International Journal of Cardiology, 31(1992) 165-168 0 1992 Elsevier Science Publishers B.V. All rights reserved
CARD10
165 0167.5273/92/$05.00
01554
Acute myocardial ischemia resulting in dynamic obstruction to the left ventricular outflow relieved by successful angioplasty C. Martinez-Useros,
E. Galve Basilio and G. Oller Cid
Hospital General de Catalunya, San Cugat del Vall& Barcelona, Spain (Received
26 May 1992; accepted
30 May 1992)
Martinez-Useros C, Galve Basilio E, Oller Cid G. Acute myocardial ischaemia resulting in dynamic obstruction to the left ventricular outflow relieved by successful angioplasty. Int J Cardiol 1992;37:165168. A patient was admitted because of an acute myocardial infarction which evolved with heart failure and postinfarction angina. A pattern consistent with dynamic left ventricular outflow obstruction was found. It disappeared after coronary angioplasty was performed on the vessel responsible for the ischemia. Key words: Dynamic obstruction
to left ventricular outflow; Myocardial ischemia; Angioplasty
Case Report A 61-yr-old female with a past history of systemic hypertension and migraine, who was receiving beta-blockers for both reasons, was admitted to our institution because of repetitive episodes of rest chest pain that had begun one week previously. Physical examination, electrocardiogram (ECG), chest X-ray and blood analysis revealed no abnormalities. She was monitored for 72 h with no complaints. Beta-adrenergic blockers were discontinued and a diagnostic treadmill exercise test was performed. The patient exercised to stage 3 of a Bruce protocol and experienced angina in the postexercise period associated with persistent 7 mm ST-
Correspondence tot Dra. Carmen Martinez-Useros, C/ Rectoria, 38, 1” 2a. 08031 Barcelona, Spain. Tel. (93) 427.35. 67; (93) 589.12.12 (hospital)
segment elevation in leads V3 and V4. She was transferred to the Coronary Care Unit and fibrinolysis instituted. Anterior acute myocardial infarction was confirmed by serial ECGs and enzymes. Total creatine kinase rose to a peak of 494 U (normal values 24-190) while MB isoenzyme rose to a peak of 17 U (normal values l-2). Physical examination disclosed a grad.e 3 systolic murmur at the left sternal border in the fourth intercostal space and a loud fourth heart sound. During the next 48 h she experienced recurrent episodes of postinfarction angina and developed overt heart failure. Cardiac catheterization revealed a left ventricular outflow gradient of 52 mmHg between the body of the ventricle and a subaortic chamber. The gradient showed striking enhancement after premature ventricular contractions and during Valsalva maneuver. Left ventriculography demonstrated localized apical akinesia with tendency to the formation of aneurysm, and mild mitral regurgitation, while
166
the ejection fraction was 51%. Coronary arteriography disclosed a tight (95%) stenosis in the mid portion of the left descending artery. Doppler echocardiography confirmed the findings (Fig. 1): the left ventricle was mildly hypertrophic (interventricular septum: 15 mm, posterior wall 10 mm); there was a localized area of akinesia at the apex while the basal areas near the outflow tract had a vigorous motion, the ejection fraction being 61% (Fig. 2); there was systolic anterior motion of both mitral leaflets and midsystolic closure of the aortic valve; Doppler disclosed a subaortic gradient of 45 mmHg and mild mitral regurgitation. Percutaneous transluminal coronary angioplasty was successfully performed and the symptoms subsided. A Doppler echocardiogram recording
performed before discharge showed no subaortic gradient while systolic anterior motion of the mitral valve and midsystolic closure of the aortic valve had both disappeared (Fig. 3). During follow-up the patient has been well. Initial ECGs showed an extensive anterior ischemia pattern (Fig. 4) that gradually disappeared. Six months after angioplasty a new cardiac catheterization was performed. The left anterior descending coronary artery showed patency without evidence of restenosis. Global and segmentary left ventricular motion had returned to normal. There was no outflow gradient either at rest or under (after) maneuvers. By that time the ECG (Fig. 4) had normalized.
