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6 Fig. 3. Right anterior oblique (A) and left anterior oblique (B) views of the left coronary artery showing a large dissec- tion (arrows) of the proximal and mid LAD.

lose their normal corrugation, reticular fibers fragment, there is a decrease in acid mucopolysaccharide ground substance, and smooth muscle hypertrophy and hyperpla- sia occur.6 These changes have been attributed primarily to progesterone excess and may be exacerbated at the time of delivery by the release of relaxin. Such biochemical and histologic abnormalities may predispose to coronary artery dissection. While all of the aforementioned pathogenic mechanisms may contribute to coronary occlusion, the precise cause of the initial occlusion in this patient is un- clear. Whether coronary artery dissection occurred de novo or resulted from PTCA also is uncertain; however, it is likely that coronary artery dissection contributed to sub- sequent coronary artery occlusions. It is reasonable to speculate that postpartum patients undergoing PTCA may be at increased risk for coronary artery dissection due to the presence of the previously discussed biochemical and his-

tologic coronary artery abnormalities in such individuals. While the rationale exists for the use of emergency PTC’A in acute MI due to coronary atherosclerosis, the presence of a hypercoagulable state and the loss of normal structural integrity of the coronary arteries suggest that PTCA will he of limited usefulness in the management of postpartum MI.

REFERENCES

1.

2.

3.

Beary JF, Summer WR, Bulkley BH. Postpartum myocardial infarction: a rare occurrence of uncertain etiology. Am J Car- diol 1979;43:158-61. Bornstein A, et al. Acute myocardial infarction in a thirty-six year old postpartum female. Angiology 1984;35:591-4. Iffy L, Tentlove W, Frisoli G. Acute myocardial infarction in the puerperium in patients receiving bromocriptine. Am .I Obstet Gynecol 1986;155:371-2. Bell WR. Hematologic abnormalities in pregnancy. Med Clin North Am 1977;61:165-91. Smith JC. Dissecting aneurysms of coronary arteries. Arch Path01 Lab Med 1975;99:117-21. Menalo-Estrella P, Barker AE. Histopathologic findings in human aortic media associated with pregnancy. Arch Pathol Lab Med 1967;83:336-41.

Dipyridamole-induced negative U waves: Scintigraphic evidence of severe anterior myocardial ischemia

Michele Galli, MD, Enzo Bosimini, MD, Andrea Campi, MD,* and Luigi Tavazzi, MD. Veruno and Novara, Italy

Among the electrocardiographic signs of transient myocar- dial ischemia, negative U waves in the precordial leads have been reported to be very specific for coronary artery disease and to be almost hallmark of left anterior descending (LAD) coronary stenosis’ or spasm.2 Although the mecha- nism of U wave negativity remains unclear,3 recently Ya- makado et a1.4 postulated that myocardial ischemia asso- ciated with transient negative U waves could be less severe than that associated with ST segment elevation or depres- sion. We report the case of a patient with both spontane- ous and dipyridamole-induced negative U waves and the scintigraphic evidence of severe anterior myocardial is- chemia causing such an electrocardiographic (ECG) find- ing.

A previously well 34-year-old man was admitted to a nearby hospital because of prolonged chest pain with ECG evidence of ST segment elevation in precordial leads Vs to Vs. Pain promptly ceased and the ECG reverted to normal

From Clinica de1 Lavoro Foundation, Institute of Care and Research, Divi- sion of Cardiology, Veruno Medical Center, Veruno (No); and Hemody- namic Laboratory,* Ospedale della Carita’, Novara.

Reprint requests: Michele Galli, MD, Cardiology Division, Centro Medico. Veruno (No), 28010 Italy. 4/4/139’76

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Number 3 Brief Communications 6 17

Fig. 1A. Twelve-lead ECG at rest, during a spontaneous angina1 attack, and at the third minute of dipyridamole in- fusion. During chest pain at rest and after dipyridamole, negative U waves are clearly evident (arrows), whereas no significant ST-T changes are noted during exercise (see Fig. 1B). HR, Heart rate; BP, blood pressure. (Modified limb leads were used for exercise and dipyridamole ECG.)

