Increased right ventricular wall thickness in left ventricular pressure overload: echocardiographic determination of hypertrophic response of the "nonstressed" ventricle.

Left ventricular hypertrophy in left ventricular pressure overload occurs in response to excessive work load imposed on the left ventricle by increased impedance to ejection. Right ventricular hypertrophy may occur in patients with these findings, but has been considered to be secondary to pulmonary hypertension. To determine the frequency of right ventricular hypertrophy and its relation to increased left ventricular wall thickness in patients with left ventricular pressure overload, right ventricular wall thickness was measured using M-mode echocardiography with two-dimensional echocardiographic guidance in 65 patients with left ventricular pressure overload; 49 patients had essential hypertension and 16 had aortic valve stenosis. These measurements were compared with data from 13 patients with "thin-walled" dilated cardiomyopathy and 20 normal subjects. Average right ventricular wall thickness in hypertensive patients (7 +/- 2 mm) and patients with aortic stenosis (6 +/- 2 mm) was significantly greater than that in normal subjects (4 +/- 1 mm) and patients with dilated cardiomyopathy (4 +/- 1 mm) who had normal left ventricular wall thickness, even though left ventricular mass was increased in all patient groups. Increased right ventricular wall thickness was present in 40 (80%) of 49 patients with hypertension and 10 (63%) of 16 patients with aortic stenosis. The magnitude of increase in right ventricular wall thickness was linearly correlated (r = 0.76, p less than 0.005) with left ventricular wall thickness, but was not associated with pulmonary hypertension. It is concluded that increased right ventricular wall thickness is common in patients with left ventricular pressure overload, is directly related to increases in left ventricular wall thickness, and is independent of right ventricular hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adverse acute and chronic effects of electrical defibrillation and cardioversion on implanted unipolar cardiac pacing systems.

Six cases are presented in which a transient or chronic rise in the stimulation threshold of a permanently implanted unipolar pacemaker resulted in the loss of effective pacing after therapeutic defibrillation or cardioversion. Although damage to the pulse generator may still occur, leading to a loss of function as demonstrated in a seventh patient, improvements in the internal protection circuits of the present generation of pacemakers makes this less likely while possibly predisposing to endocardial burns and increased fibrosis at the electrode-endocardial interface. The theoretical explanations for this phenomenon are discussed, along with recommendations for the prospective and retrospective management of the pacemaker patient who requires defibrillation or cardioversion.

Prevalence and significance of nonsustained ventricular tachycardia in patients with premature ventricular contractions and heart failure treated with vasodilator therapy. Department of Veterans Affairs CHF STAT Investigators.

OBJECTIVES: This study sought to determine the prevalence and significance of nonsustained ventricular tachycardia (NSVT) in patients with premature ventricular contractions (PVCs) and heart failure treated with vasodilator therapy. BACKGROUND: Heart failure patients with ventricular arrhythmia and NSVT have a significantly increased risk of premature cardiac death. Recently there has been the question of whether these arrhythmias are expressions of a severely compromised ventricle or are they independent risk factors. We, therefore, determined the prevalence and significance of NSVT in patients with PVCs and heart failure and on vasodilator therapy. METHODS: Twenty-four hour ambulatory recordings were done at randomization, at 2 weeks, at months 1, 3, 6, 9 and 12 and then every 6 months in 674 patients with heart failure and on vasodilator therapy. The median period of follow-up was 45 months (range 0 to 54). RESULTS: Nonsustained ventricular tachycardia was present in 80% of all patients. Patients without (group 1) and with (group 2) NSVT were balanced for variables: age, etiology of heart disease, New York Heart Association (NYHA) functional class, use of amiodarone and diuretics and left ventricular diameter by echocardiogram. However, group 1 patients had significantly less beta-adrenergic blocking agent use and higher ejection fraction (EF) (p < 0.002 and p < 0.001, respectively). Survival analysis for all deaths showed a greater risk of death among group 2 patients (p=0.01). Similarly, sudden death was increased in group 2 patients (p=0.02, risk ratio 1.8). After adjusting for the above variables, only EF (p=0.001) and NYHA class (p=0.01) were shown to be independent predictors of survival. Nonsustained ventricular tachycardia showed a trend (p=0.07) as an independent predictor for all-cause mortality but not for sudden death. Only EF was an independent predictor for sudden death. CONCLUSIONS: Nonsustained ventricular tachycardia is frequently seen in patients with heart failure and may be associated with worsened survival by univariate analysis. However, after adjusting other variables, especially for EF, NSVT was not an independent predictor of all-cause mortality or sudden death. These results have serious implications in that suppression of these arrhythmias may not improve survival.

