Stress Thallium-201 Myocardial Scintigraphy in Patients With Complete Occlusion of the Left Main Coronary Artery

Stress Thallium-201 Myocardial Scintigraphy in Patients With Complete Occlusion of the Left Main Coronary Artery

induced pulmonary edema, which may be caused by hypoxic-induced pulmonary venous constriction and cytokine activation. Echocardiography and/or measure...

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induced pulmonary edema, which may be caused by hypoxic-induced pulmonary venous constriction and cytokine activation. Echocardiography and/or measurements of cardiac output and intravascular filling pressures in heart failure patients during hyperbaric oxygen treatment might be informative regarding the etiology of pulmonary edema. These patients were all treated in the single-person, monoplace oxygen-filled hyperbaric chamber (Sechrist; Anaheim, CA), necessitating the patient to be in a supine position, which might increase the risk of pulmonary edema. A difference in the incidence of pulmonary edema associated with hyperbaric oxygen therapy in supine patients vs upright patients is unknown. Fluid overload could contribute to pulmonary edema associated with hyperbaric oxygen therapy. Death due to postoperative pulmonary edema following excess fluid retention has been reported10; the authors concluded that careful attention to fluid balance was imperative. Our cases occurred in outpatients who were functional. None of these patients had recent surgery or overt manifestations of heart failure. Nevertheless, if the hyperbaric service recommends hyperbaric oxygen therapy in patients with compromised LV function, careful attention to fluid balance during their course of therapy is advised. In case 3, it is possible that the patient’s history of radiation therapy made her disease process more complicated than just ischemic coronary disease and aortic stenosis. Radiation therapy causes tissues to become hypovascular, hypocellular, and hypoxic.11 This scarred fibrotic tissue might have altered her pericardium or her cardiac function. Furthermore, her aortic stenosis may have contributed to increased afterload to a marginal left ventricle. It is interesting and of concern that this patient had no symptoms compatible with congestive heart failure and had good exercise tolerance. Acute pulmonary edema is not expected in patients treated with hyperbaric oxygen therapy, yet pulmonary edema may occur in certain patients with heart failure. Most patients treated with hyperbaric oxygen have hypoxic wounds, which often occur in patients with ischemic cardiovascular disease who may be at risk for acute pulmonary edema during hyperbaric oxygen therapy. Unfortunately, we cannot identify in whom or when acute pulmonary edema may develop. Caution is recommended in treating heart failure patients with hyperbaric oxygen. ACKNOWLEDGMENT: We thank Laura Ogaard for manuscript preparation. We also thank Drs. C. Gregory Elliott, Terry P. Clemmer, and Brent Muhlstein for thoughtful reviews.

References 1 Abel FL, McNamee JE, Cone DL, et al. Effects of hyperbaric oxygen on ventricular performance, pulmonary blood volume, and systemic and pulmonary vascular resistance. Undersea Hyperb Med 2000; 27:67–73 2 Riddick MF. Sternal wound infections, dehiscence, and sternal osteomyelitis: the role of hyperbaric oxygen therapy. In: Kindwall EP, Whelan HT, eds. Hyperbaric medicine practice. 2nd ed. Flagstaff, AZ: Best Publishing, 1999; 617– 640

