Aortopulmonary fistula caused by an infected thoracic aortic false aneurysm rupturing after endovascular stent placement.

We report a case of 74-year-old man presenting with a rupture of a thoracic aortic false aneurysm after undergoing conventional total arch replacement for aortic arch aneurysm (62 mm) and endovascular stent placement for descending aortic aneurysm (70 mm). His chief complaints at the present admission were fever and sensation of dyspnea and we put him on a course of antibiotics for stent graft infection. However he died of massive hemoptysis. From a standpoint of autopsy findings, a thoracic aortic false aneurysm formed at the just proximal landing zone owing to type Ia endoleak, and simultaneously stent graft infection lead to make fistula formation between the false aneurysm and the lung. We examined ourselves that stent graft infection and aortopulmonary fistula caused by an infected thoracic aortic false aneurysm rupturing into the lung should be promptly treated such as complete removal of the stent and another revascularization in a reasonable period of time except if there are complications such as comorbid1ities or withholding of consent. We experienced and reported one rare case associated with a rupture of thoracic aortic false aneurysm caused by stent graft infection and the fistulization between the lung and the stent graft.

[Fungal endocarditis found at onset of lower limb acute aortic occlusion; report of a case].

Fungal endocarditis caused by Candida species is associated with high morbidity and mortality. A combination of surgical resection and antifungal drug therapy is the golden standard for treatment. We reported a case of fungal endocarditis due to Candida lusitaniae found at onset of lower limb acute aortic occlusion cured by emergency operation. This case suggests that Candida endocariditis can be managed medically with antifungal drug therapy in life time.

Inhibition of carnitine synthesis modulates protein contents of the cardiac sarcoplasmic reticulum Ca2+-ATPase and hexokinase type I in rat hearts with myocardial infarction.

It was previously reported that inhibition of carnitine synthesis by 3-(2,2,2-trimethyl-hydrazinium) propionate (MET-88) restores left ventricular (LV) systolic and diastolic function in rats with myocardial infarction (MI). Preservation of the calcium uptake function of sarcoplasmic reticulum Ca2+-ATPase (SERCA2) is one of the possible mechanisms by which MET-88 alleviates hemodynamic dysfunction. To test this hypothesis, the effects of MET-88 on protein content of SERCA2 were evaluated using the same rat model of heart failure. Myocardial protein content of hexokinase, which is one of the key enzymes of glucose utilization, was also measured. Either MET-88 (MET-88 group) or a placebo (MI group) was administered for 20 days to rats with MI induced by coronary artery ligation. The control group underwent sham surgery (no ligation) and received placebo. In LV myocardial homogenates, the myocardial SERCA2 protein content was 32% lower (p<0.05) in the MI group than in the control group. However, in the MET-88 group myocardial SERCA2 content was the same as in the control group. Hexokinase I protein content was 29 % lower (p<0.05) in the MI group compared with the control. In contrast, hexokinase II protein content did not differ significantly among the three groups. Consequently, inhibition of carnitine synthesis ameliorates depression of SERCA2 and hexokinase I protein content which may reduce tissue damage caused by MI.

End-tidal CO2 pressure decreases during exercise in cardiac patients: association with severity of heart failure and cardiac output reserve.

OBJECTIVES: We measured end-tidal CO2 pressure (PETCO2) during exercise and investigated the relationship between PETCO2 and exercise capacity, ventilatory parameters and cardiac output to determine the mechanism(s) of changes in this parameter. BACKGROUND: It is unclear whether PETCO2 is abnormal at rest and during exercise in cardiac patients. METHODS: Cardiac patients (n = 112) and normal individuals (n = 29) performed exercise tests with breath-by-breath gas analysis, and measurement of cardiac output and arterial blood gases. RESULTS: PETCO2 was lower in patients than in normal subjects at rest and decreased as the New York Heart Association class increased, whereas the partial pressure of arterial CO2 did not differ among groups. Although PETCO2 increased during exercise in patients, it remained lower than in normal subjects. PETCO2 in relation to cardiac output was similar in patients and normal subjects. PETCO2 at the respiratory compensation point was positively correlated with the O2 uptake (r = 0.583, p < 0.0001) and the cardiac index at peak exercise (r = 0.582, p < 0.0001), and was negatively correlated with the ratio of physiological dead space to the tidal volume. The sensitivity and specificity of PETCO2 to predict an inadequate cardiac output were 76.6% and 75%, respectively, when PETCO2 at respiratory compensation point and a cardiac index at peak exercise that were less than the respective control mean-2 SD values were considered to be abnormal. CONCLUSIONS: PETCO2 was below normal in cardiac patients at rest and during exercise. PETCO2 was correlated with exercise capacity and cardiac output during exercise, and the sensitivity and specificity of PETCO2 regarding decreased cardiac output were good. PETCO2 may be a new ventilatory abnormality marker that reflects impaired cardiac output response to exercise in cardiac patients diagnosed with heart failure.

