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Biomedical subjects

H R Schelbert

Publications and source records attributed to H R Schelbert.

At least 37 records · Page 2Linked to original sources
PubMed1998

The usefulness of positron emission tomography.

The evaluation of myocardial blood flow, especially in conjunction with studying either residual oxidative metabolism or glucose uptake, accurately identifies potentially reversible myocardial dysfunction. It also reliably distinguishes between an irreversible and reversible impairment in left ventricular wall motion. The presence of metabolic abnormalities as evidence of reversible dysfunction is associated with an increased risk for cardiac-related morbidity and death and thus identifies patients likely to gain most from surgical revascularization. Restoration of blood flow to reversibly dysfunctional myocardium that occupies at least 15% to 20% of the left ventricle reduces long-term mortality, improves congestive heart failure-related symptoms, and enhances left ventricular performance. Blood flow-metabolism imaging can be especially useful for patients with ischemic cardiomyopathy who are evaluated for cardiac transplantation. A PET-driven management algorithm aids in identifying those patients likely to benefit most from revascularization. Such identification can reduce significantly the cost of managing patients with end-stage coronary artery disease.

Coronary Circulation↗
PubMed1998

Simultaneous measurement of myocardial oxygen consumption and blood flow using [1-carbon-11]acetate.

UNLABELLED: [1-Carbon-11]acetate has been used as a tracer for oxidative metabolism with PET. The aim of this study was to validate, in humans, a previously proposed two-compartment model for [1-11C]acetate for the noninvasive measurement of myocardial oxygen consumption (MVO2) and myocardial blood flow (MBF) with PET. METHODS: Twelve healthy volunteers were studied with [13N]ammonia, [1-11C]acetate and PET. Myocardial oxygen consumption was invasively determined by the Fick method from arterial and coronary sinus O2 concentrations and from MBF obtained by [13N]ammonia PET. RESULTS: Directly measured MVO2 ranged from 5.2 to 11.1 ml/100g/min, and MBF ranged from 0.48 to 0.88 ml/g/min. Oxidative flux through the tricarboxylic acid cycle, reflected by the rate constant k2, which correlated linearly with measured MVO2 [k2 = 0.0071 + 0.0074(MVO2); r = 0.74, s.e.e. = 0.015]. With this correlation, MVO2 could be estimated from the model-derived k2 value by MVO2 = 135(k2) - 0.96. The slope of this relationship was close to that previously obtained in rats and implies that the tricarboxylic acid cycle intermediate metabolite pool sizes are comparable. The net extraction (K1) of [1-11C]acetate, measured by PET, from blood into myocardium correlated closely with MBF by K1 = 0.15 + 0.73(MBF) (r = 0.93, s.e.e. = 0.033) and, thus, provided noninvasively obtainable measures of blood flow. CONCLUSION: The proposed compartment model for [1-11C]acetate fits the measured kinetics well and, with proper calibration, allows estimation of absolute MVO2 rather than only an index of oxidative metabolism. Furthermore, [1-11C]acetate-derived estimates of MBF are feasible.

Acetic Acid↗
PubMed1998

Dual spillover problem in the myocardial septum with nitrogen-13-ammonia flow quantitation.

UNLABELLED: Conventional cardiac PET modeling techniques for [13N]ammonia flow determination do not fully account for the effects of spillover of activity from the right ventricle (RV) onto the activity in the myocardial septum. The purpose of this study was to investigate and to quantitatively account and correct for this effect. METHODS: Simulations were performed to determine the error introduced by conventional quantitation using septal time-activity curves, which only account for left ventricle (LV) spillover. Furthermore, we explored two separate methods to account for the dual spillover problem: direct estimation of the RV and LV spillover fractions incorporated into the [13N]ammonia model by using the LV and RV input functions in the fit and estimation of the relative dispersion and time shift between the LV and RV input functions by fitting using only the LV input function. The simulated curves were fitted using a two-compartment [13N]ammonia model. Flow estimates from the conventional model and the models including either of the two correction procedures were compared with canine microsphere data. RESULTS: The influence of RV spillover on flow estimation in the septum is determined by several parameters (e.g., dispersion between the RV and LV input function). Depending on the value of these parameters, the septal flow may be underestimated by 0%-30%. The applied methods for correction of the dual spillover problem were comparable and allow for more accurate quantitation in the septum. The canine microsphere data revealed that flow underestimation in the septum is small but significant. CONCLUSION: Dual spillover in the myocardial septum can introduce significant errors in the estimation of flow by the conventional [13N]ammonia model fitting method, which does not properly account for the RV spillover. Adjusting for the RV spillover in one of the two proposed methods allows for more accurate quantitation of myocardial septal flow with [13N]ammonia PET data.

