(Circulation. 2000;102:611.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Acute Coronary Findings at Autopsy in Heart Failure Patients With Sudden Death
Results From the Assessment of Treatment With Lisinopril and Survival (ATLAS) Trial
From the University of Texas Medical Branch, Galveston (B.F.U.); Aarhus University Hospital, Aarhus, Denmark (K.T.); the University of Alberta, Canada (P.W.A.); the University of Hull, UK (J.G.C.); the University of Adelaide, Australia (J.D.H.); the University of California, San Francisco (B.M.M.); Columbia University, New York, NY (M.P.); Imperial College School of Medicine, University of London, UK (P.A.P); and Karolinska Institute, Stockholm, Sweden (L.R.).
Correspondence to Barry F. Uretsky, MD, 5.106 JSHA, Galveston, TX 77555-0553.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background—Sudden unexpected death frequently occurs in chronic heart failure. The importance of acute coronary events in triggering sudden death (SD) is unclear.
Methods and Results—We evaluated at autopsy the prevalence of acute coronary findings (coronary thrombus, ruptured plaque, or myocardial infarction [MI]) and their relation to SD. Autopsy results in 171 patients in the randomized ATLAS trial were reviewed. The prevalence of acute coronary findings was 33%: in 54% of patients with significant coronary artery disease (CAD) who died suddenly, 32% who died of myocardial failure, but in non-CAD patients, they were present in only 5% and 10% respectively. The percentage of patients classified as dying of MI was 28% in the autopsy group versus 4% in the nonautopsied group (P<0.0001). Of the autopsied group with acute MI, 97% (31 of 32 patients) with SD and 40% (6 of 15 patients) with myocardial failure did not have the MI diagnosed during life. When undiagnosed MI was classified as "sudden unexpected" or "myocardial failure" from clinical information only, the distribution of death causes was similar in the autopsy and nonautopsied groups.
Conclusions—Acute coronary findings are frequent and usually not clinically diagnosed in heart failure patients with CAD, particularly in those dying suddenly, suggesting the importance of acute coronary events as a trigger for SD in this setting.
Key Words: death, sudden • heart failure • ischemia
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Heart failure (HF) has become an increasingly prevalent cause of death worldwide. Despite advances in therapy, mortality rates remain high, with annual rates of 10% to 20% in patients with moderately severe to severe failure. Sudden unexpected death constitutes 30% to 50% of all deaths.1 Although sudden deaths (SD) are often considered arrhythmic, the rate of acute coronary events in this setting is uncertain. Clinical studies in patients with significant coronary artery disease (CAD) without HF have implied that a primary arrhythmia without an acute ischemic event may be the primary mechanism of SD in the majority of patients.2 In autopsy series, however, acute coronary findings are often present in patients who die suddenly, particularly those with CAD.3 4 5 6 In autopsy studies, a fresh thrombus, recent myocardial infarction (MI), or plaque rupture was found in 57% to 73% of CAD patients without HF who died suddenly.3 4
The relative importance of an acute coronary event as a
trigger for SD in patients with HF is currently unknown. Recurrent MI
is a frequent cause of terminal myocardial failure in patients with
chronic CAD but has inconsistently been described in studies of
HF patients. The frequency of recurrent MI compared with other causes
of death in HF is unclear because most large clinical trials have not
classified MI as a cause of death. As CAD accounts for 
50% of HF
patients in the Western world, it is possible that acute
coronary events contribute importantly to the progression of HF
and SD.
The ATLAS (Assessment of Treatment with Lisinopril and Survival) trial provides a unique opportunity to address this issue because there were many HF patients who underwent autopsy and were classified by means of prospectively developed definitions of mode and cause of death.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
ATLAS Trial Design and Results
The ATLAS trial was a prospective, international, multicenter, randomized, double-blind, parallel-group study comparing the effects on mortality and mortality plus morbid events of a low (2.5 to 5.0 mg) to a high (32.5 to 35 mg) dose of the ACE inhibitor lisinopril in 3164 patients with moderate to severe HF caused by systolic dysfunction followed for a median of 41.2 months with 100% complete follow-up data. Primary results showed a trend to decreased mortality rate (8%) in the high-dose group and a significant 12% reduction in the risk of all-cause mortality plus all-cause hospitalization. There were 1383 deaths during follow-up (mortality rate 43.7%). Autopsy was performed in 188; data were available to determine the cause of death in 171 (12.4%) patients (present study group).
Clinical Classification of Deaths and Ischemic Events
Definitions for cause of death and MI were as follows: Sudden
unexpected death was defined as death that was sudden and unexpected,
including observed arrhythmic deaths and those not attributable to
intractable myocardial (heart) failure or other identifiable cause.
These deaths were classified as witnessed or unwitnessed and if
unwitnessed, the time interval between death and the last time another
individual saw the patient alive: (a) <1 hour, (b) 1 to 24 hours, or
(c) >24 hours. Patients who had sudden loss of consciousness, who were
successfully resuscitated, and who ultimately died of sequelae such as
pneumonia were also classified as SD and formed the ">24-hour SD"
group. If an autopsy was performed in a patient who died suddenly and
evidence of a recent MI was found, the death was classified as
secondary to MI.
Myocardial (heart) failure was defined as death from pump failure, even
if the terminal event was an arrhythmia. Myocardial infarction
was defined as death occurring 
28 days after "definite" or
"probable" MI. Other cardiovascular was defined as
death occurring from a cardiovascular event other than
those specified in the above 3 categories, including cerebrovascular
accident, pulmonary or peripheral thromboembolism,
cardiovascular procedural deaths from cardiac surgery,
angioplasty, aortic aneurysm rupture or dissection, or other
vascular causes not covered elsewhere.
Noncardiovascular death was defined as death as the
result of any other cause not included in the categories above.
