Background: QT dispersion has been proposed to be a predictor of adverse outcomes in a variety of cardiac disease states. The objective of this study was to examine QT dispersion in patients with sickle cell disease (SCD) and to assess the effect of pulmonary hypertension (PHT) on QT dispersion. Methods: We performed Doppler echocardiographic assessments of pulmonary artery systolic pressure in 73 (mean age 18.5 ± 8.0 years) steady-state SCD patients and 25 (mean age 19.6 ± 7.2 years) healthy subjects. Resting 12-lead electrocardiogram was recorded and QT dispersion was calculated as the difference between maximum and minimum QT intervals. Bazett’s formula was used to obtain a rate-corrected value of the QT interval (QTc). Results: Maximum QTc, minimum QTc and QTc dispersion were significantly increased in SCD patients compared to the control subjects (p < 0.0001, p < 0.05, p < 0.0001, respectively). Among SCD patients, patients with PHT had higher maximum QTc and QTc dispersion than patients without PHT (p < 0.0001). However, minimum QTc showed no significant differences between the two patient groups. Conclusion: QTc dispersion is significantly increased in SCD patients, especially those with PHT indicating regional inhomogeneity of ventricular repolarization.
Aim: The primary percutaneous procedure resulted in a significant improvement in the prognosis of myocardial infarction. However, no-reflow phenomenon restrains this benefit of the process. There are studies suggesting that soluble suppression of tumorigenicity (sST2) can be valuable in the diagnosis and progression of heart failure and myocardial infarction. In this study, we aimed to investigate the effect of sST2 on no-reflow phenomenon in ST-elevated myocardial infarction (STEMI).Method: This study included 379 patients (258 men; mean age, 60 ± 11 years) who underwent primary percutaneous treatment for STEMI. sST2 levels were measured from blood samples taken at admission. Patients were divided into two groups according to Thrombolysis in Myocardial Infarction(TIMI) flow grade: group 1 consists of TIMI 0,1,2, accepted as no-reflow, and group 2 consists of TIMI 3, accepted as reflow.Results: No-reflow phenomenon occurred in 60 patients (15.8%). The sST2 level was higher in the no-reflow group (14.2 ± 4.6 vs. 11.3 ± 5.0, p = 0.003). Moreover, regression analysis indicated that diabetes mellitus, lower systolic blood pressure, multivessel vascular disease, high plaque burden, and grade 0 initial TIMI flow rate were other independent predictors of the no-reflow phenomenon in our study. Besides, when the patients were divided into high and low sST2 groups according to the cut-off value from the Receiver operating characteristics analysis, being in the high sST2 group was associated with 2.7 times increased odds for no-reflow than being in the low sST2 group.Conclusion: sST2 is one of the independent predictors of the no-reflow phenomenon in STEMI patients undergoing primary percutaneous coronary intervention.
P wave dispersion (PWD) is a sign for the prediction of atrial fibrillation (AF). The aim of this study was to assess P wave dispersion and its relation with clinical and echocardiographic parameters in patients with rheumatoid arthritis (RA). Thirty RA patients (mean age 49 +/- 10 years) and 27 healthy controls (mean age 47 +/- 8 years) were included in the study. We performed electrocardiography and Doppler echocardiography on patients and controls. Maximum and minimum P wave duration were obtained from electrocardiographic measurements. PWD defined as the difference between maximum and minimum P wave duration was also calculated. Maximum P wave duration and PWD was higher in RA patients than controls (P = 0.031 and P = 0.001, respectively). However, there was no significant difference in minimum P wave duration between the two groups (P = 0.152). There was significant correlation between PWD and disease duration (r = 0.375, P = 0.009) and isovolumetric relaxation time (r = 0.390, P = 0.006). P wave duration and PWD was found to be higher in RA patients than healthy control subjects. PWD is closely associated with disease duration and left ventricular (LV) diastolic dysfunction.
Fifty-one patients (mean age 51.6 +/- 7.1 years) with angiographically proven coronary artery disease (CAD) entered the study. In 26 patients (Group I), trimetazidine treatment started twenty-four hours after percutaneous transluminal coronary angioplasty (PTCA). Another 25 patients (Group II) without trimetazidine treatment were kept as controls. The groups were comparable by age, gender, risk factors of CAD, coronary anatomy, left ventricular performance, and heart rate variability indices at baseline state. Power spectral analysis of heart rate variability and two-dimensional and Doppler echocardiographic examinations were performed before PTCA, and twenty-four hours, ten days, thirty days, and three months after PTCA. A statistically significant improvement of left ventricular systolic performance (P < 0.001), augmentation of the parasympathetic band of heart rate variability (P < 0.001), and decline of P1/P2 ratio (P < 0.01) were evident in patients treated with trimetazidine, while no apparent changes were observed in controls. The intergroup analysis also showed marked difference between groups as recorded on the day 30 and month 3 of observation (P < 0.001). During follow-up period recurrences of angina pectoris and ischemia were registered in Group II, while no evidence of ischemia was discerned in Group I patients. In conclusion, trimetazidine modulates the autonomic control of heart rate, ie, reduces sympathetic overactivity and augments vagal influences, improves left ventricular contractility, and diminishes the clinical manifestations of ischemia in patients with CAD after PTCA.
SUMMARYA total of 168 consecutive patients with predominant rheumatic mitral stenosis were evaluated by transthoracic (TTE) and transesophageal echocardiography (TEE). Of the 168 patients, 35 had previous embolic events (group I) and 133 had no emboli (group II). A total of 77 (45.8%) patients had atrial fibrillation. The frequency of atrial fibrillation was higher in group I than group II (68.6% vs 39.8%, p<0.001). The incidence of left atrial enlargement was greater in group I (p<0.001). Mitral valve area was found to be smaller in group I compared to group II (p<0.001). In group I 83.3% and 29.2% of the patients with atrial fibrillation had left atrial spontaneous echo contrast (SEC) and left atrial thrombus, respectively, and 72.7% of the patients with sinus rhythm had left atrial SEC. In group II 79.2% and 20.8% of the patients with atrial fibrillation had left atrial SEC and left atrial thrombus whereas 28.6% and 2.6% of the patients with sinus rhythm had left atrial SEC and left atrial thrombus, respectively. The incidence of left atrial thrombus was significantly different in those patients with compared to those without embolic events (20% vs 9.7%, p<0.01). In groups I and II, 28 of 35 (80%) and 64 of 133 (48.1%) patients had left atrial SEC (p<0.01). Patients with left atrial SEC had a greater left atrial size (p<0.01) and smaller mitral valve area (p<0.01). Left atrial size was normal in 2 patients with left atrial SEC and SEC was not found in 55 patients with enlarged left atrium. Multiple logistic regression analysis showed that atrial fibrillation, mitral valve area and left atrial enlargement were independent predictors of the SEC (p<0.001) and left atrial SEC was the principal determinant of thromboembolism.These data suggest that regardless of rhythm and atrial size, left atrial SEC is a principal determinant of thromboembolic risk in mitral stenosis. TEE may be able to detect those patients with mitral stenosis at risk for emboli and guide appropriate therapy. (Jpn Heart J 1997; 38: 669-675)
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