(Circulation. 1995;92:1701-1709.)
© 1995 American Heart Association, Inc.
Articles |
Sudden Coronary Death
Frequency of Active Coronary Lesions, Inactive Coronary Lesions, and Myocardial Infarction
From the Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC.
Correspondence to Renu Virmani, MD, Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC 20306-6000.
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Abstract |
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Background The reported frequency of active coronary lesions (plaque rupture and coronary thrombosis) in sudden death due to coronary artery atherosclerosis (sudden coronary death) has varied from <20% to >80% of cases in previous series. In hearts lacking an active coronary lesion, sudden death has usually been attributed to a healed myocardial infarction. The purpose of the present study was to determine the frequency of active and inactive coronary lesions and myocardial infarction in individuals with sudden coronary death.
Methods and Results The hearts of persons who died as a result of
sudden coronary death underwent perfusion-fixation and
postmortem angiography. An active coronary lesion was defined
as a disrupted plaque, luminal fibrin/platelet thrombus, or both.
We defined an inactive lesion as having a cross-sectional luminal
stenosis of 
75% with neither plaque disruption nor luminal
thrombus. Ninety hearts were examined (from 72 men and 18 women; mean
age at the time of death, 51±10 years). Acute myocardial infarction
was present in 19 (21% [acute myocardial infarction only in 9,
both acute and healed myocardial infarction in 10]), healed myocardial
infarction only in 37 (41%), and no myocardial infarction in 34
(38%). Active coronary lesions were identified in 51 (57%):
acute thrombi plus disrupted plaques in 27, acute thrombi only in 21,
and disrupted plaques only in 3. In hearts with acute myocardial
infarction, active coronary lesions were significantly more
prevalent than in hearts with only healed myocardial infarction or
hearts lacking an acute or a healed myocardial infarction (89%, 46%,
and 50%, respectively; P<.005). Hearts without acute or
healed myocardial infarction and without active lesions were similar to
hearts with active lesions with respect to heart weight and severity of
epicardial coronary disease.
Conclusions Acute changes in coronary plaque morphology (thrombus, plaque disruption, or both) were found in 57% of cases of sudden coronary death. In hearts with myocardial scars and no acute infarction, active coronary lesions were identified in 46% of cases. Neither myocardial infarction (acute or healed) nor an active coronary lesion was present in 19% of hearts.
Key Words: death • sudden • plaque • infarction
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Introduction |
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Coronary atherosclerosis may present as cardiac angina (stable or unstable), acute myocardial infarction (MI), or sudden death. Death due to coronary atherosclerosis accounts for approximately 50% of all cardiac deaths, and 50% of coronary atherosclerosis deaths are sudden and unexpected. The pathophysiology of acute MI in the vast majority of cases involves coronary thrombosis overlying a disrupted atherosclerotic plaque. However, the frequency of unstable plaques and coronary thrombosis in sudden cardiac death secondary to atherosclerosis (sudden coronary death) is extremely variable.1 2 3 4 5 6 7 8 9 10 11 12 13 14 Specifically, the percentages of sudden coronary death cases accounted for by disrupted plaques, healed MIs, or severe coronary atherosclerosis with neither an active (acute) coronary lesion nor MI are uncertain. Davies et al14 found occlusive or nonocclusive thrombi in 73.3% of cases of sudden cardiac death, plaque fissures or intraintimal thrombi in 7.7%, and no active coronary lesions in 19%. In contrast, Warnes and Roberts13 found thrombi in only 19% of hearts from 70 persons who had died as a result of sudden coronary death. Methodological differences such as sources of cases of sudden death (medical examiner's offices versus hospitalized inpatients), autopsy protocol and histopathological techniques (postmortem angiography, serial sectioning), and exclusion criteria (absence of myocardial necrosis) between these studies may help to explain the divergent results, but the question of the frequency of active coronary artery lesions in sudden coronary death remains.
