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Related Concept Videos

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...
Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.
Dysrhythmias II: Classification of Tachyarrhythmias01:28

Dysrhythmias II: Classification of Tachyarrhythmias

Tachyarrhythmias are a type of dysrhythmia where the heart rate exceeds 100 beats per minute. Here are some common types of tachyarrhythmias:Sinus TachycardiaSinus tachycardia originates from increased impulses from the sinus node, leading to an elevated heart rate. It is often triggered by stress, fever, or exercise.Patients may experience palpitations, a sensation of a racing heart, dizziness, and chest discomfort.Causes and Risk Factors: Common causes include physical exertion, emotional...
Coronary Artery Disease III: Clinical Manifestations01:30

Coronary Artery Disease III: Clinical Manifestations

Coronary Artery Disease (CAD) is a primary health risk worldwide, leading to significant morbidity and mortality. The condition arises from the buildup of atherosclerotic plaques within the coronary arteries, resulting in diminished blood supply to the heart muscle.The clinical manifestations of CAD vary widely, from asymptomatic stages to severe, life-threatening conditions. Understanding these manifestations is crucial for early diagnosis and effective management.Angina Pectoris: The Warning...
ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias01:25

ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias

Arrhythmia is a condition characterized by an irregular heart rhythm, with ECG changes that differ based on its origin and nature. The types of arrhythmias discussed below include atrial, junctional, and ventricular arrhythmias.Atrial ArrhythmiasPremature Atrial Complexes (PACs): PACs are early atrial beats caused by stress, caffeine, alcohol, electrolyte imbalances, hypoxia, hyperthyroidism, or certain medications (e.g., bronchodilators and decongestants). The ECG shows early P waves with an...
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Rheumatic Heart Disease I: Introduction

Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...

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Related Experiment Video

Updated: Jun 3, 2026

Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation
28:13

Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation

Published on: February 26, 2013

Clinical Risks and Underlying Mechanisms of Atrial Fibrillation after Myocardial Infarction.

Tian-Peng Wei1, Xiao-Lu Zhang1, Wen-Rui Wang1

  • 1Department of Cardiology, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi 214023, China.

Current Cardiology Reviews
|June 2, 2026
PubMed
Summary

Atrial Fibrillation (AF) after Myocardial Infarction (MI) involves complex remodeling. Understanding these mechanisms can guide new treatments for post-MI AF.

Keywords:
Atrial fibrillationarrhythmia.myocardial infarction

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Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
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The WATCHMAN Left Atrial Appendage Closure Device for Atrial Fibrillation
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The WATCHMAN Left Atrial Appendage Closure Device for Atrial Fibrillation

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Last Updated: Jun 3, 2026

Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation
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Published on: February 26, 2013

Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
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The WATCHMAN Left Atrial Appendage Closure Device for Atrial Fibrillation
23:33

The WATCHMAN Left Atrial Appendage Closure Device for Atrial Fibrillation

Published on: February 28, 2012

Area of Science:

  • Cardiology
  • Electrophysiology
  • Pathophysiology

Background:

  • Atrial Fibrillation (AF) is a frequent complication post-Myocardial Infarction (MI), worsening patient outcomes.
  • The development of AF post-MI is linked to significant atrial structural and electrical changes.

Purpose of the Study:

  • To review the clinical risks and pathophysiological mechanisms of AF following MI.
  • To summarize molecular pathways driving AF in the post-infarction state.
  • To synthesize evidence on pharmacological interventions targeting AF post-MI.

Main Methods:

  • Literature review of clinical risks and pathophysiological mechanisms.
  • Analysis of molecular mechanisms contributing to AF post-MI.
  • Synthesis of current evidence on pharmacological interventions.

Main Results:

  • Post-MI AF involves maladaptive processes, including atrial remodeling, creating an arrhythmogenic substrate.
  • Key molecular mechanisms contributing to AF in this setting were identified.
  • Pharmacological interventions target anti-fibrotic effects, calcium homeostasis, hormone regulation, and inflammation.

Conclusions:

  • Elucidating the dynamic pathophysiological changes in post-MI AF is crucial.
  • Targeted therapeutic strategies for post-infarction AF can be developed based on these insights.