Discussion
Fig. 1. Top: M-mode echocardiogram showing systolic anterior motion of the mitral leaflets and hypertrophy of the interventricular septum. Bottom: Doppler flow recording through the left ventricular outflow tract demonstrating a subaortic gradient of 45 mmHg. Note the characteristic endsystolic peak velocity.
Our patient shows an unusual behavior of the dynamic left ventricular outflow gradient. The obstructive pattern appeared after an acute myocardial infarction and it was relieved after an angioplasty that restored the motion of an apical area of akinesia. We think that this patient had a mild form of hypertensive heart disease resulting in mild septal hypertrophy. The occurrence of an apical area of akinesia resulted in an increase of motion of the basal portions of the left ventricle as a compensatory mechanism, thus generating the dynamic outflow gradient. The combination of ischemia, depressed ventricular function and outflow obstruction was responsible for a dramatic clinical situation coursing with unstable angina and severe heart failure. However, the infarction was not enzymatically large, and the left anterior descending artery was patent; therefore, viability of the akinetic area could be presumed. Angioplasty resulted in relief of the ischemia, thus restoring contractility to the apex and, as a consequence, decreasing the hypercontractility of the basal areas of the left ventricle and thus obliterating the outflow obstruction. It has to be emphasized that the presence and regression of the pressure gradient was documented in the absence of positive or negative inotropic drugs that could interfere with or modify dynamic obstruction. On the other hand, the absence of abnormalities on physical examina-
167
tion, and in the initial and current ECGs, as well as in the current Doppler echocardiogram, indicate that this patient does not fulfil1 the criteria to be diagnosed hypertrophic cardiomyopathy. In fact, it has not been reported that hypertrophic cardiomyopathy could regress, although regression has been found in hypertrophy associated with hypertension or highly-trained athletes. Therefore, this case constitutes an unusual form of dynamic gradient secondary to changes in motion wall abnormalities. It has been reported that changes in ventricular activation in the Wolff-Parkinson-White syndrome can modify the degree of obstruction in hypertrophic cardiomy-
opathy [l]. It is well known that acute myocardial infarction in hypertrophic cardiomyopathy can abolish the gradient [2,3], either by involving the upper interventricular septum, or when necrosis is extensive and the left ventricle becomes dilated and globally hypokinetic. Nevertheless, the present case shows the converse mechanism, as the gradient resulted from the increase of contractility of the basal walls as a consequence of apical hypokinesia. This phenomenon has been previously reported [4], although our case is the first to have been documented by cardiac catheterization, and the first to show relief by means of coronary angioplasty.
Fig. 2. Diastolic and systolic apical views of the left ventricle showing akinesia at the apex and vigorous motion of the basal areas.
168
Fig. 3. M-mode echo and Doppler after angioplasty. Top: No systolic anterior motion of the mitral valve is registered. Bottom: Doppler recording placed at the subaortic level showing no gradient.
References 1 Angel J, ArmendLriz J, G. de1 Castillo H, Llamas C, Gausi C. Idiopathic hypertrophic subaortic stenosis and WolffParkinson-White syndrome. Chest 1975;68:248-254. 2 Come PC, Riley MF. Hypertrophic myocardiopathy. Disappearance of auscultatory, carotid pulse and echocardiographic manifestations of obstruction following myocardial infarction. Chest 1982;82:451-454. 3 Waller BF, Maron BT, Epstein SE, Roberts WC. Transmural myocardial infarction in hypertrophic cardiomyopathy. A cause of conversion from left ventricular asymmetry to symmetry and from normal-sized to dilated left ventricular cavity. Chest 1981;79:461-465. 4 Chesi G, Reverzani A, Pinelli G, Marani L. Dynamic left intraventricular obstruction in acute myocardial ischemia. Minerva Cardioangiol 1989;3787/8:351-353.
Fig. 4. Twelve-lead electrocardiogram. Top: ECG obtained during hospital admission, one day before angioplasty shows negative T waves with a pattern of extensive anterior ischaemia. Bottom: Six months after angioplasty the ECG has normalized and no signs of ischaemia are found.
