Coronary artery vasoconstriction after successful single angioplasty of the left anterior descending artery

Coronary artery vasoconstriction after successful single angioplasty of the left anterior descending artery transluminal coronary angioplasty is associated with spontaneous transient vasoconstriction. The mechanisms by which coronary vasoconstriction occurs distally to a successful dilated stenosis after coronary artery angioplasty are still unknown. The present study was planned to investigate the effect of successful coronary artery angioplasty on coronary vasomotion distal to a dilated stenosis and in the control veseel and the role of a-adrenergic receptors on coronary vasomotion after successful coronary artery angioplasty. We prospectively studied 32 consecuttve patients scheduled for elective single coronary artery angioplasty of the left anterior descending coronary artery. Only aspirin, 325 mg, or nitroglycerin was allowed in the week before the study; no premeditation with diazepam or other drugs was given. In group 1 (control patients, n = 20), quantitative coronary angiography was performed in the control state; 5 and 15 minutes after coronary artery angioplasty; and after intmcoronary nitroglycerin infusion, 300 pg. In group 2 (n = 12), intracoronary phentolamine,2 mg, was infused regionally through the balloon catheter before the coronary artery angioplasty, and coronary angiogmphy was performed at baseline, 15 minutes after balloon deflation, and after nitroglycerfn infusion. In group 1, constriction of the coronary segment distal to a dilated stenosis (2.4 + 0.8 to 2.1 -+ 0.6 mm, -14.6% vs baseline; p < 0.05) and of the circumflex coronary artery segment (2.8 f 0.7 to 2.5 + 0.6 mm, -10.7% vs baseline, p < 0.05) occurred 15 minutes after coronary artery angioplasty. The degree of vasoconstriction -wasnot correlated with the lesion severity before coronary artery angioplasty. In group 2, nonselective a-adrenergic blockade prevented distal vasoconstriction after coronary artery angioplasty (2.1 + 0.4 vs 2.2 2 0.4 mm; difference not significant), whereas significant vasoconstrlction was observed in the control circumflex segments (2.7 + 0.6 vs 2.4 -t 0.7 mm; p < 0.05). After successful coronary artery angioplasty of the left anterior descending coronary artery, constriction of the coronary segment distal to the site of balloon dilation and of the control segment in the circumflex coronary artery was observed. The degree of vasoconstriction of the segment distal to the stenosis was not correlated with lesion severity before coronary artery angioplasty. ,Pretreatment with regional a-adrenoceptor blockade abolished the coronary vasoconstriction. Therefore a generalized mechanismand a-adrenergic-mediated constriction may participate in the abnormalvasomotor changes after successful angioplasty. These findings may provide insight into the mechanisms of coronary vasoconstriction after coronary artery angioplasty. (AM HEART J 1994;128:858-64.) Pt3rCUtSneOUS

Ciro Indolfi, MD, Federico Piscione, MD, Antonio Rapacciuolo, MD, Giovanni Esposito, MD, Nicolino Esposito, MD, Roberto Ceravolo, MD, Emilio Di Lorenzo, MD, AntonGiulio Maione, MD, Mario Condorelli, MD, and Massimo Chiariello, MD Naples, Italy

Coronary vasoconstriction distal to a successful dilated stenosis is a frequent event after coronary artery angioplasty. ‘1 2 However, the mechanisms unFrom the Division of Cardiology, University of Naples Federico II. Received for publication Aug. 4,1993; accepted Feb. X,1994. Reprint requests Ciro Indolfi, MD, Cattedra di Cardiologia, University derico II, Via S. Pansini, 5,80131 Naples, Italy. Copyright @ 1994 by MO&y-Year Book, Inc. 0002s8703/94/$3.00

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derlying this phenomenon are still unknown. Fischell et al.’ first proposed that distal vasoconstriction after coronary artery angioplasty reflect3 autoregulatory vascular adaptation. In their study the severity of coronary artery vasoconstriction distal to the site of coronary artery angioplasty was closely correlated with the severity of the lesion before coronary artery angiop1asty.r However, a subsequent study by ElTamini et al3 did not confirm this finding. In addition to its role as therapeutic tool, balloon occlusion

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Table I. Patients and procedure data of group 1 Patient 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20