Ammonia↗
PubMed1997

Coronary vasodilatory capacity and flow reserve in normal myocardium supplied by bypass grafts late after surgery.

Coronary artery bypass surgery is used widely for treating myocardial ischemia. However, blood flow and flow reserve of normally perfused myocardium subtended by bypass grafts have not been evaluated late after surgery. Also, it is unknown whether pharmacologic vasodilation evokes comparable myocardial flow responses in arterial and venous conduits. Myocardial blood flow was quantified at rest and during dipyridamole hyperemia using N-13 ammonia and positron emission tomography (PET) in 15 patients 9 +/- 3 years after bypass surgery and in 10 healthy volunteers. Blood flow was analyzed in 26 territories subtended by bypass grafts with normal wall motion and normal perfusion. Myocardial blood flow at rest did not differ between patients and controls (0.65 +/- 0.14 vs 0.68 +/- 0.16 ml/ g/min) and was similar in normal myocardium subtended by saphenous vein (n = 16) and internal mammary artery grafts (n = 10; 0.64 +/- 0.13 vs 0.66 +/- 0.15 ml/g/min). However, the hyperemic response in normal myocardium supplied by bypass grafts was less than that in controls (1.61 +/- 0.33 vs 2.04 +/- 0.30 ml/g/min, p <0.005). No differences between territories supplied by venous and arterial conduits were observed (1.61 +/- 0.35 vs 1.63 +/- 0.32 ml/g/min). Normal myocardium subtended by bypass grafts exhibited a lower flow reserve than that in controls (2.54 +/- 0.51 vs 3.16 +/- 0.85, p <0.02). Myocardial flow reserve was almost identical in regions supplied by venous and arterial grafts (2.55 +/- 0.48 vs 2.52 +/- 0.58). The similar reduction in vasodilatory capacity together with the normal PET polar map findings during dipyridamole argue against flow limiting stenoses in both venous and arterial bypass conduits late after revascularization. Rather, nonobstructive proliferative fibrointimal changes of the bypass conduits or atherosclerosis of the native resistance vessels might account for this finding.

Aged↗
PubMed1997

Effects of cardiac allograft vasculopathy on myocardial blood flow, vasodilatory capacity, and coronary vasomotion.

BACKGROUND: Coronary vasculopathy is the third leading cause of death 1 year after cardiac allograft transplantation. This study was designed to assess the hemodynamic effects of transplant vasculopathy on myocardial blood flow and vasomotion. METHODS AND RESULTS: Thirty-two patients were studied 1 to 2 years after cardiac transplantation by use of positron emission tomography (n = 32), intravascular ultrasound (n = 26), coronary angiography (n = 32), and endomyocardial biopsy (n = 32). Twenty healthy individuals served as control subjects. Quantitative intravascular ultrasound was used to compute coronary lumen area, intimal thickness, and intimal index [Intima Area/(Intima + Lumen Area)]. Myocardial blood flow was quantified with the use of 13N-ammonia/positron emission tomography. Mean myocardial blood flow was higher in the transplant patients than in control subjects (0.94 +/- 0.26 versus 0.68 +/- 0.16 mL.min-1.g-1 P < .0005). Cold increased myocardial blood flow to 0.79 +/- 0.18 mL.min-1.g-1 in control subjects but not in patients (0.98 +/- 0.36 mL.g-1.min-1). Hyperemic myocardial blood flow was lower in patients than in control subjects (1.69 +/- 0.78 versus 2.30 +/- 0.32 mL.min-1.g-1; P < .05) and was inversely related to maximal intimal thickness and intimal index (all P < .05). The myocardial flow reserve was reduced in patients (1.82 +/- 0.55 versus 3.45 +/- 1.03; P < .0001). CONCLUSIONS: The degree of intimal thickening is correlated with abnormalities in coronary function in patients with diffuse cardiac allograft vasculopathy. The reduction in vasodilatory capacity and the abnormal blood flow response to cold suggest abnormalities in endothelium-dependent and -independent coronary vasodilation in transplant recipients.

Cold Temperature↗
PubMed1997

Effect of beta 1 adrenergic receptor blockade on myocardial blood flow and vasodilatory capacity.

