Clin. Cardiol. 15,928-930 (1992)
Case Reports
Acute Ischemic Exacerbation of Rheumatic Mitral Regurgitation hnv A. SIMPSON, M.D., JAMES SNEDDON, M.R.c.P.,TERIMILLANE, M.R.c.P., JOHNR. PEPPER, F.R.c.s.,DAVID E. WARD, M.D.
Departments of Cardiology and Cardiac Surgery, St. George’s Hospital, London, United Kingdom
Summary: This report describes a patient who developed acute severe exacerbation of mild rheumatic mitral regurgitation caused by ischemia in the territory of a small, nondominant circumflex coronary artery without myocardial infarction. Key words: mitral regurgitation, coronary angioplasty, rheumatic heart disease
Case Report A 63-year-old previously asymptomatic man with longstanding mild mitral regurgitation of rheumatic origin awoke with an episode of severe retrosternal chest pain. In the emergency department he was found to be in acute pulmonary edema. The electrocardiogram (ECG) demonstrated a broad complex tachycardia (subsequently confirmed as AV nodal reentry tachycardia with aberrancy) and was administered lignocaine for an assumed ventricular tachycardia which caused hemodynamic collapse. Cardiac resuscitation was successful and the patient was ventilated and stabilized following transfer to the intensive care unit where the ECG demonstrated sinus rhythm with left bundle-branch block. Arterial blood pressure was 80/50
Address for reprints:
I. A. Simpson, M.D. Wessex Cardiac Centre Southampton General Hospital Tremona Road Southampton 509 4XY, U.K. Received: December 9, 1990 Accepted: March 9, 1991
mmHg and Swan-Ganz catheterization revealed a pulmonary artery pressure of 20-40 mmHg systolic with a mean wedge pressure of 18 mmHg. Over the next 12 h the patient experienced episodes of acute fulminant pulmonary edema associated with a rise in pulmonary artery pressure to 90 mmHg. Cardia catheterization revealed dynamic left ventricular function without regional wall motion abnormalities, moderate mitral regurgitation, and a 95% stenosis of the distal portion of the circumflex coronary artery (Fig. 1) with no other significant obstructive coronary disease. Transesophageal echocardiography excluded any obstructive pathology in the pulmonary veins and left atrium and demonstrated a rheumatic mitral valve with a fixed posterior leaflet and an apparently normal anterior leaflet. We postulated papillary muscle ischemia as the mechanism of exacerbating mitral regurgitation and, in order to stabilize the situation, proceeded to coronary angioplasty with simultaneous monitoring of pulmonary artery pressures and the appearance of the mitral regurgitant jet by transesophageal color Doppler flow mapping. Immediately following apparently successful angioplasty during which the patient remained stable, the pulmonary artery pressure rose abruptly to 90 mmHg (Fig. 2). This was associated with pulmonary edema coming from the endotracheal tube and a dramatic increase in the size of the regurgitant jet on color flow mapping as compared with baseline (Fig. 3). Immediate angiography demonstrated occlusion of the circumflex artery at the site of angioplasty. Administration of intracoronary nitrates (250 pg) reestablished patency of the artery and produced an immediate fall in pulmonary pressures to baseline values. In view of the residual mitral regurgitation and the apparent instability of the circumflex lesion, the patient was referred for immediate surgery. Appearances of the mitral valve at surgery were consistent with rheumatic disease. The posterior leaflet was thickened and rolled posteriorly and there was no evidence of papillary muscle infarction. Mitral valve replacement with a 31 mm Carbomedics valve and a single coronary vein graft were performed. The patient remained hemodynamically stable postoperatively and recovery was complicat-
I. A. Simpson et al.: Acute ischemic mitral regurgitation
929
0 mmHg
FIG.1 Left coronary arteriogram in the left anterior oblique projection demonstrating a high grade stenosis of the distal left circumflex coronary artery (arrow).
ed only by mild cerebral impairment caused by prolonged hypoxia sustained during hemodynamic collapse in the emergency room. The neurological impairment recovered fully and the patient was subsequently discharged home. Mitral regurgitation associated with isolated left circumflex stenosis is well recognized' and acute ischemic mitral regurgitation has recently been successfully treated by coronary angioplasty in a small number of However, the association of acute ischemic mitral regurgitation with rheumatic mitral valve disease has not been
0 mmHg
FIG.2 (A) Aortic and pulmonary artery (PA) pressure tracings at baseline. The distal left circumflex coronary artery was demonstrated to be patent and transesophageal color flow mapping demonstrated mitral regurgitation as shown in Fig. 3A. (B) Aortic and pulmonary artery (PA) pressure tracings during occlusion of the distal left circumflex artery at the time of angioplasty. Note the dramatic rise in pulmonary artery pressure during coronary occlusion.
