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Lipomatous hypertrophy of interatrial septum is a very rare condition associated with supraventricular arrhythmias and sudden death. The authors describe two clinical cases of lipomatous hypertrophy and underline usefulness of multiplane transesophageal echocardiography in the diagnosis of this affection.

Despite the increasing number of reports on lipomatous hypertrophy of interatrial septum, a standardization of measurement of the dimensions of the interatrial septum (IAS) in the different phases of cardiac cycle has not been reported. Moreover, no data on modification of thickness with age and in specific cardiac diseases are available.Our purpose was to study whether the changes of thickness and thinning of IAS may be related to age, left atrial dimension, cardiac cycle and different cardiac diseases.248 patients (mean age 52.7 +/- 19.9 years) underwent transthoracic (TTE) and transesophageal (TEE) echocardiography. IAS was measured at the constant regions anterior and posterior to the fossa ovalis. IAS thickness (tk), thinning (th) and % thinning (% th) were measured.IAS thickness ranged from 4 to 13 mm at the time of ventricular end-systolic phase (mean 6.7 +/- 1.9 mm) and from 6 to 16 mm at the time of atrial systole (mean 9.9 +/- 1.8 mm); significant statistical difference between these values was found (P0.01). IAS thinning ranged from 1 to 7 mm (mean 3.42 +/- 1.8) while % IAS thinning from 18 to 76% (mean 36.53 +/- 16.36%). Statistical analysis showed a significant positive correlation between age and ventricular end-systolic thickness and atrial systolic thickness and thinning. An insignificant correlation was found between age and % IAS thinning and between left atrial dimension and IAS tk and th.Our results demonstrate that IAS thickness increases by age; no correlation exists between IAS thinning and age. There is no difference between IAS thickness and thinning in patients with or without cardiac disease. We believe that the thickness of IAS can be considered hypertrophic only if it exceeds the value of 15 mm during both ventricular end-systolic and atrial systolic phases of the cardiac cycle. IAS thickness and thinning might be an additional parameter to evaluate systolic atrial function particularly with regard to maintenance of synus rhythm after conversion from atrial fibrillation as well as to better understand its role in determining the filling of ventricles in different clinical conditions.

In order to assess the left ventricular systolic function we studied by echo 14 pts (8M, 6F) with complete atrioventricular septal defect (AVSD) who had undergone surgical repair. Mean age was 20.30 +/- 24.63 months, with a follow-up of 52.85 +/- 19.11%; in 6 pts Down syndrome was associated. Particularly, we tried to determine whether the following factors might affect the post-operative left ventricular systolic function: a) Down syndrome; b) residual mild mitral regurgitation; c) age of the surgical repair; d) length of the follow-up. As load-independent indexes of contractility, the left ventricular end systolic stress (LVESS)-circumferential fibre shortening velocity normalized for heart rate (VCFc) relationship and the LVESS/end systolic volume index (ESVI) ratio were chosen. All pts showed normal (mean +/- 2 standard deviations) or slightly higher values of LVESS/VCFc relationship; significantly, the only two pts with lower values had later undergone surgical repair. LVESS/ESVI ratio confirmed an inverse relationship between systolic function and age of the surgical correction (r = -0.75); no other factors (Down syndrome, residual mild mitral regurgitation, length of the follow-up) showed a significant correlation with the post-operative left ventricular systolic function. In conclusion, in our limited population, the age of the surgical repair appears to be the main factor affecting the post surgical left ventricular systolic function in pts with complete AVSD.

Twenty-five hypertensive patients (13 males/12 females) with left ventricular hypertrophy (LVH) and 12 hypertensive patients (6 males/6 females) without LVH were studied. Both groups were matched for age, sex, body mass index, percentage body fat, arterial BP and known duration of hypertension. After a seven day wash-out period from antihypertensive treatment each subject underwent: (1) an oral glucose tolerance test, (2) an euglycemic hyperinsulinaemic glucose clamp (insulin infusion rate 7.1 pM/kg per min), (3) an echocardiographic determination of left ventricular mass index, and (4) 24h ECG Holter monitoring. All tests were performed in random order and on different days. All investigators were unaware of the patient groups. Hypertensive patients with LVH had lower fasting intracellular (erythrocyte) magnesium concentrations (1.85 +/- 0.06 vs. 2.07 +/- 0.04 mM; P0.001) but higher fasting plasma insulin concentrations (86 +/- 4 vs. 59 +/- 5 pM; P0.001) Glucose clamp study demonstrated a lower insulin-mediated glucose disposal (24.8 +/- 0.4 vs. 30.1 +/- 0.3 microM/kg of lean body mass per min; P0.05) and a net change in intracellular magnesium accumulation (17.9 +/- 1.3 vs. 27.3 +/- 1.8%, P0.01) in response to insulin infusion in hypertensive patients with LVH than in those without LVH. After adjustment for fasting plasma insulin levels and insulin-mediated glucose uptake, fasting and insulin-mediated erythrocyte magnesium accumulation were no longer different between the two groups. In conclusion, hypertensive patients with LVH compared with those without LVH have a lower intracellular magnesium content due a higher degree of insulin resistance.