High dispersion of ventricular repolarization after an implantable defibrillator shock predicts induction of ventricular fibrillation as well as unsuccessful defibrillation.

OBJECTIVES: To test the hypothesis that post-shock dispersion of repolarization (PSDR) is higher in T wave shocks that induce ventricular fibrillation (VF) than in those that do not, as well as in implantable cardioverter defibrillator (ICD) defibrillation shocks which fail to terminate VF when compared with those that are successful. BACKGROUND: Ventricular fibrillation has been linked to the presence of dispersion of repolarization, which facilitates reentry. Most of the studies have been done in animals, and the mechanism underlying the generation and termination of VF in humans is speculative and remains to be determined. METHODS: Monophasic action potentials (MAPs) were recorded simultaneously from the right ventricular outflow tract (RVOT) and the right ventricular apex (RVA) in 27 patients who underwent implantation and testing of an ICD. T wave shocks were used to induce VF while the termination was attempted using internal defibrillator shocks. The post-shock repolarization time (PSRT) was measured in both the RVA and RVOT MAPs, and the difference between the two recordings was defined as the PSDR. The averages of PSDR were compared between the successful and unsuccessful inductions and terminations of VF. RESULTS: T wave shocks that induced VF generated a greater PSDR (93.4 +/- 85.1 ms) than the unsuccessful ones (45.1 +/- 55.9 ms, p < 0.001). On the other hand, shocks that failed to terminate VF were associated with a greater PSDR (59.9 +/- 41.2 ms) than shocks that terminated VF (21.1 +/- 20.1 ms), p < 0.001. CONCLUSIONS: A high PSDR following a T wave shock is associated with induction of VF; while following a defibrillating shock, it is associated with its failure and the continuation of VF. Conversely, a low PSDR is associated with failure of a T wave shock to induce VF and successful termination of VF by a defibrillating shock.

Pulmonary effect of amiodarone in patients with heart failure. The Congestive Heart Failure-Survival Trial of Antiarrhythmic Therapy (CHF-STAT) Investigators (Veterans Affairs Cooperative Study No. 320).

