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Incidence of significant coronary artery disease in rheumatic valvular heart disease
Incidence of Significant Coronary Artery Disease in Rheumatic Valvular Heart Disease
ELLIOTT
H. COLEMAN,
and LOUIS A. SOLOFF, Philadelphia,
MD MD, FACC
Pennsylvania
Thirteen percent of 77 patients who died after surgical treatment to correct valvular dysfunction were found at necropsy to have clinically significant coronary artery disease. This disorder occurred at all ages but was more common after age 40 years. It was commoner in aortic valvular disease either alone (17.7 percent) or combined with mitral valvular disease (21.1 percent) than in isolated mitral valvular disease (8.6 percent). This difference might be due to the older age at death of the patients who had aortic lesions. Because clinically significant coronary artery disease complicating valvular heart disease is difficult to recognize on clinical grounds and because it might adversely affect prognosis, coronary cinearteriography and left ventricular angiography are suggested in the overall evaluation of patients for valvular heart surgery. Such studies should be made particularly in those above age 40 years and in those with X-ray evidence of aortic calcification and with atherosclerosis detected during retrograde catheterization of the femoral artery. Atherosclerosis of the coronary arteries is the commonest cardiac disorder in adults. Its incidence increases with age. Clinical evidence of this disorder occurs particularly after the age of 40 years, the age period when most patients are subjected to surgery for correction of valvular dysfunction. Therefore it is not surprising that rheumatic heart disease and coronary artery disease may coexist. Older reports’ suggest that rheumatic fever, in addition to producing specific injuries to small coronary arterial branches, may accelerate the development of coronary atherosclerosis. Coronary artery disease may therefore be an additional and an occult cause of myocardial dysfunction in rheumatic valvular heart disease and an important factor in preventing optimal recovery after surgical correction of valvular dysfunction. This possibility has been recognized in the older patient with aortic stenosis, particularly when angina pectoris is present. However, in general it has been ignored in patients without angina pectoris and in younger patients with mitral valvular disease. This report assesses the incidence and severity of coronary artery disease in subjects who died after valvular heart surgery.
From the Division of Cardiology, Department of Medicine, Temple University Health Sciences Center, Philadelphia, Pa. This work was supported by U. S. Public Health Service Grant HE 5712-03 and by the Council for Tobacco Research, U.S.A. Manuscript received April 19, 1969, accepted August 4, 1969. Address for reprints: Louis A. Soloff, MD, Division of Cardiology, Temple University Health Sciences Center, 3401 N. Broad St., Philadelphia, Pa. 19140.
VOLUME 25, APRIL 1970
Material and Methods There were 77 necropsies in individuals who died in our hospital between 1963 and 1968 after surgical treatment for rheumatic valvular heart disease. Thirty-six of these were men and 41 were women. Eighteen were under age 40 years and 59 were older. Replacement of the mitral valve alone was the commonest operation. Combined aortic and mitral valve replacements were commoner than replacement of the aortic valve alone. Because clinical coronary artery disease de-
401
COLEMAN AND SOLOFF
TABLE
I
Age at Death in Seventy-Seven Degree of Coronary Artery Disease
volvrment of the mitral valve alone. Nonetheless, 8.6 percent of patients with isolated mitral valvular lcSons had clinically significant coronary arttry tlisease. The age ut death of these patients having aortic valvular disease alone or in combination with mitral disease was significantly higher than t’hat of ljatients who had isolated mitral disease. The average age at death was 45 years in those receiving a mitral prosthesis, whcrca? thozc opciatcd on for aoitic valvular disease and for combined aortic and mitral valve correction had an average age at death of 53 and 50 years, respectively. This difference in age might partially explain the liighci wrsociation of significant coronary artery disease in those with aortic valvular disease. Eight patients (Table I) had evidence of old myocardial infarction. Atherosclerosis was not confined to the coronary arteries in those with significant coronary occlusive disease, as evidenced by the presence of thoracic and abdominal aortic atherosclerosis described by the pathologist as moderate to severe in 7 of these 10 patients. Two of the 7 were under age 50, 1 was only 25 and t.he other 43 years old.
