58 year old female with long-standing hypertension (30 mg Benazepril daily). Wt, chol, lipids, glucose, etc. all good. Last year, my primary referred me to a Cardio for a 24 hour Holter for palpitations. The cardiologists' comment on the ECG was "non specific ST and T wave changes." This May, after resuming regular exercise (daily 2.4 mile walk uphill), following 8 weeks de-conditioning for sprained ankle, I experienced a first episode of extreme breathlessness, nausea, sweating, at peak. My primary recommended a stress echo. She administered an ECG and said, "it's not abnormal but it's not normal." The stress echo was normal, 7 Mets and 158 bpm, but I stopped it at 158bpm due to shortness of breath and sensation of throat tightening. The cardiologist's interpretation was normal with no wall motion abnormalities and no ECG suggestion of ischemia (some ST and T changes less than 1 mm, rapidly resolving). The Cardio said this could be equivocal, as throat tightening is an anginal equivalent. I next had a Myocardial Spect Perfusion test and an Echocardiogram. The echo showed mild mitral and mild tricuspid regurgitation. The perfusion scan was negative, at 99% of 159bmp, no perfusion abnormalities at rest or at peak. I did not experience throat tightening. I still occasionally experience throat tightening at peak exercise; on the inhale. The Cardio invited me to participate in a CCTA trial. Would a CCTA provide additional useful info? Apparently, false stress echo negatives are due to: not achieving 85% target rate, balanced ischemia, left anterior circumflex stenosis. Also, wall motion abnormalities occur later chronologically than perfusion abnormalities in the CAD cascade. But what causes a falsely negative Myocardial perfusion scan?
CAn the CCTA show microvascular occlusion? Given a negative stress echo and a negative perfusion scan, would a CCTA add useful information?