Myocardial infarction as an ischemic event was defined as
follows: a definite MI included (1) significant new Q waves with or
without a typical history with characteristic rise and fall of
biochemical markers, (2) a rise and fall of biochemical markers, in
which the maximum value was 2 times the normal upper limit, with or
without a typical history and/or equivocal ECG, or (3) postmortem
evidence. A probable MI was defined as typical or atypical history with
equivocal or no ECG abnormalities plus a typical rise and fall of
biochemical markers in which the maximum value was <2 times the normal
upper limit.
Clinical records were reviewed by the Endpoints Committee. If the treating physician noted the diagnosis of MI on the hospital record or biochemical markers were drawn and elevated, it was considered that the physician was aware of the possibility of an MI before death.
Autopsy Review
Each autopsy report was reviewed for the cause of death, the
presence of recent and old MI, premortem coronary thrombus,
plaque rupture, and the presence of significant (>70%
stenosis) CAD. When CAD severity was not quantified,
significant CAD was considered present if the examiner classified
CAD as "severe" or "class III or IV." Class I or II or
"mild" or "moderate" obstruction was not considered significant
CAD. MI was considered acute if there was a necrotic area related to a
vascular territory and considered "acute" by the examiner.
"Diffuse hemorrhagic areas" and "patchy necrosis" were not
considered an acute MI because these findings may have developed during
the period of terminal myocardial failure with hypotension. "Acute
coronary findings" included premortem coronary
thrombus, ruptured plaque, and/or the presence of a recent or acute
MI.
The underlying cause for HF was based on the investigator-provided case report form. The mode (sudden versus nonsudden) and cause of death were classified by the Endpoints Committee, who were blinded to the patient’s treatment. Consensus was reached in all cases, and deaths could be classified in 99.1% of cases.
Statistical Analysis
A 
2 test for categoric and 2-tailed
Student’s t test for continuous variables were used
where appropriate to compare groups.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Clinical Characteristics of the Study Group
Patients who died had, in general, worse baseline characteristics compared with survivors (full listing available from authors on request). They were older, more frequently in New York Heart Association class IV, with a longer duration of symptoms, and a higher prevalence of CAD. Patients undergoing autopsy, however, were similar as a group to patients who died and did not have an autopsy (full listing available from authors on request). The largest number of patients were from Sweden (n=42), Czech Republic (n=40), United States (n=24), United Kingdom (n=22), Canada (n=12), and Hungary (n=12). However, autopsy rates were quite variable, ranging from 2% (United States) to 27% (Czech Republic) (full listing available from authors on request).
Of the 171 study patients, there were 92 diagnosed clinically
with ischemic cardiomyopathy (ICM) alone
(54% of the study group), 17% idiopathic, 13% ICM and hypertension,
5% with no cause listed, 4% hypertension, 2% each for
valvular heart disease, ICM and valvular heart disease,
and other clinical combinations, and 0.6% for each of ICM plus
idiopathic and ICM plus hypertension plus idiopathic (Table 1
). Of those diagnosed clinically
as having ICM alone (n=92) or in combination with another diagnosis
(n=28), 83% actually had significant CAD at autopsy (Table 1).
Of the 51 patients diagnosed clinically as having a nonischemic
cause or with no diagnosis listed, 31% actually had autopsy-documented
significant CAD. In summary, there were 116 patients at autopsy with
significant CAD, 53 patients with normal or near-normal
coronary arteries, and 2 with unclear severity of CAD.
|
In patients with ICM alone or in combination with another
clinical diagnosis, mortality rate during the study was 48% (974 of
2035 patients) compared with 36% (409 of 1129) of non-ICM patients.
The causes of death in the autopsy and nonautopsy groups are shown in
Table 2 (first 2 columns). A
"correction" (third column of Table 2, discussed below)
assumed that autopsied patients were classified from clinical
information alone. For the "other cardiovascular"
and "noncardiovascular" deaths, the distribution of
causes was similar in the 2 groups. In addition, there were similar
causes of death in the patients diagnosed clinically in the ICM and
non-ICM groups except that there were fewer MI deaths in the non-ICM
group both in the entire cohort and the autopsied group (Table 3). This difference was magnified if
patients were classified by the actual presence of CAD at autopsy
rather than by clinical diagnosis (Table 3).
|
|
We investigated whether differences in causes of death could be explained by the autopsy results. Of 47 patients with MI as cause of death, 32 patients (68% of the MI group) died suddenly: In all but 1, MI was clinically unsuspected, with the autopsy findings providing the sole basis for diagnosis. Hence, if these patients had not had autopsies, they would have been classified as "sudden unexpected." Of the 15 patients with acute MI on autopsy who died of myocardial failure, 6 (40%) were not diagnosed during life as having an ischemic event. These patients without an autopsy would have been classified as "myocardial failure."
Causes of Sudden Death
SD causes in the autopsy group are shown in Table 4. Autopsy showed no specific pathology
to explain SD in 51%, suggesting a primary arrhythmia, MI in
42%, with a small percentage of SD (2%) classified as
noncardiovascular. One of the 2 patients had cancer. He
died suddenly and unexpectedly in the hospital. This death may have
reasonably been classified as "sudden unexpected." Thus, only 1
patient with unexplained SD (1.2% of cohort), with a gastrointestinal
bleed at autopsy, probably died of a noncardiovascular
cause.
|
Autopsy Findings
There were 56 patients with findings suggesting an acute
coronary event (33%). There were 7 patients with fresh
thrombus, 1 of whom had a ruptured plaque. All had significant CAD at
autopsy. There were 3 patients with fresh thrombus and acute MI; all
showed significant CAD. There were 46 patients with only recent
myocardial necrosis. Significant CAD was present in 42 (91.3%).
The 4 non-CAD patients with recent MI had the following: (1) 3 with
dilated cardiomyopathy, normal coronaries without
thrombus, and myocardial necrosis and (2) 1 with endocarditis and
mesenteric infarction. It should be noted that of these 56 patients
found to have acute coronary findings, death was classified as
MI-related in 47 patients only. Four patients were classified as
myocardial failure, 1 with severe myocarditis, believed to be the
primary cause of death, and a right coronary thrombus premortem
but considered incidental; in the other 3, the autopsy report
documenting recent MI was provided after unblinding. Had these reports
been available, these 3 deaths would have been classified by the
Endpoints Committee as "MI." One patient was classified as
"sudden unexpected" death; the autopsy report received after
unblinding showed acute MI. Four other patients had either MI (n=3) or
thrombus (n=1) but were classified as "other
cardiovascular" because another process was believed
to be the primary cause of death (2 deaths after bypass surgery, 1
cerebrovascular accident, and 1 mesenteric infarction). There were 103
(60%) patients with autopsy evidence of an old MI. Of these, 90 (87%)
had significant CAD.