OBJECTIVES: The purpose of this study was to evaluate the pulmonary effects of amiodarone in patients with heart failure, in those with chronic obstructive pulmonary disease (COPD) and in those undergoing a surgical procedure. BACKGROUND: Amiodarone has been known to cause pulmonary complications; especially in those with COPD and in those undergoing a surgical procedure. METHODS: Patients receiving vasodilator therapy for congestive heart failure were prospectively randomized to placebo or amiodarone at 800 mg/day for 14 days, 400 mg/day for 50 weeks and then 300 mg/day thereafter. Chest X-ray film and pulmonary function tests with diffuse capacity of carbon monoxide (DLCO) were obtained at baseline and annually. The power to detect a 20% difference in DLCO at 1 year exceeded 90% in all patients and in those with COPD (two-sided alpha = 0.05). The sample allowed a 75% power to detect pulmonary complications (1% vs. 5%) between the two treatment groups. RESULTS: There was no difference in baseline characteristics between patients randomized to amiodarone (n = 269) or placebo (n = 250). The DLCO measurements at randomization were 18.3 +/- 6.9 and 17.7 +/- 7.6 ml/min per mm Hg for the amiodarone and placebo groups, respectively (p = 0.3). At 1 and 2 years, DLCO measurements were 17.7 +/- 7.0 and 18.3 +/- 7.7 ml/min per mm Hg for the amiodarone group and 17.9 +/- 7.2 and 18.2 +/- 7.2 for the placebo group, respectively. There were no significant differences between the groups, with corresponding p values of 0.73 ad 0.96 at years 1 and 2, respectively. Among patients with COPD, DLCO measurements at randomization were 17.9 +/- 6.7 and 15.8 +/- 6.8 ml/min per mm Hg for the amiodarone and placebo groups, respectively. At years 1 and 2, DLCO measurements were 16.6 +/- 7.8 and 17.8 +/- 9.5 ml/min per mm Hg for the amiodarone group and 16.5 +/- 6.6 and 16.3 +/- 7.0 ml/min per mm Hg for the placebo group, with corresponding p values of 0.95 and 0.48, respectively. There was no difference in survival free of noncardiac or perioperative deaths between patients assigned to amiodarone or placebo. Pulmonary fibrosis was diagnosed in four patients (1.1%) treated with amiodarone and in three patients (0.8%) receiving placebo. CONCLUSIONS: Our study shows that amiodarone can be safely used, with an acceptable pulmonary toxicity, in patients with heart failure.

Thermal effects of laser and electrical discharge on cardiovascular tissue: implications for coronary artery recanalization and endocardial ablation.

To determine the thermal responses of cardiovascular tissues to laser and electrical ablation, and to characterize the effects of different superfusing media and temperatures on target tissue temperatures and resulting extent of tissue injury, 184 laser and 15 electrical discharges were delivered to segments of human and canine aorta and canine ventricular endocardium. Tissue temperatures were measured 2 mm from the point of contact of laser fiber tip and tissue. When superfusing media consisted of whole blood or plasma at room temperature, a standard 40 J laser discharge caused peak arterial temperatures to rise 29.2 +/- 1.6 degrees C and 30 +/- 1.4 degrees C, respectively; however, tissue cooling was significantly slower in blood than in plasma. When saline solution was superfused, tissue temperatures rose by 11.4 +/- 2.2 degrees C, and tissue cooling occurred significantly faster than with either plasma or blood. The dimensions of the resulting aortic lesions were larger when blood (1.69 +/- 0.26 mm) was superfused than when plasma (1.39 +/- 0.04 mm) or saline (0.77 +/- 0.13 mm) was superfused (p less than 0.0001). Similar findings were observed with ventricular endocardium using blood or saline as the superfusing medium. In arterial tissue, superfusion with cold blood or saline solution resulted in lower peak temperature elevations (22 +/- 3.8 degrees C and 13.5 +/- 1.3 degrees C, respectively) and faster tissue cooling after laser discharge. Corresponding aortic lesion sizes were significantly smaller (1.4 +/- 0.03 and 0.5 +/- 0.02 mm, respectively) than when blood or saline medium was superfused at room temperature (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Radiofrequency catheter ablation of ectopic atrial tachycardia using paced activation sequence mapping.

OBJECTIVES: Although ectopic atrial tachycardia is infrequent, it can be an important clinical challenge. We sought to define an alternative therapeutic approach to this refractory problem. BACKGROUND: Radiofrequency energy catheter ablation has been used to treat a variety of ventricular and supraventricular arrhythmias but has not been proved efficacious in the management of ectopic atrial tachycardia. METHODS: Ten patients (14 to 47 years of age) referred with refractory ectopic atrial tachycardia were studied. Mapping techniques included identification of earliest atrial activation, confirmation of concordance of P wave configuration during spontaneous tachycardia and pacing from the ablation catheter, and paced activation sequence mapping. The paced activation sequence mapping compared the activation sequence at multiple atrial sites during spontaneous tachycardia with that recorded during pacing from the ablation catheter. The catheter was steered to a point where pacing reproduced the spontaneous activation sequence. RESULTS: Foci were right atrial in eight patients and left atrial in two. In 8 of 10 patients, 514 +/- 97 (SE) J and 5.7 +/- 2.3 (SD) J radiofrequency energy applications ablated the ectopic focus. Seven of these eight patients presented with one focus and one had two discrete and stable foci. Ablation was unsuccessful in two patients with multiple foci. No complications occurred. An arrhythmia focus recurred in two patients and one patient underwent successful repeat ablation. The other patient was managed medically. All seven patients with successful ablation are symptom free after 6.5 +/- 3.8 months. CONCLUSIONS: Our preliminary experience suggests that with the use of both paced activation sequence mapping and standard techniques, radiofrequency ablation of ectopic atrial tachycardia may be a safe and effective form of therapy.