Cases
Age (yr) <20
21-30
31-40
41-50
51-60
61-70+
Men 0 1 2 3 None noted Total
10 0 0 0 0 1
0 0 1 0 1
13 3 0 0 1 5
4 1 1 2 11
2 3 4 3 0 12
0 4 2 0 0 6
Women 0 1 2 3 None noted Total
2 0 0 0 0 2
3 0 0 1 1 5
2 1 0 0 1 4
2 12 0 0 0 14
1 5 3 3 2 14
1 0 0 1 0 2
Total
7 (9.1%) 14 (18.2%) 7 5 3 36
(9.1%) (6.5%) (3.%) (46.%)
11 (14.3%) 18 (23.4%) 3 5 4 41
(3.9%) (6.5%) (5.2%) (53.2%)
Code for severity of coronary artery disease: 0 = no significant disease; 1 = 25-50s or more occlusion of lumen (mild); 2 = 50-75s or more occlusion of vessel lumen (moderate); 3 = >75% occlusion of vessel lumen (severe).
pends upon degree of occlusion of the coronary arteries rather than the anatomic distribution of atherosclerosis, coronary artery disease was graded as follows: 0, up to 25 percent reduction of lumen ; grade 1, up to 50 percent; grade 2, up to 75 percent; and grade 3, greater than 75 percent reduction in lumen.
Grade 3 Coronary Artery Disease
Old infarction and myocardial fibrosis: All of the 10 with grade 3 occlusive disease had atherosclerotic involvement of all three major branches of the coronary arteries. Four of the 10 had old myocardial infarctions (Cases 2,3,5 and 8, Table IV). Of these 4, 1 had calcifications in the coronary arteries with marked reduction of the lumen of the distal half of the left circumflex artery and infarction of the septum extending into the free wall of the right ventricle; 1 had occlusion of the right coronary artery with an old infarction involving the posterior wall of the left ventricle ; 1 had extreme narrowing of the right coronary artery with an old infarction of the posterior third of the intravent’ricular septum; the f0urt.h had calcification of all major branches and old infarction of the posterior wall of the left ventricle. The circumflex branch was completely replaced by calcium. Three of the 10 had microscopic regions of fibrosis not definitely attributable to a specific occlusive vessel. Of these 3, 1 had numerous plaques in the right
Results Table I shows the ages at death for both men and women and the degree of reduction of lumina of coronary arteries for each age group. Table II gives the incidence by sex for each operative procedure. Table III shows the degree of reduction of the lumina of the coronary arteries for each operative procedure. Ten patients (13.0 percent) had clinically significant (grade 3) coronary artery disease. Eight of these 10 were above 40 years of age and 2 were below 30 years. Both sexes were equally affected. Those with involvement of the aortic valve, either alone or combined with involvement of the mitral valve, had a higher percentage of complicating clinically significant coronary artery disease than did those with inTABLE
II
Sex and Type of Valve Replaced
Sex M F Total
402
in Seventy-Seven
Mitral 14 21 35
Cases
Tricuspid 0 1 1
Aortic
Mitral & Tricuspid
13 4 17
1 4 5
Mitral & Aortic
a 11 19
The American
Total 36 (46.8%) 41 (53.2%) 77 (100%)
Journal of CARDIOLOGY
CORONARY
TABLE
DISEASE
IN
VALVULAR
DISEASE
III
Degree of Coronary
Artery
Degree of Coronary Artery Disease ~~~~ ~__ 0 1 2 3
___
None
noted
Disease Related to Type of Valve Replaced in Seventy-Seven
.___
Mitral
Tricuspid
25,
APRIL
1970
Cases
Mitral & Aortic -_-_
Mitral & Tricuspid
Aortic
12 14 3 3
1 0 0 0
4 5 4 3
1 3 0 0
0 10 3 4
3
0
1
1
2
coronary artery with complete occlusion 6 cm from its orifice and spotty fibrosis in the free wall of the left ventricle; 1 had numerous ulcerative plaques in the three major branches of the coronary arteries and a small scar at t.he apex of the left ventricle; the third calcification of the anterior descending hda pipe-stem and circumflex branches of the left coronary artery and a scar in the septum. Acute myocardial infarction: Two of these 10 had recent fresh infarcts. It was not possible to be certain whether they were iatrogenically produced at the time of operation or were independent of the technical procedure. They are therefore not included in Table I. One of these 2 had a recent occlusion of the left circumflex artery, and the other had calcification of the three branches of the coronary arteries with a recent acute myocardial infarction involving the posterior and anterior wall of the left ventricle. One patient without infarction or fibrosis had atherosclerotic plaques throughout the right and left coronary arteries and t,heir major branches with calcification in t.hc left anterior descending and right coronary arteries. Additional cases of old infarctions: Four other subjects had old infarction (Cases 1, 4, 6 and 7, Table IV). Three of these 4 had evidence of myocardial infarction but, the atherosclerotic coronary artery diseast was less than significant (
VOLUME
ARTERY
Total
.~_. 18 32 10 10
(23.4%) (41.6%) (13.0%) (13.0%)
7 (9.1%)