UNLABELLED: The beta 1 receptor blockade reduces cardiac work and may thereby lower myocardial blood flow (MBF) at rest. The effect of beta 1 receptor blockade on hyperemic MBF is unknown. METHODS: To evaluate the effect of selective beta 1 receptor blockade on MBF at rest and during dipyridamole induced hyperemia, 10 healthy volunteers (8 men, 2 women, mean age 24 +/- 5 yr) were studied using 13N-ammonia PET (two-compartment model) under control conditions and again during metoprolol (50 mg orally 12 hr and 1 hr before the study). RESULTS: The resting rate pressure product (6628 +/- 504 versus 5225 +/- 807) and heart rate (63 +/- 6-54 +/- 5 bpm) declined during metoprolol (p < 0.05). Similarly, heart rate and rate pressure product declined from the baseline dipyridamole study to dipyridamole plus metoprolol (p < 0.05). Resting MBF declined in proportion to cardiac work by approximately 20% from 0.61 +/- 0.09-0.51 +/- 0.10 ml/g/min (p < 0.05). In contrast, hyperemic MBF increased when metoprolol was added to dipyridamole (1.86 +/- 0.27-2.34 +/- 0.45 ml/g/min; p < 0.05). The decrease in resting MBF together with the increase in hyperemic MBF resulted in a significant increase in the myocardial flow reserve during metoprolol (3.14 +/- 0.80-4.61 +/- 0.68; p < 0.01). CONCLUSION: The beta 1 receptor blockade increases coronary vasodilatory capacity and myocardial flow reserve. However, the mechanisms accounting for this finding remain uncertain.

Adrenergic beta-Antagonists↗
PubMed1997

Compartment model for measuring myocardial oxygen consumption using [1-11C]acetate.

UNLABELLED: Although [1-11C]acetate has been validated as a PET tracer for myocardial oxygen consumption (MVO2) in animals and humans, mono- and biexponential fitting of the tissue time-activity curve yields only estimates of MVO2. This study attempts to develop and validate a simple tracer kinetic model in vivo for estimation of regional MVO2. METHODS: Twenty-seven experiments were performed in 12 anesthetized dogs with [1-11C]acetate and serial PET images under different MBF and MVO2 (baseline, ischemia, xylazine, dobutamine and dipyridamole). Estimates of MVO2 were obtained from dynamic [1-11C]acetate PET and model fitting. MBF was measured by radiolabeled microspheres, and MVO2 was calculated by the Fick method using arterial and coronary blood samples. RESULTS: The proposed model fitted equally well for all study conditions with a multiple correlation coefficient of 0.985 +/- 0.026. Estimated MVO2 correlated linearly with measured MVO2 (y = 0.033 + 0.690x, r = 0.92, s.e. of estimates = 0.020). CONCLUSION: This study indicates that MVO2 can be assessed with PET and [1-11C]acetate over a wide range with a simple tracer kinetic model.

Acetates↗
PubMed1996

Effects of dobutamine stimulation on myocardial blood flow, glucose metabolism, and wall motion in normal and dysfunctional myocardium.

BACKGROUND: This investigation examines the effects of inotropic stimulation on myocardial blood flow (MBF) and glucose metabolism (MRGlc) in dysfunctional myocardium through the use of positron emission tomography (PET). METHODS AND RESULTS: Nineteen patients with chronic coronary artery disease and 12 normal volunteers were studied with 13N-ammonia, 18F-deoxyglucose, and PET and with two-dimensional echocardiography at baseline and during intravenous dobutamine (5 to 10 micrograms/kg per minute). At rest, MBF in mismatch regions (n = 10) averaged 0.53 +/- 0.19 mL/g per minute and increased by 41.4 +/- 46.6% (P = .01) during dobutamine, whereas in match regions (n = 16) MBF was 0.28 +/- 0.09 mL/g per minute at rest without an increase during dobutamine (26.4 +/- 47.3%; NS). Myocardium with normal rest MBF was classified as normal remote (normal wall motion, n = 8) or abnormal remote (abnormal wall motion, n = 11). Dobutamine raised MBF similarly in normal subjects and in normal remote regions (by 82 +/- 85% and 84 +/- 42%, P < .01) but by only 33 +/- 34% in abnormal remote regions. MRGlc declined by 49 +/- 28% (P < .005) with dobutamine in the normal subjects, remained unchanged in normal and abnormal remote regions of the patients, but increased in mismatch and match regions (by 49 +/- 74% and 46 +/- 77%; P < .05). Wall motion improved with dobutamine only in mismatch and abnormal remote regions but not in match regions. CONCLUSIONS: Blood flow-metabolism mismatch patterns are not consistently associated with a fixed downregulation of MBF; the increased contractile work in response to dobutamine stimulation is associated with an increase in MBF and a greater reliance on glucose utilization, possibly reflecting acute ischemia or alterations in substrate selection by chronically dysfunctional myocardium. Importantly, functionally impaired though normally perfused myocardium frequently exists in chronic coronary artery disease patients and may represent repetitively stunned or, more likely, remodeled left ventricular myocardium.