Acute coronary findings were present in 56 (36%) of 155
patients who died of a cardiovascular cause (all
cardiac except for 1 case of cerebrovascular accident with MI at
postmortem as noted above) and in no patient who died of a
noncardiovascular cause (P=0.003) (Figure 1, left). Acute coronary findings
were more prevalent in CAD patients (P=0.001) but not
confined to this group (Figure 1, middle). There was a higher
prevalence (P=0.033) of acute coronary findings in
patients dying suddenly than from myocardial failure (Figure 1, right). The prevalence of acute coronary findings was highest
in CAD patients with SD (54%), intermediate in CAD patients who died
of HF (32.1%), and infrequent in non-CAD patients dying of any cause
(P=0.0001) (Figure 2). Of the
103 patients with an old MI with autopsy-documented myocardial
scarring, the incidence of SD was somewhat higher (52%) than in
patients without an old MI (40%). Patients with an old MI who died
suddenly had an incidence of acute coronary findings (16 of 54,
30%) similar to that in patients without an old MI who died suddenly
(7 of 35, 28%).
|
|
Relation of Death Classification to Autopsy Findings
MI as a cause of death was 28% in the autopsy group and 4% in
the nonautopsy group (P<0.001). Because it was possible
that this apparent difference was due to new information obtained at
autopsy, a correction was made that assumed all patients with
autopsy-documented MI who died suddenly without MI being diagnosed
during life (31 of 32 patients) would have been classified as "sudden
unexpected," and all patients who died from myocardial failure with
unrecognized MI (6 of 15) would have been classified as "myocardial
failure" deaths. The causes of death then became similar between
"no autopsy" and "autopsy" groups (Table 2
, third
column). These data suggest strongly that the autopsy group is truly
representative of all patients who died and that the
differences in cause of death are due almost entirely to the
underappreciation of MI as a precipitant of sudden unexpected, and to a
lesser extent, myocardial failure deaths.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The present study is the first prospective, randomized, large, multicenter trial that used prespecified definitions of causes of death and a blinded Endpoints Committee to provide a relatively large sample of autopsied patients to examine causes of death in a HF population. This study demonstrates that recent coronary events are frequently unrecognized in patients with symptomatically moderate to advanced HF, especially in patients with CAD who die suddenly. These data are consistent with previous autopsy studies that have documented that a high percentage of CAD patients without HF who die suddenly also have evidence of an acute coronary event.3 4 5 6 It should be noted that recent autopsy studies of sudden cardiac death3 4 have reported a much higher incidence of ruptured plaque (57% to 81%) than we observed. However, the prevalence of acute coronary findings in CAD patients (41% in Davies’ study and 21% in Farb’s study) was similar to the present study (44%). Cuts at millimeter distances and meticulous review of each section are required to identify accurately plaque rupture and small thrombi.3 4 Because the autopsies in our study were routine clinical examinations, the degree of detail necessary to observe ruptured plaque and small thrombi was unlikely to have been performed. An alternate hypothesis is that that there was a greater delay in dying in the HF population versus the non-HF CAD group described in previous SD studies. This delay might account for the decreased prevalence of thrombus, but one would still expect the prevalence of ruptured plaque to be similar and of myocardial necrosis to be as high or even higher. This was not the case. Thus, the higher probability is that differences in methodology5 6 account for the higher prevalence of ruptured plaque and thrombus in previous studies rather than differences in patient populations or longer delay between coronary event and death.
The presence of acute coronary findings in ICM patients dying of myocardial failure is not unexpected. The most recent ischemic insult was probably the reason the patient progressed from tenuous compensation to terminal pump dysfunction. Somewhat less intuitive is the occasional patient without severe CAD at autopsy who had autopsy-documented MI. These findings may have been due to coronary embolization, an unusual sequelae of left ventricular dysfunction. In our study, patients without CAD at autopsy had a 12% prevalence of old MI, a figure similar to the 14% prevalence previously reported in patients with idiopathic dilated cardiomyopathy.7
In patients with acute MI at autopsy, 79% were undiagnosed during life, many with SD and no immediate antecedent history of chest pain. If we extrapolate the findings in this study to the general HF population, it suggests that as many as half of patients with ICM who die suddenly may have had an acute ischemic event precipitating the death. Furthermore, an additional third of CAD patients dying of terminal HF may have been precipitated by an unrecognized ischemic event.
Comparison With Other Studies
This study is the first large HF trial to systematically review
all autopsied patients. Thus, it is difficult to compare our results
with other large randomized clinical HF trials. In previous studies,
causes of death have not been described,8 9 10 MI as a
cause of death not included,11 12 13 14 mode of death not
described,9 or prespecified definitions of causes of death
not used or reported.12 13 15 16 17 That classification of
cause of death can be difficult and may be multifactorial emphasizes
the importance of maximizing methods to maintain
consistency across centers. In the ATLAS study,
classification of cause and mode of death were prospectively developed.
The End- points Committee required unanimity for classification; all
decisions were made blinded to the patient’s drug assignment. When
disagreement occurred, further information was requested and provided
by individual investigators when possible, allowing for consensus in
all cases and definitive classification in >99% of cases. An
Endpoints Committee was not used in several frequently cited
trials,12 13 15 17 18 19 leading to the likelihood of
inconsistent classification among centers.
Ability to Generalize Results
The most important issue in generalizing the results of this study
to the HF population as a whole is whether the autopsied patients are
truly representative of the spectrum of patients who
die with HF. In this study a potential shortcoming is that the
percentage of autopsied patients was low (<15% of all deaths).
