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Related Concept Videos

Acute Coronary Syndrome I: Introduction01:30

Acute Coronary Syndrome I: Introduction

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Acute Coronary Syndrome (ACS) encompasses a spectrum of heart conditions caused by sudden obstruction of coronary arteries, typically resulting from the rupture of an atherosclerotic plaque and subsequent thrombus (blood clot) formation. This obstruction can lead to partial or complete blockage of blood flow, causing varying degrees of myocardial ischemia or infarction.ACS includes the following clinical entities:Unstable Angina (UA)Non-ST-Elevation Myocardial Infarction (NSTEMI)ST-Elevation...
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Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations01:19

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

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The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...
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Acute Coronary Syndrome III: Diagnostic Studies01:30

Acute Coronary Syndrome III: Diagnostic Studies

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Diagnosing acute coronary syndrome or ACS begins with a thorough patient history. Notable symptoms include central, crushing chest pain radiating to the left arm, neck, jaw, or back, along with shortness of breath, sweating (diaphoresis), nausea, vomiting, dizziness, and palpitations.It is crucial to note any history of cardiac illnesses and assess risk factors, including age, gender, smoking, hypertension, diabetes, hyperlipidemia, and a sedentary lifestyle.During physical examination, vital...
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Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

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Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
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Blood Studies for Cardiovascular System I: Cardiac Biomarkers01:20

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Cardiac biomarkers are enzymes, proteins, and hormones released into the blood when cardiac cells are injured. They are powerful tools for triaging.
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Troponins
Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...
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Single Nucleotide Polymorphisms-SNPs01:05

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A single nucleotide polymorphism or SNP is a single nucleotide variation at a specific genomic position in a large population. It is the most prevalent type of sequence variation found in the human genome. Point mutations that occur in more than 1% of the population qualify as SNPs. These are present once every 1000 nucleotides on an average in the human genome. Replacement of a purine with another purine (A/G) or a pyrimidine with another pyrimidine (C/T) is known as a transition. In contrast,...
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A Research Method For Detecting Transient Myocardial Ischemia In Patients With Suspected Acute Coronary Syndrome Using Continuous ST-segment Analysis
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New candidate genes for ST-elevation myocardial infarction.

S Cederström1, P Lundman1, L Folkersen2

  • 1Division of Cardiovascular medicine, Department of Clinical Sciences, Karolinska Institutet Danderyd Hospital (KI DS), Stockholm, Sweden.

Journal of Internal Medicine
|October 8, 2019
PubMed
Summary

Researchers identified seven genes linked to ST-elevation myocardial infarction (STEMI) by analyzing leukocyte gene expression. This study offers new insights into coronary atherothrombosis mechanisms in STEMI patients.

Keywords:
acute myocardial infarctionatherothrombosiscardiovascular clinical researchplaque rupture

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Candidate Gene Testing in Clinical Cohort Studies with Multiplexed Genotyping and Mass Spectrometry
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Area of Science:

  • Cardiovascular Biology
  • Molecular Genetics
  • Thrombosis Research

Background:

  • Mechanisms of coronary atherothrombosis in ST-elevation myocardial infarction (STEMI) remain unclear despite extensive atherosclerosis research.
  • Investigating leukocyte gene expression in STEMI patients can elucidate underlying causes of coronary atherothrombosis.
  • Distinguishing primary gene expression changes from secondary inflammation is crucial for understanding STEMI pathogenesis.

Purpose of the Study:

  • To identify candidate genes involved in STEMI by analyzing leukocyte gene expression.
  • To differentiate primary genetic factors from secondary inflammatory responses in STEMI.
  • To uncover novel molecular targets for STEMI treatment and prevention.

Main Methods:

  • Gene expression analysis of leukocytes from 51 STEMI patients at acute phase (P1), 24-48h (P2), and 3 months (P3).
  • Utilized Affymetrix Human Transcriptome Array 2.0 for comprehensive gene expression profiling.
  • Excluded secondary inflammatory gene expression changes by comparing P1 to P3 (convalescent) samples, focusing on genes differentially expressed in P1.

Main Results:

  • Identified seven genes differentially expressed in the acute phase of STEMI compared to convalescence.
  • Three genes (ABCG1, RAB20, TMEM2) were upregulated, and four genes (ACVR1, NFATC2IP, SUN1, TTC9C) were downregulated in STEMI patients.
  • These seven candidate genes were also found to be highly expressed in carotid atherosclerotic plaques, suggesting a role in atherosclerosis.

Conclusions:

  • Seven candidate genes were identified as potentially involved in the mechanisms of STEMI.
  • The study's unique approach excluded secondary inflammatory responses, providing a clearer view of primary genetic involvement.
  • Further studies are needed to replicate these findings and validate the role of these genes in STEMI pathogenesis.