Download EP show 2

The EP show:
sudden death, part 1
Eric Prystowsky MD
Director
Clinical Electrophysiology Laboratory
St Vincent Hospital, Indianapolis, IN
Douglas P Zipes MD
Director, Division of Cardiology and
Krannert Institute of Cardiology
Indiana University School of Medicine
Indianapolis, IN
Robert J Myerburg MD
Professor of Medicine and Physiology
Director, Division of Cardiology
University of Miami School of Medicine
Miami, FL
Incidence of sudden cardiac
death
Since 1970, sudden cardiac death has been
estimated to represent about 50% of all
cardiovascular deaths, or 300 000 annually.
Although the true incidence is not known, it is
now likely to be higher given a greater
number of chronic heart disease patients at
risk in a growing and aging population.
Risk categories for sudden
death
In the adult population, aged 35 and over, the
incidence of sudden cardiac death approaches
0.1-0.2% per year or 1 in every 500-1000
individuals.
In the adolescent and adult population below
30, the incidence of sudden cardiac death is
approximately 1 in 100 000, and is slightly
higher for athletes.
Current intervention strategies
for sudden cardiac death
Other than general disease prevention
measures applicable to the population at large,
intervention strategies focus on patients who
are post-myocardial infarction, and who have
low ejection fractions and arrhythmic markers
of risk.
The highest risk groups have a 10-30% risk
per year. Many studies are now concentrating
on populations at moderate risk, eg, heart
failure patients.
Intervention strategies for the
general population
Most noninvasive electrophysiologic markers
are not helpful in determining risk in the
general population, in patients with multiple
risk factors, or in low risk post-MI patients.
Sudden death is the marker for coronary
disease in 20-30% of sudden deaths whose
etiology is ischemia.
Future noninvasive risk factors may include a
profile of inflammatory markers in addition to
genetic profiling.
Ischemia and sudden death
It has been well documented that only about
20% of the patients who are resuscitated from
ventricular fibrillation (VF) and then
hospitalized evolve transmural infarction.
Yet 3/4 of these patients are also found to have
coronary artery disease.
Also, autopsy data shows that a significant
number of patients who die from VF have
severe coronary disease, often with signs of
recent plaque disruption.
Precipitants of ventricular
fibrillation
The precipitant of VF in those patients who are
found not to have an evolving infarction or
ischemic markers is unknown.
Several possibilities include coronary
vasospasm, and transient thrombotic events in
the coronary arteries which produce ischemia
but not infarction.
An implantable ischemic sensor device which
measures wall motion abnormalities or STsegment shifts may be useful in this regard.
The evolution of the
ambulatory CCU
“But if you stop and think of how we take
care of outpatients, it's much like we took
care of the infarct 30 years ago. A patient
comes and sees you and you write a script
for whatever it is and you send the patient
home. And he comes back a month or 3
months later, if he's still alive, and then you
continue therapy.”
Douglas P Zipes MD
Indiana University School of Medicine
Indianapolis, IN
Multicenter Automatic
Defibrillator Implantation Trial
Prophylactic therapy with an implantable
cardioverter-defibrillator was compared with
conventional medical therapy in a high-risk
group of 196 post-MI patients.
Over an average follow-up of 27 months,
therapy with the ICD led to improved survival
when compared with conventional therapy
(hazard ratio for overall mortality, 0.46; 95
percent confidence interval, 0.26 to 0.82;
P=0.009).
Moss AJ, et al. N Engl J Med 1996;335:1933-1940
Multicenter Unsustained
Tachycardia Trial: protocol
Electrophysiologic studies
Registry
(n=1435)
Randomization
(n=704)
sustained VT
not inducible
sustained VT
inducible
Conservative therapy
(n=353)
EP-guided therapy
(n=351)
ACE-inhibitors and
beta-blockers
ACE-inhibitors and
beta-blockers
Buxton AE, et al. N Engl J Med 1999;341:1882-1890
MUSTT results
EP guided therapy showed a reduction in
primary endpoints:
27% reduction in arrhythmic death and
cardiac arrest
trend toward overall reduction in
mortality (20% risk reduction)
The entire benefit derived from EP-guided
therapy was due to treatment with implantable
defibrillators.
Buxton AE, et al. N Engl J Med 1999;341:1882-1890
Secondary prevention of
sudden cardiac death: CASH
The Cardiac Arrest Study, Hamburg
Survivors of cardiac arrest secondary to
documented ventricular arrhythmias were
randomized to an ICD or medical
antiarrhythmic therapy (288 patients total).
There was a nonsignificant trend toward higher
survival in patients assigned to ICD therapy.
Kuck KH, et al. Circulation 2000; 102(7):748-754
Secondary prevention of
sudden cardiac death: CIDS
The Canadian Implantable Defibrillator Study
659 patients with resuscitated VF, ventricular
tachycardia (VT), or unmonitored syncope were
randomized to ICD or amiodarone therapy.
Nonsignificant relative risk reductions of 20%
and 33% were found to occur in all-cause
mortality and arrhythmic mortality in the ICD
group compared to amiodarone.
Connolly SJ, et al. Circulation 2000; 101(11):1297-1302
Secondary prevention of
sudden cardiac death: AVID
Antiarrhythmics Versus Implantable
Defibrillators study
1016 survivors of VF or VT were randomly
assigned to either ICD or antiarrhythmic-drug
therapy.
Over three years, statistically significant
relative reductions in mortality from 27-39%
were seen in the ICD group.
The Antiarrhythmics Versus Implantable Defibrillators
(AVID) Investigators. N Engl J Med 1997;337:1576–1583
AVID data and heart failure
Combined data from secondary prevention
trials, and AVID data alone, show that patients
with ejection fractions above 35% did not
receive additional benefit from an ICD
compared to amiodarone alone.
The 2 therapies offered have equal outcomes.
Domanski MJ, et al. J Am Coll Cardiol 1999;34:1090-1095
AVID data and mortality risk
AVID registry data suggests that there is a high
mortality rate for patients with VF and VT
thought due to reversible factors, and for
patients who manifest only asymptomatic VT.
This mortality rate is similar to the rate for
more high-risk ventricular arrhythmias and
suggests that clinical judgment regarding
reversibility and recurrence risk is not very
accurate.
Anderson JL, et al. Circulation 1999;99:1692-1699
Persistence of reversibility
Early studies attributing sudden cardiac death
to MI relied on the presence of enzymes, new
Q waves and a clinical history of pain preceding
the onset of cardiac arrest.
New data are highlighting the distinction
between reversibility and persistence of
reversibility in cardiac arrest survivors.
For example, active plaque pathophysiology in
cardiac arrest victims (present in 40-70%) may
be reversible, but not permanently reversible.