[Idiopathic cardiomyopathy: pathophysiology and hemodynamics].

Idiopathic cardiomyopathy is classified into three categories, namely, hypertrophic, dilated and restrictive cardiomyopathy. Pathophysiology and hemodynamics are quite different between the three types of cardiomyopathies. Hypertrophic cardiomyopathy is hemodynamically characterized by outflow obstruction and diastolic dysfunction. In dilated cardiomyopathy, progressive dilatation and systolic dysfunction of the left ventricle are predominant. This left ventricular remodeling is strongly associated with neurohormonal activation occurred in this disease. In restrictive cardiomyopathy, left ventricular distensibility is markedly impaired and differential diagnosis from constrictive pericarditis is often difficult.

Detection of exogenous growth hormone (GH) administration by monitoring ratio of 20kDa- and 22kDa-GH in serum and urine.

We previously demonstrated that individual subjects have fairly constant ratios of serum concentrations of 20 kDa- (20K) and 22 kDa-GH (22K). The aim of this study is to demonstrate the possibility of utilizing the changes in the ratio of 20K/22K for detecting the exogenous administration of 22K. A male patient with idiopathic dilated cardiomyopathy (age 51) received 22K (4U, s.c.) every other day. The concentrations of 20K and 22K in serum and urine were measured using enzyme-linked immunosorbent assays before and after administration. The administration of 22K increased total GH concentration, and markedly decreased the ratio of 20K/22K in serum, especially 2-10 h after the administration. From calculations, it became clear that the concentration of exogenous 22K reached a peak between 2-4 h after the administration and decreased to a negligible level after 24 h. The ratio of 20K/22K in the 0-24 h urine was 5 times lower than that in the 24-48 h urine. These data suggest that, by monitoring the ratio of 20K/22K in serum or urine, it is possible to determine whether or not GH has been externally administered and to calculate the serum GH that has been administered.

Analysis of nitric oxide in the exhaled air of patients with chronic glomerulonephritis.

BACKGROUND: Nitric oxide (NO) plays an important role in renal hemodynamics and function. Although production of NO in the glomeruli has been found to be increased in animal models of glomerulonephritis, it remains unclear whether its endogenous production is enhanced in patients with chronic glomerulonephritis (CGN). SUBJECTS AND METHODS: We measured NO output in exhaled air as an indicator of its local production in the lungs and plasma and urinary nitrite plus nitrate (NO2-/NO3-) levels as indicators of its production in the whole body in 21 patients with CGN in 31 healthy controls. RESULTS: The patients exhaled higher concentrations of NO (29.5 +/- 1.4 vs. 18.7 +/- 1.0 parts per billion (ppb), mean +/- SEM, p < 0.0001) and exhaled NO output was also higher than in controls (166.6 +/- 6.8 vs. 95.5 +/- 5.6 nl/min/m2, p < 0.0001). Plasma NO2-/NO3- concentrations were also significantly greater in the patients than in the controls (81.6 +/- 7.2 vs. 41.1 +/- 4.3 micromol/l, p < 0.001). In patients with CGN, exhaled NO output correlated negatively with creatinine clearance (r = -0.62, p < 0.05). Oral administration of prednisolone (60 mg/day) for two weeks did not significantly affect the exhaled NO output in the patients (160 +/- 7 vs. 200 +/- 30 nl/min/m2, p = NS) despite a decrease in urinary protein excretion (12.0 +/- 2.9 vs. 1.4 +/- 0.6 g/day, p < 0.01). CONCLUSION: These findings suggested that endogenous NO production is increased in patients with CGN. Increased endogenous NO production may play some pathophysiological role in these patients.

Insulin action on heart and skeletal muscle FDG uptake in patients with hypertriglyceridemia.

