Lean tissue adjusted peak oxygen consumption in congestive heart failure.
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Adipose Tissue↗
Biomedical subjects
S D Anker
Publications and source records attributed to S D Anker.
Acquired growth hormone resistance in patients with chronic heart failure: implications for therapy with growth hormone.
OBJECTIVES: We aimed to determine whether growth hormone (GH) resistance is present in patients with chronic heart failure (CHF) and whether it may be linked to the biochemical response to GH treatment. BACKGROUND: Acquired GH resistance is a feature of severe illness, in particular, cachexia. In patients with CHF, the response to GH therapy appears to be variable. METHODS: Biochemical markers of the GH-insulin-like growth factor-I (IGF-I) axis were compared in 21 cachectic patients with CHF, 51 noncachectic patients and 26 healthy control subjects. In separate studies, the predictive value of baseline biochemical variables for the IGF-I response to GH treatment was analyzed. RESULTS: Cachectic patients showed an increase of total GH and immunologically intact GH (p < or = 0.0002) and a decrease of GH-binding protein (BP) (p = 0.005), IGF-BP3 (p = 0.01) and IGF-I (p = 0.06), compared with noncachectic patients. Similar changes were found when the cachectic group was compared with the control group. No differences were found between noncachectic patients and control subjects. Levels of GH-BP correlated with the IGF-I/GH ratio in all subgroups (all p < or = 0.002). Baseline GH-BP levels were related to the increase of IGF-I levels in response to GH treatment in patients with CHF after 24 h (r = 0.83, p = 0.005; n = 9; study 2), 44 days (r = 0.52, p = 0.007; n = 25; study 3) and 96 days (r = 0.54, p = 0.006; n = 24; study 3). CONCLUSIONS: Most cachectic and some noncachectic patients with CHF show features of acquired GH resistance. The principal predictors of the biochemical features of GH resistance and of the poor biochemical response to short-term and longer-term GH treatment are GH-BP plasma levels. The presence of GH resistance is potentially a major factor determining the response to GH therapy in patients with CHF.
Biomarkers↗
Preservation of exercise capacity and lack of peripheral changes in asymptomatic patients with severely impaired left ventricular function.
AIMS: To establish the extent, if any, of peripheral changes in asymptomatic patients with severe left ventricular dysfunction. METHODS ANS RESULTS: Nine asymptomatic and nine symptomatic patients with left ventricular ejection fraction, <25%, matched for age and left ventricular ejection fraction (asymptomatic vs symptomatic, age: 52+/-1.5 vs 55.9+/-2.5 years [Mean+/-SEM], left ventricular ejection fraction: 16+/-2 vs 19+/-2%P=0.23 and 0.48, respectively) were studied and compared with 26 age-matched normal controls. We assessed exercise capacity, leg blood flow (occlusion plethysmography), respiratory muscle strength, quadriceps maximal isometric strength, fatigue and CT cross-sectional muscle area at mid thigh. Fatigue was expressed as the percentage reduction in maximal strength following a 20 min fatiguing protocol. There was a graded increase in peak oxygen consumption comparing symptomatic, asymptomatic and control groups (16.6+/-1.3 vs 27.1+/-1.6 vs 32.8+/-1.3 ml x min(-1) x kg(-1)respectively, ANOVA P<0.0001). Between the three groups there was significant variation in muscle strength (P<0.0001), endurance (P=0.0002) and cross-sectional area (P=0.0003) and in peak blood flow (P=0.027) and respiratory muscle strength (P<0.05). When asymptomatic patients and controls were compared no significant differences existed. CONCLUSIONS: Patients with severe left ventricular dysfunction may have near normal exercise capacity and no peripheral changes. Exercise capacity may depend less upon left ventricular function than on the presence or absence of peripheral factors.
Exercise Test↗
The role of C-type natriuretic peptide in cardiovascular medicine.
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Animals↗
The 6-minute walk test and prognosis in chronic heart failure--the available evidence.
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Exercise Test↗
Ventricular assist device in severe heart failure: effects on cytokines, complement and body weight.