Introduction Microbubbles (MBs) or cavitation is high-velocity, echo-bright findings present during the closing or opening of a mechanical valve (MVP). Cavitation bubble growth or gas emboli are less frequently described. We evaluated the hemodynamic parameters involved in the formation of gas emboli and the impact of gas emboli on requests for additional investigations. Methods and results Transthoracic echocardiographic studies (TTE) of 57 patients (31 males, mean age 46.8 ± 13.8 years) with gas emboli were evaluated after heart valve replacement surgery. The majority (72%, n = 42) had a mitral or combined mitral/aortic MVP, with 28% (n = 16) an aortic MVP. The last TTE with and without gas emboli were considered for the same patient and the no emboli group was the control group (42 patients). The patient's blood pressure (BP) and heart rate (HR) were available for each TTE. Comparing the two TTEs, the systolic and diastolic BP, transmitral and aortic gradients, and left ventricular ejection fraction were similar but the HR (80.9 ± 18.7 vs 72.5 ± 13.9 bpm, P = .02) was significantly higher in the group with gas emboli. A TEE was performed 52 times in 27 patients, due to gas emboli, with one case positive for thrombus/vegetation. For 19 patients, a brain CT was requested. In two patients, the indication for the brain CT was gas emboli but the result was negative. Conclusion Gas emboli are frequently present and associated to an increased HR. They can cause the misdiagnosis of endocarditis or thrombus formation with significant additional requests for diagnostic examinations.

Left ventricular (LV) adaptation to aging is currently poorly understood. We aimed to characterize age related changes in LV structure and function by studying a large group of healthy subjects across a wide age range. Prospectively enrolled healthy volunteers (n = 778, 327 females; age 18 to 100 years, mean age 49.8 ± 18.1 years), were divided into 4 age groups: 18 to 34 years (n = 165); 35 to 49 years (n = 242), 50 to 79 years (n = 334) and ≥ 80 years (n = 40). All subjects underwent clinical examination, as well as comprehensive transthoracic echocardiogram [TTE]. Body mass index, systolic blood pressure (BP), and left atrial volume (p < 0.0001) increased with age while diastolic BP (p < 0.0001) decreased over time. LV mass/body surface area (BSA) and relative wall thickness increased with age (p < 0.0001) coincident with worsening parameters of diastolic function (E/A and E/Em, p < 0.0001). The ejection fraction and Sm did not change significantly. Stroke volume, ejection time index, flow rate and stroke work significantly increased with age (p < 0.01). The arterial elastance (Ea), a measure of ventricular afterload, and ventricular elastance (Ees), an index of LV systolic stiffness did not change with age nor did their ratio (Ees/Ea) the latter being an expression of ventricular-arterial coupling. Age, gender and LVM were the main independent variables associated with LV systolic function. In conclusion, LV adaptation to aging in a healthy cohort is characterized by concentric LV remodeling, increased contractility and preserved ventricular-arterial coupling.

The management of patent foramen ovale (PFO) still remains controversial. According to the newest scientific evidences, the assessment of the PFO size and the shunt has paramount importance for further management [1]. Although two-dimensional (2D) transesophageal (TE) echocardiography (E) contrast study has been considered to be the gold standard imaging modality for diagnosing PFO for a long time, new evidences underscore that its accuracy may have been over-valued [1,2]. Three-dimensional (3D) TEE imaging has emerged as a diagnostic technique that overcome some of the limitations of 2DE. 3D TEE allows an anatomical imaging for a comprehensive echocardiographic assessment of the left atrium, atrial septum and of PFO morphology [3,4]. However, it has never been reported about its diagnostic usefulness in detecting the bubbles passage during contrast study. We report a case where it has been possible to detect the passage of bubbles across the PFO thanks to 3D TEE.