3 Side effects. In: Hampson NB, ed. Hyperbaric oxygen therapy: 1999 committee report. Kensington, MD: Undersea and Hyperbaric Medical Society, 1999; 73–75 4 Whalen RE, Saltzman HA, Holloway DH Jr, et al. Cardiovascular and blood gas responses to hyperbaric oxygenation. Am J Cardiol 1965; 15:638 – 646 5 Haque WA, Boehmer J, Clemson BS, et al. Hemodynamic effects of supplemental oxygen administration in congestive heart failure. J Am Coll Cardiol 1996; 27:353–357 6 Kaneko M, Beamish RE, Dhalla NS. Depression of heart sarcolemmal Ca2⫹ -pump activity by oxygen free radicals. Am J Physiol 1989; 255:H368 –H374 7 Rubanyi GM, Vanhoutte PM. Superoxide anions and hyperoxia inactivate endothelium-derived relaxing factor. Am J Physiol 1986; 250:H822–H827 8 Paulus WJ, Vantrimpont PJ, Shah AM. Acute effects of nitric oxide on left ventricular relaxation and diastolic dispensability in humans: assessment by bicoronary sodium nitroprusside infusion. Circulation 1994; 89:2070 –2078 9 Clark J, Whelan H. Oxygen toxicity. In: Kindwall EP, Whelan HT, eds. Hyperbaric medicine practice. 2nd ed. Flagstaff, AZ: Best Publishing, 1999; 69 – 82 10 Arieff AI. Fatal postoperative pulmonary edema. Chest 1999; 115:1371–1377 11 Marx RE, Johnson RP. Studies on the radiobiology of osteoradionecrosis and their clinical significance. Oral Surg 1987; 64:379 –390

Stress Thallium-201 Myocardial Scintigraphy in Patients With Complete Occlusion of the Left Main Coronary Artery* Takashi Hatori, MD; Takuji Toyama, MD; Tomoyuki Yokoyama, MD; Masashi Arai, MD; Masahiko Kurabayashi, MD; Tsugiyasu Kanda, MD; and Shigeru Oshima, MD

Complete occlusion (CO) of the left main coronary artery (LMCA) is a rare but often fatal condition. The diagnosis is frequently missed because the signs and symptoms are often obscure and diverse. We describe three patients with CO-LMCA who showed unusual myocardial scintigraphic findings. The patients had extensive right-to-left collateral channels and decreased uptake and washout rates at the basal anterior and anterolateral portions of the heart wall during stress thallium-201 scintigraphy. The basal anterior to anterolateral portion of the heart wall is the most distant from the collateral artery and should be the most ischemic area shown during exercise, resulting in this scintigraphic pattern. This scintigraphic finding may be useful for the noninvasive diagnosis of CO-LMCA. (CHEST 2001; 120:1409 –1412) Key words: complete occlusion; left main coronary artery; stress 201 Tl myocardial single photon emission CT; washout rate Abbreviations: CO ⫽ complete occlusion; EF ⫽ ejection fraction; LAD ⫽ left anterior descending artery; LCX ⫽ left circumCHEST / 120 / 4 / OCTOBER, 2001

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flex artery; LMCA ⫽ left main coronary artery; LV ⫽ left ventricle, ventricular; LVEDP ⫽ left ventricular end-diastolic pressure; RCA ⫽ right coronary artery; SPECT ⫽ single photon emission CT

occlusion (CO) [atherosclerotic] of the left C omplete main coronary artery (LMCA) is an extremely rare (incidence, 0.043 to approximately 0.067%) but often fatal condition.1– 4 Patients with CO-LMCA are at risk for massive myocardial infarctions and sudden death. Immediate revascularization is recommended in an effort to prolong life and to alleviate symptoms in these patients.

For related article see page 1212 However, the diagnosis is still frequently missed until the patient undergoes selective coronary arteriography because the signs and symptoms can be obscure at times and the clinical manifestations are often diverse.4 – 6 In this report, we describe three patients with CO-LMCA who had characteristic findings on stress thallium-201 myocardial scintigraphy.

