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Relation of left ventricular dilation during acute myocardial infarction to systolic performance, diastolic
A A Seals1, C M Pratt, J J Mahmarian
1Department of Medicine, Baylor College of Medicine, Houston, Texas.
Insights
Left ventricular dilation occurs early after acute myocardial infarction (AMI), especially in anterior cases. Diastolic dysfunction is common, even with normal systolic function, as the heart dilates to maintain stroke volume.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Myocardial Infarction Research
Background:
- Acute myocardial infarction (AMI) significantly impacts left ventricular (LV) function.
- Understanding early LV remodeling and dysfunction is crucial for patient outcomes.
Purpose of the Study:
- To quantify LV volumes and assess their relationship with systolic/diastolic dysfunction post-AMI.
- To evaluate the impact of infarct location on LV remodeling.
- To investigate the correlation between infarct size and LV volumetric changes.
Main Methods:
- Blood pool radionuclide angiography in 54 first-time AMI patients.
- Assessment of LV end-diastolic, end-systolic, and stroke volume indexes, ejection fraction, and peak diastolic filling rate.
- Infarct size estimation using plasma MB creatine kinase activity.
Main Results:
- Significant LV dilation observed within 24 hours of AMI.
- Anterior AMI patients showed greater LV dilation (end-diastolic and end-systolic volumes) than inferior AMI patients.
- Low peak diastolic filling rates were noted, irrespective of ejection fraction.
- LV volumes increased further by day 10, while ejection fraction and diastolic filling rate remained unchanged.
- No significant correlation between infarct size and LV volumetric indices.
Conclusions:
- LV dilation is an early event following AMI, more pronounced in anterior infarcts.
- Significant LV diastolic dysfunction is prevalent, even with preserved systolic function.
- Early LV dilation serves as a compensatory mechanism to maintain stroke volume despite reduced LV function.
Abstract:
The quantification of left ventricular (LV) volumes and assessment of their relation to systolic and diastolic dysfunction, infarct size and anatomic location were performed in 54 patients with a first acute myocardial infarction (AMI). Blood pool radionuclide angiography was used to assess LV end-diastolic, end-systolic, and stroke volume indexes, ejection fraction and peak diastolic filling rate. Infarct size was estimated from plasma MB creatine kinase activity. Substantial LV dilation occurred within the initial 24 hours of AMI. The peak diastolic filling rate was low, even in those patients with a normal ejection fraction. In comparison with inferior AMI (n = 25), patients with anterior AMI (n = 29) had a larger end-diastolic volume index (105 +/- 8 vs 81 +/- 4 ml/m2, p less than 0.01) and end-systolic volume index (64 +/- 7 vs 37 +/- 4 ml/m2, p less than 0.001), but similar stroke volume index (41 +/- 3 vs 43 +/- 2 ml/m2, difference not significant). No significant relation was noted between infarct size estimated by MB creatine kinase and any volumetric index. On repeat study (day 10 after AMI), end-diastolic and end-systolic volume indexes increased further (p less than 0.05 vs day 1) but ejection fraction and peak diastolic filling rate were unchanged. It was concluded that: (1) LV dilation occurs within hours of AMI in both inferior and anterior AMI, but is more marked in the latter; (2) significant LV diastolic dysfunction is the rule, even in patients with preserved LV systolic function; and (3) LV dilation is an early compensatory mechanism that maintains normal stroke volume, even in patients with severely reduced LV function.