BRACKGROUND: The most important determinant of long-term survival in patients with idiopathic pulmonary fibrosis is the right ventricular (RV) adaptation to the increased pulmonary vascular resistance. Our aim was to explore RV contractile reserve during stress echocardiography in early-stage IPF.METHOD: Fifty early-stage patients with IPF and 50 healthy control patients underwent rest and stress echocardiography, including RV two-dimensional speckle tracking echocardiography. At peak exertion, blood gas analysis and spirometry were also assessed.RESULTS: At rest, RV diameters were mildly increased in IPF; however, although RV conventional systolic function indexes were similar between the IPF and control groups, RV global longitudinal strain and RV lateral wall longitudinal strain (LWLS) were significantly reduced in the IPF cohort. During physical exercise, patients with IPF showed a reduced exercise tolerance with lower maximal workload (P < .01), level of oxygen saturation (P < .001), and peak heart rate (P < .01). Systolic and diastolic BP values were similar in both groups. Systolic pulmonary artery pressure (PAPs) increase (Delta PAPs) during exertion was higher in IPF vs healthy subjects (P < .0001); RV LWLS increase (Delta RV LWLS) during exercise was lower in patients with IPF vs control patients (P < .00001). By multivariable analysis, RV LWLS at rest and Delta RV LWLS were directly related to peak exertion capacity, PAPs, and blood oxygen saturation level (Spo(2) ; P < .0001). Delta RV LWLS was directly related to diffusion lung carbon monoxide (P < .0001).CONCLUSION RV myocardial dysfunction is already present at rest in early-stage IPF and worsens during exertion as detected by two-dimensional speckle-tracking echocardiography. The RV altered contractile reserve appears to be related to reduced exercise tolerability and impaired pulmonary hemodynamic.

Antihypertensive efficacy, effects on left ventricular mass index (LVMI) and tolerability of telmisartan, an angiotensin II receptor blocker, were compared with those of hydrochlorothiazide (HCTZ). Adult patients with mild-to-moderate hypertension and an optimal acoustic window by two-dimensional echocardiography were randomised at baseline to 12 months' double-blind, once-daily treatment with telmisartan 80 mg or HCTZ 25 mg. Two-dimensional echocardiography and freehand precordial three-dimensional echocardiography and 24-h ambulatory blood pressure monitoring were performed at baseline and after treatment. Of the 41 telmisartan group patients and 28 HCTZ group patients, 40 and 25, respectively, completed the study. Following treatment, 24-h mean SBP (telmisartan 157 +/- 11 vs 133 +/- 7 mmHg, P

Thirty elderly (mean +/- SEM: 73.8 +/- 2.1 y) nondiabetic, moderately obese (body mass index = 28.3 +/- 0.6 kg/m2) patients with stable effort angina underwent an oral-glucose-tolerance test and a euglycemic hyperinsulinemic glucose clamp before and after vitamin E supplementation (900 mg/d for 4 mo). The study was of a randomized, placebo-controlled, double-blind, and crossover design. Anthropometric indexes were stable throughout the study. Despite similar fasting and 2-h plasma glucose concentrations, vitamin E administration (compared with placebo) lowered fasting (88 +/- 14 and 68 +/- 9 pmol/L, P < 0.02) and 2-h (348 +/- 43 and 263 +/- 28 pmol/L, P < 0.05) plasma insulin concentrations, plasma triglyceride concentrations (1.34 +/- 0.06 and 1.07 +/- 0.03 mmol/L, P < 0.05), and the ratio of plasma LDL to HDL cholesterol (7.64 +/- 0.31 and 5.52 +/- 0.38, P < 0.02). Vitamin E administration was associated with higher nonoxidative glucose metabolism (18.1 +/- 0.5 and 10.6 +/- 0.7 mumol.kg lean body mass-1.min-1, P < 0.03) than was placebo administration during the euglycemic glucose clamp. We conclude that chronic intake of pharmacological doses of vitamin E might be useful in the therapy of elderly insulin-resistant patients with coronary heart disease.

