Congestive Heart Failure Arrhythmias Research Articles

THE EFFECT OF VOLUME OVERLOADED STATE ON THE TRANSMURAL DISPERSION OF REPOLARIZATION IN A FAILING HEART

Volume overloaded state is suspected of increasing the risk of ventricular arrhythmias in congestive heart failure (CHF). The T peak to T end interval (Tpe) as measured on the surface electrocardiogram (EKG) is presumed to represent global dispersion of ventricular repolarization and has been shown

Tumor necrosis factor-α: a new mechanism of ischemic ventricular fibrillation?

Tumor necrosis factor-α: a new mechanism of ischemic ventricular fibrillation?

Left Stellate Ganglion and Vagal Nerve Activity and Cardiac Arrhythmias in Ambulatory Dogs With Pacing-Induced Congestive Heart Failure

The purpose of this study was to determine the patterns of autonomic nerve activity in congestive heart failure (CHF). The relationship between autonomic nerve activity and cardiac arrhythmias in CHF is unclear. We implanted radiotransmitters in 6 dogs for continuous (24/7) simultaneous monitoring of left stellate ganglion nerve activity (SGNA), vagal nerve activity (VNA), and electrocardiography before and after pacing-induced CHF. Congestive heart failure increased both SGNA and VNA. The SGNA but not VNA manifested a circadian variation pattern. There was extensive sinus node fibrosis. We analyzed 2,263 episodes of prolonged (>3 s) sinus pauses (PSP) and 1,420 long (>10 s) episodes of paroxysmal atrial tachycardia (PAT). Most (95.3%) PSP episodes occurred at night, and 56% were preceded by a short burst of SGNA that induced transient sinus tachycardia. Long PAT episodes were typically (83%) induced by simultaneous SGNA and VNA discharge, followed by VNA withdrawal. Premature ventricular contractions and ventricular tachycardia were preceded by elevated SGNA. The reduction of sympathovagal balance at night in ambulatory dogs was due to reduced sympathetic discharge rather than a net increase of vagal discharge. The tachybrady syndrome in CHF might be triggered by an intermittent short burst of SGNA that resulted in tachycardia and sinus node suppression. Simultaneous sympathovagal discharge is a cause of long PAT episodes. These data indicate that there is an association between the specific patterns of autonomic nerve discharges and cardiac arrhythmia during CHF.

Developments in the Management of Atrial Arrhythmias in Congestive Heart Failure

Developments in the Management of Atrial Arrhythmias in Congestive Heart Failure

Selective Aldosterone Blockade Suppresses Atrial Tachyarrhythmias in Heart Failure

Renin-angiotensin-aldosterone system activation may be involved in the pathogenesis of atrial arrhythmias in congestive heart failure (CHF). The effects of aldosterone blockade on atrial tachyarrhythmias have not been evaluated. This study's aim was to determine whether selective aldosterone blockade suppresses atrial tachyarrhythmia inducibility and modifies atrial electrical and/or structural remodeling in a canine model of rapid ventricular pacing (RVP)-induced CHF. Dogs were assigned randomly to treatment with oral placebo or eplerenone (50 mg/day) and divided into four groups: two sham-operated (no RVP) and two RVP groups. After 5 weeks of no RVP or RVP at 230 beats/min along with concurrent placebo or eplerenone treatment, dogs underwent electrophysiologic and echocardiographic studies. Sustained atrial tachyarrhythmia inducibility (>10-minute duration), atrial effective refractory periods (ERPs), systolic and diastolic function, and left atrial and left ventricular (LV) chamber sizes were assessed. Placebo-treated RVP dogs developed CHF with LV systolic and diastolic dysfunction, left atrial and LV enlargement, increased atrial ERPs, and inducible sustained atrial tachyarrhythmias. Eplerenone treatment in RVP dogs significantly suppressed sustained atrial tachyarrhythmia inducibility, nonuniformly prolonged atrial ERPs and attenuated LV diastolic dysfunction without modifying left atrial or LV dilation or ejection fractions in CHF. Isoproterenol (2-4 microg/min) reversed eplerenone's atrial antiarrhythmic and ERP prolonging effects in CHF. Eplerenone did not alter atrial ERPs in sham (no RVP) dogs without CHF. Eplerenone suppresses inducibility of sustained atrial tachyarrhythmias, selectively prolongs atrial ERPs, and attenuates LV diastolic remodeling in RVP-induced CHF. Aldosterone blockade may be a promising new approach for atrial tachyarrhythmia prevention in CHF.

