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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 region- al 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 dipyrida- mole hyperaemia. Twelve healthy control subjects were in- cluded 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, myo- cardial 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 un- changed 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. [ABSTRACT FROM AUTHOR]

Flow quantitation with nitrogen-13 ammonia ([sup 13]NH[sub 3]) and positron emission tomography (PET) is dependent on an accurate blood time-activity curve. This is conveniently derived from the PET images by drawing a region of interest in the left ventricular cavity. The blood time-activity curve obtained in this way, however, may contain spillover from the myocardial wall. The purpose of this study was to analyse the effect of wall to blood pool spillover. Additionally, we analysed the application of a left atrial input function. Using computer simulations, we investigated the effect of spillover from the myocardial wall to the left ventricular input function and the effect of time delay on the left ventricular input function. An oxygen-15 carbon monoxide PET study of seven normal volunteers was used to investigate possible recovery issues regarding the left atrial input function. Finally, [sup 13]NH[sub 3] studies of 31 normal volunteers during rest and dipyridamole stimulation were analysed using either a left atrial or a left ventricular input function. The simulation studies showed that myocardial wall to blood pool spillover causes a considerable underestimation of the regional blood flow values in hyperaemic flow studies. Neither time delay nor recovery issues prevent flow quantitation with a left atrial input function. The [sup 13]NH[sub 3] studies revealed no significant difference between the resting blood flow values, whereas the hyperaemic blood flow values were underestimated by 8% (P<0.01) on average (up to 40% individually) when using a left ventricular input function compared with a left atrial input function. Spillover of activity from the left ventricular wall to the blood time-activity curve is of importance in hyperaemic flow studies using [sup 13]NH[sub 3]. Application of a left atrial input function is a possible solution to these issues. [ABSTRACT FROM AUTHOR]

The purpose of the present study was to evaluate the effect of spillover of activity from the right ventricle (RV) on quantitation of the regional myocardial blood flow in the septum. Thirty-one healthy volunteers, 31 patients with ischemic heart disease, 7 patients with severe congestive heart failure, and 6 heart transplant patients underwent positron emission tomography (PET) with nitrogen-13 ammonia. Quantitation of the regional myocardial blood flow in the septum was performed using both a conventional two-compartment model and a previously validated two-compartment model taking RV spillover into account. Unaccounted RV spillover resulted in significant underestimation of the regional myocardial blood flow in the septum. The amount of underestimation was primarily dependent on the magnitude of spillover and the dispersion between the right and the left ventricular input functions. In healthy volunteers, the flow error was small but significant: on average 6% (range 5%–29%, P<0.00001), compared with 27% (range 0%–88%, P<0.002) in the group of patients with severe congestive heart failure, who had the most considerable amount of RV spillover. In the group of patients with ischemic heart disease and the group of heart transplant patients the flow errors were 10% (range 0%–55%, P<0.00001) and 6% (range 1%–19%, P<0.01), respectively. It is concluded that flow quantitation in the septum is significantly affected by RV spillover, resulting in a considerable underestimation of the septal blood flow unless correction is performed. [ABSTRACT FROM AUTHOR]

The aim of this study was to assess regional and global variability of insulin-stimulated myocardial glucose uptake in healthy elderly subjects and to evaluate potentially responsible factors. Twenty men with a mean age of 64 years, no history of cardiovascular disease, and normal blood pressure, bicycle exercise test, electrocardiogram and echocardiography were studied [P(coronary artery disease) <5%]. Whole-body insulin sensitivity and insulin-stimulated myocardial glucose uptake were measured during hyperinsulinaemic euglycaemic glucose clamp with fluorine-18 fluorodeoxyglucose, and myocardial rest and hyperaemic blood flow during dipyridamole infusion were measured with nitrogen-13 ammonia and positron emission tomography in 16 left ventricular myocardial segments. Intra-individual and inter-individual variability of insulin-stimulated myocardial glucose uptake [relative dispersion = (standard deviation/mean)] was 13% and 29% respectively. Although inter-individual variability of glucose uptake and blood flow at rest was of the same magnitude, no correlation was found between these measures. Regional and global insulin-stimulated myocardial glucose uptake correlated linearly with whole-body insulin sensitivity (r=0.51, P<0.05 and r=0.56, P<0.01). The strongest independent association by multivariate linear regression analysis was found between myocardial glucose uptake and hyperaemic blood flow (r=0.63, P<0.005). We conclude that in healthy elderly subjects, insulin-stimulated myocardial glucose uptake is homogeneous throughout the left ventricle, but has moderate inter-individual variability. Inter-individual variability of insulin-stimulated myocardial glucose uptake is primarily explained by variability in coronary vascular reactivity and tissue insulin sensitivity. [ABSTRACT FROM AUTHOR]

We tested the hypothesis that low whole-body insulin sensitivity in patients with ischaemic heart disease and impaired left ventricular (LV) function is associated with abnormalities of insulin-mediated myocardial glucose uptake affecting outcome after coronary bypass surgery (CABG). We studied 29 patients with ischaemic heart disease and impaired LV ejection fraction (EF) and age-matched healthy volunteers (n = 30). As assessed by euglycaemic glucose-insulin clamp, 15 patients had a low and 14 a normal whole-body insulin sensitivity. Using positron emission tomography, patterns of fluorine-18 fluorodeoxyglucose and nitrogen-13 ammonia uptake in addition to quantified glucose uptake, blood flow and hyperaemic blood flow were assessed before CABG in 16 myocardial segments of the left ventricle. Major adverse cardiac events and LVEF were evaluated 7 months after CABG. Glucose uptake in normokinetic PET-normal myocardium was found to be higher in patients with normal whole-body insulin sensitivity (P < 0.001), whereas in patients with low whole-body insulin sensitivity more segments displayed a pattern of reduced glucose uptake in normoperfused myocardium (PET-reverse mismatch) (P < 0.05). Hyperaemic blood flow was impaired in both patient groups. A major cardiac event after CABG could partly be predicted by the LV extent of normoperfused segments with PET-reverse mismatch. We conclude that low whole-body insulin sensitivity in patients with ischaemic heart disease and impaired LV function is associated with impaired insulin-mediated myocardial glucose uptake, which is partially predictive of a worse outcome after CABG. [ABSTRACT FROM AUTHOR]