Patients with chronic heart failure syndrome may develop a myopathy contributing to muscle wasting and exercise intolerance. Little is known about skeletal muscle pathology in patients with dilated cardiomyopathy (DCM). To correlate skeletal muscle biopsy (SMB) findings with endomyocardial biopsy (EMB) and clinical/functional data in DCM patients. SMBs and EMBs were morphometrically and morphologically analysed in 30 consecutive patients aged 40.7 ± 14 years (16-63), including 25 in NYHA classes I and II. Four had familial DCM. Serum creatine-phosphokinase (sCPK) was normal in 23 and slightly increased in seven. All the SMBs showed morphological (including non-recurrent changes different from those in the EMBs) and morphometric changes, with atrophic fibres in all cases (atrophy factor >150 in six NYHA II patients) and necrotic fibres in three. The SMBs of two patients with EMB-proven myocarditis showed inflammation. Plotting the morphometric factors against age at symptom onset, age at diagnosis, follow-up, clinical outcome, ejection fraction and sCPK levels showed that only sCPK >180 mU/ml correlated with atrophy factor. The use of SMB in DCM patients documents some aspecific subclinical muscle damage that is unrelated to the functional class and duration of the DCM. However, this information does not contribute to identify the aetiology or managing the disease.
Cardiomyology: an attempt to link structural cardiac and skeletal muscle damage in patients with dilated cardiomyopathy
FERRARI, RobertoPenultimo
;
2004
Abstract
Patients with chronic heart failure syndrome may develop a myopathy contributing to muscle wasting and exercise intolerance. Little is known about skeletal muscle pathology in patients with dilated cardiomyopathy (DCM). To correlate skeletal muscle biopsy (SMB) findings with endomyocardial biopsy (EMB) and clinical/functional data in DCM patients. SMBs and EMBs were morphometrically and morphologically analysed in 30 consecutive patients aged 40.7 ± 14 years (16-63), including 25 in NYHA classes I and II. Four had familial DCM. Serum creatine-phosphokinase (sCPK) was normal in 23 and slightly increased in seven. All the SMBs showed morphological (including non-recurrent changes different from those in the EMBs) and morphometric changes, with atrophic fibres in all cases (atrophy factor >150 in six NYHA II patients) and necrotic fibres in three. The SMBs of two patients with EMB-proven myocarditis showed inflammation. Plotting the morphometric factors against age at symptom onset, age at diagnosis, follow-up, clinical outcome, ejection fraction and sCPK levels showed that only sCPK >180 mU/ml correlated with atrophy factor. The use of SMB in DCM patients documents some aspecific subclinical muscle damage that is unrelated to the functional class and duration of the DCM. However, this information does not contribute to identify the aetiology or managing the disease.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.