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Left ventricular aneurysm without coronary arterial obstruction or occlusion
Left Ventricular Aneurysm Without Coronary Arterial Obstruction or Occlusion
The most comnion cause of left ventricular aneurysm is severe obstruction or occlusion of a major coronary artery. Among the last 2,500 patients studied in our laboratory with selective coronary cinearteriography and left ventriculography, we found 9 with unquestionable evidence of left ventricular aneurysm and no or minimal coronary arterial obstruction. Eight of the nine patients had a history of previous myocardial infarction and classic electrocardiographic changes. We believe that in these patignts coronary arterial obstruction had led to the development of left ventricular aneurysm. Later, complete or partial regression of the coronary obstruction ensued, leaving a normal or a minimally compromised vascular lumen.
PAOLO ESENTE, MD* GOFFREDO G. GENSINI, MD, FACC PETER P. HUNTINGTON, MD ANN E. KELLY, MS ASHER BLACK, MD, FACC Syracuse, New York
Left ventricular aneurysm can be caused by chest trauma,l rheumatic fever,2 syphilis,2 mycosis,2 Chagas’ disease,3 sarcoidosis4 and congenital defects.5 The aneurysm may be associated with normal coronary arteries, but it is most commonly caused by severe obstruction or occlusion of a major coronary artery secondary to coronary atherosclerosis. Occasionally, severe obstruction or occlusion of a large coronary branch may be related to embolism, primary dissecting aneurysm of the coronary arteries or one of various forms of arteritis. Since the development and widespread application of coronary arteriography, a great deal of controversy has been generated by the discovery of patients with a seemingly clear-cut history of typical angina pectoris and normal coronary arteries.6-g A problem that has been even more difficult to resolve is the finding of normal coronary arteries in patients with an unquestionable previous history of myocardial infarction.‘O-l3 This report concerns a small group of nine patients whose findings are at the extreme end of this spectrum: all nine had a ventricular aneurysm by left ventriculography, yet two of the nine had normal coronary arteries and seven had minimal coronary artery disease at the time of study. Material
From the Msgr. Toomey Cardiovascular Laboratory and Research Department, St. Joseph’s Hospital, Syracuse, N. Y. Manuscript accepted June 19, 1974. Address for reprints: Goffredo G. Gensini, MD, Cardiovascular Laboratory, St. Joseph’s Hospital, 301 Prospect Ave., Syracuse, N. Y. 13203. Present address: lstituto di Cardiologia. Ospedale Civile, 33 100-Udine, Italy. l
655
November 1974
The Amerkan
and Methods
Among the last 2,500 patients studied in our laboratory with selective coronary cinearteriography and left ventriculography, 11 had unquestionable evidence of left ventricular aneurysm and normal coronary arteries or minimal coronary artery disease (50 percent stenosis or less). Left ventricular aneurysm was considered present when there was paradoxical motion of a well defined myocardial segment that had distinct borders and a thinned wall. Two of these patients had a positive history of chest trauma and were excluded from this series. The other nine patients were free of any history of chest trauma and had no systemic, congenital, infectious or parasitic disease that could account for the aneurysm. Results
Table I summarizes the pertinent clinical, electrocardiographic and angiographic findings. Eight of the nine patients had an unquestion-
Jotirnal ol CARDIOLOGY
Volume 34
VENTRICULAR
ANEURYSM
WITHOUT CORONARY
OBSTRUCTION-ESENTE
ET AL.
TABLE I Clinical,
Electrocardiographic
and Angiographic
Case no.
Age (yr) & Sex
Months After
1
4SF
11
2
50M
...
3
40F
1
4
38F
11
5 6
42M 38M
60 15
7
39M 55M 54M 44.9
122 8 24 21
8 9 Mean
Findings in Nine Cases Aneurysm ~~~~__..
