Vous êtes sur la page 1sur 6

Clin. Cardiol.

15,760-765 (1992)

ClCnlcal Pathologlc Correlations


This section edited by Bruce Waller;M D.

Cardiac Pathology in 2007 Consecutive Forensic Autopsies


BRUCEF. WALLER,
M.D., MICHELE
J. CATELLIER,
M.D.,* MICHAEL
A. CLARK,
M.D.,* DEAN
A. HAWLEY,
M.D.,*
JOHNE. PLESS,M.D.*

The Cardiovascular Pathology Registry, St. Vincent Hospital and Health Care Center, Nasser, Smith & Pinkerton Cardiology, Inc.;
*Division of Forensic Pathology, Department of Pathology, Indiana University School of Medicine, Indianapolis,Indiana, USA

Summary: The incidence of various types of cardiovascular disease was evaluated in 2007 consecutive forensic
patients. Cardiovascular deaths accounted for 22.8% of the
study patients and atherosclerotic coronary heart disease
was the most common type of cardiac disease (18%).
Among subjects dying of atherosclerotic coronary disease,
sudden death was three times more frequent than acute
myocardial infarction. Expected cardiac findings included
the incidence of severe coronary atherosclerosis (21%),
floppy mitral valves (5%), and congenital bicuspid aortic
valves (1%). Major cardiac findings occurred in 32% and
minor cardiac findings were found in 40%. Only 17% of
hearts were anatomically normal. An unexpected cardiac
necropsy finding included the high frequency of myocardial bridges (23%). Unexpected cardiac findings included
the low incidence of acute myocarditis (0.6%) and common finding of tunneled epicardial coronary arteries
(myocardial bridges) (23%).

Introduction
Cardiovascular disease remains the number one killer in
the United States. More than half of these deaths are sudden,
unexpected; or both24 and thus fall into the realm of forensic pathology. In 1987 we began a systematic evaluation of
consecutive hearts from forensic autopsies to determine various types of cardiac abnormalities. Our first evaluation of
consecutive 470 hearts has been reported previously? The
present study, now encompassing over 2000 consecutive
forensic cardiac evaluations, expands the initial report fivefold. These cardiac observations (expected and unexpected)
provide a database for the frequency with which they may be
found in a group of nonhospitalized decedents.

Methods
Site and Population

Key words: cardiac disease, forensic, atherosclerosis,


valve disease, cardiomyopathy, sudden death, congenital
heart disease

This study was based upon forensic autopsies conducted in the Marion County Coroners system derived from an
area including the city of Indianapolis, Indiana, and surrounding townships. This population base is estimated at
1.5 million. Of 21 19 cardiac specimens examined between
1987 and 1991, 112 (5%)were excluded from this analysis because of severe decomposition or skeletonization.
Evaluation of Hearts and Collection of Data

Address for reprints:


B. F. Waller, M.D.
8402 Harcourt Road
Suite 400
Indianapolis, IN 46260, USA

Received: March 2, 1992


Accepted with revision: May 5, 1992

All of the hearts evaluated in this study were initially


examined by a forensic pathologist, then re-examined in
detail by a cardiac pathologist (BFW).All gross findings
were recorded and logged into a computer database.
Routine cardiac histology was performed on all hearts and
served to c o n f m or establish the cardiac diagnosis. Cardiac observations were subsequently divided into the following categories: (1) normal versus abnormal hearts, (2)

B. F. Waller et al.: Cardiac pathology in forensic autopsies

congenital versus acquired cardiac abnormalities, and (3)


