Acute glucose dysmetabolism in the elderly with ST elevation myocardial infarction submitted to mechanical revascularization

Abstract

Though age is a predictor of adverse events after acute coronary syndrome, including in-hospital and posthospital mortality rates, elderly patients are under-represented in randomized trials evaluating strategies of early coronary revascularization in acute myocardial infarction. Several factors can account for the unfavorable outcome of the elderly, comprising increased glucose values. Diabetes is more common in the elderly patients with acute myocardial infarction in respect to younger patients and elevated glucose, though common, are rarely treated and associated with increased mortality, particularly in those without recognized diabetes. Age itself is thought to affect the acute glucose response to stress. Human aging is associated with impaired β-cell sensitivity to glucose and impaired β-cell compensation to insulin resistance and older people exhibit an impaired glucose response after injury characterized by a more marked increases in endogenous glucose production. In the early phase of ST elevation myocardial infarction (STEMI), the acute glucose response to stress comprises not only hyperglycemia but also insulin-resistance (assessed by the Homeostatic Model Assessment). Recently it has been documented in 346 STEMI patients submitted to mechanical revascularization that the acute glucose response to myocardial injury differs in respect to age, since older patients showed the highest glucose levels and the poorest glycemic control during ICCU stay in the lack of differences in insulin resistance incidence. Taking into account that aging impairs the acute glucose response to stress in elderly STEMI patients, further studies are needed to establish whether a different (more aggressive) therapeutic regime is needed in this subgroup of patients at higher risk.

Impact of newly diagnosed abnormal glucose regulation on long-term prognosis in low risk patients with ST-elevation myocardial infarction: A follow-up study

“…Furthermore, the patients included were relatively young and previous studies have shown a close relationship between newly diagnosed abnormal glucose regulation and age [8,26-28]. Additionally, a high proportion of our patients were diagnosed with single-vessel disease during coronary angiography [10], which may have contributed to the low event-rate observed in both groups.…”

The glucose dysmetabolism in the acute phase of non-diabetic ST-elevation myocardial infarction: from insulin resistance to hyperglycemia

“…Criteria used for the definition of insulin resistance are in accordance with the recently published guidelines proposed by the European Group of the study of Insulin Resistance (EGIR) [25,26]. HOMA was calculated according to the following formula: {[fasting insulin (microU/ml)] 9 [fasting glucose (mmol/l)]}/22.5 [27].…”

ST-elevation myocardial infarction with preserved ejection fraction: The impact of worsening renal failure

“…On ICCU admission, after PCI, the following parameters were measured [5][6][7][8][9][10][11]: glucose (mg/dl), insulin values (mIU/l), glycated hemoglobin (HbA1c, %), troponin I (ng/ml), C-reactive protein (mg/dl) (normal values b 9), NT-pro Brain Natriuretic Peptide (NT-pro BNP) (pg/ml), erythrocyte sedimentation rate (ESR), microalbuminuria (mg/dl), uric acid (mg/dl), leukocytes (*10 3 /μl), fibrinogen (mg/dl). Glucose, creatinine and Tn I were measured three times a day during ICCU stay and peak values for each variable were considered.…”

“…Glucose, creatinine and Tn I were measured three times a day during ICCU stay and peak values for each variable were considered. Acute insulin resistance was measured by means of homeostatic model assessment (HOMA) [5,[9][10][11][12]. (Table 1).…”

“…They also exhibited a worse in-hospital glycemic control (as inferred by peak glycemia) and a higher inflammatory activation (as indicated by higher values of hs-CRP, microalbuminuria). These factors are known to be associated with a worse prognosis at short term in STEMI patients [5,6,[10][11][12].…”