Background Cigarette smoking and abnormal serum cholesterolconcentrations are risk factors for acute coronary syndromes,but the underlying mechanisms are poorly understood. We studiedwhether cigarette smoking and abnormal cholesterol values mayprecipitate acute coronary thrombosis and sudden death resultingfrom either rupture of vulnerable coronary plaques or erosionof plaques.
Methods We examined the hearts of 113 men with coronary diseasewho had died suddenly and also analyzed their coronary riskfactors. We found an acute coronary thrombus in each of 59 men,and severe narrowing of the coronary artery by an atheroscleroticplaque without acute thrombosis (stable plaque) in 54. Casesof acute thrombosis were divided into two groups: 41 resultingfrom rupture of a vulnerable plaque (a thin fibrous cap overlyinga lipid-rich core), and 18 resulting from the erosion of a fibrousplaque rich in smooth-muscle cells and proteoglycans. Vulnerableplaques that had not ruptured were counted in each heart.
Results Cigarette smoking was a risk factor in 44 (75 percent)of the men with acute thrombosis, as compared with 22 (41 percent)of the men with stable plaques (P<0.001). The mean (±SD)ratio of serum total cholesterol to high-density lipoprotein(HDL) cholesterol was markedly elevated in the men who diedof acute thrombosis with plaque rupture (8.5±4.0) butonly mildly elevated in the men without acute thrombosis (5.5±2.4,P<0.001) and in the men with thrombi overlying eroded plaques(5.0±1.8, P<0.001). Multivariate analysis showed anassociation between an elevated ratio of serum total cholesterolto HDL cholesterol and the presence of vulnerable plaques (P<0.001).
Conclusions Among men with coronary disease who die suddenly,abnormal serum cholesterol concentrations — particularlyelevated ratios of total cholesterol to HDL cholesterol —predispose patients to rupture of vulnerable plaques, whereascigarette smoking predisposes patients to acute thrombosis.
Cigarette smoking and hypercholesterolemia are well-known riskfactors for atherosclerotic heart disease.1 In addition to itsassociation with premature atherosclerosis,2 cigarette smokingis a risk factor for acute myocardial infarction3 and possiblysudden death from coronary disease.4 Likewise, elevated serumcholesterol concentrations and low serum high-density lipoprotein(HDL) cholesterol concentrations are associated with an increasedrisk of acute coronary events and premature atherosclerosis.2,3Recently, it has been established that cholesterol-loweringtherapy decreases the frequency of acute myocardial infarction,especially in secondary-prevention trials.5
Sudden death, a frequent result of severe coronary disease,is often precipitated by acute coronary thrombosis. Plaque rupture,the most frequent cause of coronary thrombosis,6,7 has beenimplicated in the episodic progression of coronary stenosisas demonstrated by sequential angiography and is often associatedwith unstable angina.8 Atherosclerotic plaques that are vulnerableto rupture have a dense infiltrate of macrophages and, to alesser extent, lymphocytes8 within a fibrous cap that overliesa crescentic acellular mass of lipids. Another mechanism ofcoronary thrombosis, plaque erosion, has recently been identifiedas an important cause of sudden coronary death.9 Eroded plaquesdiffer from ruptured plaques in that they have a base rich insmooth-muscle cells and proteoglycans.9
Antithrombotic treatment is an integral part of the preventionof recurrent coronary events,10 and both cigarette smoking11and hypercholesterolemia12 have been linked to coronary thrombosis.Despite the evidence linking acute coronary events and coronarythrombosis to the risk factors of cigarette smoking and elevatedcholesterol concentrations, autopsy studies have not yet addressedthe association of the risk factors with the frequency and typeof acute coronary thrombosis in men who die suddenly.
This study addressed the following questions: Are risk factorsfor coronary disease associated with acute thrombosis in suddencoronary death? And are those risk factors associated with oneof the two major mechanisms of acute coronary thrombosis —plaque rupture and plaque erosion? The answers may help explainwhy cholesterol-lowering therapy and antithrombotic drugs preventacute coronary events in patients with severe coronary atherosclerosis.