after the intravenous administration of nitrates and hep- arin; a modest but consistent serum myocardial enzyme release was noted (peak creatine kinase [CK], 490 U/L; peak MB isoenzyme of CK, 20 U/L). In the following days the patient remained symptom-free and a pre-discharge treadmill test with oral nitrate therapy only failed to induce chest pain or significant ECG abnormalities (max- imal heart rate and blood pressure values achieved = 170 beats/min and 190/90 mm Hg, respectively, at the sixth stage of the Bruce protocol). During the next few days, however, the patient experienced a return of mild chest discomfort at rest and was admitted to our hospital. In the course of a new episode of mild spontaneous chest pain,

transient negative U waves and peaked T waves were doc- umented in leads V3 to Vg (Fig. 1A); angina and ECG ab- normalities rapidly disappeared after the administration of sublingual nitroglycerin. Nifedipine was initiated and in the following days a new bicycle exercise test with nitrates and nifedipine caused neither angina nor significant ECG abnormalities (maximal heart rate and blood pressure val- ues achieved were 125 beats/min and 180/80 mm Hg, respectively, at 75 W for 3 minutes) (values at the third minute, Fig. 1B).

A dipyridamole (0.56 mg/kg in 4 minutes) thallium-201 scan was carried out after 12 hours of drug withdrawal. At the third minute of dipyridamole infusion (heart rate, 88 beats/min; blood pressure, 110/80 mm Hg), negative U waves in precordial leads Vz to V5 were observed (Fig. lA), and the patient experienced worsening angina. Dipyrida- mole infusion was interrupted, thallium was injected, and 5 minutes later intravenous aminophylline, 200 mg, was administered with rapid relief of pain. Thallium images (Fig. 2) disclosed a transmural perfusion defect of the an- terior and apical regions, with filling in of the tracer defect at 4 hours of delayed scans, suggesting transient severe is- chemia induced by dipyridamole. The mild persistent thallium defect in the distal anterior and apical regions agreed both with the clinical evidence of recent non-Q wave infarction and with the severe degree of transient ischemia. Coronary angiography (Fig. 3) revealed stenosis of the proximal LAD involving its first diagonal branch and the occlusion of the second LAD diagonal branch. Circumflex and right coronary arteries appeared normal; mild apical hypokinesia was noted at ventriculography. Because of the multiple LAD stenotic lesions, surgical revascularization was preferred.

The mechanism of U wave generation is disputed and includes Purkinje fiber repolarization or ventricular after- potentials during the relaxation phase.3 Negative U waves are a very specific but poorly understood sign of valvular, hypertensive, and ischemic heart disease. Their ischemic genesis has been postulated due to the angiographic evidence of LAD stenosis in patients with exercise inver- sion of U waves,l because of their appearance during vari- ant angina,2t 4 and because of their regression following successful angioplasty.5 Although the occurrence of nega- tive U waves during exercise is uncommon,l the true inci- dence may be underestimated due to the difficult recogni- tion of this phenomenon at a faster heart rate; indeed, this ECG finding may be more common during vasospastic an- ginal attacks, frequently in the absence of ST segment changes.2 Other uncommon ECG ischemic findings, such as transient positivity of negative T waves” or exercise- induced ST segment elevation in leads without Q waves7 have been documented to indicate severe transient myo- cardial ischemia, as suggested by the thallium-201 perfu- sion pattern; to our knowledge, the scintigraphic finding associated with negative U waves has not been previously reported, nor has such an ischemic ECG sign after dipy- ridamole been recorded.

A recent angiographic study by Yamakado et a1.4 during ergonovine-induced vasospastic angina documented in one

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American Heart Journal

Fig. 2. Early post-dipyridamole (above) and delayed (below) thallium-201 images in the three common projections. A severe perfusion defect (large arrows) is present at early images in the anterior and apical regions, with less severe hypoperfusion of septal segments (small arrow). Incomplete redistribution of the isotope is present in the distal anterior and apical regions at the delayed images. LAO, Left anterior ob- lique projection.

patient less severe LAD narrowing associated with U wave waves could be less severe than that associated with ST inversion and a further spastic LAD narrowing with segment changes. However, we documented negative U

delayed distal filling of the vessel associated with transient waves associated with angina and a severe anterior perfu- ST segment depression; from this the authors speculated sion defect, as indicated by the transmural thallium uptake that myocardial ischemia associated with only negative U defect with incomplete delayed redistribution. Further-

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Number 3 Brief Communications 6 19

Fig. 3. Selective left coronary angiograms showing stenoses of proximal anterior descending coronary (large arrows), of its first diagonal branch, and the occlusion of a second diagonal branch (small arrow).

more, assessment of the severity of ischemia on angio- graphic findings alone is not reliable.