Adult↗
PubMed1996

Noninvasive quantification of myocardial blood flow in humans. A direct comparison of the [13N]ammonia and the [15O]water techniques.

BACKGROUND: [13N]Ammonia has been validated in dog studies as a myocardial blood flow tracer. Estimates of myocardial blood flow by [13N]ammonia were highly linearly correlated to those by the microsphere and blood sample techniques. However, estimates of myocardial blood flow with [13N]ammonia in humans have not yet been compared with those by an independent technique. This study therefore tested the hypothesis that the [13N]ammonia positron emission tomographic technique in humans gives estimates of myocardial blood flow comparable to those obtained with the [15O]water technique. METHODS AND RESULTS: A total of 30 pairs of positron emission tomographic flow measurements were performed in 30 healthy volunteers; 15 volunteers were studied at rest and 15 during adenosine-induced hypermia. Estimates of average and of regional myocardial blood flow by the [13N]ammonia and the [15O]water approaches correlated well (y = 0.02 + 1.02x, r = .99, P < .001 SEE = 0.023 for average and y = 0.06 + 1.00x, r = .97, P < .001, SEE = 0.025 for regional values) over a flow range of 0.45 to 4.74 mL.min-1.g-1. At rest, mean myocardial blood flow was 0.64 +/- 0.09 mL.min-1.g-1 for [13N]ammonia and 0.66 +/- 0.12 mL.min-1.g-1 for [15O]water (P = NS). For adenosine-induced hyperemia, mean myocardial blood flow was 2.63 +/- 0.75 mL.min-1.g-1 for [13N]ammonia and 2.73 +/- 0.77 mL.min-1.g-1 for [15O]water (P = NS). The coefficient of variation as an index of the observed heterogeneity of myocardial blood flow averaged, for [13N]ammonia, 9 +/- 4% at rest and 12 +/- 7% during stress and, for [15O]water, 14 +/- 11% at rest and 16 +/- 9% during stress. The coefficients of variation for [15O]water were significantly higher than those for [13N]ammonia (P = .004 at rest and P = .03 during stress). CONCLUSIONS: The two approaches yield comparable estimates of myocardial blood flow in humans, which supports the validity of the [13N]ammonia method in human myocardium previously shown only in animals. However, the [15O]water approach reveals a greater heterogeneity (presumably method-related), which might limit the accuracy of sectorial myocardial blood flow estimates in humans.

Adenosine↗
PubMed1996

Dobutamine positron emission tomography: absolute quantitation of rest and dobutamine myocardial blood flow and correlation with cardiac work and percent diameter stenosis in patients with and without coronary artery disease.

OBJECTIVES: This study sought to measure myocardial blood flow at rest and during dobutamine infusion and to correlate flow with cardiac work and severity of coronary artery disease. BACKGROUND: Dobutamine is used with cardiac imaging to induce possible ischemia in patients with known or suspected coronary artery disease. Positron emission tomography permits noninvasive quantitation of myocardial blood flow. METHODS: Fifteen patients with quantitative coronary arteriography were studied at rest and during dobutamine infusion using nitrogen-13 ammonia flow imaging with positron emission tomography. Myocardial blood flow was determined in regions corresponding to the three major coronary arteries for myocardium with and without dobutamine flow defects and with and without a > 50% diameter stenosis. RESULTS: Eight patients had at least one dobutamine flow defect; four of whom had a previous myocardial infarction. One patient with > 50% diameter stenosis had no flow defects, and one with < 50% diameter stenosis (48%) had one defect. Dobutamine significantly increased myocardial blood flow in regions with and without a dobutamine flow defect or > 50% diameter stenosis, with a greater increase when a defect or > 50% diameter stenosis was not present. Rest and dobutamine flows in regions without > 50% diameter stenosis were 0.93 +/- 0.20 (mean +/- SD) and 2.16 +/- 0.52 ml/min per g (p < 0.01), respectively. The corresponding flows in regions without a defect were 0.94 +/- 0.21 and 2.17 +/- 0.53 ml/min per g (p < 0.01), respectively. This 2, 4-fold increase in flow was significantly correlated (p < 0.001) with a 2.2-fold increase in rate-pressure product induced by dobutamine. The rest and dobutamine flows for regions subtended by a vessel with > 50% diameter stenosis were 0.70 +/- 0.33 and 1.20 +/- 0.54 ml/min per g (p < 0.05), respectively, whereas the corresponding values for regions with a dobutamine flow defect were 0.69 +/- 0.33 ml/min per g at rest and 1.23 +/- 0.54 ml/min per g during dobutamine (p < 0.05). Dobutamine increased flow inversely proportional to percent diameter stenosis. The rest flow for regions with a dobutamine flow defect were not significantly different from that in regions without defects. CONCLUSIONS: Dobutamine resulted in a significant increase in myocardial blood flow that correlated significantly with both increased cardiac work and degree of stenosis.