Methods
Selection of Cases
The hearts of men who died suddenly of causes that were initiallyunexplained were examined prospectively in consultation withthe Office of the Chief Medical Examiner of the state of Marylandto establish the cause and manner of death of each of the men.Sudden death was defined as that occurring within 6 hours ofthe onset of symptoms (witnessed cardiac arrest) or within 24hours of the time that the victim was last seen alive in hisnormal state of health. Death from coronary causes was definedas a luminal narrowing of a major epicardial coronary arteryby at least 75 percent by an atherosclerotic plaque or acutethrombus when noncardiac causes of death could be ruled outby a complete forensic autopsy and the results of postmortemtoxicologic testing. From an initial series of 125 cases, atotal of 113 remained after cases with gross hemolysis or inadequatecells for the measurement of glycosylated hemoglobin were excluded.
Evaluation of the Hearts
All the hearts were studied under the supervision of the medicalexaminer; information on 26 cases has been published previouslywithout data on risk factors other than hypertension.13 In everycase, coronary arteries were perfusion-fixed with formalin at100 mm Hg.14 The coronary arteries were studied by serial sectioningat 3-mm intervals after decalcification, if necessary. Any 3-mmsegment that showed narrowing of more than 50 percent was submittedfor histologic analysis. In every artery with luminal narrowingof more than 50 percent and a necrotic core, the mean thicknessof the fibrous cap was measured by ocular micrometry.
Definitions
The culprit plaque was defined as the plaque with an acute thrombusor, in the absence of an acute thrombus, the one with the greatestdegree of luminal narrowing relative to the internal elasticlamina at the narrowest segment. An acute plaque rupture consistedof a luminal platelet–fibrin thrombus continuous withan underlying lipid-rich core (Figure 1A and Figure 1B). Theconnection between the thrombus and the lipid core was througha disrupted thin fibrous cap infiltrated by macrophages. A plaqueerosion (Figure 1C and Figure 1D) was defined as an acute thrombusin direct contact with the intimal plaque without rupture ofa lipid pool, as demonstrated by serial sections. A vulnerableplaque (Figure 2A and Figure 2B) was defined as a fibrous capless than 65 µm thick with an infiltrate of macrophages(>25 per high-magnification [0.3-mm-diameter] field), withor without plaque rupture. The 65-µm thickness in caseswithout rupture was chosen as a criterion for vulnerabilitybecause in arteries with ruptured plaque, the mean (±SD)cap thickness was 23±19 µm (95 percent of the capsmeasured less than 64 µm). Stable plaque was defined ascross-sectional luminal narrowing of at least 75 percent inthe absence of a luminal thrombus and could be vulnerable ornonvulnerable. An infarct was defined as previously described.14
Panel A shows a cross section of the epicardial coronary artery, demonstrating a rupture of the shoulder region of the plaque with a luminal thrombus (x30). Panel B, at a higher magnification than Panel A, shows a ruptured thin cap densely infiltrated by macrophages and an adjacent fibrin–platelet thrombus (black reflects the postmortem injection of contrast material) (x120). In Panel C, showing an eroded plaque, a subocclusive luminal thrombus is visible in a cross section of the epicardial coronary artery (x20). Panel D, at a higher magnification, demonstrates a luminal thrombus (left) overlying smooth-muscle-cell fibrin-rich plaque (x100). (Movat pentachrome.)
Panel A shows a cross section of the epicardial coronary artery, demonstrating a thin fibrous cap (arrowheads) overlying a crescentic, lipid-rich core (x30). Panel B, with a higher magnification of the margin of the cap, demonstrates dense infiltration by foamy macrophages (x300). (Hematoxylin and eosin.)
Serum and Blood Studies
Serum samples were analyzed for total cholesterol, HDL cholesterol,and thiocyanate, and blood cells were analyzed for glycosylatedhemoglobin, as previously described.15,16 The mean postmorteminterval was 19±8 hours. A history of smoking was assumedif the serum thiocyanate concentration was at least 90 µmolper liter.16 Henceforth, "smoking" will denote "presumed smoking."Hypertension was determined on the basis of the history andby microscopical analysis of renal vasculature.13 Hypercholesterolemiawas defined as a serum total cholesterol concentration of atleast 210 mg per deciliter (5.46 mmol per liter) or a ratioof total cholesterol to HDL cholesterol greater than 5.0.