Age (yr) 62 55 62 52 46 57 51 47 79 69 65 48 46 55 51 58 48 61 53 55

Sex M M M F M M M

M F F

F M M M M M M M M F

Balloon 3.0 2.5 3.0 2.5 3.0 3.0 2.5 2.5 2.5 2.0 2.0 2.5 2.0 3.0 3.0 2.5 2.0 2.5 2.5 2.0

during coronary artery angioplasty provides a model for the study of acute reversible regional ischemia in humans4 The temporary coronary occlusion during balloon inflation may be associated with anginal pain, ischemic ST-segment changes, regional wall motion abnormalities, and increases in plasma norepinephrine levels.5 Activation of cardiac sympathetic afferent nerves during myocardial ischemia has been extensively described in animal preparation@-* and in humans,g and it is well known that sympathetic stimulation may produce coronary vasoconstriction. In fact, Gerova et aLlo demonstrated that sympathetic activation induced by electrical stimulation of the right and left stellate ganglia produces significant vasoconstriction of the large coronary arteries. This effect is known to be cu-adrenoceptor-mediated because it is prevented by phentolamine.1° On the other hand, Vatner et all1 demonstrated in conscious dogs that norepinephrine produces remarkable coronary vasoconstriction. The present study was planned to investigate the mechanisms underlying coronary vasoconstriction after successful angioplasty of a stenosis of the left anterior descending coronary artery. Accordingly, we assessed the effects of coronary artery angioplasty on coronary vasoconstriction in the distal vessel after successful coronary artery angioplasty of the left anterior descending coronary artery and on a circumflex control coronary segment not manipulated by the balloon catheter or guide

size

Minimal diameter

stenosis (mm) 1.4 1.5 1.2 1.1 1.3 1.4 1.1 1.2 1.6 0.7 0.8 1.2 0.9 1.2 1.3 1.0 0.9 1.0 1.2 1.1

Pressure

inflation (atm) 4 6 4 4 5 4 6 4 4 6 6 6 6 3 4 4 6 4 6 4

wire. The role of a-adrenoceptor antagonist agents on distal segment vasoconstriction after successful coronary artery angioplasty also was assessed. METHODS Population. Thirty-two patients scheduled for elective single coronary artery angioplasty of the left anterior descending coronary artery were prospectively included in the study. The study was approved by the Institutional Review Board of the University of Naples, and written informed consent was obtained from all patients before the study. No patients had unstable angina, angina at rest, previous or acute myocardial infarction, diabetes mellitus, hypertrophic cardiomyopathy, systemic hypertension, congestive heart failure, or grade 3 collateral filling of the target vessel before coronary artery angioplasty. All patients had evidence of exercise-induced myocardial &hernia despite medical therapy. Only aspirin, 326 mg/day, or sublingual nitroglycerin when needed was allowed in the week preceding the study. Patients who required nitroglycerin in the 6 hours before the study or who required any other drug were excluded from the study, as were patients with unsuccessful coronary artery angioplasty or technically in-

adequate coronary arteriograms. No premeditation

with

diaxepam or other drugs was given before the procedure. All patients underwent right- and left-sided heart catheterization in the morning after an overnight fast. After administration of local anesthesia, 8F femoral art&a1 and 7F femoral venous sheaths were placed, and intravenous heparin, 5000 U, was given. Diagnostic coronary angiography was performed by a standard percutaneous femoral approach with the Judkins technique. After diagnostic

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Table II. Patients and procedure data of group 2 Patient 1 2 3 4 5 6 7 8 9 10 I1 12

Age (yr) 55 48 55 68 48 62 45 56 61 53 51 50

Sex

Balloon size

Minimal stenosis diameter (mm)

M

2.5 3.0 2.5 3.0 3.0 2.0 3.0 2.5 2.5 2.5 2.5 2.0

0.9 1.1 0.7 1.3 1.2 0.5 1.2 1.1 0.8 1.3 1.2 0.8

M M M M M

M M M M M F

coronary angiographicstudiesperformed to selectthe best projection (where the stenosiswas dilated and the distal and control vesselsrecorded), a secondintravenous bolus of heparin, 5000U, wasadministered, followed by intravenous administration of acetylsalicylic acid lysine salt, 500 mg. The angioplasty wasperformed with an over-the-wire balloon catheter system.Balloon size waschosento match the diameter of the “normal” coronary segmentadjacent to the stenosisto be dilated, asduring routine angioplasty. To keeptotal ischemictissueconstant, the inflation time of the balloon wasalways 60 seconds,and only the first inflation wasusedto assess the effect of angioplasty on coronary vasomotion. Patient selection and study protocol Group 1: Control patients. This group included 20 patients (15men and 5 women)aged46 to 79 (mean55 & 8) years. Quantitative coronary angiography was performed in the control state; 5 and 15minutes after the first balloon inflation; and after intracoronary administration of nitroglycerin, 300 pg. Procedure data are reported in Table I. Group 2: Patients pretreated with intracoronary phentolamine. Twelve patients (11 men and 1 woman) aged45