______-. Electrocardiogram
Ml
Left atrial enlargement; old anterior MI; ventricular aneurysm Complete left bundle branch block Left anterior hemiblock; old anteroseptal and high lateral Ml Left anterior hemiblock; left atrial enlargement; old lateral Ml Old anterolateral Ml Periinfarction block: left atrial enlargement; old anterior MI Old anterolateral Ml Old anterolateral Ml Old diaphragmatic Ml
Heart Failure
-__
Site
Size
No
Anterolateral
L
No
Diaphragmatic
S
Yes
Anteroapical
L
No*
Anterolateral
L
No Yes
Anterolateral Anterolateral,
No No No
Anteroapical Anterolateral Apical
apical
S L
L S S
* No clinical evidence of congestive heart failure. L = large; Ml = myocardial infarction: S = small.
FIGURE 1 (top). Case 3. Left ventriculogram during systole, right anterior oblique view. A well defined anteroapical aneurysm (proved at operation) is outlined by arrows. FIGURE 2 (right). Case 9. Coronary arteriograms. A, right coronary artery, right anterior oblique view; 6, left coronary artery, left anterior oblique view. A 50 percent reduction in lumen diameter is observed in the mid-segment of the right coronary artery (arrow). The left coronary artery is entirely normal despfte the presence of an apical aneurysm.
able history of acute myocardial infarction from 6 weeks to 10 years (mean 32 months) before the diagnostic studies; only two had a history of heart failure. In seven patients, the left ventricular aneurysm involved the apex or the anterolateral wall, or both (Fig. I), a type commonly seen with severe proximal involvement of the left anterior descending artery. One patient (Case 2) had left ventricular aneurysm of
November 1974
The American Journal of CARDIOLOGY
Volume 34
659
VENTRICULAR
ANEURYSM
WITHOUT CORONARY
OBSTRUCTION-ESENTE
the diaphragmatic wall, and one (Case 9) had an apical aneurysm. Although seven of the nine patients had coronary arterial involvement, none had more than 50 percent constriction of the lumen diameter of any vessel (Fig. 2).14 A meticulous review of the coronary arteriograms of all these patients excluded to our satisfaction the possibility of flush occlusion of a variant coronary arterial branch at its origin-l5 Discussion In reviewing cases of left ventricular aneurysm with normal or functionally unimpaired coronary circulation, only two hypotheses may be considered: (1) The aneurysms were caused by factors other than coronary arterial occlusion, or (2) coronary arterial occlusion had occurred but was no longer present at the time of study. The first hypothesis does not appear likely in our nine patients since none had a history of trauma or signs associated with other possible causative factors. The second hypothesis is supported by the history of previous myocardial infarction with classic electrocardiographic changes found in seven of the nine patients and by the results of repeated cinearteriographic studies made in one. In this latter patient (Case 7), a young man with a large anteroapical left ventricular aneurysm, a single subocclusive lesion of the left anterior descending artery regressed after 10 years, leaving a lumen that was only 50 percent obstructed. lap17 Coronary arteriography performed at repeated intervals may help to explain the possible sequence of events leading to the phenomenon of unstable angina,ls-lS as well as infarction (and eventually aneu-
ET AL.
rysm) without coronary occlusion (Case 7). Regression of coronary artery disease occurs in at least 2 percent of patients. l7 We have studied with serial coronary arteriograms a few patients, not included in the present group, with unstable angina of sudden onset that began to subside a few hours before coronary arteriography. lg Two of these patients had arteriographic evidence of an ulcerated plaque at the origin of a major vessel; 1 year later their coronary arteriograms revealed a diminution in the ulceration. In another case moderate coronary arterial obstruction (75 percent) rapidly progressed to occlusion requiring surgery and then regressed to less than 75 percent reduction of lumen diameter by the time of the postoperative arteriogram, 3 months later. Regression of coronary arterial thrombosis is another possibility and has been demonstrated in experimental conditions.20 Coronary spasm occurring subsequent to an ulcerated plaque may also be postulated.lgv21 We interpreted our findings in these cases as severe obstruction due to hemorrhage into a plaque that either suddenly ruptured, causing fragmentation of the atheroma, or regressed, causing the obstruction to disappear before myocardial necrosis had time to occur. Our experience and previously published data indicate that coronary arterial occlusion must be regarded as a dynamic phenomenon. Selective coronary arteriography defines the extent and severity of coronary arterial occlusion at the time of the procedure. Predictions based on one selective coronary arteriogram are statistically valid for a large patient population but cannot be utilized to foretell the future of the atherosclerotic plaque or to construct the temporal sequence of past events in any one case.
