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Recovery of severe ischemic ventricular dysfunction after coronary artery bypass grafting
650
BRIEF
REPORTS
RCA during PTCA results in a dramatic decrease of RV global function and a 38% decrease of RV.ej ection fraction. This is comparable to the response of the left ventricle to &hernia chamber volumes and end-diastolic pressure increases, which show a low tolerance of the human right ventricle even to short heriods of ischemia. Therefore, in patients with an acute proximal occlusion of the RCA the clinical course may be influenced by the occurrence of RV failure. 1. Serruys PW, Wijns W, van den Brand M. Left ventricular performance, regional blood flow, wall motion and lactate metabolism during transluminal ongioplasty. Circulation 1984;70:25-36.
Recovery of Severe, lsehemic Ventiicular Dysfunltion Aft&r Coronary Artery Bypass Grafting DAVID A. BRILL, MD LAWRENCE,I. DECKELBAUM, MD MICHAEL S. REMETZ, MD ROBERTSOUFER,MD JOHN A. ELEFTERIADES,MD BARRY L. ZARET, MD
2. JaskiBE, Serruys PW. Epicardial wall motion and left ventricular fun&n during coronary graft angioplasty in humans. JACC 1985;6:695-700. 3. Arcilla RA, Tsai P. Thilenius 0, Ranninger K. Angiographic method for volume estimation of right and left ventricles. Chest 1971;60:446-454. 4. Karliner JS,Bouchard RI, Gault HG. Hemodynamic effects of angiographic contrast material
in man: a beat by beat analysis. Br Heart J 1972;34:347-353.
5. Brooks H, Kirk E, Vokonas P, Urschel C, Sonnenblick E. Performance of the sight ventricle
under stress: relation
to right coronary
pow. J Clin Invest
1971;5O:2176-2182.
6. Brooks H, Holland R, Al-Sader J. Right ventricular ischemia:
an anatomic
performance dtiring analvsis. Am T Phvsiol 1977;233:
and hemodvnamic
H505-H512.
7. Berger HJ, Johnstone .DE, Sands JM, Go&chalk A, Zaret BL. Response of right ventricular ejection fraction to upright bicycle exercise in coronary artery disease. Circulation 1979:60:1292-1299. 8. Ferlinz J,Gorlin R, Cohn PF, Herman MV. Right ventricular performance in patients with coronary artery disease. Circulation 1975;52:608-615.
to-
A LVEF
27
%
LVEF
63
%
9-
Iv-
o-
Y-
V
entricular wall motion abnormalities at rest aie believed to be indicative of myocardial scar and fibrous tissue. Although patients may have reversible wall motion abnormalities at rest during periods of ischemia, recent evidence suggests that reversible ventricular dysfunction can persist after a major ischerqic insu1t.Q Braunwald and Rutherford3 distinguish between stunned and hibernating myocardium and suggest that in either situation, revascularization can reverse exercise-induced ischemic dysfunction.4,5 However, reversal of prolonged resting ventricular dysfunction is not as clear. We report a patient with severe coronary artery disease without myocardial infarction who had complete reversal of marked left ventricular (LV) dysfunction. A @year-old man was healthy, physically active and free of any symptoms of cardiac dysfunction until 2 wekks before admission when he developed exertional dyspnea and angina pectoris. His symptoms increased, leading to hospitalization. He had had a pulmonary embolus at age 25 after knee surgery. His only medications were chlorproniazine 500 mg daily and temazepam 60 mg daily for post-traumatic stress disorder. He smoked a pack of cigarettes a day and had a From the Department of Medicine, Cardiology Section, and the Department of Surgery, Yale University School of Medicine, New Haven, and the Veterans Administration Medical Center, West Haven, Connecticut. Manuscript received August 17,1987; revised manuscript received and accepted October 27,1987.
T-
B
FIGURE 1. Left ventrkulography before and after coronary artery bypasS graflihg. Diastolic and systolic ventricular outlines from right anterior oblique angiocardiograms are shown from the irkal (A) and follow-up (e) catheterizations. Regional wall motion is represented by the chords that plot the excursion of each perimeter segment. Improved regional contraction involving all segmknts resulted in a global ejection fraction increase from 27 % preoperatively to 63 % 2 months postoperatively.