However, the autopsied patients were very similar in baseline
characteristics to the nonautopsied patients who died. In the
nonautopsied group, the causes of death mirror the published
literature.11 20 On the other hand, the proportions of the
adjudicated causes of death was different in the autopsied versus the
nonautopsied group with a higher percentage of MI as cause of death in
the autopsied series. The correction that we used, that is, eliminating
the influence of any new information obtained at autopsy, produced a
classification of death causes that was almost identical in the
autopsied and nonautopsied groups. Without this correction, the
difference was due almost entirely to the underappreciation of MI as
the immediate precipitant of sudden unexpected, and to a lesser extent,
myocardial failure deaths. Thus, it may be surmised that our autopsy
patients were, in fact, likely to be representative of
the broad spectrum of HF patients included in ATLAS. The results
underscore the importance of addressing the consequences of CAD in an
attempt to decrease mortality rates in HF patients.
Definition of SD
The definitions of sudden unexpected death and other death causes
are crucial in placing our results in perspective. The present
study differs in some minor respects from the most frequently used
definition of SD, requiring death to occur within 1 hour and be
witnessed with some caveat to deal with an unwitnessed
death.1 The underlying concept was, however, retained in
this study. Our definition tacitly acknowledged the reality that many
SD are not witnessed and that the circumstances surrounding the event
require evaluation to determine if the death was truly unexpected and
sudden. In the present study, we also included patients who died
in-hospital from sequelae of earlier sudden collapse after successful
resuscitation. This was done under the assumption that the sudden
hemodynamic destabilization from the collapse was the
direct precipitant of the terminal event. The CAST and CAMIAT trials
considered any successful resuscitation as an end point, whereas we
counted only those patients who eventually died after
resuscitation.21 22 If we would have used a more
restricted definition of <1 hour with or without witnesses, our
results would not have substantially changed as <5% of the SD
patients had "delayed SD." It should also be noted that in several
studies in the HF population, there have been modifications of the
definition of SD. Death occurring during sleep in an ambulatory patient
with unchanged symptoms was assumed to be sudden in most cases in our
series; it probably has been considered as such in other studies but
has rarely been explicitly stated. Unwitnessed deaths with adequate
circumstantial information suggesting SD were so classified in several
other studies.4 8 15
Other Triggers and Causes of SD
The similar frequency of SD in the non-CAD and CAD patients
without acute coronary findings at autopsy emphasizes that
triggers other than an acute coronary event are clearly
operative in SD in HF patients. Our data also demonstrate that
unexpected SD may on occasion be related to a vascular catastrophe and
only very rarely to a noncardiovascular cause.
Therapeutic Implications
Our findings have important therapeutic implications. Death may be
precipitated in approximately one third of HF patients from acute
coronary events. Therefore, improved strategies to prevent or
more adequately treat ischemia may be important. It should be
emphasized that the accuracy of diagnosing CAD clinically was only
moderate in this study. If differentiating a coronary from
noncoronary cause has therapeutic implications,
coronary arteriography should be recommended whenever a
HF-related cause is in doubt. In the ATLAS trial, although two thirds
of the patients had ICM clinically as their cause of HF, only 40% were
taking aspirin. Furthermore, the interaction of aspirin and an ACE
inhibitor remains unclear,23 and other
antiplatelet agents such as clopidogrel may have more of a role
when an ACE inhibitor is used. ß-Blockers were used
in only a small fraction of cases, although they have been found to be
efficacious in improving symptoms and longevity.1 15
Similarly, cholesterol-lowering agents may be appropriate
in view of data showing a decrease in secondary coronary events
in patients with elevated or average cholesterol levels,
although data in HF patients are limited.
Study Limitations
Limitations of this study include the relatively low percentage of
autopsies and the varying degrees of description and detail on autopsy
reports. The possibility exists that autopsies were done for special
reasons, and the study group is not representative.
This possibility is lessened by the similar clinical characteristics of
the autopsied and nonautopsied groups, the broad geographic area
represented by study patients, the common disease process,
and modes of death. The relative underrepresentation of North
American patients autopsied may have affected the findings, but this is
unlikely because 
20% of all study patients were from North
America.
Conclusions
In summary, acute coronary events are frequent in HF
patients who die suddenly and may be a trigger of sudden, and to a
lesser extent, progressive myocardial failure deaths, particularly in
patients with ICM. Careful attention to this issue, including a more
aggressive use of agents known to be protective against subsequent
ischemic events, may allow for improvement in prognosis.
|
Acknowledgments |
|---|
We express our appreciation for the statistical assistance of Pam Rennie of Zeneca Pharmaceuticals and the facilitation of this project by many individuals at Zeneca Pharmaceuticals, including Michael Arnstein, Ross Pownall, Betty Black, Sandra Fitt, and Dr Hilary Marlowe.
Received September 21, 1999; revision received March 2, 2000; accepted March 10, 2000.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Uretsky BF, Sheahan RG. Primary prevention of sudden cardiac death in heart failure: will the solution be shocking? J Am Coll Cardiol. 1997;30:1589–1597.[Abstract]
2.
Meissner MD, Akhtar M, Lehmann MH. Nonischemic
sudden tachyarrhythmic death in atherosclerotic heart disease.
Circulation. 1991;84:905–912.
3. Davies MJ. Anatomic features in victims of sudden coronary death: coronary artery pathology. Circulation. 1992;85(suppl I):I-19–I-24.
4.
Farb A, Tang AL, Burke AP, et al. Sudden
coronary death: frequency of active coronary lesions,
inactive coronary lesions, and myocardial infarction.
Circulation. 1995;92:1701–1709.
5. Baba N, Bashe WJ Jr, Keller MD, et al. Pathology of atherosclerotic heart disease in sudden death, I: organizing thrombosis and acute coronary vessel lesions. Circulation. 1975;53(suppl III):III-53–III-59.
6. Bashe WJ Jr, Baba N, Keller MD, et al. Pathology of atherosclerotic heart disease in sudden death, II: the significance of myocardial infarction. Circulation. 1975;53(suppl III):III-63–III-69.
