Arrhythmia profile in acromegaly.

In a controlled study, the cardiac involvement and arrhythmia profile of 32 patients with acromegaly were correlated with endocrine parameters (somatomedine C, growth hormone), clinical score and duration of the disease. Data were compared with those of 50 controls free of cardiac disease. Stress ECG, 24 h Holter monitoring and echocardiography were performed. Supraventricular premature complexes occurred no more often in acromegalics than in controls. Both prevalence and severity of ventricular arrhythmia, however, were significantly higher in patients compared to controls (P less than 0.01). 15/32 (48%) acromegalic patients had complex ventricular arrhythmias (Lown III-IV) as compared with 6/50 (12%) normal subjects (P less than 0.01). Repetitive ventricular arrhythmias (Lown IV a/b) occurred in 10/32 (31%) patients, but only in 4/50 (8%) controls (P less than 0.01). Furthermore, the frequency of ventricular premature complexes increased with duration of acromegaly (P less than 0.01). No correlation was found between the severity of ventricular arrhythmia and hormone levels. Left ventricular muscle mass was significantly increased (285 +/- 139 g, P less than 0.02) due to concentric hypertrophy. Severity of ventricular arrhythmias correlated with left ventricular mass and with clinical activity score (P less than 0.01). Thus, compared to controls, acromegalic patients show more frequent and complex ventricular arrhythmias and left ventricular hypertrophy. Duration of the disease rather than hormone levels seems to be relevant for these pathological changes.

Sudden cardiac death while wearing a Holter monitor.

The Holter tapes of 61 patients (46 men, mean age +/- standard deviation 65 +/- 11 years) with sudden cardiac death while being monitored were analyzed. Thirty-eight patients were known to have coronary artery disease, 5 had cardiomyopathy, and 7 had aortic valve disease. Etiology remained unknown in 11 patients. Mean New York Heart Association functional class was 2.5 +/- 0.7. Thirty patients had received antiarrhythmic drugs and 32 had received digitalis. Sudden death occurred at rest in 73%. In the hours before death, repetitive ventricular arrhythmias were found in 50 patients (82%), with atrial fibrillation in 34%. Patients with bradyarrhythmic death (18%) had less complex ventricular activity compared to patients with tachyarrhythmic death (p less than 0.01). Lethal arrhythmias--monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, torsades de pointes, primary ventricular fibrillation, and 1:1 conducting atrial tachycardia--were found in 26 (43%), 15 (25%), 5 (8%), 3 (5%), and 1 patient, respectively. The coupling interval of the final ventricular tachycardia correlated inversely with the initial frequency of ventricular tachycardia (p less than 0.05). For patients with tachyarrhythmic death, an increase of heart rate within the last 3 hours was noted (83 vs 89 beats/min, p less than 0.05). Ventricular premature complexes and the proportion of patients with greater than 2 couplets and greater than 2 triplets increased significantly only within the last hour before death.(ABSTRACT TRUNCATED AT 250 WORDS)

Combination of calcium channel blocker and thrombolytic therapy in acute myocardial infarction.

To evaluate the protective effect of nifedipine on ischemic myocardium, in addition to thrombolytic therapy, a total of 149 patients with acute myocardial infarction were included in a double-blind controlled study in which they received 20 mg sublingual nifedipine (74 patients in group 1) or placebo (75 patients in group 2) in the emergency ward, either intracoronary nifedipine, 0.2 mg before and 0.2 mg after reperfusion of the infarct-related vessel and 20 mg three times/day during the hospital stay, or placebo. Combined intravenous and intracoronary thrombolytic therapy was initiated by means of mechanical recanalization in nonreperfused vessels. There were no differences between group 1 and 2 with regard to age, sex, body weight, or location of infarct. Evolution of CK-MB release and cumulative CK-MB was higher in group 1 than in group 2. Changes with regard to regional and global left ventricular function and coronary anatomy were not significantly different (NS) between the two groups. Reocclusion occurred in 15 of 74 (20%) and 10 of 75 (13%) patients in groups 1 and 2, respectively. During the reperfusion period, second- and third-degree atrioventricular block occurred in 5.4% and 6.7% (NS), ventricular couplets in 17.6% and 24% (NS), ventricular tachycardia in 2.7% and 9.3%, and ventricular fibrillation in 2.7% and 8% of the patients, respectively. Mortality rates were 13% and 8%. The study demonstrates that even very early administration of nifedipine combined with intracoronary administration does not enhance the salvage of ischemic myocardium achieved by reperfusion.

Long-term prognostic significance of ventricular arrhythmias in idiopathic dilated cardiomyopathy.

The prognostic significance of ventricular arrhythmias in idiopathic dilated cardiomyopathy is controversial. Thus, 73 patients with idiopathic dilated cardiomyopathy who had both 24-hour Holter monitoring and angiography were followed for greater than or equal to 3 years. Twenty-eight patients (38%) died, 14 patients (19%) due to pump failure and 14 patients (19%) due to sudden death. Univariate analysis revealed ventricular tachycardias as a major risk indicator, among others. However, multivariate analysis determined the major independent risk factors in the following order: patients who died from pump failure, left ventricular filling pressure, left bundle branch block, the number of beats in the longest episode of ventricular tachycardia and left ventricular ejection fraction; patients who died from sudden death, left bundle branch block and left ventricular ejection fraction, but not any form of ventricular arrhythmias. Reclassification by means of the risk factors resulted in a meaningful identification of patients who died from pump failure; however, patients who died from sudden death could not be separated from survivors. Thus, in the present study Holter monitoring was unable to distinguish between patients who died from subsequent pump failure and patients who died from subsequent sudden death.