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At least 397 records · Page 22Linked to original sources
PubMed1995

Assessment of autonomic tone over a 24-hour period in patients with congestive heart failure: relation between mean heart rate and measures of heart rate variability.

Patients with congestive heart failure (CHF) are characterized by an imbalance of the autonomic nervous system, which may contribute to the progression of circulatory failure and influence survival. However, it is still unclear whether CHF is characterized by a suppression of the diurnal variation in autonomic tone that is observed in normal subjects. To characterize the circadian variation in autonomic tone in patients with ventricular failure, ambulatory 24-hour Holter monitor recordings were obtained in 20 patients with CHF; 4-minute epochs of data from every hour of each 24-hour recording were selected. For each epoch we calculated the mean heart rate (HR) and, by applying spectral analysis of heart rate variability (HRV), we quantified the magnitude of the total (0.02 to 0.9 Hz), sympathetically governed low frequency variability (0.02 to 0.1 Hz), and parasympathetically mediated high-frequency variability (0.1 to 0.9 Hz). These areas were also expressed as a ratio to total variability and a ratio of high to low variability. A highly significant change in the mean HR over 24 hours was observed (p = 0.0001); no changes in the measures of HRV were obtained (p < 0.3). No significant correlation was found between mean HR and any frequency domain measures. We conclude that the sustained imbalance of autonomic tone over a 24-hour period, as shown by the spectral analysis of HRV, may promote the progression of circulatory failure and predispose patients with CHF to malignant ventricular arrhythmias and sudden cardiac death.(ABSTRACT TRUNCATED AT 250 WORDS)

Autonomic Nervous System↗
PubMed1982

The contributions of sympathetic tone and the renin-angiotensin system to severe chronic congestive heart failure: response to specific inhibitors (prazosin and captopril).

The contribution of sympathetic tone and the renin-angiotensin system to the pathogenesis of chronic heart failure was evaluated. In 20 paired studies of the same 10 patients, the baseline hemodynamic and humoral correlates of congestive heart failure, and the response to alpha adrenergic blockade (prazosin) and angiotensin converting enzyme inhibition (captopril) were assessed. Despite the extent of failure, baseline plasma renin activity ranged from normal to very high. In contrast, baseline plasma catecholamine levels were always elevated. Baseline plasma norepinephrine reflected the severity of heart failure, correlating inversely with baseline cardiac index before administration of both drugs. Comparable improvement in left ventricular function was noted after acute therapy. Baseline renin and norepinephrine did not predict the response to prazosin, but baseline renin did predict the response to captopril: pulmonary wedge pressure (r=-0.776, p less than 0.01), stroke index (r=0.752, p less than 0.02), systemic vascular resistance (r=-0.673, p less than 0.05). In summary, elevated levels of plasma norepinephrine were inversely correlated with baseline cardiac function but norepinephrine levels did not change despite improved hemodynamics with specific prazosin therapy. The renin-angiotensin system exhibited a wide spectrum of activity and hemodynamic improvement with captopril was related to this activity. Absence of a correlation between plasma norepinephrine and plasma renin activity suggested that their contributions to vasoconstriction were not interdependent. Increased sympathetic tone was consistent in severe heart failure, whereas renin-angiotensin activity differed widely. The response to captopril can be used to identify a subset of patients with severe heart failure and adverse angiotensin-mediated vasoconstriction.

Aged↗
PubMed1983

Association of hyponatremia with increased renin activity in chronic congestive heart failure: impact of diuretic therapy.