addition, there were two fibrotic lesions in the anterior and lateral walls of the left ventricle. The heart weighed 600 g, and the left ventricle was 2.2 cm thick. There was moderate atherosclerosis of the thoracic and abdominal aorta. In addition, there was a traumatic dissecting a,neurysm arising 3 cm above the insertion of a catheter in the right femoral artery. Thr traumatic aneurysm extended into the arch of the aorta and terminated in the region of the right innominate artery. The last (Case 1, Table IV) had patent coronary arteries with minimal atherosclerosis (grade 1). The patient was 63 years old and had had aortic valvular disease. There were two distinct areas differing in color in the left ventricular wall. One, consisting of brown hemorrhagic areas in the anterior wall of the left ventricle, appeared to be due to acute myocardial infarction. The ot,her, fibrous yellow areas, was considered to represent oltl infarction. One heart was lost in transit to the cardiac pathologist (Case 7, Table IV). The resident pathologist had noted the presence of an old myocardial infarction. This patient died after replacement of his aortic valve for aort,ic stenosis. Clinically, there was evidence of high grade ventricular hypertrophy, anal
TABLE
IV
Eight Patients Who Had Evidence of Past Myocardial at Necropsy
Age & Sex
Infarction
Degree of Coronary Artery Disease
1
63
M
Valve Replaced _-__._ Aortic
2
66
F
Aortic
3
3
54
M
Mitral
3 2
Case
4
56
M
Aortic
5
54
F
Mitral
6
57
F
Aortic
7
49
M
Aortic
8
58
M
Mitral
1
3 & mitral
2 Unknown 3
403
COLEMAN
AND
SOLOFF
X-ray study showed left ventricular enlargement and calcification of the aortic valve. The electrocardiogram showed left ventricular hypertrophy and S-T segment and T wave abnormalities of a coronary ischemic type. There was moderate atherosclerosis of the thoracic and abdominal aorta with foci of calcification. Two additional patients had ventricular aneurysms coexistent with mitral valvular disease but without significant coronary artery disease. The cause of these aneurysms was unexplained. They might have been due to previous embolization of the coronary arteries.
Discussion Severe coronary artery disease was found at necropsy in 13.0 percent of patients who had died after surgical treatment to correct valvular dysfunction. This incidence may be compared to Gardner and White’s report2 of 7 percent, to Kaufman and Poliakoff’s3 report of 10 percent and other reports up to 21.2 percent.4-6 These differences in occurrence could be related to differences in age groups, in definition of clinically significant coronary artery disease and in thoroughness of the anatomic examination. Clinical evidence of significant coronary artery disease in individuals with valvular heart disease may be difficult or impossible to recognize. Suggestive symptoms may be few or absent. Symptoms of myocardial ischemia could be due to myocardial limitation imposed by the valvular disorder and intrinsic myocardial rheumatic defects rather than coronary atherosclerosis.7-9 In this analysis findings of fibrosis and ventricular aneurysm in patients with minimal coro-
nary atherosclerosis might be cxplaincd by the presence of cliffuse rheumatic ]~athOl0gic ciiseasc in t.he nlyocardiun~. Postopcrativc failure of the pnticnt’s contlit,ion to improve or to improve optimally after surgery might be clue to clinically significant coronary disease. Thus, Peterson et al.“’ observed that 7 of 17 patients whose condition did not improve clinically after surgery had severe coronary artery disease with infarction and fibrosis diagnosed at necropsy. Linhart and Wheat’l in an analysis of 20 postoperative patients with aortic valvular disease noted that 14 had hemodynamic evidence of ventricular dysfunction. Of these 14, 9 had severe coronary artery disease diagnosed by coronary cinearteriography. These studies are primarily concerned wit’h aortic valvular disease. Our study indicates that clinically significant coronary artery disease also occurs in isolated mitral valvular disease. Clinical implications : Clinically significant coronary artery disease occurs in a high percentage of older patients with valvular heart disease. The ischemic lesions themselves may limit improvement of the patient’s condition after valvular surgery and presumably require their own specific treatment. Therefore, coronary arteriography and left ventricular angiography are suggested as routine procedures on all patients over the age of 40 years who are to undergo valvular heart surgery. One should consider the likelihood of significant coronary artery disease in the younger patient with rheumatic heart disease if there is roentgenographic evidence of aortic calcification and if the presence of atherosclerosis is recognized or suggested during retrograde catheterization of the femoral artery.