UNLABELLED: Abnormal heart and skeletal muscle 18F-fluorodeoxyglucose (FDG) uptake in patients with insulin resistance has been demonstrated. Although the existence of whole-body insulin resistance has been reported in hypertriglyceridemics, its specific role in heart and skeletal muscle FDG uptake in hypertriglyceridemics has not been clarified. METHODS: We compared heart and skeletal muscle FDG uptake using PET and the whole-body glucose disposal rate (GDR) during insulin clamping in 17 hypertriglyceridemics and 12 age-matched control subjects to increase our knowledge of whole-body insulin resistance and its relationship to heart and skeletal muscle FDG uptake in hypertriglyceridemics. RESULTS: GDR was significantly reduced in hypertriglyceridemics compared with control subjects (4.50 +/- 1.37 mg/min/kg versus 10.0 +/- 2.97 mg/min/kg, P = 0.00001), as were the skeletal muscle FDG Ki = (k1 x k3)/(k2 + k3) (SFKi: 0.007 +/- 0.003 mL/min/g versus 0.018 +/- 0.01 mL/min/g, P = 0.0001) and skeletal muscle FDG uptake ([SMFU] 0.725 +/- 0.282 mg/min/100 g versus 1.86 +/- 1.06 mg/min/100 g, P = 0.00023). However, myocardial FDG Ki (MFKi) tended to be reduced in hypertriglyceridemics compared with that in control subjects (0.062 +/- 0.017 mL/min/g versus 0.068 +/- 0.015 mL/min/g), but the difference was statistically insignificant (P = 0.3532). Moreover, myocardial FDG uptake (MFU) in hypertriglyceridemics (6.47 +/- 1.72 mg/min/100 g) tended to be reduced compared with that in control subjects (6.97 +/- 1.73 mg/min/100 g), but the difference was statistically insignificant (P = 0.4485). GDR was significantly correlated with SFKi (r = 0.69, P = 0.0022), SMFU (r = 0.612, P = 0.009), MFKi (r = 0.57, P = 0.0174) and MFU (r = 0.505, P = 0.0385) in hypertriglyceridemics. CONCLUSION: Both heart and skeletal muscle glucose utilization were related to insulin resistance in hypertriglyceridemics. However, the less severe reduction in MFU (compared with SMFU) suggests that myocardium may have a mechanism to oppose insulin resistance in hypertriglyceridemics.

Improvement of impaired myocardial vasodilatation due to diffuse coronary atherosclerosis in hypercholesterolemics after lipid-lowering therapy.

BACKGROUND: Diminished myocardial vasodilatation (MVD) in hypercholesterolemics without overt coronary stenosis has been reported. However, whether the diminished MVD of angiographically normal coronary arteries in hypercholesterolemics can be reversed after lipid-lowering therapy is not known. METHODS AND RESULTS: A total of 27 hypercholesterolemics and 16 age-matched controls were studied. All patients had >1 normal coronary artery, and those segments that were perfused by anatomically normal coronary arteries were studied. Myocardial blood flow (MBF) was measured during dipyridamole loading and at baseline using positron emission tomography and 13N-ammonia, after which MVD was calculated before and after lipid-lowering therapy. Total cholesterol was significantly higher in hypercholesterolemics (263+/-33.8) than in controls (195+/-16.6), and it normalized after lipid-lowering therapy (197+/-19.9). Baseline MBF (ml. min-1. 100 g-1) was comparable among hypercholesterolemics (both before and after therapy) and controls. MBF during dipyridamole loading was significantly lower in hypercholesterolemics before therapy (189+/-75.4) than in controls (299+/-162, P<0.01). However, MBF during dipyridamole loading significantly increased after therapy (226+/-84.7; P<0.01). MVD significantly improved after therapy in hypercholesterolemics (2.77+/-1.35 after treatment [P<0.05] versus 2. 02+/-0.68 before treatment [P<0.01]), but it remained significantly higher in controls (3.69+/-1.13, P<0.01). There was a significant relationship between the percent change of total cholesterol and the percent change of MVD before and after lipid-lowering therapy (r=-0. 61, P<0.05). CONCLUSIONS: Diminished MVD of anatomically normal coronary arteries in hypercholesterolemics can be reversed after lipid-lowering therapy.

Kinetics of oxygen uptake at onset of exercise related to cardiac output, but not to arteriovenous oxygen difference in patients with chronic heart failure.

Patients with chronic heart failure performed exercise tests to evaluate the relation of kinetics of oxygen uptake to cardiac output and arteriovenous oxygen difference at the onset of exercise. The kinetics of oxygen uptake are primarily determined by cardiac output; these kinetics are useful in evaluating exercise intolerance and cardiac output response during exercise.

The sarcoplasmic reticulum Ca2+-ATPase (SERCA2) gene promoter activity is decreased in response to severe left ventricular pressure-overload hypertrophy in rat hearts.

