Karthik Shekha,
MD, Joydeep Ghosh, MD, Deepak Thekkoott, MD,
MRCP (UK), Yisachar Greenberg MD
Department of Cardiology and Clinical Electrophysiology, Maimonides
Medical Center (Mount Sinai Health System), Brooklyn, New York.
Address for
correspondence: Dr Deepak Thekkoott MD, MRCP (UK), Department of
Cardiology
Maimonides Medical Center (Mount Sinai Health System), 4802 Tenth
Avenue, Brooklyn, New York 11219. E-mail:
Dkthekkoott@aol.com
Non ischemic dilated
cardiomyopathy (NIDCM) is a disorder of myocardium. It has varying
etiologies. Albeit the varying etiologies of this heart muscle
disorder, it presents with symptoms of heart failure, and rarely as
sudden cardiac death (SCD). Manifestations of this disorder are in many
ways similar to its counterpart, ischemic dilated cardiomyopathy
(IDCM). A proportion of patients with NIDCM carries a grave prognosis
and is prone to sudden cardiac death from sustained ventricular
arrhythmias. Identification of this subgroup of patients who carry the
risk of sudden cardiac death despite adequate medical management is a
challenge .Yet another method is a blanket treatment of patients with
this disorder with anti arrhythmic medications or anti tachyarrhythmia
devices like implantable cardioverter defibrillators (ICD). However
this modality of treatment could be a costly exercise even for affluent
economies. In this review we try to analyze the existing data of risk
stratification of NIDCM and its clinical implications in practice.
Key Words: Non
Ischemic Dilated Cardiomyopathy; Ischemic Dilated Cardiomyopathy; Risk
Stratification; Implantable cardioverter defibrillator; Sudden Cardiac
Death
Non-ischemic dilated
cardiomyopathy (NIDCM) is a primary disease of the myocardium,
characterized by dilatation of all four chambers of the heart, but
primarily the left ventricle, with associated systolic
dysfunction. The incidence of dilated cardiomyopathy is 5 – 8 /
100,000 / year1,2.
In an international heart failure study it was found that 18% of
symptomatic patients with ejection fraction less than 30% were
diagnosed with NIDCM3.
The age-adjusted mortality in patients with NIDCM ranges from 0.10 per
10,000 person-years among men aged 35-39 up to 1.16 per 10,000
person-years among men aged 55-572.
Currently, mortality in NIDCM is 12-13% at 3 years4. Independent risk factors for death
include smoking, diabetes mellitus, and high diastolic blood pressure2. Patients with NIDCM suffer from
heart failure mortality and sudden cardiac death in near equal numbers5. Sudden cardiac death (SCD) may
well be the first manifestation of NIDCM, and idiopathic NIDCM is
responsible for 10% of all sudden cardiac deaths in adults6. Survivors of SCD with NIDCM often
have recurrent ventricular fibrillation as their clinical arrhythmia7.
The majority
of SCDs occur among patients that are classically defined as low risk,
including those with NYHA functional class II or I. In the
MERIT-HF trial (NYHA heart failure class II-IV, EF < 40%), the most
common cause of mortality in patients with NYHA functional classes II
and III was sudden cardiac death8.
The incidence of SCD in NYHA class IV heart failure is also high but
the competing risk of pump failure makes it the second cause of death
in this very sick category of patients.
With the
advent of the implantable cardioverter defibrillator (ICD) and their
near-perfect termination of lethal arrhythmias, a determination needs
to be made of which patients would benefit most from ICD
insertion. In order to balance the potential risks of device
implantation and the associated cost, many investigators have sought to
establish risk factors to select patients with NIDCM who would benefit
most from ICD implantation.
Secondary Prevention Trials
Patients with
symptomatic NIDCM and documented ventricular tachycardia or ventricular
fibrillation (VT/VF) have a mortality rate of up to 22% in the first
two years after diagnosis. This is comparable to a similar group
of patients in the AVID registry with CAD9.
