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Related Concept Videos

Acute Coronary Syndrome I: Introduction01:30

Acute Coronary Syndrome I: Introduction

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...
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations01:19

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

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...
Acute Coronary Syndrome III: Diagnostic Studies01:30

Acute Coronary Syndrome III: Diagnostic Studies

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...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Myocarditis I: Introduction01:21

Myocarditis I: Introduction

Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
Blood Studies for Cardiovascular System I: Cardiac Biomarkers01:20

Blood Studies for Cardiovascular System I: Cardiac Biomarkers

Cardiac biomarkers are enzymes, proteins, and hormones released into the blood when cardiac cells are injured. They are powerful tools for triaging.
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
Troponins
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Related Experiment Video

Updated: May 21, 2026

Myocardial Infarction and Functional Outcome Assessment in Pigs
12:03

Myocardial Infarction and Functional Outcome Assessment in Pigs

Published on: April 25, 2014

Sex differences in cardiac structure and function following ST-segment elevation myocardial infarction.

Kim W L M Ricken1, Kyriakos Panaou1, Chris Lenselink1

  • 1Department of Cardiology, University Medical Center Groningen, Hanzeplein 1, Groningen, 9713 GZ, The Netherlands.

Scientific Reports
|May 19, 2026
PubMed
Summary

Sex differences in cardiac remodelling after ST-elevation myocardial infarction (STEMI) are unclear. This study found similar post-STEMI cardiac remodelling trajectories between women and men, despite baseline differences.

Keywords:
Cardiac remodellingEchocardiographySTEMISex Differences

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Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
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In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography
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In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography

Published on: February 16, 2016

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Last Updated: May 21, 2026

Myocardial Infarction and Functional Outcome Assessment in Pigs
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Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
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Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs

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In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography
08:13

In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography

Published on: February 16, 2016

Area of Science:

  • Cardiology
  • Cardiovascular Research
  • Clinical Medicine

Background:

  • Post-STEMI cardiac remodelling significantly impacts long-term patient outcomes.
  • Existing research highlights sex disparities in STEMI presentation, treatment, and outcomes, but less is known about sex-specific cardiac remodelling.
  • Understanding these differences is crucial for tailored patient management.

Purpose of the Study:

  • To investigate sex-based differences in cardiac remodelling following STEMI.
  • To compare the evolution of cardiac structure and function between women and men post-myocardial infarction.
  • To assess if baseline sex differences influence long-term remodelling trajectories.

Main Methods:

  • Analysis of 379 patients (95 women, 284 men) from the GIPS-III trial (metformin vs. placebo in STEMI without diabetes).
  • Transthoracic echocardiography performed during hospitalization and at four months post-STEMI.
  • Evaluation of left ventricular dimensions, volumes, ejection fraction, E/e' ratio, and adverse remodelling incidence.

Main Results:

  • Women had higher rates of hypertension, lower hemoglobin, and elevated NT-proBNP compared to men.
  • Women presented with smaller LV dimensions/volumes and higher LVEF, but similar adverse remodelling rates and LV geometry at four months.
  • Despite baseline differences, cardiac remodelling trajectories over four months did not significantly differ between sexes.

Conclusions:

  • While baseline cardiac characteristics post-STEMI differ between sexes, the subsequent remodelling process appears broadly similar.
  • These findings suggest current post-STEMI monitoring and management strategies may be applicable across sexes.
  • Further research could explore the clinical implications of these similar remodelling patterns.