Old MI is commonly observed (approximately 40% to 80%) in persons with sudden coronary death.2 3 5 7 8 9 10 13 14 However, even when there is evidence of healed MI, sudden death has often been attributed to active coronary lesions (coronary thrombi and disrupted plaques).15 16 17 In contrast, acute MI is much less common (20% to 40%), even when acute coronary thrombosis is found,2 3 5 7 8 9 10 14 which probably reflects the time needed to develop gross and histological changes of myocardial necrosis. When no active coronary lesion is found in sudden death, cardiomegaly has been suggested as a potential cause of lethal cardiac dysrhythmias.14
To our knowledge, no large study of sudden coronary death from a series of cases derived from a single medical examiner's office has been performed recently in the United States with methodologies similar to those of Davies et al.12 14 The goals of the present study were to define the association of coronary thrombosis and disrupted coronary plaques in sudden coronary death victims with and without MI. In this study, both postmortem angiography and serial coronary artery sectioning were used to optimize identification of significant coronary stenosis, thrombosis, and disrupted coronary plaques.
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Methods |
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Selection of Cases
Cases of sudden coronary death were reviewed in consultation at the State of Maryland Medical Examiner's Office over a 12-month period. Sudden coronary death was defined as witnessed sudden unexpected death within 6 hours of the onset of symptoms from a stable medical condition or death of an individual who had been seen in stable condition less than 24 hours antemortem. To be included in the study, at least one major coronary artery had to have a histologically confirmed luminal thrombus or be narrowed
75% in cross-sectional area by plaque with or without
plaque rupture (details given later). No other potentially lethal
cardiac or noncardiac cause of death could be present, including
toxicology screening. Associated nonlethal medical conditions were
recorded. Cases of mechanical cardiac complications secondary to
acute MI (eg, free wall, septal, or papillary muscle rupture) were
excluded. All hearts were examined fresh and uncut, with fixation and
postmortem angiography performed on the day of autopsy. No previously
cut hearts were included in the study.
Tissue Handling and Processing
Hearts with a short segment of
attached aortic stump were
excised and weighed. The coronary arterial tree was
perfusion-fixed with 10% neutral-buffered formalin for 15
minutes at 100 mm Hg. Postmortem coronary angiography was
performed by selective injection of the left and right ostia with a
mixture of barium gelatin followed by radiography after
15 minutes of additional fixation. The major epicardial
coronary arteries (left main, left anterior descending, left
circumflex, and right coronary arteries) and their main
branches (left diagonals, left obtuse marginals, and posterior
descending coronary artery) were cut transversely at 2-mm
intervals and decalcified before sectioning if necessary. Segments that
had a >50% cross-sectional luminal stenosis by visual
inspection were submitted for light microscopy,
histological examination, and morphometric
measurements. Arterial segments were dehydrated in a series
of graded alcohols, cleared with xylene, embedded in paraffin, cut at 4
µm, and stained with hematoxylin and eosin and Movat's
pentachrome stains. The severity and extent of coronary
atherosclerosis determined the number of
histological sections examined per case. From one to
six arterial segments were placed in each cassette.
The right and left ventricles were cut at 1.0-cm intervals parallel to the posterior atrioventricular groove from apex to base. The myocardium was examined for the presence of healed and/or acute MI and extent of infarction. In hearts without gross evidence of MI (acute or healed), at least one section of the myocardium was submitted (from the midventricular slice) from the anterior left ventricular wall, lateral wall, posterior wall, interventricular septum, and posterior right ventricular wall (for a total of five myocardial sections). In hearts with MI identified on gross examination, sections from all acute and healed infarcts in addition to the above-listed sections were submitted. Each myocardial section was approximately 1.5 to 2.0 cm in length and extended from the endocardium to epicardium.