References 1. Zeek P:
2. 3. 4. 5. 6.
404
Studies in atherosclerosis. II. Atheroma and its sequelae in rheumatic heart disease. Amer J Med Sci l&$:356-364, 1932 Coronary occlusion and myoGardner FE, White PD: cardial infarction associated with chronic rheumatic heart disease. Ann Intern Med 31:1003-1009, 1949 Studies of the aging heart. The Kaufman P, Poliakoff H: pattern of rheumatic heart disease in old age. Ann Intern Med 32:889-904, 1950 Pfister CW. Plice SG. Do&worth J: The coexistence of rheumatic *heart disease and myocardial infarction. L$s.s:e;t 37:240-242, 1960 : Aortic stenosis and the so called rheumatic valvular disease in a post mortem material. Acta Med Stand 156:241-261, 1950 The coexistance of rheumatic Chasnbff J, Silver A: and arteriosclerotic heart disease in patients over the
age of 40 years. Amer Heart J 42:809-813, 1951 Manchester JH, Amsterdam EA, Kemp HG, et al: Coronary artery disease in valvular heart disease (abstr). Circulation 38: Suppl 6:132, 1968 Oakley C, Yusef R, Hollman A: Coronary embolism and angina in mitral stenosis. Brit Heart J 23:357-369, 1961 Grismer JT, Anderson WR, Weiss L: Chronic occlusive rheumatic coronary vasculitis and myocardial dysfunction. Amer J Cardiol 20:734-745, 1967 10. Peterson CR, Herr R. Cruera RV, et al: The failure of hemodynamic improvement after valve surgery. Ann Intern Med 66:1-24. 1967 11. Linhart JW, Wheat MW: Myocardial dysfunction following aortic valve replacement. The significance of coronary artery disease. J Thorac Cardiovasc Surg 54:259-264, 1967
The
American
Journal
of
CARDIOLOGY
ELLIOTT
H. COLEMAN,
and LOUIS A. SOLOFF, Philadelphia,
MD MD, FACC
Pennsylvania
Thirteen percent of 77 patients who died after surgical treatment to correct valvular dysfunction were found at necropsy to have clinically significant coronary artery disease. This disorder occurred at all ages but was more common after age 40 years. It was commoner in aortic valvular disease either alone (17.7 percent) or combined with mitral valvular disease (21.1 percent) than in isolated mitral valvular disease (8.6 percent). This difference might be due to the older age at death of the patients who had aortic lesions. Because clinically significant coronary artery disease complicating valvular heart disease is difficult to recognize on clinical grounds and because it might adversely affect prognosis, coronary cinearteriography and left ventricular angiography are suggested in the overall evaluation of patients for valvular heart surgery. Such studies should be made particularly in those above age 40 years and in those with X-ray evidence of aortic calcification and with atherosclerosis detected during retrograde catheterization of the femoral artery. Atherosclerosis of the coronary arteries is the commonest cardiac disorder in adults. Its incidence increases with age. Clinical evidence of this disorder occurs particularly after the age of 40 years, the age period when most patients are subjected to surgery for correction of valvular dysfunction. Therefore it is not surprising that rheumatic heart disease and coronary artery disease may coexist. Older reports’ suggest that rheumatic fever, in addition to producing specific injuries to small coronary arterial branches, may accelerate the development of coronary atherosclerosis. Coronary artery disease may therefore be an additional and an occult cause of myocardial dysfunction in rheumatic valvular heart disease and an important factor in preventing optimal recovery after surgical correction of valvular dysfunction. This possibility has been recognized in the older patient with aortic stenosis, particularly when angina pectoris is present. However, in general it has been ignored in patients without angina pectoris and in younger patients with mitral valvular disease. This report assesses the incidence and severity of coronary artery disease in subjects who died after valvular heart surgery.