major versus minor cardiac findings.
Definitions

Major cardiac findings were defined as those recognized


as responsible for death or as a potential cause of death.
Minor cardiac findings were those that were present but
not responsible for death and in most circumstances were
classified as incidental. Coronary atheroscleroticheart disease was defined as at least one major epicardial coronary
narrowed > 75% in cross-sectionalarea by atherosclerotic
plaque, thrombus, or both on gross examination. Sudden
coronary death was defined as death occurring within six
hours of onset of symptoms, if any, and at necropsy where
at least one major coronary artery was narrowed >75% in
cross-sectionalarea by plaque. The six-hour time span was
chosen to exclude gross and histologic evidence of myocardial necrosis (acute myocardial infarction) as a cause
of
Idiopathic dilated cardiomyoparhy was defined
as dilation of all four chambers with increased heart weight
but unassociated with valvular, coronary, or severe pulcardiomyopathy was dimonary d i ~ e a s eHypertrophic
.~~~
agnosed by asymmetric septal hypertrophy (a ratio of ventricular septum to free wall thickness of at least 1.3 to 1.O),
increased heart weight, normal or small left ventricular
cavity size, and histologic evidence of myocardial fiber
Inflammatory cardiomyopathy (myocardisorgani~ation.~.~
ditis) was established by histologic evaluation. Each myocardial section needed to contain massive areas of lymphocytic infiltrate associated with myocardial necrosis.
Rheumatic valvular heart disease was defined in the presence of mitral stenosis (fused commissures,diffuse leaflet
fibrosis). Aortic stenosis was classified as rheumatic when
the mitral valve was also stenotic and there was fusion of
one or more aortic valve commissures.Degenerative aortic
valve stenosis was defined as a three-cuspid aortic valve
unassociated with commissural fusion, containing heavy
mounds of calcific deposits in one or more sinuses of Valsalva, associated with an anatomically normal mitral valve;
the subject was aged > 65 years. A mitral valve was considered jloppy (mitral valve prolapse) on gross examination if it demonstrated thickening of leaflets with an increased leaflet area and dilated annulus. Additional findings

76 1

such as elongated chordae tendineae, interchordal hooding, or redundancy of valve leaflets and endocardial friction lesions were supportive, if present, but not required
for establishing this diagnosis.
Primary aortic dissection or ruptured aortic aneurysm
was diagnosed in the absence of any trauma and no other
potential cardiac cause of death. Complex congenital heart
disease was defined as conditions such as hypoplastic ventricles, valve atresia, primary endocardial fibroelastosis,
and a combination of two or more simple congenital defects such as atrial or ventricular septal defect (e.g., tetralogy of Fallot). A coronary artery ostium was considered in
a high take-ofposition if its ostium arose 5 mm or more
above the aortic sinotubular junction. A conal coronary
artery was defined as an accessory or third coronary vessel
arising in the right sinus of Valsalva and supplying the outflow tract of the right ventricle (i.e., conus). Segments of
epicardial coronary arteries which became covered by
myocardium (intramural segment), then returned to the
epicardial surface after at least 1 mm of depth and distance
were designated as tunneled coronary arteries (myocardial bridges). Hearts were classified as demonstrating
excess epicardial fat (cardiac adiposity) when 100% of
the right ventricular surface and adjacent atrioventricular
sulcus was covered by epicardial fat. Primary neoplastic
lesions seen in this study were all benign papillomas (papillary fibroelastoma).

Results
Demographics

The study population consisted of 1345 males (67%)


and 662 females (33%). The dominance of male gender
persisted over the four-year study: 1987 = 65%; 1988 =
69%; 1989 = 67%; 1990 = 66%. Ages of the study population ranged from newborn to 100 years (mean 41.3 years)
and the mean age was similar for each of the four years of
study. There was no significant difference in mean ages
between men and women, but the study subjects were
much younger than the decedent population of Marion
County as a whole (mean of the former = 41 years, mean
of the latter = 69 years).