FIG.3 (A) Transesophageal color Doppler flow mapping at baseline with patent distal left circumflex artery demonstrating a jet of mitral regurgitation within the left atrium (la). Iv = left ventricle. (B) Transesophageal color Doppler flow mapping during occlusion of the distal left circumflex coronary artery. Note the marked increase in the spatial jet distribution of mitral regurgitation within the left atrium. Instrumentation factors remained unaltered between the two images.
930
Clin. Cardiol. Vol. 15. December 1992
reported previously. Since operation for acute ischemic mitral regurgitation carries a significant m~rtality,'.~ the possibility of acute ischemic exacerbation of mitral regurgitation in patients with rheumatic valve disease should be considered and subsequent treatment by angioplasty may be appropriate in some patients.
2. Shawl FA, Forman MB, Punja S, Goldbaum TS: Emergent coronary angioplasty in the treatment of acute ischemic mitral regurgitation: Long-term results in five cases. J Am Coll Cardi01 14,986-991 (1989)
3, Heuser RR, Maddoux GL, Goss JE, Ram0 BW, Ruff GL, Shadoff N: Coronary angioplasty for acute mitral regurgitation due to myocardial infarction. Ann Intern Med 107, 852-855 (1987)
References 4. Pinson CW, Cobanoglu A, Metzolorff MT, Grunkemeier GL,
I. Rankin JS, Hickey MStJ, Smith LR, Muhlbaier L, Reves JG, Pryor DB, Wechsler AS: Ischemic mitral regurgitation. Circulurion 79(suppl I), 1116-1121 (1989)
Kay PH, Starr A: Late surgical results for ischemic mitral regurgitation: Role of wall motion score and seventy of regurgitation. J Thoruc Curdiovusc Surg 88,663-672 (1984)
Case Reports
Acute Ischemic Exacerbation of Rheumatic Mitral Regurgitation hnv A. SIMPSON, M.D., JAMES SNEDDON, M.R.c.P.,TERIMILLANE, M.R.c.P., JOHNR. PEPPER, F.R.c.s.,DAVID E. WARD, M.D.
Departments of Cardiology and Cardiac Surgery, St. George’s Hospital, London, United Kingdom
Summary: This report describes a patient who developed acute severe exacerbation of mild rheumatic mitral regurgitation caused by ischemia in the territory of a small, nondominant circumflex coronary artery without myocardial infarction. Key words: mitral regurgitation, coronary angioplasty, rheumatic heart disease
Case Report A 63-year-old previously asymptomatic man with longstanding mild mitral regurgitation of rheumatic origin awoke with an episode of severe retrosternal chest pain. In the emergency department he was found to be in acute pulmonary edema. The electrocardiogram (ECG) demonstrated a broad complex tachycardia (subsequently confirmed as AV nodal reentry tachycardia with aberrancy) and was administered lignocaine for an assumed ventricular tachycardia which caused hemodynamic collapse. Cardiac resuscitation was successful and the patient was ventilated and stabilized following transfer to the intensive care unit where the ECG demonstrated sinus rhythm with left bundle-branch block. Arterial blood pressure was 80/50
Address for reprints:
I. A. Simpson, M.D. Wessex Cardiac Centre Southampton General Hospital Tremona Road Southampton 509 4XY, U.K. Received: December 9, 1990 Accepted: March 9, 1991
mmHg and Swan-Ganz catheterization revealed a pulmonary artery pressure of 20-40 mmHg systolic with a mean wedge pressure of 18 mmHg. Over the next 12 h the patient experienced episodes of acute fulminant pulmonary edema associated with a rise in pulmonary artery pressure to 90 mmHg. Cardia catheterization revealed dynamic left ventricular function without regional wall motion abnormalities, moderate mitral regurgitation, and a 95% stenosis of the distal portion of the circumflex coronary artery (Fig. 1) with no other significant obstructive coronary disease. Transesophageal echocardiography excluded any obstructive pathology in the pulmonary veins and left atrium and demonstrated a rheumatic mitral valve with a fixed posterior leaflet and an apparently normal anterior leaflet. We postulated papillary muscle ischemia as the mechanism of exacerbating mitral regurgitation and, in order to stabilize the situation, proceeded to coronary angioplasty with simultaneous monitoring of pulmonary