The sarcoplasmic reticulum Ca2+-ATPase (SERCA2) pump plays a key role in the contraction-relaxation cycle of the myocardium by controlling the intracellular Ca2+ concentration. SERCA2 protein and mRNA expression levels, as well as, SR Ca2+ uptake function are depressed in hypertrophied and failing myocardium. At this time, the molecular mechanisms regulating SERCA2 gene transcription during hypertrophy and heart failure are not completely understood, especially in vivo. Direct gene transfer into adult cardiac tissue has recently been shown to be a useful technique to study in vivo gene regulation. In this study, SERCA2 promoter-luciferase (Luc) reporter constructs of various lengths were injected into the beating left ventricular apex of adult rats (groups = compensated hypertrophy, heart failure, and controls) and the expression level was analysed. Our SERCA2 promoter analyses revealed three positive regulatory regions between -1810 bp and -1110 bp, -658 bp and -284 bp, and -267 bp and -72 bp and a negative regulatory region between -1110 bp and -658 bp, important for in vivo expression in rat hearts. SERCA2 promoter activity was also assessed in rat hearts with compensated pressure-overload hypertrophy (induced by the DOCA-salt treatment) and heart failure (induced by severe ascending aortic constriction). In the DOCA-salt-induced hypertrophy model, SERCA2 promoter activity was similar to that of sham controls. In contrast, severe constriction of the ascending aorta decreased the expression of the -1810 Luc and -1110 Luc constructs by 92.8% and 64.3%, respectively. This study suggests that only severe pressure-overload hypertrophy produces a significant decrease in SERCA2 promoter activity, and the promoter region extending to -1810 bp is sufficient for the down regulation of SERCA2 gene expression.

Effect of inhaled nitric oxide on gas exchange in patients with congestive heart failure. A randomized, controlled trial.

BACKGROUND: Conventional vasodilators increase ventilation-perfusion mismatch and do not improve gas exchange even though they reduce pulmonary hypertension. However, the effects of nitric oxide inhalation on ventilatory and gas exchange values in patients with congestive heart failure are not known. OBJECTIVE: To investigate the effect of nitric oxide inhalation on gas exchange in patients with congestive heart failure. DESIGN: Randomized, controlled trial. SETTING: University hospital. PATIENTS: 16 patients with congestive heart failure (New York Heart Association class II or III). INTERVENTIONS: Patients inhaled nitric oxide gas at graded concentrations (n = 8) or were given intravenous isosorbide dinitrate, 2.5 mg (n = 8). MEASUREMENTS: Hemodynamic and ventilatory variables and blood gases were measured 5 minutes after inhalation of different doses of nitric oxide and 10 minutes after administration of isosorbide dinitrate. RESULTS: Nitric oxide inhalation reduced the mean pulmonary arterial pressure in a dose-dependent manner without altering the mean arterial pressure or cardiac output. At a dose of 40 parts per million, nitric oxide inhalation increased PaO2 (change from baseline, 12.0 mm Hg [95% CI, 2.3 to 21.7 mm Hg]; P = 0.014) and decreased the alveolar-arterial difference in partial pressure of oxygen (change, -8.6 mm Hg [CI, -16.8 to -0.4 mm Hg]; P = 0.038) and the ventilatory equivalent for carbon dioxide output (change, -6.7 [CI, -10.3 to -3.1]; P < 0.001). Although isosorbide dinitrate similarly decreased pulmonary arterial pressure, it did not alter gas exchange or ventilatory variables. CONCLUSIONS: Because nitric oxide inhalation improved gas exchange, it may be used as a supportive therapy when other conventional vasodilators worsen gas exchange.

Increased excretion of nitric oxide in exhaled air of patients with chronic renal failure.