An animal model of arrhythmogenesis in congestive heart failure

Background: Patients with congestive heart failure (CHF) frequently die from arrhythmias, but models to study arrhythmogenic mechanisms during progressive CHF are lacking. Consequently we examined the feasibility of using dogs with an ischemic insult followed by rapid pacing to study ventricular arrhythmias in CHF. Methods: Eighteen chronically instrumented dogs had ischemic damage induced by inflating a balloon tipped catheter in a coronary artery for 90 min. After 2 weeks recovery, electrophysiologic studies were performed on no drugs, during esmolol infusion, and during isoproterenol infusion. The pacer was turned on at 250 bpm in 12 dogs, but not in six controls, and studies repeated bi-weekly for up to 6 weeks. Results: Serial echocardiograms documented progressive CHF, and serial signal averaged electrocardiograms demonstrated prolongation of total QRS, increased duration of terminal QRS<40 mv, and decreased RMS voltage of the terminal 20 ms of QRS in paced dogs. Arrhythmia severity increased as CHF progressed, but responses were quite variable, unaffected by esmolol, and minimally altered by isoproterenol. Conclusions: Ischemic left ventricular damage followed by rapid ventricular pacing in dogs produces a model that closely mimics patients with CHF and ventricular arrhythmias, including a heterogeneous pathophysiologic response to intervention.

Suppressing sympathetic activation with clonidine on ventricular arrhythmias in congestive heart failure

This randomized, double-blind, placebo-controlled study examines the effects of clonidine (a centrally acting sympathoinhibitor) on ventricular arrhythmias in 35 patients with congestive heart failure (CHF) by using the 24-h ambulatory electrocardiographic recording. After baseline examination and Holter recording, patients were balanced and 18 patients were randomized to clonidine group and 17 patients to placebo group. After four weeks of clonidine (given as a transdermal patch) or matching placebo therapy, a second Holter recording was obtained. The placebo group showed no change in the frequency of ventricular arrhythmias whereas the clonidine-treated group showed a significant decrease in the frequency of ventricular premature beats by 68% ( P<0.01), couplets by 63% ( P<0.01) and episodes of non-sustained ventricular tachycardia by 60% ( P<0.05). Clonidine also decreased heart rate and arterial blood pressure, but left ventricular ejection fraction was slightly improved. It is concluded that sympathetic suppression with clonidine reduces the frequency of ventricular arrhythmias in patients with CHF, which suggests that sympathetic activation plays a role in arrhythmogenesis in these patients.

I defibrillation threshold

The purpose of this study was to determine the patterns of autonomic nerve activity in congestive heart failure (CHF).The relationship between autonomic nerve activity and cardiac arrhythmias in CHF is unclear.We implanted radiotransmitters in 6 dogs for continuous (24/7) simultaneous monitoring of left stellate ganglion nerve activity (SGNA), vagal nerve activity (VNA), and electrocardiography before and after pacing-induced CHF.Congestive heart failure increased both SGNA and VNA. The SGNA but not VNA manifested a circadian variation pattern. There was extensive sinus node fibrosis. We analyzed 2,263 episodes of prolonged (>3 s) sinus pauses (PSP) and 1,420 long (>10 s) episodes of paroxysmal atrial tachycardia (PAT). Most (95.3%) PSP episodes occurred at night, and 56% were preceded by a short burst of SGNA that induced transient sinus tachycardia. Long PAT episodes were typically (83%) induced by simultaneous SGNA and VNA discharge, followed by VNA withdrawal. Premature ventricular contractions and ventricular tachycardia were preceded by elevated SGNA.The reduction of sympathovagal balance at night in ambulatory dogs was due to reduced sympathetic discharge rather than a net increase of vagal discharge. The tachybrady syndrome in CHF might be triggered by an intermittent short burst of SGNA that resulted in tachycardia and sinus node suppression. Simultaneous sympathovagal discharge is a cause of long PAT episodes. These data indicate that there is an association between the specific patterns of autonomic nerve discharges and cardiac arrhythmia during CHF.

Heart rate variability and its relation to ventricular arrhythmias in congestive heart failure.