to 68 (mean 54 -r- 7) years were included in this group. Phentolamine, 2 mg bolus, was subselectively infused through the balloon catheter, positioned just adjacent to the stenosis,before the dilation. Quantitative coronary angiography was performed before balloon inflation (immediately after phentolamine infusion), 15 minutes after balloon deflation, and after intracoronary administration of nitroglycerin, 300rg. Procedure data are reported in Table II. Quantitative coronary angiography. Coronary angiography was performed after injection of 6 to 8 ml of nonionic contrast medium (Omnipaque 350, ‘WinthropBreon Laboratories, New York, N. Y.). Cineangiograms were recorded with a radiographic system (Siemens,Erlangen, Germany) at 50frames/set. The projection that allowed the best visualization of the coronary artery under study was chosenand was used throughout the study for quantitative analysis.End-diastolic tine frames were vid-

Pressure inflation (atm) 4 3 6 6 6 4 5 5 6 6 5 6

eodigitized by an investigator blind to the study condition and were stored in an image analysis system (Mipron, Kontron Electronics, Eching, Germany) in a 512 x 512 matrix with an eight-bit gray scaleand a 12cm field of view, resulting in a pixel density of 7.3 pixels/mm2.12~ l3 Automatic vessel-segmentcontour detection was performed by a previously described geometric edge differentiation technique. l2 In brief, after interactive determination of a center line within the vesselto ensure the reproducibility of the measurements,5 mm segmentsof the coronary artery were selected. In the segment to be measured, the computer automatically generated scan lines perpendicular to the center line. The first and second derivative functions of densogramsalong each scan line were then computed and the contour point defined as70 % of the distance betweenthe extrema of the first and second derivatives. With the use of the detected contour points, the computer then automatically generated a refined center line of the vesselsegment,and the edgedetection algorithm wasrepeated. The diameter of the guiding catheter in the field of view was usedto convert the imaging data from pixels to millimeters.12*13 Drugs. Phentolamine (Regitin), 10 mg/ml, was purchasedfrom Ciba, Saronno, Italy. Intracoronary nitroglycerin 100 pg/ml, wasprepared by the addition of 25 mg nitroglycerin (Venitrin, Astra-Simes, S.p.A., Milano, Italy) to 250 ml 0.9% sodium chloride solution. Statistical analysis. Results are expressedas means+SD. Statistical analysiswasperformed by analysisof variance for repeated measureswith a SYSTAT (Evanston, Ill.) program.I4 When a significant overall effect was detected, Tukey’s test wasapplied to comparesinglemean values.15Significant differenceswere assumedto be present when p was <0.05. RESULTS Group 1: Effects of coronary artery angioplasty on coronary tiasomotion. In two patients coronary diameter distal to the stenosis was not measured because the quality of angiograms was unsatisfactory. The

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Fig. 1. Spontaneous changes in basal coronary diameter (millimeters) in distal dilated left anterior descendingcoronary artery (LAD) and in control circumflex vessels(CX) before percutaneoustransluminal coronary artery angioplasty (PTCA) (baseline);5 and 15 minutes after PTCA, and after intracoronary (in left main) nitroglycerin (NTG) . Significant vasoconstriction occurred after successfulPTCA. *p < 0.05 vs baselineand 5 and 15 minutes; **p < 0.05 vs baselineand NTG; @p < 0.05 vs NTG. time course of the distal

