C Gruppi

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.

Ablação com radiofreqüência de extra-sístoles da via de saída do ventrículo direito

OBJECTIVES: To evaluate if radiofrequency catheter ablation is an effective procedure for the treatment of right ventricular outflow tract premature ventricular contractions (RVOT-PVC) and ascertain if it results in an improvement of symptoms. METHODS: A prospective study with 30 consecutive patients (mean age 40 ± 13 years, 25 females), with no apparent structural cardiopathy, with very frequent (mean density of 1,263 ± 593/h) RVOT-PVC, symptomatic for more than one year (mean = 74 months) and resistant to antiarrhythmic drugs (3 ± 1.7, including beta-blockers), who underwent radiofrequency catheter ablation. RESULTS: After the first procedure, there were 23 initial successful cases (76.6%) and 7 initial failures (23.4%). Four patients experienced relapses, two of whom did not undergo the second procedure. The second procedure was carried out in 9 patients (7 initial failures and 2 relapses), and there was success in 5 additional patients, one of them by epicardial access. The final success rate was 80% (24/30), and there were no major complications. After a mean follow-up of 14 ± 6 months, in the successful group there was a reduction greater than 90% in density of premature ventricular contractions (PVC) (24/24; p<0.0001) and a resulting absence of symptoms in the majority of patients (23/24; p<0.001). CONCLUSION: Radiofrequency catheter ablation is a safe and effective treatment for patients with persistent and symptomatic PVC with RVOT morphology.

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.

Left ventricular hypertrophy predicts outcome of hypertension regardless of the type of ventricular arrhythmia present

Left ventricular hypertrophy is associated with an increased cardiovascular mortality in hypertension. A potential role of ventricular arrhythmias is debated but not yet determined. The purpose of this study was to evaluate whether the presence of arrhythmias would ascribe any additional risk to cardiovascular mortality beyond that related to the presence of left ventricular hypertrophy. From November 1988 to February 1991, 40 mild to severe hypertensive patients (mean SBP, DBP 183/117 mm Hg) were submitted to clinical, echocardiographic and electrocardiographic evaluations complemented by 24-h Holter monitoring and then followed until November 1996. The Kaplan–Meier method supplemented by the Cox multiple regression model were performed to identify the variable(s) associated with fatal cardiovascular outcome. Twelve cardiovascular fatalities occurred as a consequence of sudden death (n = 4), stroke (n = 4), heart failure (n = 2) and myocardial infarction (n = 2). In comparison with patients who survived, those dying from cardiovascular causes had a greater percentage of electrocardiographic left ventricular hypertrophy (83 vs 36%, P = 0.0037) and couplets of ventricular ectopic beats (58 vs 18%, P = 0.0467). In addition, they showed larger left ventricular diastolic diameter (60 ± 10 vs 53 ± 8 mm), mass index (248 ± 67 vs 154 ± 57 g/m2) and posterior wall thickness (12 ± 2 vs 10 ± 2 mm), as well as shorter left ventricular fractional shortening (0.23 ± 0.8 vs0.32 ± 0.9). Univariate analysis showed that electrocardiographic left ventricular hypertrophy and strain, mass index, end-systolic wall stress, fractional shortening and the presence of couplets were significantly related to cardiovascular mortality. However, only mass index was shown to be independently associated with cardiovascular death. In conclusion, left ventricular hypertrophy predicts cardiovascular outcome, regardless of the presence of other signs of cardiac damage, including ventricular arrhythmia.

Effects of chlorthalidone and diltiazem on myocardial ischemia in elderly patients with hypertension and coronary artery disease

OBJECTIVE Antihypertensive therapy with thiazides decreases coronary events in elderly patients. However, the influence of diuretics on myocardial ischemia has not been fully investigated. The aim of this study was to compare the effect of chlorthalidone and diltiazem on myocardial ischemia. METHODS Following a randomized, double-blind, crossover protocol, we studied 15 elderly hypertensive patients aged 73.6+/-4.6 years with myocardial ischemia. All patients had angiographically documented coronary artery disease. We measured patients using 48- hour ambulatory electrocardiogram monitoring and exercise testing. After a 2-week period using placebo, patients received chlorthalidone or diltiazem for 4 weeks. RESULTS Both treatments lowered systolic and diastolic blood pressures. The number of ischemic episodes on ambulatory electrocardiogram recordings was reduced with the use of chlorthalidone (2.5+/-3.8) and diltiazem (3.2+/-4.2) when compared with placebo (7.9+/-8.8; p<0.05). The total duration of ischemic episodes was reduced in both treatments when compared with placebo (chlorthalidone: 19.2+/-31.9min; diltiazem: 19.3+/-29.6min; placebo: 46.1+/-55.3min; p<0.05). CONCLUSION In elderly hypertensive patients with coronary artery disease, chlorthalidone reduced myocardial ischemia similarly to diltiazem. This result is consistent with epidemiological studies and suggests that reduction of arterial blood pressure with thiazide therapy plays an important role in decreasing myocardial ischemia.

Isquemia silenciosa na doença coronariana estável em vigência de tratamento medicamentoso

BACKGROUND Few data are available on the behavior of myocardial ischemia during daily activities in patients with coronary artery disease receiving antianginal drug therapy. OBJECTIVE To study the mechanism generating myocardial ischemia by evaluating blood pressure and heart rate changes in patients with stable atherosclerotic disease receiving drug therapy and with evidence of myocardial ischemia. METHODS Fifty non-hospitalized patients (40 males) underwent 24-hour electrocardiographic monitoring synchronized with blood pressured monitoring. RESULTS Thirty five episodes of myocardial ischemia were detected in 17 patients, with a total duration of 146.3 minutes; angina was reported in five cases. Twenty nine episodes (100.3 minutes) occurred during wakefulness, with 11 episodes (35.3 + 3.7 min) in the period from 11 a.m. to 3 p.m. Blood pressure and heart rate evaluation in the three ten-minute intervals following the ischemic episodes showed a statistically significant difference (p< 0.05), unlike that shown for the three intervals preceding the episodes. However, during the ischemic episode, a higher than 10-mmHg elevation in blood pressure and 5 beats per minute in heart rate were observed when compared with the time interval between 20 and 10 minutes before the episode. The mean heart rate at the onset of ischemia during the exercise test performed before the study was 118.2 + 14.0, and 81.1 + 20.8 beats per minute on the 24-hour electrocardiogram (p < 0.001). CONCLUSION The incidence of silent myocardial ischemia is high in stable coronary artery disease and is related to alterations in blood pressure and heart rate, with different thresholds for ischemia for the same patient.