Positron-emission tomography offers the possibility of quantifying noninvasively absolute myocardial perfusion in humans. However, since the heart walls are relatively thin compared with the spatial resolution of most imaging devices and tissue tracer concentrations are underestimated, it is not possible to assess the transmural distribution of myocardial perfusion. In patients with hypertrophic cardiomyopathy the left ventricular myocardium may be extremely thick. This anatomic feature offers a unique opportunity to assess perfusion of the subendocardial and subepicardial layers of the left ventricle, overcoming the technical constraints imposed by the current positron cameras. In this study the possibility of measurement of the transmural distribution of coronary perfusion was assessed in two patients with hypertrophic cardiomyopathy and very thick interventricular septa (maximal septal thickness, 39 and 31 mm). Regional myocardial perfusion at rest and after pharmacologically induced vasodilation (intravenous dipyridamole, 0.56 mg/kg over 4 minutes) was measured by means of 13N-ammonia and dynamic positron-emission tomography. The subendocardial-subepicardial flow ratios at rest and after dipyridamole were measured in a total of eight regions of interest (four per patient; two in the septum and two in the anterior wall). At baseline a focal deficit of perfusion, probably reflecting an area of scar at the base of the anterior papillary muscle, was demonstrated in patient 1. In both patients, however, transmural distribution of perfusion was homogeneous and the subendocardial-subepicardial flow ratios were close or equal to unity. After dipyridamole, myocardial perfusion increased significantly more in subepicardial than in subendocardial myocardium in the septum and in one of the two anterior regions in patient 1. In patient 2 myocardial perfusion after dipyridamole was reduced transmurally, below the respective baseline values, in one of the two septal regions, whereas it was more severely reduced in the left ventricular subendocardium of the second septal region and in both the anterior regions. A subendocardial-subepicardial flow ratio equal to or lower than 0.7 was demonstrated in five of eight regions of interest after dipyridamole. To our knowledge, this is the first quantitative assessment of the transmural distribution of myocardial perfusion that has been performed in humans by means of positron-emission tomography. Our results suggest that dipyridamole-induced flow maldistribution in patients with hypertrophic cardiomyopathy is for the most part the result of relative or even absolute subendocardial underperfusion.
DIPYRIDAMOLE-INDUCED SUBENDOCARDIAL UNDERPERFUSION IN HYPERTROPHIC CARDIOMYOPATHY ASSESSED BY POSITRON-EMISSION TOMOGRAPHY
CAMICI , PAOLO;
1991-01-01
Abstract
Positron-emission tomography offers the possibility of quantifying noninvasively absolute myocardial perfusion in humans. However, since the heart walls are relatively thin compared with the spatial resolution of most imaging devices and tissue tracer concentrations are underestimated, it is not possible to assess the transmural distribution of myocardial perfusion. In patients with hypertrophic cardiomyopathy the left ventricular myocardium may be extremely thick. This anatomic feature offers a unique opportunity to assess perfusion of the subendocardial and subepicardial layers of the left ventricle, overcoming the technical constraints imposed by the current positron cameras. In this study the possibility of measurement of the transmural distribution of coronary perfusion was assessed in two patients with hypertrophic cardiomyopathy and very thick interventricular septa (maximal septal thickness, 39 and 31 mm). Regional myocardial perfusion at rest and after pharmacologically induced vasodilation (intravenous dipyridamole, 0.56 mg/kg over 4 minutes) was measured by means of 13N-ammonia and dynamic positron-emission tomography. The subendocardial-subepicardial flow ratios at rest and after dipyridamole were measured in a total of eight regions of interest (four per patient; two in the septum and two in the anterior wall). At baseline a focal deficit of perfusion, probably reflecting an area of scar at the base of the anterior papillary muscle, was demonstrated in patient 1. In both patients, however, transmural distribution of perfusion was homogeneous and the subendocardial-subepicardial flow ratios were close or equal to unity. After dipyridamole, myocardial perfusion increased significantly more in subepicardial than in subendocardial myocardium in the septum and in one of the two anterior regions in patient 1. In patient 2 myocardial perfusion after dipyridamole was reduced transmurally, below the respective baseline values, in one of the two septal regions, whereas it was more severely reduced in the left ventricular subendocardium of the second septal region and in both the anterior regions. A subendocardial-subepicardial flow ratio equal to or lower than 0.7 was demonstrated in five of eight regions of interest after dipyridamole. To our knowledge, this is the first quantitative assessment of the transmural distribution of myocardial perfusion that has been performed in humans by means of positron-emission tomography. Our results suggest that dipyridamole-induced flow maldistribution in patients with hypertrophic cardiomyopathy is for the most part the result of relative or even absolute subendocardial underperfusion.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