TABLE
I Categories of death
Year
Cardiovascular
Cardiac
Aorta
Traumatic
Other

1987
n = 470 (%)
87
85
2
273
110

(18.4)
(18.0)
(0.4)
(58)
(23)

1988
n = 583 (%)

n = 483 (%)

1990
n = 531 (%)

n = 2007 (%)

126
125
1
319
78

98
95
3
304
81

146
143
3
324
61

457
448
9
1220
330

(24.2)
(24.0)
(0.2)
(61)
(15)

1989
(20.6)
(20.0)
(0.6)
(63)
(17)

(27.5)
(26.9)
(0.6)
(61)
(11)

Total
(22.8)
(22.3)
(0.45)
(61.0)
(16)

Clin. Cardiol. Vol. 15, October 1992

762

TABLEIl Cardiovascular causes of death


1987

Year

n = 470 (%)

Cardiac disease
Coronary heart disease
Sudden coronary death
Acute myocardial
infarction
Cardiomyopathy
Acute myocarditis
Rheumatic heart
disease
Degenerative aortic
stenosis
Floppy mitral valve
(sudden death)
Anomalous coronary
artery
Complex congenital
heart disease
Subtotal
Aortic disease
Primary aortic
dissection

Rupture aortic
aneurysm
Subtotal

Total

64 (13.6)
49
15
6 (1.3)
4 (0.8)

Total

1988
n = 523 (%)

1989
n = 483 (%)

1990
n = 531 (%)

n = 2007 (%)

101 (19.3)
72

79 (16.4)
53

119 (22.4)
101

363 (18.1)
275 (13.7)

18
9 (1.7)
4 (0.8)

88 (4.4)
31 (1.5)
13 (0.6)

29
12 (2.3)
2 (0.4)

26
4
3

(0.8)
(0.6)

1 (0.2)

1 (0.2)

1 (0.2)

1 (0.2)

(0.4)

(0.4)

6 (0.3)

5 (1.1)

3 (0.6)

(0.8)

(0.9)

17 (0.8)

1 (0.2)

1 (0.2)

2 (0.1)

3 (0.6)
143 (26.9)

14 (0.7)
448 (22.3)

4 (0.8)
85 (18.0)

5 (1.0)
125 (24.0)

2 (0.4)

1 (0.2)

0
2 (0.4)
87 (18.4)

0
1 (0.2)
126 (24.2)

Causes of Death

Causes of death for the 2007 forensic patients were classified as cardiovascular (heart and aorta); traumatic
(including homicides, suicides, and accidents); and other
noncardiac (noncardiac natural, sudden infant death syndrome, neoplastic, stroke, etc.). Cardiovascular causes of
death constituted 22.8% of the deaths (Tables I, II). The
most common type of cardiac death was coronary heart
disease (18%), followed by cardiomyopathy (1.5%), acute
myocarditis (0.6%), floppy mitral valve (0.8%), anomalous coronary artery (0.1%), and rheumatic heart disease
(0.1%) (Tables I, II). Diseases of the aorta as a cause of
death constituted only an additional 0.45%. Among the
subjects dying from atherosclerotic coronary disease, sudden coronary death was a more frequent mode of death
compared with acute myocardial infarction (14 versus 4%)
(Table 11).

2 (0.4)
95 (20.0)

(0.4)

1 (0.2)
3 (0.6)
146 (27.5)

3 (0.6)
98 (20.6)

8 (0.4)
1 (0.05)
9 (0.45)
457 (22.8)

mon (76%). Cardiomyopathy and valvular heart disease


constituted another 3.6% of acquired conditions. Cardiac
trauma (nonisolated trauma) occurred in 7.4% of subjects.
Major congenital cardiac conditions occurred in 140 cases
(7%) (Table IV). The most common major congenital cardiac anomaly was the floppy mitral valve (5%) followed

1
I

Major and Minor Cardiac Findings (Tables III-V)


Major acquired cardiac abnormalities occurred in 649
cases (32%) (Table III). The most common major acquired
finding was atherosclerotic coronary heart disease (20.6%)
(Fig. 1). Triple vessel (left anterior descending, left circumflex, right coronary arteries) disease was most com-

(0.6)

2 (0.1)

Tunneled
coronary

artery

4.9

Probe Coronary Floppy cardio- Bicuspid Acute Anomalous


mitral myopathy aortic myowditis coronary
patent heart
foramen disease valve
valve
artery
oval9

FIG. 1 Frequency of certain acquired and congenital cardiac


conditions in 2007 consecutive forensic necropsy subjects.

