Case Reports

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Patient 1

A 56-year-old man with a history of mild hypertension treated with enalapril (Vasotec, Merck & Co., West Point, Pennsylvania), 10 mg daily, came to a local emergency room complaining of pressure-like chest pain that awakened him from sleep. Results of his 12-lead electrocardiogram were normal despite persistent chest pain. Intravenous nitroglycerin was begun, and the patient was titrated up to 40 µg/min without relief. Intravenous heparin was begun and intravenous demerol was used to provide partial pain relief. Metoprolol (Lopressor, Ciba-Geigy Co., Woodbridge, New Jersey), 25 mg twice daily, was also begun orally. During the course of 12 hours, the chest pain recurred intermittently. Results of three additional 12-lead electrocardiograms during this time remained normal. The creatinine kinase levels measured on arrival and 6 hours later were normal, but a third creatinine kinase level was 12.5 µkat/L with a 6% MB fraction.

At this point, helicopter transfer was arranged to our hospital for urgent diagnostic cardiac catheterization. On arrival, the patient's blood pressure was 110/68 mm Hg, the jugular venous pressure was not increased, and the Kussmaul sign was absent. Another 12-lead electrocardiogram remained within normal limits, but the chest pain persisted. Contrast left ventriculography showed an ejection fraction of 60% with normal regional wall motion. Selective injections of the left coronary artery showed a left dominant system without coronary narrowing. Contrast injection of the right coronary artery showed total proximal obstruction Figure 1 A. Because of the presence of persistent chest pain, a 2.5-mm balloon catheter (Cordis Corporation, Miami Lakes, Florida) and a 0.014-inch (30.8-mm) floppy guidewire (ACS, Santa Clara, California) were used to restore flow to the nondominant right coronary artery Figure 1 B. Branches supplying only the right ventricle were present. The patient had complete relief of chest pain within minutes. After the patient arrived in the coronary care unit, an electrocardiogram with right side chest leads was done; it showed a 0.75-mm ST-segment elevation in lead V4R. The creatinine kinase level peaked at 28.9 µkat/L, 11 hours after the angioplasty. A transthoracic echocardiogram showed normal left ventricular regional and normal global systolic function. The right ventricle was dilated and globally hypokinetic. Slight tricuspid regurgitation was present. The patient was discharged without recurrent chest pain on the fourth hospital day. At a 1-month follow-up visit, he was well and did not have recurrent symptoms.

View larger version (85K): [in this window] [in a new window]   Figure 1. Contrast coronary angiogram from Patient 1. Left. Selective injection of the right coronary artery in the left, anterior oblique projection. Total proximal obstruction is seen (arrow). Right. After percutaneous transluminal coronary angioplasty, flow is restored to this nondominant artery supplying only the right ventricle.

A 69-year-old man with a history of diabetes mellitus, hypertension, and hypercholesterolemia came to a local emergency room complaining of three episodes of pressure-like chest pain that day. Each episode had lasted 10 minutes. On arrival he was pain free. His chronic medications included hydrochlorothiazide and glyburide (Diaßeta; Hoechst-Roussel, Somerville, New Jersey). His initial 12-lead electrocardiogram was normal, and subsequent tracings remained normal. The jugular venous pressure was normal. During the next 12 hours, the creatinine kinase level increased to 6.62 µkat/L with a 9% MB fraction that was diagnostic of myocardial infarction. He had an episode of recurrent chest pain that evening and had atrial fibrillation with a ventricular response rate of 150 beats/min. He was treated with intravenous nitroglycerin and heparin, and he also received digitalis. He reverted to sinus rhythm by the next morning. On the third hospital day, he had recurrent chest pain at rest; results of another 12-lead electrocardiogram during pain were normal.

He was transferred to our hospital for diagnostic cardiac catheterization. Contrast left ventriculography showed an ejection fraction of 55% with normal regional wall motion. The left coronary artery was the dominant artery for circulation, and it was normal. The nondominant right coronary artery had a subtotal stenosis in its proximal third Figure 2 A and supplied branches only to the right ventricle. A 2.5-mm balloon catheter (Cordis Corp.) and a 0.014-inch (30.8-mm) floppy guidewire (ACS) were used to dilate the stenosis to a narrowing of less than 20% Figure 2 B. The sheath was removed the next day and the patient was discharged on the fifth hospital day. At a 1-month follow-up visit, he was well without recurrent symptoms.