vasoconstriction observed after coronary artery angioplasty is illustrated in Fig. 1. The basal coronary diameter of the segment distal to the stenosis was 2.4 -t- 0.8 mm before coronary artery angioplasty, 2.3 + 0.7 mm after 5 minutes, and 2.1 +_0.6 mm (-14.6% vs baseline, p < 0.05) 15 minutes after coronary artery angioplasty. After intracoronary administration of nitroglycerin the distal coronary segment was 2.7 + 0.8 mm (p < 0.05 vs baseline and 5 and 15 minutes). The diameter of control segment was 2.8 rt 0.7 mm at baseline before coronary artery angioplasty and 2.7 + 0.8 mm (p < 0.05) 5 minutes after and 2.5 + 0.6 mm (-10.7% vs baseline, p < 0.05) 15 minutes after coronary artery angioplasty. The diameter of control segment after nitroglycerin was 3.2 -r- 0.8 (p < 0.05 vs baseline and 5 and 15 minutes) (Fig. 1). In this group 8 patients had angina pectoris, and 13 had STsegment changes. Fig. 2 shows the relation between minimal lesion severity and the degree of vasoconstriction distal to the stenosis after coronary artery angioplasty. The degree of vasoconstriction was not correlated with lesion severity before coronary artery angioplasty. Group 2: Effects of pretreatment with intracoronary phentolamine on angioplasty-induced changes in hemodynamics and coronary vasomotion. The regional

infusion of phentolamine did not induce changes in aortic pressure or heart rate. In this group 8 patients

had chest pain, and 10 had ST-segment changes. Regional pretreatment with phentolamine prevented coronary artery angioplasty-induced coronary constriction distal to the balloon dilation (2.1 * 0.4 vs 2.2 -C 0.4 mm, difference not significant) but not in the control segment (2.7 +- 0.6 vs 2.4 -t- 0.7 mm, p < 0.05). Intracoronary infusion of nitroglycerin increased distal left anterior descending coronary artery diameter to 2.3 t 0.3 mm (p < 0.05 vs baseline) and circumflex control coronary diameter to 3.1 f 0.7 mm (p < 0.05 vs baseline and 15 minutes). DISCUSSION

The major findings of the present study are that after successful coronary artery angioplasty of the left anterior descending coronary artery, constriction occurred in the coronary segment distal to the site of balloon dilation and in the control segment in the circumflex coronary artery, and the distal coronary vasoconstriction after coronary artery angioplasty was prevented by intracoronary cY-adrenergic blockade. In our study, the first performed in a selected population with a single left anterior descending coronary artery stenosis with pharmacologic wash-out, we found significant coronary vasoconstriction also in the control circumflex segment. This finding suggests that the mechanisms of this phenomenon involve more than just a regional event or the release of vasoactive substances from aggregating platelets

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10

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‘m

m

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Minimal lesion diameter

30

40

(mm)

Fig. 2. Relation between lesion severity (minimal stenosis

diameter) on degree of vasoconstriction (percentage) in left anterior descending coronary artery distal to stenosis 15 minutes after percutaneous transluminal coronary angioplasty. No significant relation between stenosis severity and vasoconstriction was found.

to the site of endothelial injury. Likewise, in a previous study performed in patients with stenosis of the left anterior descending coronary artery, the right or circumflex arteries showed coronary constriction in the control segment of about 13%.2 However, perhaps because of the small number of patients (n = 5) and the different study protocol used, statistical significance was not achieved.2 Thus neural and hormonal mechanisms may participate to the coronary constriction associated with a successful coronary angioplasty. In this regard, Malliani et al6 first described a cardiocardiac spinal sympathetic reflex during ischemia. Transient coronary occlusion induces an increase in discharge of most of the fibers isolated from the left third thoracic ramus communicans, which is known to contribute to the efferent innervation of the heart6 Activation of cardiac sympathetic aRerent nerves has been described in humans.g It also has been demonstrated, in an animal model, that the constriction distal to a severe coronary stenosis during sympathetic stimulation is produced by an activation of az-adrenoceptors.16 Thus balloon occlusion producing sympathetic activation may contribute to coronary vasoconstriction after coronary artery angioplasty.lo Previous studies