Statistical Analysis
We divided the 113 hearts into two groups: 59 hearts with acutethrombi and 54 hearts without acute thrombi. The effects ofsmoking and race on the presence of thrombosis were assessedby using a two-by-two contingency table (Fisher's exact test),and the effects of age, serum total cholesterol concentration,serum HDL cholesterol concentration, and glycosylated hemoglobinconcentration were assessed by using Student's two-tailed t-test(unpaired). For multivariate analysis, the effects of age, race,serum total cholesterol concentration, HDL cholesterol concentration,the presence or absence of hypertension, and glycosylated hemoglobinconcentration on whether there was acute thrombosis were analyzedin all 113 cases by using stepwise logistic regression (significancelevel for removing the variable from analysis = 0.4, for enteringthe variable = 0.2).
We further divided the 59 hearts with acute thrombi into thosewith eroded plaques (18 hearts) and those with ruptured plaques(41). The two groups were compared in terms of age, the glycosylatedhemoglobin value, serum total cholesterol concentration, andserum HDL cholesterol concentration by using Student's t-test,and the effect of cigarette smoking was assessed with a two-by-twocontingency table (Fisher's exact test). For multivariate analysis,the effects of the risk factors on plaque rupture were evaluatedby stepwise logistic regression. To evaluate the associationbetween plaque rupture and the ratio of total to HDL cholesterol,the analysis was repeated, with total cholesterol and HDL cholesterolomitted as independent variables.
For each of the 113 hearts, we tabulated the total number ofvulnerable plaques and determined a mean value. Using Student'st-test, we compared the mean number of vulnerable plaques accordingto cigarette-smoking status, race, the presence or absence ofhypertension, and serum cholesterol concentrations; using simpleregression, we related the number of vulnerable plaques to age,concentrations of total cholesterol and HDL cholesterol, theratio of total to HDL cholesterol, and the glycosylated hemoglobinvalue. For multivariate analysis, we used analysis of varianceto assess the effects of the risk factors age and race on thenumber of vulnerable plaques.
The mean heart weight among the categories of culprit plaqueand the mean ages among risk-factor categories were comparedby using Student's t-test.
All data are expressed as means ±SD. For multivariateanalyses, the serum total cholesterol and HDL cholesterol concentrations,the ratio of total HDL to cholesterol, and the glycosylatedhemoglobin value were considered as continuous variables.
Results
Descriptive Information
The mean age of the 113 patients at the time of death was 50±10years. There were 86 whites and 27 blacks. In 68 men (60 percent)the cardiac arrests had been witnessed, whereas 45 men (40 percent)had been found unresponsive. The mean body weight was 87.0±20.7kg. Acute coronary thrombi were present in 59 cases; of those,41 represented plaque ruptures and 18, plaque erosions. Theculprit plaques were stable in the remaining 54 cases; in 29of these an old myocardial infarction was present. Acute myocardialinfarcts were present in 8 of the 41 cases of plaque rupture,in 2 of the 18 cases of eroded plaque, and in 2 of the 54 heartswith stable plaque. The mean heart weight (normal range, 277to 481 g for an 87-kg man)17 was 485±120 g in cases ofacute thrombosis and 495±103 g in cases of stable plaque(P = 0.64). In hearts with stable plaque, the mean heart weightwas 522±84 g in the presence of a healed infarct and465±116 g in hearts without a healed infarct (P = 0.04).In hearts with acute thrombi, the mean heart weight was 499±122g for those with plaque ruptures and 455±112 g for thosewith eroded plaque (P = 0.20).
The mean age of the men who died with acute thrombi was 47±9years, as compared with 53±11 years for those with stableplaque (P = 0.005). The mean age of the smokers was 47±8years, as compared with 54±11 years for the nonsmokers(P< 0.001); the mean age of the men with hypertension was55±13 years, as compared with 48±8 years for thenormotensive men (P<0.001); and the mean age of the men withelevated serum total cholesterol and an elevated ratio of totalto HDL cholesterol was 48±9 years, as compared with 53±10years for those without elevated values (P = 0.05).