7. Roberts WC, Siegel RJ, McManus BM. Idiopathic dilated cardiomyopathy: analysis of 152 necropsy patients. Am J Cardiol. 1987;60:1340–1355.[Medline] [Order article via Infotrieve]
8. Hendrix GH, Bommer WJ, Elkayam U, et al, for the PROMISE Study Research Group. Effect of oral milrinone on mortality in severe chronic heart failure. N Engl J Med. 1991;325:1468–1474.[Abstract]
9. Acute Infarction Ramipril Efficacy (AIRE) Study Investigators. Effect of ramipril on mortality and morbidity of survivors of acute myocardial infarction with clinical evidence of heart failure. Lancet. 1993;2:821–827.
10.
Packer M, O’Connor CM, Ghali JK, et al. Effect of
amlodipine on morbidity and mortality in severe chronic heart failure.
N Engl J Med. 1996;335:1107–1114.
11. CONSENSUS Trial Study Group. Effects of enalapril on mortality in severe congestive heart failure: results of the Cooperative North Scandinavian Enalapril Survival Study. N Engl J Med. 1987;316:1429–1435.[Abstract]
12. Cohn JN, Johnson G, Ziesche S, et al. A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Engl J Med. 1991;325:303–310.[Abstract]
13.
Digitalis Investigative Group. The effect of digoxin on
mortality and morbidity in patients with heart failure. N
Engl J Med. 1997;336:525–533.
14. Doval HC, Nul DR, Grancelli HO, et al. Randomised trial of low-dose amiodarone in severe congestive heart failure. Lancet. 1994;344:493–498.[Medline] [Order article via Infotrieve]
15.
Packer M, Bristow MR, Cohn JN, et al. The effect of
carvedilol on morbidity and mortality in patients with chronic heart
failure. N Engl J Med. 1996;334:1349–1355.
16.
Singh SN, Fletcher RD, Fisher SG, et al.
Amiodarone in patients with congestive heart failure and
asymptomatic ventricular arrhythmia.
N Engl J Med. 1995;333:77–82.
17. Pfeffer MA, Braunwald E, Moye LA, et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med. 1992;327:669–677.[Abstract]
18. SOLVD Investigators. Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl J Med. 1992;327:685–691.[Abstract]
19. Cohn JN, Archibald DG, Ziesche S, et al. Effect of vasodilator therapy on mortality in chronic congestive heart failure: results of a Veterans Administration Cooperative Study. N Engl J Med. 1986;314:1547–1557.[Abstract]
20. SOLVD Investigators. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med. 1991;325:293–302.[Abstract]
21. Echt DS, Liebson PR, Mitchell LB, et al, and the CAST Investigators. Mortality and morbidity in patients receiving encainide, flecainide, or placebo: the Cardiac Arrhythmia Suppression Trial. N Engl J Med. 1991;324:781–788.[Abstract]
22. Cairns JA, Roberts R, Gent M, for the Canadian Amiodarone Myocardial Infarction Arrhythmia Trial Investigators. Randomised trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarisations. Lancet. 1997;349:675–682.[Medline] [Order article via Infotrieve]
23.
Al-Khadra AS, Salem DN, Rand WM, et al.
Antiplatelet agents and survival: a cohort analysis for the
Studies of Left Ventricular Dysfunction (SOLVD) trial.
J Am Coll Cardiol. 1998;31:419–425.
This article has been cited by other articles:
 |
|
 |
|
  D. L. Packer, J. M. Prutkin, A. S. Hellkamp, L. B. Mitchell, R. C. Bernstein, F. Wood, J. P. Boehmer, M. D. Carlson, R. P. Frantz, S. E. McNulty, et al. Impact of Implantable Cardioverter-Defibrillator, Amiodarone, and Placebo on the Mode of Death in Stable Patients With Heart Failure: Analysis From the Sudden Cardiac Death in Heart Failure Trial Circulation, December 1, 2009; 120(22): 2170 - 2176. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. A. Hunt, W. T. Abraham, M. H. Chin, A. M. Feldman, G. S. Francis, T. G. Ganiats, M. Jessup, M. A. Konstam, D. M. Mancini, K. Michl, et al. 2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the International Society for Heart and Lung Transplantation J. Am. Coll. Cardiol., April 14, 2009; 53(15): e1 - e90. [Full Text] [PDF]
|
|
|
|
|
|
M. Jessup, W. T. Abraham, D. E. Casey, A. M. Feldman, G. S. Francis, T. G. Ganiats, M. A. Konstam, D. M. Mancini, P. S. Rahko, M. A. Silver, et al. 2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the International Society for Heart and Lung Transplantation J. Am. Coll. Cardiol., April 14, 2009; 53(15): 1343 - 1382. [Full Text] [PDF]
|
|
|
|
|
|
2009 WRITING GROUP TO REVIEW NEW EVIDENCE AND UPDA, M. Jessup, W. T. Abraham, D. E. Casey, A. M. Feldman, G. S. Francis, T. G. Ganiats, M. A. Konstam, D. M. Mancini, P. S. Rahko, et al. 2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: Developed in Collaboration With the International Society for Heart and Lung Transplantation Circulation, April 14, 2009; 119(14): 1977 - 2016. [Full Text] [PDF]
|
|
|
|
|
|
2005 WRITING COMMITTEE MEMBERS, S. A. Hunt, W. T. Abraham, M. H. Chin, A. M. Feldman, G. S. Francis, T. G. Ganiats, M. Jessup, M. A. Konstam, D. M. Mancini, et al. 2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: Developed in Collaboration With the International Society for Heart and Lung Transplantation Circulation, April 14, 2009; 119(14): e391 - e479. [Full Text] [PDF]
|
|
|
|
 |
|
 W. A. Ahmed, P. J. Tully, R. A. Baker, and J. L. Knight Survival After Isolated Coronary Artery Bypass Grafting in Patients With Severe Left Ventricular Dysfunction Ann. Thorac. Surg., April 1, 2009; 87(4): 1106 - 1112. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A. Konstam Antithrombotic Therapy in Heart Failure: WATCHful Wondering Circulation, March 31, 2009; 119(12): 1559 - 1561. [Full Text] [PDF]
