Management of SCD survivors has changed since the 
use of ICDs, which offer better survival than traditional
treatment with anti-arrhythmic drugs. None of the 
criteria used to test the risk of arrythmia recurrence 
has been proved reliable. The recurrence rate is very 
high and the sense of security gotten from EPS testing is 
unjustified.
	Those who are in the worst condition will simply 
be saved from sudden death to die from other forms of 
cardiac death in about the same amount of time. One must 
answer the question of whether this is useful or not.
	On one end are patients with little structural 
disease, whose only risk factor *can* be controlled by ICD.
	In the middle, a majority of patients deserve 
various approaches which can improve their long term 
outcome. In this group, to select ICD instead of anti-
arrhythmic drug treatment can affect survival. Such 
patients with an ICD are not exposed to drug side-effects
and can be treated with lower doses, or with beta-blockers
and ACE inhibitors because of their ICD.
	In recent years, much has been learned about SCD 
and we know the mechanisms to be complex. However, 
guidelines for management of SCD survivors are simpler 
than they used to be, thanks mainly to ICDs. The main 
condition leading to SCD is coronary artery disease (CAD),
which accounts for more than 80% of total cases. SCD is 
the first sign of CAD in 25% of them. Cardiomyopathies, 
inflammatory diseases, drug toxicity, and electrolyte 
disorders such as long QT syndrome are responsible for 
another 10-15%. The remainder are patients with no 
apparent heart disease, who have lethal abnormalities. 
The "Brugada syndrome" is one example.
	EF, and, perhaps more important, functional class,
are the main prognosis indicators. Patients with very low 
EF of less than 25%, and Class 3-4 are at highest risk for 
death. Their survival does not usually seem improved even 
by ICD, which stops lethal arrhythmias but leave the 
underlying disease unchanged. The result is a shift from 
SCD to non-SCD, without benefit on overall survival.
	On the opposite end are SCD survivors with slight 
or no apparent heart disease at all. Their long-term 
outcome depends totally on getting rid of this risk factor.
In this area, efforts should be concentrated on correct 
specific diagnoses, so any underlying condition is 
properly treated.
	Between these 2 extremes lie most patients, with 
structural heart disease and balanced risk of SCD and non-
SCD. Their outcome can be improved both by treating the 
underlying disease and by arrhythmia prevention.
	Ventricular fibrillation (VF), ventricular flutter 
and fast polymorphic ventricular tachycardia (VT) cause 
most Sudden Cardiac Death. SCD survivors may not have an 
inducible arrhythmia. VF is the first arrhythmia in 88% of 
cases.
	Despite the strong relationship between the number 
and complexity of recorded premature ventricular beats and
the risk of SCD, Holter has not turned out to be a 
reliable indicator. There is high day-to-day variability in
many arrhythmias. CAST and other studies have proved that 
even successful suppression with class 1 drugs can retain 
deadly risk of late pro-arrhythmia. Ambulatory monitoring 
has lost most of its impact on the decision making process.
	Inducibility of ventricular arrhythmias with EP 
testing has been widely used as a reliable way to confirm 
an arrhythmia, select type of treatment and confirm the 
treatment's effectiveness. Several problems emerged which 
greatly reduced the predictive value of EP testing for 
managing SCD survivors.
	First, re-examination has shown that all-type 
inducibility in true aborted SCD patients is less than 50%,
as compared with more than 80% in patients with re-entrant
monomorphic VT.
	Second, the rate of suppression of any type of 
ventricular arrhythmia with anti-arrhythmic drug is highly
variable (22-78%) owing to many factors: different patient
populations, EF, low reproducibility, co-existence of 
different mechanisms and more.
	Third, although suppression of inducibility 
(obtained in 26-78% of cases) seems to predict better 
recurrence-free survival than persistent inducibility, the 
cost/ benefit ratio of invasive EP guided treatment 
appears unfavourable when compared with non-drug approaches.