Introduction: Atrial remodelling, leading to atrial fibrillation (AF), is mediated by the renin.angiotensin.aldosterone system. Methods: Mild hypertensive outpatients (systolic/diastolic blood pressure 140.159/90.99 mmHg) in sinus rhythm who had experienced . 1 electrocardiogram (ECG)-documented AF episode in the previous six months received randomly telmisartan 80 mg/day or carvedilol 25 mg/day. Blood pressure and 24-hour ECG were monitored monthly for one year; patients were asked to report symptomatic AF episodes and to undergo an ECG as early as possible. Results: One hundred and thirty-two patients completed the study (telmisartan, n=70; carvedilol, n=62). Significantly fewer AF episodes were reported with telmisartan versus carvedilol (14.3% vs. 37.1%; p

Ten healthy subjects and 30 non-insulin-dependent (type II) diabetic patients matched for age, gender ratio, body mass index, lean body mass (LBM), waist to hip ratio, and arterial blood pressure volunteered for the study. In all subjects, fasting plasma free radical (O2-) levels and basal membrane lipid fluidity (MLF) and protein mobility (MPM) were determined. The whole group of subjects underwent a euglycemic hyperinsulinemic glucose clamp with simultaneous indirect calorimetry for substrate oxidation determination. Diabetic patients versus controls displayed higher fasting plasma glucose (8.3 +/- 0.4 v 5.1 +/- 0.4 mmol/L, P +/- .001), O2- (0.48 +/- 0.02 v 0.16 +/- 0.02 mumol/L x min), and hemoglobin A1c ([HbA1C] 7.9% +/- 0.4% v 5.7% +/- 0.3%, P < .03) levels and a stronger reduction in basal MLF (0.243 +/- 0.006 v 0.318 +/- 0.009, P < .003) and basal MPM (0.348 +/- 0.003 v 0.518 +/- 0.010, P < .002). Whole-body glucose disposal (WBGD) and oxidative and nonoxidative glucose metabolism were also significantly lower in diabetics than in controls. In diabetic patients (n = 30), plasma O2- levels correlated with basal MLF (r = -.59, P < .005), basal MPM (r = -.84, P < .001), fasting plasma insulin level (r = .51, P < .004), WBGD (r = -.53, P < .002), and nonoxidative (r = -.45, P < .01) glucose metabolism. In conclusion, our results demonstrate that a relationship between plasma O2- levels and insulin action occurs in non-insulin-dependent diabetics.

Twenty elderly (77 +/- 0.4 y), nonobese [body mass index (in kg/m2) 26.4 +/- 0.5] subjects with normal glucose tolerance were submitted to a euglycemic hyperinsulinemic (3.5 pmol.min/kg) glucose clamp in a double-blind, crossover, randomized procedure after 4 mo treatment with either vitamin E (900 mg d-alpha-tocopherol/d, Ephynal; Roche, Milan, Italy) or placebo. Body mass index was practically unchanged throughout the study. After the glucose clamp, insulin-mediated stimulation 2 of whole-body glucose disposal (18.4 +/- 0.5 vs 26.1 +/- 0.6 mumol.min/kg lean body mass P < 0.02) was significantly potentiated by vitamin E rather than placebo administration. Furthermore, net changes in plasma vitamin E concentrations correlated with net changes in insulin-stimulated whole-body glucose disposal (r = 0.60 P < 0.003). Plasma vitamin E concentrations seem to play an important role in the modulation of insulin action in elderly people.

BACKGROUND Many studies have shown a significant association between the magnitude of insulin resistance and the plasma insulin levels in non-diabetic patients. It has also been shown that all major cardiovascular risk factors are associated with the presence of hyperinsulinemia or insulin resistance. However, studies have not addressed the possible metabolic differences in insulin action that can occur in patients with and without coronary heart disease (CHD) but with a superimposable cluster of risk factors. METHODS Three groups of patients matched for age, sex, and lean body mass, but different in their absence of risk factors (group A; n = 8), presence of risk factors but no clinical and electrocardiographic signs of CHD (group B; n = 12), and the presence of risk factors, family history of CHD, and clinical and electrocardiographic signs of CHD (group C; n = 14) volunteered for the study. Patients in groups B and C were also matched for main risk factors. All patients were submitted to a euglycemic hyperinsulinemic glucose clamp during which a an infusion of 3H-glucose and indirect calorimetry facilitated the determination of glucose turnover parameters and substrate oxidation. RESULTS Patients with CHD (group C) had the highest fasting plasma insulin levels (98 +/- 13 pmol/l) compared with patients in group B (86 +/- 4 pmol/l; P < 0.05) and in group A (63 +/- 4 pmol/l; P < 0.05) and the lowest insulin-mediated stimulation in non-oxidative glucose metabolism. Fasting lipid oxidation was similar in the three groups, but a stronger insulin-mediated inhibition in the control patients (group A) was found. Multiple regression analysis of the pooled data from the patients in groups B and C (n = 26) demonstrated that all risk factors considered correlated (t = 1.58, P < 0.04) with total body glucose disposal (TBGD) and accounted for 77% of the variability in TBGD. Furthermore, a separate analysis for groups B and C demonstrated a different contribution of all risk factors (89% and 65% for groups B and C, respectively) to the variability in TBGD. In group C patients, a multiple logistic regression analysis encompassing all risk factors studied, but also the family history of CHD, explained 92% of the variability in TBGD. CONCLUSION In patients with and without CHD but with similar risk factors, a significant reduction in non-oxidative glucose metabolism occurs; nevertheless, such impaired glucose handling seems to be worsened in the presence of CHD. Further studies will be needed to determine the cause of such differences.