Histological Analysis and
Definitions
The presence of acute thrombi (collections of platelets,
fibrin, and trapped erythrocytes and white blood cells) and disrupted
coronary plaques (disruption of the luminal fibrous cap with
fissure or rupture into a lipid core) was noted. An active
coronary lesion was defined by the presence of a disrupted
coronary plaque, luminal thrombus, or both (luminal thrombus in
the area of a ruptured plaque). An inactive lesion had a luminal
stenosis of 75% but lacked both plaque disruption and
thrombus. Segments that demonstrated luminal thrombus but no rupture
into a lipid core underwent serial step-sectioning and staining (at
every 40 µm) to determine whether rupture of a fibrous cap was
present deeper in the section. Organized thrombi consisted of
granulation tissue and recannalized channels within the
arterial lumen with or without fibrin.
In cases in which there were no
active coronary lesions (ie,
absence of plaque disruption and intraluminal thrombus), the most
severely narrowed arterial segment underwent serial
step-sectioning and staining so we would not overlook
extremely focal active lesions. Deep hemorrhage into plaque
(foci of erythrocytes in plaque that did not communicate with the
lumen) was noted, and a large plaque hemorrhage was defined as
a hemorrhage occupying 25% of the total plaque area.
Arterial segments that had a large, deep plaque
hemorrhage also underwent serial step sectioning to identify
any communication of the hemorrhage with the lumen.
All active coronary lesions and the most severely narrowed inactive coronary lesions from each major coronary artery were magnified and digitized. The following computerized morphometric measurements were performed on histological sections (IPLAB image analysis software, version 2.5): arterial size (defined by the area within the internal elastic lamina), lumen area, and percent arterial stenosis [100x(1-lumen area/arterial size)].
Healed MI was identified by focal macroscopic replacement of the myocardium by scarring, with histological confirmation. Acute MI was diagnosed by the presence of coagulation necrosis of myocytes with or without an associated inflammatory infiltrate. The presence of intramyocardial artery embolization was recorded.
Statistical Analysis
Values are given as mean±1 SD.
Continuous variables were
compared with the use of ANOVA, and categorical variables were
compared with the use of 
2 test
(STATVIEW software, version 4.01). A value of
P
.05 was considered significant.
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Results |
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Patient Characteristics
Ninety hearts were collected that met criteria for sudden coronary death. The hearts were from 72 men and 18 women (66 white 24 black); the mean age at the time of death was 51±10 years (range, 34 to 89 years). The age distribution of the individuals in this study was as follows: 30 to 39 years, n=12; 40 to 49 years, n=33; 50 to 59 years, n=32; 60 to 69 years, n=9; 70 to 79 years, n=2; and 80 to 89 years, n=2. The circumstances at death were as follows: 42 patients were found dead, and 48 had a witnessed collapse. Of those with a witnessed collapse, 13 had chest pain, dyspnea, or both; 5 abdominal or back pain; and 30 had no symptoms immediately before collapse. Of the 90 cases, 9 were previously diagnosed as having coronary artery disease; hypertension was present in 11, hypercholesterolemia in 4, diabetes in 9, and miscellaneous conditions in 11 (cerebrovascular disease [n=3], asthma [n=2], peptic ulcer disease [n=2], hypothyroidism [n=1], mitral valve prolapse [n=1], multiple sclerosis [n=1], and chronic renal disease [n=1]).
Myocardial Pathology
Examination of the myocardium revealed
acute MI only
in 9 hearts (10%), both acute and healed MI in 10 (11%), healed MI
only in 37 (41%), and no MI in 34 (38%) (Table 1
). In
hearts with acute MI, the infarct was identified on gross inspection in
9 of 19 cases. Of these 9, the infarct was transmural in 8 and
subendocardial in 1. The 10 acute infarcts identified by histology only
were subendocardial. Platelet-fibrin emboli in small
intramyocardial coronary arteries were found in 7 hearts (8%)
and only in cases with an acute coronary thrombus.