References 1. Klllen DA, Gobbel WG Jr, France R, et ak Post-traumatic aneurysm of the left ventricle. Circulation 39: 10 I- 108, 1989 2. Gould SE: Pathoiogy of the Heart. Springfield, Ill, Charles C Thomas, 1980, p 815-818 3. Ahseknl A, Molelro F, Suarez R, et al: Ventricular aneurysms in acute experimental Chagas myocardiopathy. Chest 59:854858, 1971 4. Lull RJ, Dunn BE, Gregorator 0, et al: Ventricular aneurysm due to cardiac sarcoldosis with surgical cure of refractory ventricutar tachycardta. Am J Cardiol30:282-287, 1972 F, Bergogllo S, et al: Congenital aneurysm 5. Dada JC, fhpez of the left ventricle. Ann Thorac Sum 1:897-710. 1985 8. Llkoff W, Segal BL, Kasparlan H: Paradox of normal selective coronary artedograms in patients considered to have unmtstakable coronary heart disease. N Engl J Med 278:1083-1088, 1987 7. Nelff WA, Kassebaum DG, Judkh MP: Myocardiil hypoxia as the basis for angina pectoris in a patient with normal coronary arterbgrams. N Engl J Med 279:789-792.1988 8. Dwyer EM, Welner L, Cox JW: Angina pectoris in patients with normal and abnormal coronary arteriograms. Am J Cardiol 23: 839-848. 1989 9. Eliot RS, Bratt 0: The paradox of myocardfal ischemh and necrosis in young women with normal coronary arteriograms. Relation to abnormal hemogloblnsxygen dissociation. Am J Cardol23:833-838. 1989 10. Klmblrls D, Segal BL, Munlr M, et al: Myocardial infarction in patients with normal patent coronary arteries as visualized by cinearteriography. Am J Cardiol 29:724-728, 1972 11. Sfdd JJ, Kemp HO, Gorlln R: Acute myocardhl infarction in a
680
November 1974
lhe American Journal of CARDIOLOGY
12. 13.
14.
15.
18. 17. 18.
19. 20.
21.
Volw
nineteen-year-old student in the absence of coronary obstructive disease. N Engl J Med 282:1308-1307, 1970 Llkoff W: Myocardial infarction in subjects with normal coronary arteriograms. Am J Cardlol 28:742-743, 1971 Glancy DL, Marcus ML, Epstein SE: Myocardial infarction in young women with normal coronary arteriograms. Circulation 44:495-502, 1971 Proudfit WL, Shfrey EK, Sones FY: Selective cinecoronary arteriography. Correlation with clinical findings in 1,000 patients. Circulation 33:901-910, 1988 Carlson RG, Fleming RJ, Llllehel CW: Postinfarction ventricuhr aneurysm with “normal” coronary arteriogram. NY State J Med 70:1970-1973.1970 Gendnl 00, Kelly AE, Esente P: lnckfenza e progressione delI’aterosclerosi corona&a. G ital Cardiol2:778-783, 1972 Genslnl GO, KeHy AE: Incidence and progression of coronary artery disease. Arch Intern Med 129:814-827, 1972 Henderson RR, Hanelng CE, Razavl M, et al: Resolution of an obstructive coronary lesion as demonstrated by selective angiography in a patient with transmural myocardtal infarction. Am J Cardiol31:785-788, 1973 Gensfnl GO: Coronary Arteriography, Mt Kisko. NY, Futura Publishing, in press Webs0 AB. Lehan PH, Ettlnger PO, et al: The fate of experimentally induced coronary artery thrombosis. Am J Cardiol 23: 229-237, 1989 Genslnl 06, DlGfergl S, Murad-NeHo S, et al: Arteriographic demonstration of coronary artery spasm and Its release after the use of a vasodilator in a case of angina pectoris and in the experimental animal. J Vast Dis 13:550-553. 1982
34
The most comnion cause of left ventricular aneurysm is severe obstruction or occlusion of a major coronary artery. Among the last 2,500 patients studied in our laboratory with selective coronary cinearteriography and left ventriculography, we found 9 with unquestionable evidence of left ventricular aneurysm and no or minimal coronary arterial obstruction. Eight of the nine patients had a history of previous myocardial infarction and classic electrocardiographic changes. We believe that in these patignts coronary arterial obstruction had led to the development of left ventricular aneurysm. Later, complete or partial regression of the coronary obstruction ensued, leaving a normal or a minimally compromised vascular lumen.