AIMS: Inflammatory and immune activation and body wasting are important features of end-stage chronic heart failure. It is not known whether restoration of cardiac output by assist device implantation can improve these abnormalities. METHODS: We studied 48 patients (39 males; age 45+/-2 years) with NYHA class IV heart failure. All patients underwent ventricular assist device implantation for end-stage heart failure as a bridge to cardiac transplantation. Plasma levels of tumour necrosis factor alpha, and its receptors, interleukin-6, elastase, activated complement, and soluble CD14 receptors were measured at the time of operation and in survivors at 1 week (n=46), 40 days (n=35) and 90 days (n=26). Follow-up was for a minimum of 1 year. RESULTS: One-year survival was 35% (95% CI: 22-49%). Body mass index was the only predictor of survival (body mass index >25 (n=16); survival 63 (39-86) %; body mass index <25 (n=32); survival 22 (7.5-36) %: P=0.003). Tumour necrosis factor alpha fell from 9.66+/-1.33 pg x ml(-1) to 4.2+/-1.0 at 1 week (P=0.008), but returned to pre-operative levels at 90 days. Interleukin-6, activated complement and elastase fell progressively to 40 days, but were rising at 90 days. There was no change in tumour necrosis factor receptor. There was a gradual rise in CD14 (3.99+/-0.15 microg x ml(-1) at baseline, 5.02+/-0.39 at 90 days, P=0.006). After surgery, body weight fell from 80+/-2 to 73+/-2 kg by 1 month (P<0.001) and to 72+/-2 kg at 90 days. CONCLUSIONS: Ventricular assist device implantation results in a short-term fall in tumour necrosis factor alpha and interleukin-6, but no change in CD14 or tumour necrosis factor receptor, suggesting that the pathophysiological process resulting in inflammation was not altered by left ventricular assist device implantation. Low body mass index is related to poor outcome after assist device implantation, and no weight gain.
Body Weight↗
Uric acid in cachectic and noncachectic patients with chronic heart failure: relationship to leg vascular resistance.
BACKGROUND: Chronic heart failure (CHF) is a hyperuricemic state, and capillary endothelium is the predominant site of xanthine oxidase in the vasculature. Upregulated xanthine oxidase activity (through production of toxic free radicals) may contribute to impaired regulation of vascular tone in CHF. We aimed to study the relationship between serum uric acid levels and leg vascular resistance in patients with CHF with and without cachexia and in healthy control subjects. METHODS: In 23 cachectic and 44 noncachectic patients with CHF (age, 62 +/- 1 years, mean +/- SEM) and 10 healthy control subjects (age, 68 +/- 1 years), we assessed leg resting and postischemic peak vascular resistance (calculated from mean blood pressure and leg blood flow by venous occlusion plethysmography). RESULTS: Cachectic patients, compared with noncachectic patients and control subjects, had the highest uric acid levels (612 +/- 36 vs 459 +/- 18 and 346 +/- 21 micromol/L, respectively, both P <.0001) and the lowest peak leg blood flow and vascular reactivity (reduction of leg vascular resistance from resting to postischemic conditions: 83% vs 88% and 90%, both P <.005). In all patients, postischemic vascular resistance correlated significantly and independently of age with uric acid (r = 0.61), creatinine (r = 0.47, both P <.0001), peak VO2 (r = 0.34), and New York Heart Association class (r = 0.33, both P <.01). This correlation was not present in healthy control subjects (r = -0.04, P =.9). In multivariate and stepwise regression analyses, serum uric acid emerged as the strongest predictor of peak leg vascular resistance (standardized coefficient = 0.61, P <.0001) independent of age, peak VO2, creatinine, New York Heart Association class, and diuretic dose. CONCLUSIONS: Hyperuricemia and postischemic leg vascular resistance are highest in cachectic patients with CHF, and both are directly related independent of diuretic dose and kidney function. The xanthine oxidase metabolic pathway may contribute to impaired vasodilator capacity in CHF.
Adult↗
Chronic heart failure in the very elderly: clinical status, survival, and prognostic factors in 188 patients more than 70 years old.