Case Reports Case 1 A 62-year-old man first noted the onset of retrosternal discomfort at the beginning of an morning walk 6 months prior to hospital admission. Subsequently, he experienced almost weekly angina at work. He had a history of hypertension, diabetes mellitus, and cigarette smoking. A physical examination revealed a BP of 166/92 mm Hg and a pulse of 66 beats/min. The resting ECG showed only nonspecific ST-T abnormalities, and the chest radiograph revealed no abnormalities. The result of a Master’s two-step test was positive with a 2-mm ST-segment depression. The patient was admitted to our hospital and was hospitalized for further evaluation in May 1987, at which time a stress 201Tl myocardial single photon emission CT (SPECT) scan was performed. An exercise-induced 201Tl perfusion defect was observed only in the basal anterolateral wall of the left ventricle (LV), and the defect was redistributed at rest (Fig 1, top, A). The myocardial 201Tl washout rate, displayed in a bull’s-eye-view map (Fig 1, top, A), was decreased in the basal anterolateral wall. Based on circumferential profile analysis using apical, midventricular, and basal short-axis images, the circumferential washout rate curve for the base was significantly decreased in the anterolateral segment (Fig 2, top, A). At the time of cardiac catheterization, the LV end-diastolic pressure (LVEDP) was 6 mm Hg and the ejection fraction (EF) was 0.68. Left ventriculography revealed mild anterior wall hypokinesis. The LMCA was completely occluded, and the left *From the Second Department of Internal Medicine (Drs. Hatori, Toyama, Yokoyama, Arai, and Kurabayashi) and the Department of General Medicine (Dr. Kanda), Gunma University School of Medicine, Gunma, Japan; and the Department of Cardiovascular Medicine (Dr. Oshima), Gunma Prefectural Cardiovascular Center, Maebashi, Gunma, Japan. Manuscript received September 14, 2000; revision accepted April 5, 2001. Correspondence to: Takuji Toyama, MD, Second Department of Internal Medicine, Gunma University School of Medicine, 3–39-15 Showa-Machi, Maebashi, Gunma 371-0034, Japan; email: [email protected] 1410

Figure 1. Short-axis images and bull’s-eye-view maps of stress 201 Tl myocardial SPECT scans from patients with CO-LMCA (patient 1, top, A; patient 2, middle top, B; patient 3, middle bottom, C) and from a 60-year-old woman with classic angina pectoris whose coronary arteriography results showed a proximal stenotic lesion of the LAD (bottom, D). Stress ⫽ stress image; rest ⫽ resting image; apical ⫽ apical slice; mid ⫽ mid-ventricular slice; basal ⫽ basal slice; WR ⫽ washout rate.

anterior descending artery (LAD) and left circumflex artery (LCX) were easily visualized during right coronary artery (RCA) injection via extensive intercoronary collateral channels (Fig 3). The collateral pathways were mainly formed by interventricular septal branches, the distal posterior descending artery connecting around the cardiac apex to the distal LAD and the distal posterior lateral ventricular branch of the RCA. The RCA was a dominant vessel with noncritical stenoses. The patient underwent coronary artery bypass grafting of the LAD and the LCX. Three months later, the grafts were found to be patent, and the stress 201Tl myocardial SPECT scan showed no perfusion abnormality. Case 2 A 73-year-old woman with an 8-year history of hypertension and a 3-year history of diabetes consulted a physician for the treatment of hypertension. She had smoked one pack of cigarettes per day for 35 years. She had no anginal symptoms. On physical examination, the BP was 174/94 mm Hg, the pulse was 68 beats/min, and the lung fields were clear. Chest radiography showed a normal heart size and normal pulmonary vascular markings. The resting ECG showed evidence of left ventricular Selected Reports

Figure 2. Circumferential profile curves of the washout rates for patients with CO-LMCA (patient 1, top, A; patient 2, middle top, B; patient 3, middle bottom, C) and for a 60-year-old woman with a proximal LAD lesion (bottom, D). The washout rate curves for the basal region (yellow lines) in the patients with CO-LMCA showed most prominent decreases in the anterior and/or anterolateral segments, while the curve for the apical region (green line) in the patient with a proximal LAD lesion showed the most prominent decrease in the anterior segment. Blue line ⫽ washout rate curve for the mid-ventricular region.