A correlation between hyponatremia and increased plasma renin activity (PRA) has been reported in patients with severe congestive heart failure (CHF), implying both clinical and pathophysiologic significance. To determine the impact of diuretic therapy on this relation, we evaluated the correlation of serum sodium, prerenal azotemia (blood urea nitrogen/creatinine ratio [BUN/Cr] ), and PRA in 44 patients with severe CHF who were maintained on diuretic therapy. Serum sodium level was inversely related to PRA (r = -0.389, p less than 0.02). However, a significant correlation also existed between the BUN/Cr ratio and PRA (r = 0.365, p less than 0.025) and an inverse correlation between serum sodium level and the BUN/Cr ratio (r = 0.332, p less than 0.025). Multiple regression analysis of the 3 variables yielded significant interdependence (p less than 0.01). To evaluate the effect of diuretic therapy, 12 patients with severe CHF discontinued diuretic therapy and received, for 1 week each, 10 and 100 mEq sodium diets in balance studies. PRA ranged from 0.14 to 16 ng/ml/h. Despite this range, there was no significant correlation between either serum sodium or BUN/Cr ratio and PRA. It is concluded that the presence of marked hyponatremia and prerenal azotemia in patients with diuretic-treated CHF may suggest increased PRA. However, substantial patient-to-patient variability limits the predictive value of these correlations. Although some clinical value may be derived from such correlations, they should not be used to draw major inferences regarding the severity of CHF or the pathophysiology of water balance in CHF.

Adult↗
PubMed1985

Acute dose range study of milrinone in congestive heart failure.

To determine the magnitude and time course of the optimal acute hemodynamic response to oral milrinone, an ascending dose range study was performed in 34 patients with severe chronic congestive heart failure (2.5 to 10 mg, n = 21; 7.5 to 15 mg, n = 13). With the 7.5- and 10-mg doses in both groups, cardiac index increased 26%, pulmonary capillary wedge pressure decreased 25% and systemic vascular resistance decreased 20%, with peak effect at 90 minutes. The hemodynamic improvement with 10 mg was sufficient to normalize cardiac index in 29% of patients. There was a clear dose-response relation, with the largest increases of cardiac index seen with the 15-mg dose (1.67 +/- 0.10 to 2.31 +/- 0.11; p less than 0.005). This dose-response relation was confirmed by the correlation of drug levels and change in cardiac index. However, some patients had significant hypotension and tachycardia with the 15-mg dose. Thus, although 10 mg appears to be optimal for most patients, the dose of milrinone should be individualized for all patients.

Administration, Oral↗
PubMed1985

Immediate converting-enzyme inhibition with intravenous enalapril in chronic congestive heart failure.

To test the hypothesis that intravenous enalapril is a useful pharmacologic probe of the renin angiotensin system, intravenous enalapril was administered to 9 patients with severe congestive heart failure (CHF). This produced abrupt and complete blockade of converting enzyme, with peak effect occurring at 30 minutes, as reflected by increases of plasma renin activity (from 16.8 +/- 6 to 86.6 +/- 23 ng/ml/hour) and decreases of plasma aldosterone levels (from 46 +/- 14 to 25 +/- 6 ng%) (both p less than 0.05). With reduction of angiotensin II--mediated vasoconstriction, systemic vascular resistance decreased markedly (from 1,974 +/- 233 to 1,400 +/- 136 dyne s cm-5) and cardiac index was improved (from 1.88 +/- 0.9 to 2.20 +/- 0.21 liters/min/m2) (both p less than 0.05). The time course of angiotensin II levels suggested that the lack of a cumulative effect from additive doses of intravenous enalapril was a reflection of complete inhibition of converting enzyme. One patient did not respond to enalapril; despite comparable hemodynamic severity of CHF, the renin-angiotensin system was not activated in this patient. Thus, intravenous enalapril is capable of rapid and complete inhibition of converting enzyme for the accurate assessment of angiotensin II--mediated vasoconstriction in patients with severe CHF.

Adult↗
PubMed1985

Arrhythmias in ischemic and nonischemic dilated cardiomyopathy: prediction of mortality by ambulatory electrocardiography.