PAOLO ESENTE, MD* GOFFREDO G. GENSINI, MD, FACC PETER P. HUNTINGTON, MD ANN E. KELLY, MS ASHER BLACK, MD, FACC Syracuse, New York
Left ventricular aneurysm can be caused by chest trauma,l rheumatic fever,2 syphilis,2 mycosis,2 Chagas’ disease,3 sarcoidosis4 and congenital defects.5 The aneurysm may be associated with normal coronary arteries, but it is most commonly caused by severe obstruction or occlusion of a major coronary artery secondary to coronary atherosclerosis. Occasionally, severe obstruction or occlusion of a large coronary branch may be related to embolism, primary dissecting aneurysm of the coronary arteries or one of various forms of arteritis. Since the development and widespread application of coronary arteriography, a great deal of controversy has been generated by the discovery of patients with a seemingly clear-cut history of typical angina pectoris and normal coronary arteries.6-g A problem that has been even more difficult to resolve is the finding of normal coronary arteries in patients with an unquestionable previous history of myocardial infarction.‘O-l3 This report concerns a small group of nine patients whose findings are at the extreme end of this spectrum: all nine had a ventricular aneurysm by left ventriculography, yet two of the nine had normal coronary arteries and seven had minimal coronary artery disease at the time of study. Material
From the Msgr. Toomey Cardiovascular Laboratory and Research Department, St. Joseph’s Hospital, Syracuse, N. Y. Manuscript accepted June 19, 1974. Address for reprints: Goffredo G. Gensini, MD, Cardiovascular Laboratory, St. Joseph’s Hospital, 301 Prospect Ave., Syracuse, N. Y. 13203. Present address: lstituto di Cardiologia. Ospedale Civile, 33 100-Udine, Italy. l
655
November 1974
The Amerkan
and Methods
Among the last 2,500 patients studied in our laboratory with selective coronary cinearteriography and left ventriculography, 11 had unquestionable evidence of left ventricular aneurysm and normal coronary arteries or minimal coronary artery disease (50 percent stenosis or less). Left ventricular aneurysm was considered present when there was paradoxical motion of a well defined myocardial segment that had distinct borders and a thinned wall. Two of these patients had a positive history of chest trauma and were excluded from this series. The other nine patients were free of any history of chest trauma and had no systemic, congenital, infectious or parasitic disease that could account for the aneurysm. Results
Table I summarizes the pertinent clinical, electrocardiographic and angiographic findings. Eight of the nine patients had an unquestion-
Jotirnal ol CARDIOLOGY
Volume 34
VENTRICULAR
ANEURYSM
WITHOUT CORONARY
OBSTRUCTION-ESENTE
ET AL.
TABLE I Clinical,
Electrocardiographic
and Angiographic
Case no.
Age (yr) & Sex
Months After
1
4SF
11
2
50M
...
3
40F
1
4
38F
11
5 6
42M 38M
60 15
7
39M 55M 54M 44.9
122 8 24 21
8 9 Mean
Findings in Nine Cases Aneurysm ~~~~__..
