Increased myocardial ischemia during supine compared to erect exercise demonstrated by thallium-201 myocardial perfusion imaging

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18. Chandra MS, Raines RD, Doty DB, Kioschas JM: Postinfarction ventricular septal defect with posterior ventricular aneurysm. Chest 661837, 1975. 19. Hill JD, Lary D, Kirth WJ, Gerbode F: Acquired ventricular septal defects: Evaluation of an operation, surgical technique and results. J Thorac Cardiovasc Surg 70:440, 1975. 20. Kitamura S, Mendez A, Kay JH: Ventricular septal defect following myocardial infarction: Experience with surgical repair through a left ventriculotomy and review of- the literature. J Thorac Cardiovasc Sura 61:186. 1971. 21. Schumaker AB: Suggestions concerning operative management of postinfarction septal defects. J Thorac Cardiovasc Surg 64~452, 1972. 22. Donahoo JS, Brawley RK, Taylor D, Gott VL: Factors influencing survival following post-infarction on ventricular septal defects. Ann Thorac Surg 19:648, 1975. 23. Davidson C. Davidson CL: VSD followine mvocardial infarction (letter): Circulation 52:522, 1975. - d 24. Graham AF, Stimson EB, Dailey PO, Harrison DC: Ventricular septal defects after myocardial infarction: Early operative treatment. JAMA 225:708, 1973. 25. Montoya L, McKeever L, Scanlon P, Sullivan HJ, Gunnar RM, Pifarre R: Early repair of ventricular septal rupture after infarction. Am J Cardiol 45:345, 1980. 26. Edmundson HA, Hoxie HJ: Hypertension and cardiac rupture. AM HEART J 24:719, 1942. 27. Daggett WM, Mundth ED, Gold HK, Leinbach RC, Buckley MJ, Austin MG: Early repair of ventricular septal defect complicating inferior myocardial infarction (abstr). Circulation SO(Supp1 III):lll, 1974. occur28. Gowda KS, Loh CW, Roberts R: The simultaneous rence of a ventricular septal defect and mitral insufficiency after myocardial infarction. AM HEART J 92:234, 1976. 29. Prinzmetal M, Kennamer R, Merliss R, Wada T, Bor N: Angina pectoris. I. A variant form of angina pectoris: Preliminary report. Am J Med 27:375, 1959. E: Coronary artery spasm. N Engl J 30. Hillis LD, Braunwald Med 299:695, 1978. 31. Silverman ME, Flamm MD: Variant angina pectoris: Anatomic findings and prognostic implications. Ann Intern Med 75339, 1971. HR: The advantages of a vasospastic cause of 32. Hellstrom myocardial infarction (editorial). AM HEART J 90:545, 1975.

Maseri A, L’Abbate A, Chierchia S, Parodi 0, Severi S, Biagini A, Distante A, Marzilla M, Ballerstra AM: Significance of spasm in the pathogenesis of ischemic heart disease. Am J Cardiol 44~788, 1979. 34. Kirshenbaum HD, Ockene IS, Alpert JS: The spectrum of coronary artery disease: The variable variant. JAMA 246:354, 1981. 35. Cheng TO, Bashour R, Kelser GA, Weiss L, Bacos J: Variant angina of Prinzmetal with normal coronary arteriograms: A variant of the variant. Circulation 47:476, 1973. 36. Seizer A, Langston M, Ruggeroli C: Clinical syndrome of variant angina with normal coronary arteriogram. N Engl J Med 295:1343, 1976. 37. Kemp HG, Vokonas PS, Cohn PF, Gorlin R: The angina1 syndrome associated with normal coronary arteriograms: Renort of a six-vear exnerience. Am J Med 54:735. 1973. 38. Chkng TO, Bashour T; Singh BK, Kelser GA: Myocardial infarction in the absence of coronary arteriosclerosis: Result of coronary spasm (?). Am J Cardiol 30~680, 1972. 39. Kimbiris D, Segal BL, Munir M, Katz M, Likoff W: Myocardial infarction in patients with normal patent coronary arteries as visualized by cinearteriography. Am J Cardiol 29:724, 1972. 40. Johnson AD, Detwiler JH: Coronary spasm, variant angina, and recurrent myocardial infarctions. Circulation 55:947, 1977. 41. Khahn AH, Haywood LJ: Myocardial infarction in nine patients with radiographically patent coronary arteries. N Engl J Med 291:427, 1974. 33.