It has been clearly established that patients with symptomatic
sustained ventricular tachycardia and underlying structural heart
disease benefit from ICD implantation irrespective of the etiology of
their heart disease10-21.
Data from the AVID registry reveal a similar mortality rate in
patient’s surviving symptomatic VT or VF regardless of the underlying
nature of cardiac disease. The AVID trial, on the other hand,
randomized patients resuscitated from ventricular arrhythmias to either
ICD therapy or treatment with class III antiarrhythmic agents
(primarily amiodarone)22.
Patients were randomized (n=1016) and 3117 patients were followed in
the AVID registry. The registry comprised 73% of the patients
with CAD, while the remaining 27% were diagnosed as NIDCM. 54% of
NIDCM patients received ICDs, while 48% of CAD patients received ICDs.
Analysis of the registry revealed that the overall 2-year survival of
patients with NIDCM was 78.2%, which was similar to those with CAD.
Primary Prevention
Primary
prevention of sudden cardiac death is an important goal in the NIDCM
population. Two trials using amiodarone in a randomized fashion against
placebo have been performed in the NIDCM population. The GESICA trial
randomized 516 patients with predominantly non-ischemic
cardiomyopathies and ejection fraction <35% on optimal medical
therapy to amiodarone or placebo23.
The trial demonstrated a substantial reduction in all cause mortality
in patients treated with amiodarone (33.5% vs. 41.4% RR reduction 28%,
95% CI 4-45%) independent of the presence of ventricular arrhythmias.
Although the trial was randomized, it was criticized for its
non-blinded enrollment. Also many patients enrolled in this trial had
cardiomyopathy from Chaga’s disease, which is a very different group of
patients compared to NIDCM patients in the US or other parts of the
world.
Similarly,
CHF-STAT evaluated the use of amiodarone in a predominantly though not
exclusively ischemic cardiomyopathy population with > 10 PVCs /hr.
Although the overall study showed no mortality benefit of amiodarone
therapy, subgroup analysis of the 193 non-ischemic participants
demonstrated a trend towards reduction in all cause mortality24, with a P value of 0.07. One of the
intriguing findings of this randomized, double blind trial was that
arrhythmia suppression with amiodarone had no effect on survival.
The
Cardiomyopathy Trial (CAT) randomized 104 patients with NIDCM to ICD
placement versus optimal medical management and followed them for
greater than five years (5.5 ± 2.2 years). ICD therapy had
no significant benefit in comparison to medical therapy25. The trial may have been
underpowered to detect a survival benefit, as the overall mortality did
not reach the anticipated 30% in the control group.
The Amiodarone
Versus Implantable Cardioverter-Defibrillator in patients with
non-ischemic dilated cardiomyopathy and asymptomatic nonsustained
ventricular tachycardia (AMIOVIRT trial) evaluated empiric amiodarone
therapy vs. prophylactic ICD implantation in 103 patients with NIDCM,
EF <35%, and
asymptomatic NSVT. The three-year survival rate was 89% in both
arms of the study with no significant difference between amiodarone and
ICD placement in either survival or quality of life endpoints (the
trial was stopped at the first interim analysis). Patients
treated with amiodarone, however, showed a trend toward improved
arrhythmia-free survival compared to the ICD arm.
