Myocardial perfusion in type 2 diabetes with left ventricular hypertrophy: normalisation by acute angiotensin-converting enzyme inhibition

Birger Hesse, Christian Meyer, Flemming S Nielsen, Asako Sato, Jens D Hove, Soeren Holm, Lia E Bang, Klaus F Kofoed, Tage L Svendsen, Hans-Henrik Parving, Lionel H Opie

15 Citationer (Scopus)

Abstrakt

The purpose of this study was to assess whether acute angiotensin-converting enzyme (ACE) inhibition would improve myocardial perfusion and perfusion reserve in a subpopulation of normotensive patients with diabetes and left ventricular hypertrophy (LVH), both independent risk factors of coronary disease. Using positron emission tomography (PET), we investigated the response of regional myocardial perfusion to acute ACE inhibition with i.v. infusion of perindoprilat (vs saline infusion as control, minimum interval 3 days) in 12 diabetic patients with LVH. Myocardial perfusion was quantified with PET using nitrogen-13 ammonia infused at rest and during dipyridamole hyperaemia. Twelve healthy control subjects were included in the study, five of whom were also studied with perindoprilat. Mean blood pressure in normo-albuminuric, asymptomatic patients was 123+/-7/65+/-9 mmHg. Compared with controls, maximal perfusion was reduced in patients (1.8+/-0.6 vs 2.5+/-1.0 ml min(-1) g(-1); P<0.05), and perfusion reserve was also lower, at borderline significance (2.7+/-1.0 vs 3.6+/-1.3; P=0.059). During perindoprilat infusion, myocardial perfusion reserve in patients increased to 3.9+/-0.9 ( P<0.001) due to normalisation of maximal perfusion (2.3+/-0.5 ml min(-1) g(-1), P<0.01). In the five control subjects both resting and hyperaemic perfusion remained unchanged during perindoprilat infusion. It is concluded that acute ACE inhibition with perindoprilat improves maximal achieved myocardial perfusion in non-hypertensive patients with diabetes and LVH.

OriginalsprogEngelsk
TidsskriftEuropean Journal of Nuclear Medicine and Molecular Imaging
Vol/bind31
Udgave nummer3
Sider (fra-til)362-8
Antal sider7
ISSN1619-7070
DOI
StatusUdgivet - mar. 2004

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