Effect on coronary artery anatomy of radiofrequency catheter ablation of atrial insertion sites of accessory pathways.

OBJECTIVES: The purpose of this study was to analyze the effects of radiofrequency catheter ablation of the atrial insertion site of accessory pathways on the angiographic appearance of coronary arteries. BACKGROUND: Radiofrequency catheter ablation of accessory pathways requires the application of energy to the endocardial surface of the atrioventricular groove adjacent to the major epicardial coronary arteries. A systematic analysis of the effect of radiofrequency ablation on coronary arteries has not previously been demonstrated. METHODS: Seventy consecutive patients with 76 accessory pathways (7 right free wall, 44 left free wall, 12 posteroseptal, 8 anteroseptal and 5 midseptal) were studied. Quantitative coronary angiography was performed before, immediately after and a mean of 69 +/- 42 days after radiofrequency catheter ablation. RESULTS: Coronary artery diameter adjacent to the ablating electrode was 2.6 +/- 0.9 mm before ablation, 2.7 +/- 0.9 mm immediately after ablation and 2.7 +/- 1.0 mm at the time of follow-up study. Angiographic findings were unchanged from baseline in 69 of 70 patients immediately after ablation and in all 70 patients at the time of follow-up study. CONCLUSIONS: Radiofrequency catheter ablation of the atrial insertion site of accessory pathways does not result in short-term angiographic changes in coronary artery anatomy.

Thiazide therapy is not a cause of arrhythmia in patients with systemic hypertension.

Forty-four patients with uncomplicated systemic hypertension underwent 48-hour electrocardiographic monitoring before and after four weeks of treatment with hydrochlorothiazide, 100 mg daily. Plasma potassium concentration decreased from 4.07 +/- 0.26 mmol/L (4.07 +/- 0.26 mEq/L) to 3.36 +/- 0.44 mmol/L (3.36 +/- 0.44 mEq/L). The average number of premature ventricular contractions, couplets, or ventricular tachycardia episodes did not change significantly. Twenty patients had more than minimal ventricular ectopy (class 2 to 5) before and 17 after diuretic therapy. Further analysis revealed that following diuretic therapy, neither patients with plasma potassium levels of 3.4 mmol/L or less (less than or equal to 3.4 mEq/L) nor patients with left ventricular hypertrophy had increased ectopy as compared with baseline. At baseline, patients with left ventricular hypertrophy had more arrhythmias than patients without. We conclude that the results of this study provide no evidence that diuretic therapy or diuretic-induced hypokalemia results in increased ventricular ectopy, and that patients with left ventricular hypertrophy may have more ventricular ectopy than patients without, but these arrhythmias are not adversely effected by diuretic therapy.

Acebutolol and left ventricular function: assessment by radionuclide angiography.