These two
smaller trials, evaluating optimal medical therapy25 and amiodarone4
against prophylactic ICD placement, have suggested medical therapy to
be as effective as ICD implantation in preventing all cause mortality
in asymptomatic patients with NIDCM and non-sustained ventricular
tachycardia (NSVT). A more definitive assessment of the benefit of
prophylactic ICD implantation in the NIDCM population was, however,
performed in the Defibrillators in Non-ischemic Cardiomyopathy
Treatment Evaluation (DEFINITE) trial. DEFINITE compared the use
of the ICD with standard oral medical therapy vs. medical therapy only
of patients with NIDCM and NSVT. Inclusion criteria for the trial
included EF <35%,
symptomatic heart failure, and documented ventricular ectopy (> 10
PVCs/hour) or NSVT on Holter monitor or telemetry within the last 6
months26. The trial
randomized 458 patients. Arrhythmia mortality accounted for 33% of
deaths. At 2 years, mortality in the medical therapy arm was
13.8%, and was reduced to 8.1 % in the ICD arm (p=0.06). The ICD
group had a 74% reduction in arrhythmic deaths (p < 0.05). The trial’s
primary endpoint (total mortality) failed to reach statistical
significance; however, ICD’s were associated with a significantly lower
rate of arrhythmic death, the study’s secondary endpoint. Subgroup
analysis found that male patients, EF < 20%, QRS duration > 120
msec, and NYHA Class III received the greatest benefit from ICD
implantation. NYHA class III was associated with a 67% risk reduction
in all cause mortality (p=0.009). The DEFINITE trial has also been
criticized for being underpowered.
The Sudden
Cardiac Death in Heart Failure Trial (SCD-HeFT) is a recently published
primary prevention trial. It enrolled patients with EF < 36%
and NYHA class II or III heart failure27
into three arms, medical therapy vs. medical therapy plus amiodarone
vs. medical therapy plus ICD. The endpoint of the study was
all-cause mortality. About half of the 2521 patients enrolled had
an underlying diagnosis of NIDCM. The five-year all-cause
mortality in the ICD group was 28.9%, compared to 34.1% in the
amiodarone group and 35.8% in the placebo group. This resulted in
a reduction in five-year all-cause mortality by 23% with ICD use
compared with the control group. Amiodarone had no effect on
survival. The conclusion is that ICD implantation saves lives
(but amiodarone doesn't) in patients with class 2 or 3 heart failure,
irrespective of the etiology of heart failure. It is interesting to
note that in patients with class III heart failure, irrespective of
etiology, ICD implantation was associated with a significant survival
advantage when compared to amiodarone but not when compared to placebo.
As a result of this large randomized, double-blind trial incorporating
a placebo arm, prophylactic ICD implantation in NIDCM patients with a
LVEF <36% and NYHA functional class II or III seems justified and
risk stratification in this group of patients may no longer be
required. Other patient groups (eg. LVEF 36-40% or NYHA class I
functional status) will, however, still need risk stratification.
Risk Stratification
Based on the primary
prevention
trials there seems to be still some controversy regarding improved
survival with ICD therapy in patients with NIDCM. It is believed that
benefit would be more readily achievable if a higher risk subgroup
could be selected instead of allocating this expensive therapy to the
broad population of patients with NIDCM. A number of diagnostic methods
have been used to risk stratify patients with cardiomyopathy for
elevated risk for sudden death. History of syncope28-30,
Electrocardiographic monitoring31-36, programmed electrical stimulation
(PES)37-56,
signal-averaged ECG (SAECG)56-58,
heart rate
variability48-59,
QT dispersion46, and
baroreceptor sensitivity
testing60, heart rate
turbulence63-65
have all been evaluated.
Syncope
Syncope may be
a harbinger of SCD. Comparisons of patients without documented
VT/VF but with a history of unexplained syncope and patients who have
survived documented cardiac arrest reveal similar mortality29. In one
particular trial 23 patients with NIDCM and syncope were compared to a
similar group of 201 patients that did not have syncope28. This
trial was non-randomized, with more frequent use of amiodarone in the
syncope group (p < 0.04). During the follow-up, there was no
statistical difference in mortality between the two groups.
However, 83% of the mortality in the syncope group was due to sudden
death, compared to 32% in the control group (P < 0.025).
Knight et al.
prospectively followed 14 patients who presented with unexplained
syncope and who were diagnosed with NIDCM, and had negative
electrophysiology study29
along with a control group of 19 patients
with NIDCM who sustained a cardiac arrest. All patients in both
arms of the study received an ICD. During the 24 ± 13
months of follow-up, 50% of patients with unexplained syncope received
appropriate ICD shocks in comparison to 42% of the patients who
received an ICD for cardiac arrest (P=0.1). Time to first
appropriate ICD shock actually occurred earlier in the syncope patients
as compared to those with cardiac arrest (32+7 vs. 72+12 months, p
=0.01). Due to the small number of patients in this study, the
results were not statistically significant. However, the trend
suggests that syncope is a marker for arrhythmic death in patients with
NIDCM.
