Fragmented QRS is predictive of myocardial dysfunction, pulmonary hypertension and severity in mitral stenosis.

Reliable non-invasive new indices reflecting severity of rheumatic valve disease would be highly beneficial. Recently, presence of fragmented QRS (fQRS) in ECG was accepted as a marker of myocardial fibrosis. fQRS is defined as the presence of RSR' patterns such as additional R wave (R'), notching in the R wave or the S wave in 2 contiguous leads. Purpose of our study was to establish frequency of fQRS in isolated rheumatic mitral stenosis compared with control group. We studied 193 patients with mitral stenosis and age/gender matched 97 healthy subjects. Patients were categorized according to the New York Heart Association (NYHA) functional class. Severity of mitral stenosis, left ventricular ejection fraction, and pulmonary artery pressure were obtained by means of echocardiography. fQRS was defined on routine 12-lead ECG. fQRS was more frequent in subjects with mitral stenosis than in control group (p < 0.001). fQRS was associated with low ejection fraction, pulmonary hypertension, poor functional NYHA class, increased mean mitral valve gradient and decreased mitral valve area (R = 0.1, p = 0.02; R = 0.1, p = 0.001; R = 0.1, p = 0.01; R = 0.1, p = 0.04; and R = -0.1, p = 0.009, respectively). Mitral valve area was the only independent predictor of fQRS in multiple logistic regression analysis. In conclusion, fQRS is predictive of severe mitral stenosis, lower ejection fraction, increased pulmonary artery pressure, and poor functional class. fQRS might be considered as a novel indicator of mitral stenosis severity and associated complications.

Acute sleep deprivation is associated with increased QT dispersion in healthy young adults.

BACKGROUND: Sleep deprivation (SD) is known to be associated with worse cardiovascular outcome including mortality. We investigated the association between acute SD and electrocardiographic maximum QT interval (QTmax), QT, and corrected QT dispersion (QTd/cQTd), which are known to be among predictors of ventricular arrhythmias and sudden death. METHODS: We obtained electrocardiograms of 37 healthy young volunteers (age: 28.45 +/- 7.97 years; 11 women) after a night with regular sleep and repeated after a night with sleep debt. We measured minimum QT interval (QTmin), QTmax, QTd, and cQTd in milliseconds. RESULTS: Average sleep time of the subjects were 7.7 +/- 0.8 hours during regular sleep and 1.7 +/- 1.6 hours during a night with sleep debt (P < 0.001). Subjects had similar values of QTmin in milliseconds after a night of sleep debt when compared to after regular sleep (347.56 +/- 29.75 vs 344.59 +/- 20.89; P = 0.51), whereas they had significantly higher values of QTmax, QTd, and cQTd (396.48 +/- 30.11 vs 378.10 +/- 23.90; P = 0.001, 49.45 +/- 9.11 vs 33.51 +/- 10.05; P < 0.001 and 54.92 +/- 10.42 vs 37.23 +/- 10.81; P < 0.001, respectively). In Pearson's correlation analysis, QTmax, QTd, and cQTd were inversely correlated with sleep time (P = 0.012, r =-0.291; P < 0.001, r =-0.625 and P < 0.001, r =-0.616, respectively) CONCLUSIONS: In conclusion, we clearly demonstrated that even one night of SD is associated with significant increase in QTmax, QTd, and cQTd in healthy young adults despite remaining within normal limits. These electrocardiographic changes in acute SD might contribute to development and/or recurrence of arrhythmias. This implication deserves further studies for clarifying the possible linkage between SD and arrhythmias.

Acute sleep deprivation is associated with increased electrocardiographic P-wave dispersion in healthy young men and women.

BACKGROUND: Sleep deprivation (SD) is associated with worse cardiovascular outcome including mortality. Prolonged P-wave duration and P-wave dispersion (Pd) are known to represent inhomogeneous conduction of sinus impulses and are known to be electrophysiologic predictors of atrial fibrillation. Pd in normal subjects has been reported to be influenced by the autonomic tone. Because autonomic tone is affected by sleep and sleep duration, we evaluated the effect of acute SD on P-wave duration and Pd in healthy young adults and whether the effect was gender selective. METHODS: We obtained electrocardiograms of 37 healthy young volunteers (age: 28.45 +/- 7.97; 11 women) after a night of regular sleep and repeated after a night with sleep debt. We measured minimum and maximum P-wave durations (Pmin, Pmax) and Pd in milliseconds. RESULTS: Average sleep time of the subjects were 7.7 +/- 0.8 hours during regular sleep and 1.7 +/- 1.6 hours during a night of sleep debt (P < 0.001). Subjects had significantly lower values of Pmin in milliseconds after a night of sleep debt when compared to regular sleep (65.13 +/- 8.03 vs 74.86 +/- 10.95; P < 0.001), whereas they had significantly higher values of Pmax and Pd (102.16 +/- 9.46 vs 95.13 +/- 11.21; P < 0.001 and 37.02 +/- 8.11 vs 20.27 +/- 11.42; P < 0.001, respectively). In Pearson's correlation analysis Pmin was positively and Pmax and Pd were negatively correlated with sleep time (P < 0.001, r = 0.465; P = 0.003, r =-0.336 and P < 0.001, r =-0.698 respectively). Effect of SD on P-wave duration and Pd was similar for both men and women. CONCLUSIONS: In conclusion, prolongation of Pmax and Pd in acute SD suggests that acute SD might contribute to development and/or recurrence of atrial fibrillation.