myocardial infarction/protease

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Unmet needs in the management of acute myocardial infarction: role of novel protease-activated receptor-1 antagonist vorapaxar.

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Platelet activation with subsequent aggregation is a complex process leading to thrombus formation, which remains a key component for atherothrombotic manifestations, in particular myocardial infarction. Therefore, antiplatelet therapies are pivotal for the treatment of these patients. Current oral

Acute myocardial infarction elevates serine protease activity in saliva of patients with periodontitis.

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OBJECTIVE There are indications that acute myocardial infarction (AMI) may have an effect on the oral environment, which is reflected in the expression of salivary and gingival proteinases. According to our knowledge, no studies have been carried out to investigate the effect of AMI on the

Incidence of myocardial infarction in randomized clinical trials of protease inhibitor-based antiretroviral therapy: an analysis of four different protease inhibitors.

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Protease inhibitor (PI) therapy for patients infected with the human immunodeficiency virus has been associated with lipid disorders and insulin resistance. We compared the incidence of myocardial infarction (MI) among participants receiving treatment with PIs with or without nucleoside reverse

Protease-activated receptor 2 deficiency in hematopoietic lineage protects against myocardial infarction through attenuated inflammatory response and fibrosis.

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Ischaemic heart disease is one of the leading causes of death. Protease-activated receptor 2 (PAR2) is widely expressed within the cardiovascular system and is known to mediate inflammatory processes in various immunocytes, such as macrophages, mastocytes and neutrophils. Here, we investigated

Calcium-activated neutral protease inhibitor (E-64c) and reperfusion for experimental myocardial infarction.

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We examined the efficacy of the combination of coronary reperfusion and calcium-activated neutral protease (CANP) inhibitor (E-64c) for the treatment of acute myocardial infarction in dogs. In 34 dogs, the left anterior descending artery (LAD) was occluded and reperfused after 1 hour (Groups A and

Reduction of experimentally produced acute myocardial infarction size by a new synthetic inhibitor, NCO-700, against calcium-activated neutral protease.

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Calcium-activated neutral protease (CANP) might be involved in the irreversible degradation of myocardial proteins in the ischemic region, leading to the loss of contractility. The new compound, NCO-700, and its analogues were synthetized against CANP. Among these analogues, NCO-700 was the most

Pentraxin 3, ficolin-2 and lectin pathway associated serine protease MASP-3 as early predictors of myocardial infarction - the HUNT2 study.

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The lectin complement pathway is suggested to play a role in atherogenesis. Pentraxin-3 (PTX3), ficolin-1, ficolin-2, ficolin-3, MBL/ficolin/collectin-associated serine protease-3 (MASP-3) and MBL/ficolin/collectin-associated protein-1 (MAP-1) are molecules related to activation of the lectin

Role of PMN elastase on ischemic myocardial injury in evolving myocardial infarction: correlation with clinical parameters and intervention by protease inhibitor ulinastatin.

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The purposes of this study were to investigate the sequential changes of PMN elastase during evolving myocardial infarction, and also to ascertain whether or not ulinastatin (UL), a clinically useful protease inhibitor, would affect the extent of ischemic myocardial injury. The levels of plasma PMN

Mouse Mast Cell Protease 4 Deletion Protects Heart Function and Survival After Permanent Myocardial Infarction.

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Chymase, a mast cell serine protease involved in the generation of multiple cardiovascular factors, such as angiotensin II and endothelin-1 (ET-1), is elevated and participates in tissue degeneration after permanent myocardial infarction (PMI). Anesthetized 4-month old male wild-type (WT) C57BL/6J

A homogeneous assay system of aspartate aminotransferase iso-enzymes using proteases and application for clinical evaluation of myocardial infarction.

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We designed a rapid, homogeneous assay for human aspartate aminotransferase (AST) isoenzymes, by a selective proteolysis of soluble AST (s-AST), using chymotrypsin and protease 401. The linearity of mitochondrial (m-AST) was elongated up to 4000 U/l. m-AST values from the human liver, and determined

[Use of natural kallikrein-protease inhibitors (contrical and gordox) in the therapy of acute myocardial infarct].

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The paper reports on the efficacy of the protease inhibitors Contrycal and Hordox in acute myocardial infarction. The authors observed 154 patients, of whom 50 constituted the control group. They used to watch the process in the myocardium with biochemical, radioimmune and electrocardiographic

[Kallikrein-protease inhibitors (contrical, gordox) in the complex treatment of myocardial infarction].

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One hundred and forty-nine of 199 patients with myocardial infarction (MI) were treated with varying doses of kallikrein-protease inhibitors (KPI), contrical or gordox, for 4 to 5 days as part of combined treatment. KPI added to combined treatment at early dates of MI contributed significantly to

[Myocardial infarction in the course of antiretroviral therapy with protease inhibitor].

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The use of protease inhibitors (PIs) in the antiretroviral therapy (ART) of HIV-1 infection has reduced the rate of morbidity and mortality; but, unfortunately, this therapy has several side effects and a long term toxicity. Unexpected lipid abnormalities and cardiovascular complications are

Attenuation of increased secretory leukocyte protease inhibitor, matricellular proteins and angiotensin II and left ventricular remodeling by candesartan and omapatrilat during healing after reperfused myocardial infarction.

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While secretory-leukocyte-protease-inhibitor (SLPI) may promote skin wound healing, its role in infarct healing after reperfused myocardial infarction (RMI) remains unclear. Short-term intravenous angiotensin II (AngII) receptor blocker therapy with candesartan (CN) attenuates increased SLPI and

[Acute myocardial infarct in HIV-positive patients in treatment with protease inhibitors].

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We report the case of a 40-year-old HIV-positive man, undergoing three-drug antiretroviral therapy for 2 years that included a protease inhibitor (ritonavir). The patient was admitted to our Coronary Care Unit with an acute anterior myocardial infarction. He smoked 20 cigarettes/day and had a family

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