Effect of spironolactone on ventricular arrhythmias in congestive heart failure secondary to idiopathic dilated or to ischemic cardiomyopathy.

Epidemiologic studies have shown an important increase in the high mortality of patients with congestive heart failure (CHF) despite optimal medical management. Ventricular arrhythmia was recognized as the most common cause of death in this population. Electrolyte imbalance, myocardial fibrosis, left ventricular dysfunction, and inappropriate neurohumoral activation are presumed responsible for sudden cardiac death. In this study, we focused on the deleterious effects of the overproduction of aldosterone that occurs in patients with CHF. Secondary hyperaldersteronism can be part of several factors thought to be responsible for sudden cardiac death. We randomized 35 patients (32 men, aged 48 +/- 9 years) with systolic dysfunction (ejection fraction 33 +/- 5%) and New York Heart Association class III CHF secondary to dilated or ischemic cardiomyopathy into 2 groups. The treatment group received spironolactone, an aldosterone receptor antagonist, along with standard medical management using furosemide, angiotensin-converting enzyme inhibitors, and digoxin. The control group received only the standard medical treatment. Holter monitoring was used to assess the severity of ventricular arrhythmia. After 20 weeks, patients who received spironolactone had a reduced hourly frequency of ventricular premature complexes (VPCs) (65 +/- 18 VPCs/hour at week 0 and 17 +/- 9 VPCs/hour at week 16) and episodes of nonsustained ventricular tachycardia (VT) (3.0 +/- 0.8 episodes of VT/24-hour period at week 0, and 0.6 +/- 0.3 VT/24-hour period at week 16). During monitored treadmill exercise, a significant improvement in ventricular arrhythmia was found in the group receiving spironolactone (39 +/- 10 VPCs at week 0, and 6 +/- 2 VPCs at week 16). These findings suggest that aldosterone may contribute to the incidence of ventricular arrhythmia in patients with CHF, and spironolactone helps reduce this complication.

Blood pressure and the risk of complex arrhythmia in renal insufficiency, hemodialysis, and renal transplant patients.

Complex arrhythmia is frequent in hemodialysis patients but it is not clear if this is a consequence of dialysis or uremia or is secondary to the hemodynamic and cardiovascular alterations often associated with chronic renal failure. The incidence of complex ventricular arrhythmia (frequent multiform premature beats, couplets, and runs) in 31 subjects who had their uremic status recently corrected by renal transplant (Group 1) and in 23 predialysis (Group 2) and 73 hemodialysis (Group 3) chronic renal failure patients were studied with 24-h Holter monitoring. Patients were not receiving antiarrhythmic drugs or digitalis and significant coronary artery disease was excluded by clinical and noninvasive methods. Complex arrhythmia was two times more frequent in dialysis patients but the difference did not reach statistical significance (Group 1: 16%; Group 2: 17%; Group 3: 34%; chi2 4.9, P = .086). The stepwise model of logistic regression analysis identified systolic blood pressure (odds ratio 1.015, 95% confidence interval [CI] 1.001-1.027, P = .03) and left ventricular systolic dysfunction (odds ratio 7.04, 95% CI 1.3-36.7, P = .02) as the only factors that independently influenced the probability of complex arrhythmia. Age, gender, race, diabetes, smoking status, body mass index, diastolic blood pressure, serum creatinine, hematocrit, left ventricular mass index, and use of diuretics, beta-blockers, angiotensin converting enzyme (ACE) inhibitors, sympatolytics, and calcium channel blockers did not influence the occurrence of complex arrhythmia. The data indicate that blood pressure and myocardial dysfunction are more important determinants of complex arrhythmia than dialysis or uremia in chronic renal disease patients.

Prognostic significance of silent myocardial ischemia after a first uncomplicated myocardial infarction.

Forty asymptomatic patients were studied after a first uncomplicated myocardial infarction. They were 36 men and 4 women, with a mean age of 52.6 yr; the location of myocardial infarction was in the anterior wall in 18 (45%) patients and in the inferior wall in 22 (55%). The patients were submitted to: (1) 48-h Holter monitoring, during the 2nd and 8th weeks after the acute event; (2) exercise testing during the same periods; (3) cardiac catheterization and coronary arteriography. Patients with clinical conditions associated with cardiac rhythm disturbances or repolarization abnormalities were excluded. The electrocardiographic methods identified 11 (27.5%) patients with silent myocardial ischemia. Patients with and without silent ischemia were similar in relation to sex, age, coronary risk factors, arrhythmias, left ventricular function and follow-up. Patients with silent ischemia had more inferior wall myocardial infarctions, but the difference was not statistically significant. Patients with silent ischemia had significantly more extensive coronary artery disease (45.5% multivessel disease) when compared to those without ischemia (14.8% multivessel disease) (p < 0.05). After a 2-yr follow-up, 4 (36.4%) patients with and 1 (3.4%) without silent ischemia had a coronary event (p < 0.05). Kaplan-Meier analysis demonstrated a significantly higher cumulative probability of not experiencing a new coronary event for the patients without silent ischemia (96.5%) as compared to those with silent ischemia (62.3%) (p < 0.01). Our results suggest that silent myocardial ischemia after a first uncomplicated myocardial infarction carries an adverse prognosis and should be routinely investigated.

[Variability of the heart rate and silent ischemia after myocardial infarction]. / Variabilidade da freqüência cardíaca e isquemia silenciosa após infarto do miocárdio.

PURPOSE: To show a possible relation between heart rate and silent myocardial ischemia. METHODS: Forty-nine ischemic episodes were registered in six patients during a total period of 576-hour Holter monitoring. Those patients were selected from a group of 40 asymptomatic individuals after a first uncomplicated myocardial infarction; 11 (27.5%) showed ischemia during daily activities or exercise, the six selected patients had myocardial ischemia on Holter monitoring. RESULTS: The silent episodes consisted 92% of the total ischemic burden; they lasted from 1 min 30 s to 20 min and the ST-segment depression varied from -1.1 mm to 3.3 mm. Thirty-five (72%) episodes occurred at rest or during light physical activities; nine (18.5%) occurred between 7:00 AM and 12:00 PM; eight (16.5%), between 12:00 PM and 6:00 PM; 17 (35%) between 6:00 PM and 12:00 AM and 15 (30%), between 12:00 AM and 7:00 AM. There was no significant change (more than 20%) in heart rate at the onset of ischemic episodes in relation to the heart rate 1 minute before (94.63 +/- 9.79 bpm and 99.47 +/- 10.99 bpm, respectively). Complex ventricular arrhythmias occurred in all patients and only one of them had an episode of nonsustained ventricular tachycardia related to silent ischemia. CONCLUSION: Our results suggest that there is no relation between heart rate, arrhythmias and silent ischemia.