Association between Risk Factors and Acute Thrombosis
The men who died with acute thrombosis were more likely to besmokers (44 of 59, or 75 percent) than the men who died withstable plaque (22 of 54, or 41 percent; P<0.001) (Table 1).According to the multivariate analysis, cigarette smoking wasassociated with acute thrombosis (odds ratio, 3.6; P = 0.004).In contrast, the serum HDL cholesterol concentration (odds ratiofor each additional milligram per deciliter, 1.01), hypertension(odds ratio, 0.5), age (odds ratio for each additional year,1.0), black race (odds ratio, 0.6), glycosylated hemoglobinvalue (P>0.4), and serum total cholesterol concentration(P>0.4) were not significantly associated with acute thrombosis(Table 1).
Table 1. Risk Factors and the Presence of Acute Coronary Thrombosis in 113 Men Who Died Suddenly with Severe Coronary Artery Disease.
Effect of Risk Factors on the Type of Coronary Thrombus
According to the univariate analysis, plaque rupture was associatedwith low serum HDL cholesterol concentrations (P = 0.008), elevatedserum total cholesterol concentrations (P = 0.01), and an elevatedratio of total to HDL cholesterol (P = 0.001) (Table 2). Themean total:HDL cholesterol ratio in the men who died of plaquerupture was 8.5±4.0, as compared with 5.5±2.4in the men who died with stable plaque (P<0.001). By multivariateanalysis, the serum concentrations of total cholesterol (oddsratio, 1.02) and HDL cholesterol (odds ratio, 0.92) and theratio of total to HDL cholesterol (odds ratio, 1.78) were independentlyassociated with plaque rupture (P = 0.003) (Table 2). Hypertension(odds ratio, 0.09), smoking (odds ratio, 0.28), age (odds ratio,1.04), glycosylated hemoglobin value (P>0.4), and race (P>0.4)were not significantly associated with plaque rupture.
Table 2. Risk Factors and the Type of Coronary Thrombosis in 59 Cases of Sudden Death from Coronary Causes with Acute Thrombosis.
Effect of Risk Factors on Vulnerable Plaques
According to the univariate analysis, the numbers of vulnerableplaques were associated with the serum total cholesterol concentration(r2 = 0.08, P = 0.003) and the serum HDL cholesterol concentration(r2 = 0.04, P = 0.03), with the ratio of total to HDL cholesterol(r2 = 0.11, P<0.001), and with white race (P = 0.02); therewas no association between the glycosylated hemoglobin valueand the number of vulnerable plaques (r2 = 0.002, P = 0.65).The mean numbers of vulnerable plaques were lower in the blackmen and higher in the men with elevated serum cholesterol concentrations(Table 3). The mean number of vulnerable plaques in the menwith hypertension was 1.0±1.0, as compared with 1.3±1.6in the normotensive men (P = 0.33); in the smokers, the numberwas 1.1±1.3, as compared with 1.4±1.7 in the nonsmokers(P = 0.33). According to multivariate analysis, the total cholesterolconcentration (F = 19.7, P<0.001) and the HDL cholesterolconcentration (F = 7.3, P = 0.008) were associated with thenumbers of vulnerable plaques; there was no significant associationbetween smoking status (F = 4.4, P = 0.09), race (F = 1.7, P= 0.18), glycosylated hemoglobin value (F = 0.28, P = 0.60),age (F = 0.00, P = 0.94), or the presence or absence of hypertension(F = 0.02, P = 0.88) and the numbers of vulnerable plaques.
Table 3. Mean Numbers of Vulnerable Plaques and Serum Cholesterol Concentrations in 113 Men Who Died Suddenly with Severe Coronary Artery Disease.