March
paternal family history of ischemic cardiac disease. He had bibasilar rales, a fourth heart sound and a soft systolic ejection murmur. The electrocardiogram revealed sinus rhythm at a rate of 95/min with biphasic T waves in leads I, aVL and V4 through Vs. His chest x-ray was normal. He was admitted to the coronary care unit and was treated with lidocaine and nitroglycerin ointment. Serum creatine kinase levels remained within normal limits and his electrocardiogram did not change from admission. He had no further angina. Cardiac catheterization on the third hospital day revealed globally depressed LV function with an ejection fraction of27% [Figure IA). He had a 90% diameter stenosis of the left main coronary artery. The right coronary, left circumflex and left anterior descending arteries had insignificant narrowings. An equilibrium radionuclide angiocardiogram on the same day revealed an LV ejection fraction of 17% with severe generalized hypokinesis. On the fourth hospital day he underwent coronary artery bypass grafting (CABG) ’ with a left internal mammary graft to the left anterior descending artery and a saphenous vein graft to the left circumflex artery. At surgery, inspection of his heart revealed no evidence of acute myocardial infarction. He recovered uneventfully. A repeat equilibrium radionuclide angiocardiogram on the tenth hospital day revealed an LV ejection fraction of 36% without discrete regional wall motion abnormalities. The results of exercise tolerance test performed 5 weeks postoperatively were normal. An equilibrium radionuclide angiocardiogram performed 6 weeks postoperatively revealed an LV ejection fraction of 52%. The patient was readmitted to the hospital 8 weeks postoperatively with atypical chest pain and no electrocardiographic changes. Cardiac catheterization at that time revealed patent grafts and an LV ejection fraction of 63% [Figure IB). This report documents total reversal of severe global LV dysfunction as a result of CABG. Reversal of regional wall motion abnormalities at rest4 and improvement in exercise LV ejection fraction5 have been reported after CABG. However, the initial ejection fractions in these reports were normal or minimally abnormal and improved only modestly. Akins et al6
1,1988
THE
AMERICAN
JOURNAL
OF CARDIOLOGY
Volume
61
651
reported 2 patients with previous history of myocardial infarction and severely depressed LV ejection fraction but without bvidence of acute ischemia. Both patients had improvement in ejection fraction after revascularization (15 to 27% in 1 patient and 15 to 33% in the other). No previous report has documented complete reversal of severe LV dysfunction at rest following CABG. The improvement in ejection fraction over 6 weeks from 17 to 52% (an increase of 206%) in our patient is a dramatic example of the potential for reversible ischemic dysfunction. The pathophysiology of persistent myocardial dysfunction in ischemic heart disease is not well understood. Matsuzaki et al2 demonstrated in a’ dog model that prolonged partial occlusion of coronary arteries (5 hours] resulted in sustained myocardial dysfunction lasting several days before recovery. Braunwald and Klonerl in their review of stunned myocardium concluded that similar effects could be produced by repetitive ischemic episodes or brief total occlusion of the circulation. Ventricular dysfunction in our patient was most likely the result of either stunned myocardium secondary to an ischemic event, ongoing silent ischemia [hibernating myocardium] or both. The patient’s repeated episodes of angina may have induced prolonged depression of systolic LV function. The recovery of LV dysfunction following CABG suggests that the myocardium was chronically ischemic and hibernating, not necrotic. The serial improvement in ejection fraction suggests myocardial stunning with the gradual return of function of postischemic reperfused myocardium. 1. Braunwald E, Kloner RA. The stunned myocardium: prolonged, postischemic ventricular dysfunction. Circulation 1982;66:1146-1149. 2. Matsuzaki M, Gallagher KP, Kemper WS, White F, Ross J Jr. Sustained regional dysfunction produced by prolonged coronary stenosis: gradual recovery after reperfusion. Circulation 1983;68:170-182. 3. Braunwald E, Rutherford JD. Reversible ischemic left ventricular dysfunction: evidence for the “hibernating myocordium.” rACC 1986;8:1467-1470. 4. Rankin JS, Newman GE, Muhlbaier LH, Behar VS, Fedor JM, Sabiston DC Jr. The effects of coronary revascularization on left ventricular function in ischemic heart disease. J Thorac Cardiovasc Surg 1985;90:818-832. 5. Kent KM, Bgrer JS, Green MV, Bacharach SL, McIntosh CL, Conkle DM, Epstein SE. Effects of coronary-artery bypass on global and regional left ventricular function during exercise. N Engl J Med 2978;298:1434-1439. 6. Akins CW, Pohost GM, DeSanctis RW, Block PC. Selection of angina-free patients with severe left ventricular dysfunction for myocardial revosculorization. Am J Cardiol 1980;46:695-700.