We assessed the effects of acebutolol, a cardioselective beta blocker, on global and regional left ventricular function in 26 patients with chronic angina pectoris. All patients underwent rest and maximal supine bicycle exercise radionuclide angiography while on placebo and oral acebutolol (400 mg three times a day). Resting ejection fraction on placebo was 51 +/- 3% and on acebutolol was 54 +/- 3% (p less than 0.05). No resting ejection fraction decreased greater than or equal to 7%. Only one patient (resting ejection fraction 28% on placebo and 21% on acebutolol) developed signs of fluid retention. Exercise nuclear studies on placebo revealed responses consistent with coronary artery disease (abnormal ejection fraction response to exercise and regional wall motion abnormalities) in 24 of 26 patients. Peak exercise ejection fraction was of the same order on placebo and acebutolol (51 +/- 3% and 54 +/- 3%, p = NS). In four patients the ejection fraction response to exercise became normal and in five patients all regional wall motion abnormalities became normal on acebutolol. Cardioselective beta blockade with acebutolol in effective antianginal doses is safe and may improve resting and exercise ventricular function.

Glucose and lipid metabolism during acebutolol and propranolol therapy of angina in nondiabetic patients.

The metabolic effects of acebutolol, a cardioselective beta-adrenergic blocker, and of propranolol, a nonselective beta blocker, were evaluated. Our subjects were 20 men with chronic stable angina; none had diabetes. An initial 4-wk, single-blind control phase was followed by two drug treatment periods, each a 3-wk double-blind titration phase (using increasing doses of acebutolol or propranolol), followed by a 5-wk double-blind maintenance phase. Metabolic studies were performed at the end of the control and maintenance phases. Propranolol induced elevation in basal serum glucose concentrations and both propranolol and acebutolol decreased glucose tolerance at 2.5 and 3 hr. There was no noticeable effect on insulin secretion by either drug. Neither propranolol nor acebutolol induced hyperlipidemia. There was a small decrease in total serum cholesterol after propranolol. Both drugs decreased low-density lipoprotein cholesterol. No effects were noted on the levels of serum triglycerides, high-density lipoprotein cholesterol, or free fatty acids.

Class III drugs and congestive heart failure: focus on the congestive heart failure-survival trial of antiarrhythmic therapy.

Patients with congestive heart failure frequently have ventricular arrhythmias on ambulatory electrocardiographic recordings and sudden cardiac death is seen in almost 50% of such patients. Many antiarrhythmic agents have been approved to suppress the arrhythmia in an effort to improve survival. Some sodium-channel blockers not only failed to improve survival but have been shown to be harmful. This led to the development of potassium-channel blockers, such as d-sotalol, amiodarone, dofetilide, and azimilide. d-Sotalol was associated with excess mortality in patients with left ventricular dysfunction; amiodarone seems to be potentially beneficial; and dofetilide has a neutral effect on mortality. The Sudden Cardiac Death Heart Failure Trial (SCD HEFT) is testing the implantable cardioverter defibrillator (ICD) against amiodarone and placebo. The ICDs appear to be superior to antiarrhythmic drugs in certain high-risk patients, although not proved in unstratified patients with heart failure.

M-mode echocardiograms for determination of optimal left atrial timing in patients with dual chamber pacemakers.

To determine if the A wave of the mitral valve echocardiogram can be used as a marker for left atrial (LA) activity and assist in the programming of dual chamber pacemakers, 156 echocardiograms with the mitral A wave present were obtained from 23 patients with dual chamber pacemakers, all of whom had bipolar esophageal recordings of LA depolarization. Twelve of these patients also underwent hemodynamic study with cardiac function determined at 5 different pacemaker settings: ventricular demand pacing and dual chamber sequential pacing at 0 or 25, 150, 200 and 250 ms programming atrioventricular (AV) delay. The time delay from right atrial pacing artifact to onset and peak of mitral A wave was linearly related to the time from atrial pacing artifact to LA depolarization on the esophageal lead (p less than 0.001). As pacing mode changed from dual chamber sequential pacing (DVI) mode to atrial synchronous-ventricular pacing (VDD), the A wave came earlier relative to the ventricular pacing spike, linearly related to the LA to ventricular extension with mode change determined with the esophageal lead (r = 0.94, p less than 0.001). The time from atrial pacing to peak of A wave was shorter in patients whose optimal programmed AV delay was 150 ms compared with those whose optimal AV delay was 200 or 250 ms (p less than 0.02). At the optimal programmed delay for cardiac output, the peak of the A wave was an average of 13 +/- 36 ms after the ventricular pacing spike.(ABSTRACT TRUNCATED AT 250 WORDS)

Importance of left atrial timing in the programming of dual-chamber pacemakers.

