Causes of Transient Dilatation of the Left Ventricle During Myocardial Perfusion Imaging
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).
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).
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.
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).
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.
Footnote
Address correspondence to V. J. B. Robinson.
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
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
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
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
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
7.
Inoue T, Sakai Y, Morooka S, et al. Coronary flow reserve in patients with dilated cardiomyopathy. Am Heart J 1993; 125:93-98
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
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© American Roentgen Ray Society.
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Submitted: July 12, 1999
Accepted: September 29, 1999
First published: November 23, 2012
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