Of relevance in this case was the fact that repeated exercise tests did not induce angina nor ECG ischemic changes, although the heart rate-blood pressure products achieved during effort were remarkably greater than those achieved at the third minute of dipyridamole infusion. This suggests that an absolute decrease in myocardial oxygen supply rather than increased oxygen demand in the jeopardized LAD territory was the prevalent cause of angina and negative U waves. In view of the good exercise tolerance of the patient (he was able to go to the sixth stage of the 3ruce protocol completely symptom-free), the possibility of LAD coronary spasm during the dipyridamole test should be considered.

REFERENCES

1.

2.

3.

4.

5.

6.

7.

Gerson MC, Phillips JF, Morris SN, McHenry PL. Exercise- induced U-wave inversion as a marker of stenosis of the left anterior descending coronary artery. Circulation 1979;60:1014. Kishida H, Cole JS, Surawicz B. Negative U wave: a highly specific but poorly understood sign of heart disease. Am J Cardiol 1982;49:2030. Miwa K, Murakami T, Kambara H, Kawai C. U wave inver- sion during attacks of variant angina. Br Heart J 1983;50:378. Yamakado T, Nakano T, Masuda T, Takezawa HD. Coronary angiographic findings associated with U-wave inversion dur- ing coronary artery spasm. Am J Cardiol 1987;60:188. Scholl JM. Waaniart P. Morice MC. Charlier P. Morin B. Daffos C. Elimiiation ofisolated exercise-induced’u wave in: version after successful percutaneous transluminal coronary angioplasty of left anterior descending artery. AM HEART J 1987;114:166. Parodi 0, Uthurralt N, Severi S, Bencivelli W, Michelassi C, L’Abbate M, Maseri A. Transient reduction of regional myo- cardial perfusion during angina at rest with ST-segment de- pression or normalization of negative T waves. Circulation 1981;63:1238. Dunn RF, Bailey IK, Uren R, Kelly DT. Exercise-induced ST segment elevation: correlation of thallium-201 myocardial perfusion scanning and coronary arteriogrpahy. Circulation 1980;61:989.

Echocardiographic diagnosis of an aortocoronary venous bypass graft aneurysm

Vlad Dzavik MD, FRCPC, Michel Lemay MD, FRCPC, and Kwan-Leung Chan MD, FRCPC. Otttawa, Ontario, Canada

First recognized in 1975, aneurysmal dilatation of the sa- phenous vein graft is a rare complication of coronary artery bypass surgery.’ Previous cases have been diagnosed at angiography.1-6 We report the case of an aneurysm of a sa- phenous vein graft to the right coronary artery that was vi- sualized by means of transesophageal echocardiography.

A 54-year-old man with long-standing hypertension and an 80 pack year smoking history presented with angina in 1975. He was found to have multivessel coronary artery disease and underwent a saphenous vein grafting proce- dure of the left anterior descending, first diagonal, and right coronary arteries. Over the past 7 years he was com- pletely asymptomatic. His angina recurred in August 1988, and in September 1988 he suffered an inferior wall myo- cardial infarction. Because of post-infarctional angina, an angiogram was performed. This showed inferior hypokine- sis of the left ventricle, proximal occlusion of the left an- terior descending and right coronary arteries, and diffuse disease of the circumflex artery. The graft to the first diag- onal artery was patent. The left anterior descending graft was tortuous but also patent. The graft to the right coro-

From the University of Ottawa Heart Institute, Ottawa Civic Hospital. Reprint requests: Kwan-Leung Chan MD, FRCPC, Diagnostic Centre, University of Ottawa Heart Institute, Ottawa Civic Hospital, 1053 Carling Ave., Ottawa, Ontario, Canada KlY 4EW. 414113975