BACKGROUND: Chronic heart failure (CHF) is a frequent disease with a dismal prognosis, but little is known about survival in the very elderly. There are no data on the prognostic value of cardiopulmonary exercise testing in this population. We aimed to assess exercise capacity, survival, and prognostic parameters in elderly patients with CHF. METHODS: We evaluated 188 patients with CHF >70 years old (mean 77 +/- 4 years, range 70-94 years) seen at our heart failure clinic between March 1992 and June 1998. A cardiopulmonary exercise test was performed in 102 patients (peak VO2 15.3 +/- 4.7, VE/VCO2 slope 39.6 +/- 15.01). All patients were followed up for at least 12 months. The prognostic end point of the study was all-cause mortality. RESULTS: At the end of follow-up (16 +/- 10 mo, range 12-41 mo), 67 patients (35.6%) had died (1-year mortality rate 26% [95% confidence interval 20-32]). In univariate analysis New York Heart Association class (NYHA) (relative risk [RR] = 2.56, P <.0001), VE/VCO2 (RR = 1.041, P <.0001), peak VO2 (RR = 0.87, P =.0007), and fractional shortening (RR = 0.95, P <.0001) predicted mortality. Peak VO2 predicted mortality independently of age, NYHA class, and left ventricular ejection fraction. A subgroup of 12 patients with dynamic left ventricular outflow tract obstruction during stress had an excellent outcome, with a 100% survival at the end of follow-up (mean 16 +/- 7 mo, range 12-39 mo). CONCLUSIONS: The prognosis in elderly patients with CHF is poor. Valid exercise testing results can be obtained in more than 50% of elderly patients with CHF. NYHA class and peak VO2 are the strongest prognostic factors in this population.
Aged↗
Raised urinary glucocorticoid and adrenal androgen precursors in the urine of young hypertensive patients: possible evidence for partial glucocorticoid resistance.
OBJECTIVE: To evaluate urinary glucocorticoid excretion profiles in a cohort of recently diagnosed young hypertensive patients. METHODS: After excluding patients with secondary causes, 60 individuals with premature hypertension were recruited (diagnosed by ambulatory blood pressure monitoring before the age of 36 years). In addition, 30 older hypertensive controls (age of onset > 36 years, "middle aged hypertensive controls"), and 30 normal controls (age matched to the young hypertensive group) were studied. All provided 24 hour urine collections for mass spectrometry for total cortisol metabolites and total androgen metabolites by gas chromatography. RESULTS: Among male patients, those with premature hypertension had higher total urinary excretion of cortisol metabolites (mean (SD), 13 332 (6472) microg/day) than age matched normal controls (7270 (1788) microg/day; p = 0.00001) or middle aged hypertensive controls (8315 (3565) microg/day; p = 0.002). A similar increase was seen among the female patients, although the absolute concentrations were lower. There was no significant difference between middle aged hypertensive patients and normal controls. Urinary total androgen excretion profiles in female patients also showed an unusual increase in the premature hypertension group (2958 (1672) microg/day) compared with the other groups (middle aged hypertensive controls, 1373 (748) microg/day, p = 0.0003; normal controls, 1687 (636) microg/day, p = 0.002). In all subjects, serum sodium and creatinine concentrations were within the normal range; serum potassium concentrations were found to be low before the start of treatment. CONCLUSIONS: Individuals presenting with premature hypertension have an abnormally high excretion of glucocorticoid metabolites in the urine. While the mechanism remains uncertain, these findings are compatible with partial resistance of the glucocorticoid receptors, with a compensatory increase in cortisol and androgen metabolites. The mineralocorticoid effects of the latter (sodium and water retention) may contribute to an abnormally high blood pressure and may have implications for targeted selection of first line treatment in young hypertensive patients.
Adult↗
Wasting as an independent predictor of mortality in patients with cystic fibrosis.