To test the hypothesis that ventricular arrhythmias detected by ambulatory electrocardiography can stratify mortality risk in patients with ischemic and those with nonischemic dilated cardiomyopathy, clinical, hemodynamic and neurohumoral findings were evaluated in 31 patients. By Kaplan-Meier analysis, the total population had 51% survival at 12 months and 19% survival at 25 months. Subgroups based on peak complexity of ventricular arrhythmias included 9 patients with simple ventricular arrhythmias (peak Lown grades 1 to 3) and 22 patients with complex ventricular arrhythmias (peak Lown grades 4 or 5). Clinical variables and baseline catecholamine levels and renin-angiotensin system activity were similar in the simple and complex arrhythmia subgroups. Patients with simple and those with complex arrhythmias were comparable by all hemodynamic indexes except for a higher mean pulmonary capillary wedge pressure in the complex arrhythmia subgroup. Survival was strikingly related to arrhythmias: mortality was 11% (1 of 9) in the simple ventricular arrhythmia subgroup and 59% (13 of 22) in the complex ventricular arrhythmia subgroup (p less than 0.025 by log-rank test). Twelve patients died suddenly and 2 patients died in circulatory failure, and the risk of death was not affected by the etiology of cardiomyopathy. The higher mortality among the patients with complex arrhythmia could not be explained by the presence of elevated filling pressures alone. Thus, ambulatory electrocardiography can stratify mortality risk among patients with severe ischemic and nonischemic dilated cardiomyopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Clinical and hemodynamic experience with enalapril in congestive heart failure.

The renin-angiotension system is activated in many patients with congestive heart failure (CHF), resulting in angiotensin-mediated vasoconstriction and aldosterone-mediated sodium and water retention. To evaluate the effectiveness of enalapril, a new converting enzyme inhibitor, enalapril was administered to patients either orally or intravenously in a single dose, and hemodynamic and hormonal responses were measured. Patients were then placed on oral enalapril therapy for 1 month, and treadmill exercise duration and invasive hemodynamics were compared with baseline pretreatment data. With single-dose administration, both oral and intravenous enalapril reduced systemic vascular resistance and increased cardiac output. However, the effects of oral enalapril were not manifest for 3 to 4 hours, because oral enalapril is a pro-drug form that requires hepatic deesterification. In contrast, intravenous enalapril resulted in significant hemodynamic and hormonal changes 15 to 30 minutes after administration. During long-term therapy, enalapril was associated with improved symptomatology, increase of treadmill exercise duration and sustained hemodynamic improvement. Enalapril was effective therapy for chronic CHF. Optimal short-term response may require coadministration of both intravenous and oral preparations of enalapril; however, the magnitude of the short-term response was comparable for both preparations. Long-term therapy is most effective when the drug is administered as a twice-daily regimen.

Administration, Oral↗
PubMed1985

Value of programmed stimulation and exercise testing in predicting one-year mortality after acute myocardial infarction.

The ability of programmed ventricular stimulation and exercise testing to predict 1-year mortality after acute myocardial infarction (AMI) was investigated in 228 clinically well survivors of AMI. Patients with inducible ventricular tachycardia (VT) or ventricular fibrillation (VF) had a higher mortality rate than those without inducible arrhythmias (26% vs 6%, p less than 0.001). Exercise-induced ST-segment change of 2 mm or more was associated with a higher mortality rate than ST change of less than 2 mm (11% vs 4%, 0.05 less p less than 0.10). Of patients who had both tests, 62% had no inducible ventricular tachycardia or ventricular fibrillation and ST change of less than 2 mm, and only 1% died during the first year. Thus, in clinically well survivors of AMI, programmed stimulation is a powerful predictor of first-year mortality; programmed stimulation and exercise testing together predict virtually all deaths within the first year, and they can identify a large group of patients with a very low mortality rate.

Adult↗
PubMed1986

Effect of antiarrhythmic therapy on delayed potentials detected by the signal-averaged electrocardiogram in patients with ventricular tachycardia after acute myocardial infarction.