Mitral annular calcium (MAC) is a condition that often occurs in patients with systemic hypertension. To evaluate the effectiveness of nifedipine in preventing MAC, 223 patients with systemic hypertension of recent onset and without MAC were selected and randomly enrolled in 3 groups: group 1 (76 patients) received nifedipine; group 2 (72 patients) received enalapril; and group 3 (75 patients) received atenolol. After 5 years, these treatments significantly reduced systolic (p0.001) and diastolic (p0.05) blood pressure (BP) in 3 treated groups. M-mode echocardiography revealed MAC only in 2 patients in the nifedipine group (2.6%), in 13 in the enalapril group (18%) and in 15 in the atenolol group (20%). The degree of MAC was mild (5 mm) in the 2 patients in group 1, in 5 of the 13 in group 2, and in 6 of the 15 in the group 3, whereas it was severe (5 mm) in the remaining 8 in the enalapril group and in the other 9 in the atenolol group. There was also a significant correlation in the degree of MAC, left atrial enlargement and mitral regurgitation. In addition, atrial fibrillation and atrioventricular conduction defects were associated with severe MAC. These results indicate that nifedipine is an effective drug both in the long-term management of systemic hypertension and in preventing or delaying MAC.

In 3231 prosthetic valves implanted between January 1975 and November 1990, we observed 61 cases of prosthetic obstruction of biological origin with clinical and laboratory findings of severe functional impairment which required surgery as emergency treatment. The hospital mortality was 19.67% (12/61). The obstruction was due to a primary thrombosis in all 5 bioprostheses which were not anticoagulated and in 11/56 (19.64%) mechanical prostheses of which 3 were not anticoagulated and 4 were not properly anticoagulated. The obstruction was due to fibrous tissue overgrowth in the other 45 mechanical prostheses (80.35%) with secondary thrombosis in 34 cases (60.71%) and no thrombosis in 11 (19.64%); 71.11% of these prostheses were adequately anticoagulated. Of the 61 obstructed prostheses, 53 were mitral and 8 were aortic. No tricuspid obstruction was observed. A statistical assessment by multiple correspondence, cluster and chi square analysis was performed in two groups of patients with different models of mechanical mitral prostheses. The 5-year actuarial incidence of obstruction was 6.08%. Significant risk factors were: tilting disc prostheses, prostheses without pyrocarbon coating, large prostheses, tilting disc prostheses with a small orifice posteriorly oriented, atrial fibrillation, enlarged left atrium, time from implant greater than 4 years, age between 40 and 50 years. In our opinion, prosthetic obstruction may be referred to a primary thrombosis only in cases where it may be prevented by adequate anticoagulation. In most cases, the obstruction is produced by periprosthetic fibroblastic proliferation which may develop in spite of adequate anticoagulation in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