Discussion
Cholesterol-lowering therapy reduces the risk of acute coronaryevents, especially in secondary-prevention trials.5,18 Becausethe decrease in serum cholesterol is not associated with a largedecrease in the luminal narrowing of coronary arteries,19,20these benefits are assumed to be due to the stabilization ofvulnerable plaques rather than to plaque regression. The currentstudy demonstrates that an elevated serum cholesterol concentrationis associated with the rupture of vulnerable plaques. A possiblecorollary is that the benefit of cholesterol-lowering therapylies in reducing the frequency of plaque rupture. We have alsodemonstrated, in cases of sudden coronary death, that thereis a strong correlation between serum cholesterol and the numberof vulnerable plaques within the coronary tree that is independentof other risk factors.21,22,23,24
A decrease in serum cholesterol may result in the stabilizationof plaque by removing cholesterol from macrophage foam cells.25Lowering cholesterol may decrease the volume of soft, cholesteryl-ester–richnecrotic core, lessening the risk of plaque rupture by a "passive"mechanism involving mechanical factors.19,20,26 Lowering cholesterolmay also reduce the risk of thrombosis by decreasing plateletreactivity12 and endothelium-mediated vasoconstriction.27 Becausecoronary angioscopy allows an in vivo diagnosis of plaque thrombosis28and thermal probes may detect vulnerable plaques,29 it may bepossible in the future to identify the patients who will benefitmost from cholesterol-lowering strategies.
This study demonstrates that cigarette smoking in men is associated,independently of other risk factors, with coronary thrombosisin cases of sudden death from coronary causes. Cigarette smokingwas associated with thrombosis regardless of the mechanism ofplaque disruption (erosion or rupture) and was not associatedwith the number of vulnerable plaques. The mechanism of coronarythrombosis in cigarette smokers may be related to increasedplatelet aggregation and plasma epinephrine concentrations.11In addition to cigarette smoking, a variety of thrombotic factorshave been implicated in the development of coronary-artery atherosclerosisand thrombosis, including abnormal levels of fibrinogen,30 vonWillebrand factor antigen,30 and tissue plasminogen activator,30and the presence of anticardiolipin antibodies,31 cross-linkedfibrin-degradation products,32 and polymorphism of a plateletglycoprotein receptor.33
Our study demonstrates a decreased frequency of acute thrombosisin hypertension-related sudden death due to coronary eventsand shows that the mean age of men with hypertension who diesuddenly from coronary disease is greater than that of normotensivemen. The importance of left ventricular hypertrophy and microvasculardisease in sudden death with hypertension, relative to epicardialcoronary disease, has yet to be fully studied.13 The older ageof the men with hypertension reflects the relatively young ageof cigarette smokers, men who died with acute thrombosis, andmen with hypercholesterolemia; clinical studies have shown anassociation between premature death from coronary disease andthe risk factors of smoking and hypercholesterolemia.2
We did not find an association between glucose intolerance andsudden death with acute coronary thrombosis. In people withdiabetes who have unstable angina, however, coronary thrombosisis more frequent than in those without diabetes,34 indicatingthat in living patients with acute coronary syndromes, diabetesis strongly associated with acute thrombosis.34 The absenceof an association between diabetes mellitus and acute plaquedisruption in our study may suggest that, as is the case withhypertensive heart disease, noncoronary mechanisms related toglucose intolerance may be factors in the precipitation of suddendeath from coronary disease. The roles of renal disease, microvasculardisease, and diabetic cardiomyopathy in sudden death in patientswith diabetes remain to be elucidated.
The chief limitations of the current study include the inherentbias in the selection of patients for autopsy and the exclusiveselection of men who died suddenly. Therefore, the results mustbe interpreted cautiously when applied to patients who surviveacute coronary events, and may not apply to women. Because theseassociations corroborate clinical and experimental findings,however, we propose that among men who die suddenly, hypercholesterolemiahas predisposed them to the rupture of vulnerable plaques andcigarette smoking has predisposed them to acute thrombosis.Cholesterol lowering may be particularly beneficial to patientswith vulnerable plaques, and antithrombotic therapy may be especiallyeffective in cigarette smokers at risk for sudden death dueto coronary events.
The opinions or assertions contained herein are the privateviews of the authors and are not to be construed as officialor as reflecting the views of the Department of the Army, theDepartment of the Air Force, or the Department of Defense.
Source Information
From the Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, D.C. (A.P.B., A.F., Y.L., R.V.); Louisiana State University, New Orleans (G.T.M.); and the University of Maryland, Baltimore (J.S.).
Address reprint requests to Dr. Virmani at the Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC 20306-6000.
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