BACKGROUND: Cystic fibrosis (CF) is the most common life threatening autosomal recessive disorder in the white population. Wasting has long been recognised as a poor prognostic marker in CF. Whether it predicts survival independently of lung function and arterial blood gas tensions has not previously been reported. METHODS: 584 patients with CF (261 women) of mean (SD) age 21 (7) years were studied between 1985 and 1996, all of whom were being followed up in a tertiary referral centre. Lung function tests, body weight, arterial blood oxygen (PaO(2)) and carbon dioxide (PaCO(2)) tensions were measured. The weight was calculated as a percentage of the ideal body weight for age, height, and sex. RESULTS: Forced expiratory volume in one second (FEV(1)) recorded at the start of the study was 1.8 (1.0) l (52 (26)% predicted FEV(1)), PaO(2) 9.8 (1.9) kPa, PaCO(2) 5.0 (0.9) kPa, and % ideal weight 92 (18)%. During the follow up period (45 (27) months) 137 patients died (5 year survival 72%, 95% CI 67 to 73). FEV(1), % predicted FEV(1), PaO(2), % ideal weight (all p<0.0001), and PaCO(2) (p=0.04) predicted survival. In multivariate analysis, % predicted FEV(1) (p<0.0001), % ideal weight (p=0.004), and PaCO(2) (p=0.02) were independent predictors of outcome. Patients with >85% ideal body weight had a better prognosis at 5 years (cumulative survival 84%, 95% CI 79 to 89) than those with < or =85% ideal weight (survival 53%, 95% CI 45 to 62), p<0.0001. Percentage predicted FEV(1) (area under curve 0.83; 95% CI 0.78 to 0.87) and % ideal weight (area under curve 0.74; 95% CI 0.68 to 0.79) were accurate predictors of survival at 5 years follow up (receiver-operating characteristic analysis). CONCLUSIONS: Body wasting is a significant predictor of survival in patients with CF independent of lung function, arterial blood oxygen and carbon dioxide tensions.
Adolescent↗
Leptin, insulin sensitivity and growth hormone binding protein in chronic heart failure with and without cardiac cachexia.
OBJECTIVE: Regulation of growth hormone (GH) receptor expression and hence tissue GH sensitivity may be important for the conflicting results found in treatment studies with recombinant growth hormone in chronic heart failure (CHF). Growth hormone-binding protein (GHBP) corresponds to the extracellular domain of the GH receptor and is closely related to measures of body composition and, specifically, to size of visceral fat tissue. Leptin, the adipocyte specific (ob) gene product, has been proposed as the signal linking adipose tissue and GHBP/GH-receptor expression. CHF has recently been shown to be a hyperleptinaemic and insulin-resistant state regardless of aetiology. This study aimed to examine the influence of leptin on GHBP in CHF patients with and without cardiac cachexia compared with healthy control subjects. METHODS: We studied 47 male patients with CHF (mean age 61+/-2 years, New York Heart Association (NYHA)-class 2.7+/-0.1, left ventricular ejection fraction (LVEF) 28+/-2%, peak oxygen consumption 16.8+/-0.9 ml/kg/min) and 21 male healthy controls of similar age. Of the CHF patients, 19 were cachectic (cCHF; non-oedematous weight loss >7.5% over at least 6 months) and 28 non-cachectic (ncCHF; similar for age and LVEF). Insulin sensitivity was assessed by an intravenous glucose tolerance test using the minimal model approach. RESULTS: Compared with healthy controls, patients had elevated levels of leptin (7.6+/-0.7 vs 4.8+/-0.7 ng/ml, P<0.05), insulin (76.2+/-8.9 vs 41.4+/-6.0 pmol/l, P<0.01), and reduced insulin sensitivity (2.43+/-0.2 vs 3.48+/-0.3 min(-1).microU.ml(-1).10(4), P<0.005) but similar GHBP levels (901+/-73 vs 903+/-95 pmol/l). Leptin levels were increased in ncCHF (9.11+/-1.0 ng/ml, P=0.001) but were not different from normal in cCHF (5.32+/-0.7 ng/ml, P>0.5). After correction for total body fat mass, both ncCHF and cCHF were hyperleptinaemic (41.8+/-3.8 and 37.9+/-0.38 vs 24.4+/-2.1 ng/ml/100 g, ANOVA P=0.001). In both patients and controls there was a direct correlation between leptin levels and GHBP (r=0.70 and r=0.71 respectively, both P<0.0001). This relationship was stronger than between GHBP and several parameters of body composition (body mass index (BMI), total and regional body fat mass or % body fat) and held true when sub-groups were tested individually (ncCHF r=0.62, P<0.001; cCHF r=0.79, P<0.0001). In multivariate regression analysis in all CHF patients, serum leptin levels emerged as the strongest predictor of GHBP, independent of age, BMI, total and regional fat mass or % body fat, fasting insulin level and insulin sensitivity. CONCLUSION: Fat mass corrected leptin levels are elevated in CHF patients with and without cachexia. Reduced total fat mass may account for lower leptin levels in cachectic CHF patients compared with non cachectic patients. Leptin strongly predicts GHBP levels in CHF regardless of its hyperleptinaemic state or severely altered body composition as in cardiac cachexia. Leptin could be the signalling link between adipose tissue and GHBP/GH receptor expression in CHF.