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Coronary Artery Pathology |
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The total number of arterial segments examined was 1825 (mean of 20 arterial segments per case; range, 8 to 51). Of these 90 cases of sudden coronary death, there were 172 major coronary arteries that had
75% cross-sectional
luminal narrowing. The distribution of these vessels was left main in
4, left anterior descending coronary artery in 68, left
diagonal in 3, left circumflex in 31, left obtuse marginal in 9, ramus
intermedius in 4, right coronary artery in 50, and posterior
descending coronary artery in 3. The mean percent luminal area
stenosis for these 172 arteries was 89±10%. The extent of
coronary atherosclerosis was one-vessel
disease (single coronary artery cross-sectional lumen area
narrowed 75% by atherosclerotic plaque) in 40 (44%), two-vessel
disease in 29 (32%), three-vessel disease in 20 (22%), and
four-vessel disease in 1 (1%).
The distribution of coronary lesions for the entire group of
hearts was acute thrombus in 48 (53%), disrupted coronary
plaque (with or without an acute thrombus) in 30 (33%), and organized
thrombus in 36 (40%). In aggregate, accounting for the
simultaneous presence of thrombus and disrupted plaque in
some arteries, there were 51 active coronary lesions in the 90
cases (57%); no case had an active lesion in more than one
coronary artery. The association of thrombus and disrupted
coronary plaque was as follows: acute thrombus with plaque
disruption was seen in 27 (30% of all hearts) and acute thrombus
without plaque disruption was seen in 21 (23% of all hearts).
Disrupted plaque without acute thrombus was identified in 3 cases (3%
of all hearts) among the 172 coronary lesions with 75%
luminal stenosis. Plaque hemorrhage of any size was
present in 52 cases (58%); of these, plaque hemorrhage
occupying 25% of total plaque area was identified in 28 (54%).
The association of active coronary lesions with MI is shown in
Table 1
. Not unexpectedly, 16 of 19 cases (84%) with an acute
MI had
an acute coronary thrombus (8 [42%] associated with and 8
[42%] without a disrupted plaque). One acute-MI case (5%) had a
disrupted plaque without a thrombus, and 2 acute-MI cases (11%) had no
active coronary lesion. Of the 37 healed-MI-only cases (ie, no
acute MI), 8 (22%) had an acute thrombus with a disrupted plaque, 7
(19%) had an acute thrombus without a disrupted plaque, and 2 (5%)
had a disrupted plaque without a thrombus. Twenty healed-MI-only cases
(54%) had no active coronary lesion. Of the 34 cases without
an MI (acute or healed), 11 (32%) had an acute thrombus with a
disrupted plaque, and 6 (18%) had an acute thrombus without a
disrupted plaque. Seventeen hearts (50%) without acute or healed MI
lacked active coronary lesions. An active coronary
lesion (thrombus, disrupted plaque, or both) was more frequently
identified in acute-MI cases than in cases with only a healed MI or
those without MI (89%, 46%, and 50%, respectively,
P<.005). Acute thrombi without plaque disruption were more
common in acute-MI cases than in healed-MI cases or no-MI cases (42%,
19%, and 18%, respectively) but did not reach statistical
significance (P=.09). Representative
postmortem angiography and pathology are shown in Figs 1 through
4.
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Thus, of the 90 total cases, sudden coronary death could be
attributed to active coronary lesions (thrombus, disrupted
plaque, or both) in 51 cases (57%). There were 22 cases (24%) without
an active coronary lesion that had an acute (n=2) or healed
(n=20) MI. In the 34 cases without an acute or a healed MI, 17 (50%)
had only inactive coronary artery lesions, ie, severe
atherosclerosis without acute coronary
thrombosis or plaque disruption. These hearts were otherwise similar to
hearts with active coronary lesions with respect to heart
weight and vessel disease (Table 2). A coronary
stenosis score was calculated based on the mean percent
stenosis of all major epicardial arteries with 75% luminal
narrowing. The coronary stenosis score was 86±10% in
hearts with active coronary lesions versus 83±9% in hearts
lacking both active coronary lesions and MI (P=NS).
Therefore, sudden cardiac death in 50% of hearts that lack acute or
healed MI (19% of the entire group of sudden coronary death
victims) cannot be explained by active coronary lesions (ie,
thrombus or plaque disruption).