BACKGROUND: The hypothesis that left ventricular hypertrophy regression in hypertension relates to blood pressure (BP) control and to non-antihypertensive activity of some drugs was tested by comparing the effects of telmisartan and carvedilol on 24-h mean ambulatory BP and left ventricular mass (LVM) regression, measured using three-dimensional echocardiography (3-DECHO) and magnetic resonance imaging (MRI). METHODS: A total of 82 patients with mild-to-moderate hypertension and an optimal echocardiographic acoustic window were randomized to receive once-daily telmisartan 80 mg or carvedilol 25 mg for 44 weeks. RESULTS: Ten patients withdrew from the study because office diastolic BP remained >90 mm Hg. The 24-h mean ambulatory systolic/diastolic BP reductions were similar in both treatment groups (telmisartan, from 159.6 +/- 10.2/97.8 +/- 5.4 to 128.6 +/- 6.5/78.2 +/- 5.8 mm Hg; carvedilol, from 157.8 +/- 11.1/95.7 +/- 11.9 to 128.2 +/- 5.6/78.7 +/- 5.2 mm Hg). However, night-time and last 6-h mean BP reductions were nonsignificantly greater with telmisartan. Using 3-DE, telmisartan (P< .001) and carvedilol (P< .001) progressively reduced LVM index by 21.97 +/- 5.84 (15.7%) and 12.31 +/- 3.14 (9.1%) g/m2, respectively, at week 44. Similar magnitudes of reductions were observed using MRI (15.5% and 9.6%, respectively). Reductions in LVM index achieved with telmisartan were statistically superior to carvedilol (P< or = .001). CONCLUSIONS: The superior LVM regression with telmisartan versus carvedilol suggests telmisartan has a mechanism that may be beyond that of lowering BP in hypertensive patients.

In hypertensive patients the presence of left ventricular (LV) hypertrophy has been associated with a more severe degree of insulin resistance. Whether myocardial wall thickness or LV geometry are associated with a different degree of insulin resistance is still unknown in essential hypertensives. For this reason 26 men with new diagnosed essential hypertension were enrolled. All patients underwent echocardiographic examination and euglycemic hyperinsulinemic glucose clamp combined with indirect calorimetry. According to LV mass and relative wall thickness data, all patients were categorized in four groups: 1) patients with a normal geometric LV pattern (n = 8) (PAT = 0); 2) patients with concentric remodeling LV mass (n = 8) (PAT = 1); 3) patients with eccentric LV hypertrophy (n = 3) (PAT = 2); and 4) patients with concentric LV hypertrophy (n = 7) (PAT = 3). All groups were similar for anthropometric characteristics. Patients with normal echocardiographic LV pattern (PAT = 0) had higher whole body glucose disposal (WBGD), oxidative and nonoxidative glucose metabolism, and lower lipid oxidation than patients with abnormal echocardiographic LV patterns (PAT = 1 to 3). Nevertheless, no significant differences among the groups with abnormal echocardiographic patterns were found. After controlling for age, body mass index (BMI), waist/hip ratio (WHR), and mean arterial blood pressure, only sum of the wall thickness was significantly correlated with fasting plasma insulin (r = -0.38, P < .05), WBGD (r = - 0.50, P < .009), and NOGM (r = - 0.48, P < .02). In multivariate analysis, a model made by age, BMI, WHR, systolic and diastolic blood pressure, and WBGD explained 38% of the echocardiographic pattern variability. In this model, WBGD (P < .02) was significantly and independently associated with echocardiographic patterns explaining 19% of the echocardiographic pattern variability. In conclusion, our data demonstrate that in arterial hypertension hyperinsulinemia/insulin resistance mainly affects myocardial wall thickness, whereas only a trivial association with LV geometry occurs.

Hypertensive patients with left ventricular hypertrophy (LVH) have a higher degree of hyperinsulinaemia than hypertensive patients without LVH. Obese patients with LVH have also been demonstrated to have a very low glucose disappearance rate after an intravenous glucose bolus. No studies have investigated the difference in insulin action and substrate oxidation in hypertensive patients with and without LVH. For this reason 36 subjects were enrolled for our study: (1) healthy control subjects (n = 10); (2) hypertensive patients without LVH (n = 12); and (3) hypertensive patients with LVH (n = 14). All subjects underwent an oral glucose tolerance test (OGTT, 75 g of glucose) and a euglycaemic hyperinsulinaemic glucose clamp (insulin infusion rate, 7.1 pmol (kg min)-1 for 120 min). In this latter test indirect calorimetry allowed substrate oxidation determination. Echocardiographic methods allowed LVH assessment. Hypertensive patients with LVH had the lowest insulin-mediated nonoxidative glucose metabolism compared to hypertensive patients without LVH (P < 0.01) and to healthy subjects (P < 0.001). In the whole group of hypertensive patients (n = 26), partial correlations showed left ventricular mass index (LVMI) associated with fasting plasma insulin levels (r = 0.44 P < 0.005), insulin-mediated whole body glucose disposal (r = -0.41 P < 0.01) and nonoxidative glucose metabolism (r = -0.33 P < 0.04) independently of age, body weight, systolic blood pressure and plasma catecholamines levels. In conclusion, our data provide evidence that LVH in hypertensive patients is associated with a worsening in nonoxidative glucose metabolism.

