TY - JOUR
T1 - Persistence of coronary vasodilator responsivity after cardiac transplantation
AU - Senneff, Martha J.
AU - Hartman, Judy
AU - Sobel, Burton E.
AU - Geltman, Edward M.
AU - Bergmann, Steven R.
N1 - Funding Information:
From the Cardiovascular Division, Washington University School of Medicine, St. Louis, Missouri. This study was supported in part by the National Heart, Lung and Blood Institute (Specialized Center of Research Coronary Vascular Disease Grant HL17646) of the National Institutes of Health, Bethesda, Maryland. Dr. Senneff was supported in part by a Mallinckrodt/Society of Nuclear Medicine Fellowship and by a Squibb Diagnostic/Society for Cardiac Angiography and Interventions Fellowship. Manuscript received July 23, 1992; revised manuscript received August 24, 1992, and accepted August 30. Address for reprints: Steven R. Bergmann, MD, PhD, Cardiovascular Division, Washington University School of Medicine, Box 8086, 660 South Euclid Avenue, St. Louis, Missouri 63 110.
PY - 1993/2/1
Y1 - 1993/2/1
N2 - Accelerated graft atherosclerosis is a major cause of death after cardiac transplantation. Although its detection currently requires surveillance angiography, loss of vasodilator responsivity may precede obstructive lesions and be detectable by noninvasive assessment of myocardial perfusion. Thirty-five allograft recipients were studied an average of 31 ± 19 (mean ± SD) months after transplantation. All were free from angiographically definable macrovascular obstructive coronary artery lesions. Nutritive myocardial perfusion at rest, estimated in absolute terms by positron emission tomography with oxygen-15 water averaged 1.63 ± 0.51 ml/g/min in patients and was greater than that in 26 healthy volunteers (1.17 ± 0.33 ml/g/min, p < 0.001). The increase correlated with increased cardiac work at rest in transplant recipients with arterial hypertension and tachycardia. Peak myocardial perfusion induced by intravenous administration of dipyridamole was normal in the transplant recipients (3.49 ± 1.70 ml/g/min compared with 3.60 ± 1.41 ml/g/min in volunteers). Because of the high flow at rest, myocardial perfusion reserve (the ratio of hyperemic flow to flow at rest) was diminished (2.3 ± 1.2 compared with 3.3 ± 1.5 in volunteers, p < 0.005). These results indicate that the responsivity to vasodilator stimulation is well preserved in transplant recipients devoid of macroscopic coronary arterial lesions obviating detection of early vascular dysfunction in individual subjects. Positron emission tomography may be useful, however, in quantifying the magnitude of the increase in flow at rest secondary to increased cardiac work - a potentially remedial cause of accelerated coronary vascular disease induced by high shear force activation of platelets in the coronary bed, and in detecting impaired perfusion once macrovascular vascular disease is extant.
AB - Accelerated graft atherosclerosis is a major cause of death after cardiac transplantation. Although its detection currently requires surveillance angiography, loss of vasodilator responsivity may precede obstructive lesions and be detectable by noninvasive assessment of myocardial perfusion. Thirty-five allograft recipients were studied an average of 31 ± 19 (mean ± SD) months after transplantation. All were free from angiographically definable macrovascular obstructive coronary artery lesions. Nutritive myocardial perfusion at rest, estimated in absolute terms by positron emission tomography with oxygen-15 water averaged 1.63 ± 0.51 ml/g/min in patients and was greater than that in 26 healthy volunteers (1.17 ± 0.33 ml/g/min, p < 0.001). The increase correlated with increased cardiac work at rest in transplant recipients with arterial hypertension and tachycardia. Peak myocardial perfusion induced by intravenous administration of dipyridamole was normal in the transplant recipients (3.49 ± 1.70 ml/g/min compared with 3.60 ± 1.41 ml/g/min in volunteers). Because of the high flow at rest, myocardial perfusion reserve (the ratio of hyperemic flow to flow at rest) was diminished (2.3 ± 1.2 compared with 3.3 ± 1.5 in volunteers, p < 0.005). These results indicate that the responsivity to vasodilator stimulation is well preserved in transplant recipients devoid of macroscopic coronary arterial lesions obviating detection of early vascular dysfunction in individual subjects. Positron emission tomography may be useful, however, in quantifying the magnitude of the increase in flow at rest secondary to increased cardiac work - a potentially remedial cause of accelerated coronary vascular disease induced by high shear force activation of platelets in the coronary bed, and in detecting impaired perfusion once macrovascular vascular disease is extant.
UR - http://www.scopus.com/inward/record.url?scp=0027388889&partnerID=8YFLogxK
U2 - 10.1016/0002-9149(93)90801-I
DO - 10.1016/0002-9149(93)90801-I
M3 - Article
C2 - 8427178
AN - SCOPUS:0027388889
SN - 0002-9149
VL - 71
SP - 333
EP - 338
JO - The American journal of cardiology
JF - The American journal of cardiology
IS - 4
ER -