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Causes of Transient Dilatation of the Left Ventricle During Myocardial Perfusion Imaging

¹ Department of Medicine, Section of Cardiology, Medical College of Georgia, 1120 15th St., BIH 2227, Augusta, GA 30912-3105.
² Department of Radiology, Section of Nuclear Radiology, Medical College of Georgia, Augusta, GA 30912-3105.
³ Cardiovascular Care Department, Specialty Care Line, Veterans Affairs Medical Center, Augusta, GA 30904-6285.

Received July 12, 1999; accepted after revision September 29, 1999.

 
Address correspondence to V. J. B. Robinson.

Introduction

Top Introduction References

 
Beginning with Stolzenberg [1] in 1980 and later popularized by Weiss et al. [2] in 1987, the apparent dilatation of the left ventricular cavity on myocardial perfusion imaging in the presence of extensive epicardial vessel stenoses has been referred to as transient ischemic dilation. Iskandrian et al. [3] provided evidence that the mechanism of this apparent dilatation may involve subendocardial ischemia by revealing increased wall thickness on the delay images when cavity dilatation with myocardial thinning was seen during stress. The severely ischemic, count-poor subendocardium at stress appears as part of the left ventricular cavity with an external rim of slightly better perfused epicardium. The result is a relatively dilated left ventricular cavity during stress imaging. Transient ischemic left ventricular cavity dilatation during stress myocardial perfusion imaging has become a generally accepted marker of severe, extensive myocardial ischemia [2]. However, a number of studies and case reports suggest other causes of global subendocardial ischemia with apparent transient ischemic dilatation of the left ventricle in the absence of any significant epicardial coronary artery stenoses.

Preliminary evidence suggests that severe hypertensive heart disease is an additional cause of global subendocardial ischemia resulting in transient ischemic dilatation of the left ventricular cavity seen on myocardial perfusion imaging [4]. The development of diffuse subendocardial ischemia with stress in hypertensive patients is likely caused by a combination of factors: namely, delayed diastolic left ventricular relaxation, significant endothelial dysfunction in the coronary arteries, decreased capillary density in hypertrophied myocardium, and elevated end-diastolic pressure in the left ventricle. The latter increases the epicardial diastolic pressure required to perfuse the full thickness of the myocardium. Although in cases of severe left ventricular hypertrophy, the epicardial coronary arteries may show compensatory dilatation, as the hypertensive heart disease progresses, there appears to be patchy transmural ischemia in the myocardium, in addition to subendocardial ischemia, unassociated with any epicardial stenoses [5] (Fig. 1A,1B,1C,1D,1E,1F).

View larger version (153K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1A. —59-year-old woman with 6-year history of hypertension and hypercholesterolemia and family history of coronary artery disease who presented with chest and shoulder "tiredness" and shortness of breath. Midventricular short-axis slices of 201Tl myocardial perfusion images obtained during stress (A) and after 3-hr delay (B) show apparent global increase in size of left ventricular cavity in stress image that is associated with thinner left ventricular wall than that seen on delay image. Ratio of wall thickness to size of cavity on delay images exceeds 2:1, which suggests left ventricular hypertrophy.

View larger version (169K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1B. —59-year-old woman with 6-year history of hypertension and hypercholesterolemia and family history of coronary artery disease who presented with chest and shoulder "tiredness" and shortness of breath. Midventricular short-axis slices of 201Tl myocardial perfusion images obtained during stress (A) and after 3-hr delay (B) show apparent global increase in size of left ventricular cavity in stress image that is associated with thinner left ventricular wall than that seen on delay image. Ratio of wall thickness to size of cavity on delay images exceeds 2:1, which suggests left ventricular hypertrophy.

View larger version (172K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1C. —59-year-old woman with 6-year history of hypertension and hypercholesterolemia and family history of coronary artery disease who presented with chest and shoulder "tiredness" and shortness of breath. Midventricular vertical long-axis slices of 201Tl myocardial perfusion images obtained during stress (C) and after 3-hr delay (D) show anterior breast attenuation artifact. Also note larger ventricular cavity in stress image, with smaller cavity and thicker walls on 3-hr delay image. No segmental perfusion defects are seen.

View larger version (171K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1D. —59-year-old woman with 6-year history of hypertension and hypercholesterolemia and family history of coronary artery disease who presented with chest and shoulder "tiredness" and shortness of breath. Midventricular vertical long-axis slices of 201Tl myocardial perfusion images obtained during stress (C) and after 3-hr delay (D) show anterior breast attenuation artifact. Also note larger ventricular cavity in stress image, with smaller cavity and thicker walls on 3-hr delay image. No segmental perfusion defects are seen.