November 1 C!94 Heart Journal

have shown that large epicardial coronary arteries are innervated with sympathetic adrenergic nerve fibers.17p i8 In addition, welg recently found an increase in coronary and aortic plasma norepinephrine levels after coronary artery angioplasty, as has been described by McCance and Forfar. Their study showed that the cardiac spillover of noradrenaline did not change during balloon occlusion but increased almost threefold during early reperfusion; therefore during the balloon occlusion there was an increase in overall sympathetic tone.5 A well-controlled experimental study by Vatner et al.ll demonstrated that in normal dogs norepinephrine induces a significant a-adrenergic-mediated coronary vasoconstriction despite increases in left ventricular end-diastolic pressure and left ventricular contractility. Several laboratories have demonstrated that cyi- and az-adrenoceptors mediate constriction of epicardial coronary arteries.20-23 For instance, in conscious calves intracoronary infusion of the selective cui-receptor agonist phenylephrine or the selective cuz-receptor agonist BHT 920 produced equivalent reductions in epicardial coronary artery diameter.21 Finally, the presence of cY2-adrenoceptormediated vasoconstriction has been documented in peripheral and coronary human vessels. 13,24125Therefore, norepinephrine-mediated coronary constriction may be one of the mechanisms by which coronary constriction occurs after coronary artery angioplasty, especially in the presence of atherosclerosis that enhances adrenergic constriction.26t 27 a-Adrenergic vasoconstrictor tone after coronary artery angioplasty may result from both direct sympathetic nerve outflow or from circulating catecholamines. It has been demonstrated that coronary vasoconstriction induced by cold or smoking is prevented by a-adrenoceptor blockade. 28y2g In one study, generalized sympathetic activation induced by the cold pressor test constricted the distal segment before coronary artery angioplasty, whereas no significant vasoconstriction to the cold pressor test was found after coronary artery angioplasty.3 This finding supports the hypothesis that sympathetic activation already exists after coronary artery angioplasty, therefore preventing further vasoconstriction by cold exposure. On the other hand, the finding that intracoronary phentolamine was able to prevent coronary vasoconstriction also suggests that an Lu-adrenergic mechanism may be involved in the changes in coronary diameter after coronary artery angioplasty. In the present study the degree of vasoconstriction was not correlated with lesion severity before coronary artery angioplasty. This finding supports the

Volume 128, Number 5 American Heart Journal

hypothesis that in our group of patients the “reset” of autoregulation is unlikely to be the major mechanism by which successful coronary artery angioplasty may provoke reflex vasoconstriction.3 Another possible explanation for angioplasty-induced coronary vasoconstriction is an increase in the concentration of vasoactive substances released from platelets aggregating at the site of balloon injury.30 However, this is unlikely to be the only phenomenon that occurs in our patients because (1) coronary vasoconstriction also occurred in control segment; (2) the serotonin antagonist LY 53857 does not prevent distal vasoconstriction after coronary artery angioplasty31; and (3) thromboxane concentration in the coronary sinus does not increase after coronary artery angioplasty. 32Although several additional vasoactive substances (such as endothelin or thrombin) released in the dilated vessel may be involved in the mechanisms of the observed constrictor response after coronary artery angioplasty, it is unlikely that these substances produce coronary vasoconstriction of the control circumflex segments. Therefore the vasoconstriction observed after successful coronary artery angioplasty may result from the action of several mechanisms. Advantages and limitations. In the present study, we used quantitative angiography to assess coronary diameter. This method, previously validated in our12, l3 and other laboratories,2, 3 is a reliable method to measure coronary diameter. In addition, we used the over-the-wire balloon catheter for the subselective infusion of drugs. Intracoronary administration of selective drugs allowed the study of the regional effects of a-adrenoceptor blockade agents with no effect on global hemodynamics. In addition, this is the first study performed in conditions of pharmacologic wash-out to eliminate the possible influence of therapy on angioplasty-induced vasomotor changes. However, we did not follow the effect on coronary artery angioplasty on coronary vasoconstriction for >15 minutes. A more pronounced coronary vasoconstriction may occur in the late stages of intervention. Clinical and pathophysiologic relevance. The demonstration that generalized coronary vasoconstriction occurs after coronary artery angioplasty of the left anterior descending coronary artery and that intracoronary a-adrenergic blockade prevents this phenomenon may have important pathophysiologic and clinical implications. Our results provide evidence that cu-adrenergic-mediated vasoconstriction occurs and that sympathetic stimulation may participate in the abnormal vasomotor changes observed after successful angioplasty. The observation coronary vaso-

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constriction in the control vessel strongly suggests that the mechanisms of vasoconstriction involves more than just production of local substances by balloon injury. We thank Massimo Volpe, MD, for his suggestions and Salvatore Buonerba, Giuseppe D’Alise, and Arturo Bruno for excellent technical assistance.