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The significance of isolated deep hemorrhage into plaque
without plaque disruption at the luminal surface is uncertain as it is
commonly seen in atherosclerotic plaques not associated with acute
clinical events.18 The frequency of isolated large plaque
hemorrhage (without disrupted plaque or coronary
thrombosis) was small and was similar among cases with MI or without MI
(Table 1). Organized thrombi were present in 9 acute-MI cases
(47%) and 22 healed-MI-only cases (59%), significantly more frequent
than hearts lacking an acute or a healed MI (5 cases [15%],
P=.0005, Table 1). There were no cases of an
acute
thrombosis in a coronary arterial segment that
contained an organized thrombus.
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Discussion |
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Present Study
In this series of sudden coronary death, 57% of hearts had an active coronary artery lesion consisting of coronary thrombosis, plaque disruption, or both. These active coronary lesions were seen approximately twice as often when there was evidence of an acute MI compared with hearts with myocardial scarring or hearts without acute or healed MI. Only 46% of hearts with a healed MI had an active coronary artery lesion identified at the time of sudden coronary death. Sudden coronary death without an active coronary lesion and without an MI (acute or healed) was not uncommon in the present study as it accounted for 17 of 90 cases (19%). Of the 34 cases without an acute or a healed MI, 17 cases (50%) lacked an active coronary artery lesion. The mechanism of sudden death in this group is uncertain. It may be postulated that vasospasm or increased susceptibility to ventricular fibrillation in the setting of chronic myocardial ischemia is responsible for sudden death in these instances.
Frequency of Active Lesions in Sudden Coronary Death:
Previous Studies
Studies by Davies et al12 14
are most directly
comparable to the present study based on methodological
similarities. In their reports, coronary arteries were
analyzed by postmortem angiography and serial
histological sectioning at 3-mm intervals. In a
consecutive series of 100 sudden cardiac death cases in London, UK,
these authors identified active arterial lesions, defined
as coronary artery thrombi or atherosclerotic plaque fissuring,
in 95% of hearts and intraluminal thrombi in 74%.12 In
26 cases without luminal thrombi, intraintimal thrombus, defined as
platelets and fibrin within the intima, was identified in 21, and
plaque fissure was identified in 19. Only 5 cases (5%) had neither an
intraluminal thrombus nor plaque fissure. Of all thrombi, 90% were
associated with plaque fissuring. The mean percent cross-sectional
luminal stenosis was 79% in arteries with luminal thrombi;
65% of cases had 75% luminal stenosis. When thrombi
occurred in arteries with <50% stenosis, a major fissure of a
lipid-rich plaque was seen. In a subsequent study of 168 cases of
sudden coronary death, 73.3% were associated with plaque
fissuring and a mural or occlusive thrombus.14 An
additional 7.7% of these cases had a plaque fissure without luminal
thrombus so that >80% of their sudden coronary deaths had an
active coronary artery lesion.14 The difference in
the incidence of active coronary lesions in the reports by
Davies et al and that in the present study, in which 57% of hearts
had acute coronary thrombosis, disrupted plaque, or both, is
uncertain. One-vessel disease was more frequent in the present
study (44% of cases) than in the study by Davies et al
(26%).14 The number of cases with three-vessel
disease in Davies et al (30%14 ) was greater than in the
present study (23%). These differences are somewhat unexpected as
one could postulate that there would be a higher incidence of
three-vessel disease and a lower incidence of one-vessel
disease in studies that report a relatively high rate of cases that
lack both an active coronary lesion and previous infarction.
The number of cases with acute MI was 40% in Davies et
al14 versus 21% in the present study.