View larger version (149K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1E. —59-year-old woman with 6-year history of hypertension and hypercholesterolemia and family history of coronary artery disease who presented with chest and shoulder "tiredness" and shortness of breath. Angiograms of right coronary artery (E) and left coronary artery (F) show no evidence of significant coronary obstruction. Note tortuosity of left anterior descending artery (arrows, F). Also note tortuosity of circumflex artery (arrowheads, F), which is seen as "beading" of artery when viewed along same plane as posterior epicardial surface on which it lies. In this patient, hypertensive heart disease caused global subendocardial reduction in 201Tl uptake on stress imaging, which was reversed on delay imaging.

View larger version (147K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1F. —59-year-old woman with 6-year history of hypertension and hypercholesterolemia and family history of coronary artery disease who presented with chest and shoulder "tiredness" and shortness of breath. Angiograms of right coronary artery (E) and left coronary artery (F) show no evidence of significant coronary obstruction. Note tortuosity of left anterior descending artery (arrows, F). Also note tortuosity of circumflex artery (arrowheads, F), which is seen as "beading" of artery when viewed along same plane as posterior epicardial surface on which it lies. In this patient, hypertensive heart disease caused global subendocardial reduction in 201Tl uptake on stress imaging, which was reversed on delay imaging.

In a recent review of 237 consecutive single-center myocardial perfusion scans, 23 scans revealed global transient ischemic dilatation of the left ventricle [4]. Nine of these 23 patients had transient ischemic dilatation of the left ventricle in the absence of segmental perfusion defects and multivessel coronary artery disease. In seven of these nine patients, there was evidence of left ventricular hypertrophy by either thallium-201 or electrocardiographic criteria.

In severe multivessel coronary atherosclerosis, a similar combination of elevated left ventricular end-diastolic pressure and inadequate diastolic epicardial perfusion pressure exists. In this instance, end-diastolic pressures are elevated because of ischemia-induced systolic and diastolic myocardial dysfunction. The inadequate diastolic epicardial perfusion pressure is a result of multiple severe epicardial stenoses. Redistribution of blood flow away from the subendocardium in the presence of coronary stenosis has been documented in experimental animals [6]. A severe reduction in epicardial diastolic perfusion pressure creates a transmyocardial perfusion gradient that is visible on ²⁰¹Tl myocardial perfusion imaging. This marked decrease in subendocardial perfusion during stress results in minimal uptake of radionuclide and, thus, an apparent dilatation of the left ventricular cavity on the stress images (Fig. 2A,2B,2C,2D,2E,2F).

View larger version (122K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2A. —59-year-old man with long history of smoking and hypertension who presented with atypical chest pain. Echocardiogram (not shown) showed left ventricular ejection fraction of 55% with basal posterior and inferior hypokinesis. Midventricular short-axis slices of 201Tl myocardial perfusion images obtained during stress (A) and after 3-hr delay (B) show severe ischemia in septum and inferior, lateral, and anterior walls. Left ventricular cavity is globally dilated on stress image and is decreased in size on 3-hr delay image with increasing wall thickness, especially in septum. This patient shows transient ischemic dilatation of left ventricle caused by severe multivessel epicardial coronary artery atherosclerosis.

View larger version (126K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2B. —59-year-old man with long history of smoking and hypertension who presented with atypical chest pain. Echocardiogram (not shown) showed left ventricular ejection fraction of 55% with basal posterior and inferior hypokinesis. Midventricular short-axis slices of 201Tl myocardial perfusion images obtained during stress (A) and after 3-hr delay (B) show severe ischemia in septum and inferior, lateral, and anterior walls. Left ventricular cavity is globally dilated on stress image and is decreased in size on 3-hr delay image with increasing wall thickness, especially in septum. This patient shows transient ischemic dilatation of left ventricle caused by severe multivessel epicardial coronary artery atherosclerosis.

View larger version (131K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2C. —59-year-old man with long history of smoking and hypertension who presented with atypical chest pain. Echocardiogram (not shown) showed left ventricular ejection fraction of 55% with basal posterior and inferior hypokinesis. Midventricular vertical long-axis slices of 201Tl myocardial perfusion images obtained during stress (C) and after 3-hr delay (D) show severe inferior, inferoapical, apical, mid, and distal anterior perfusion defects with substantial reversibility at 3 hr. Left ventricular cavity is also reduced in size on delay image. Also, note mid and distal anterior wall flaring outward on stress image, creating divergence of anterior wall at anteroapex (arrow, C). This ischemia-induced wall motion abnormality results in transient apical aneurysm seen only on stress image. This patient shows transient ischemic dilatation of left ventricle caused by severe multivessel epicardial coronary artery atherosclerosis.