Fonarow et al.
evaluated 147 patients with NIDCM, syncope, and severely decreased left
ventricular function30.
Twenty-five patients underwent ICD
implantation and were compared to 122 controls that were treated
medically. The 2-year survival was 84.9% in the ICD group
compared to 66.9% in the medically treated group (P=0.04). While
this trial was non-randomized, the ICD group had significantly improved
2-year survival although they had more frequent ventricular arrhythmias
during monitoring (56% vs. 15% P=0.0001).
These studies
suggest that unexplained syncope in patients with NIDCM is a grave
prognostic indicator with a significant proportion benefiting from ICD
implantation; however that is not to imply that absence of syncope
confers any protection from sudden death.
Electrocardiographic Monitoring
The prognostic
influence of electrocardiographic monitoring for the presence of
ventricular arrhythmias has been debated for nearly two decades. The
incidence of NSVT in patients with NIDCM varies from 33 to
79%31,32.
Survival in such patients at one year is 92%, and
decreases to 88% at two years4.
Huang et al. followed 35 patients
with recently diagnosed NIDCM that had ambulatory electrocardiographic
monitoring to evaluate for ventricular arrhythmias33. At baseline, 83%
had frequent PVCs, 93% had complex PVCs and 60% of patients had
NSVT. During follow-up of 34 ± 17 months there were 4
deaths, two of which were sudden. Of the two patients who suffered
sudden death during follow-up, one had no evidence of ventricular
arrhythmias at baseline. While this study showed a high incidence
of NSVT in the NIDCM population, it was not powered to show any
correlation between NSVT and sudden death.
Olshausen et
al. followed a group of 73 patients with NIDCM for a minimum of 3
years34. All patients
received ambulatory holter monitoring at
baseline. During follow-up, 38% of patients expired. The
deaths were evenly divided between those that died of pump failure and
those that died due to sudden death. NSVT was a risk factor for
death due to pump failure, but was not for sudden death. On the other
hand, Becker et al. followed 256 patients with NIDCM35. Of those,
99 patients had documented asymptomatic NSVT, while 157 controls with
NIDCM were free of documented ventricular arrhythmias. During the
22 ± 14 months of follow-up, both overall mortality and
mortality due to sudden death were higher in patients with NSVT than
those without arrhythmias (34.2 vs. 9.8%, P=0.0001 and 15.8 vs. 3.7%,
P=0.0037).
Grimm et al.
recently assessed a cohort of 343 patients with NIDCM using multiple
diagnostic tests to assess risk for sudden death36. During the 52
± 21 months of follow-up, 13% of patients had a major arrhythmic
event (sustained VT, VF, or sudden death). Ejection fraction was
found to be the only significant predictor of a major arrhythmic event,
with a relative risk reduction of 2.3 for every 10% increase in
ejection fraction (95% CI, 1.5 to 3.3, p=0.0001). The finding of
NSVT on holter monitoring was associated with a trend towards an
increased risk of major arrhythmic events (RR 1.7, 95% CI 0.9 to 3.3,
p=0.11).
The prognostic
value of NSVT or frequent ventricular arrhythmias remains unclear. The
weight of evidence suggest that it is predominantly a marker of risk
for all cause mortality but is not very effective in selecting a high
risk group for sudden arrhythmic death.
Electrophysiologic Testing
Programmed
electrical stimulation (PES) has been evaluated in NIDCM. The
studies performed were often non-randomized and had small numbers of
patients (Table 1). In
addition, the variability of stimulation
protocols makes assessment of predictive values difficult. Sustained
ventricular arrhythmias (monomorphic and polymorphic VT, or VF) may be
induced in up to 38% of patients with NIDCM undergoing PES, but this
may have limited clinical significance37.
