Mark Jenkins, M.D.;([unkeyable]) Da...

Mark Jenkins, M.D.;([unkeyable]) David Tate, M.D.;([unkeyable]) and Avanindra Jain, M.D.([unkeyable])

A patient with normal coronary arteriography who experienced a non-Q myocardial infarction is described. The temporal relationship of ischemic symptoms, ECG changes, and rise in creatine phosphokinase (CPK) support a relationship to an exercise treadmill test

It is estimated that through the whole extent of 500,000 cardiovascular stress tests are performed annually in this country[1] Complications of these courses are unusual but include myocardial infarction, arrhythmias, and death. These issues tend to occur in patients with plain cardiac abnormalities.[1] We report a patient who experienced a nonfatal, non-Q myocardial infarction related to a diagnostic exercise touchstone in whom no abnormality was set up on coronary angiography.

CASE REPORT

A 38-year-old man was referr for evaluation of chest pain of fresh onset. Five days prior to admission he had an episode of chest pain lasting 5 min while lifting a 225-kg woven fabric roll. This recurred the following day while walking and lasted 30 min. The pain was a substernal tightness without radiation further with mild nausea. He was admitted to a local hospital, where serial ECG and cardiac isoenzyme values were normal. He was treated with propranolol, 40 mg bid, nifedipine, 10 mg qid, and aspirin, 1 qd with no renewed symptoms and was referred four days later for further evaluation. He had a history of mild hypertension not requiring medication, and smok cigarettes, 1 pack/day. The consequence s of physical examination showed line pressure of 120/100 mm Hg if it were not that otherwise unremarkable. An ECG was within normal limits. An exercise criterion was performed using the standard Bruce protocol, without discontinuation of his present medications, in which he exercised for 10 min to a heart rate of 151 bpm and family pressure of 152/110 mm Hg He experienced fatigue still no chest pain. At peak exercise there were 2 mm of upsloping ST depression in leads 2 3 and aVF, and a 1-mm slowly upsloping ST depression in [Vsub6] At 5 min into restoration these changes became horizontal to downsloping, and he complained of substernal chest tightness. The ECG changes and chest pain resolv from one side of to the other 19 min after treatment with 2 sublingual nitroglycerin tablets (04 mg)

Cardiac isoenzymes were abnormal, the CPK peaking at 227 (nl 38-125) and an 8 percent MB fraction 12 h after the exercise criterion Serial ECGs showed no change from the resting normal tracing. Cardiac catheterization performed 22 h after the exercise proof showed normal coronary arteries (Fig 1) and normal left ventriculography. As part of the catheterization manner of proceeding graduated doses of ergonovine (005 01 02 and 02 mg) were serially administered IV and accrueed in no symptoms or ECG changes. A technetium-pyrophosphate infarct scan showed uptake in the anteroapical area at 72 h after the exercise trial (Fig 2). An M-mode and 2D echocardiogram showed normal chamber dimensions, normal LV contraction, borderline LV wall thickness (12 mm septum and posterior) and normal valves.

COMMENTS

To our knowledge, this is the first reported case of myocardial infarction complicating exercise stres testing in a patient with normal coronary arteriography. Despite the absence of large bottom coronary artery disease, our patient experienced myocardial ischemia simple enough to cause myocardial injury, as documented at the rise in CPK-MB and uptake of pyrophosphate.

Brown et al[2] described a patient who experienced an acute inferior myocardial infarction after completion of an exercise treadmill criterion in which the patient experienced chest pain without ST portion changes. Coronary arteriography performed three month later showed a 40 percent proximal narrowing of the left circumflex artery and a 40 percent lesion in the midportion of a dominant right coronary artery.

Possible mechanisms for the myocardial infarction in our patient include flush occlusion of a branch utensil not visualized by angiography and thrombosis with spontaneous thrombolysis. In addition, the negative answer to ergonovine administration does not bar the possibility of coronary spasm. The temporal relationship of the CPK peak to the symptoms and ECG changes observ during the exercise proof implicates this procedure as the probable inciting issue During the exercise example there was an abnormal family pressure response and elevation of the diastolic progeny pressure with exertion. This finding refer tos an abnormality of the normal vasodilation that fall outs in the peripheral vasculature in reply to exercise. Such an abnormality in the coronary circulation could terminate in myocardial ischemia, as has been allude toed by the studies of Cannon et al[3] in patients with chest pain, normal coronary arteriography, and abnormal vasodilator reserve

ACKNOWLEDGMENT: We gratefully acknowledge the assistance of Leonard Gette MD in reviewing this manuscript.