It has been shown that heart rate variability is decreased in patients with congestive heart failure and that depressed heart rate variability is associated with a propensity to ventricular arrhythmias. Little is known, however, about heart rate variability in patients with both congestive heart failure and ventricular arrhythmias. Spectral heart rate variability was analysed from 24 hour ambulatory electrocardiograms in 15 controls, 15 patients with non-sustained ventricular tachycardia associated with clinically normal hearts (NHVT group), and 40 patients with congestive heart failure (CHF group) secondary to either ischaemic heart disease (n = 15) or idiopathic dilated cardiomyopathy (n = 25). Of the 40 patients with congestive heart failure 15 had no appreciable ventricular arrhythmias (ventricular extrasystoles < 10 beats/h and no salvos) and formed the CHF-VA- group. Another 15 patients with congestive heart failure and non-sustained ventricular tachycardia formed the CHF-NSVT group. Heart rate variability was significantly lower in the CHF group than in controls (mean (SD) total frequency 23 (12) v 43 (13) ms; low frequency 12 (8) v 28 (9) ms; high frequency 8 (5) v 14 (7) ms; p < 0.001). The differences in heart rate variability between controls and the NHVT group, between ischaemic heart disease and dilated cardiomyopathy, and between the CHF-VA- and CHF-NSVT groups were not significant. In the CHF group heart rate variability was significantly related to left ventricular ejection fraction but not associated with ventricular arrhythmias. The frequency of ventricular extrasystoles was significantly related to the high frequency component of heart rate variability (r = 0.54, p < 0.05) in the NHVT group. Stepwise multiple regression analysis showed that in the CHF group, heart rate variability was predominantly related to left ventricular ejection fraction (p < 0.05). There was no significant difference in heart rate variability between survivors (n = 34) and those who died suddenly (n = 6) at one year of follow up in the CHF group. In patients with congestive heart failure, heart rate variability is significantly decreased. The depressed heart rate variability is principally related to the degree of left ventricular impairment and is independent of aetiology and the presence of ventricular arrhythmias. The data suggest that analysis of heart rate variability does not help the identification of patients with congestive heart failure at increased risk of sudden death.

Sudden death in patients with congestive heart failure: future directions.

Sudden, unexpected cardiac death continues to be a major clinical problem in patients with congestive heat failure. This review summarizes the current state of knowledge regarding the identification and management of these patients. The roles of ambulatory ECG monitoring, electrophysiological testing, signal-averaged ECG, and other methods of predicting increased risk of sudden death are discussed. The modes of sudden cardiac death and the potential mechanisms of ventricular arrhythmias in congestive heart failure are reviewed. Current therapeutic options including antiarrhythmic drugs, neurohormonal blockade, and automatic implantable cardioverter defibrillators are discussed. Finally, future directions and ongoing clinical investigations of the management of these complex patients are considered.

Short-term effects of oral enoximone on hemodynamics, exercise capacity, anaerobic threshold, and arrhythmias in congestive heart failure

Enoximone, a phosphodiesterase-inhibitor, is a potent inotropic vasodilator agent that causes a marked improvement in hemodynamics in patients with congestive heart failure. The acute effects of oral enoximone on rest and exercise hemodynamics, ejection fraction, aerobic metabolism, exercise capacity, and arrhythmias were studied in 11 patients with moderate to moderately severe dilative cardiomyopathy after 8 days of enoximone (100 mg tid) in addition to baseline therapy (diuretics and digitalis). The cardiac index increased from 2.44 +/- 0.45 to 2.72 +/- 0.50 l/min/m2 (p less than 0.01) at rest and from 4.00 +/- 0.96 to 4.75 +/- 0.95 l/min/m2 (p less than 0.005) during exercise. Pulmonary wedge pressure decreased from 16.8 +/- 7.3 to 12.5 +/- 6.5 mmHg (p less than 0.005) at rest and from 28.2 +/- 8.0 to 24.5 +/- 10.3 mmHg (p less than 0.05) during exercise. Systemic vascular resistance decreased from 1608 +/- 243 to 1495 +/- 300 dynes*sec*cm-5 (p less than 0.05) at rest and from 1152 +/- 155 to 1027 +/- 236 dynes*sec*cm-5 (ns) during exercise. The anaerobic threshold, which was recorded simultaneously, increased from 13.2 +/- 2.7 to 15.5 +/- 2.5 ml/kg/min VO2 (p less than 0.02). The radionuclide ventriculography ejection fraction improved from 21.7 +/- 5.0 to 28.1 +/- 9.1% (p less than 0.01) during exercise; the changes at rest were not significant (20.8 +/- 6.2 vs 25.8 +/- 8.4%). Exercise tolerance showed an increase of 16% (492 +/- 133 to 573 +/- 135 sec, p less than 0.005). The resting heart rate remained unchanged (81.8 +/- 13.4 vs 81.8 +/- 11.9). Interestingly, 24-h Holter monitoring revealed more or new repetitive arrhythmias in 9/11 patients.