The ability of class I and class II antiarrhythmic drugs to either abolish delayed potentials or modify their timing was investigated in 39 patients with spontaneous ventricular tachycardia (VT) after myocardial infarction. Before the study all patients had delayed potentials on the signal-averaged electrocardiogram and inducible VT with programmed stimulation. These investigations were repeated during 67 trials of oral antiarrhythmic therapy (mexiletine 25, quinidine 24, metoprolol 13, disopyramide 2, procainamide 1, drug combinations 2). Delayed potentials were abolished in only 5 trails (7%), which was within the baseline variability of 8.5% for detection of delayed potentials. In the 7 trials in which VT inducibility was suppressed, delayed potentials persisted in 6 and mean ventricular activation time was virtually unchanged (151 ms before drug therapy, 152 ms after). Quinidine, mexiletine and metoprolol caused no consistent change in ventricular activation time. There was also no change in mean ventricular activation time (164 ms before and 163 ms after drug treatment) in patients in whom spontaneous VT did not recur with drug therapy during follow-up. Thus, the tested antiarrhythmic drugs had no consistent effects on presence or timing of delayed potentials on the signal-averaged electrocardiogram, even when VT inducibility was suppressed or recurrence of spontaneous VT was prevented.

Action Potentials↗
PubMed1986

Effect of nicardipine on rest and exercise hemodynamics in chronic congestive heart failure.

The hemodynamic response to vasodilation induced by the new calcium channel antagonist nicardipine was studied in 10 patients with severe, chronic congestive heart failure. Rest and exercise hemodynamics were evaluated in the baseline state and after 1 week of oral nicardipine therapy (30 mg 3 times daily). In addition, respiratory gas exchange and arteriovenous oxygen difference were measured to assess changes in oxygen utilization. The responses of the sympathetic nervous system were evaluated by measuring plasma norepinephrine concentrations at rest and during maximal exercise. At rest, nicardipine administration was associated with significant reductions in mean systemic arterial pressure, systemic vascular resistance, pulmonary artery wedge pressure and pulmonary arterial pressure, and significant increases in cardiac index and stroke volume index. These effects were maintained during exercise. In contrast to findings with other calcium channel antagonists, no negative inotropic effect of nicardipine was identified. Nicardipine administration was associated with reduction of arteriovenous oxygen difference. Nicardipine had no effect on plasma norepinephrine concentrations, suggesting absence of reflex sympathetic nervous activation. Thus, nicardipine-mediated vasodilation leads to significant improvements in both rest and exercise cardiac performance.

Adult↗
PubMed1987

Use of invasive ergometric exercise to assess the hemodynamic response to nicardipine.

The calcium antagonists are potent vasodilators. This physiologic property suggests that these agents have a potential role in the treatment of patients with hypertension and congestive heart failure. Although the clinical response to calcium antagonism in hypertension is promising, the response in patients with congestive heart failure is less than hoped for; this is due to the fact that this class of agents may induce a hemodynamically important degree of negative inotropic effect. To test the hemodynamic response to nicardipine, a second-generation dihydropyridine, the hemodynamic response to maximal ergometric exercise was evaluated in a group of patients with moderate to severe chronic congestive heart failure. One week of nicardipine therapy was associated with a significant reversal of vasoconstriction at rest and during peak exercise with a secondary increase of cardiac index, and a decrease in pulmonary wedge pressure. The reversal of vasoconstriction was associated with a decrease in mean arterial pressure, with no change in the heart rate. There was no change in oxygen consumption or carbon dioxide production; however, there was a decrease in arteriovenous oxygen difference, consistent with a reduction of oxygen extraction. This short-term study identified the potent vasodilator properties of nicardipine in patients with chronic congestive heart failure; a hemodynamically significant negative inotropic effect could not be identified. Although the use of calcium antagonists for the treatment of congestive heart failure may have a limited role, this study nonetheless suggests that nicardipine may have a favorable vasodilator effect without an overt negative inotropic effect. This would be of considerable advantage in the treatment of hypertension, when compared with beta-adrenergic blocking agents.

Adult↗
PubMed1987

Identification of normal neurohormonal activity in mild congestive heart failure and stimulating effect of upright posture and diuretics.