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Increased myocardial ischemia during supine compared to erect exercise demonstrated by thallium-201 myocardial perfusion imaging Michael J. Kelly, F.R.A.C.P., Philip J. Currie, M.B.B.S., Victor Kalff, F.R.A.C.P., JamesGardiner, M.D., F.R.A.C.P., and Aubrey Pitt, M.D., F.R.A.C.P. Melbourne, Australia

Thallium-201 (Tl-201) myocardial perfusion imaging following erect exerciseis an acknowledgedmeansof demonstrating myocardial ischemiadue to coronary artery disease.’ We have recently observed a number of patients with normal erect bicycle exercise Tl-201 and ECG tests but markedly abnormal ECG and radionuclide ventriculography (RVG) results during supinebicycle exercise.2In order to clarify the possiblerelevance of posture to these findings, we present the results obtained in a patient with this discordant combination of findings, who had repeat exercise Tl-201 imaging following supine exercise. A 71-year-old woman with no history of prior myocardial infarction underwent selective coronary angiography becauseof disabling angina refractory to medical therapy. A single severecoronary stenosisof 90% luminal narrowing wasfound in the left anterior descending(LAD) vessel. One week after coronary angiography, the patient underwent exercise and redistribution Tl-201 imaging in conjunction with maximal erect bicycle exercise. This was followed by three more maximal exercise procedures: supine bicycle exercise RVG, a treadmill ECG test, and finally repeat Tl-201 stress testing with supine bicycle exercise. Beta-blocking medications and verapamil were discontinued 48 hours and nitrates 12 hours before exercise testing. For RVG imaging a biplanar collimator was used to enable both right anterior oblique (RAO) ECGgated first-pass and left anterior oblique (LAO) equilibrium RVG.3 All bicycle exercise procedures used the same bicycle ergometer for continuous graded exercise with an initial work load of 150 kpm/min, each work load being sustained for 4 minutes. The maximal exercise treadmill ECG test was performed with the use of the Bruce protocol.4 A lo-lead ECG was recorded continuously before, during, and after all exercise procedures.On both occasionsTl-201 imaging used an identical protocol. Two millicuries of Tl-201 was injected intravenously 2 minutes prior to cessation of exercise. Consecutive myocardial perfusion images were obtained in the 4.5degree LAO,

From the Department of Nuclear Medicine and the Cardiology Service, Alfred Hospital. Supported by a Postgraduate Research Scholarship from the National Heart Foundation of Australia and by the Alfred Hospital Whole Time Medical Specialists Reprint requests: Dr. Michael Kelly, Department of Nuclear Medicine, Alfred Hospital, Commercial Rd., Prahran, Victoria, Australia 3181.

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Erect

bicycle (*o’Tf

Supine bicycle (RVG)

)

v4

Treadmill

Supine bicycle

1. ECG lead V, at maximal exercisefrom the four exercisetests: Top left = erect bicycle exercisefor initial Tl-201 imaging; top right = supine bicycle exerciseduring radionuclide ventriculography (RVG); bottom left = erect treadmill exercise; bottom right = repeat supine bicycle exercise for repeat Tl-201 imaging. Fig.