______-. Electrocardiogram
Ml
Left atrial enlargement; old anterior MI; ventricular aneurysm Complete left bundle branch block Left anterior hemiblock; old anteroseptal and high lateral Ml Left anterior hemiblock; left atrial enlargement; old lateral Ml Old anterolateral Ml Periinfarction block: left atrial enlargement; old anterior MI Old anterolateral Ml Old anterolateral Ml Old diaphragmatic Ml
Heart Failure
-__
Site
Size
No
Anterolateral
L
No
Diaphragmatic
S
Yes
Anteroapical
L
No*
Anterolateral
L
No Yes
Anterolateral Anterolateral,
No No No
Anteroapical Anterolateral Apical
apical
S L
L S S
* No clinical evidence of congestive heart failure. L = large; Ml = myocardial infarction: S = small.
FIGURE 1 (top). Case 3. Left ventriculogram during systole, right anterior oblique view. A well defined anteroapical aneurysm (proved at operation) is outlined by arrows. FIGURE 2 (right). Case 9. Coronary arteriograms. A, right coronary artery, right anterior oblique view; 6, left coronary artery, left anterior oblique view. A 50 percent reduction in lumen diameter is observed in the mid-segment of the right coronary artery (arrow). The left coronary artery is entirely normal despfte the presence of an apical aneurysm.
able history of acute myocardial infarction from 6 weeks to 10 years (mean 32 months) before the diagnostic studies; only two had a history of heart failure. In seven patients, the left ventricular aneurysm involved the apex or the anterolateral wall, or both (Fig. I), a type commonly seen with severe proximal involvement of the left anterior descending artery. One patient (Case 2) had left ventricular aneurysm of
November 1974
The American Journal of CARDIOLOGY
Volume 34
659
VENTRICULAR
ANEURYSM
WITHOUT CORONARY
OBSTRUCTION-ESENTE
the diaphragmatic wall, and one (Case 9) had an apical aneurysm. Although seven of the nine patients had coronary arterial involvement, none had more than 50 percent constriction of the lumen diameter of any vessel (Fig. 2).14 A meticulous review of the coronary arteriograms of all these patients excluded to our satisfaction the possibility of flush occlusion of a variant coronary arterial branch at its origin-l5 Discussion In reviewing cases of left ventricular aneurysm with normal or functionally unimpaired coronary circulation, only two hypotheses may be considered: (1) The aneurysms were caused by factors other than coronary arterial occlusion, or (2) coronary arterial occlusion had occurred but was no longer present at the time of study. The first hypothesis does not appear likely in our nine patients since none had a history of trauma or signs associated with other possible causative factors. The second hypothesis is supported by the history of previous myocardial infarction with classic electrocardiographic changes found in seven of the nine patients and by the results of repeated cinearteriographic studies made in one. In this latter patient (Case 7), a young man with a large anteroapical left ventricular aneurysm, a single subocclusive lesion of the left anterior descending artery regressed after 10 years, leaving a lumen that was only 50 percent obstructed. lap17 Coronary arteriography performed at repeated intervals may help to explain the possible sequence of events leading to the phenomenon of unstable angina,ls-lS as well as infarction (and eventually aneu-
ET AL.
rysm) without coronary occlusion (Case 7). Regression of coronary artery disease occurs in at least 2 percent of patients. l7 We have studied with serial coronary arteriograms a few patients, not included in the present group, with unstable angina of sudden onset that began to subside a few hours before coronary arteriography. lg Two of these patients had arteriographic evidence of an ulcerated plaque at the origin of a major vessel; 1 year later their coronary arteriograms revealed a diminution in the ulceration. In another case moderate coronary arterial obstruction (75 percent) rapidly progressed to occlusion requiring surgery and then regressed to less than 75 percent reduction of lumen diameter by the time of the postoperative arteriogram, 3 months later. Regression of coronary arterial thrombosis is another possibility and has been demonstrated in experimental conditions.20 Coronary spasm occurring subsequent to an ulcerated plaque may also be postulated.lgv21 We interpreted our findings in these cases as severe obstruction due to hemorrhage into a plaque that either suddenly ruptured, causing fragmentation of the atheroma, or regressed, causing the obstruction to disappear before myocardial necrosis had time to occur. Our experience and previously published data indicate that coronary arterial occlusion must be regarded as a dynamic phenomenon. Selective coronary arteriography defines the extent and severity of coronary arterial occlusion at the time of the procedure. Predictions based on one selective coronary arteriogram are statistically valid for a large patient population but cannot be utilized to foretell the future of the atherosclerotic plaque or to construct the temporal sequence of past events in any one case.