In contrast, Warnes and Roberts13 studied hearts from 70 victims of sudden death due to coronary artery disease, of whom only 13 (19%) had coronary artery thrombi. In this study,13 coronary arteries were sectioned at 5-mm intervals, and postmortem angiography was not performed. Thus, small localized areas of plaque rupture may have been missed.19 20 Unlike in the present study and studies by Davies et al, Warnes and Roberts excluded all hearts in which ventricular myocardial coagulation necrosis was present. The number of sudden coronary death hearts that had myocardial coagulation necrosis and were excluded from analysis was not stated. This most likely resulted in a decreased frequency of active coronary lesions. For example, in the present study, 25% of all cases with acute coronary thrombosis had evidence of acute myocardial necrosis. Of the 13 arteries with thrombi in the study by Warnes and Roberts, 7 had superficial plaque rupture, and only 3 thrombosed arteries had plaque containing pultaceous debris, suggesting that most of these plaques were predominately fibrous. Unlike the present study and those by Davies et al,12 14 all significantly narrowed arteries were not specifically analyzed for the presence of plaque fissure, so active coronary lesions consisting of coronary fissure without thrombus (which comprised 8% of sudden death hearts in the series by Davies et al) were not accounted for. Furthermore, Warnes and Roberts defined coronary thrombus as a collection of fibrin or platelets within the residual lumen. In contrast, in Davies et al,12 21% of sudden cardiac death victims had intraintimal thrombi without intraluminal thrombi.
A summary of previous large studies of cardiac pathology in
sudden
coronary death is presented in Table 3. The definition of
sudden death
has included various intervals of duration of symptoms before collapse,
and most recent studies have used a 6-hour time period. In the
present study, we used a 6-hour symptom interval in individuals
with witnessed collapse and have also included cases of persons found
dead within 24 hours of being alive and known to be in stable
condition. Davies17 claims that after 6 hours, there is a
greater likelihood that patients with ischemic heart disease
will die secondary to complications of infarction such as cardiogenic
shock. If this were true, one might have expected a higher frequency of
acute MI in the present study. However, the incidence of acute MI
was 21% in the present study versus 40% in the report by Davies
et al.14 Also, the accuracy of symptom duration may be
questioned as individuals may have symptoms that are not reported
before sudden collapse. In general, most studies did not use postmortem
angiography. Furthermore, few studies specifically identified disrupted
plaques as important components of coronary artery pathology in
sudden coronary death.
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The following are factors that may explain differences in results compared with previous studies of sudden cardiac death:
1. Chest pain or other evidence of myocardial ischemia: The presence of antemortem chest pain identifies a cohort with an increased frequency of coronary thrombi.17 In contrast, the inclusion of individuals with a history of old MI reduces the frequency of acute thrombi in autopsy studies of sudden cardiac death.17 Of 47 cases of sudden death due to coronary atherosclerosis reported by Falk,11 prodromal chest pain was present in 42 (89%), and plaque rupture with coronary thrombosis was noted in 40 (85%). Of 168 sudden death victims reported by Davies et al,14 116 (69%) had prodromal chest pain, and of these, 97 (84%) had coronary thrombi. Chest pain or a potential anginal equivalent was noted in only 18 of 48 (38%) cases in the present study with witnessed collapse; this clinical historical factor may help to explain the lower prevalence of active coronary lesions in the present study.
2. Increased heart weight: Davies et al14 noted significantly increased heart weight in sudden death cases that lacked both MI and an active coronary lesion. Similar results were not found in the present study; the mean heart weight in cases with an active coronary artery lesion was 471±110 versus 423±72 g (P=NS) in hearts with neither an active coronary artery lesion nor MI. The results of the present study suggest that the presence of cardiomegaly cannot explain the mechanism of sudden coronary death in these individuals.
3. Tissue handling: The methods used for preparing heart specimens in the present study are similar to those of Davies et al—perfusion-fixation, postmortem angiography, and serial sectioning of the coronary arteries at narrow intervals. It should be recognized that active coronary lesions are typically quite focal in nature. The entire lesion may occupy less than a few hundred microns of tissue, so sectioning at 3- to 5-mm intervals may not be sufficiently sensitive to reliably identify the true frequency of all arterial lesions.21
Clinical Implications
Individuals with sudden coronary death
but without
an active coronary lesion may be divided into two groups: those
with MI and those without myocardial scarring. Risk factors for sudden
death in persons with previous MI have been identified and include
depressed left ventricular function and spontaneous complex
ventricular arrhythmias,22 23 24 and
perhaps abnormal signal-averaged ECG25 26 and
inducible sustained ventricular tachycardia by
electrophysiological
testing.27 In contrast, the cohort of individuals with
stable severe coronary atherosclerosis without
previous MI who are at increased risk of sudden death may be difficult
to identify without provocative screening tests (ie, stress
tests) since they may be asymptomatic or not cognizant
of symptoms as manifestations of ischemia and are unlikely to
have an abnormal ECG.