Effect of milrinone on ventricular arrhythmias in congestive heart failure

M ilrinone is a nonglycoside, noncatecholamine inotropic agent that has been shown to exhibit inotropic and vasodilatory effects in patients with severe congestive heart failure (CHF).’ 4 It is a bipyridine analog of amrinone that has been shown in experimental studies to be significantly more potent than the parent compound on a per weight basis. Although its mechanism of action has not been fully delined, it has been suggested that enhancement of calcium ion fluxes in the myocardial cell is contributory.5 Heart failure secondary to verapamil or propanolol can be improved with milrinone and its inotropic effect can be detected despite concomitant therapy with either catecholamine or glycoside agents. The effect of milrinone on ventricular arrhythmias has not been completely delined. Several studies have suggested that ventricular arrhythmias can be exacerbated in some patients treated with either amrinone6 or milrinone.’ L, Ventricular arrhythmias, including complex features such as nonsustained ventricular tachycardia (VT), are common in patients with CHF and have been implicated in the high mortality of the disease. lo We attempted to determine if chronic treatment with milrinone affects the prevalence and complexity of ventricular arrhythmias in patients with CHF.

Significance of arrhythmias in congestive heart failure.

Patients with CHF are commonly encountered in clinical practice. Cardiac arrhythmias, particularly complex ventricular premature contractions, often occur in these patients. The presence of ventricular tachyarrhythmia, especially ventricular tachycardia, denotes a poor prognosis. Patients with CHF already have a limited life span, and the presence of ventricular arrhythmia further increases an already high death rate. Although previous reports failed to show any significant effect of treatment on mortality in patients with CHF, results of recent studies are encouraging. Several reports have shown that treatment with angiotensin converting enzyme inhibitors and newer antiarrhythmic agents reduces the frequency of ventricular arrhythmia and decreases mortality. It is hoped that the results of these studies will be confirmed in well-controlled, large-scale, prospective trials.

Factors causing arrhythmias in chronic congestive heart failure

Severe congestive heart failure (CHF) is a common syndrome with a high mortality rate (about 50% in 1 year among patients with symptoms at rest). Severity of left ventricular dysfunction is the most important adverse prognostic factor. Serious arrhythmias are common in CHF and also increase the mortality rate. Sudden death is the mode of death in about 40% of patients with severe heart failure. Multiple factors contribute to arrhythmias in CHF, including left ventricular dysfunction, myocardial ischemia, catecholamines, electrolyte disturbances, and drugs used to treated the heart failure. Minimizing or correcting these influences may be important in reducing serious arrhythmias. Antiarrhythmic drugs may be important in reducing the incidence of sudden doath among patients with severe heart failure, although this has not yet been proved.

Effect of enalapril on ventricular arrhythmias in congestive heart failure

Twenty-four-hour Holter electrocardiographic recordings were used to measure the effects of a converting-enzyme inhibitor, enalapril, given for 12 weeks, on the frequency of cardiac arrhythmias in 10 patients with congestive heart failure (New York Heart Association functional class II to III) receiving maintenance therapy with digoxin and furosemide. Nine patients were given placebo, and both study groups were conducted in a double-blind, parallel manner. The placebo group had no change in the frequency of arrhythmias, whereas enalapril-treated patients showed a significant decrease in the frequency of premature ventricular complexes, ventricular couplets and ventricular tachycardia. A minor, nonsignificant reduction in atrial premature complexes was seen in patients who received enalapril. Compared with placebo patients, those who received enalapril had an increase in plasma potassium levels of 0.33 mmol/liter, a decrease in plasma digoxin, and decreases in pulmonary artery wedge, mean pulmonary artery and right atrial pressures. However, none of these indexes were correlated with the concomitant decline in cardiac arrhythmias. It is concluded that enalapril reduces the frequency of ventricular arrhythmias in congestive heart failure, although the underlying mechanisms are not known.