|
|
|
|
|
|
B. M. Massie, J. F. Collins, S. E. Ammon, P. W. Armstrong, J. G.F. Cleland, M. Ezekowitz, S. M. Jafri, W. F. Krol, C. M. O'Connor, K. A. Schulman, et al. Randomized Trial of Warfarin, Aspirin, and Clopidogrel in Patients With Chronic Heart Failure: The Warfarin and Antiplatelet Therapy in Chronic Heart Failure (WATCH) Trial Circulation, March 31, 2009; 119(12): 1616 - 1624. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. N. Sharikabad, J. M. Aronsen, E. Haugen, J. Pedersen, A.-S. W. Moller, H. K. Mork, H. C. D. Aass, O. M. Sejersted, I. Sjaastad, and O. Brors Cardiomyocytes from postinfarction failing rat hearts have improved ischemia tolerance Am J Physiol Heart Circ Physiol, March 1, 2009; 296(3): H787 - H795. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. D. Flaherty, J. J. Bax, L. De Luca, J. S. Rossi, C. J. Davidson, G. Filippatos, P. P. Liu, M. A. Konstam, B. Greenberg, M. R. Mehra, et al. Acute heart failure syndromes in patients with coronary artery disease early assessment and treatment. J. Am. Coll. Cardiol., January 20, 2009; 53(3): 254 - 263. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. A. Mehta, S. W. Dubrey, H. F. McIntyre, D. M. Walker, S. M.C. Hardman, G. C. Sutton, T. A. McDonagh, and M. R. Cowie Mode of death in patients with newly diagnosed heart failure in the general population Eur J Heart Fail, November 1, 2008; 10(11): 1108 - 1116. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. C. Becker, T. W. Meade, P. B. Berger, M. Ezekowitz, C. M. O'Connor, D. A. Vorchheimer, G. H. Guyatt, D. B. Mark, and R. A. Harrington The Primary and Secondary Prevention of Coronary Artery Disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition) Chest, June 1, 2008; 133(6_suppl): 776S - 814S. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Kuner, A. S. Barth, M. Ruschhaupt, A. Buness, L. Zwermann, E. Kreuzer, G. Steinbeck, A. Poustka, H. Sultmann, and M. Nabauer Genomic analysis reveals poor separation of human cardiomyopathies of ischemic and nonischemic etiologies Physiol Genomics, June 1, 2008; 34(1): 88 - 94. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Torabi, J. G.F. Cleland, N. K. Khan, P. H. Loh, A. L. Clark, F. Alamgir, J. L. Caplin, A. S. Rigby, and K. Goode The timing of development and subsequent clinical course of heart failure after a myocardial infarction Eur. Heart J., April 1, 2008; 29(7): 859 - 870. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Kjekshus, E. Apetrei, V. Barrios, M. Bohm, J. G.F. Cleland, J. H. Cornel, P. Dunselman, C. Fonseca, A. Goudev, P. Grande, et al. Rosuvastatin in Older Patients with Systolic Heart Failure N. Engl. J. Med., November 29, 2007; 357(22): 2248 - 2261. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. J. Remme, J. G. Cleland, L. Erhardt, P. Spark, C. Torp-Pedersen, M. Metra, M. Komajda, C. Moullet, M. A. Lukas, P. Poole-Wilson, et al. Effect of carvedilol and metoprolol on the mode of death in patients with heart failure Eur J Heart Fail, November 1, 2007; 9(11): 1128 - 1135. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Patel and J. T. Heywood Mode of Death in Patients With Systolic Heart Failure Journal of Cardiovascular Pharmacology and Therapeutics, June 1, 2007; 12(2): 127 - 136. [Abstract] [PDF]
|
|
|
|
|
|
J. G.F. Cleland, R. Shelton, N. Nikitin, S. Ford, L. Frison, and M. Grind Prevalence of markers of heart failure in patients with atrial fibrillation and the effects of ximelagatran compared to warfarin on the incidence of morbid and fatal events: A report from the SPORTIF III and V trials Eur J Heart Fail, June 1, 2007; 9(6-7): 730 - 739. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. J. Bunch, S. H. Hohnloser, and B. J. Gersh Mechanisms of Sudden Cardiac Death in Myocardial Infarction Survivors: Insights From the Randomized Trials of Implantable Cardioverter-Defibrillators Circulation, May 8, 2007; 115(18): 2451 - 2457. [Full Text] [PDF]
|
|
|
|
|
|
A.-Y. Chong and G. Y.H. Lip Viewpoint: The prothrombotic state in heart failure: A maladaptive inflammatory response? Eur J Heart Fail, February 1, 2007; 9(2): 124 - 128. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. J. Goldberger, H. Subacius, A. Schaechter, A. Howard, R. Berger, A. Shalaby, J. Levine, A. H. Kadish, and for the DEFINITE Investigators Effects of Statin Therapy on Arrhythmic Events and Survival in Patients With Nonischemic Dilated Cardiomyopathy J. Am. Coll. Cardiol., September 19, 2006; 48(6): 1228 - 1233. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Gheorghiade, G. Sopko, L. De Luca, E. J. Velazquez, J. D. Parker, P. F. Binkley, Z. Sadowski, K. S. Golba, D. L. Prior, J. L. Rouleau, et al. Navigating the Crossroads of Coronary Artery Disease and Heart Failure Circulation, September 12, 2006; 114(11): 1202 - 1213. [Full Text] [PDF]
|
|
|
|
 |
|
 R Klingenberg, C Zugck, R Becker, D Schellberg, G Heinze, R Kell, A Remppis, W Schoels, H A Katus, and T J Dengler Raised B-type natriuretic peptide predicts implantable cardioverter-defibrillator therapy in patients with ischaemic cardiomyopathy. Heart, September 1, 2006; 92(9): 1323 - 1324. [Full Text] [PDF]
|
|
|
|
|
|
L. R. Goldberg and M. Jessup Stage B Heart Failure: Management of Asymptomatic Left Ventricular Systolic Dysfunction Circulation, June 20, 2006; 113(24): 2851 - 2860. [Full Text] [PDF]
|
|
|
|
 |
|
