Ventricular Arrhythmias and Sudden Death in Heart Failure: Evaluation and
Management
by Prakash Deedwania, MD, FACC, FACP

	May 14, 1999 - "The very presence of heart failure indicates a high
risk for sudden cardiac death." This was the consensus of expert panelists
from all over the world, who unanimously agreed about heart failure patients'
risk of cardiac death, especially sudden death. Studies have shown that CHF
patients have as high as 50% mortality over a 5 year follow-up period.
Patients with CHF can die from many causes, but death due to pump failure or
cardiac arrhythmia is the primary cause in most CHF patients.

Cause of death in CHF:

Ventricular tachycardia
Ventricular fibrillation
Bradyarrhythmia/asystole
Pump failure
Recurrent ischemia
Electromechanical dissociation
Strokes/ebolic phenomenon
Pulmonary/renal complication

	Ventricular tachyarrhythmias are thought to be mainly responsible for
sudden death in CHF patients. Arrhythmias are common in CHF patients. Some
studies have shown as many as 80% of CHF patients have ventricular
arrhythmias. It is now known that PVCs (preventricular complexes) are not a
risk marker for SCD (sudden cardiac death). However, several studies have
shown that NSVT (nonsustained ventricular tachycardia) is associated with
substantial risk of SCD (sudden cardiac death). So, NSVT is now accepted as a
risk marker for SCD in CHF. As many as 50-60% of patients with class 3-4 CHF
may have episodes of NSVT on 24-hour Holter monitoring.
	During the 20th Scientific Sessions of NASPE, discussion took place
about the best test for identifying SCD risk in CHF patients: Holter
monitoring, exercise testing, heart-rate variability, signal-averaged ECG, QT
interval, T wave alternans or a combination of tests.
	There was agreement that LVEF measurement is a powerful predictor of
increased SCD risk. Although most non-invasive tests give useful information,
the panel agreed that it is best to use a test measuring multiple factors
during the same test. In this regard, ECG monitoring by 24-hour Holter was
considered the best because it provides information about arrhythmias,
signal-averaged ECG, QT interval, and HRV (heart rate variability). The
panelists agreed that HRV analysis is critical and gives substantial
information about risk level. (Jon's note: low HRV is not good!)
	Richard Verrier of Boston and Stefan Hohnloser of Frankfurt presented
data about microvolt T-wave alternans. Both showed evidence that this new
technology may greatly help identify those at risk for SCD. In the study done
by Hohnloser in 107 CHF patients, it was shown that presence of T-wave
alternans is highly predictive of SCD risk.
	Based on data from studies done during the last 15 years, it was
suggested that inducing ventricular tachycardia via EPS (electrophysiology
study/testing) does not correspond to real-life risk of SCD. Also, NOT being
able to induce an arrhythmia via EPS does not mean a lower risk of SCD.
Patients with non-ischemic cardiomyopathy are a difficult subset, because
EPS has very low predictive value in them.

Treatment for Sudden Death in Heart Failure

	There was considerable discussion about treatments for reducing SCD
in CHF patients. All agreed that the generally accepted therapy for CHF also
reduces SCD risk. Current therapy for CHF is ACE inhibitors, beta-blockers,
diuretics, digoxin, and vasodilators. Although this reduces overall mortality,
many patients are still at risk of SCD. A comparison of several recent trials
with ACE inhibitors in CHF patients have shown that as many as 1/3 of
patients remain at risk of sudden death.
	In the VHeFT-II study it was shown that treatment with enalapril
(Vasotec) was associated with significant reduction in SCD risk. Even in
heart attack patients with LV dysfunction, studies like SAVE and TRACE show
significant reduction in SCD risk with ACE inhibitor use.
	In the RALES-IV trial, we have seen that spironolactone (Aldactone)
on top of ACE inhibitor use further reduced risk of cardiac death. This
benefit was much stronger in patients taking digoxin. The greater effect of
spironolactone in patients taking digoxin suggests that it reduces risk of
digitalis-induced arrhythmia.
	Beta-blockers improve EF and heart function. Although first seen with
Coreg, studies with bisprolol and metoprolol-XL (CIBIS-II and MERIT-HF
studies) have shown that benefit is more due to beta-blockers than any single
brand name. In addition to reducing overall mortality, the risk of sudden
death was also significantly reduced (up to 60% in MERIT-HF).

Mechanisms of sudden death reduction by beta-blockers in CHF:

Heart rate slowing
Prevention of catecholamine-induced myocyte toxicity/apoptosis
Anti-arrhythmic effects
Anti-fibrillatory actions
Anti-ischemic effects
Up-regulation of beta-receptor sensitivity
Decreased sympathetic outflow

Anti-arrhythmic Drugs In CHF Patients

	It is now known that there is no role for class 1 anti-arrhythmic
drugs in CHF patients. Indeed, some studies have shown increased toxicity
and pro-arrhythmic effects of type 1 anti-arrhythmic drugs in CHF patients.
	Several recent studies have shown that amiodarone treatment is safe
in most CHF patients. With the lower doses used in most studies, risk of
serious side effects (such as pulmonary or thyroid toxicities) has been
reduced. In the GESICA trial, treatment with amiodarone reduced cardiac
mortality, especially in those with resting heart rate less than 90 beats per
minute. However, amiodarone had no effect on overall survival or risk of
sudden death, despite reducing ventricular arrhythmias. This raises important
questions about the current arrhythmia suppression model.
	The EMIAT and CAMIAT trials showed that taking both amiodarone and a
beta-blocker is far more effective than taking one or the other. Data from a
recent meta-analysis also suggest that in patients with nonischemic dilated
cardiomyopathy, amiodarone can reduce cardiac mortality.

ICDs in CHF

	Some recent studies have shown significant reduction in SCD risk
with ICDs (implantable cardioverter defibrillators). A recent publication
from the CABG-Patch study suggests that while ICD may reduce risk of
arrhythmic death, the overall benefit is neutralized by increased risk of
non-arrhythmic death (pump failure) in the ICD group.
	This suggests that proper patient selection is critical for ICD use
in CHF patients. This point is also made in the AVID study, which was a
secondary prevention trial (all patients had cardiac arrest or syncope before
entering the trial). The benefits of ICD were far greater in patients with EF
less than 35%.

Conclusions

	Patients with heart failure are at substantial risk of sudden death.
A number of therapies are now available to reduce risk of sudden death in CHF.
The most critical among them are ACE inhibitors and beta-blockers. Amiodarone
might be useful in selected patients. The role of ICD therapy will not be
precisely answered until the results of SCD-HeFT become available.

20th Annual Scientific Sessions of the North American Society of Pacing and
Electrophysiology