REFERENCES

1. F&hell TA, Bausback KN, McDonald TV. Evidence for altered epicardial coronary artery autoregulation as a cause of distal coronary vasoconstriction after successful percutaneous transluminal coronary angioplasty. J Clm Invest 1990;86:5’75-84. 2. Fischell TA, Derby G, Tse TM, Stadius ML. Coronary artery vasoconstriction routinely occurs after percutaneous transluminal coronary angioplasty. Circulation 1988;78:1323-34. 3. El-Tamini A, Davis GJ, Hackett D, Sritara P, Bertrand 0, Crea F, Maseri A. Abnormal vasomotor changes early after coronary angioplasty. Circulation 1991;94:1198-202. 4. Perry RA, Seth A, Hunt A, Smith SCH, Westwood E, Woolgar N, Shiu MF. Balloon occlusion during coronary angioplasty as a model of myocardial ischemia: reproducibility of sequential inflations. Eur Heart J 1989;10:791-800. 5. McCance AJ, Forfar CJ. Coronary venous noradrenaline during coronary angioplasty. Int J Cardiol 1991;33:89-98. 6. Malliani A, Schwartz P, Zanchetti P. A sympathetic reflex elicited by experimental coronary occlusion. Am J Physiol 1969;217:703-9. 7. Lombardi F, Casalone L, Della Bella P, Malfatto G, Pagani M, Malliani A. Global versus regional myocardial ischemia: differences in cardiovascular and sympathetic responses in eats. Cardiovasc Res 1984;18:1423.

8. Minisi A, Thames MD. Activation of cardiac sympathetic afIerenta during coronary occlusion: evidence for reflex activation of sympathetic nervous system during transmural myocardial ischemia in the dog. Circulation 1991;84:357-67. 9. Webb SW, Adgey AAJ, Pantridge JF. Autonomic disturbance at onset of acute myocardial infarction. Br Med J 1972;3:89-92. 10. Gerova M, Barta E, Gero J. Sympathetic control of major coronary artery diameter in the dog. Circ Res 1979;44:459-67. 11. Vatner SF, Higgins CB, Braunwald E. Effects of norepinephrine on coronary circulation and left ventricular dynamics in the conscious dog. Circ Res 1974;24:812-23. 12. Indolfi C, Piscione F, Russolillo E, Villari B, Golino P, Ambrosini V, Condorelli M, Chiariello M. Digoxin-induced vasoconstriction of normal and atherosclerotic coronary arteries in man. Am J Cardiol 1991;68:1274-8. 13. Indolfi C, Piscione F, Villari B, Russolillo E, Rendina V, Golino P, Condorelli M, Chiariello M. Role of as-adrenoceptors in normal and atherosclerosis human coronary circulation. Circulation 1992;86:111624.

14. Wilkinson L. SYSTAT: the system for statistics. Evanst,on, Ill.: SYSTAT, 1988. 15. Dixon WJ, Massey J Jr. Introduction to statirricai analysis. New York: McGraw-Hill. 1969231.43. 16. Heusch G, Deussen A. The effects of cardiac sympathetic nerve stimulation on the perfusion of stenotic coronary arteries in the dog. Circ Res 1983;53:8-15. 17. Feigl EO. Coronary physiology. Physiol Rev 1983;63:1-205. 18. Denn MJ, Stone HL. Autonomic innervation of dog coronary arteries. J Appl Physiol 1976;41:30-5. 19. Indolfi C, Piscione F, Esposito G, Rapacciuolo, Maione AG, Esposito N, Gargiulo G, Chiariello M. Mechanisms of coronary vasoconstriction after successful single angioplasty of the left. anterior descending artery [Abstract]. J Am Co11 Cardiol 1993;21:340A. 20. Heusch G, Deussen A, Schipke J, Thamer V. ui and ols-Adrenoceptormediated vasoconstriction of large small canine coronary arteries in viva. d Cardiovasc Pharmacol 1984&961-8.

