TY - JOUR
T1 - Iodine-123 phenylpentadecanoic acid myocardial scintigraphy in patients with left ventricular hypertrophy
T2 - Alterations in left ventricular distribution and utilization
AU - Wolfe, Christopher L.
AU - Kennedy, Patrick L.
AU - Kulkarni, Padmaker V.
AU - Jansen, Donald E.
AU - Gabliani, Gregory I.
AU - Corbett, James R.
N1 - Funding Information:
Many investigators have attempted to identify metabolic or biochemical factors that might contribute to the development of cardiac hypertrophy in the hope of gaining insight into the pathogenesis of the disease process. Altered levels of adenosine triphosphate (ATP) and creatine phosphate, increased amino acid Radiology,U niversityo f Texas Health ScienceC enter, and the Divisiono f Cardiology,U niversityo f California. Supported in part by National Heart, Lung, and Blood Institute Ischemic SCOR grant HL 17669,t he Moss Heart Fund, Dallas, Texas,a nd a Clinical Investigator Award (HL-01972-03)f rom the National Heart, Lung, and Blood Institute (Dr. Wolfe). Received for publication April 17, 1989; acceptedJ an. 8, 1990. Reprint requests: ChristopherL . Wolfe,M D, CardiologyD ivision,U niver-sity of Californiaa t San Francisco, San Francisco,C A 94143. 4/1/19440 transport, and enhanced ribonucleic acid and protein synthesis have all been described in various experimental models of hypertrophy. 1-5 Recently Yonekura et al. 6 showed that regional cardiac uptake of fatty acids and glucose was altered in rats with hypertension. They found that rats with severe hypertension had decreased fatty acid uptake and enhanced glucose uptake in the subendocardial region of the left ventricle despite normal myocardial perfusion. Other investigators have shown that both animals and humans with left ventricular hypertrophy (LVH) have increased susceptibility to ischemic injury in the absence of coronary artery disease, probably because of decreased coronary vasodilator reserve. 7-1~ Because ischemia causes a shift from oxidative phosphorylation to anaerobic glycolysis, this might account for a shift from fatty acid to glucose as the preferred sub-
PY - 1990/6
Y1 - 1990/6
N2 - Regional alterations in myocardial substrate uptake and/or utilization have been demonstrated in rats with hypertension. To determine whether alterations in left ventricular fatty acid uptake and/or utilization are present in patients with left ventricular hypertrophy (LVH), we compared the results of rest and exercise iodine-123 phenylpentadecanoic acid (IPPA) myocardial scintigraphy in 10 patients with hypertension who had concentric LVH without evidence of coronary artery disease and in 15 normal subjects. Patients with LVH had more heterogeneous left ventricular activity of IPPA compared to normal subjects after exercise but not at rest (23±8% versus 13±5% difference in maximum segmental activity at 4 minutes after exercise; p=0.005). Although IPPA clearance was similar in both patients with LVH and normal subjects, postexercise washout in segments showing decreased initial IPPA uptake was reduced compared to washout at rest in patients with LVH (11.7±7.5% versus 21.5±8.4% at 20 minutes after injection, n=15; p=0.005). Exercise thallium-201 (Tl-201) scintigraphy was normal in all seven patients with LVH tested. Patients with LVH showed significantly greater heterogeneity in IPPA uptake compared to TI-201 uptake immediately after exercise (25±5% versus 16±6%; p=0.013). We conclude that (1) compared to normal subjects, patients with LVH show heterogeneous myocardial IPPA activity after exercise but not at rest; (2) postexercise washout of IPPA was decreased in segments with reduced uptake after exercise in patients with LVH; and (3) the distribution of IPPA is more heterogeneous than that of TI-201 immediately after exercise in patients with concentric LVH. The postexercise heterogeneity in IPPA uptake and delayed washout in segments with reduced initial uptake is consistent with exercise-induced myocardial ischemia in patients with LVH.
AB - Regional alterations in myocardial substrate uptake and/or utilization have been demonstrated in rats with hypertension. To determine whether alterations in left ventricular fatty acid uptake and/or utilization are present in patients with left ventricular hypertrophy (LVH), we compared the results of rest and exercise iodine-123 phenylpentadecanoic acid (IPPA) myocardial scintigraphy in 10 patients with hypertension who had concentric LVH without evidence of coronary artery disease and in 15 normal subjects. Patients with LVH had more heterogeneous left ventricular activity of IPPA compared to normal subjects after exercise but not at rest (23±8% versus 13±5% difference in maximum segmental activity at 4 minutes after exercise; p=0.005). Although IPPA clearance was similar in both patients with LVH and normal subjects, postexercise washout in segments showing decreased initial IPPA uptake was reduced compared to washout at rest in patients with LVH (11.7±7.5% versus 21.5±8.4% at 20 minutes after injection, n=15; p=0.005). Exercise thallium-201 (Tl-201) scintigraphy was normal in all seven patients with LVH tested. Patients with LVH showed significantly greater heterogeneity in IPPA uptake compared to TI-201 uptake immediately after exercise (25±5% versus 16±6%; p=0.013). We conclude that (1) compared to normal subjects, patients with LVH show heterogeneous myocardial IPPA activity after exercise but not at rest; (2) postexercise washout of IPPA was decreased in segments with reduced uptake after exercise in patients with LVH; and (3) the distribution of IPPA is more heterogeneous than that of TI-201 immediately after exercise in patients with concentric LVH. The postexercise heterogeneity in IPPA uptake and delayed washout in segments with reduced initial uptake is consistent with exercise-induced myocardial ischemia in patients with LVH.
UR - http://www.scopus.com/inward/record.url?scp=0025366958&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0025366958&partnerID=8YFLogxK
U2 - 10.1016/S0002-8703(05)80184-X
DO - 10.1016/S0002-8703(05)80184-X
M3 - Article
C2 - 2141221
AN - SCOPUS:0025366958
SN - 0002-8703
VL - 119
SP - 1338
EP - 1347
JO - American Heart Journal
JF - American Heart Journal
IS - 6
ER -