A 57-year-old man presented to the emergency department after he had a syncopal episode while at home alone. The patient stated that he had no prodrome and was unaware as to how long he was unconscious. He described substantial midsternal chest pain and shortness of breath on awakening. Although he had a history of coronary artery disease, the chest discomfort differed from his typical angina. The patient stated that, in the weeks before presenting to the emergency department, he had increasing fatigue as well as episodic chest pain and shortness of breath unrelated to physical activity.
The patient's medical history was significant for coronary artery disease, hyperlipidemia, hypertension, depression, and renal insufficiency. The patient had three intracoronary stents placed more than 3 years earlier: two in the left anterior descending artery and one in the right coronary artery. The patient had no known history of myocardial infarction, cardiomyopathy, arrhythmia, or central nervous system disease. He had a 6-year history of minimal tobacco use (approximately 1 pack per year), admitted to occasional alcohol consumption, and denied illegal drug use. His prescribed medications included clopidogrel bisulfate, 75 mg/d, for coronary artery disease; metoprolol tartrate, 50 mg twice a day, for hypertension; isosorbide mononitrate, 60 mg/d, for angina; lansoprazole, 30 mg/d, for heart burn; amitriptyline hydrochloride, 25 mg at bedtime, and citalopram hydrobromide, 20 mg/d, for depression; inhaled beclomethasone dipropionate, 42 μg twice a day, as a prophylaxis for asthma; and aspirin, 325 mg/d, for cardiac protection.
On examination, the patient's blood pressure was 123/80 mm Hg in the supine and orthostatic positions; oxygen saturation, 96%; and heart rate, 111 beats per minute and regular. He appeared to be well nourished. Although he was in mild respiratory distress, the patient was able to complete full sentences. His trachea was midline and his lung fields were clear. No jugular venous distension was noted. Cardiac examination revealed tachycardia and a grade 1 or 2 early-peaking systolic murmur at the lower left sternal border without an audible third heart sound and no parasternal heave. Findings from the abdominal examination were unremarkable. The patient's extremities were warm with normal pulses and without edema.
Laboratory data revealed near-baseline serum electrolyte levels and unremarkable complete blood cell count (
Figure 2). The patient had a mildly elevated creatinine level of 1.6 mg/dL and a brain-type natriuretic peptide level of 21 pg/mL. Troponin I was normal (0.03 ng/mL). Results from the initial ECG demonstrated sinus tachycardia with first-degree block in the interval from atrial stimulus to succeeding ventricular stimulus, incomplete right bundle-branch block, and subtle ST-segment elevation in the anteroseptal leads. Inverted T waves were noted in the right precordial and inferior leads (
Figure 3). Chest X-ray findings were unremarkable.
The patient was admitted to the telemetry unit for further laboratory testing, including serial cardiac enzyme measurements. Intravenous heparin was administered as a 5000 U bolus dose followed by an infusion of 1000 U/hr. Partial thromboplastin time was measured after 1 hour, and the infusion was adjusted according to a previously established nomogram. Several hours later, the patient again experienced substantial midsternal chest discomfort (rated 8 on a 10-point scale, with 10 being “the worst pain imaginable”) and shortness of breath similar to that prompting his admission. After initiating transdermal nitroglycerin therapy, the patient's blood pressure decreased from 110/70 mm Hg to 78/40 mm Hg. Nitroglycerin was removed, and intravenous fluids were administered. A second ECG revealed substantial ST-segment elevation and pathologic Q waves consistent with AMI (
Figure 4). As a result, therapy for acute coronary syndrome was initiated and arrangements were made for emergency cardiac catheterization for suspected acute coronary occlusion.
Results from an angiogram, however, failed to reveal critical obstructive coronary disease. In fact, all of the patient's stents were widely patent with only mild to moderate atherosclerotic disease in the left anterior descending coronary artery, circumflex artery, and right coronary artery (
Figure 5). Although the ECG changes suggested compromised anterior circulation, the patient's response to nitroglycerin suggested right ventricular injury. However, the angiogram revealed a preserved vascular supply to the right ventricle.
After cardiac catheterization, transthoracic echocardiogram revealed dramatic right ventricular enlargement and displacement of the interventricular septum into the left ventricle (
Figure 6); however, left ventricular systolic function was normal. In addition, cardiac pressures on the right side were elevated, and right ventricular systolic function was mildly reduced. The patient did not demonstrate “McConnell's sign,” which is described as ventricular freewall hypokinesis with preservation of right ventricular apical function.
5 McConnell's sign has been reported in instances of massive PE.
5
As a result of the patient's renal insufficiency and contrast load from angiography, a ventilation-perfusion (V/Q) scan was promptly ordered instead of a computed tomography scan to evaluate for PE. The V/Q scan demonstrated large bilateral ventilation-perfusion mismatches highly suggestive of PE (
Figure 7). The patient's troponin I level increased to a peak of 2.6 ng/mL, and creatine kinase-MB increased to 18.3 ng/mL.
After continuation of intravenous heparin therapy and hydration, the patient's condition stabilized. The remainder of the patient's hospital stay was unremarkable. Three days after presentation, a second echocardiogram revealed normalization of the right ventricular cavity size and a decrease in estimated pulmonary artery pressures (
Figure 8). Likewise, the anterior ST-segment changes and conduction defects resolved without the occurrence of pathologic Q waves. The right precordial T-wave inversions also improved (
Figure 9). All cardiac enzyme markers normalized. Ten grams of coumadin was adminstered on the day before discharge, and 7.5 mg on the day of patient's discharge. Arrangements were made with the patient's internist for follow-up care.