Adipose Tissue↗
The importance of tumor necrosis factor and lipoproteins in the pathogenesis of chronic heart failure.
Elevated levels of proinflammatory cytokines, such as tumor necrosis factor (TNF) and interleukin-6 (IL-6), have been demonstrated in patients with chronic heart failure (CHF). Evidence suggests that cytokines such as these may play a central role in the pathogenesis of this syndrome. TNF has several properties that are particularly detrimental in CHF, such as negatively inotropic effects, the promotion of left ventricular remodelling, and the induction of dilated cardiomyopathy in humans. Furthermore, TNF can cause skeletal muscle wasting and apoptosis, and, therefore, may be important in the development of cardiac cachexia. Although the precise stimulus for immune activation in CHF is unknown, one hypothesis is that endotoxin may be a significant trigger for cytokine release. This is supported by the finding that decompensated CHF patients have elevated endotoxin levels that normalize on diuretic therapy. The factors that influence endotoxin responsiveness in patients with CHF, in particular the potential importance of serum lipoproteins, will be discussed in this review.
Biomarkers↗
Plasma cytokine parameters and mortality in patients with chronic heart failure.
BACKGROUND: Inflammatory immune activation is an important feature in chronic heart failure (CHF). Little is known about the prognostic importance of tumor necrosis factor-alpha (TNF-alpha), soluble TNF-receptor 1 and 2 (sTNF-R1/sTNF-R2), interleukin-6 (IL-6), and soluble CD14 receptors (sCD14) in CHF patients. METHODS AND RESULTS: In 152 CHF patients (age 61+/-1 years, New York Heart Association [NYHA] class 2.6+/-0.1, peak VO(2) 17.3+/-0.6 mL. kg(-1). min(-1), mean+/-SEM) plasma concentrations of immune variables were prospectively assessed. During a mean follow-up of 34 months (>12 months in all patients), 62 patients (41%) died. Cumulative mortality was 28% at 24 months. In univariate analyses, increased total and trimeric TNF-alpha, sTNF-R1, and sTNF-R2 (all P</=0.0001), sCD14 (P=0.0007), and IL-6 (P=0.005) predicted 24-month mortality. With multivariate analysis and receiver operating characteristics, sTNF-R1 emerged among all cytokine parameters as the strongest and most accurate prognosticator in this CHF population, regardless of follow-up duration and independently of NYHA class, peak VO(2), VE/VCO(2) slope, left ventricular ejection fraction, and wasting (P<0.001). The receiver operating characteristic area under the curve for sTNF-R1 was greater than for sTNF-R2 at 6, 12, and 18 months (all P<0.05). CONCLUSIONS: sTNF-R1 was the strongest and most accurate prognosticator, independent of established markers of CHF severity. Assessment of sTNF-R1 may be useful in identifying patients who are at high risk of death and in monitoring patients undergoing anti-TNF-alpha treatment.
Adult↗
The endotoxin-lipoprotein hypothesis.
The advent of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins) has revolutionised the treatment of hypercholesterolaemia. Statin treatment, by lowering the atherogenic lipoprotein profile, reduces morbidity and mortality in patients with cardiovascular disease. Treatment with simvastatin causes a reduction of events of new-onset heart failure, but this may be attributable to properties other than its lipid-lowering effects. There is some evidence that lower serum cholesterol concentrations (as a surrogate for the totality of lipoproteins) relate to impaired survival in patients with chronic heart failure (CHF). Inflammation is a feature in patients with CHF and increased lipopolysaccharide may contribute substantially. We postulate that higher concentrations of total cholesterol are beneficial in these patients. This is potentially attributable to the property of lipoproteins to bind lipopolysaccharide, thereby preventing its detrimental effects. We hypothesise there is an optimum lipoprotein concentration below which lipid reduction would, on balance, be detrimental. We also propose that, in patients with CHF, a non-lipid-lowering statin (with ancillary properties such as immune modulatory and anti-inflammatory actions) could be as effective or even more beneficial than a lipid-lowering statin.
Animals↗
Echocardiographic determinants of mortality in patients >67 years of age with chronic heart failure.
