Meta-analysis of corticosteroid treatment in acute myocardial infarction

Giugliano, Gregory R.; Giugliano, Robert P.; Gibson, C. Michael; Kuntz, Richard E.

doi:10.1016/s0002-9149(03)00148-6

Cited by 168 publications

(120 citation statements)

References 22 publications

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“…In this context an elevated leukocyte count is an independent predictor for mortality after acute cardiac events (10,11). Immunosuppression by using steroids for example has shown mixed results in various trials (39). It has therefore been proposed that a balance is crucial as insufficient as well as exaggerated leukocyte presence may lead to impaired healing (28).…”

Section: Discussionmentioning

confidence: 99%

Therapeutic hypothermia impacts leukocyte kinetics after cardiac arrest

Dufner

André

Stiepak³

et al. 2016

Cardiovasc. Diagn. Ther.

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Background: Patients admitted to the hospital after primarily successful cardiopulmonary resuscitation (CPR) are at a very high risk for neurologic deficits and death. Targeted temperature management (TTM) for mild therapeutic hypothermia has been shown to improve survival compared to standard treatment.Acute cardiovascular events, such as myocardial infarction (MI), are a major cause for cardiac arrest (CA) in patients who undergo CPR. Recent findings have demonstrated the importance and impact of the leukocyte response following acute MI.Methods: In this retrospective, single center study we enrolled 169 patients with CA due to non-traumatic causes and primarily successful CPR. A total of 111 subjects (66%) underwent TTM aiming for a target temperature of 32-34 ℃.Results: Analysis of 30 day follow up showed a significantly improved survival of all patients who received TTM compared to patients without hypothermia (P=0.0001). Furthermore TTM was an independent variable of good neurological outcome after 6 months (P=0.0030). Therapeutic hypothermia was found to be beneficial independent of differences in age and sex between both groups. While a higher rate of pneumonia was observed with TTM, this diagnosis had no additional impact on survival or neurological outcome. The beneficial effect on mortality remained significant in patients with the diagnosis of an acute cardiac event (P=0.0145). Next, we evaluated the kinetics of leukocytes in this group over the course of 7 days after CA.At presentation, patients showed a mean level of 16.5±6.7 of leukocytes per microliter. While this level stayed stable in the group of patients without hypothermia, patients who received TTM showed a significant decline of leukocyte levels resulting in significantly lower numbers of leukocytes on days 3 and 5 after CPR. Interestingly, these differences in leukocyte counts remained beyond the time period of TTM while C-reactive protein (CRP) levels were suppressed only during ongoing cooling, but differences between the groups were diminished after TTM was terminated (from day 3 on, P>0.2). Finally, patients who received TTM and showed a leukocyte count of less than 12.7/μL on day 3 had an improved survival (P=0.0214) and neurological outcome (P=0.0049) compared to patients above that level.Conclusions: Our data underline the beneficial effects of TTM and demonstrate an impact of hypothermia on leukocyte counts after CA.

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Section: Discussionmentioning

confidence: 99%

Therapeutic hypothermia impacts leukocyte kinetics after cardiac arrest

Dufner

André

Stiepak³

et al. 2016

Cardiovasc. Diagn. Ther.

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“…Most of these were conducted in the 1970s with suboptimal methodology, but a recent meta-analysis suggests a small beneficial effect on mortality (136). The increased incidence of heart failure amongst glucocorticoid users in the pharmacoepidemiology studies described above (99,100,137), however, raises the possibility that longer term glucocorticoid therapy has an adverse effect on vascular remodelling.…”

Section: Recovery From Myocardial Infarctionmentioning

confidence: 99%

Glucocorticoids and Cardiovascular Disease

Walker¹

2007

European Journal of Endocrinology

476

386

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Chronic excessive activation of glucocorticoid receptors induces obesity, insulin resistance, glucose intolerance, dyslipidaemia and hypertension. Subtle abnormalities of the hypothalamic-pituitaryadrenal axis and/or of tissue sensitivity to glucocorticoids are also associated with these cardiovascular risk factors in patients with the metabolic syndrome. Furthermore, glucocorticoids have direct effects on the heart and blood vessels, mediated by both glucocorticoid and mineralocorticoid receptors and modified by local metabolism of glucocorticoids by the 11b-hydroxysteroid dehydrogenase enzymes. These effects influence vascular function, atherogenesis and vascular remodelling following intravascular injury or ischaemia. This article reviews the systemic and cardiovascular effects of glucocorticoids, and the evidence that glucocorticoids not only promote the incidence and progression of atherogenesis but also modify the recovery from occlusive vascular events and intravascular injury. The conclusion is that manipulation of glucocorticoid action within metabolic and cardiovascular tissues may provide novel therapeutic avenues to combat cardiovascular disease.European Journal of Endocrinology 157 545-559

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“…18 -24 However, the more longterm effects of glucocorticoids on the outcome of ischemia/ reperfusion are more controversial. 25 In the present study, we examined the effect of methylprednisolone, given either before or after established coronary microembolization, on the myocardial inflammatory reaction and the progressive contractile dysfunction over a period of 8 hours. In addition, in chronically instrumented conscious dogs, we determined the more long-term effects of glucocorticoids, when given as a single dose after microembolization, on the progressive contractile dysfunction and its eventual recovery.…”

mentioning

confidence: 99%

Glucocorticoid Treatment Prevents Progressive Myocardial Dysfunction Resulting From Experimental Coronary Microembolization

et al. 2004

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Background-The frequency and importance of microembolization in patients with acute coronary syndromes and during coronary interventions have recently been appreciated. Experimental microembolization induces immediate ischemic dysfunction, which recovers within minutes. Subsequently, progressive contractile dysfunction develops over several hours and is not associated with reduced regional myocardial blood flow (perfusion-contraction mismatch) but rather with a local inflammatory reaction. We have now studied the effect of antiinflammatory glucocorticoid treatment on this progressive contractile dysfunction. Methods and Results-Microembolization was induced by injecting microspheres (42-m diameter) into the left circumflex coronary artery. Anesthetized dogs were followed up for 8 hours and received placebo (nϭ7) or methylprednisolone 30 mg/kg IV either 30 minutes before (nϭ7) or 30 minutes after (nϭ5) microembolization. In addition, chronically instrumented dogs received either placebo (nϭ4) or methylprednisolone (nϭ4) 30 minutes after microembolization and were followed up for 1 week. In acute placebo dogs, posterior systolic wall thickening was decreased from 20.0Ϯ2.1% (meanϮSEM) at baseline to 5.8Ϯ0.6% at 8 hours after microembolization. Methylprednisolone prevented the progressive myocardial dysfunction. Increased leukocyte infiltration in the embolized myocardium was prevented only when methylprednisolone was given before microembolization. In chronic placebo dogs, progressive dysfunction recovered from 5.0Ϯ0.7% at 4 to 6 hours after microembolization back to baseline (19.1Ϯ1.6%) within 5 days. Again, methylprednisolone prevented the progressive myocardial dysfunction. Conclusions-Methylprednisolone, even when given after microembolization, prevents progressive contractile dysfunction.

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Meta-analysis of corticosteroid treatment in acute myocardial infarction

Cited by 168 publications

References 22 publications

Therapeutic hypothermia impacts leukocyte kinetics after cardiac arrest

Therapeutic hypothermia impacts leukocyte kinetics after cardiac arrest

Glucocorticoids and Cardiovascular Disease

Glucocorticoid Treatment Prevents Progressive Myocardial Dysfunction Resulting From Experimental Coronary Microembolization

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