 E. Vanoli and P. B. Adamson What does the future hold for the management of chronic heart failure? Eur. Heart J. Suppl., June 1, 2006; 8(suppl_C): C51 - C57. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. P. Daubert, W. Zareba, W. J. Hall, C. Schuger, A. Corsello, A. R. Leon, M. L. Andrews, S. McNitt, D. T. Huang, A. J. Moss, et al. Predictive Value of Ventricular Arrhythmia Inducibility for Subsequent Ventricular Tachycardia or Ventricular Fibrillation in Multicenter Automatic Defibrillator Implantation Trial (MADIT) II Patients J. Am. Coll. Cardiol., January 3, 2006; 47(1): 98 - 107. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Carson, I. Anand, C. O'Connor, B. Jaski, J. Steinberg, A. Lwin, J. Lindenfeld, J. Ghali, J. H. Barnet, A. M. Feldman, et al. Mode of Death in Advanced Heart Failure: The Comparison of Medical, Pacing, and Defibrillation Therapies in Heart Failure (COMPANION) Trial J. Am. Coll. Cardiol., December 20, 2005; 46(12): 2329 - 2334. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Lamblin, F. Mouquet, B. Hennache, J. Dagorn, S. Susen, C. Bauters, and P. de Groote High-sensitivity C-reactive protein: potential adjunct for risk stratification in patients with stable congestive heart failure Eur. Heart J., November 1, 2005; 26(21): 2245 - 2250. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Demers, J. J. V. McMurray, K. Swedberg, M. A. Pfeffer, C. B. Granger, B. Olofsson, R. S. McKelvie, J. Ostergren, E. L. Michelson, P. A. Johansson, et al. Impact of Candesartan on Nonfatal Myocardial Infarction and Cardiovascular Death in Patients With Heart Failure JAMA, October 12, 2005; 294(14): 1794 - 1798. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Kjekshus, P. Dunselman, M. Blideskog, C. Eskilson, A. Hjalmarson, J. V. McMurray, F. Waagstein, H. Wedel, P. Wessman, J. Wikstrand, et al. A statin in the treatment of heart failure? Controlled rosuvastatin multinational study in heart failure (CORONA): Study design and baseline characteristics Eur J Heart Fail, October 1, 2005; 7(6): 1059 - 1069. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. M. Massie Aspirin Use in Chronic Heart Failure: What Should We Recommend to the Practitioner? J. Am. Coll. Cardiol., September 20, 2005; 46(6): 963 - 966. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Senior, R. Janardhanan, P. Jeetley, and L. Burden Myocardial Contrast Echocardiography for Distinguishing Ischemic From Nonischemic First-Onset Acute Heart Failure: Insights Into the Mechanism of Acute Heart Failure Circulation, September 13, 2005; 112(11): 1587 - 1593. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. D. Solomon, S. Zelenkofske, J. J.V. McMurray, P. V. Finn, E. Velazquez, G. Ertl, A. Harsanyi, J. L. Rouleau, A. Maggioni, L. Kober, et al. Sudden Death in Patients with Myocardial Infarction and Left Ventricular Dysfunction, Heart Failure, or Both N. Engl. J. Med., June 23, 2005; 352(25): 2581 - 2588. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A Y Patwala and D J Wright Device based treatment of heart failure Postgrad. Med. J., May 1, 2005; 81(955): 286 - 291. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. G. Ray, Y. Gong, K. Sykora, and J. V. Tu Statin Use and Survival Outcomes in Elderly Patients With Heart Failure Arch Intern Med, January 10, 2005; 165(1): 62 - 67. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. D. Sosin, G. S. Bhatia, R. C. Davis, and G. Y.H. Lip Heart failure--the importance of ethnicity Eur J Heart Fail, December 1, 2004; 6(7): 831 - 843. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A M A Shehab, R J MacFadyen, M McLaren, R Tavendale, J J F Belch, and A D Struthers Sudden unexpected death in heart failure may be preceded by short term, intraindividual increases in inflammation and in autonomic dysfunction: a pilot study Heart, November 1, 2004; 90(11): 1263 - 1268. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. D. Solomon, D. Wang, P. Finn, H. Skali, L. Zornoff, J. J.V. McMurray, K. Swedberg, S. Yusuf, C. B. Granger, E. L. Michelson, et al. Effect of Candesartan on Cause-Specific Mortality in Heart Failure Patients: The Candesartan in Heart failure Assessment of Reduction in Mortality and morbidity (CHARM) Program Circulation, October 12, 2004; 110(15): 2180 - 2183. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Nichol, P. Kaul, E. Huszti, and J. F.P. Bridges Cost-Effectiveness of Cardiac Resynchronization Therapy in Patients with Symptomatic Heart Failure Ann Intern Med, September 7, 2004; 141(5): 343 - 351. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. A. McAlister, J. A. Ezekowitz, N. Wiebe, B. Rowe, C. Spooner, E. Crumley, L. Hartling, T. Klassen, and W. Abraham Systematic Review: Cardiac Resynchronization in Patients with Symptomatic Heart Failure Ann Intern Med, September 7, 2004; 141(5): 381 - 390. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. A. Harrington, R. C. Becker, M. Ezekowitz, T. W. Meade, C. M. O'Connor, D. A. Vorchheimer, and G. H. Guyatt Antithrombotic Therapy for Coronary Artery Disease: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy Chest, September 1, 2004; 126(3_suppl): 513S - 548S. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Thygesen and B. F Uretsky Acute ischaemia as a trigger of sudden cardiac death Eur. Heart J. Suppl., August 1, 2004; 6(suppl_D): D88 - D90. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M McDermott The continuing decline of autopsies in clinical trials: is there any way back? Arch. Dis. Child. Fetal Neonatal Ed., May 1, 2004; 89(3): F198 - F199. [Full Text] [PDF]