From the Division of Cardiology, Department of Medicine, Temple University Health Sciences Center, Philadelphia, Pa. This work was supported by U. S. Public Health Service Grant HE 5712-03 and by the Council for Tobacco Research, U.S.A. Manuscript received April 19, 1969, accepted August 4, 1969. Address for reprints: Louis A. Soloff, MD, Division of Cardiology, Temple University Health Sciences Center, 3401 N. Broad St., Philadelphia, Pa. 19140.
VOLUME 25, APRIL 1970
Material and Methods There were 77 necropsies in individuals who died in our hospital between 1963 and 1968 after surgical treatment for rheumatic valvular heart disease. Thirty-six of these were men and 41 were women. Eighteen were under age 40 years and 59 were older. Replacement of the mitral valve alone was the commonest operation. Combined aortic and mitral valve replacements were commoner than replacement of the aortic valve alone. Because clinical coronary artery disease de-
401
COLEMAN AND SOLOFF
TABLE
I
Age at Death in Seventy-Seven Degree of Coronary Artery Disease
volvrment of the mitral valve alone. Nonetheless, 8.6 percent of patients with isolated mitral valvular lcSons had clinically significant coronary arttry tlisease. The age ut death of these patients having aortic valvular disease alone or in combination with mitral disease was significantly higher than t’hat of ljatients who had isolated mitral disease. The average age at death was 45 years in those receiving a mitral prosthesis, whcrca? thozc opciatcd on for aoitic valvular disease and for combined aortic and mitral valve correction had an average age at death of 53 and 50 years, respectively. This difference in age might partially explain the liighci wrsociation of significant coronary artery disease in those with aortic valvular disease. Eight patients (Table I) had evidence of old myocardial infarction. Atherosclerosis was not confined to the coronary arteries in those with significant coronary occlusive disease, as evidenced by the presence of thoracic and abdominal aortic atherosclerosis described by the pathologist as moderate to severe in 7 of these 10 patients. Two of the 7 were under age 50, 1 was only 25 and t.he other 43 years old.
Cases
Age (yr) <20
21-30
31-40
41-50
51-60
61-70+
Men 0 1 2 3 None noted Total
10 0 0 0 0 1
0 0 1 0 1
13 3 0 0 1 5
4 1 1 2 11
2 3 4 3 0 12
0 4 2 0 0 6
Women 0 1 2 3 None noted Total
2 0 0 0 0 2
3 0 0 1 1 5
2 1 0 0 1 4
2 12 0 0 0 14
1 5 3 3 2 14
1 0 0 1 0 2
Total
7 (9.1%) 14 (18.2%) 7 5 3 36
(9.1%) (6.5%) (3.%) (46.%)
11 (14.3%) 18 (23.4%) 3 5 4 41
(3.9%) (6.5%) (5.2%) (53.2%)
Code for severity of coronary artery disease: 0 = no significant disease; 1 = 25-50s or more occlusion of lumen (mild); 2 = 50-75s or more occlusion of vessel lumen (moderate); 3 = >75% occlusion of vessel lumen (severe).
pends upon degree of occlusion of the coronary arteries rather than the anatomic distribution of atherosclerosis, coronary artery disease was graded as follows: 0, up to 25 percent reduction of lumen ; grade 1, up to 50 percent; grade 2, up to 75 percent; and grade 3, greater than 75 percent reduction in lumen.