hypertrophy, and a treadmill exercise ECG using a Bruce protocol was positive with 1.5 mm of additional ST-segment depression. However, the patient did not experience chest pain during exercise. She was referred for further evaluation and was hospitalized. During a stress 201Tl myocardial SPECT scan, an exerciseinduced 201Tl perfusion defect, which redistributed at rest (Fig 1, middle top, B), was observed in the basal anterior and midanterolateral wall of the LV. A distinct decrease in myocardial 201 Tl washout rate was noted in the basal anterior and midanterolateral wall of the LV on the bull’s-eye-view map (Fig 1, middle top, B) and the circumferential profile curve (Fig 2, middle top, B). The patient subsequently underwent cardiac catheterization. Left ventriculography revealed mild hypokinesis of the basal anterior wall. The LVEDP was 9 mm Hg, and the EF was 0.72. Coronary arteriography revealed CO-LMCA with extensive right-to-left collateral channels filling the LAD and the LCX. The dominant RCA had a noncritical narrowing. The

Figure 3. Top, A: left main coronary artery viewed in the left anterior oblique projection revealing a total occlusion at the ostium (arrow). Bottom, B: selective right coronary angiogram in the left anterior oblique projection revealed extensive collateral channels between the RCA and the left coronary system.

patient underwent bypass grafting of the LAD and LCX the next month. When the patient underwent coronary angiography 3 months later, the grafts were patent, and the LAD and LCX were partially opacified during RCA injection with relatively poor collateral channels. A stress 201Tl myocardial SPECT scan showed no abnormal findings. Case 3 A 72-year-old man with a 1-year history of classic angina pectoris had noticed a marked reduction in exercise tolerance and an increase in the frequency and duration of angina over a 6-month period. He had a history of subendocardial infarction of the anterior wall 7 years before presentation. On examination, the BP was 140/60 mm Hg and the pulse was 61 beats/min. The physical examination was unremarkable. The resting ECG showed complete right bundle-branch block. He was hospitalized in June 1998 for further evaluation. A stress 201Tl myocardial SPECT scan showed an exerciseinduced perfusion defect, which redistributed at rest (Fig 1, bottom middle, C), in the basal anterior wall of the LV. A distinct decrease in the myocardial 201Tl washout rate in the basal anterior wall on the bull’s-eye map (Fig 1, bottom middle, C) and the circumferential profile curve also were noted (Fig 2, bottom middle, C). Cardiac catheterization revealed a LVEDP of CHEST / 120 / 4 / OCTOBER, 2001

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9 mm Hg and an EF of 0.62. Left ventriculography showed mild hypokinesis of the basal anterior wall. Coronary arteriography revealed CO-LMCA with extensive right-to-left collateral channels filling the LAD and LCX. The dominant RCA had a proximal 75% stenosis. The patient underwent bypass grafting of the LAD and the LCX. The grafts were patent 3 months later, and the patient has been free of symptoms during exertion. A stress 201Tl myocardial SPECT scan showed no abnormality.

transaxial emission computed tomography: quantitative versus qualitative analysis for evaluation of coronary artery disease. J Am Coll Cardiol 1984; 4:1213–1221 9 Topaz O, Disciascio G, Cowley MJ, et al. Complete left main coronary artery occlusion: angiographic evaluation of collateral vessel patterns and assessment of hemodynamic correlates. Am Heart J 1991; 121:450 – 456

Discussion The patients described in this report had characteristic scintigraphic findings on stress 201Tl myocardial SPECT scans. A distinct decrease in the 201Tl washout rate was most prominent in the basal anterior and/or anterolateral wall, where a decreased 201Tl washout rate is not usually observed in patients with ischemic heart disease. In the setting of proximal stenosis of the LAD, the most prominent redistribution and decreased washout rate are commonly found in the mid to apical region of the anterior LV wall distal to the lesion on stress 201Tl myocardial SPECT scanning7,8 (Fig 1, bottom, D and Fig 2, bottom, D). In contrast, in the setting of CO-LMCA with extensive right-to-left collateral channels, the LAD and the LCX territories are perfused in a retrograde manner by collateral flow. Therefore, the basal anterior and anterolateral wall of the LV, which is closest to the LMCA and furthest from the RCA, should be the most ischemic area during exercise.9 This could explain the unique scintigraphic pattern seen in the patients with CO-LMCA. The differences in the scintigraphic patterns between patient 1 and patient 3 might be caused by the extent of the collateral channels to LCX, which were less extensive in patient 1. In summary, we described three patients with COLMCA who had decreased uptake and washout rates in the basal anterior and anterolateral wall of the LV on stress 201 Tl myocardial SPECT scans. We suggested that this unusual characteristic scintigraphic pattern may be a specific finding for this rare condition and may be useful for the noninvasive diagnosis of CO-LMCA.