View larger version (132K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2D. —59-year-old man with long history of smoking and hypertension who presented with atypical chest pain. Echocardiogram (not shown) showed left ventricular ejection fraction of 55% with basal posterior and inferior hypokinesis. Midventricular vertical long-axis slices of 201Tl myocardial perfusion images obtained during stress (C) and after 3-hr delay (D) show severe inferior, inferoapical, apical, mid, and distal anterior perfusion defects with substantial reversibility at 3 hr. Left ventricular cavity is also reduced in size on delay image. Also, note mid and distal anterior wall flaring outward on stress image, creating divergence of anterior wall at anteroapex (arrow, C). This ischemia-induced wall motion abnormality results in transient apical aneurysm seen only on stress image. This patient shows transient ischemic dilatation of left ventricle caused by severe multivessel epicardial coronary artery atherosclerosis.

View larger version (133K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2E. —59-year-old man with long history of smoking and hypertension who presented with atypical chest pain. Echocardiogram (not shown) showed left ventricular ejection fraction of 55% with basal posterior and inferior hypokinesis. Angiogram of right coronary artery shows severe (90%) midvessel stenosis (arrow). This patient shows transient ischemic dilatation of left ventricle caused by severe multivessel epicardial coronary artery atherosclerosis.

View larger version (118K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2F. —59-year-old man with long history of smoking and hypertension who presented with atypical chest pain. Echocardiogram (not shown) showed left ventricular ejection fraction of 55% with basal posterior and inferior hypokinesis. Angiogram of left coronary artery shows severe midvessel stenosis (solid arrow) of left anterior descending artery with diffuse disease distally. Note occlusion of all obtuse marginal branches and severe diffuse disease of terminal circumflex coronary artery (open arrow). This patient shows transient ischemic dilatation of left ventricle caused by severe multivessel epicardial coronary artery atherosclerosis.

Forty percent of the patients in a single-center study with transient ischemic dilatation did not have multivessel coronary artery disease [4]; thus, transient ischemic dilatation is not a specific marker for severe multivessel coronary artery disease in a population with a high prevalence of hypertensive or hypertrophic heart disease.

Transient ischemic dilatation was noted in some patients with dilated cardiomyopathy in the absence of epicardial vessel stenoses (Fig. 3A,3B,3C,3D). These patients had a variable history of hypertension, but none were observed to be hypertensive at the time of perfusion imaging. Preliminary data point to limited coronary flow reserve as a possible explanation for transient ischemic dilatation of the left ventricle in patients with dilated cardiomyopathy [7]. Patchy perfusion defects afecting the entire thickness of the myocardium in these patients are generally believed to be caused by prior myocarditis, underlying myocardial fibrosis, or small-vessel disease.

View larger version (123K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3A. —70-year-old woman with diabetes who had biventricular heart failure caused by cardiotoxicity after having undergone adriamycin therapy for non-Hodgkin's lymphoma. Echocardiogram (not shown) showed global hypokinesis with left ventricular ejection fraction of 20%. Patient presented with prolonged chest pain. Midventricular short-axis slices of 201Tl myocardial perfusion images obtained during stress (A) and after 3-hr delay (B) show large anteroseptal defect with significant reversibility on delay image (arrows). This patient shows dilated cardiomyopathy, which was caused by adriamycin cardiotoxicity, with both segmental perfusion defect and mild transient dilatation of left ventricular cavity during stress. Echocardiography (not shown) showed no discrete wall motion abnormality in area of perfusion defect. This perfusion defect in anteroseptal segment could result from coronary flow reserve abnormalities caused by diabetic microangiopathy, but this remains unproven.

View larger version (155K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3B. —70-year-old woman with diabetes who had biventricular heart failure caused by cardiotoxicity after having undergone adriamycin therapy for non-Hodgkin's lymphoma. Echocardiogram (not shown) showed global hypokinesis with left ventricular ejection fraction of 20%. Patient presented with prolonged chest pain. Midventricular short-axis slices of 201Tl myocardial perfusion images obtained during stress (A) and after 3-hr delay (B) show large anteroseptal defect with significant reversibility on delay image (arrows). This patient shows dilated cardiomyopathy, which was caused by abriamycin cardiotoxicity, with both segmental perfusion defect and mild transient dilatation of left ventricular cavity during stress. Echocardiography (not shown) showed no discrete wall motion abnormality in area of perfusion defect. This perfusion defect in anteroseptal segment could result from coronary flow reserve abnormalities caused by diabetic microangiopathy, but this remains unproven.