Grade 3 Coronary Artery Disease
Old infarction and myocardial fibrosis: All of the 10 with grade 3 occlusive disease had atherosclerotic involvement of all three major branches of the coronary arteries. Four of the 10 had old myocardial infarctions (Cases 2,3,5 and 8, Table IV). Of these 4, 1 had calcifications in the coronary arteries with marked reduction of the lumen of the distal half of the left circumflex artery and infarction of the septum extending into the free wall of the right ventricle; 1 had occlusion of the right coronary artery with an old infarction involving the posterior wall of the left ventricle ; 1 had extreme narrowing of the right coronary artery with an old infarction of the posterior third of the intravent’ricular septum; the f0urt.h had calcification of all major branches and old infarction of the posterior wall of the left ventricle. The circumflex branch was completely replaced by calcium. Three of the 10 had microscopic regions of fibrosis not definitely attributable to a specific occlusive vessel. Of these 3, 1 had numerous plaques in the right
Results Table I shows the ages at death for both men and women and the degree of reduction of lumina of coronary arteries for each age group. Table II gives the incidence by sex for each operative procedure. Table III shows the degree of reduction of the lumina of the coronary arteries for each operative procedure. Ten patients (13.0 percent) had clinically significant (grade 3) coronary artery disease. Eight of these 10 were above 40 years of age and 2 were below 30 years. Both sexes were equally affected. Those with involvement of the aortic valve, either alone or combined with involvement of the mitral valve, had a higher percentage of complicating clinically significant coronary artery disease than did those with inTABLE
II
Sex and Type of Valve Replaced
Sex M F Total
402
in Seventy-Seven
Mitral 14 21 35
Cases
Tricuspid 0 1 1
Aortic
Mitral & Tricuspid
13 4 17
1 4 5
Mitral & Aortic
a 11 19
The American
Total 36 (46.8%) 41 (53.2%) 77 (100%)
Journal of CARDIOLOGY
CORONARY
TABLE
DISEASE
IN
VALVULAR
DISEASE
III
Degree of Coronary
Artery
Degree of Coronary Artery Disease ~~~~ ~__ 0 1 2 3
___
None
noted
Disease Related to Type of Valve Replaced in Seventy-Seven
.___
Mitral
Tricuspid
25,
APRIL
1970
Cases
Mitral & Aortic -_-_
Mitral & Tricuspid
Aortic
12 14 3 3
1 0 0 0
4 5 4 3
1 3 0 0
0 10 3 4
3
0
1
1
2
coronary artery with complete occlusion 6 cm from its orifice and spotty fibrosis in the free wall of the left ventricle; 1 had numerous ulcerative plaques in the three major branches of the coronary arteries and a small scar at t.he apex of the left ventricle; the third calcification of the anterior descending hda pipe-stem and circumflex branches of the left coronary artery and a scar in the septum. Acute myocardial infarction: Two of these 10 had recent fresh infarcts. It was not possible to be certain whether they were iatrogenically produced at the time of operation or were independent of the technical procedure. They are therefore not included in Table I. One of these 2 had a recent occlusion of the left circumflex artery, and the other had calcification of the three branches of the coronary arteries with a recent acute myocardial infarction involving the posterior and anterior wall of the left ventricle. One patient without infarction or fibrosis had atherosclerotic plaques throughout the right and left coronary arteries and t,heir major branches with calcification in t.hc left anterior descending and right coronary arteries. Additional cases of old infarctions: Four other subjects had old infarction (Cases 1, 4, 6 and 7, Table IV). Three of these 4 had evidence of myocardial infarction but, the atherosclerotic coronary artery diseast was less than significant (
VOLUME
ARTERY
Total
.~_. 18 32 10 10
(23.4%) (41.6%) (13.0%) (13.0%)
7 (9.1%)
addition, there were two fibrotic lesions in the anterior and lateral walls of the left ventricle. The heart weighed 600 g, and the left ventricle was 2.2 cm thick. There was moderate atherosclerosis of the thoracic and abdominal aorta. In addition, there was a traumatic dissecting a,neurysm arising 3 cm above the insertion of a catheter in the right femoral artery. Thr traumatic aneurysm extended into the arch of the aorta and terminated in the region of the right innominate artery. The last (Case 1, Table IV) had patent coronary arteries with minimal atherosclerosis (grade 1). The patient was 63 years old and had had aortic valvular disease. There were two distinct areas differing in color in the left ventricular wall. One, consisting of brown hemorrhagic areas in the anterior wall of the left ventricle, appeared to be due to acute myocardial infarction. The ot,her, fibrous yellow areas, was considered to represent oltl infarction. One heart was lost in transit to the cardiac pathologist (Case 7, Table IV). The resident pathologist had noted the presence of an old myocardial infarction. This patient died after replacement of his aortic valve for aort,ic stenosis. Clinically, there was evidence of high grade ventricular hypertrophy, anal
TABLE
IV
Eight Patients Who Had Evidence of Past Myocardial at Necropsy
Age & Sex
Infarction
Degree of Coronary Artery Disease
1
63
M
Valve Replaced _-__._ Aortic
2
66
F
Aortic
3
3
54
M
Mitral
3 2
Case
4
56
M
Aortic
5
54
F
Mitral
6
57
F
Aortic
7
49
M
Aortic
8
58
M
Mitral
1
3 & mitral
2 Unknown 3
403
COLEMAN
AND
SOLOFF
X-ray study showed left ventricular enlargement and calcification of the aortic valve. The electrocardiogram showed left ventricular hypertrophy and S-T segment and T wave abnormalities of a coronary ischemic type. There was moderate atherosclerosis of the thoracic and abdominal aorta with foci of calcification. Two additional patients had ventricular aneurysms coexistent with mitral valvular disease but without significant coronary artery disease. The cause of these aneurysms was unexplained. They might have been due to previous embolization of the coronary arteries.
