[Simply ... move!].
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Biomedical subjects
Publications and source records attributed to Jean-François Aupetit.
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BACKGROUND: In animal models, brief periods of ischemia performed just at the time of reperfusion can reduce infarct size, a phenomenon called postconditioning. In this prospective, randomized, controlled, multicenter study, we investigated whether postconditioning may protect the human heart during coronary angioplasty for acute myocardial infarction. METHODS AND RESULTS: Thirty patients, submitted to coronary angioplasty for ongoing acute myocardial infarction, contributed to the study. Patients were randomly assigned to either a control or a postconditioning group. After reperfusion by direct stenting, control subjects underwent no further intervention, whereas postconditioning was performed within 1 minute of reflow by 4 episodes of 1-minute inflation and 1-minute deflation of the angioplasty balloon. Infarct size was assessed by measuring total creatine kinase release over 72 hours. Area at risk and collateral blood flow were estimated on left ventricular and coronary angiograms. No adverse events occurred in the postconditioning group. Determinants of infarct size, including ischemia time, size of the area at risk, and collateral flow, were comparable between the 2 groups. Area under the curve of creatine kinase release was significantly reduced in the postconditioning compared with the control group, averaging 208 984+/-26 576 compared with 326,095+/-48,779 (arbitrary units) in control subjects, ie, a 36% reduction in infarct size. Blush grade, a marker of myocardial reperfusion, was significantly increased in postconditioned compared with control subjects: 2.44+/-0.17 versus 1.95+/-0.27, respectively (P<0.05). CONCLUSIONS: This study suggests that postconditioning by coronary angioplasty protects the human heart during acute myocardial infarction.
PHARMACOLOGICAL MODIFICATIONS TO BE TAKEN INTO ACCOUNT: In elderly patients, there is a modification in the distribution columns of drugs, an alteration in glomerular filtration (doses require adaptation) and tubular function (greater sensitivity to low salt diet and diuretics), and a reduction in the hepatic elimination capacity. FOR SYSTOLIC HEART FAILURE: The choice of drugs is in practice the same as that for younger patients: diuretics, antialdosterone agents, converting enzyme inhibitors, angiotensin II receptor antagonists, beta-blockers and digitalics. FOR DIASTOLIC HEART FAILURE: The therapeutic approach combines an etiologic treatment (blood pressure, myocardial ischaemia), prevention and the rapid treatment of the decompensation factors (atrial arrhythmia), a pharmacological treatment (converting enzyme inhibitors, angiotensin II receptor antagonists, and bradycardia lowering agents). Non-pharmacological measures include dietary restrictions, regular physical exercise, and education for the patient and the family.