View larger version (167K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3C. —70-year-old woman with diabetes who had biventricular heart failure caused by cardiotoxicity after having undergone adriamycin therapy for non-Hodgkin's lymphoma. Echocardiogram (not shown) showed global hypokinesis with left ventricular ejection fraction of 20%. Patient presented with prolonged chest pain. Midventricular vertical long-axis slices of 201Tl myocardial perfusion images obtained during stress (C) and after 3-hr delay (D) show anterior reversible perfusion defect (arrows). Also note grossly dilated cavity on stress image with mild decrease in size and mild increase in myocardial wall thickness on 3-hr delay image. Angiograms of right coronary artery and left coronary artery (not shown) revealed no abnormalities. This patient shows dilated cardiomyopathy, which was caused by adriamycin cardiotoxicity, with both segmental perfusion defect and mild transient dilatation of left ventricular cavity during stress. Echocardiography (not shown) showed no discrete wall motion abnormality in area of perfusion defect. This perfusion defect in anteroseptal segment could result from coronary flow reserve abnormalities caused by diabetic microangiopathy, but this remains unproven.

View larger version (164K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3D. —70-year-old woman with diabetes who had biventricular heart failure caused by cardiotoxicity after having undergone adriamycin therapy for non-Hodgkin's lymphoma. Echocardiogram (not shown) showed global hypokinesis with left ventricular ejection fraction of 20%. Patient presented with prolonged chest pain. Midventricular vertical long-axis slices of 201Tl myocardial perfusion images obtained during stress (C) and after 3-hr delay (D) show anterior reversible perfusion defect (arrows). Also note grossly dilated cavity on stress image with mild decrease in size and mild increase in myocardial wall thickness on 3-hr delay image. Angiograms of right coronary artery and left coronary artery (not shown) revealed no abnormalities. This patient shows dilated cardiomyopathy, which was caused by adriamycin cardiotoxicity, with both segmental perfusion defect and mild transient dilatation of left ventricular cavity during stress. Echocardiography (not shown) showed no discrete wall motion abnormality in area of perfusion defect. This perfusion defect in anteroseptal segment could result from coronary flow reserve abnormalities caused by diabetic microangiopathy, but this remains unproven.

A variant of transient ischemic dilatation in which cavity dilatation is localized to a small segment of the ventricle has been described [8]. Preliminary findings show localized stress dilatation of the ventricular cavity at the site of a perfusion defect correlates very strongly with a 70% or greater obstruction of the subtending artery. In 13 patients who had this finding, 12 had a stenosis of 90% or greater in the subtending coronary artery. The remaining patient had an 80% stenosis. As noted in multivessel coronary artery disease, a visible transmyocardial perfusion gradient is occurring, but it is localized to the territory of the severely stenosed subtending coronary artery. This local transient cavity dilatation within a perfusion defect hence becomes a specific marker of severe subtending epicardial vessel obstruction (Fig. 4A,4B,4C,4D,4E,4F).

View larger version (119K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 4A. —40-year-old woman with class III anginal symptoms according to Canadian Cardiovascular Society classification system [9]. Midventricular short-axis slices of 201Tl myocardial perfusion images obtained during stress (A) and after 3-hr delay (B) show anterior, entire septal, and inferior reversible perfusion defects (arrows, A). Also note thinning of these walls on stress image as compared with that of lateral wall, which is of normal thickness. In both short-axis and vertical long-axis slices, anteroseptal and inferior defects show thinned walls in regions supplied by left anterior descending and right coronary arteries, and there is larger cavity seen on stress image as compared with delay image.

View larger version (120K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 4B. —40-year-old woman with class III anginal symptoms according to Canadian Cardiovascular Society classification system [9]. Midventricular short-axis slices of 201Tl myocardial perfusion images obtained during stress (A) and after 3-hr delay (B) show anterior, entire septal, and inferior reversible perfusion defects (arrows, A). Also note thinning of these walls on stress image as compared with that of lateral wall, which is of normal thickness. In both short-axis and vertical long-axis slices, anteroseptal and inferior defects show thinned walls in regions supplied by left anterior descending and right coronary arteries, and there is larger cavity seen on stress image as compared with delay image.