EP testing can uncover other arrhythmias, like monomorphyc 
VT, which may co-exist and can be treated.
	The effectiveness of drug treatment in preventing 
SCD is limited and such drugs can be dangerous, 
particularly in patients with low EF treated with Class 1 
sodium channel blocking anti-arrhythmic agents. Treatment 
with such drugs, either guided by EP testing, or by 
ambulatory monitoring is significantly less effective than 
ICD. Class 3 drugs - amiodarone and sotalol - are associated
with longer survival than Class 1 A,B and C agents, as 
shown by CASCADE and ESVEM trials.
	Recurrence rates in patients treated with 
amiodarone can be as high as 31% and there are cardiac side
effects. The ESVEM trial, from which sotalol gained much of 
its popularity, included only 22% SCD survivors. Sotalol 
remains to be proven the outcome of SWORD trial is not a good 
indicator for its safety profile, regarding its Class 3 
action in high risk patients.
	Empiric treatment with beta-blockers is as good as 
EP guided treatment. Beta-blockers are valuable to control 
"environmental" triggers for VF in patients who tolerate them.
Beta-blockers are not pro-arrhythmic. A similar favourable 
effect can be had from ACE inhibitors.
	ICDs have greatly improved. Operative mortality is 
now less than 1%. ICDs can now be implanted by cardiologists
without surgical support. New software allows many patients
to remain free of shocks. Pacemaker backup is an option, 
highly beneficial and life-saving in some cases, notably in 
bradyarrhthmia. The added complexity of devices, instead of 
leading to adverse effects, has turned out to improve survival.
	Recent studies in patients with VF or fast ventricular
tachycardia (VT) and low EF have provided strong evidence that
ICD is superior to all anti-arrhythmic drugs in terms of 
survival from arrhythmic sudden death. In some cases, ICDs 
even protect from non-arrhythmic heart death. The AVID study 
compared ICD and anti-arrhythmic treatment (amiodarone in most 
cases and sotalol). Survival at 1 and 3 years was 89% and 75%
in the ICD group versus 82% and 64% in the drug treatment 
group, which means a 38% improvement of risk for ICD.
	In patient populations with very low EF (less than 
25%), the presence of Class 3-4 heart failure is the main 
indicator of poor outcome. One study showed that these 
patients receiving an ICD have longer survival on the medium 
term, compared with those on anti-arrhythmic drugs. Those with
ICD have an outcome only slightly worse than those who had 
anti-arrhythmic surgery. Therefore, the benefit of ICD 
treatment is not predictable in these patients and the 
choice cannot be cost-effective in most cases, unless it is 
intended as a "bridge" towards definite intervention such as
transplant.
	An unexpected result of these studies is that ICD 
patients have better survival rates not only in terms of 
arrhythmic death, but also general cardiac mortality. This 
raises criticism on the design of the trials. There are 
some logical explanations: ICD patients benefit from regular
visits at the outpatient clinic and those not treated with 
drugs probably benefit both from not being exposed to the 
side effects of drugs, and from being better treated with 
beta-blockers and ACE inhibitors, which are rarely used in 
combination with anti-arrhythmic drugs.
	Despite the advantages of ICD, the number of implants
vary from nation to nation and even among institutions. 
This reflects cultural and technical differences but more 
importantly, economic concerns about the high cost of the 
devices and of the patients' follow-up, which many health 
care systems cannot afford.

Title: Management of Sudden Cardiac Death Survivors
Authors: Andrea Finzi MD, Ruggero Manfredini MD, Paola 
Montanari MD, Ferdinando Maria Massari MD, Francesco 
Ambrosini MD, Fulvio Bellocci MD* and Salvatore Romano MD
From: the Department. of Cardiovascular Sciences, 
Ospedale Maggiore di Milano, IRCCS, Milan, Italy and the 
Institute of Cardiology, Policlinico Universitario "A. 
Gemelli", Rome, Italy
From: HeartWeb 4(1), 1998