Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Results of early studies support the concept that steroid treatment may reduce mortality from acute myocardial infarction. This double-blind, randomized, 1118-patient study was performed to determine if methylprednisolone sodium succinate (MPSS, Solu-Medrol Sterile Powder, The Upjohn Company) reduced 28-day mortality following myocardial infarction complicated by cardiac failure. Treatment with 30 mg/kg intravenous MPSS (maximum dose, 3 g) resulted in 28-day mortality rates of 11.7% with MPSS and 9.9% with placebo when treatment was initiated within six hours of the onset of chest pain (Group 1). Mortality rates at 28 days were 10.4% with MPSS and 14.7% with placebo when the treatment was initiated 6-12 hours after onset of chest pain (Group 2). In the late-treatment group, six-month mortality rates were 13.7% with MPSS and 20.3% with placebo (p = 0.08). Analysis of data by life table methods showed similar survival rates between MPSS- and placebo-treated patients in Group 1. In Group 2, survival rates were increased in MPSS-treated patients in the intervals from 48 hours through seven days (p = 0.04) and from three months through six months (p = 0.03). A Cox regression analysis showed that the relative risk of death for Group 1 patients was similar, regardless of treatment; Group 2 patients on MPSS had a significantly decreased relative risk of death (p less than 0.01). MPSS treatment was not associated with increased incidence of myocardial rupture, cardiac aneurysm, early malignant ventricular arrhythmias, or other adverse cardiac events.
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PMID:Methylprednisolone as an intervention following myocardial infarction. The Solu-Medrol Sterile Powder AMI Studies Group. 287 3

In studies of patients with cardiac failure following an acute myocardial infarction, 1114 patients were followed for 7-day mortality. In the 45% of patients receiving diuretics on day 1, the death rate was twice that of patients not receiving diuretics. In patients treated 6 to 12 hours following the onset of chest pain, mortality was 2.8 times that of patients treated within 6 hours of the onset of chest pain. Randomization to methylprednisolone sodium succinate (MPSS, Solu-Medrol Sterile Powder, The Upjohn Company) did not improve the low mortality rates of those patients who did not need diuretics nor who were treated early. However, patients who were treated late and who needed diuretics and who were randomized to MPSS had a death rate half that of those who received placebo.
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PMID:Positive synergism between diuretics and methylprednisolone following acute myocardial infarction. 352 10

Methylprednisolone sodium succinate (MPSS) administered during reperfusion may improve myocardial function. These effects have been related to adrenergic stimulation. The present study investigated (1) the effects of ischemia and reperfusion on the beta-adrenergic response system and (2) the ability of MPSS to modify the ischemic effects on the beta-adrenergic system. Isolated perfused rat hearts were used. The ischemic protocol consisted of aerobic perfusion (20 minutes) followed by total, global normothermic (37 degrees C) ischemia (30 minutes) and reperfusion (30 minutes) with MPSS (0, 100, 500, or 1,000 mg/L). The non-ischemic protocol consisted of aerobic perfusion (20 minutes) followed by aerobic perfusion (20 minutes) with MPSS (0, 100, 500, or 1,000 mg/L). At the end of the experiments all hearts were rapidly frozen in liquid nitrogen. Crude sarcolemmal membranes were prepared and stimulated at the beta-receptor, at the coupling (G.- or N-) protein, or directly at the adenylate cyclase enzyme (AC). Results were assessed by cyclic adenosine monophosphate (cAMP) production. Tissue specimens were analyzed for myocardial content of cAMP and methylprednisolone (MP). In the ischemic protocol, the responsiveness of the beta-adrenergic system was significantly reduced at the G.-protein level. The treatment with MPSS (100 or 500 mg/L) during reperfusion preserved the beta-adrenergic response. MPSS (1,000 mg/L) offered no protection. In the non-ischemic protocol, MPSS reduced the response of the beta-adrenergic system in a dose-dependent manner at the same level. The hearts in the ischemic protocol had significantly higher contents of MP than the hearts in the non-ischemic protocol at corresponding concentrations of MPSS. The present study suggests that postischemic cardiac failure may result in part from beta-adrenergic dysfunction. This loss of function, probably at the level of the protein connecting the receptor and AC, can successfully be prevented by an optimal dose of MPSS during reperfusion after ischemia.
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PMID:Steroids protect the beta-adrenergic system during reperfusion after ischemia: effects of methylprednisolone on the beta-adrenergic response system. 1717 88