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Updated: Jul 16, 2026

Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
The relationship of myocardial infarct size and prognosis
Insights
Patients experiencing cardiogenic shock within 6 hours of acute myocardial infarction had larger necrotic areas and more occluded arteries. This rapid-onset shock may be less responsive to current therapies compared to slow-onset cases.
Area of Science:
- Cardiology
- Pathophysiology
- Medical Research
Background:
- Cardiogenic shock is a critical complication of acute myocardial infarction.
- Understanding the factors influencing shock onset and severity is crucial for patient outcomes.
Purpose of the Study:
- To investigate the relationship between the timing of cardiogenic shock onset after acute myocardial infarction and infarct characteristics.
- To compare pathological findings in patients with rapid-onset versus slow-onset cardiogenic shock.
Main Methods:
- Patients with cardiogenic shock post-acute myocardial infarction were divided into two groups based on shock onset (within 6 hours vs. >6 hours).
- Infarct size, epicardial artery occlusion sites, and collateral flow were assessed.
- Postmortem X-ray examination was utilized to evaluate collateral circulation.
Main Results:
- Rapid-onset shock (within 6 hours) was associated with significantly larger areas of myocardial necrosis (48% vs. 28%).
- Patients with rapid-onset shock exhibited more sites of total epicardial artery occlusion (3.5 vs. 1.6).
- Less visible collateral flow was observed in rapid-onset shock cases compared to slow-onset cases.
Conclusions:
- The timing of cardiogenic shock onset correlates with infarct size, arterial occlusion, and collateral circulation.
- Slow-onset cardiogenic shock appears more amenable to current therapeutic interventions than rapid-onset shock.
Abstract:
Patients with cardiogenic shock were arbitrarily divided into groups, those in whom shock appeared within 6 hours after the onset of acute infarction and those in whom the symptoms appeared more than 6 hours after the onset of acute infarction. The patients with more rapidly developing shock had larger areas of necrosis (average 48%) than the slow-onset group (average 28%). The former group had more sites of total occlusion of the epicardial arteries (3.5 vs 1.6) than the slow-onset group. By postmortem X-ray examination less collateral flow was visible in the rapid-onset shock patients than the slow-onset ones. These observations suggest that slow-onset shock is more likely to respond to presently available therapeutic interventions than the cases with rapid-onset shock.
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