BRIEF
REPORTS
RCA during PTCA results in a dramatic decrease of RV global function and a 38% decrease of RV.ej ection fraction. This is comparable to the response of the left ventricle to &hernia chamber volumes and end-diastolic pressure increases, which show a low tolerance of the human right ventricle even to short heriods of ischemia. Therefore, in patients with an acute proximal occlusion of the RCA the clinical course may be influenced by the occurrence of RV failure. 1. Serruys PW, Wijns W, van den Brand M. Left ventricular performance, regional blood flow, wall motion and lactate metabolism during transluminal ongioplasty. Circulation 1984;70:25-36.
Recovery of Severe, lsehemic Ventiicular Dysfunltion Aft&r Coronary Artery Bypass Grafting DAVID A. BRILL, MD LAWRENCE,I. DECKELBAUM, MD MICHAEL S. REMETZ, MD ROBERTSOUFER,MD JOHN A. ELEFTERIADES,MD BARRY L. ZARET, MD
2. JaskiBE, Serruys PW. Epicardial wall motion and left ventricular fun&n during coronary graft angioplasty in humans. JACC 1985;6:695-700. 3. Arcilla RA, Tsai P. Thilenius 0, Ranninger K. Angiographic method for volume estimation of right and left ventricles. Chest 1971;60:446-454. 4. Karliner JS,Bouchard RI, Gault HG. Hemodynamic effects of angiographic contrast material
in man: a beat by beat analysis. Br Heart J 1972;34:347-353.
5. Brooks H, Kirk E, Vokonas P, Urschel C, Sonnenblick E. Performance of the sight ventricle
under stress: relation
to right coronary
pow. J Clin Invest
1971;5O:2176-2182.
6. Brooks H, Holland R, Al-Sader J. Right ventricular ischemia:
an anatomic
performance dtiring analvsis. Am T Phvsiol 1977;233:
and hemodvnamic
H505-H512.
7. Berger HJ, Johnstone .DE, Sands JM, Go&chalk A, Zaret BL. Response of right ventricular ejection fraction to upright bicycle exercise in coronary artery disease. Circulation 1979:60:1292-1299. 8. Ferlinz J,Gorlin R, Cohn PF, Herman MV. Right ventricular performance in patients with coronary artery disease. Circulation 1975;52:608-615.
to-
A LVEF
27
%
LVEF
63
%
9-
Iv-
o-
Y-
V
entricular wall motion abnormalities at rest aie believed to be indicative of myocardial scar and fibrous tissue. Although patients may have reversible wall motion abnormalities at rest during periods of ischemia, recent evidence suggests that reversible ventricular dysfunction can persist after a major ischerqic insu1t.Q Braunwald and Rutherford3 distinguish between stunned and hibernating myocardium and suggest that in either situation, revascularization can reverse exercise-induced ischemic dysfunction.4,5 However, reversal of prolonged resting ventricular dysfunction is not as clear. We report a patient with severe coronary artery disease without myocardial infarction who had complete reversal of marked left ventricular (LV) dysfunction. A @year-old man was healthy, physically active and free of any symptoms of cardiac dysfunction until 2 wekks before admission when he developed exertional dyspnea and angina pectoris. His symptoms increased, leading to hospitalization. He had had a pulmonary embolus at age 25 after knee surgery. His only medications were chlorproniazine 500 mg daily and temazepam 60 mg daily for post-traumatic stress disorder. He smoked a pack of cigarettes a day and had a From the Department of Medicine, Cardiology Section, and the Department of Surgery, Yale University School of Medicine, New Haven, and the Veterans Administration Medical Center, West Haven, Connecticut. Manuscript received August 17,1987; revised manuscript received and accepted October 27,1987.
T-
B
FIGURE 1. Left ventrkulography before and after coronary artery bypasS graflihg. Diastolic and systolic ventricular outlines from right anterior oblique angiocardiograms are shown from the irkal (A) and follow-up (e) catheterizations. Regional wall motion is represented by the chords that plot the excursion of each perimeter segment. Improved regional contraction involving all segmknts resulted in a global ejection fraction increase from 27 % preoperatively to 63 % 2 months postoperatively.