B. E Waller et al.: Cardiac pathology in forensic autopsies

763

TABLEIII Major acquired cardiac findings

Year
Atherosclerotic coronary
heart diseasea
Left main disease
Single vessel
Double vessel
Triple vessel
Acute myocardial
infarction (1) rupture

Healed myocardial
infarction
Left ventricular aneurysm
Ruptured papillary muscle
Sudden coronary death

1987
n=470 (%)

1988
n=523 (%)

1989
n=483 (%)

77 (16.0)
4
3
11
59
15 (3.2)
[OI

124 (23.7)
6
5
14
99
29 (5.5)

Total

1990
n=531 (a)

n = 2007 (%)

103 (21.3)
3
8
16
76
26 (5.4)
111

110 (21.0)
5
9
15
81
18 (3.4)
[I1

414 (20.6)
18
25
56
315
88 (4.4)
131 (0.2)

(9.0)
(0.4)
(0.2)
(14.1)

39 (8.1)
0
0
60 (12.4)

56 (10.5)
1
0
83 (15.6)

172 (8.6)
4 (0.2)
1 (0.05)
261 (13.0)

4 (0.8)
2 (0.4)
0

11 (2.1)
1 (0.2)
0

3 (0.6)
1 (0.2)
0

7 (1.3)
2 (0.4)
0

25 (1.2)
6 (0.3)
0

4 (0.8)

2 (0.4)

3 (0.6)

4 (0.8)

13 (0.6)

3
8
1
7

(0.6)
(1.7)
(0.2)
(1.5)

0
5 (1.0)
0
5 (1.0)

1 (0.2)
8 (1.6)
0
8 (1.6)

0
5 (0.9)
0
5 (0.9)

4
26
1
25

2 (0.4)
0
36 (8.0)

1 (0.2)
0
51 (9.8)

3 (0.6)
0
22 (4.6)

2 (0.4)
1 (0.2)
40 (7.5)

8 (0.4)
1 (0.05)
149 (7.4)

0
1 (0.2)

2 (0.2)
2 (0.2)

30 (6.0)
1 (0.2)
0
44 (9.4)

HI
47
2
1
74

Cardiomyopathyb

Idiopathic dilated
Hypertrophic
Amyloid

Inflammatory
(acute myocarditis)
Valve diseaseC
h4itral stenosis
Aortic stenosis
Rheumatic
Degenerative
Primary (nontraumatic)
aortic dissection
Ruptured aortic aneurysm
Cardiac trauma
Neoplasm
Primary
Metastatic

2 (0.2)
0

1 (0.2)

0
0

(0.6)
(1.3)
(0.05)
(1.25)

O414 hearts (20.6%).


b44hearts (2.2%).
29 hearts (1.4%).

by the bicuspid aortic valve (0.8%). Minor acquired cardiac abnormalities including excessive epicardial fat, left
ventricular hypertrophy, and mitral annular calcium were
found in 802 (40%)hearts (Table V) and minor congenital
defects, including conal arteries and probe patent foramen
ovale defects, occurred in 1378 (68%)of hearts (Table V).
Only 339 hearts (17%) were free of the acquired or congenital lesions sought.

Discussion
The major goal of this and our previous study5 was to
focus on cardiac findings in a forensic pathology population. To our knowledge this remains the only study which
sequentially evaluates general gross cardiac findings in
forensic necropsy patients. Previous studies have evaluat-

ed a series of subjects for specific items such as sudden


aging changes,I5floppy mitral valves,1619athletic deaths,20 and myocarditis in children,21 but do not
describe other cardiac findings. Limitations of the present
study which may influence the results if applied to the general population include the overrepresentation of males and
low incidence of cardiac deaths. The male gender skew
could result in under- or over-representation of any of the
conditions evaluated. The low frequency of cardiac deaths
on this study contrasts with the estimated 48% of cardiovascular causes of death in the U.S.12or 30-35% in Marion County, Indiana.22An explanation for this difference is
the number of forensic cases signed out without autopsies which were attributed to cardiovascular deaths. In
1988,38%of signout cases in the Marion County Coroners Office were considered cardiovascular death^.^ Conversely, death certificates, which are the basis for most

