Coronary Vasospasm Inducing Dynamic Left Ventricular Outflow Tract Obstruction

Abstract

An 80-year-old man was admitted to the emergency department of our institution due to acute, anterior-wall myocardial infarction and cardiogenic shock. Two-dimensional echocardiography revealed systolic anterior motion of the mitral leaflets with severe left ventricular outflow tract obstruction. Although coronary angiography showed normal coronary arteries, an ergonovine provocation test induced diffuse coronary constriction of the left coronary artery, with chest pain, and ST-T changes seen on the electrocardiogram. These clinical signs caused us to suspect coronary spasm.

The present case serves as a reminder that coronary vasospasm may be a factor in the development of dynamic left ventricular outflow tract obstruction. Early detection and intensive efforts to relieve vasospasm, including emergency coronary angiography and intracoronary injection of nitroglycerin, are essential.

People with coronary vasospastic angina usually experience it at rest, between midnight and early morning, or under special conditions, such as cigarette smoking, ¹ cocaine use, ² or alcohol withdrawal. ³ The diagnosis is difficult to document because results of conventional laboratory tests and electrocardiograms (ECGs) usually fall within normal limits except during attacks of coronary vasospasm. In addition to considering the patient's age and risk factors, physicians should conduct a thorough review of the clinical history in order to detect this disease.

Coronary vasospasm is often associated with a fixed atherosclerotic lesion but occasionally occurs in normal arteries. A severe attack of vasospasm may progress to myocardial infarction ⁴ or sudden death, ⁵ although this is rare. The unusual presentation of dynamic left ventricular outflow obstruction during coronary vasospasm in elderly patients reminds us of the need for a special treatment strategy should this rare condition occur.

Case Report

In August 1999, an 80-year-old man arrived at the emergency room of our institution at 8:20 AM due to severe prolonged chest pain, which had begun 5 hours earlier. A 12-lead electrocardiogram (ECG) showed ST-segment elevation in leads II, III, aVF, and V₁ through V₆ (Fig. 1A). The initial blood pressure was 76/43 mmHg, the heart rate was 67 beats/min, and the respiration rate was 24 breaths/min. Physical examination revealed a grade 3 systolic murmur at the left sternal border in the 4th intercostal space. The lungs were clear. Tissue plasminogen activator was administered at 9:20 AM for suspected acute myocardial infarction but was discontinued after less than an hour because the patient's gums were bleeding. The patient had severe hypotension, and therefore was given dopamine (15 μg/kg per minute) instead of nitroglycerin. Two-dimensional echocardiography revealed a dilated left ventricle with akinetic changes at the apical, anteroseptal, and lateral walls, and a left ventricular ejection fraction of 33%. Vigorous contraction was observed at the basal areas near the left ventricular outflow tract (LVOT), with marked systolic anterior motion of the mitral leaflets (Figs. 1C and 1D). Doppler echocardiography revealed a subaortic pressure gradient of 159 mmHg (Fig. 1E). Serial ECGs and cardiac enzyme levels confirmed the diagnosis of acute myocardial infarction. The cardiac troponin I level was 2.12 ng/mL (normal range, <0.1 ng/mL) at the emergency department, and the peak creatine kinase level was 598 U/L (normal range, 15–130 U/L) with an MB isoenzyme fraction of 11.1%.

Fig. 1 Twelve-lead electrocardiogram (ECG) showed ST-segment elevation at anterior, lateral, and inferior wall leads (A); repeated ECG, 10 days after admission, showed diffuse T wave inversion (B); 2-dimensional echocardiography in the parasternal long-axis view showed normal closure of the mitral valves in the early systolic phase (C) and marked systolic anterior motion of the mitral leaflets (arrow) in the late systolic phase (D), with a subaortic pressure gradient of 159 mmHg (E).