March
paternal family history of ischemic cardiac disease. He had bibasilar rales, a fourth heart sound and a soft systolic ejection murmur. The electrocardiogram revealed sinus rhythm at a rate of 95/min with biphasic T waves in leads I, aVL and V4 through Vs. His chest x-ray was normal. He was admitted to the coronary care unit and was treated with lidocaine and nitroglycerin ointment. Serum creatine kinase levels remained within normal limits and his electrocardiogram did not change from admission. He had no further angina. Cardiac catheterization on the third hospital day revealed globally depressed LV function with an ejection fraction of27% [Figure IA). He had a 90% diameter stenosis of the left main coronary artery. The right coronary, left circumflex and left anterior descending arteries had insignificant narrowings. An equilibrium radionuclide angiocardiogram on the same day revealed an LV ejection fraction of 17% with severe generalized hypokinesis. On the fourth hospital day he underwent coronary artery bypass grafting (CABG) ’ with a left internal mammary graft to the left anterior descending artery and a saphenous vein graft to the left circumflex artery. At surgery, inspection of his heart revealed no evidence of acute myocardial infarction. He recovered uneventfully. A repeat equilibrium radionuclide angiocardiogram on the tenth hospital day revealed an LV ejection fraction of 36% without discrete regional wall motion abnormalities. The results of exercise tolerance test performed 5 weeks postoperatively were normal. An equilibrium radionuclide angiocardiogram performed 6 weeks postoperatively revealed an LV ejection fraction of 52%. The patient was readmitted to the hospital 8 weeks postoperatively with atypical chest pain and no electrocardiographic changes. Cardiac catheterization at that time revealed patent grafts and an LV ejection fraction of 63% [Figure IB). This report documents total reversal of severe global LV dysfunction as a result of CABG. Reversal of regional wall motion abnormalities at rest4 and improvement in exercise LV ejection fraction5 have been reported after CABG. However, the initial ejection fractions in these reports were normal or minimally abnormal and improved only modestly. Akins et al6
1,1988
THE
AMERICAN
JOURNAL
OF CARDIOLOGY
Volume
61
651
reported 2 patients with previous history of myocardial infarction and severely depressed LV ejection fraction but without bvidence of acute ischemia. Both patients had improvement in ejection fraction after revascularization (15 to 27% in 1 patient and 15 to 33% in the other). No previous report has documented complete reversal of severe LV dysfunction at rest following CABG. The improvement in ejection fraction over 6 weeks from 17 to 52% (an increase of 206%) in our patient is a dramatic example of the potential for reversible ischemic dysfunction. The pathophysiology of persistent myocardial dysfunction in ischemic heart disease is not well understood. Matsuzaki et al2 demonstrated in a’ dog model that prolonged partial occlusion of coronary arteries (5 hours] resulted in sustained myocardial dysfunction lasting several days before recovery. Braunwald and Klonerl in their review of stunned myocardium concluded that similar effects could be produced by repetitive ischemic episodes or brief total occlusion of the circulation. Ventricular dysfunction in our patient was most likely the result of either stunned myocardium secondary to an ischemic event, ongoing silent ischemia [hibernating myocardium] or both. The patient’s repeated episodes of angina may have induced prolonged depression of systolic LV function. The recovery of LV dysfunction following CABG suggests that the myocardium was chronically ischemic and hibernating, not necrotic. The serial improvement in ejection fraction suggests myocardial stunning with the gradual return of function of postischemic reperfused myocardium. 1. Braunwald E, Kloner RA. The stunned myocardium: prolonged, postischemic ventricular dysfunction. Circulation 1982;66:1146-1149. 2. Matsuzaki M, Gallagher KP, Kemper WS, White F, Ross J Jr. Sustained regional dysfunction produced by prolonged coronary stenosis: gradual recovery after reperfusion. Circulation 1983;68:170-182. 3. Braunwald E, Rutherford JD. Reversible ischemic left ventricular dysfunction: evidence for the “hibernating myocordium.” rACC 1986;8:1467-1470. 4. Rankin JS, Newman GE, Muhlbaier LH, Behar VS, Fedor JM, Sabiston DC Jr. The effects of coronary revascularization on left ventricular function in ischemic heart disease. J Thorac Cardiovasc Surg 1985;90:818-832. 5. Kent KM, Bgrer JS, Green MV, Bacharach SL, McIntosh CL, Conkle DM, Epstein SE. Effects of coronary-artery bypass on global and regional left ventricular function during exercise. N Engl J Med 2978;298:1434-1439. 6. Akins CW, Pohost GM, DeSanctis RW, Block PC. Selection of angina-free patients with severe left ventricular dysfunction for myocardial revosculorization. Am J Cardiol 1980;46:695-700.