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)

The purpose of the present study was to examine the effects of a long-acting calcium antagonist, amlodipine, on the development of cardiac remodeling. Dihydropyridine calcium antagonists have been used widely for many years in the treatment of hypertension and angina pectoris. It has been reported, however, that a prototype of dihydropyridines, nifedipine, does not reduce mortality of patients with ischemic heart disease, possibly because of reflex stimulation of the sympathetic nervous system. A calcium antagonist, amlodipine, has been reported to have potential benefits by virtue of a gradual onset of action and a long duration of effects. Amlodipine (8 mg/kg per day, once a day) or nifedipine (24 mg/kg per day, three times a day) was administered to spontaneously hypertensive 12-week-old rats for 12 weeks. Left ventricular wall thickness was measured by echocardiography, and relative amounts of myosin heavy chain isoforms were assessed by pyrophosphate gels. Expressions of "fetal type" genes and type 1 collagen gene were examined by Northern blot analysis. Amlodipine and nifedipine both markedly reduced systolic blood pressure. However, the decrease in systolic blood pressure caused by nifedipine continued for no more than 8 hours, whereas the blood pressure-lowering effect of amlodipine continued for more than 16 hours post dose. Amlodipine markedly reduced left ventricular wall thickness, whereas nifedipine only weakly attenuated an increase in the wall thickness. Amlodipine, but not nifedipine, prevented an increase in the relative amount of V3 myosin heavy chain isoform and suppressed an increase in mRNA levels of beta-myosin heavy chain, skeletal alpha-actin, and type 1 collagen. Unlike nifedipine, amlodipine effectively prevented cardiac remodeling secondary to high blood pressure at biochemical levels and morphological levels. These results suggest that a long-acting calcium antagonist is more effective than a short-acting one in preventing organ injury in hypertensive subjects.
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PMID:Efficient inhibition of the development of cardiac remodeling by a long-acting calcium antagonist amlodipine. 944 87

Plasma myosin heavy chain assay, which can be easily performed during the acute phase of myocardial infarction, is a recent method allowing quantitative assessment of the extent of infarction. However, to our knowledge, its prognostic value has not been studied in contrast with serum myosin light chain assay. We monitored the state of health of 40 patients (including 37 men with a mean age of 56 years) for two years after a first myocardial infarction, thrombolized during the acute phase. Their survival (mortality) and the development of "cardiac events" (MI, angina, sudden death, etc.) were evaluated at 2 years. The results observed at 2 years were correlated with the initial plasma myosin assay results and other direct and indirect methods of assessment of the extent of infarction, performed during the acute phase of myocardial infarction (cardiac enzymes, contrast angiography). The main result of this study is the demonstration that an unusual plasma myosin release kinetic (complex appearance) is predictive for the medium-term development of heart failure (p = 0.04) and/or destabilization of coronary insufficiency (p = 0.02). These results need to be emphasized, as with only 5 serum myosin assays performed over a 10-day period, it seems possible to identify a group of patients at high risk of medium-term complications, who possess a complex release kinetic during the acute phase of myocardial infarction and a value for area under the curve greater than 10.470 microliters U/L (cut-off value, p = 0.043).
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PMID:[Mid-term prognostic value of plasma heavy-chain myosin in thrombolysed myocardial infarction]. 1255 65