LETTERS TO THE EDITOR

pressure. However, in two patients we made the following angiographic findings: Upon low pressure injection of radi- opaque material into the left coronary artery and with- drawal of the catheter, there was significant retrograde flow in the large saphenous vein only during ventricular contraction. Experimentally, coronary blood flow may cease or there may actually be retrograde coronary blood flow during systole owing to increased intramural pres- sures. We observed in these two patients that the blood flow was reversed in the shunt only during systole. The large saphenous vein may act as a low-resistance reservoir during this time, thus diverting blood from the native coro- nary circulation. It is conjectural whether this phenomenon is a mechanism for angina pectoris because its effect on myocardial blood flow is unknown.

In another patient with persistent angina pectoris after bypass surgery, the arteriogram revealed a moderate degree of obstruction in the proximal portion of a graft to the left anterior descending coronary artery. During injection into the left main coronary artery, radiopaque material was di- verted from the left anterior descending coronary artery with resultant retrograde filling of the large saphenous vein. Presumably this occurred because the proximal ob- struction caused a significant decrease in pressure in the distal portion of the graft and the resistance to flow was then less to the graft than to the native coronary circula- tion. The pressure in the aorta was of course greater than in the saphenous vein and retrograde flow did not reach the aorta.

Theoretically, there may be a third mechanism in pa- tients with progressive distal atherosclerosis; blood flow may be diverted away from the high-resistance coronary circulation into the low-resistance large saphenous vein during all phases of the cardiac cycle. We have not ob- served this phenomenon.

Bernard L. Segal, MD, FACC William Likoff, MD, FACC Moosa Najmi, MD Joseph W. Linhart, MD, FACC The Hahnemann Medical College and Hospital Philadelphia, Pennsylvania

UNSTABLE ANGINA PECTORIS VS. PREOCCLUSION SYNDROME

In the recent article by Conti et al.’ on unstable angina pectoris, myocardial infarction developed in only 1 of 10 patients considered to be in the preocclusion state. This finding is in contrast to the experience of many cardiolo- gists.

Many seasoned clinicians prefer the term “preocclusion syndrome” to “unstable angina” because of their experi- ence with a high percentage of patients whose condition progresses to myocardial infarction. In our office 75 to 80 percent of patients with the diagnosis of preocclusion syn- drome later have myocardial infarction. This wide discrep- ancy between our data and those of Conti et al. can be sim- ply explained by the selection of patients. They list their criteria as one or more episodes of ischemic cardiac pain consistent with unstable angina and also admission to a coronary care unit because of a suspected impending myo- cardial infarction. Apparently discrepancy arises on the basis of how strictly or loosely patients are classified by these criteria.

Many patients have various degrees of exacerbation of

their angina without the development of myocardial infarc- tion. The unwary or inexperienced physician could easily be erroneously diagnosing the so-called preocclusion syn- drome in many of these cases. By applying stricter criteria of what represents the preocclusion ischemic pain pattern one can obtain a higher percentage of patients with unsta- ble angina or preocclusion syndrome whose condition pro- gresses to infarction, and thereby demonstrate a distinct pattern of behavior of this disease.

In our office the diagnosis of preocclusion syndrome re- quires a pain pattern with the following characteristics: (1) severity, as manifested by sweat, pallor and nausea; (2) poor relief by nitroglycerin; (3) intense radiation with new pathways of radiation; (4) pain without any of the usual provoking factors; (5) very poor relief with rest; (6) unduly prolonged pain; (7) distinct ischemic abnormalities of the electrocardiogram with or without pain (usually during pain), including the Prinzmetal variation.

Asher Black, MD, FACC Syracuse, New York

Reference

1. Cod CR, Brawky RK, Grlflith LSC, et al: Unstable angina pectoris: morbidity and mortality in 57 consecutive patients evaluated angicgraphically. Am J Cardiol 32: 745-750. 1973

REPLY

I have the following comments in reply to the letter by Dr. Black. First, 2 of the 10 patients with unstable angina who were treated medically had major complications. One had a myocardial infarction and survived and another died from a myocardial infarction during hospitalization. This is a 20 percent complication rate. This experience is similar to that of Krauss et al. who reported the occurrence of six myocardial infarctions and one hospital death in a group of 104 patients with acute coronary insufficiency admitted to their coronary care unit.

Second, we prefer the term “unstable angina” to “preoc- elusion” or “preinfarction” because we believe that a given syndrome of ischemic cardiac pain and electrocardiograph- ic changes can be termed preinfarction or preocclusion only retrospectively. It is difficult to find a term on which there is universal agreement but we believe that the term prein- farction or preocclusion is undesirable because it implies a knowledge of the future that we do not have. Black reports that an average of 75 to 80 percent of patients with the di- agnosis of preocclusion syndrome later have myocardial in- farction. It is possible that these patients are not really in a preocclusion state but rather have early occlusion with re- sulting early myocardial infarction. I would be interested in knowing what Black calls the 20 to 25 percent of patients whose condition did not progress to myocardial infarction but who presented with a similar syndrome.

Third, we readily admit that our patients are selected since many of them are referred to us from other coronary care units in the city. We do not know how frequently myo- cardial infarction ensues in similar patients in other insti- tutions. Our criteria for selection are not loose. All of our patients met the definition of unstable angina as described in our paper, and all but one patient had angina at rest. In addition, all patients had transient electrocardiographic abnormalities associated with episodes of chest pain.

Fourth, Black states that many patients have various de- grees of exacerbations of angina without the development of myocardial infarction. We agree wholeheartedly with

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