Congestive heart failure is a condition associated with increased plasma norepinephrine levels, which have been demonstrated to impair glucose handling. In the present study, 10 patients suffering from congestive heart failure and 10 healthy age- and body mass index-matched subjects were submitted to a hyperinsulinemic (insulin infusion rate, 0.5 mU/kg.min-1) glucose clamp, while simultaneous D-3H-glucose infusion and indirect calorimetry allowed for determination of glucose turnover parameters and substrate oxidation, respectively. On a separate day, basal local (myocardial) indirect calorimetry was also performed. Our data demonstrate that in congestive heart failure, fasting myocardial glucose oxidation (Gox) was inhibited with a simultaneous increase in lipid oxidation (Lox). In our patients, a significant decrease in total-body insulin-stimulated glucose metabolism (31.0 +/- 0.5 v 20.3 +/- 0.4 mumol/kg.min-1, P < .01) and nonoxidative glucose metabolism (18.9 +/- 1.1 v 11.0 +/- 0.5 mumol/kg.min-1, P < .05) was also found. Such latter changes were also associated with a simultaneous overdrive of Lox (0.4 +/- 0.2 v 1.9 +/- 0.2 mumol/kg.min-1, P < .02) that was correlated with an enhanced availability of plasma free fatty acids (FFAs).

In aged healthy (n = 10) and non-insulin-dependent (type II) diabetic (n = 10) subjects matched for age [67.3 +/- 0.5 vs. 68.0 +/- 0.4 yr, P = not significant (NS)], body mass index (25.7 +/- 0.7 vs. 26.0 +/- 0.2 kg/m2, P = NS), gender ratio [6 males (M)/4 females (F) vs. 5 M/5 F], and mean arterial blood pressure (104 +/- 6 vs. 105 +/- 9 mmHg, P = NS), we determined the changes in insulin secretion and action after vitamin C infusion and the relative increase in plasma vitamin C levels. At the highest vitamin C infusion rate (0.9 mmol/min) the increase in plasma vitamin C levels did not affect B cell response to glucose, but it improved Conard's K values and whole body glucose disposal in healthy subjects and in diabetic patients. In both groups of subjects vitamin C-mediated increase in insulin action was mainly due to an improvement in nonoxidative glucose metabolism. After fasting, plasma vitamin C levels correlated with basal whole body glucose disposal (r = -0.44, P < 0.05; n = 20). After vitamin C infusion, percent change in plasma vitamin C level correlated with the percent decline in membrane microviscosity (r = 0.53, P < 0.01; n = 20) and increase in whole body glucose disposal (r = 0.63, P < 0.003; n = 20). In conclusion, plasma vitamin C levels seem to play a role in the modulation of insulin action in aged healthy and diabetic subjects.

In forty healthy subjects with normal glucose tolerance divided by age into four groups (group A, subjects with mean age25 years [n = 10]; group B, subjects with mean age40 years [n = 9]; group C, subjects with mean age60 years [n = 11]; group D, subjects with mean age75 years [n = 10]) and were matched for body mass index (BMI), lean body mass (LBM), mean arterial blood pressure, and sedentary life style, we determined the plasma O2- production, reduced to oxidized glutathione level ratio (GSH/GSSG), and plasma membrane microviscosity. Euglycemic hyperinsulinemic (1 mU/kg.min-1 for 120 minutes) glucose clamp with simultaneous D-3-H glucose infusion and indirect calorimetry allowed determination of glucose turnover parameters and substrate oxidation. In the oldest group of subjects, a significant increase in plasma O2-production and membrane microviscosity associated with a significative reduction in glucose disappearance rate (Rd), total body glucose disposal (TBGD), and nonoxidative glucose metabolism was found. In group D subjects (n = 10), all of these changes were correlated with one another. In a multiple regression analysis of the pooled data from all study subjects (n = 40), only plasma O2- production levels displayed a statistically significant relation with TBGD and nonoxidative glucose metabolism. In conclusion, in aged patients a significant relationship between free radical production and insulin action seems to exist.