go-degree LAO, anterior, and left lateral projections, starting within 5 minutes of ceasingexercise. All imaging was performed with the patient in the supine posture except for the left lateral images,which used the right decubitus posture on both occasions. Gamma camera uniformity was verified prior to each study by a uniform flood study. The first image was acquired for 300,000 counts and all subsequent imageswere collected for an identical time, including the redistribution images obtained 3 hours later. Digital imageswere obtained in a 128x 128matrix with identical mild background subtraction (20%); no other processinghas been used for interpretation. An abnormal perfusion defect was diagnosed when it was compatible with coronary distribution and confirmed by either visualization in more than one projection or by the presenceof significant redistribution. The highest work load, heart rate, and rate-pressure product levels were obtained with the erect bicycle exercise test used for the initial Tl-201 scan, and the lowest heart rate responsewas obtained with the secondsupine bicycle exercise test used for the second Tl-201 scan (Table I). All exercise tests were limited by leg fatigue, and the only occasionon which chest pain developed was immediately after the initial supine exercise test. The ECG responsesdiffered markedly with posture; neither of

the erect exercise procedures produced significant ST segment depression either during exercise or during a period of postexercisemonitoring in the supine posture; in contrast, both supine exercise procedures produced marked ST segmentdepression,which began during the first exercise level and which was maximal at 4.0 mm in lead V, (Fig. 1) during the highest work load on each occasion. The radionuclide equilibrium left ventricular ejection fraction dropped progressively during supine exercisefrom 59% at rest to 43% at the end of the second work load. A marked exercise-induced anteroseptal wall motion abnormality alsodeveloped in both LAO and RAO views. The TI-201 imageswere analyzed by three independent blinded observers with unanimity. The initial erect Tl-201 imagesshowedno significant abnormality. However, the repeat Tl-201 myocardial imagesfollowing supine exercise showed a marked anteroseptal perfusion defect, best seen in the 60-degree LAO projection, and correspondedto the territory of the LAD coronary vesse1.5 This exercise-inducedperfusion defect had filled in at the time of redistribution imaging 3 hours later (Fig. 2). As only supine exercise produced a significant Tl-201 perfusion defect, it seemslikely that the degree of exercise-induced myocardial &hernia was greater during the supine than erect posture. This was supported by the

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Table I. Work loads, heart rate, and blood pressureduring four maximal exercisetests Time, 9 AM,

Posture Exercise type Radionuclide test Work loads kpmlmin (min) Peak heart rate (hpm) Peak blood pressure (mm I-k)* Peak ratepressure product (mm Hg/min/ lOOH

11/g

1 PM,

11/g

date 9 AM,

ll/lo

9 AM,

11/16

Erect Bicycle Tl-201

Supine Bicycle RVG

Erect Treadmill Nil

Supine Bicycle Tl-201

150 (4) 300 (4) 350 (4) 150

150 (4) 250 (4)

150 (4) 300 (4)

140

Stage Stage Stage 150

200/100

195/105

17Of90

185195

300

273

255

231

1 (3) 2 (3) 3 (1)

125

RVG = radionuclide ventriculography; TI-201 = thallium-201 myocardial perfusion imaging. *Blood pressure measured with a calibrated sphygmomanometer is expressed as systolic/diastolic pressure. tRate-pressure product was calculated as peak heart rate x peak systolic blood pressure.

development of 4.0 mm ST segment depression during both supine exercise procedures but no significant ST depressionduring either erect exercise test. These findings occurred despite the patient achieving greater heart rate and rate-pressure product levels during the erect Tl-201 stresstest (Table I). Additional evidence was that supine exercise produced an anteroseptal wall motion abnormality on RVG, which matched the supine exercise Tl-201 defect. Spontaneous variability is not thought likely to have causedthe secondTl-201 scan to become positive, asrepeat Tl-201 scanswith erect exercise 1 week apart in patients with ischemic heart diseasehave not beenreported to result in any new perfusion defects in the secondprocedure” Other reports have indicated that supineposture accentuates exercise-induced cardiac abnormalities in patients with ischemicheart disease.Thadani et a1.7found that left ventricular filling pressureswere higher during supine than erect exercise,with the development of chest pain at lower rate-pressureproducts in the supine posture. Levey et a1.8found the development of 1 mm ST depressionwas more frequently seenduring supine than equivalent erect exercise. We have recently reported that for equivalent work load, heart rate, and rate-pressure product supine exercise produced twice the magnitude of ST segment depression on average as erect exercise? In contrast to these reports are those in which exercise RVG studies noted a similar frequency of exercise-inducedabnormali-

