title: Positron emission tomographic evaluation of regulation of myocardial perfusion in physiological (elite athletes) and pathological (systemic hypertension) left ventricular hypertrophy.
abstract: Myocardial perfusion (MP) may differ in physiologic and pathologic left ventricular hypertrophy (LVH). We compared MP in LVH in elite athletes and patients with hypertension with healthy, age-matched subjects. We included 12 rowers with LVH, 19 patients with hypertension with LVH, and 2 age-matched groups of healthy subjects (n = 11 and n = 12). The left ventricular mass index was determined echocardiographically. MP was measured by N-13 ammonia positron emission tomography. The maximal perfusion and perfusion reserve were studied using dipyridamole, and endothelial function was assessed by a cold pressor test. The degree of LVH was similar in athletes and those with hypertension. Compared with controls, athletes had 20% lower baseline MP (p <0.05), a similar response to the cold pressor test, and a higher perfusion reserve (31%, p <0.05). The patients with hypertension had a 25% higher baseline MP (p <0.05), a reduced increase during the cold pressor test (12% vs 25% in controls, p <0.05), and a reduced perfusion reserve (27% lower, p <0.001). The peak global perfusion (MP x left ventricular mass index) was 62% higher in athletes (p <0.05) than in controls, but the peak global perfusion in patients with hypertension did not differ from that of controls. In conclusion, physiologic LVH in athletes is suited for a high peak workload at the cost of only a small increase in basal myocardial oxygen consumption. In contrast, LVH in the presence of hypertension is a good adaptation to the increased baseline workload with maintained maximal cardiac performance. Endothelial dysfunction may contribute to the reduced perfusion reserve seen in hypertensive LVH.
authors.affiliation: Department of Clinical Physiology, Nuclear Medicine and PET, Rigshospitalet University Hospital, Copenhagen, Denmark. kjaer@mfi.ku.dk
authors.forename: Andreas
authors.initials: A
authors.lastname: Kjaer
authors.forename: Christian
authors.initials: C
authors.lastname: Meyer
authors.forename: Kristian
authors.initials: K
authors.lastname: Wachtell
authors.forename: Michael Hecht
authors.initials: MH
authors.lastname: Olsen
authors.forename: Hans
authors.initials: H
authors.lastname: Ibsen
authors.forename: Lionel
authors.initials: L
authors.lastname: Opie
authors.forename: Søren
authors.initials: S
authors.lastname: Holm
authors.forename: Birger
authors.initials: B
authors.lastname: Hesse
mesh_terms: D000328:Adult; D000368:Aged; D003326:Coronary Circulation / Q000502:physiology*; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology; D004176:Dipyridamole / Q000008:administration & dosage; D004452:Echocardiography; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging*; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography; D013177:Sports / Q000502:physiology*; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000627:therapeutic use; D016276:Ventricular Function
chemical_list: D014665:Vasodilator Agents; D004176:Dipyridamole