View larger version (106K): [in this window] [in a new window]   Figure 2. Contrast coronary angiogram from Patient 2. Left. Selective injection of the right coronary artery in the left, anterior oblique projection. A subtotal obstruction is present in the proximal portion of this nondominant artery (arrow) supplying only the right ventricle. Right. After percutaneous transluminal coronary angioplasty, the narrowing improved.

Discussion

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Another explanation for the infrequent diagnosis of isolated right ventricular infarction may relate to the difficulty in accurately diagnosing the condition. Both of our patients, along with several others [6, 8], had normal or only slightly abnormal 12-lead electrocardiography, which can lead to considerable diagnostic confusion. Although ST-segment elevation in right-sided precordial leads, especially V4R, has been reported [9] to have increased sensitivity and specificity for the diagnosis of right ventricular infarction accompanying inferior left ventricular infarction, the diagnostic accuracy in isolated right ventricular infarction is unknown. In Patient 1, nearly 1 mm of ST elevation was found in V4R, suggesting that right-sided chest leads may also be useful in the diagnosis of isolated right ventricular infarction. A further limitation of right-sided electrocardiography is that, in the absence of inferior ST-segment changes, it may rarely be requested (as in the case of patient 2). Right precordial electrocardiography should be done routinely in patients with prolonged anginal symptoms and normal results of a standard electrocardiogram. An elevated jugular venous pressure and Kussmaul sign are often found during hemodynamically important right ventricular infarctions [10] and should be looked for during the physical examination of patients with prolonged anginal symptoms.

Echocardiography and radionuclide angiography have been used to identify right ventricular infarction accompanying inferior left ventricular infarction [1, 2]. In Patient 1, two-dimensional echocardiography confirmed dysfunction of the right ventricle with normal left ventricular function. Echocardiography, in particular, may be useful in the early confirmation of acute myocardial infarction in patients in whom clinical uncertainty exists. In patients with prolonged anginal-type chest pain who have nondiagnostic electrocardiograms, urgent two-dimensional echocardiography might show isolated right ventricular infarction, pericardial effusions, aortic dissections, and cardiomyopathies that may alter the treatment plan.

Our two patients with isolated right ventricular infarction were the first patients in whom coronary angioplasty was used to restore arterial patency. In Patient 1, cardiac catheterization was done emergently because of persistent anginal chest pain and diagnostic uncertainty. Coronary angioplasty resulted in immediate relief of chest pain. Intravenous thrombolytic therapy was not considered to be appropriate due to the normal 12-lead electrocardiogram and the considerable diagnostic uncertainty. In Patient 2, cardiac catheterization was done because of postinfarction angina; coronary angioplasty of the stenotic nondominant right coronary artery relieved his symptoms. The considerations in doing coronary angioplasty differed from procedures in larger arteries only in that surgical standby for emergency revascularization (that is, coronary bypass surgery) was not arranged because of the limited distribution of the target vessels.

An additional symptom in Patient 2, which has not been previously reported, is the development of atrial fibrillation during isolated right ventricular infarction. This fibrillation presumably developed due to right atrial ischemia or infarction. Recurrent ventricular tachycardia has been reported previously in isolated right ventricular infarction [6].

Isolated right ventricular infarction due to occlusion of nondominant right coronary arteries may lead to prolonged anginal pain even in the absence of changes in the 12-lead electrocardiogram. Right precordial electrocardiography should be done routinely in such patients to determine if ST-segment elevation is present in lead V4R. Although the usual clinical course of isolated right ventricular infarction is incompletely described, in general it would probably be benign. Urgent cardiac catheterization and coronary angioplasty can probably be limited to a minority of patients with ongoing clinical instability. Awareness of this syndrome should lead to more frequent diagnosis and more appropriate management.