Fig. 2. Exercise (Ex) and redistribution (Redn) Tl-201 myocardial imagesobtained in the 60-degreeleft anterior oblique (LAO) projection, using erect exercise (top row) and supine exercise (lower row). The patient was supine during the actual acquisition of both sets of images.The myocardial images show no significant defect following erect exercise. There is an anteroseptal perfusion defect following supine exercise which redistributes.

ties in the upright and supine positionslOall;it is not clear to what extent these reported discrepanciesare due to different patient selection, different study design, or physiologic differences in the way ECG ST segment changes, angina1threshold, left ventricular filling pressures,and indices of left ventricular contraction respond to changesin posture. It is not known how frequently exercise-induced myocardial perfusion abnormalities are accentuated by supine posture. If it is as common as the reported accentuation by supine posture of left ventricular filling pressures7and ECG ST segmentchanges>Qthe sensitivity of exercise Tl-201 myocardial imaging may then be increased significantly. This possibility needsto be explored with a formal study comparing supine with erect exercise Tl-201 imaging. REFERENCES

1. Bailey IK, Griffith LSC, Rouleau J. Strauss HW. Pitt B: Thallium-201 myocardial perfusion imaging at rest and during exercise. Comparative sensitivity to electrocardiography in coronary artery disease. Circulation 66:79, 1977. 2. Currie P, Kelly MJ, Anderson ST, Pitt A: Comparison of exercise thallium, radionuclide ventriculography and ECG in detecting myocardial ischemia in single vessel CAD. Aust NZJ Med 12:310, 1982. 3. Lim YL, Kalff V, Kelly MJ, Mason PJ, Currie PJ, Harper RW, Anderson ST, Federman J, Stirling GR, Pitt A: Radionuclide angiographic assessment of global and segmental left ventricular function at rest and during exercise following coronary artery bypass graft surgery. Circulation 66:972, 1982.

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Bruce RA: Exercise testing of patients with coronary heart disease. Principles and normal standards for evaluation. Ann Clin Res 3:323, 1971. Dunn RF, Freedman B, Bailey IK, Bernstein L, Kelly DT: Exercise thallium imaging: Location of perfusion abnormalities in single vessel coronary disease. J Nucl Med 21:717, 1980. McLaughlin PR, Martin R, Doherty P, Daspit S, Gloris M, Haskell W, Lewis S, Kriss JP, Harrison DC: Reproducibility of thallium-201 myocardial imaging. Circulation 55:497, 1977. Thadani U, West RO, Mathew TM, Parker JO: Hemodynamits at rest and during supine and sitting bicycle exercise in patients with coronary artery disease. Am J Cardiol 39:776, 1977. Levey M, Rozanski A, Valovis R, Ford D, Morris D, Pantaleo N, Maddahi J, Swan HJC, Berman D: Comparative ability of upright and supine bicycle exercise electrocardiography to detect coronary artery disease (abstr). Am J Cardiol 49:945, 1982. Currie P, Kelly M, Pitt A: Is it valid to compare the sensitivity of a supine exercise nuclear imaging procedure with that of an erect exercise ECG (abstr)? Aust NZ J Med 12:668, 1982. Freeman MR, Berman DS, Staniloff H, Elkayam U, Maddahi J, Swan HJC, Forrester J: Comparison of upright and supine bicycle exercise in the detection and evaluation of extent of coronary artery disease by equilibrium radionuclide ventriculography. AM HEART J 102:182, 1981. Manyari DE, Kostuk WJ, Purves PP: Left and right ventricular function at rest and during bicycle exercise in the supine and sitting positions in normal subjects and patients with coronary artery disease: Assessment by radionuclide ventriculography. Am J Cardiol 51:36, 1983.