|
|
|
|
|
|
P. de Groote, N. Lamblin, F. Mouquet, D. Plichon, E. McFadden, E. Van Belle, and C. Bauters Impact of diabetes mellitus on long-term survival in patients with congestive heart failure Eur. Heart J., April 2, 2004; 25(8): 656 - 662. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Cardinal, G. Rousseau, C. Bouchard, M. Vermeulen, J.-G. Latour, and P. L. Page Myocardial electrical alteration in canine preparations with combined chronic rapid pacing and progressive coronary artery occlusion Am J Physiol Heart Circ Physiol, April 1, 2004; 286(4): H1496 - H1506. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. B. Horwich, W. R. MacLellan, and G. C. Fonarow Statin therapy is associated with improved survival in ischemic and non-ischemic heart failure J. Am. Coll. Cardiol., February 18, 2004; 43(4): 642 - 648. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R.A. Anderson, G.R. Ellis, Y.Y. Chirkov, A.S. Holmes, N. Payne, D.J. Blackman, S.K. Jackson, M.J. Lewis, J.D. Horowitz, and M.P. Frenneaux Determinants of platelet responsiveness to nitric oxide in patients with chronic heart failure Eur J Heart Fail, January 1, 2004; 6(1): 47 - 54. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Bello, D. J. Shah, G. M. Farah, S. Di Luzio, M. Parker, M. R. Johnson, W. G. Cotts, F. J. Klocke, R. O. Bonow, R. M. Judd, et al. Gadolinium Cardiovascular Magnetic Resonance Predicts Reversible Myocardial Dysfunction and Remodeling in Patients With Heart Failure Undergoing {beta}-Blocker Therapy Circulation, October 21, 2003; 108(16): 1945 - 1953. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.A. McCrohon, J.C.C. Moon, S.K. Prasad, W.J. McKenna, C.H. Lorenz, A.J.S. Coats, and D.J. Pennell Differentiation of Heart Failure Related to Dilated Cardiomyopathy and Coronary Artery Disease Using Gadolinium-Enhanced Cardiovascular Magnetic Resonance Circulation, July 8, 2003; 108(1): 54 - 59. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.G.F. Cleland, N. Freemantle, S.G. Ball, R.S. Bonser, P. Camici, S. Chattopadhyay, D. Dutka, J. Eastaugh, J. Hampton, S. Large, et al. The heart failure revascularisation trial (HEART): rationale, design and methodology Eur J Heart Fail, June 1, 2003; 5(3): 295 - 303. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. W. Lytle The role of coronary revascularization in the treatment of ischemic cardiomyopathy Ann. Thorac. Surg., June 1, 2003; 75(90060): S2 - 5. [Full Text] [PDF]
|
|
|
|
|
|
P A Poole-Wilson, B F Uretsky, K Thygesen, J G F Cleland, B M Massie, and L Ryden Mode of death in heart failure: findings from the ATLAS trial Heart, January 1, 2003; 89(1): 42 - 48. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P.A. Poole-Wilson Who are the enemies? Lack of oxygen Eur. Heart J. Suppl., November 1, 2002; 4(suppl_G): G15 - G19. [Abstract] [PDF]
|
|
|
|
|
|
P.R. Kalra, P.P. Ponikowski, and S.D. Anker Sympathetic activation and malignant ventricular arrhythmias: a molecular link? Eur. Heart J., July 2, 2002; 23(14): 1078 - 1080. [Full Text] [PDF]
|
|
|
|
|
|
H. Krum and J. J. McMurray Statins and chronic heart failure: do we need a large-scale outcome trial? J. Am. Coll. Cardiol., May 15, 2002; 39(10): 1567 - 1573. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. C. Allman, L. J. Shaw, R. Hachamovitch, and J. E. Udelson Myocardial viability testing and impact of revascularization on prognosis in patients with coronary artery disease and left ventricular dysfunction: a meta-analysis J. Am. Coll. Cardiol., April 3, 2002; 39(7): 1151 - 1158. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S Orn and K Dickstein How do heart failure patients die? Eur. Heart J. Suppl., April 1, 2002; 4(suppl_D): D59 - D65. [Abstract] [PDF]
|
|
|
|
|
|
G. M. Felker, L. K. Shaw, and C. M. O'Connor A standardized definition of ischemic cardiomyopathy for use in clinical research J. Am. Coll. Cardiol., January 16, 2002; 39(2): 210 - 218. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. G F Cleland, J. John, J. Dhawan, and A. Clark What is the optimal medical management of ischaemic heart failure? Br. Med. Bull., October 1, 2001; 59(1): 135 - 158. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S.G. Priori, E. Aliot, C. Blomstrom-Lundqvist, L. Bossaert, G. Breithardt, P. Brugada, A.J. Camm, R. Cappato, S.M. Cobbe, C. Di Mario, et al. Task Force on Sudden Cardiac Death of the European Society of Cardiology Eur. Heart J., August 2, 2001; 22(16): 1374 - 1450. [PDF]
|
|
|
|
|
|
D. L. Dries, N. K. Sweitzer, M. H. Drazner, L. W. Stevenson, and B. J. Gersh Prognostic impact of diabetes mellitus in patients with heart failure according to the etiology of left ventricular systolic dysfunction J. Am. Coll. Cardiol., August 1, 2001; 38(2): 421 - 428. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Isnard and M. Komajda Thromboembolism in heart failure, old ideas and new challenges Eur J Heart Fail, June 1, 2001; 3(3): 265 - 269. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. M. Spooner, C. Albert, E. J. Benjamin, R. Boineau, R. C. Elston, A. L. George Jr, X. Jouven, L. H. Kuller, J. W. MacCluer, E. Marban, et al. Sudden Cardiac Death, Genes, and Arrhythmogenesis : Consideration of New Population and Mechanistic Approaches From a National Heart, Lung, and Blood Institute Workshop, Part I Circulation, May 15, 2001; 103(19): 2361 - 2364. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||