Nitric oxide exerts multiple effects on renal function. It remains unclear whether endogenous nitric oxide production is increased or decreased in patients with chronic renal failure. To evaluate endogenous nitric oxide production in these patients we studied exhaled nitric oxide output by an ozone chemiluminescence method and plasma NO2(-)/NO3(-) levels by the Griess method in 40 patients with end-stage chronic renal failure who underwent regular continuous ambulatory peritoneal dialysis (n=30) or haemodialysis (n=10), and in 28 healthy subjects. Patients with chronic renal failure had a higher exhaled nitric oxide concentration [39+/-3 versus 19+/-1 parts per billion, (mean+/-S.E.M.), P<0.0001], a greater nitric oxide output (177+/-11 versus 96+/-7 nl.min-1.m-2, P<0.001) and a higher plasma NO2(-)/NO3(-) concentration (96+/-14 versus 33+/-4 micromol, P<0.01) than controls. These values did not differ between patients on haemodialysis and those on continuous ambulatory peritoneal dialysis. Patients with chronic renal failure had significantly higher plasma concentrations of both interleukin-1beta and interferon-gamma than controls. The exhaled nitric oxide output did not correlate with plasma NO2(-)/NO3(-) or with peritoneal dialysate NO2(-)/NO3(-), but plasma NO2(-)/NO3(-) correlated with dialysate NO2(-)/NO3(-) in patients who underwent continuous ambulatory peritoneal dialysis (r=0.77, P<0.01). Haemodialysis for 4 h acutely decreased plasma NO2(-)/NO3(-) (92+/-17 versus 50+/-8 micromol, P<0.05) and cGMP concentration (16.5+/-4.3 versus 5.1+/-1. 7 pmol/ml, P<0.01), but did not decrease exhaled nitric oxide output. The increase in exhaled nitric oxide with the simultaneous increase in circulating cytokines suggests that nitric oxide synthase seems to be induced significantly in patients with chronic renal failure. Increased endogenous nitric oxide production may have a pathophysiological role in patients with uraemia.

Role of positron emission tomography using fluorine-18 fluoro-2-deoxyglucose in predicting improvement in left ventricular function in patients with idiopathic dilated cardiomyopathy.

Improvement in left ventricular (LV) function in patients with idiopathic dilated cardiomyopathy (DCM) by medical treatment has been suggested. Thus, it is important to evaluate which patients will respond to medical therapy. Positron emission tomography (PET) with fluorine-18 fluoro-2-deoxyglucose (FDG) and cardiac catheterization were performed in 20 patients with DCM before the initiation of medical therapy. The regional myocardial glucose utilization rate (rMGU) was measured with FDG PET. Subjects were divided into two groups, group 1 (event-free patients, n=10) and group 2 (clinical cardiac events, n=10). Haemodynamic and PET parameters before the initiation of medication were compared between the two groups and between patients with and patients without improvement in LV function. Ejection fraction (EF) was significantly higher in group 1 (35.8%+/-9.0%) than in group 2 (24.8%+/-7.0%) and LV end-diastolic pressure (LVEDP) was significantly lower in group 1 (8.4+/-1.7 mmHg) than in group 2 (11.6+/-3.5 mmHg). Average rMGU (mg min-1 100 g-1) was similar in group 1 (11.2+/-2.5 mg min-1 100 g-1) and group 2 (11.2+/-2.9 mg min-1 100 g-1), while %CV of rMGU was significantly lower in group 1 (11.1%+/-6.3%) than in group 2 (29. 9%+/-13.9%, P<0.01). Furthermore, LV function normalized in seven patients in group 1. In these seven patients, EF (35.1%+/-10.9%), LVEDP (8.2+/-2.0 mmHg) and average rMGU (11.8+/-2.7 mg min-1 100 g-1) were comparable with those in patients without LV functional improvement (EF: 31.6%+/-9.1%; LVEDP: 10.7+/-3.3 mmHg; average rMGU: 10.8+/- 2.7 mg min-1 100 g-1). However,% CV of rMGU in patients with LV functional improvement (9.6%+/-5.6%) was significantly lower than in those without such improvement (26.3%+/-14.1%, P<0.01). %CV of rMGU <13.6% predicted prognosis with a sensitivity of 80%, a specificity of 100% and an accuracy of 90%. %CV of rMGU <13.6% also predicted improvement in LV function, with a sensitivity of 75%, a specificity of 92% and an accuracy of 85%. However, EF failed to predict improvement of LV function. In is concluded that homogeneous myocardial glucose utilization rate can predict both prognosis and improvement in LV function achieved by medical therapy in patients with DCM.

Comparison of unitary displacements and forces between 2 cardiac myosin isoforms by the optical trap technique: molecular basis for cardiac adaptation.