Adult↗
PubMed1996

Myocardial viability: methods of assessment and clinical relevance.

Myocardial hibernation is hypoperfused dysfunctional myocardium that has the potential to recover function after coronary revascularization. Although recovery of regional function after revascularization is the gold standard for assessing the diagnostic accuracy of various techniques, improvements of EF, symptoms, and survival are fundamental end points. Despite important differences in the markers of viability by positron-emission tomography, single-photon emission tomography, two-dimensional echocardiography, and magnetic resonance imaging, their positive and negative predictive values in nonrandomized studies are fairly comparable. Assessment of myocardial viability may be clinically important in many patients but especially in those with EF < 30% and congestive heart failure. The degree of improvement in EF after coronary revascularization depends on the extent of hibernation, the suitability of coronary structure for revascularization, the lack of perioperative infarction, the completeness of revascularization, and the long-term patency of grafts.

Cardiac Catheterization↗
PubMed1996

Inhibition of glyceraldehyde-3-phosphate dehydrogenase in post-ischaemic myocardium.

OBJECTIVE: Myocardial reperfusion following brief period of ischaemic is associated with prolonged, reversible periods of metabolic dysfunction. As the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is inhibited in vitro by reactive oxygen species, we hypothesized that production of reactive oxygen species during reperfusion would lead to inhibition of GAPDH in post-ischaemic myocardium. METHODS: Anaesthetized closed-chest-dogs were subjected to 20 min balloon occlusion of the left anterior descending coronary artery. Biopsy samples were taken after 3 and 24 h of reperfusion, to determine the activity of GAPDH and the concentrations of glycolytic intermediates in post-ischaemic and remote, non-ischaemic territories. RESULTS: A significant reduction in GAPDH activity was observed in post-ischaemic relative to remote tissue after 3 h reperfusion (4.8 +/- 0.5 vs. 2.9 +/- 0.2 mumol/min/mg protein; P < 0.01). Western blotting revealed no reduction in the levels of GAPDH protein. Analysis of enzyme kinetics showed the loss of activity to be associated with decreased Vmax (5.9 +/- 0.5 vs. 3.2 +/- 0.2 mumol/min/mg protein; P < 0.01) with no significant change in the Km for glyceraldehyde-3-phosphate (GAP). Incubation of the inhibited enzyme under both mild and strong reducing conditions failed to reactivate the enzyme. The acute reduction in enzyme activity in post-ischaemic tissue was accompanied by regional differences in glycolytic intermediates, notably a twofold accumulation of GAP (P < 0.05), and a reduction in the glucose metabolic rate (GMR) determined by positron emission tomography and [18F]2-fluorodeoxyglucose. By 24 h reperfusion, no regional differences in GAPDH activity, reaction Vmax or Km, GAP concentrations or GMR were detectable. CONCLUSIONS: These results suggest that inhibition of GAPDH activity may represent an important point at which glycolysis is limited during reperfusion, and further, that the mechanisms of enzyme inhibition do not involve simple oxidation or S-thiolation of critical active site thiol groups.

Animals↗
PubMed1996

Reproducibility of measurements of regional resting and hyperemic myocardial blood flow assessed with PET.

