title: Adverse effects of corticosteroids on the cardiovascular system.
abstract: OBJECTIVE
  To review the potential adverse effects of glucocorticoid therapy on the cardiovascular system and to provide insight into the mechanisms of these effects.
  
  
  METHODS
  Case reports and studies demonstrating adverse effects of glucocorticoid therapy on the cardiovascular system were examined from a MEDLINE search. Animal data and in vitro studies were identified to provide insight on the mechanisms of these effects.
  
  
  RESULTS
  Undesirable effects identified were dyslipidemia, hypertension and left ventricular free wall rupture after myocardial infarction. Elevations of total plasma cholesterol, triglycerides, low density lipoprotein cholesterol and high density lipoprotein cholesterol are often reported. The elevation of various lipid subfractions is likely mediated by increased plasma insulin levels, impaired lipid catabolism and increased lipid production in the liver. Hypertension was shown to be more prevalent in patients treated with high doses of glucocorticoid. The mechanisms are complex, but final pathways include increased systemic vascular resistance, increased extracellular volume and increased cardiac contractility. Glucocorticoids were demonstrated to increase the incidence of left ventricular free wall rupture by delaying myocardial scar formation in the postmyocardial infarction period.
  
  
  CONCLUSIONS
  The major adverse effects of glucocorticoids on the cardiovascular system include dyslipidemia and hypertension. These effects may predispose treated patients to coronary artery disease if high doses and prolonged courses are used. Accordingly, corticosteroids should be employed judiciously in patients with other risk factors for cardiovascular disease, and attention should be paid to risk modification. Low dose and alternate day therapy may reduce the incidence of complications in corticosteroid therapy. The mechanisms of these adverse effects are complex and have not yet been fully explained.
authors.affiliation: University of Alberta, Edmonton, Canada.
authors.forename: D E
authors.initials: DE
authors.lastname: Sholter
authors.forename: P W
authors.initials: PW
authors.lastname: Armstrong
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000139:chemically induced; D005938:Glucocorticoids / Q000009:adverse effects* / Q000627:therapeutic use; D006321:Heart / Q000187:drug effects; D006342:Heart Rupture, Post-Infarction / Q000139:chemically induced*; D006801:Humans; D006949:Hyperlipidemias / Q000139:chemically induced*; D006973:Hypertension / Q000139:chemically induced*; D019851:Thrombophilia / Q000139:chemically induced
chemical_list: D005938:Glucocorticoids