The
reproducibility of programmed stimulation is greater in patient’s who
presented with clinical VT as opposed to those with ventricular
fibrillation. Milner et al. performed programmed stimulation in
19 patients with NIDCM and symptomatic ventricular arrhythmias; 10 had
survived an out-of-hospital cardiac arrest, 8 had monomorphic VT
(MMVT), and 1 had NSVT38.
The mean ejection fraction in this
group was 26 ± 9%. 13 (68%) of these patients had their
clinical arrhythmia reproduced in the EP lab. The most frequently
reproduced rhythm was MMVT (92%), while VF was reproducible in only one
patient (8%). Monomorphic VT induced with programmed stimulation
does appear to predict future occurrence of spontaneous monomorphic VT
of a similar rate and configuration38,39.
Nevertheless,
the diagnostic yield of PES in the NIDCM population has been poor.
Stamato et al. performed PES in 15 patients with NIDCM and heart
failure40. The mean
EF in this group was 17%, and they all had
NSVT on cardiac monitoring. PES in this group failed to produce a
sustained ventricular arrhythmia in any patients. Similarly, Das
et al. performed PES in 24 patients with NIDCM and a mean ejection
fraction of 25 ± 12%. While ventricular arrhythmias were
induced in 42% of patients, MMVT was seen in only 8% of the group.
Furthermore
the specificity of induced arrhythmias has been called into question.
The most common finding with PES in patients with NIDCM is inducible
polymorphic VT or VF37,41,39. Meinertz et al. evaluated 42
patients with NIDCM and performed PES in all patients41. 86% of
the study group had polymorphic ventricular arrhythmias, with three or
more beats of PMVT induced in 26% of the study group. During the
16 ± 7 months of follow-up, 5% of patients died of sudden
death. None of the patients who suffered sudden death had an
induced arrhythmia during PES. This suggests that the positive
predictive value of induced polymorphic ventricular arrhythmias is low
in the NIDCM population.
The use of PES
for risk stratification in the NIDCM population has not provided
satisfying results. Aside from the rare occasion of inducible MMVT, PES
may frequently result in the induction of non-specific
arrhythmias. The negative predictive value of a normal study is
poor as well.
Signal Averaged ECG
Several groups
have evaluated the performance of the signal averaged ECG (SAECG) to
stratify risk for SCD. Many of these studies did not
differentiate between CAD and non-ischemic causes of cardiomyopathy,
and were not powered for mortality in the NIDCM population. Galinier et
al. prospectively followed 151 patients with CHF, 48% of which were
diagnosed with NIDCM42.
At baseline, late potentials were
detected in 32.5% of the total patient population. 34% of the
NIDCM patients were found to have late potentials (similar to the
incidence of late potentials in patient’s with CAD). Late
potentials were not found to be predictive of overall mortality or
sudden cardiac death but did improve risk stratification for sustained
ventricular tachycardia.
In a group of
NIDCM patients, Fauchier et al. performed SAECG in 131 patients with
mean ejection fraction of 33 ± 12% and followed them for 54
± 41 months43.
Late potentials were present in 27% of the
patients. During follow-up, 15% of the patients had major
arrhythmic events. Patients with late potentials were found to be
at increased risk of all-cause cardiac death (RR 3.3, 95% CI 1.5 to
7.5, P = 0.004) and of arrhythmic events (RR 7.2, 95% CI 2.6 to 19.4, P
= 0.0001), but not sudden death.
The studies of
SAECG in the NIDCM population are complicated by the inclusion of
individuals with bundle branch blocks(BBB), which compromises the
utility of the SAECG as an adequate method for risk stratification in
this population. Mancini et al. evaluated 114 patients with NIDCM
with SAECG44. In the
first year of follow-up, survival was 95% in
patients with a normal SAECG, 88% in patients with a BBB, and only 39%
in patients with an abnormal SAECG (P < 0.001). During
follow-up, of the 20 patients with an abnormal SAECG, 5 (20%) suffered
a sudden death, and three others either died from progressive heart
failure or required urgent cardiac transplantation. This suggests
that an abnormal SAECG confers an increased risk for an arrhythmic
episode within a relatively short follow-up period. This study
was flawed, however, because of the non-uniform implantation of ICDs in
the study group, with patients with BBB having significantly more ICDs
placed at baseline (P < 0.05).