To determine the hemodynamic effect of different programmed atrioventricular (AV) delays and the importance of the actual timing of left atrial (LA) depolarization, 16 patients with dual-chamber pacemakers were studied and all were found to have an optimal programmed AV delay for cardiac function. However, randomly chosen AV delays of 150, 200 or 250 ms actually provided worse stroke volume than VVI pacing in 7 patients. The optimal programmed AV delay was variable between patients and was related to the interatrial conduction delay, measured as the time from right atrial pacing artifact to LA depolarization (mean 144 +/- 82 ms, range 70 to 380.) Patients with short interatrial delays (less than or equal to 90 ms) were served better by shorter programmed AV delays (150 ms), and patients with longer interatrial delays (greater than or equal to 120 ms) were served better by longer programmed AV delays (greater than or equal to 200 ms) (p less than 0.05). Furthermore, as pacing mode changed from dual-chamber sequential pacing (DVI) to atrial synchronous ventricular pacing (VDD), the LA to ventricular sequence increased from 6 +/- 81 ms to 137 +/- 50 ms (p less than 0.001). This change in the LA to ventricular sequence with mode change produced a significant decrease in stroke volume (p less than 0.05). Thus, the optimal programmed AV delay in patients with dual-chamber pacemakers is predicted by the relation of LA and ventricular activation. Because interatrial conduction delays vary widely, optimal programming requires knowledge of the LA to ventricular sequence.(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiographic assessment by computer-assisted analysis of diastolic left ventricular function and hypertrophy in borderline or mild systemic hypertension.

Systemic hypertension is a common cause of congestive heart failure. However, left ventricular (LV) systolic function remains normal for many years in patients with mild or moderate hypertension. In this study, high-quality M-mode echocardiograms were recorded in 7 patients with borderline hypertension, 14 patients with mild hypertension and 15 normal persons. Measures of systolic and diastolic LV function and the degree of LV hypertrophy were studied with the assistance of a tablet digitizer and dedicated microcomputer. Average blood pressure was 125 +/- 10/77 +/- 7 mm Hg in normal subjects, 146 +/- 18/92 +/- 2 mm Hg in patients with borderline hypertension and 150 +/- 11/102 +/- 4 in patients with mild hypertension. Indexes of systolic LV function were similar in all 3 groups. The peak rate of early relaxation of the LV posterior wall was significantly decreased in the group of patients with mild hypertension (4.7 vs 6.6 sec-1, p less than 0.01). The mitral valve closure rate was 150 +/- 32 mm/s in normal subjects, 119 +/- 35 mm/s in patients with borderline hypertension and 106 +/- 26 mm/s (p less than 0.001) in patients with mild hypertension. Mild LV hypertrophy was present in 6 of 7 patients with borderline and 13 of 14 patients with mild hypertension. The degree of hypertrophy and the level of blood pressure correlated poorly.(ABSTRACT TRUNCATED AT 250 WORDS)

Noninvasive electrophysiologic study using standard permanent pacemakers in patients with spontaneous sustained ventricular tachycardia or ventricular fibrillation.

Permanent pacemakers capable of noninvasive electrophysiologic testing were used to study and treat 26 patients with spontaneous sustained ventricular tachycardia (VT) or fibrillation (VF). One hundred nine episodes of sustained VT or VF were induced in these patients. In 8 patients spontaneous VT was reverted by noninvasive means. Drug changes based on noninvasive testing were made in 12 patients. In the 1- to 67-month follow-up period, drug therapy based on noninvasive electrophysiologic testing was predictive of outcome in patients with spontaneous arrhythmias. Thus, noninvasive electrophysiologic testing using permanent pacemakers is a useful method for studying and treating patients with recurrent sustained ventricular arrhythmias.