Charney et al. 21. Young MA, Vatner DE, Knight DR, Graham RM, Homey CJ, Vatner SF. ol-Adrenergic vasoconstriction and receptor subtypes in large coronary arteries of calves. Am J Physiol 1988;255:H1452-9. 22. Chen DG, Dai XZ, Bathe RJ. Postsynaptic adrenoceptor-mediated vasoconstriction in coronary and femoral vascular beds. Am J Physiol 1988;23:H984-92. 23. Woodman OL, Vatner SF. Coronary Vasoconstriction mediated by oland us-adrenoceptors in conscious dogs. Am J Physiol1987;253:388-93. 24. Seitelberger R, Guth BD, Heusch G, Katayama L, Ross J Jr. Intracoronary os-adrenergic receptor blockade attenuates ischemia in conscious dogs during exercise. Circ Res 1988;62:436-42. 25. Taddei S, Salvetti A, Pedrinelli R. Further evidence of the existence of as-mediated adrenergic vssoconstriction in human vessels. Eur J Clin Pharmacol 1988;34:407-10. 26. Heistad DD, Armstrong ML, Marcus ML, Piegors DJ, Mark AL. Augmented responses to vssoconstrictor stimuli in hypercholesterolemic and atherosclerotic monkeys. Circ Res 1984;54:711-8. 27. Young MA, Vatner SF. Enhanced adrenergic constriction of iliac artery with removal of endothelium in conscious dogs. Am J Physiol 1986; 250:H892-7.

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28. Kern MJ, Horowitz JD, Ganz P, Gaspar J, Colucci WS, Lore11 BH, Barry WH, Mudge GH. Attenuation of coronary vascular resistance by selective alphal-adrenergic blockade in patients with coronary artery disease. J Am Co11 Cardiol 1988;5:840-6. 29. Winniford MD, Wheelan KR, Kremers MS, Ugolini V, Van Den Berg E, Niggemann EH, Jansen DE, Hillis LD. Smoking-induced coronary vasoconstriction in patients with atherosclerotic coronary artery disease: evidence for adrenergically mediated alterations in coronary tone. Circulation 1986;73:662-7. 30. Lam JY, Chesebro JH, Steele PM, Badimon L, Fuster V. Is vasospasm related to platelet deposition? relation in a porcine preparation of arterial injury in viva. Circulation 1987;75:243-5. 31. Sigal SLIJ, Sanrembock PJ, LaVeau PJ, Yang TL, Ezekowits MO. A specific serotonin receptor antagonist prevents proximal but not distal spasm following balloon angioplasty. Circulation 19%;1-278-87. 32. Peterson MB, Machaj V, Block PC, Palacios I, Philbin D, Watkins D. Thromboxane release during percutaneous coronary angioplasty. AM HEART J 1986:111:1-6.

Dobutamine echocardiography and resting-redistribution thallium-201 scintigraphy predicts recovery of hibernating myocardium after coronary revascularization The value of dobutamine echocardiography and resting thallium-201 rcintigraphy to predict reversal of regional left ventricular wail motion dysfunction after revascuiarization in patients with chronic coronary artery disease was assessed. improvement in wail motion during dobutamine echocardiography and normal or mildly decreased uptake on thallium-201 scanning are strong predictors of reversible left ventricular dysfunction. Dobutamine echocardiography and resting thallium-201 scanning are simple and safe methods of assessing hibernating myocardium. (AM HEART J 1994;128:864-9.)

Richard Charney, MD,” Matthew E. Schwinger, MD,a Jenny Chun, MD,” Michael V. Cohen, MD,a Michele Nanna, MD,a Mark A. Menegus, MD,a John Wexler, MD, PhD,b Hugo Spindola France, MD: and Mark A. Greenberg,

MD”

Bronx, N. Y.

Revascularization with coronary artery bypass surgery and percutaneous transluminal coronary angioFrom the BDiviaion of Cardiology, Department of Medicine, and the Departments of bNuclear Medicine and Radiology, Mont&ore Medical Center/Albert Einstein College of Medicine. Received for publication Oct. 26, 1993; accepted Feb. 14, 1994 Reprint requests: Richard Charney, MD, Division of Cardiology, Department of Medicine, Montefiore Medical Center, 111 E. 210th St., Bronx, NY 10467. Copyright Q 1994 by Mosby-Year Book, Inc. 0002-8703/94/$3.00 + 0 4/l/68129

plasty has been shown to reverse ischemic regional wall motion dysfunction.1-3 The identification of chronically ischemic hibernating myocardium may be important in the decision-making process regarding revascularization.4 Positron emission tomography has been used to assess hibernating myocardium but is only available in a few centers.5p6 Exercise thallium-201 scanning with 24-hour follow-up and reinjection has also been used to identify dysfunctional but viable myocardium.7, 8