artery pressures and the appearance of the mitral regurgitant jet by transesophageal color Doppler flow mapping. Immediately following apparently successful angioplasty during which the patient remained stable, the pulmonary artery pressure rose abruptly to 90 mmHg (Fig. 2). This was associated with pulmonary edema coming from the endotracheal tube and a dramatic increase in the size of the regurgitant jet on color flow mapping as compared with baseline (Fig. 3). Immediate angiography demonstrated occlusion of the circumflex artery at the site of angioplasty. Administration of intracoronary nitrates (250 pg) reestablished patency of the artery and produced an immediate fall in pulmonary pressures to baseline values. In view of the residual mitral regurgitation and the apparent instability of the circumflex lesion, the patient was referred for immediate surgery. Appearances of the mitral valve at surgery were consistent with rheumatic disease. The posterior leaflet was thickened and rolled posteriorly and there was no evidence of papillary muscle infarction. Mitral valve replacement with a 31 mm Carbomedics valve and a single coronary vein graft were performed. The patient remained hemodynamically stable postoperatively and recovery was complicat-
I. A. Simpson et al.: Acute ischemic mitral regurgitation
929
0 mmHg
FIG.1 Left coronary arteriogram in the left anterior oblique projection demonstrating a high grade stenosis of the distal left circumflex coronary artery (arrow).
ed only by mild cerebral impairment caused by prolonged hypoxia sustained during hemodynamic collapse in the emergency room. The neurological impairment recovered fully and the patient was subsequently discharged home. Mitral regurgitation associated with isolated left circumflex stenosis is well recognized' and acute ischemic mitral regurgitation has recently been successfully treated by coronary angioplasty in a small number of However, the association of acute ischemic mitral regurgitation with rheumatic mitral valve disease has not been
0 mmHg
FIG.2 (A) Aortic and pulmonary artery (PA) pressure tracings at baseline. The distal left circumflex coronary artery was demonstrated to be patent and transesophageal color flow mapping demonstrated mitral regurgitation as shown in Fig. 3A. (B) Aortic and pulmonary artery (PA) pressure tracings during occlusion of the distal left circumflex artery at the time of angioplasty. Note the dramatic rise in pulmonary artery pressure during coronary occlusion.
FIG.3 (A) Transesophageal color Doppler flow mapping at baseline with patent distal left circumflex artery demonstrating a jet of mitral regurgitation within the left atrium (la). Iv = left ventricle. (B) Transesophageal color Doppler flow mapping during occlusion of the distal left circumflex coronary artery. Note the marked increase in the spatial jet distribution of mitral regurgitation within the left atrium. Instrumentation factors remained unaltered between the two images.
930
Clin. Cardiol. Vol. 15. December 1992
reported previously. Since operation for acute ischemic mitral regurgitation carries a significant m~rtality,'.~ the possibility of acute ischemic exacerbation of mitral regurgitation in patients with rheumatic valve disease should be considered and subsequent treatment by angioplasty may be appropriate in some patients.
2. Shawl FA, Forman MB, Punja S, Goldbaum TS: Emergent coronary angioplasty in the treatment of acute ischemic mitral regurgitation: Long-term results in five cases. J Am Coll Cardi01 14,986-991 (1989)
3, Heuser RR, Maddoux GL, Goss JE, Ram0 BW, Ruff GL, Shadoff N: Coronary angioplasty for acute mitral regurgitation due to myocardial infarction. Ann Intern Med 107, 852-855 (1987)
References 4. Pinson CW, Cobanoglu A, Metzolorff MT, Grunkemeier GL,
I. Rankin JS, Hickey MStJ, Smith LR, Muhlbaier L, Reves JG, Pryor DB, Wechsler AS: Ischemic mitral regurgitation. Circulurion 79(suppl I), 1116-1121 (1989)
Kay PH, Starr A: Late surgical results for ischemic mitral regurgitation: Role of wall motion score and seventy of regurgitation. J Thoruc Curdiovusc Surg 88,663-672 (1984)
