A 70 year old white female with hypertension, diabetes and chronic renal failure presented with prolonged chest pain, shortness of breath, diaphoresis and weakness. Pain was relieved by two sublingual nitroglycerin tablets. Prior to admission her symptoms were consistent with class III angina. Her previous coronary angiography (C. angio) in 1996 and 2000 showed non-obstructive coronary artery disease. Physical examination revealed BP 165/70 mm Hg, heart rate 86/min, 1+ lower extremity edema, jugular venous pressure of 7 cm above sternal angle and fine bilateral basilar crackles. Peripheral pulses were 2+ bilaterally. Chest x-ray showed vascular redistribution and her serial cardiac enzymes were equivocal. Electrocardiogram (ECG) showed minor ST-T angle changes inferiorly and anterolateraly. Echocardiogram showed a fall in ejection fraction (EF) to 25% from 50% (in 2000) and new hypokinesis of anterior and anteroseptal walls. In view of ACS with decrease in her EF, C. angio was performed showing 30% distal left main (LM) stenosis and diffuse non-obstructive left anterior descending (LAD) stenosis. Surprisingly, when compared to her angiogram of 2000 there were no changes in coronary obstruction. Given the diagnostic conundrum, dipyridamole MPI was done. Stress ECG showed non-diagnostic ST-T changes in lateral leads. A reversible MPI defect in the LAD territory involving 20% of total myocardial volume was seen. This defect was associated with hypokinesis of the anterior wall and localized transient ischemic dilation of the ventricular cavity. In view of the discrepancy between MPI and C. angio the intravascular ultrasonography (IVUS) of the LM and LAD arteries was done that showed a distal 70% LM stenosis (< 4 mm2). The IVUS catheter momentarily got “stuck” while traversing this tight LM stenosis. A 50% proximal LAD stenosis was also noted. The patient underwent two-vessel coronary artery bypass grafting and was discharged after two weeks. Two years later MPI showed no perfusion defect and EF stable at 44%. This case highlights the inability of C. angio to pick up significant obstructive lesions in certain cases. The irregular (geographic) nature of the lumen obstruction and atherosclerotic positive remodeling effect, before and after culprit stenosis, makes it difficult to identify significant stenosis on routine C. angio using orthogonal views. In these cases both MPI and IVUS can be utilized for better clarification of significance of stenosis as was done in our case.
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