References 1. Klllen DA, Gobbel WG Jr, France R, et ak Post-traumatic aneurysm of the left ventricle. Circulation 39: 10 I- 108, 1989 2. Gould SE: Pathoiogy of the Heart. Springfield, Ill, Charles C Thomas, 1980, p 815-818 3. Ahseknl A, Molelro F, Suarez R, et al: Ventricular aneurysms in acute experimental Chagas myocardiopathy. Chest 59:854858, 1971 4. Lull RJ, Dunn BE, Gregorator 0, et al: Ventricular aneurysm due to cardiac sarcoldosis with surgical cure of refractory ventricutar tachycardta. Am J Cardiol30:282-287, 1972 F, Bergogllo S, et al: Congenital aneurysm 5. Dada JC, fhpez of the left ventricle. Ann Thorac Sum 1:897-710. 1985 8. Llkoff W, Segal BL, Kasparlan H: Paradox of normal selective coronary artedograms in patients considered to have unmtstakable coronary heart disease. N Engl J Med 278:1083-1088, 1987 7. Nelff WA, Kassebaum DG, Judkh MP: Myocardiil hypoxia as the basis for angina pectoris in a patient with normal coronary arterbgrams. N Engl J Med 279:789-792.1988 8. Dwyer EM, Welner L, Cox JW: Angina pectoris in patients with normal and abnormal coronary arteriograms. Am J Cardiol 23: 839-848. 1989 9. Eliot RS, Bratt 0: The paradox of myocardfal ischemh and necrosis in young women with normal coronary arteriograms. Relation to abnormal hemogloblnsxygen dissociation. Am J Cardol23:833-838. 1989 10. Klmblrls D, Segal BL, Munlr M, et al: Myocardial infarction in patients with normal patent coronary arteries as visualized by cinearteriography. Am J Cardiol 29:724-728, 1972 11. Sfdd JJ, Kemp HO, Gorlln R: Acute myocardhl infarction in a
680
November 1974
lhe American Journal of CARDIOLOGY
12. 13.
14.
15.
18. 17. 18.
19. 20.
21.
Volw
nineteen-year-old student in the absence of coronary obstructive disease. N Engl J Med 282:1308-1307, 1970 Llkoff W: Myocardial infarction in subjects with normal coronary arteriograms. Am J Cardlol 28:742-743, 1971 Glancy DL, Marcus ML, Epstein SE: Myocardial infarction in young women with normal coronary arteriograms. Circulation 44:495-502, 1971 Proudfit WL, Shfrey EK, Sones FY: Selective cinecoronary arteriography. Correlation with clinical findings in 1,000 patients. Circulation 33:901-910, 1988 Carlson RG, Fleming RJ, Llllehel CW: Postinfarction ventricuhr aneurysm with “normal” coronary arteriogram. NY State J Med 70:1970-1973.1970 Gendnl 00, Kelly AE, Esente P: lnckfenza e progressione delI’aterosclerosi corona&a. G ital Cardiol2:778-783, 1972 Genslnl GO, KeHy AE: Incidence and progression of coronary artery disease. Arch Intern Med 129:814-827, 1972 Henderson RR, Hanelng CE, Razavl M, et al: Resolution of an obstructive coronary lesion as demonstrated by selective angiography in a patient with transmural myocardtal infarction. Am J Cardiol31:785-788, 1973 Gensfnl GO: Coronary Arteriography, Mt Kisko. NY, Futura Publishing, in press Webs0 AB. Lehan PH, Ettlnger PO, et al: The fate of experimentally induced coronary artery thrombosis. Am J Cardiol 23: 229-237, 1989 Genslnl 06, DlGfergl S, Murad-NeHo S, et al: Arteriographic demonstration of coronary artery spasm and Its release after the use of a vasodilator in a case of angina pectoris and in the experimental animal. J Vast Dis 13:550-553. 1982
34