The Pathogenesis of Cardiac Cachexia

Pittman, Joseph G.; Cohen, Phin

doi:10.1056/nejm196408202710807

Cited by 180 publications

(48 citation statements)

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“…Metabolic alterations in HF. Wasting of subcutaneous fat and skeletal muscle is relatively common in HF and suggests an increased use of noncarbohydrate substrates for energy production (32,33). In fact, fasting blood ketone bodies (34) as well as fat oxidation during exercise (35) have been shown to be increased in patients with HF.…”

Section: Discussionmentioning

confidence: 99%

A Randomized Clinical Trial of Trimetazidine, a Partial Free Fatty Acid Oxidation Inhibitor, in Patients With Heart Failure

Fragasso

Palloshi

Puccetti

et al. 2006

Journal of the American College of Cardiology

222

148

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Section: Discussionmentioning

confidence: 99%

A Randomized Clinical Trial of Trimetazidine, a Partial Free Fatty Acid Oxidation Inhibitor, in Patients With Heart Failure

Fragasso

Palloshi

Puccetti

et al. 2006

Journal of the American College of Cardiology

222

148

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“…The causes of cardiac cachexia in CHF patients and the precise pathophysiological mechanisms remain unclear. Four mechanisms, however, appear to enhance muscle wasting: these include anorexia, malabsorption, hypermetabolism and possibly a dysfunctional uptake of nutrients into the cell [9][10][11]. Another possible explanation has recently emerged.…”

Section: Introductionmentioning

confidence: 99%

Collagen accumulation and dysfunctional mucosal barrier of the small intestine in patients with chronic heart failure

Arutyunov

Kostyukevich

Серов

et al. 2008

International Journal of Cardiology

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“…A number of hypotheses have been put forth to explain muscle atrophy in heart failure (4,37,45). Each of the mechanisms forwarded in these hypotheses must ultimately affect the regulation of skeletal muscle protein or cell mass.…”

mentioning

confidence: 99%

Effect of heart failure on the regulation of skeletal muscle protein synthesis, breakdown, and apoptosis

Persinger

Janssen–Heininger²,

Wing³

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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. Effect of heart failure on the regulation of skeletal muscle protein synthesis, breakdown, and apoptosis. Am J Physiol Endocrinol Metab 284: E1001-E1008, 2003. First published February 11, 2003 10.1152/ajpendo.00517.2002.-Heart failure is often characterized by skeletal muscle atrophy. The mechanisms underlying muscle wasting, however, are not fully understood. We studied 30 Dahl salt-sensitive rats (10 male, 20 female) fed either a high-salt (HS; n ϭ 15) or a low-salt (LS; n ϭ 15) diet. This strain develops cardiac hypertrophy and failure when fed a HS diet. LS controls were matched to HS rats for gender and duration of diet. Body mass, food intake, and muscle mass and composition were measured. Skeletal muscle protein synthesis was measured by isotope dilution. An additional group of 27 rats (HS, n ϭ 16; LS; n ϭ 11) were assessed for expression of genes regulating protein breakdown and apoptosis. Gastrocnemius and plantaris muscles weighed less (16 and 22%, respectively) in HS than in LS rats (P Ͻ 0.01). No differences in soleus or tibialis anterior weights were found. Differences in muscle mass were abolished after data were expressed relative to body size, because HS rats tended (P ϭ 0.094) to weigh less. Lower body mass in HS rats was related to a 16% reduction (P Ͻ 0.01) in food intake. No differences in muscle protein or DNA content, the protein-to-DNA ratio, or muscle protein synthesis were found. Finally, no differences in skeletal muscle gene expression were found to suggest increased protein breakdown or apoptosis in HS rats. Our results suggest that muscle wasting in this model of heart failure is not associated with alterations in skeletal muscle metabolism. Instead, muscle atrophy was related to reduced body weight secondary to decreased food intake. These findings argue against the notion that heart failure is characterized by a skeletal muscle myopathy that predisposes to atrophy. atrophy; isotope; ubiquitin proteasome pathway; cytokine IN BOTH HUMAN AND ANIMAL MODELS, heart failure is frequently characterized by skeletal muscle atrophy (14,22,33,40,43). Loss of skeletal muscle contributes to exercise intolerance (20, 43), a cardinal symptom of heart failure, and increases morbidity (1, 39) and mortality (5). Knowledge of the mechanisms underlying muscle atrophy in heart failure, however, is limited.A number of hypotheses have been put forth to explain muscle atrophy in heart failure (4, 37, 45). Each of the mechanisms forwarded in these hypotheses must ultimately affect the regulation of skeletal muscle protein or cell mass. Muscle atrophy can occur during net negative protein balance, in which protein breakdown exceeds synthesis, during net negative muscle cell balance, in which the loss of muscle cells exceeds replacement, or during a combination of these two events. Studies in both humans and animal models suggest that heart failure is associated with alterations in the regulation of skeletal muscle protein synthesis (40), protein breakdown (36), and apoptosis (47) that may predispose to s...

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The Pathogenesis of Cardiac Cachexia

Cited by 180 publications

References 48 publications

A Randomized Clinical Trial of Trimetazidine, a Partial Free Fatty Acid Oxidation Inhibitor, in Patients With Heart Failure

A Randomized Clinical Trial of Trimetazidine, a Partial Free Fatty Acid Oxidation Inhibitor, in Patients With Heart Failure

Collagen accumulation and dysfunctional mucosal barrier of the small intestine in patients with chronic heart failure

Effect of heart failure on the regulation of skeletal muscle protein synthesis, breakdown, and apoptosis

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