CARD10
165 0167.5273/92/$05.00
01554
Acute myocardial ischemia resulting in dynamic obstruction to the left ventricular outflow relieved by successful angioplasty C. Martinez-Useros,
E. Galve Basilio and G. Oller Cid
Hospital General de Catalunya, San Cugat del Vall& Barcelona, Spain (Received
26 May 1992; accepted
30 May 1992)
Martinez-Useros C, Galve Basilio E, Oller Cid G. Acute myocardial ischaemia resulting in dynamic obstruction to the left ventricular outflow relieved by successful angioplasty. Int J Cardiol 1992;37:165168. A patient was admitted because of an acute myocardial infarction which evolved with heart failure and postinfarction angina. A pattern consistent with dynamic left ventricular outflow obstruction was found. It disappeared after coronary angioplasty was performed on the vessel responsible for the ischemia. Key words: Dynamic obstruction
to left ventricular outflow; Myocardial ischemia; Angioplasty
Case Report A 61-yr-old female with a past history of systemic hypertension and migraine, who was receiving beta-blockers for both reasons, was admitted to our institution because of repetitive episodes of rest chest pain that had begun one week previously. Physical examination, electrocardiogram (ECG), chest X-ray and blood analysis revealed no abnormalities. She was monitored for 72 h with no complaints. Beta-adrenergic blockers were discontinued and a diagnostic treadmill exercise test was performed. The patient exercised to stage 3 of a Bruce protocol and experienced angina in the postexercise period associated with persistent 7 mm ST-
Correspondence tot Dra. Carmen Martinez-Useros, C/ Rectoria, 38, 1” 2a. 08031 Barcelona, Spain. Tel. (93) 427.35. 67; (93) 589.12.12 (hospital)
segment elevation in leads V3 and V4. She was transferred to the Coronary Care Unit and fibrinolysis instituted. Anterior acute myocardial infarction was confirmed by serial ECGs and enzymes. Total creatine kinase rose to a peak of 494 U (normal values 24-190) while MB isoenzyme rose to a peak of 17 U (normal values l-2). Physical examination disclosed a grad.e 3 systolic murmur at the left sternal border in the fourth intercostal space and a loud fourth heart sound. During the next 48 h she experienced recurrent episodes of postinfarction angina and developed overt heart failure. Cardiac catheterization revealed a left ventricular outflow gradient of 52 mmHg between the body of the ventricle and a subaortic chamber. The gradient showed striking enhancement after premature ventricular contractions and during Valsalva maneuver. Left ventriculography demonstrated localized apical akinesia with tendency to the formation of aneurysm, and mild mitral regurgitation, while
166
the ejection fraction was 51%. Coronary arteriography disclosed a tight (95%) stenosis in the mid portion of the left descending artery. Doppler echocardiography confirmed the findings (Fig. 1): the left ventricle was mildly hypertrophic (interventricular septum: 15 mm, posterior wall 10 mm); there was a localized area of akinesia at the apex while the basal areas near the outflow tract had a vigorous motion, the ejection fraction being 61% (Fig. 2); there was systolic anterior motion of both mitral leaflets and midsystolic closure of the aortic valve; Doppler disclosed a subaortic gradient of 45 mmHg and mild mitral regurgitation. Percutaneous transluminal coronary angioplasty was successfully performed and the symptoms subsided. A Doppler echocardiogram recording
performed before discharge showed no subaortic gradient while systolic anterior motion of the mitral valve and midsystolic closure of the aortic valve had both disappeared (Fig. 3). During follow-up the patient has been well. Initial ECGs showed an extensive anterior ischemia pattern (Fig. 4) that gradually disappeared. Six months after angioplasty a new cardiac catheterization was performed. The left anterior descending coronary artery showed patency without evidence of restenosis. Global and segmentary left ventricular motion had returned to normal. There was no outflow gradient either at rest or under (after) maneuvers. By that time the ECG (Fig. 4) had normalized.