The patient's general condition stabilized gradually under aggressive medical treatment that included oral isosorbide dinitrate, aspirin, and intravenous heparin and dopamine infusion. Carvedilol was also prescribed on the 2nd day after admission. However, during the early morning hours of the 4th and 6th days, similar chest pain recurred. On the morning of the 7th day, cardiopulmonary resuscitation was required after an episode of severe chest pain with ST-segment elevation in the precordial leads; the patient went into shock. After his condition was stabilized, coronary angiography was performed and disclosed normal coronary arteries (Fig. 2A). However, an intracoronary injection of 5 μg methylergonovine provoked severe diffuse coronary spasm at the left anterior descending and circumflex coronary arteries with chest pain and ST-T changes on ECG (Fig. 2B), which were immediately reversed by intracoronary nitroglycerin. After withdrawal of carvedilol and administration of a long-acting calcium channel blocker (verapamil) and oral isosorbide dinitrate, the patient became well and was free of angina. Two-dimensional echocardiography showed a left ventricular ejection fraction of 0.65 without any abnormal wall motion and no pressure gradient at the LVOT. Electrocardiography showed no ST-segment elevation, but diffuse T wave inversion remained (Fig. 1B).

Fig. 2 Coronary angiography showed normal left coronary arteries (A), which became diffusely constricted after intracoronary injection of ergonovine (B).

Discussion

This patient had multiple symptoms that were consistent with acute myocardial infarction, including recurrent episodes of chest pain with cardiogenic shock, a positive cardiac isoenzyme, and typical changes on ECG. Despite the results of coronary angiography, which showed normal coronary arteries, coronary vasospasm was strongly suspected because of the patient's clinical presentation.

Except for hypertrophic obstructive cardiomyopathy, the most frequently reported cause of LVOT obstruction is a hyperdynamic state resulting from dobutamine administration, dehydration, sepsis, vasodilatation, or mitral valve repair. ^6,7 Martinez-Useros and colleagues ⁸ once reported the case of a patient who had a severe fixed stenotic lesion in the left anterior descending coronary artery that led to dynamic obstruction of the LVOT; the condition was relieved by coronary angioplasty. However, to our knowledge, ours is the first report of dynamic obstruction of the LVOT caused by severe coronary spasm. The pathogenesis of this condition in our patient was most likely associated with vasospasm of left coronary arteries, which resulted in poor distal coronary blood flow with extensive akinetic changes at the anterior-apical wall. Meanwhile, the left ventricular basal area compensated with hypercontraction and eventually induced LVOT obstruction.

Inotropic agents are often used to maintain the systemic blood pressure in the presence of shock. However, for patients with dynamic LVOT obstruction, such treatment aggravates the dynamic obstruction and myocardial ischemia. For this reason, it is important to identify such a condition early in patients with acute myocardial infarction. In our patient, the extensive anterior wall ischemia, a new murmur at the left sternal border, and hypotension suggested dynamic outflow tract obstruction or ventricular septal rupture rather than ischemia-related mitral regurgitation. Two-dimensional echocardiography is useful, when patients are in cardiogenic shock, to reveal causes such as myocardial failure, acute mitral insufficiency, septal rupture, and LVOT obstruction.

Our patient was unusual in that he experienced severe hypotension without the compensation of a rapid heart rate. Such an increase in parasympathetic activity has been shown to be important for the induction of coronary vasospasm. ^9,10 A situation such as this should alert the physician to the possibility of coronary spasm in patients with early morning chest pain and extensive anterior wall ischemia. Nitroglycerin and calcium channel blockers are normally mandatory for the treatment of coronary spasm; however, severe hypotension, as in the present case, may contraindicate the use of such agents via either the sublingual or the intravenous route before the patient is stabilized. Emergency coronary angiography is needed to identify the underlying cause and to assist in deciding whether to perform rescue coronary angioplasty or to initiate prompt treatment by intracoronary nitroglycerin injection. Early diagnosis may also avert the potential deleterious effect of the β-blocker, as was administered in this patient.

In summary, the present case of acute myocardial infarction was complicated by both transient dynamic LVOT obstruction and cardiogenic shock. This case should serve as a reminder that coronary spasm may be a factor in dynamic LVOT obstruction. Relief of the vasospasm, including emergency coronary angiography and intracoronary injection of nitroglycerin, is essential.