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Heterozygous familial hypercholesterolaemia is associated with pathological exercise‐induced leakage of muscle proteins, which is not aggravated by simvastatin therapy
Author(s) -
SMIT J. W. A.,
BÄR P. R.,
GEERDINK† R. A.,
ERKELENS D. W.
Publication year - 1995
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1995.tb01530.x
Subject(s) - simvastatin , pathological , medicine , endocrinology , bioinformatics , cardiology , biology
. The objective of this study was to assess the relationship between therapy with the HMG‐CoA reductase inhibitor simvastatin and muscle damage and the possible causal role of hypercholesterolaemia. The exercise‐induced release of muscle proteins as a parameter of muscle damage was studied in two equicholesterolaemic groups of male patients with heterozygous familial hypercholesterolaemia (FH); one group without treatment, the second group on simvastatin. To assess the role of cholesterol, a third group of healthy male volunteers was studied as well. The study took place at the Lipid Clinic of an 800‐bed University Hospital. One group of 21 male patients with heterozygous FH did not receive treatment, except for a lipid‐lowering diet. A second group of 13 male FH patients were treated with 40 mg simvastatin day ‐1 for at least 1 year and matched for cholesterol levels with the first group. A third group consisted of 25 normocholesterolaemic male controls. All subjects underwent a 45 min lean body mass (LBM) standardized ergometer muscle provocation test (2 Watt/kg LBM). Levels of creatine kinase (CK) and myoglobin (Mb) were assessed before and 1 and 8 h after exercise and compared with baseline levels. The exercise‐induced release of muscle proteins is reflected by peak CK and Mb levels expressed as a percentage of baseline levels. The exercise‐induced increase in Mb and CK levels did not differ between untreated and simvastatin‐treated FH patients. However, the increase in Mb 1 h after exercise in untreated FH patients (181% of baseline level) and in simvastatin‐treated patients (144% of baseline level) differed significantly from controls (107% of baseline level, P < 0.025, Mann‐Whitney test). We conclude that hypercholesterolaemia may be associated with muscle damage, and the CK rises observed under therapy with HMG‐CoA reductase inhibitors might be attributed to hypercholesterolaemia per se .