Identifying older diabetic patients at risk of poor glycemic control

BACKGROUND: Optimal glycemic control prevents the onset of diabetes complications. Identifying diabetic patients at risk of poor glycemic control could help promoting dedicated interventions. The purpose of this study was to identify predictors of poor short-term and long-term glycemic control in older diabetic in-patients. METHODS: A total of 1354 older diabetic in-patients consecutively enrolled in a multicenter study formed the training population (retrospective arm); 264 patients consecutively admitted to a ward of general medicine formed the testing population (prospective arm). Glycated hemoglobin (HbA1c) was measured on admission and one year after the discharge in the testing population. Independent correlates of a discharge glycemia ≥ 140 mg/dl in the training population were assessed by logistic regression analysis and a clinical prediction rule was developed. The ability of the prediction rule and that of admission HbA1c to predict discharge glycemia ≥ 140 mg/dl and HbA1c > 7% one year after discharge was assessed in the testing population. RESULTS: Selected admission variables (diastolic arterial pressure < 80 mmHg, glycemia = 143–218 mg/dl, glycemia > 218 mg/dl, history of insulinic or combined hypoglycemic therapy, Charlson's index > 2) were combined to obtain a score predicting a discharge fasting glycemia ≥ 140 mg/dl in the training population. A modified score was obtained by adding 1 if admission HbA1c exceeded 7.8%. The modified score was the best predictor of both discharge glycemia ≥ 140 mg/dl (sensitivity = 79%, specificity = 63%) and 1 year HbA1c > 7% (sensitivity = 72%, specificity = 71%) in the testing population. CONCLUSION: A simple clinical prediction rule might help identify older diabetic in-patients at risk of both short and long term poor glycemic control

[The arrhythmogenicity of alpha 1-adrenergic stimulation following myocardial acidosis]

Ischemia is associated with myocardial acidosis which recovers upon reperfusion. In such conditions, alpha 1-adrenergic stimulation is arrhythmogenic. We used single cardiac myocytes loaded with the pH fluorescent dye, SNARF-1, to determine if a modulation of pH could explain the effect of alpha 1-adrenergic stimulation. Cells were exposed to acidosis (CO2 15%) for 15 min and then normocapnia restored. During acidosis, alpha 1-adrenergic stimulation caused an increase in pH which was abolished by blocking Na+/H+ exchange with ethylisopropylamiloride (EIPA). After removal of acidosis aftercontractions were manifest in 8 out of 10 and 1 out of 5 cells in the presence of an alpha 1-adrenergic agonist and in control, respectively (p < 0.001). EIPA abolished the occurrence of after contractions. Thus, the arrhythmogenicity of alpha 1-adrenergic stimulation depends on activation of Na+/H+ exchanger

[Myocardial protection in hypothermia depends on the modulation of intracellular Ca2+ homeostasis]

The effect of a mild hypothermia (30 degrees C) on sarcoplasmic reticulum (SR) Ca2+ content and release has been evaluated in single cardiac cells loaded with the fluorescent indicator, indo-1. SR Ca2+ content, assessed by rapid caffeine application, is more pronounced at 30 than at 37 degrees C. However, hypothermia reduces the occurrence of spontaneous SR Ca2+ oscillations. In fact, following electrical stimulation, the time to onset of first SR Ca2+ oscillation was increased and their frequency reduced. Since spontaneous SR Ca2+ releases are implicated on the genesis of certain forms of ventricular arrhythmias, the protection provided by a mild hypothermia may be dependent on the modulation of intracellular Ca2+ homeostasis

Adverse outcomes of underuse of beta-blockers in elderly patients

Letter to the Edito

Risk of stroke after myocardial infarction

Risk of stroke after myocardial infarctio

Right bundle-branch block associated with left posterior hemiblock. Clinical, vectorcardiographic and electrophysiological study

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