Tali T. Bashour

Variant Angina of Prinzmetal with Normal Coronary Arteriograms A Variant of the Variant

Variant angina of Prinzmetal has been generally presumed to be caused by a significant focal obstruction in a single major coronary artery which should be an ideal lesion for aortocoronary saphenous vein bypass graft. Recognition of this clinical syndrome would then be of particular diagnostic and therapeutic importance if such a consistent association can be demonstrated. Of five patients with variant angina studied in our cardiac catheterization laboratories, four had normal coronary arteriograms. Two important conclusions may be derived from this study. First, identical ECG changes may be observed both in the presence and absence of pain and thus the incidence and severity of the variant angina could be underestimated. Second, until a larger series of patients with variant angina is studied by coronary arteriography, one must exercise reservation in assuming that all patients with the clinical syndrome are operative candidates for saphenous vein bypass surgery.

Myocardial infarction in the absence of coronary arteriosclerosis: Result of coronary spasm (?)

Abstract An acute inferior wall myocardial infarction apparently resulted from a severe spasm of the left circumflex artery during selective coronary arteriography in a 52 year old woman who had a normal coronary arteriogram on a subsequent examination. Some of the possible mechanisms of production of myocardial infarction without arteriographic obstruction are discussed, such as coronary embolism or recanalization of a thrombus. It is believed that myocardial infarction without evidence of obstructive coronary disease may be caused by coronary spasm.

An Unusual Effect of Atropine on Overdrive Suppression

To the Editor: By their elegant assessment of sinoatrial conduction during premature atrial stimulation, Strauss et al. (CIRCULATION 47: 86, 1973) have uncovered one major limitation of the rapid atrial pacing as a method of evaluating sinoatrial node automaticity by post drive suppression. This and probably other yet undiscovered facts may account for the inconsistent results obtained by this technique including those from our center.1 During the past year we have been repeating the studies after the administration of 1 mg atropine intravenously. On several occasions we have noticed an apparent paradoxical prolongation after atropine of a previously normal post overdrive sinoatrial recovery time in patients who had the classical clinical picture of the sick sinus node syndrome.2 Most recently, we have evaluated a 64-year-old woman with sinus bradyeardia, frequent sinus arrest, congestive heart failure, palpitations, and two previous episodes of near syncope occurring after usual activity. Premature atrial stimulation indicated high grade sinoatrial entrance block as outlined by Strauss et al. Sinus post overdrive recovery time was normal at rates 80, 100, 110/min for pacing durations of 30 see, 60 see, and 180 sec each time. Only after pacing at a rate of 120 for one minute, did recovery time increase to 2.92 sec (fig. 1). Following 1 mg atropine intravenously, pacing at a rate of 120/mim for one minute resulted in marked post drive suppression and an escape junctional rhythm with retrograde atrial capture of 4.9 sec. Sinus activity was apparent only after 18.3 sec (fig. 2). Although actual sinus recovery may have occurred anytime between 4.9 and 18.3 sec and was suppressed by the retrograde junctional activity, nevertheless, this still represents marked delay. We postulate that sinoatrial entrance block was reversed or significantly reduced by atropine, thus allowing more constant discharge of the sinoatrial node during atrial pacing which has unmasked its profound post drive suppression. We are currently in the process of evaluating this phenomenon in other patients; meanwhile we believe atropine should be given and recovery time reassessed whenever rapid atrial pacing fails to elicit a prolongation of sinoatrial recovery time in patients with the sick sinus node syndrome. TALI BASHOUR, M.D. RAUL HEMB, M.D. RAJASEKARAN WICKRAMESEKARAN, M.D.

Acute Severe Mitral Regurgitation from Papillary Muscle Dysfunction in Acute Myocardial Infarction Successful Early Surgical Treatment by Combined Mitral Valve Replacement and Aortocoronary Saphenous Vein Bypass Graft

A patient with acute severe mitral regurgitation resulting from papillary muscle dysfunction which developed on the third day of acute myocardial infarction underwent early successful mitral valve prosthetic replacement with concomitant aortocoronary saphenous vein bypass. The concept of acute severe mitral regurgitation due to an infarcted papillary muscle which has not actually ruptured and an aggressive approach to such a catastrophic event early in the course of acute myocardial infarction are emphasized. The risk is well worth the gratifying result obtained in our patient who successfully underwent such a combined operative procedure for one of the early complications of acute myocardial infarction.

Complete heart block with normal QRS duration occurring distal to the his bundle in acute inferior myocardial infarction.

A patient with acute inferior myocardial infarction developed on the second day complete heart block with normal QRS duration, and the block was found to be distal to the His bundle. To our knowledge, this is the first such documented case in the English literature. Failure of the preceding Wenckebach periods and of complete heart block to respond to intravenous atropine may be a clinical clue to the nature of this type of heart block. The implications and possible explanations are discussed in the light of recent knowledge concerning the nature of heart block in inferior wall myocardial infarction.