels are increased in patients with unstable angina (UA). METHODS Soluble E-, P- and L-selectin levels were measured by enzyme-linked immunoassay in the peripheral blood of 23 patients with UA, 26 patients with stable angina (SA) and 15 control patients with angiographically normal coronary arteries. RESULTS Soluble E-selectin levels were significantly higher in patients with UA (45+/-11 ng/ml) than in controls (30+/-8 ng/ml, P<0.001), or patients with SA (34+/-8 ng/ml, P=0.001). Similarly, plasma levels of P- and L-selectin were significantly higher in patients with UA (427+/-144 and 772+/-160 ng/ml, respectively) than in patients with SA (278+/-79 and 643+/-94 ng/ml, respectively, P<0.005 vs. UA for both), or control patients (189+/-43 and 601+/-126 ng/ml, respectively, P=0.001 vs. UA for both). CONCLUSIONS Plasma levels of soluble selectins were increased in patients with UA compared with patients with SA or patients without angiographically visible coronary artery disease. Measurements of these adhesion molecules may be helpful as non-invasive markers of coronary plaque destabilization in UA.

Acute Anterior Myocardial Infarction Following a Mild Nonpenetrating Chest Trauma A Case Report

Myocardial infarction in patients under age 45 years is a relatively unusual phenomenon; blunt chest trauma is one of the nonatherosclerotic mechanisms leading to acute myocardial infarc tion in young adults. The authors report a rare case of anterior myocardial infarction in a 22-year- old man following a mild nonpenetrating chest trauma whose left chest was elbowed during a soccer game.

Left Ventricular Long-Axis Function Is Reduced in Patients with Rheumatic Mitral Stenosis

Left ventricular long‐axis function evaluated by M‐mode or tissue Doppler echocardiography has been shown to be useful indexes of left ventricular systolic function; however it has not been evaluated in patients with mitral stenosis. We examined the left ventricular long‐axis function of the patients with pure mitral stenosis and normal global systolic function as assessed by fractional shortening of the left ventricle (LV). Fifty‐two patients with pure mitral stenosis and twenty‐two healthy controls were evaluated by echocardiography. Although there was no statistically significant difference in global systolic function, M‐mode derived systolic motion of the septal side and (12 ± 3 vs 14.4 ± 1.5 mm, P = 0.016) the lateral side of mitral annulus (13.2 ± 3 vs 16.8 ± 2 mm, P = 0.001) were both significantly lower in the patients with mitral stenosis than control subjects. Similarly tissue Doppler systolic velocity of the septal annulus (7.6 ± 1.1 vs 10.4 ± 3.2 cm/s, P = 0.03) and lateral mitral annulus (7.6 ± 1.1 vs 10.4 ± 3.2 cm/s, P = 0.003) were also significantly lower in patients with mitral stenosis than in controls. There was a statistically significant correlation between septal annular motion and annular velocity (r = 0.643, P = 0.002). Septal annular motion and annular velocity were also correlated with left atrial ejection fraction (r = 0.338, P = 0.005 and r = 0.676, P = 0.001, respectively). Thus, patients with mitral stenosis had significantly impaired long‐axis function evaluated by M‐mode or tissue Doppler echocardiography despite normal global systolic function. (ECHOCARDIOGRAPHY, Volume 21, February 2004)

Assessment of Heart Rate Turbulence in the Acute Phase of Myocardial Infarction for Long-Term Prognosis

SADE, E., et al.: Assessment of Heart Rate Turbulence in the Acute Phase of Myocardial Infarction for Long‐Term Prognosis. This study is designed to assess the value of heart rate turbulence (HRT) in the acute phase of MI for prediction of long‐term mortality risk. The study included 128 consecutive acute MI patients with 24‐hour Holter recordings to evaluate HRT (turbulence onset and slope), SDNN, mean RR interval, and ventricular premature beat frequency. LVEF was evaluated by two‐dimensional echocardiography. Data from 117 patients (mean age 58 ± 11 years) were available for further analysis. Twelve patients died during follow‐up (mean 312 ± 78 days). Although SDNN < 70 ms was the most powerful predictor of mortality among all presumed risk factors (hazard ratio 20 [95% CI 2.6–158]; P = 0.004) in univariate Cox regression analysis, in multivariate analysis LVEF ≤ 0.40 and turbulence slope ≤2.5 ms/RR interval were the only independent predictors of mortality (hazard ratio 6.9 [95% CI 1.8–26]; P = 0.006, hazard ratio 7.3 [95% CI 1.4–37]; P = 0.016, respectively). Addition of HRT parameters for LVEF increased remarkably the positive predictive value (60%) without any decrease in the negative predictive value (92%). Blunted HRT reaction within the first 24 hours of acute MI is an independent predictor of long‐term mortality. Furthermore, its predictive power is comparable and also additive to that of LVEF. (PACE 2003; 26[Pt. I]:544–550)