An abnormal
result on SAECG may be a marker of increased risk of sustained
ventricular tachycardia or death43,44. As such, the SAECG
appears to have an excellent negative predictive value, with the caveat
that the presence of bundle branch block may significantly decrease the
specificity of SAECG45.
However, the poor positive predictive
value for arrhythmic events and decreased specificity in the
significant number of patients with bundle branch block lessens the
value of this test.
QT Dispersion
QT dispersion
(QTd) has been studied in the risk stratification of SCD in patients
with NIDCM. Few studies have been done, and the results have been
unfavorable. Grim et al. performed QT dispersion and related measures
in 107 patients with NIDCM and 100 controls without structural heart
disease and followed them for 13 ± 7 months46. During
follow-up, 11% of patients with NIDCM had an arrhythmic event, defined
as sustained VT, VF, or sudden death. QT dispersion was noted to
be increased in patients with arrhythmic events compared to patients
without an arrhythmia during follow-up (76 ± 17 vs 60 ±
26 ms, P=0.03). On the other hand, corrected QT dispersion (QTc)
and adjusted QTc were not statistically different between those with
and those without arrhythmias during follow-up (80 ± 21 vs 75
± 35 ms, and 27 ± 6 vs 24 ± 10 ms). This modality
is limited due to the overlap between groups with positive and negative
results. The Marburg Cardiomyopathy Study36,
confirmed that QT
dispersion does not significantly risk stratify patients for sudden
death.
HR Variability
Measures of
autonomic function have been evaluated to assess risk for SCD.
Heart rate variability is an indirect measure of autonomic tone.
Previous studies have shown that heart rate variability (HRV) is
predictive of arrhythmic events following myocardial infarction (Table 2). The ATRAMI
(Autonomic Tone and Reflexes After
Myocardial Infarction) study showed that both decreased HRV and
baro-receptor sensitivity, another measure of autonomic tone, are
associated with worse outcomes in patients after myocardial
infarction47.
HRV was
evaluated in 70 patients with NIDCM and prophylactic ICD
implantation. Patients with sustained ventricular arrhythmias as
recorded by their defibrillator had similar HRV to those who had no
arrhythmic events48.
Other trials have shown that in patients
with NIDCM, HRV was predictive of cardiac death but not ventricular
arrhythmias49,50.
Patients with NIDCM have decreased heart rate
variability. However, this decrease is associated with systolic
ventricular function, and does not correlate with increased risk of
ventricular arrhythmias49. The weight of the evidence suggests
that due to the poor positive predictive value of HRV, this test has no
role in the risk stratification for sudden death of patients with
NIDCM48-50.
Baroreceptor Sensitivity Testing
Studies of
baroreceptor sensitivity (BRS) in the NIDCM population have not focused
on risk stratification for sudden death until recently36. Menz et al.
compared BRS against heart rate variability in a series of 179 patients
including those with CAD (27%) and NIDCM (73%)51.
This trial was
designed to determine if there were any differences in these two
diagnostic tests in a baseline group of patients with decreased
EF. It was not designed for assessment of prognostic value.
Baroreceptor sensitivity was comparable in patients with CAD and NIDCM
(6.1 ± 3 vs 6.9 ± 5 ms/mmHg, P=NS).
Grimm, et at.
Performed an exhaustive trial of risk stratification techniques in
patients with NIDCM, including BRS36.