Clin. Cardiol. Vol. 15, October 1992

764

TABLE
IV MaioP congenital cardiac findings
Year
Complex
Floppy mitral valve
Bicuspid aortic valve
Atrial septal defect only
Ventricular septal defect only
Congenital coronary anomaly
Single coronary artery
Right from left sinus
Left from right sinus
Absent left main
(separate origin left
anterior descending
and left circumflex)
Slit-like coronary ostium
a

1987
n = 470 (%)
4
22
3
1
1
2

(0.8)
(5.0)
(0.6)
(0.2)
(0.2)
(0.4)

(0.4)

1988
n = 523 (%)

5
31
6
1
0
2

(1.0)
(5.9)
(1.1)
(0.2)
(0.4)

1989
n=483 (%)
2
27
4
0
0
1

(0.4)
(5.6)
(0.8)

(0.2)

1990
n=531(%)
3
19
3
1
0
2

(0.6)
(3.6)
(0.6)
(0.2)
(0.4)

Total
n = 2007 (%)
14
99
16
3
1
7

(0.7)
(4.9)
(0.8)
(0.1)
(0.05)
(0.3)

1 (0.2)
0
1 (0.2)

0
0
1 (0.2)

0
1 (0.2)
0

1 (0.05)
1 (0.05)
4 (0.20)

1 (0.2)

1 (0.05)

140 hearts (7%).

TABLE
V Minor acquired and congenital cardiac findings
Year
Minor acquireda
Cardiac adipoisty
Left ventricular hypertrophy
(>1.5cm wall thickness)
Mitral valve annular calcium
Minor congentialb
Conal right coronary artery
Probe patient foramen ovale
High takeoff coronary ostium
Bicuspid pulmonic valve
Quadracuspid pulmonic valve
Tunneled epicardial coronary

Totals

1987
n=470 (%)

1988
n=523 (%)

1989
n = 483 (%)

1990
n=531(%)

n=2007 (%)

101 (22.0)
61 (13.0)

141 (27.0)
82 (15.7)

128 (26.5)
77 (15.9)

137 (25.8)
91 (17.1)

507 (25.3)
311 (15.5)

18 (4.0)

29 (5.5)

26 (5.4)

21 (4.0)

94

(4.7)

148 (28.3)
101 (19.3)
27 (5.2)

162 (33.5)
113 (23.4)
23 (4.8)

195 (36.7)
129 (24.3)
19 (3.6)

625
429
108
1
1
463

(31.1)
(21.4)
(5.4)
(0.5)
(0.5)
(23.1)

120
86
39
1
1
138

(26.0)
(18.0)
(8.0)
(0.2)
(0.2)
(29.0)

0
0

0
0

122 (23.3)

107 (22.1)

0
0

96 (18.1)

802 hearts (40%).


1378 hearts (68%).

death rate statistics, are notoriously inaccurate and perhaps


overestimate the frequency of cardiac deaths.
Expected Findings

Observations in this study which were expected included: (1) coronary atherosclerosis as the major cardiac disease and leading cardiac cause of death; (2) the necropsy
frequency for floppy mitral valve (5%),17the frequency of
conal coronary arteries (38%)23and congenitally bicuspid
aortic valves (1%), and the low frequency of stenotic mitral valves (0.2%) and congenital coronary artery anomalies (0.3%).23

Unexpected Findings

TWO unexpected cardiac findings in this forensic necropsy study were: (1) a low frequency of fatal acute myocarditis (0.6%), and (2) high frequency of tunneled coronary
arteries (myocardial bridges) (23%). Several studies have
reported an incidence of myocarditis ranging from 7-12%,
particularly in pediatric cases.21124-26Differences in myocarditis definitions and the number of histologic sections
evaluated could explain this difference. Nearly 25% of the
hearts in this study contained a tunneled segment of a
major coronary artery (most commonly the left anterior
descending). This high frequency suggests tunneled coronary arteries are a common entity and mitigates against the

B. F. Waller et al.: Cardiac pathology in forensic autopsies

likelihood of its being relevant to myocardial injury or cardiac death.