Discussion
Fig. 1. Top: M-mode echocardiogram showing systolic anterior motion of the mitral leaflets and hypertrophy of the interventricular septum. Bottom: Doppler flow recording through the left ventricular outflow tract demonstrating a subaortic gradient of 45 mmHg. Note the characteristic endsystolic peak velocity.
Our patient shows an unusual behavior of the dynamic left ventricular outflow gradient. The obstructive pattern appeared after an acute myocardial infarction and it was relieved after an angioplasty that restored the motion of an apical area of akinesia. We think that this patient had a mild form of hypertensive heart disease resulting in mild septal hypertrophy. The occurrence of an apical area of akinesia resulted in an increase of motion of the basal portions of the left ventricle as a compensatory mechanism, thus generating the dynamic outflow gradient. The combination of ischemia, depressed ventricular function and outflow obstruction was responsible for a dramatic clinical situation coursing with unstable angina and severe heart failure. However, the infarction was not enzymatically large, and the left anterior descending artery was patent; therefore, viability of the akinetic area could be presumed. Angioplasty resulted in relief of the ischemia, thus restoring contractility to the apex and, as a consequence, decreasing the hypercontractility of the basal areas of the left ventricle and thus obliterating the outflow obstruction. It has to be emphasized that the presence and regression of the pressure gradient was documented in the absence of positive or negative inotropic drugs that could interfere with or modify dynamic obstruction. On the other hand, the absence of abnormalities on physical examina-
167
tion, and in the initial and current ECGs, as well as in the current Doppler echocardiogram, indicate that this patient does not fulfil1 the criteria to be diagnosed hypertrophic cardiomyopathy. In fact, it has not been reported that hypertrophic cardiomyopathy could regress, although regression has been found in hypertrophy associated with hypertension or highly-trained athletes. Therefore, this case constitutes an unusual form of dynamic gradient secondary to changes in motion wall abnormalities. It has been reported that changes in ventricular activation in the Wolff-Parkinson-White syndrome can modify the degree of obstruction in hypertrophic cardiomy-
opathy [l]. It is well known that acute myocardial infarction in hypertrophic cardiomyopathy can abolish the gradient [2,3], either by involving the upper interventricular septum, or when necrosis is extensive and the left ventricle becomes dilated and globally hypokinetic. Nevertheless, the present case shows the converse mechanism, as the gradient resulted from the increase of contractility of the basal walls as a consequence of apical hypokinesia. This phenomenon has been previously reported [4], although our case is the first to have been documented by cardiac catheterization, and the first to show relief by means of coronary angioplasty.
Fig. 2. Diastolic and systolic apical views of the left ventricle showing akinesia at the apex and vigorous motion of the basal areas.
168
Fig. 3. M-mode echo and Doppler after angioplasty. Top: No systolic anterior motion of the mitral valve is registered. Bottom: Doppler recording placed at the subaortic level showing no gradient.
References 1 Angel J, ArmendLriz J, G. de1 Castillo H, Llamas C, Gausi C. Idiopathic hypertrophic subaortic stenosis and WolffParkinson-White syndrome. Chest 1975;68:248-254. 2 Come PC, Riley MF. Hypertrophic myocardiopathy. Disappearance of auscultatory, carotid pulse and echocardiographic manifestations of obstruction following myocardial infarction. Chest 1982;82:451-454. 3 Waller BF, Maron BT, Epstein SE, Roberts WC. Transmural myocardial infarction in hypertrophic cardiomyopathy. A cause of conversion from left ventricular asymmetry to symmetry and from normal-sized to dilated left ventricular cavity. Chest 1981;79:461-465. 4 Chesi G, Reverzani A, Pinelli G, Marani L. Dynamic left intraventricular obstruction in acute myocardial ischemia. Minerva Cardioangiol 1989;3787/8:351-353.
Fig. 4. Twelve-lead electrocardiogram. Top: ECG obtained during hospital admission, one day before angioplasty shows negative T waves with a pattern of extensive anterior ischaemia. Bottom: Six months after angioplasty the ECG has normalized and no signs of ischaemia are found.
