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Changes in coronary anatomy and left ventricular function from the acute to the chronic stage of myocardial
Insights
Coronary angiography reveals that myocardial infarction (MI) can lead to persistent vessel narrowing or occlusion. Ventricular volumes increase post-MI, impacting cardiac function and remodeling.
Area of Science:
- Cardiology
- Interventional Cardiology
- Cardiac Imaging
Background:
- Myocardial infarction (MI) frequently results in significant coronary artery stenosis or occlusion.
- Assessing the natural course of infarct-related arteries and associated cardiac remodeling is crucial for understanding long-term outcomes.
Purpose of the Study:
- To evaluate the angiographic changes in infarct-related arteries following acute myocardial infarction.
- To assess changes in left ventricular volumes and function in the chronic phase after MI.
Main Methods:
- Coronary angiography was performed in 65 patients during the acute phase of MI.
- Follow-up angiography was conducted in 18 patients (55 +/- 46 days post-MI).
- Left ventricular volumes (end-diastolic and end-systolic indices) and ejection fraction were analyzed.
Main Results:
- In the chronic stage, some previously occluded vessels showed improved antegrade flow, though significant narrowing persisted (80-95%).
- Left ventricular end-diastolic volume index (LVEDVI) and end-systolic volume index (LVESVI) significantly increased post-MI.
- Correlation analysis showed a relationship between LVESVI and akinetic segment length (AKS) in both acute and chronic phases, with ejection fraction correlating with AKS in the chronic phase.
Conclusions:
- Infarct-related arteries often remain significantly narrowed or occluded in the chronic phase after MI.
- Significant left ventricular dilation occurs after MI, indicated by increased LVEDVI and LVESVI.
- Cardiac remodeling, including increased ventricular volumes and impaired function, is a key feature of the chronic phase following myocardial infarction.
Abstract:
Coronary angiography was performed in the acute stage of myocardial infarction in 65 patients. The infarct-related vessel was occluded in 50 patients; it was narrowed greater than 90% in the remaining 15 patients. Control angiography was performed 55 +/- 46 d after acute myocardial infarction in 18 patients. In the chronic stage, five of thirteen previously occluded vessels showed antegrade filling of the distal segment. The narrowing at the site of previous obstruction was 80--95%. In two of five patients with a subtotal stenosis, the lumen of the infarct-related vessel was clearly larger in the chronic stage. The end-diastolic volume index increased significantly from 86 +/- 23 ml/m2 in the acute stage to 110 +/- 35 ml/m2 in the chronic stage (p less than 0.001). The increase in the end-systolic volume index from 42 +/- 15 ml/m2 to 63 +/- 31 ml/m2 was also statistically significant (p less than 0.005). Stroke volume index, ejection fraction, and the length of the akinetic segment (AKS) did not change significantly. There was a weak correlation between the end-systolic volume index and the length of the AKS in the acute stage (r = 0.489, p less than 0.05) and a better correlation in the chronic stage (r = 0.602, p less than 0.01). The ejection fraction and the length of the AKS correlated in the chronic stage only (r = 0.795, p less than 0.001).