References 1 Frye RL, Gura GM, Chesebro JH, et al. Complete occlusion of the left main coronary artery and the importance of coronary collateral circulation. Mayo Clin Proc 1977; 52:742–745 2 Goldberg S, Grossman W, Markis JE, et al. Total occlusion of the left main coronary artery. Am J Med 1978; 64:3– 8 3 Greenspan M, Iskandrian AS, Segal BL, et al. Complete occlusion of the left main coronary artery. Am Heart J 1979; 98:83– 86 4 Zimmern SH, Rogers WJ, Bream PR, et al. Total occlusion of the left main coronary artery: the coronary artery surgery study (CASS) experience. Am J Cardiol 1982; 49:2003–2010 5 DePace NL, Kimbiris D, Iskandrian AS, et al. Total occlusion of left main coronary artery without angina pectoris. Arch Intern Med 1983; 143:1064 –1065 6 Topatz O. Total left main coronary artery occlusion: the acute, the chronic, and the iatrogenic. Chest 1992; 101:843–846 7 Rigo P, Bailey IK, Griffith LSC, et al. Value and limitations of segmental analysis of stress thallium myocardial imaging for localization of coronary artery disease. Circulation 1980; 61:973–981 8 Tamaki N, Yonekura Y, Mukai T, et al. Stress thallium-201 1412

Stenting To Reverse Left Ventricular Ischemia Due To Left Main Coronary Artery Compression in Primary Pulmonary Hypertension* Stuart Rich, MD, FCCP; Vallerie V. McLaughlin, MD; and William O’Neill, MD

Angina is a common symptom of severe pulmonary hypertension. Although many theories for the source of this pain have been proposed, right ventricular ischemia is the one most commonly accepted as the cause. We report on two patients with primary pulmonary hypertension who had angina with normal activity or on provocation. One patient had severe left ventricular dysfunction. Both were found to have severe ostial stenosis of the left main coronary artery as a result of compression from a dilated pulmonary artery. Both patients underwent stenting of the left main coronary artery with excellent angiographic results, and complete resolution of the signs and symptoms of angina and left ventricular ischemia. Left ventricular ischemia due to compression of the left main coronary artery may be a much more common mechanism of angina and left ventricular dysfunction in patients with pulmonary hypertension than previously acknowledged. Stenting of the coronary artery can be done safely with the resolution of these symptoms. (CHEST 2001; 120:1412–1415) Key words: coronary artery stenting; left main coronary stenosis; primary pulmonary hypertension Abbreviation: PPH ⫽ primary pulmonary hypertension

like chest pain, commonly has been associated A ngina, with the development of primary pulmonary hyper-

tension (PPH).1 The etiology of the chest pain has been debated, with theories ranging from painful dilatation of *From the Section of Cardiology (Drs. Rich and McLaughlin), Rush Medical College, Chicago, IL; and the Division of Cardiology (Dr. O’Neill), William Beaumont Hospital, Royal Oak, MI. Manuscript received November 28, 2000; revision accepted March 27, 2001. Correspondence to: Stuart Rich, MD, FCCP, the Rush Heart Institute, Center For Pulmonary Heart Disease, Rush-Presbyterian-St. Luke’s Medical Center, 1725 West Harrison St, Suite 020, Chicago, IL 60612-3824; e-mail: [email protected] Selected Reports