To characterize further the pathophysiology of the neurohormonal vasoconstrictor pathways in congestive heart failure (CHF), plasma renin activity, plasma norepinephrine, blood pressure, blood volume and renal hemodynamics were measured in 12 patients with mild to moderate CHF. In addition, the response to the gravitational stress of head-up tilt and the influence of 3 weeks of furosemide treatment as stimuli of neurohormonal activity were assessed. Supine plasma renin activity before diuretics was relatively normal at 1.94 +/- 1.6 ng/ml/hr and was significantly increased to 3.9 +/- 2.7 ng/ml/hr after diuretics. During tilt, there was a significant reflex increase in plasma renin activity both before and after diuretics. Plasma norepinephrine was also relatively normal before diuretics (325 +/- 211 pg/ml), did not increase after diuretics, but showed significant increases during tilt both before and after diuretics. Diuretic administration led to decreases in both systolic and diastolic blood pressures, but there was no change in body weight or total blood volume. In addition, diuretic administration did not result in any significant changes of renal blood flow (546 +/- 119 to 634 +/- 204 ml/min/1.73m2), glomerular filtration rate (81 +/- 22 to 90 +/- 27 ml/min/1.73m2) or filtration fraction (0.26 to 0.25). The present study demonstrates that the renin-angiotensin system and the sympathetic nervous system were not activated in the early symptomatic stages of CHF and that baroreceptor stimulation of these pathways during head-up tilt was relatively preserved. Renin secretion increased during diuretic administration, suggesting that the macula densa signal for renin release was also preserved in patients with relatively mild CHF.

Aged↗
PubMed1987

Correlation between signal-averaged electrocardiogram and programmed stimulation in patients with and without spontaneous ventricular tachyarrhythmias.

This study examined the incidence of delayed ventricular activation on signal-averaged electrocardiograms and the incidence of inducible sustained ventricular tachycardia (VT) at programmed stimulation (1 or 2 extrastimuli) in patients with and patients without spontaneous ventricular tachyarrhythmias. The correlation between delayed ventricular activation and inducible VT was investigated in 371 patients with acute myocardial infarction (AMI). In 32 patients with no ventricular disease and no spontaneous arrhythmias (group I), ventricular activation time averaged 115 +/- 2 ms, compared with 166 +/- 3 ms (p less than 0.001) for 65 patients with spontaneous ventricular tachyarrhythmias late after AMI (group II). In AMI patients with no spontaneous arrhythmias, ventricular activation time averaged 133 +/- 2 ms for 306 patients studied 1 to 4 weeks after AMI (group III) and 130 +/- 2 ms for 67 patients studied 3 to 12 months after AMI (group IV). The values for group III and group IV patients were each significantly higher than for group I (p less than 0.001), but lower than that for group II (p less than 0.001). The incidence of delayed ventricular activation was 89% for group II, 26% for group III and 18% for group IV. Sustained VT was not inducible in group I patients, but was inducible in 78% of group II (p less than 0.001 vs group I) and 20% of group III (p less than 0.05 vs group I; p less than 0.001 vs group II) (group IV was not studied).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Renal and hormonal effects of phosphodiesterase III inhibition in congestive heart failure.

Evaluation of the impact of therapeutic interventions in congestive heart failure (CHF) with compounds such as the phosphodiesterase (PDE) III inhibitors must include the determination of regional blood flow and functional changes. Thus, whereas PDE III inhibitors produce a significant increase in cardiac output and reduction of systemic vascular resistance, it is necessary to understand their effects on the kidney and neurohormonal parameters. The evaluation of these effects must take into consideration both the baseline renal and neurohormonal abnormalities in CHF, and the cellular actions of PDE III inhibition, which include an increase in cyclic adenosine monophosphate and cytosolic calcium. In a group of 13 patients with CHF, milrinone therapy for 1 month did not increase renal blood flow or glomerular filtration rate, or favorably affect neurohormonal parameters. However, forearm blood flow increased proportionately with cardiac output. Therefore PDE III inhibition produces a preferential increase in skeletal muscle blood flow, which may be a relative shunting of blood from the kidney. Alternatively, PDE III inhibition may activate renal cellular mechanisms that offset the anticipated favorable response to the increase of cardiac output produced by milrinone.

Aldosterone↗