Coronary revascularization by bypass surgery has reduced overall mortality in selected subsets of patients (eg, individuals with left main disease and three-vessel disease and severe ischemia or left ventricular dysfunction)28 29 30 31 but, in general, not the incidence of subsequent MI.30 32 33 The data from the present study and previous clinical observations may help to explain this phenomenon. In individuals dying suddenly with advanced coronary atherosclerosis but with neither an active coronary lesion nor MI (19% of the cases in the present report), the mechanism of sudden death probably involves the generation of a lethal arrhythmia by severe myocardial ischemia. In these cases, the plaque itself is unchanged, and it is the myocardium that experiences the ischemic insult, perhaps via increased oxygen demand or increased vascular tone. One may postulate that it is these persons whose prognoses are improved by coronary revascularization to reduce the extent of myocardial ischemia. In contrast, plaque rupture and thrombosis are acute events that cause a dramatic change in plaque morphology. When active coronary lesions occur, some individuals will die suddenly, whereas others will present with acute MI or unstable angina. It has been well documented that clinicians are limited in their ability to predict which specific plaques are susceptible to plaque rupture and thrombosis based on angiographic findings.34 35 It could be expected that revascularization would not substantially reduce later MI since bypass is performed on coronary lesions present at the time of the procedure, and non–critically stenosed but potentially vulnerable plaques are likely to be ignored. Therefore, improvements in the identification and treatment of plaques at risk for acute rupture and thrombosis may hold promise for the prevention of both acute MI and sudden coronary death.
Study Limitations
It has generally been agreed that at least
one of the major
epicardial coronary arteries must be narrowed 75% for death
to be ascribed to ischemic heart disease. However, the
prevalence of significant coronary artery disease in
individuals who do not die secondary to their severe coronary
atherosclerosis must be recognized. In an autopsy study
by Thomas et al,36 among 124 men (age range, 50 to 69
years) who died of noncardiac causes, 10.3% had one-vessel, 2.8%
had two-vessel, and 1.4% had three-vessel coronary
disease. Even active coronary lesions have been observed in
cases of noncardiac sudden death; a plaque fissure and intraintimal
thrombus (without intraluminal thrombus) were present in 8.9% of
69 cases of noncardiac sudden death.14 Thus, it is with
some conjecture that death was truly due to inactive coronary
artery lesions in the present study in which neither
coronary thrombosis nor plaque rupture was present,
especially in the 8 cases of one-vessel disease without MI. In a
recent study by Corrado et al,37 sudden cardiac death was
attributed to one-vessel disease in 33 of 37 young persons, with
coronary thrombosis noted in only 27%. Spontaneous
thrombolysis may theoretically reduce the incidence of
coronary thrombi found at autopsy. However, plaque rupture or
fissure would still be apparent. With careful examination and serial
sectioning in the present study, we sought to minimize the chance
that coronary thrombi or disrupted plaques could have been
overlooked. Finally, autopsy studies may be inherently biased because
of patient selection for postmortem examination.
Conclusions
In sudden coronary death, approximately 60% of
individuals have an active coronary artery lesion at autopsy,
with previous myocardial scarring found in another 20%. The remaining
20% of individuals have severe coronary artery disease with
inactive plaques and no MI. Improvements in the ability to identify
individuals in these subgroups at risk for sudden coronary
death may improve their long-term survival.
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Footnotes |
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The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or reflecting the views of the Department of the Army or the Department of Defense.
Received February 19, 1995; revision received April 10, 1995; accepted April 16, 1995.
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