Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study investigates the systemic hemodynamic effects of intravenous Isosorbidi Dinitras, Isoket (ISDN) in 20 patients with coronary arterial disease to test the validity of the hypothesis concerning the relief of myocardial ischemia. Patients were eligible for the study if they had angina with coronary angiographic records or if they were cases of post-myocardial infarction. Before and after ISDN infusion the following measurements were recorded or calculated: heart rate (HR); systolic, diastolic and mean aortic pressure (ASP, ADP, AP); systolic and mean pressure of the left ventricle (LVSP, LVP); end-diastolic pressure in the LV (LVEDP); left ventricular contractility (dp/dt max); the double products (DP, HR x LVSP) and myocardial perfusion pressure in the LV (LVPP). After ISDN the ASP, AP and LVEDP decreased while HR, ADP, dp/dt and DP showed no significant changes. However, LVEDP was significantly decreased from 20 +/- 7 to 12 +/- 5 mmHg (P less than 0.01) with increased LVPP from 49 +/- 12 to 56 +/- 13 mmHg (P less than 0.01), which may be favourable for the relief of myocardial ischemia. There was no significant change of dp/dt max with decreased LVEDP after ISDN. It is suggested that the left ventricle can maintain normal performance at lower intracardial volume (preload) in these patients.
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PMID:Hemodynamic assessment of intravenous Isosorbidi Dinitras in coronary heart disease. 159 78

This review summarizes available evidence on the role of serum complement component 3 (C3), produced by liver, adipocytes and activated macrophages at inflammation sites, and C3 cleavage products linking lipoproteins and metabolism to immunity. C3 and cleavage products are modified in several associated metabolic disorders including obesity, insulin resistance, type-2 diabetes, dyslipidemia, and cardiovascular diseases. Circulating C3 is independently and linearly associated with serum triglycerides, C-reactive protein (CRP), waist circumference and in some populations inversely with current smoking. The complement cascade is activated during myocardial ischemia and likely mediates immune and inflammatory responses in ischemic myocardium. Serum complement activation is elevated in unstable rather than stable angina pectoris suggesting added contribution to damage extension in acute coronary syndromes. In logistic regression models for incident metabolic syndrome (MetS), increasing C3 concentrations predicted MetS in women, after adjusting for continuous values of 3 major MetS components and other confounders, with a relative risk similar in magnitude to an established component suggesting elevated C3 likely constitutes part of the cluster of MetS in women. C3 interacts with MetS in men for independently conferring risk of incident type-2 diabetes and coronary heart disease (CHD). In women, though C3 is equally predictive of cardiometabolic risk, it is less so additively to MetS components or to CRP. Evidence suggests that circulating C3 might serve as a signal for an immune process that enhances - via mediation of increased apolipoprotein (apo) E levels - the development of dysfunctional apoA-I particles rendering them diabetogenic and atherogenic in populations prone to MetS or subsets of populations harboring impaired glucose tolerance. C3 activation also leads to production of chemoattractants C3a and C5a, and acylation stimulating protein (ASP, C3adesArg), a lipogenic hormone, which contribute additionally to the metabolic phenotypes generated. These observations have clinical and public health implications.
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PMID:Complement C3 and cleavage products in cardiometabolic risk. 2141 12