Mode of onset of torsade de pointes in congenital long QT syndrome.

OBJECTIVES: We sought to describe the mode of onset of spontaneous torsade de pointes in the congenital long QT syndrome. BACKGROUND: Contemporary classifications of the long QT syndrome (LQTS) refer to the congenital LQTS as "adrenergic dependent" and to the acquired LQTS as "pause dependent." Overlap between these two categories has been recognized, and a subgroup of patients with "idiopathic pause-dependent torsade" has been described. However, it is not known how commonly torsade is preceded by pauses in the congenital LQTS. METHODS: We reviewed the electrocardiograms (ECGs) of all our patients with congenital LQTS evaluated for syncope or sudden death (30 patients). Documentation of the onset of torsade de pointes was available for 15 patients. All these patients had "definitive LQTS" by accepted clinical and ECG criteria. RESULTS: Pause-dependent torsade de pointes was clearly documented in 14 of the 15 patients (95% confidence interval 68% to 100%). The cycle length of the pause leading to torsade was 1.3 +/- 0.2 times longer than the basic cycle length, and most pauses leading to torsade were unequivocally longer than the preceding basic cycle length (80% of pauses were > 80 ms longer than the preceding cycle length). CONCLUSIONS: The "long-short" sequence, which has been recognized as a hallmark of torsade de pointes in the acquired LQTS, plays a major role in the genesis of torsade in the congenital LQTS as well. Our findings have important therapeutic implications regarding the use of pacemakers for prevention of torsade in the congenital LQTS.

Postextrasystolic U wave augmentation, a new marker of increased arrhythmic risk in patients without the long QT syndrome.

OBJECTIVES: We attempted to determine the correlation between the presence of postextrasystolic changes in the STU segment and a history of sustained ventricular arrhythmias. BACKGROUND: Postextrasystolic U wave augmentation (a marked increment in U wave amplitude after premature ventricular complexes [PVCs]) is an adverse prognostic sign in the "pause-dependent long QT syndrome." However, the prevalence of postextrasystolic changes in patients without the long QT syndrome is unknown. METHODS: We compared the configuration of the STU segment of the postextrasystolic beat (the sinus beat after a PVC) with the STU configuration during sinus rhythm in three patient groups: 1) 41 patients with spontaneous ventricular tachycardia/fibrillation (VT/VF) (VT/VF group), 2) 63 patients with heart disease and high grade ventricular arrhythmias (control group), and 3) 29 patients with high grade ventricular arrhythmias but no heart disease (reference group). RESULTS: Postextrasystolic T wave changes did not correlate with a history of ventricular tachyarrhythmias. However, postextrasystolic U wave changes were more common among the patients with VT/VF than among control subjects (39% vs. 8.7%, p < 0.001). By logistic multiple regression analysis, a low left ventricular ejection fraction (p < 0.001) and postextrasystolic U wave changes (p < 0.005) were independent predictors of ventricular tachyarrhythmias. CONCLUSIONS: Postextrasystolic T wave changes are common and lack predictive value. Postextrasystolic U wave changes may be a specific marker of a tendency to the development of spontaneous ventricular arrhythmias. Prospective studies should be performed to confirm this association.

Treatment with beta-adrenergic blocking agents after myocardial infarction: from randomized trials to clinical practice.

OBJECTIVES: Our aim was to determine the percent of patients with myocardial infarction who are treated with beta-adrenergic blocking agents in dosages proved to be effective in preventing death after a heart attack. BACKGROUND: In the prospective randomized trials showing that beta-blocker treatment improves survival rates after myocardial infarction, relatively high dosages of these agents were used. However, it is not known whether these dosages are used in current clinical practice. METHODS: In a retrospective analysis of clinical data from 606 consecutive survivors of myocardial infarction at four university hospitals in three countries, we assessed the number of infarct survivors receiving prospectively defined "effective dosages" of beta-blockers. We defined these dosages as those that demonstrated improved survival rates of infarct survivors who received active drug in large, prospective, double-blind, placebo-controlled trials. RESULTS: Only 58% of infarct survivors with no contraindications to beta-blockers received these drugs at the time of hospital discharge, and only 11% received dosages equivalent to > 50% of the effective dosages. Independent predictors of failure to prescribe beta-blockers to infarct survivors without contraindications to these drugs were the use of diuretic agents, transient heart failure, impaired left ventricular function and increased patient age. Among patients receiving beta-blockers, only the use of propranolol predicted prescription of a low beta-blocker dosage. CONCLUSIONS: Failure to prescribe beta-blockers after myocardial infarction is common but in most cases is not due to clear contraindications. Many patients not receiving beta-blockers belong to subgroups that would derive the greatest benefit from such treatment. Finally, even when beta-blockers are prescribed, the dosages used are considerably lower than those proved to be effective in preventing death after myocardial infarction.

Circadian rhythm of acute pulmonary edema.

We found that the onset of acute pulmonary edema demonstrates circadian periodicity. Most episodes occur in the morning or at night. Pulmonary edema occurs more frequently during the colder months.

Delayed development of a pseudoaneurysm in the left circumflex artery following angioplasty and stent placement, treated with intravascular ultrasound-guided stenting.

Three months following satisfactory angioplasty and stent placement, a patient developed restenosis and a pseudoaneurysm of a coronary artery segment proximal to the previously stented area. The restenosis and the pseudoaneurysm were successfully treated with intravascular ultrasound-guided primary stenting. The delay in the appearance of the pseudoaneurysm attests to the chronic nature of the lesion.