343 patients with NIDCM
underwent BRS testing, with 26 patients (10%) being excluded due to
insufficient response to phenylephrine during BRS testing. No
correlation was noted between BRS results and sudden death during the
52 ± 21 months of follow-up. The evidence to date suggests that
BRS is not a reliable risk stratifier for sudden death in NIDCM, and
may not have additional benefit over other markers of autonomic tone,
such as heart rate variability.
Microvolt T Wave Alternans
Microvolt T
Wave Alternans (TWA) is due to beat-to-beat alterations in cellular
repolarization due to changes in action potential duration. Kitamura et
al described an increased risk of SCD or sustained VT/VF in patients
with a history of NIDCM with occurrence of microvolt level TWA at
sufficiently low heart rate52.
Onset of TWA with heart rates
below 100/minute conferred increased risk of SCD or sustained VT/VF,
with a predictive accuracy of 78%52.
The onset HR of patients
with TWA is independent of the more standard risk factors, including LV
ejection fraction, gender, systolic or diastolic BP, or NYHA functional
class. This makes it attractive in risk stratifying patients with
NIDCM. Unfortunately TWA can be indeterminate in as many as 20%
of patients with NIDCM52, 53.
Combining it with the presence of
late potentials on SAECG54
may increase the sensitivity of TWA.
A recent study
by Hohnloser et al looked at 137 patients with NIDCM referred to a
single center for diagnosis or management of heart failure or
evaluation of symptomatic arrhythmias55.
The follow-up was 14
± 6 months, with endpoints defined as sudden death and
hemodynamically unstable VT or VF. 37 patients in the study had
prior ICD implantation. TWA at heart rates <110/minutes had a
positive predictive value of 22% ± 5% and a negative predicative
value of 94% ± 4%. The strong negative predictive value of
sustained TWA demonstrated in this study at heart rates <110 bpm
suggests a role of TWA testing in risk stratification of patients with
NIDCM (Table 3). Further
studies to look at larger, more
diverse populations, long-term follow-up, and the benefits of serial
TWA measurements will clarify the role of this test in risk
stratification of patients with NIDCM.
Heart Rate Turbulence
Heart rate
turbulence is an emerging risk profiling method in patients
with heart disease63-65.
It is a method which is based on the
electrical property of the heart after a ventricular ectopic beat and
can be measured from a 12 lead electrocardiogram or holter monitoring.
Immediately post ventricular ectopic beat the native ventricular
response accelerates (due to baroreflex activity because of decreased
cardiac output) and followed by a slow deceleration back to normalcy.
Measurement of these variables when studied along with other risk
factors has shown superior risk prediction for sudden cardiac death.
This method however will need to be validated with prospective clinical
studies.
Conclusion
As the
treatment of heart failure from Non-ischemic dilated
cardiomyopathy CHF becomes more refined, it is expected that
death from pump failure will be delayed, and risk stratification of
these patients for arrhythmic death will become more important.
Proper risk stratification based on symptoms, signs, and judicious use
of noninvasive and invasive testing is important to determine the
subgroup of patients that would benefit most from ICD
implantation.
The most
effective treatment and prophylaxis for SCD is implantation of an
ICD. Due to the considerable cost considerations of these devices
it would probably be uneconomical to place these devices in all
patients with NIDCM. While it may be expected that the price of
these devices individually will decrease over time, due to the
increasing number of expected implantations the overall cost to the
healthcare system is not likely to diminish. More over majority of the
health systems cannot afford these expensive devices on a “blanket”
basis. When compared to similar patients with ischemic cardiomyopathy,
it appears that the non-ischemic dilated cardiomyopathy patient has a
less certain clinical course in terms of sudden cardiac death.
Most of the current trials of risk stratification for patients with
NIDCM, with the exception of the SCD-HeFT trial, are underpowered and
non-randomized. Clearly further studies that define the precise
role of various risk stratification modalities need to be performed.
Current indications for ICD implantation miss a fairly large number of
patients at risk for sudden death. Appropriate primary prevention and
secondary prevention of cardiac arrest in this population will require
effective risk stratification to allow delivery of life saving therapy
in an economically reasonable fashion.
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