Effect of balloon-induced acute ischaemia on P wave dispersion during percutaneous transluminal coronary angioplasty.

AIMS: P wave dispersion is a recent ECG marker that reflects discontinuous and inhomogeneous conduction of sinus impulses, which has been studied in a limited number of cardiac conditions. The aim of our study was to investigate the effects of angioplasty induced-ischaemia on atrial conduction abnormalities as estimated by P maximum and P dispersion. METHODS AND RESULTS: The study consisted of 67 consecutive patients (41 men, mean age 58 +/- 11 years) with 1-vessel coronary artery disease who underwent elective single vessel coronary angioplasty (left anterior descending (LAD) coronary artery in 28 patients, the right coronary artery (RCA) in 22 patients and the left circumflex coronary artery (LCx) in 17 patients. All patients underwent 12-lead surface ECG before the first inflation (baseline) and then 60 s after intra-coronary balloon inflation. The maximum P wave duration, the minimum P wave duration, and P wave dispersion (Pd=Pmax - Pmin) were calculated from 12-lead surface ECGs. Baseline P wave duration measurements were not significantly different among the patients with LAD, RCA and LCx coronary artery disease (P>0.05). P dispersion and P maximum were significantly higher during balloon occlusion compared with the baseline condition in all three types of coronary dilatation procedures. However, P minimum was not found to differ between baseline and during balloon occlusion (P>0.05). CONCLUSION: The prolongation of P wave dispersion may be a useful and simple additional marker for myocardial ischaemia.

What is the optimal evaluation time of the QT dispersion after acute myocardial infarction for the risk stratification?

The sequential changes of the corrected QT dispersion (QTcD) were studied in 136 patients 1 day to 30 days after a transmural acute myocardial infarction (AMI) to investigate the optimal measurement time of QT dispersion for risk stratification. The study group included 136 patients (89 men; mean age, 57+/-10 years) with transmural AMI who were treated with thrombolytics (Tr+ group, n = 73) or not (Tr- group, n = 63) and 65 healthy controls (43 men; mean age, 56+/-7 years). Fourteen patients in whom ventricular tachycardia (VT), ventricular fibrillation (VF), or sudden cardiac death developed during the 30-day period were also evaluated as major cardiac arrhythmia (MCA) group. ECGs were obtained for each patient on days 1, 3, 5, 10, 15, and 30 after AMI. QTc dispersion in patients with AMI (for every period of QTcD after MI) was significantly more prolonged than in normal controls (49.3+/-16.3 ms) (p<0.001). QTcD was significantly greater in patients without thrombolytics than in patients with thrombolytics for every period (days 1, 3, 5, 10, 15, and 30) of QTcD after MI (p<0.001). The mean of QTcD was significantly greater in patients with MCA than in patients without MCA group for every period (days 1, 3, 5, 10, 15, and 30) of QTcD after MI (p < 0.05). Maximal QTcD was seen on day 10 (p < 0.05 1st vs day 10 for each group) after myocardial infarction, and then reached a plateau for an each group. The ideal time to measure the QTD for risk stratification is at least 10 days after AMI.

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 infarction 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.

Is ventricular repolarization heterogeneity a cause of serious ventricular tachyarrhythmias in aortic valve stenosis?

BACKGROUND: It is well known that there is a close relation between sudden cardiac death and serious ventricular tachyarrhythmias in patients with aortic valve stenosis (AS). QT dispersion (QTd) reflects the ventricular repolarization heterogeneity and has been proposed as an indicator for ventricular arrhythmias. HYPOTHESIS: This study investigated the QTd and its relevance to the clinical and echocardiographic variables. METHODS: In all, 51 patients (33 men, 18 women, mean age 56 +/- 12) with isolated AS and 51 age- and gender-matched healthy controls comprised the study group. Left ventricular mass index (LVMI) was calculated by the Devereux formula, and we used continuous-wave Doppler (n = 15) and cardiac catheterization (n = 36) for the determination of the maximum aortic valve pressure gradient (PG). RESULTS: Corrected QTd (QTcd) (89 +/- 39 vs. 49 +/- 15 ms, p < 0.001) and LVMI (176 +/- 69 g/m2 vs. 101 +/- 28 g/m2, p < 0.001) in patients with AS were significantly different from those in the control group. The group of 21 patients had a significantly greater number of 24-h mean ventricular premature beats (VPB) and mean number of couplet VT episodes than did the control group (p < 0.05). QTcd also correlated significantly well with LVMI (r = 0.58, p < 0.001), PG (r = 0.41, p = 0.003), and number of 24-h VPB (r = 0.56, p = 0.008). With respect to symptoms (e.g., angina, syncope, and dyspnea) patients without symptoms (n = 19) displayed less QTcd (71 +/- 31 vs. 100 +/- 39 ms, p = 0.007) and less LVMI (144 +/- 80 g/m2 vs. 195 +/- 57 g/m2, p = 0.01) than patients with symptoms. Statistical analysis was similar for all variables with uncorrected QTd values. CONCLUSION: We found that ventricular repolarization heterogeneity was greater in patients with AS than in controls. Our findings also showed that QTd in the patient group correlates well with LVMI, severity of AS, and PG. The present results suggest that serious ventricular arrhythmias in patients with AS may be due to spatial ventricular repolarization abnormality.

Thrombosis involving the major veins with heterozygote factor V Leiden mutation as the only risk factor.

A 27-year-old man was admitted to our hospital with the complaints of swelling of his face and lower limbs. Echocardiography showed minimal pericardial effusion accompanied by disordered diastolic function. Cardiac catheterization was performed to rule out constrictive pericarditis. Normal pressure tracings of the right heart rule out constrictive pericarditis, however, a narrowing of the inferior vena cava was observed. Venographies of the inferior and superior vena cavae showed extensive thrombotic involvement of these great veins. Protein C, protein S, anticardiolipin antibodies, fibrinogen, antithrombin-III, activated protein C resistance, and factor V levels were in normal limits. Heterozygosity for factor V Leiden mutation was detected. We conclude that factor V Leiden mutation can cause extensive thrombotic involvement of major veins and should be considered in idiopathic thrombosis of them.