scholarly journals Cocaine-Associated Myocardial Infarction: Should They All Be Stented?

2011 ◽  
Vol 2011 ◽  
pp. 1-2 ◽  
Author(s):  
Sazzli Kasim ◽  
Ronan O'Donabhain ◽  
Eugene Mcfadden
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Chest Pain ◽  
Platelet Activation ◽  
Atherosclerotic Plaque ◽  
Acute Coronary Syndromes ◽  
Plaque Rupture ◽  
Coronary Syndromes ◽  
Atherosclerotic Plaque Rupture ◽  
Catheterization Procedure

Cocaine use is a known cause of chest pain and acute myocardial infarction and frequently leads to cardiac catheterization procedure. The treatment of cocaine-related acute coronary syndromes presents unique challenges because a variety of mechanisms including atherosclerotic plaque rupture, platelet activation, and coronary vasospasm may contribute to the pathogenesis. Our case highlights important considerations taken in dealing with this acute scenario

scholarly journals Thrombosis, physical activity, and acute coronary syndromes

2011 ◽  
Vol 111 (2) ◽  
pp. 599-605 ◽  
Author(s):  
Arun Kumar ◽  
Subrata Kar ◽  
William P. Fay
Keyword(s):  
Physical Activity ◽  
Atherosclerotic Plaque ◽  
Clinical Studies ◽  
Acute Coronary Syndromes ◽  
Plaque Rupture ◽  
Thrombus Formation ◽  
Coagulation Cascade ◽  
Plaque Disruption ◽  
Coronary Syndromes ◽  
Atherosclerotic Plaque Rupture

Acute coronary syndromes (ACS) are common, life-threatening cardiac disorders that typically are triggered by rupture or erosion of an atherosclerotic plaque. Platelet deposition and activation of the blood coagulation cascade in response to plaque disruption lead to the formation of a platelet-fibrin thrombus, which can grow rapidly, obstruct coronary blood flow, and cause myocardial ischemia and/or infarction. Several clinical studies have examined the relationship between physical activity and ACS, and numerous preclinical and clinical studies have examined specific effects of sustained physical training and acute physical activity on atherosclerotic plaque rupture, platelet function, and formation and clearance of intravascular fibrin. This article reviews the available literature regarding the role of physical activity in determining the incidence of atherosclerotic plaque rupture and the pace and extent of thrombus formation after plaque rupture.

scholarly journals 768-2 Non-culprit Lesions in Acute Myocardial Infarction: Implications for Multiple Plaque Rupture in Acute Coronary Syndromes

1995 ◽  
Vol 25 (2) ◽  
pp. 280A
Author(s):  
Hugo H. Castaño ◽  
Herman K. Gold ◽  
Tsunehiro Yasuda ◽  
Hiroyuki Matsuura ◽  
Robert D. Dinsmore ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Acute Coronary Syndromes ◽  
Plaque Rupture ◽  
Coronary Syndromes

Abstract 128: Serum Anti-MAA Antibody Titers are Associated with Acute Myocardial Infarction and MMP-9

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Faisal Ahmed ◽  
Michael J Duryee ◽  
Scott W Shurmur ◽  
Michael D Johnston ◽  
Carlos D Hunter ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Atherosclerotic Plaque ◽  
Inflammatory Responses ◽  
Plaque Rupture ◽  
Protein Antigens ◽  
Serum Samples ◽  
Antibody Isotypes ◽  
Antibody Titers ◽  
Atherosclerotic Plaque Rupture

Introduction Atherosclerotic plaque rupture is the leading cause of acute myocardial infarction (AMI). Malondialdehyde acetaldehyde (MAA) modified proteins have recently been implicated in this process by their ability to initiate inflammatory responses. Matrix metalloproteinase 9 (MMP-9) is increased following AMI and has been associated with the disease due to its ability to degrade the fibrotic cap that forms on some plaques. Objective The purpose of this study was to evaluate the relationship between MMP-9 and anti-MAA antibody isotypes in patients experiencing acute myocardial infarction (AMI). Methods Serum samples from AMI patients (n=10) were collected and tested for the presence of anti-MAA antibody isotypes, peak CK, peak troponin, and MMP-9 levels. Samples were collected at the time of AMI, 24 and 48 hours post event. Data was correlated to determine relationships with antibody isotypes directed against MAA protein antigens. Results MMP-9 increased significantly from the initial presentation at 24 hours post-AMI (p=0.006) and 48 hours post-AMI (p= 0.044). Anti-MAA IgM decreased significantly (p= 0.021) between initial and 24 hours post AMI. A similar significant decrease was observed for anti-MAA IgG (p= 0.006). Anti-MAA IgA levels did not change significantly post-AMI. Significant correlations were demonstrated between peak CK and anti-MAA IgG 24 hours post AMI (r= -0.819, p= 0.013), between peak troponin and anti-MAA IgG 24 hours post AMI (r= -0.860, p= 0.006) and between MMP-9 levels 24 hours post AMI and anti-MAA IgM levels 24 hours post MI ( r= 0.0712, p=0.021). Conclusions The negative correlation of anti-MAA IgG to cardiac enzymes is suggestive that myocardial infarction and tissue necrosis results in the release of the MAA antigen from infarcted myocardium and clearance of anti-MAA antibodies. Additionally, anti-MAA IgM and MMP-9 are positively correlated with each other 24 hours post-AMI, suggesting that anti-MAA IgM titers may correlate to the severity of the AMI and thus CAD. Implications Anti-MAA antibodies might serve as important biomarkers of impending atherosclerotic plaque rupture and subsequent AMI and warrants further investigation in a larger cohort of patients.

scholarly journals Applicability of Recent Dyslipidemia Guidelines in Clinical Practice

2019 ◽  
Vol 5 (1 (P)) ◽  
pp. 43
Author(s):  
Erwinanto Erwinanto
Keyword(s):  
Myocardial Infarction ◽  
Atherosclerotic Plaque ◽  
Coronary Flow ◽  
Cardiovascular Events ◽  
Ldl Cholesterol ◽  
Plaque Rupture ◽  
Heart Association ◽  
Plaque Stabilization ◽  
Plaque Regression ◽  
Atherosclerotic Plaque Rupture

Atherosclerotic plaque rupture is closely related to acute coronary syndromes.Stabilization of atherosclerotic plaque which slashes plaque rupture is as importantas regression ofplaque size for reducing cardiovascular events. Dyslipidemia therapy targeting to decrease LDL cholesterol reduces cardiovascular events such as acute myocard infarct, stroke, and death which are suggested to be the result of plaque stabilization. Dyslipidemia therapy also regress atherosclerotic plaque into a smaller volume. Plaque regression improves coronary flow responsible for the reduction of myocardial infarction incidence in patients with coronary heart disease (CHD).This paper consists of two parts. The first part discusses the evidence of cardiovascular event reduction with statin. The second part describes dyslipidemia management based on the 2017 Indonesian Heart Association (PERKI) Guideline on the Management of Dyslipidemia

Sign in / Sign up

Export Citation Format

Share Document