UNLABELLED: PET with 13N-ammonia permits the noninvasive quantification of myocardial blood flow (MBF) in humans. The present study was done to assess the reproducibility of quantitative blood flow measurements at rest and during pharmacologically induced hyperemia in healthy individuals. METHODS: Thirty healthy volunteers (26 men, 4 women) were studied. Paired measurements of MBF at rest (n = 21), during adenosine (n = 15) and during dipyridamole (n = 7) were performed using a two-compartment model for 13N-ammonia PET. The mean difference between baseline and follow-up blood flow (% difference) was calculated to assess reproducibility. RESULTS: No significant difference was observed between resting blood flow at baseline or follow-up (15.8% +/- 15.8%; p = ns). Baseline and follow-up resting blood flow were linearly correlated (r = 0.63, p < 0.005). Normalization of resting blood flow to the rate pressure product improved the reproducibility significantly (15.8% +/- 15.8% versus 10.1% +/- 10.5%, p < 0.05). Baseline and follow-up hyperemic myocardial blood flow did not differ (11.8% +/- 9.4%; p = ns) and were linearly correlated (r = 0.69, p < 0.0005). CONCLUSION: MBF at rest can be measured reproducibly with 13N-ammonia PET. The individual response to pharmacologic stress appears to be relatively consistent. Thus, serial blood flow measurements with 13N-ammonia PET can be used to quantify the effect of various interventions on MBF and vasodilatory reserve.

Adenosine↗
PubMed1996

Derivation of input function from FDG-PET studies in small hearts.

UNLABELLED: The extraction of pure arterial time-activity curves (TACs) from dynamic PET images of a small animal heart using factor analysis of dynamic structures (FADS) was found to be unsuccessful due to the small size of the cardiac chamber that causes extensive mixture of TACs of different structures. METHODS: In this study, we used digital phantoms of the left ventricle (LV cavity size: 1-2 cm) and small monkey (LV cavity size: approximately 2 cm) dynamic FDG PET studies to evaluate FADS for extracting the pure blood-pool TACs by adding a single blood sample (taken at a late scan time) constraint. RESULTS: In the digital phantom studies, spillover fractions in the extracted blood-pool TACs using FADS without a blood sample constraint (FADS(-)) and with a blood sample constraint (FADS(+)) were 3%-91% and < 3%, respectively. In the monkey studies (n = 4), FADS(+) extracted blood-pool TACs matched well with the arterialized well counter measurements (% differences of curve integration; FADS(-) < 82%; FADS(+) < 9%). The microparameters (K1*, k2*, k3*, k4*) and macroparameters (Knlr), obtained from the FADS(+) blood-pool TACs, were similar to those obtained from plasma samples in a three-compartment model fitting (% differences of Knlr:phantom studies < 5%; monkey studies < 9%). CONCLUSION: The FADS technique with a single-blood sample has the potential to extract the pure blood-pool TACs directly from dynamic PET images of a small animal without multiple blood sampling, region of interest definition or spillover correction.

Animals↗
PubMed1996

Coronary vasodilatory capacity is impaired in patients with dilated cardiomyopathy.

Increases in wall stress because of left ventricular enlargement and/or alterations in coronary vasomotor tone might affect myocardial blood flow and vasodilatory capacity in patients with dilated cardiomyopathy. To test this hypothesis myocardial blood flow was measured at rest and during intravenous administration of dipyridamole (0.56 mg/kg) using dynamic nitrogen 13-ammonia positron emission tomography (two-compartment model) in 10 patients with dilated cardiomyopathy (mean left ventricular ejection fraction 28 +/- 8% 1 woman, 9 men; 47 +/- 13 years of age). Ten age and gender matched healthy volunteers served as controls. Coronary artery disease was ruled out by coronary angiography and left ventricular hypertrophy by two dimensional-echocardiography. Baseline heart rate (70 +/- 13 v 64 +/- 12 bpm), systolic blood pressure (111 +/- 20 v 114 +/- 12 mm Hg) and rate pressure product (7,686 +/- 1264 v 7,306 +/- 1,645) were similar in patients and controls. During dipyridamole administration, the rate pressure product increased similarly in both groups. Myocardial blood flow at rest did not differ between groups of patients and volunteers (0.69 +/ -0.27 v 0.67 +/- 0.17 mL/g/min) but correlated with the rate pressure product only in controls (myocardial blood flow, 0.18 + 0.000068214; rate pressure product, .67; P < .05). Hyperemic myocardial blood flow was lower in patients (1.57 +/- 0.39 v 1.92 +/- 0.31 mL/g/min, p < .05, whereas myocardial flow reserve did not differ between groups of patients and controls (2.57 +/- 1.15 v 3.02 +/- 0.94). Coronary vasodilatory capacity is reduced in patients with severe nonischemic cardiomyopathy. Increases in extravascular compressive forces or increased serum catecholamine levels, which in turn induce coronary vasoconstriction, might account for this finding.

Adult↗