References
1. 1988 Heart Facts, American Heart Association, Dallas, Texas,
1988
2. Gillum RF: Sudden coronary death in the United States 19801985. Circulation 79,756-765 (1989)
3. Rajs J: Cardiovascular abnormalities in children: A 10-year
forensic pathology study. J Forens Sci 30, 1157-1178 (1985)
4. Kannel WB, Schatzkin A: Sudden death: Lessons from subsets
in population studies. J A m Coll Cardiol5, 141B-149B (1985)
5. Catellier MJ, Waller BF, Clark MA, Pless JE, Hawley DA,
Nyhuis AW Cardiac pathology in 470 consecutive forensic
autopsies. J Forens Sci 35, 1042-1054 (1990)
6. Waller B: Pathology of acute myocardial infarction: Definition,
location, effects of reperfusion, complications and sequelae.
Cardiol Clin 6, 1-28 (1988)
7. Virmani R, Roberts WC: Sudden cardiac death. Hum Pathol
18,485-492 (1987)
8. Waller BF: Pathology of the cardiomyopathies. J A m Soc Echo
1 , 4 1 9 (1988)
9. Edwards WD: Cardiomyopathies. Hum Pathol 18, 625-635
(1987)
10. Luke J, Helpern M: Sudden unexpected death from natural
causes in young adults. Arch Pathol85, 10-17 (1968)
11. Penttila A, Ahonen A The epidemiology of autopsies in cardiovascular deaths of middle-aged men in Finland in 1973. Forens
Sci Int 13,239-251 (1973)
12. Roberts WC, Jones A: Quantitation of coronary arterial narrowing at necropsy in sudden coronary death. Am J Cardiol44,
3 9 4 5 (1979)

765

13. Baroldi G, Falzi G, Mariani F: Sudden coronary death: A postmortem study in 208 selected cases compared to 97 control subjects. Am Heart J 98,20-31 (1979)
14. Marek Z: Morphological changes in the myocardium as substrate of functional asymmetry in sudden death. Forens Sci 1,
427-436 (1972)
15. Pomerance A Aging changes in human heart valves. Br Heurt
J 29,222-231 (1967)
16. Virmani R, Atkinson JB, Forman MB, Robinowitz M: Mitral
valve prolapse. Hum Pathol 18,596-602 (1987)
17. Lucas R, Edwards J: The floppy mitral valve. Curr Pmbl Curdiol7,5-48 (1982)
18. Davies MJ, Moore BP, Brainbridge M V The floppy mitral
valve. Br Heart J 40,468-48 1 (1978)
19. Scala-Barnett D, Donoghue E: Sudden death in mitral valve
prolapse. JForens Sci 33,84-91 (1988)
20. Virmani R, Robinowitz M: Cardiac pathology and sports medicine. Hum PathoZ18,493-501 (1987)
21. Akman D, Berenson GS, Blonde CV, Webber LS, Stopa AR:
Heart disease in a total population of children: The Bogalusa
heart study. SouthMedJ75,1177-1181 (1982)
22. Health Department Data, Marion County, Indiana, 1987
23. Blake HA, Manion WC, Mattingly TW, Baroldi G: Coronary
artery anomalies. Circulation 30,927-940 (1964)
24. Noren GR, Staley NA, Bandt CM, Kaplan EL: Occurrence of
myocarditis in sudden death in children. J Forens Sci 22,
188-196 (1977)
25. Topaz 0, Edwards J: Pathologic features of sudden death in
children, adolescents and young adults. Chest 87, 416-482
(1985)
26. Schwartz CJ, Walsh WJ: The pathologic basis of sudden death.
Prog CardiovascDis 13,465-481 (1971)

Vous aimerez peut-être aussi