Discussion Severe coronary artery disease was found at necropsy in 13.0 percent of patients who had died after surgical treatment to correct valvular dysfunction. This incidence may be compared to Gardner and White’s report2 of 7 percent, to Kaufman and Poliakoff’s3 report of 10 percent and other reports up to 21.2 percent.4-6 These differences in occurrence could be related to differences in age groups, in definition of clinically significant coronary artery disease and in thoroughness of the anatomic examination. Clinical evidence of significant coronary artery disease in individuals with valvular heart disease may be difficult or impossible to recognize. Suggestive symptoms may be few or absent. Symptoms of myocardial ischemia could be due to myocardial limitation imposed by the valvular disorder and intrinsic myocardial rheumatic defects rather than coronary atherosclerosis.7-9 In this analysis findings of fibrosis and ventricular aneurysm in patients with minimal coro-
nary atherosclerosis might be cxplaincd by the presence of cliffuse rheumatic ]~athOl0gic ciiseasc in t.he nlyocardiun~. Postopcrativc failure of the pnticnt’s contlit,ion to improve or to improve optimally after surgery might be clue to clinically significant coronary disease. Thus, Peterson et al.“’ observed that 7 of 17 patients whose condition did not improve clinically after surgery had severe coronary artery disease with infarction and fibrosis diagnosed at necropsy. Linhart and Wheat’l in an analysis of 20 postoperative patients with aortic valvular disease noted that 14 had hemodynamic evidence of ventricular dysfunction. Of these 14, 9 had severe coronary artery disease diagnosed by coronary cinearteriography. These studies are primarily concerned wit’h aortic valvular disease. Our study indicates that clinically significant coronary artery disease also occurs in isolated mitral valvular disease. Clinical implications : Clinically significant coronary artery disease occurs in a high percentage of older patients with valvular heart disease. The ischemic lesions themselves may limit improvement of the patient’s condition after valvular surgery and presumably require their own specific treatment. Therefore, coronary arteriography and left ventricular angiography are suggested as routine procedures on all patients over the age of 40 years who are to undergo valvular heart surgery. One should consider the likelihood of significant coronary artery disease in the younger patient with rheumatic heart disease if there is roentgenographic evidence of aortic calcification and if the presence of atherosclerosis is recognized or suggested during retrograde catheterization of the femoral artery.
References 1. Zeek P:
2. 3. 4. 5. 6.
404
Studies in atherosclerosis. II. Atheroma and its sequelae in rheumatic heart disease. Amer J Med Sci l&$:356-364, 1932 Coronary occlusion and myoGardner FE, White PD: cardial infarction associated with chronic rheumatic heart disease. Ann Intern Med 31:1003-1009, 1949 Studies of the aging heart. The Kaufman P, Poliakoff H: pattern of rheumatic heart disease in old age. Ann Intern Med 32:889-904, 1950 Pfister CW. Plice SG. Do&worth J: The coexistence of rheumatic *heart disease and myocardial infarction. L$s.s:e;t 37:240-242, 1960 : Aortic stenosis and the so called rheumatic valvular disease in a post mortem material. Acta Med Stand 156:241-261, 1950 The coexistance of rheumatic Chasnbff J, Silver A: and arteriosclerotic heart disease in patients over the
age of 40 years. Amer Heart J 42:809-813, 1951 Manchester JH, Amsterdam EA, Kemp HG, et al: Coronary artery disease in valvular heart disease (abstr). Circulation 38: Suppl 6:132, 1968 Oakley C, Yusef R, Hollman A: Coronary embolism and angina in mitral stenosis. Brit Heart J 23:357-369, 1961 Grismer JT, Anderson WR, Weiss L: Chronic occlusive rheumatic coronary vasculitis and myocardial dysfunction. Amer J Cardiol 20:734-745, 1967 10. Peterson CR, Herr R. Cruera RV, et al: The failure of hemodynamic improvement after valve surgery. Ann Intern Med 66:1-24. 1967 11. Linhart JW, Wheat MW: Myocardial dysfunction following aortic valve replacement. The significance of coronary artery disease. J Thorac Cardiovasc Surg 54:259-264, 1967
The
American
Journal
of
CARDIOLOGY