To provide information on the mechanism of cardiac adaptation at the molecular level, we compared the unitary displacements and forces between the 2 rat cardiac myosin isoforms, V1 and V3. A fluorescently labeled actin filament, with a polystyrene bead attached, was caught by an optical trap and brought close to a glass surface sparsely coated with either of the 2 isoforms, so that the actin-myosin interaction took place in the presence of a low concentration of ATP (0.5 micromol/L). Discrete displacement events were recorded with a low trap stiffness (0.03 to 0.06 pN/nm). Frequency distribution of the amplitude of the displacements consisted of 2 gaussian curves with peaks at 9 to 10 and 18 to 20 nm for both V1 and V3, suggesting that 9 to 10 nm is the unitary displacement for both isoforms. The duration of the displacement events was longer for V3 than for V1. On the other hand, discrete force transients were recorded with a high trap stiffness (2.1 pN/nm), and their amplitude showed a broad distribution with mean values between 1 and 2 pN for V1 and V3. The durations of the force transients were also longer for V3 than for V1. These results indicate that both the unitary displacements and forces are similar in amplitude but different in duration between the 2 cardiac myosin isoforms, being consistent with the reports that the tension cost is higher in muscles consisting mainly of V1 than those consisting mainly of V3.

Impaired myocardial vasodilation during hyperemic stress with dipyridamole in hypertriglyceridemia.

OBJECTIVES: This study sought to investigate the specific role of hypertriglyceridemia in the myocardial hyperemic stress with dipyridamole/rest flow ratio (MDR). BACKGROUND: Reduced MDR has been reported in hypercholesterolemic patients without evidence of ischemia. However, the specific role of hypertriglyceridemia in MDR has not been studied. METHODS: Fifteen nondiabetic normocholesterolemic hypertriglyceridemic patients and 13 age-matched control subjects were studied. Myocardial blood flow (MBF) during dipyridamole administration and baseline MBF in hypertriglyceridemic patients and control subjects were measured using positron emission tomography and nitrogen-13 ammonia, after which the MDR was calculated. RESULTS: Baseline MBF (ml/min per 100 g heart weight) in hypertriglyceridemic patients (mean +/- SD 73.6 +/- 24.1) did not differ significantly from that in control subjects (81.6 +/- 37.2). MBF during dipyridamole loading in hypertriglyceridemic patients (198 +/- 106) was significantly reduced compared with that in control subjects (313 +/- 176, p < 0.05), as was the MDR (2.71 +/- 1.07 vs. 3.73 +/- 1.14, respectively, p < 0.05). Spearman rank-order correlation analysis showed a significant relation between plasma triglyceride concentration and MDR (r = -0.466, asymptotic SE 0.157, p = 0.0125); however, no such significant relation was seen between total plasma cholesterol concentration and MDR (r = -0.369, asymptotic SE 0.130, p = 0.059). CONCLUSIONS: Impaired myocardial vasodilation was suggested in hypertriglyceridemic patients without symptoms and signs of ischemia.

Organ-specific insulin resistance in patients with noninsulin-dependent diabetes mellitus and hypertension.

UNLABELLED: Abnormal heart and skeletal muscle glucose metabolism in diabetes or essential hypertension has been demonstrated. However, the role of hypertension in heart and skeletal muscle glucose utilization in diabetes has not been clarified yet. METHODS: We compared heart and skeletal muscle glucose utilization using PET and the whole-body glucose disposal rate (GDR) during insulin clamping in 9 patients with noninsulin-dependent diabetes mellitus (NIDDM) and essential hypertension and 11 patients with NIDDM without hypertension to examine the effect of hypertension on heart and skeletal muscle glucose utilization. Results also were compared with those for 8 asymptomatic healthy control participants. RESULTS: Skeletal muscle glucose utilization rate was comparable between hypertensive NIDDM patients (61.2 +/- 55.5 micromol x min(-1) x kg(-1)) and normotensive NIDDM patients (50.9 +/- 25.2 micromol x min(-1) x kg(-1)) but was significantly reduced in both groups compared with control subjects (94.2 +/- 57.3 micromol x min(-1) x kg(-1)), as was the GDR (25.2 +/- 11.3 and 24.0 +/- 7.5 micromol x min(-1) x kg(-1)), respectively, for patients compared with 38.5 +/- 11.5 micromol x min(-1) x kg(-1) for control participants). However, the myocardial glucose utilization (MGU) rate was significantly reduced in NIDDM patients without hypertension (389 +/- 185 micromol x min(-1) x kg(-1)) than in those with hypertension (616 +/- 86.4 micromol x min(-1) x kg(-1), p < 0.01). Multivariate stepwise regression analysis has shown that MGU was significantly correlated with systolic blood pressure and plasma free fatty acid concentration. CONCLUSION: Whole-body insulin resistance was observed in NIDDM patients independent of hypertension. The MGU rate may have different properties to oppose insulin resistance than glucose utilization of skeletal muscle in hypertensive patients with NIDDM.