Acute right ventricular dilation and echocardiographic volume overload following pericardiocentesis for relief of cardiac tamponade William F. Armstrong, M.D., Harvey Feigenbaum, M.D., and JamesC. Dillon, M.D. Indianapolis, Znd.

June, 1984 Heart Journal

Recently, this phenomenonhas been noted with radionuelide angiographyP We report here the finding of acute right ventricular (RV) dilation and development of an echocardiographicRV volume overload pattern in three of six patients after removal of pericardial fluid for relief of cardiac tamponade. Exemplary cases. A 13-year-old white boy (patient No. 5, Table I) wasadmitted to the hospital with a diagnosisof germinal cell tumor. On admission,he was in mild respiratory distress. Heart rate was 130 bpm and blood pressure was 60/50 mm Hg with a palpable paradox. Two-

dimensional echocardiography @DE) revealed a large pericardial effusion with RV collapsesuggestinghemodynamic compromise.7Pericardiocentesis was performed, and 1400ml of serosanguineous fluid wasremoved. Immediately after pericardiocentesis, 2DE was repeated. The right ventricle was markedly dilated and interventricular septal motion was consistent with a RV volume overload pattern. Following pericardiocentesis,heart rate remained elevated at 140 bpm; blood pressurewas 90/70 mm Hg without paradox. Marked jugular venous distention persisted and a RV gallop was noted. Right heart catheterization revealed equalization of diastolic pressures at 40 mm

Hg. Repeat pericardiocentesis was performed and an additional 700 ml fluid was removed. The clinical picture of jugular venous distention with right heart gallop persisted.On the fifth hospital day, the patient wastaken to the operating room where a pericardial window was created. The resected pericardium was noted to be inflamed but wasnot thickened. The patient experienced gradual resolution of symptoms and evidence of venous congestionresolved. He was dischargedfollowing therapy of the malignancy. A 26-year-old white woman (patient No. 6, Table I) was admitted to the hospital in marked respiratory distress. Past medical history wassignificant for Hodgkins disease treated 11 years previously with chemotherapy and mediastinal radiation. She had no history of cardiovascular diseaseand had previously had multiple normal cardiovascular examinations. At the time of admission, the patient was an acutely ill and cachetic white woman.

The normal pericardium exerts a restraining influence on the size of the cardiac chambers.’ Dilation of the right ventricle has been reported after surgical removal of the pericardium for treatment of constrictive pericarditis and in cases of congenital absence of the pericardium.2-5

Blood pressurewas 70/50 mm Hg and heart rate was 120 bpm. An echocardiogram demonstrated the presence of moderate pericardial effusion with abnormal RV free wall motion suggestinghemodynamic compromise(Fig. 1).7A flow-directed right heart catheter documented elevation and equilibration of diastolic pressuresconsistent with cardiac tamponade. Pericardiocentesiswas performed, at which time 200 ml of serosanguineous

From Indiana

the Krannert University

Institute of Cardiology, School of Medicine.

Department

of Medicine,

Supported in part by the Herman C. Krannert Fund, Indianapolis, Ind., Grants HL-06308 and HL-07182, and by Clinical Investigator Award HL 01041-02 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.; by the American Heart Association, Indiana Affiliate, Indianapolis, Ind.; and by the Whitaker Foundation, Camp Hill, Pa. Reprint requests: William F. Armstrong, of Medicine, University Hospital N562,926 IN 46223.

M.D., Indiana W. Michigan

University School St., Indianapolis,

fluid was removed.

The systolic blood pressuresubsequently rose to 120 mm Hg; however, right heart pressuresremained elevated. Repeat M-mode and 2DE, performed immediately after pericardiocentesis, revealed increase in RV dimension from 1.2 cm to 2.6 cm. Left ventricular internal dimension decreasedfrom 3.8 cm to 3.1 cm. Interventricular septal motion becameabnormal, demonstrating the characteristic early systolic anterior motion of the interventricular septum, seen in RV volume overload (Fig. 2). 2DE revealed a markedly dilated right ventricle, with diastolic