View larger version (172K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 4C. —40-year-old woman with class III anginal symptoms according to Canadian Cardiovascular Society classification system [9]. Midventricular vertical long-axis slices of 201Tl myocardial perfusion images obtained during stress (C) and after 3-hr delay (D) show anterior, apical, and inferoapical reversible perfusion defects (arrows, C). In both short-axis and vertical long-axis slices, anteroseptal and inferior defects show thinned walls in regions supplied by left anterior descending and right coronary arteries, and there is larger cavity seen on stress image as compared with delay image.

View larger version (178K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 4D. —40-year-old woman with class III anginal symptoms according to Canadian Cardiovascular Society classification system [9]. Midventricular vertical long-axis slices of 201Tl myocardial perfusion images obtained during stress (C) and after 3-hr delay (D) show anterior, apical, and inferoapical reversible perfusion defects (arrows, C). In both short-axis and vertical long-axis slices, anteroseptal and inferior defects show thinned walls in regions supplied by left anterior descending and right coronary arteries, and there is larger cavity seen on stress image as compared with delay image.

View larger version (123K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 4E. —40-year-old woman with class III anginal symptoms according to Canadian Cardiovascular Society classification system [9]. Angiogram shows occluded dominant right coronary artery. In this patient, transient ischemic dilatation is localized to distribution of severely stenosed left anterior descending coronary artery and occluded right coronary artery.

View larger version (143K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 4F. —40-year-old woman with class III anginal symptoms according to Canadian Cardiovascular Society classification system [9]. Angiogram of left coronary artery shows long diffuse 90% proximal stenosis (between arrows) in left anterior descending artery. Also note posterior septal perforators filling from left coronary artery injection (between arrowheads); 90% stenosis found in first diagonal branch is not seen on this view. In this patient, transient ischemic dilatation is localized to distribution of severely stenosed left anterior descending coronary artery and occluded right coronary artery.

In summary, global transient ischemic dilatation of the left ventricle is associated with global subendocardial ischemia caused by either severe multivessel coronary artery disease or hypertrophic heart disease. It is rarely seen in patients with dilated cardiomyopathy who are not hypertensive at the time of imaging irrespective of history of antecedent hypertension. When transient ischemic dilatation is localized to a small segment of the left ventricle, it is a specific marker of severe stenosis of the subtending epicardial coronary artery.

References

Top Introduction References

 

1. Stolzenberg J. Dilation of the left ventricular cavity on stress thallium scan as an indicator of ischemic disease. Clin Nucl Med 1980;5:289 -291[Medline]
2. Weiss TA, Berman DS, Lew AS, et al. Transient ischemic dilation of the left ventricle on stress thallium-201 scintigraphy: a marker of severe and extensive coronary artery disease. J Am Coll Cardiol 1987;9:752 -759[Abstract]
3. Iskandrian AS, Heo J, Nguyen T, Lyons E, Paugh E. Left ventricular dilatation and pulmonary thallium uptake after single-photon emission computer tomography using thallium-201 during adenosine-induced coronary hyperemia. Am J Cardiol 1990;66:807 -811[Medline]
4. Robinson VJB, Corley JH, Gunter LE, et al. Transient ischemic dilatation occurs in patients without severe multivessel epicardial stenoses (abstr). J Investig Med 1997;45:226A
5. Houghton JL, Frank MJ, Carr AA, von Dohlen TW, Prisant LM. Relations among impaired coronary flow reserve, left ventricular hypertrophy and thallium perfusion defects in hypertensive patients without obstructive coronary artery disease. J Am Coll Cardiol 1990;15:43 -51[Abstract]
6. Duncker DJ, Bache RJ. Nitric oxide contributes to coronary vasodilation distal to a coronary artery stenosis that results in myocardial hypoperfusion during exercise. Circ Res 1994;73:629 -640[Abstract/Free Full Text]
7. Inoue T, Sakai Y, Morooka S, et al. Coronary flow reserve in patients with dilated cardiomyopathy. Am Heart J 1993;125:93 -98[Medline]
8. Robinson VJB, Marks DS, Eubig C, et al. A pattern of transient localized thinning seen on myocardial perfusion scans predicts severe single vessel stenosis (abstr). J Am Coll Cardiol 1998; 31[suppl C]:262C
9. Campeau L. Grading of angina pectoris (letter). Circulation 1976;54:522 -523[Medline]

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This Article Figures Only Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Robinson, V. J. B. Articles by Prisant, L. M. Search for Related Content PubMed PubMed Citation Articles by Robinson, V. J. B. Articles by Prisant, L. M. Social Bookmarking                      What's this? Hotlight (NEW!) What's Hotlight?