This study sought to assess the prognostic significance of echocardiographic measurements of left and right ventricular dimensions and function in patients >67 years of age with chronic congestive heart failure (CHF). This is a retrospective follow-up of elderly patients who underwent an echocardiography in the tertiary cardiac center. A total of 185 patients (131 men) aged >/=68 years (mean +/- SD 75 +/- 5) with CHF were enrolled into the study. After undergoing a detailed echocardiographic examination, all patients were followed-up for a median of 20 months (interquartile range 9 to 36). During the follow-up period 54 patients (29%) died. Left ventricular (LV) M-mode isovolumic relaxation time (IVRT), end-diastolic and end-systolic diameters, fractional shortening and mass, transmitral E:A ratio, and left atrial dimension, as well as New York Heart Association class and the age were found by Cox proportional-hazards univariate analyses to predict the outcome in these patients (all p <0.05). In multivariate analyses including these measurements, LV IVRT (p <0.04), age (p <0.03), and New York Heart Association class (p <0.001) were found to be the independent predictors of outcome. In the Kaplan-Meier analysis, patients with LV IVRT >30 ms had a better prognosis at 3 years (cumulative survival 78% [95% confidence interval 65% to 91%]) than those with LV IVRT </=30 ms (survival 52% [95% confidence interval 37% to 68%]). Measurements of LV performance, especially those obtained during diastole, are significantly related to prognosis in patients >67 years of age with CHF. LV M-mode IVRT is among the most important independent predictors of outcome in this population.
Aged↗
Superiority of endothelin-1 over norepinephrine in exercise-induced alterations of the conduit artery tone of the non-exercised arm in patients with chronic heart failure.
This study is aimed at examining the relative importance of norepinephrine and endothelin-1 in treadmill exercise-induced changes in brachial arterial tone of the non-exercised arm in patients with chronic heart failure (CHF). Brachial artery diameter and blood flow were measured before and after exercise in eight healthy volunteers and 18 patients with stable chronic heart failure by high-resolution ultrasound. Maximal exercise resulted in brachial artery dilatation in controls (4.42+/-0.39 vs. 4.77+/-0.39 mm; P<0. 0001) in contrast to constriction seen in the patients (5.27+/-0.67 vs. 5.12+/-0.66 mm; P=0.07). Both groups demonstrated a significant increase in blood flow after exercise. The pre-exercise (2.83+/-0.76 vs. 1.69+/-0.15 pmol/l; P=0.0004), post-exercise (4.15+/-1.5 vs. 2. 02+/-0.34 pmol/l; P=0.0004) and the percent increase (47.15+/-32.5 vs. 19.0+/-10.5%; P=0.02) in endothelin-1 levels were significantly greater in patients than in controls. In contrast to endothelin-1, the exercise-induced percent increase in norepinephrine was greater in controls than patients (100.7+/-51.8 vs. 49.8+/-43.4%; P=0.01). The percent change in the diameter of the brachial artery in response to maximal exercise was significantly correlated to pre- (r=0.634; P=0.003) and post-exercise (r=0.467; P=0.05) endothelin-1 levels in patients but not in controls [pre-exercise (r=0.07; P=0. 86), post-exercise (r=0.310; P=0.47)]. The change in the diameter of the brachial artery did not correlate with pre- or post-exercise plasma norepinephrine levels in either group. These findings suggest that endothelin-1 is potentially more important than norepinephrine in contributing exercise-induced brachial artery constriction in patients with chronic heart failure.
Brachial Artery↗
The role of inflammatory mediators in chronic heart failure: cytokines, nitric oxide, and endothelin-1.
There is now considerable evidence to suggest that neurohormonal and immune mechanisms may play a central role in the pathogenesis of chronic heart failure (CHF), which is likely to have important implications for the management of this condition. It has been proposed that CHF is a state of immune activation with inflammatory cytokines contributing to both the central and the peripheral manifestations of this syndrome. The immune system is the body's natural defence mechanism against infection and other stresses, which has several different components that interact with each other in a complex manner. The main components which are thought to be relevant to the pathogenesis of CHF are: cytokines, adhesion molecules, autoantibodies, nitric oxide, and endothelin-1, and this review will concentrate on these factors. This article will also discuss the potential role of anti-cytokine therapies in the treatment of CHF.
Autoantibodies↗
Insulin-mediated glucose uptake in congestive heart failure.
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Cause of Death↗