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عمومی::
سکتهی قلبی، سکته حاد قلبی، انفارکتوس میوکارد، آنفارکتوس میوکارد | سکته حاد قلبی
For example, atherosclerosis and myocardial infarction (MI): There is an association between atherosclerosis and smoking, smoking and risk for an MI, and atherosclerosis and risk for an MI.،Vasoactivity-hypertension (systemic and pulmonary) NO scavenging Gastrointestinal Pancreatic injury, hepatocellular injury, esophageal spasm,↑ AST, ↑ CPK, ↑ amylase, ↑ bilirubin Renal Heme-mediated oxidative events Hemostasis Coagulation defects, thrombosis, thrombocytopenia Cardiac Myocardial infarction Abbreviations: NO nitric oxide, AST aspartate aminotransferase, CPK creatine phosphokinase
Total adverse events instead were higher in intervention vs. control group (93 % vs. 88 %; p = 0.04); this was similar to serious adverse event, including myocardial infarction (MI) (40 % vs. 35 %; p = 0.12).
However, hypertension, MI, increase in pancreatic enzymes, and raised bilirubin were observed [25, 41, 42].
Overall analysis showed a significant increase in risk of death in treated patients (relative risk (RR), 1.30; 95 % confidence interval [CI], 1.05- 1.61) and risk of MI (RR, 2.71; 95 % [CI], 1.67-4.40).،ST-Elevation Myocardial Infarction Location and AV Block 62
AV Block With Inferior MI 62
AV Block With Inferior MI Acute inferior wall myocardial infarction (usually a right coronary artery event) may result in symptomatic second-degree or third-degree AV block with a junctional, narrow-complex escape rhythm.
These contraindications are consistent with the 2004 ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction.،Finally, nanoparticle delivery of siRNA against the transcription factor in- sulin response factor (IRF)-5, which has been associated with the M1-like phenotype, reduced expression of inflammatory genes in macrophages, reduced protease activity and promoted the resolution of inflammation after myocardial infarction in mice, with reduced subsequent left ventric- ular dilation [81].
For example, intraperitoneal injection of IL-4 in- creased the number of M2-like (CD206 + F4/80 +) macrophages in cardiac tissue following myocardial infarction in mice, and was associat- ed with increased fibroblast activation, deposition of supportive fibrous tissues, and improved prognosis [29].
Following myocardial infarction, delivery of the PS-presenting li- posomes caused a significant reduction in the infarct size and increased tissue vascularization compared to control liposomes, further highlight- ing the potential for macrophage-targeted therapies in regenerative medicine [104].
Frangogiannis, Inflammation as a therapeutic target in myocardial infarction: learning from past failures to meet future challenges, Transl.
, Macrophages mediate cardioprotective cellular postconditioning in acute myocardial infarction, J.
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روان شناسی و مشاوره::
سکته حاد قلبی
A case-crossover analysis of approximately 2000 patients admitted for a myocardial infarction (MI) indicated that experiencing anger in response to provocation increased the risk of MI more than two-fold in the 2-h following the provocation.2 In the last three decades, epidemiologists, behavioral medicine researchers and interventionists have studied the role of anger and related emotions in cardiovascular disease.3,4 The aim of this paper is to provide a selective review of empirical highlights, implications and unresolved issues in this area.
Early results, based on subcomponent analyses,11,12,18,19 showed strong associations between anger/hostility and cardiac events or mortality in prospective studies, often of approximate magnitude to traditional risk factors, but the evidence has been more mixed since then.25 In a qualitative review,25 outcomes were assessed separately for samples without known CHD (coronary heart disease) and those with CHD (fatal or non fatal MI).
as did 1 of 3 studies for trait anger33 and 5 of 9 studies for anger expression.34,12,35-37 Another 2 of 9 studies were positive for subsamples: one for women only,38 and one for 48- to 59-year-olds only.39 In populations with known CHD (15 reports, of which 14 assessed fatal or nonfatal MI), only 1 of 6 had positive results for cynical hostility,40 2 of 3 (one of those marginal) for trait anger,41,42 and 2 of 6 for anger expression.43,44 Suls and Bunde25 concluded that the effects of hostility, trait anger, and anger expression were difficult to identify or might not apply in all populations, and that results in patient samples were "very weak and inconsistent with respect to anger, hostility, and anger expression" (p. 284).
Friedman's Recurrent Coronary Prevention Project (RCPP; Friedman et al. 1986) involved a five-year, clinical trial of a group therapy intervention aimed at reducing the recurrence rate of post-coronary participants by reducing levels of hostility in individuals at risk for coronary problems in patients who had recovered from myocardial infarction.
Anger especially can trigger or increase vulnerability to serious clinical events, including myocardial ischemia, coronary thrombosis, myocardial infarction and sudden arrhythmic cardiac death in CAD patients (Mittleman, Maclure, & Sherwood, 1995; Reich, SeSilva, Lown, & Murawski, 1981; Verrier & Mittleman, 1996).
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