Presse Med
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Certain zones of ischemic, akinetic or severely hypokinetic myocardium are capable of recovering normal contractile function. This is termed myocardial viability and occurs in two different situations: myocardial stunning and myocardial hibernation. ⋯ The degree of myocardial viability in akinetic zones can be determined by assessing preserved inotropic capacity with stress echocardiography and/or evidencing metabolic activity with isotopic techniques (myocardial scintigraphy, positron emission tomography).
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SEVERAL FORMS: Congenital long QT syndrome is a clinically (with and without deafness) and genetically (recessive or dominant autosomal inheritance) heterogeneous entity characterized by a long QT interval on the ECG associated with the risk of severe ventricular arrhythmia (torsade de pointes, ventricular fibrillation) and subsequent syncope or sudden death.
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Review
[Nitric oxide (NO), vascular protection factor. Biology, physiological role and biochemistry of NO].
VASOMOTRICITY: The vascular endothelium plays a key role in vasomotricity by producing a number of factors which modulate smooth muscle relaxation and contraction. Nitric oxide (NO) has been found to be one of the most important relaxation factors. NO SYNTHESIS: Nitric oxide is synthesized from L-arginine by NO-synthetase whose activity is regulated by intracellular calcium concentration and modulated by pharmacological compounds such as acetylcholine, 5-hydroxytryptamine, bradykinin and ADP as well as the sheer forces produced by blood flow.
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AGING PROCESS: There is a large body of experimental and clinical data demonstrating that endothelial dysfunction is encountered not only in disease states such as atherosclerosis, hypertension, heart failure or diabetes, but also in the normal physiological process of aging. Currently available data show that endothelium-dependent function declines with age. The fact that this same decline is observed in patients with hypertension suggests that age is an independent factor capable of provoking changes in the vascular endothelium. CAUSAL MECHANISMS: It is often suggested that altered NO synthesis from L-arginine and/or increased production of contraction factors play a role in the aggravation of endothelial and parietal lesions and would thus affect the natural history of the disease process.