Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nt-proBNP have emerged as useful biomarker for the diagnosis and prognostic of heart failure but also recently in acute coronary syndrome. Myocardial ischemia is probably an important stimulus for Nt-proBNP release. Transient myocardial ischemia is inducing by balloon inflation during percutaneous coronary intervention (PCI). The authors propose to determine the Nt-proBNP secretion after uncomplicated coronary intervention in patients with preserved cardiac function. Ninety patients were enrolled in this study. Plasma Nt-proBNP was increased significantly from 135.5 to 157.8 pg/ml and 202.5 pg/ml at 8 and 24 hours following PCI, respectively. History of myocardial infarction and complex lesions were the most powerful predictors of higher Nt-proBNP peak concentration. Prognostic value must be evaluated in larger studies.
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PMID:[Increased secretion of Nt-proBNP immediately after percutaneous coronary intervention: about 90 cases]. 1757 71

Chronic haemodialysis (HD) patients are already primed by a large number of structural and functional peripheral vascular and cardiac abnormalities to experience demand myocardial ischaemia. Transient myocardial ischaemia may lead to left ventricular (LV) dysfunction that can persist after the return of normal perfusion. This prolonged dysfunction is known as myocardial stunning. Repetitive episodes of ischaemia can be cumulative and have been shown to lead to prolonged LV dysfunction (in patients with ischaemic heart disease). Conventional HD itself is a sufficient cardiovascular functional stressor to precipitate such recurrent ischaemic insults, leading to myocardial functional and structural changes, eventually resulting in fixed systolic dysfunction and heart failure (conferring a dismal prognosis for patients undergoing dialysis). Furthermore these same haemodynamic insults may also adversely affect other vascular beds in other vulnerable organ systems, driving an even wider range of pathophysiological processes. A variety of therapeutic manoeuvres aimed at improving the haemodynamic tolerability of treatment have been shown to reduce acute dialysis-induced myocardial ischaemia. This article aims to give an appreciation of the possibility that modification of the dialysis treatment to improve tolerability of therapy may have the potential to provide us with additional therapeutic targets, to reduce currently excessive rates of cardiovascular morbidity and mortality.
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PMID:Haemodialysis-induced myocardial stunning in chronic kidney disease - a new aspect of cardiovascular disease. 2009 13