Unstable angina with episodic ST segment elevation and minimal creatine kinase release culminating in extensive, recurrent infarction.

The syndrome of episodic angina at rest, recurrent ST segment elevation (mean = 9 mV) and nontransmural infarction characterized by minimal serum creatine kinase (CK) (mean 243 IU; upper normal limit 132 IU) was studied in 15 patients who presented with these findings. All were initially managed with intensive nitrate and beta-receptor blocker therapy. Eleven patients underwent intraaortic balloon counterpulsation for refractory angina and 13 underwent cardiac catheterization. High grade (greater than or equal to 90%) stenosis of the proximal left anterior descending coronary artery was demonstrated in 11 patients, and coronary spasm without significant, fixed occlusive disease was noted in 2 patients. Urgent aortocoronary bypass surgery was performed in seven patients with recurrent pain or electrocardiographic injury, or both, unresponsive to maximal medical therapy. The initial mean ST segment elevation and CK elevation for this group was 10 mV and 232 IU, respectively. No surgical patient developed recurrent infarction; there was one late death after reoperation. Eight patients whose condition stabilized initially on medical therapy did not undergo urgent surgery. However, five subsequently developed large transmural anterior reinfarction despite intensive medical therapy, and three died from pump failure. These patients on medical therapy did not differ from the surgical group in magnitude of ST segment elevation or increase in serum CK. Their initial mean ST segment elevation and CK elevation were 8 mV and 254 IU, respectively (difference not significant). Thus, repetitive episodes of rest angina with marked anterior wall ST segment elevation and mild CK elevations may define a subset of patients who appear to progress rapidly from minimal nontransmural necrosis to massive transmural infarction. Prompt recognition of this syndrome, followed by cardiac catheterization and urgent aortocoronary bypass surgery, may prevent extensive cardiac muscle loss.

Bioprosthetic endocarditis due to Cryptococcus neoformans.

Fungal prosthetic endocarditis continues to be a lethal complication of cardiac valve replacement. We describe a patient with culture-proved Cryptococcal endocarditis and myocarditis whose non-regurgitant xenograft aortic prosthesis was successfully replaced urgently upon the occurrence of new 1st degree A-V block in the third postoperative week. Operative intervention, including vigorous debridement of the aortic root, is effective in postoperative prosthetic fungal infections involving the myocardium. The patient described herein is now infection-free, with a non-regurgitant valve, one and one-half years following operation.

Exercise-induced coronary spasm with S-T segment depression and normal coronary arteriography.

The unique association of both exercise-induced coronary arterial spasm and S-T segment depression with normal findings on selective coronary arteriography is described. The patient had a prior history of typical effort angina that had recently progressed to angina at rest. Despite the change in anginal pattern, the electrocardiogram disclosed S-T segment depression that was consistent with subendocardial ischemia, during both exercise testing and spontaneous chest pain. Exercise thallium-201 scintigraphy demonstrated the presence of large perfusion defects of the anterior and septal walls of the left ventricle. Coronary arteriographic findings, in the absence of symptoms, were entirely normal. Severe localized, reversible coronary spasm of the proximal left anterior descending coronary artery was subsequently demonstrated during spontaneous angina, isometric arm exercise and after the administration of ergonovine maleate. After treatment with isosorbide dinitrate and nifedipine, the patient had no further chest pain or electrocardiographic changes, and a repeated thallium-201 stress test revealed normal findings and greatly improved exercise tolerance.