Effects of diuretic therapy and exercise-related arrhythmias in systemic hypertension.

The effect of aerobic exercise on cardiac arrhythmias, plasma catecholamines, potassium and magnesium in patients with systemic hypertension was assessed. Twenty patients (age 54 +/- 8 years) with uncomplicated hypertension underwent exercise treadmill testing twice while receiving placebo and twice while receiving hydrochlorothiazide 100 mg daily. Blood samples for electrolytes and catecholamines were obtained at rest, at peak exercise and 10 minutes after exercise. There were no substantial differences comparing the first to the second placebo phase or the first to the second treatment period. As expected, hydrochlorothiazide treatment caused a significant decrease in serum potassium (4.00 +/- 0.44 to 3.32 +/- 0.49 mEq/liter, p less than 0.001). Serum magnesium did not change with treatment. Serum potassium, serum magnesium and plasma catecholamines increased significantly with exercise. No rebound hypokalemia occurred during recovery. Occasional ventricular premature contractions were noted at rest during all phases of the study, with only a slight increase in frequency during exercise. Couplets were noted only rarely. No difference in the frequency or complexity of arrhythmias was noted between placebo and treatment periods. Diuretic therapy or diuretic-induced hypokalemia has no profound effect on cardiac arrhythmias during or after exercise in patients with uncomplicated systemic hypertension.

Value of the electrocardiogram in determining cardiac events and mortality in myotonic dystrophy.

Electrocardiograms were recorded at baseline and regular intervals in 53 patients with myotonic dystrophy who were followed for a mean of 6.3 +/- 4.0 years. Patients with cardiac events had a significantly prolonged PR interval (p <0.001), a later age of onset of neuromuscular symptoms (p <0.05), and were older (p <0.005).

Effects of aerobic training on exaggerated blood pressure response to exercise in African-Americans with severe systemic hypertension treated with indapamide +/- verapamil +/- enalapril.

Hypertensive patients are likely to have an exaggerated blood pressure (BP) response during physical exertion. When moderate aerobic exercise was added to medical antihypertensive therapy in patients with severe hypertension, excessive elevations in BP during physical exertion were attenuated even with a modest reduction in BP at rest.

Effects of amiodarone on the circadian pattern of sudden cardiac death (Department of Veterans Affairs Congestive Heart Failure-Survival Trial of Antiarrhythmic Therapy).

Some antiarrhythmic drugs have been shown to influence the circadian pattern of sudden cardiac death (SCD). The effect of chronic amiodarone therapy on this pattern is unknown. This study determines the circadian pattern of deaths in the Congestive Heart Failure-Survival Trial of Antiarrhythmic Therapy (CHF-STAT) and compares the distribution of SCD between the amiodarone and the placebo arms of the trial. CHF-STAT was a multicenter trial that determined whether amiodarone reduces mortality in patients with heart failure and asymptomatic ventricular arrhythmias. The time of death was retrospectively analyzed in patients who died from pump failure and SCD. In patients who died suddenly, the circadian pattern of deaths was compared between patients receiving amiodarone and those receiving placebo. In CHF-STAT, 274 patients died during follow-up. The time of death was available in 65 of the 74 patients who died from pump failure, and in 96 of the 139 patients who died suddenly. There was a circadian variation of all SCDs compared with other deaths with a distinct peak during the morning (p = 0.04). A similar morning peak of sudden cardiac death was found in both the amiodarone (n = 42) and the placebo (n = 54) groups, and the overall circadian pattern did not differ between them (p = 0.16). In contrast, death from pump failure occurred equally distributed over time. Thus, SCD occurs predominantly during the morning, whereas death from heart failure does not exhibit a morning peak. Amiodarone does not influence the circadian pattern of SCD.