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[Segmental changes in contractility of the left heart ventricle in Chagas cardiomyopathy with and without ventricular
1Hospital Universitário Prof. Edgard Santos da Faculdade de Medicina, UFBA, Salvador.
Insights
Chronic chagasic myocarditis (CCM) initially causes segmental left ventricular (LV) wall motion abnormalities. The condition progresses to LV dilatation and diffuse hypocontractility.
Area of Science:
- Cardiology
- Infectious Diseases
- Medical Imaging
Background:
- Chagasic myocarditis (CCM) is a significant cause of heart disease.
- Understanding the progression of myocardial dysfunction in CCM is crucial for patient management.
Purpose of the Study:
- To evaluate left ventricular (LV) segmental wall motion abnormalities in dilated and nondilated chronic chagasic myocarditis (CCM).
- To elucidate the progression of myocardial dysfunction in CCM.
Main Methods:
- Sixty-nine patients with CCM were divided into two groups based on LV end-diastolic dimension (LVEDD) and cardio-thoracic ratio (CTR).
- Two-dimensional echocardiogram (Echo) was used to analyze LV global and segmental contractility.
- A point score system was applied to quantify LV contractility.
Main Results:
- Segmental wall motion abnormalities were observed in 68% of patients, predominantly affecting the apex (64%) and postero-inferior wall (30%).
- Apical aneurysms were noted in 42% of patients.
- A significant correlation was found between LVDD and LV contractility score (r = 0.66; p = 0.0000).
- LV contractility was normal in 28% of patients (47% in group A, 3% in group B).
- Abnormal contractility patterns were segmental in group A and diffuse in group B (93%).
Conclusions:
- Early-stage CCM is characterized by segmental LV abnormalities, often involving the apex and postero-inferior wall, sometimes with aneurysm formation.
- CCM appears to progress from segmental wall motion abnormalities with normal LVDD to LV dilatation and diffuse hypocontractility.
Purpose:
To evaluate left ventricular (LV) segmental wall motion abnormalities in dilated and nondilated chronic chagasic myocarditis (CCM), to better understand the myocardial dysfunction progression in this pathology.
Methods:
Sixty nine patients with the CCM, 39 had normal end-diastolic left ventricular dimension (LVEDD) and normal cardio-thoracic ratio (CTR) (group A), and 30 had increased LVEDD and CTR (group B), all of them with abnormal EKG, had the LV global and segmental contractility analysed by two-dimensional echocardiogram (Echo). A point score system to the LV contractility was applied.
Results:
Segmental wall motion abnormalities were seen in 68% of the patients: apical 64%, postero-inferior 30%, septal 17%, anterior 6% and lateral 0. Apical aneurysm was observed in 42% of the patients, postero-inferior in 6% and basal septal in 3%. There was a statistically significant correlation between the LVDD and the LV score of contractility (r = 0.66; p = 0.0000). The LV contractility was normal in 28% of the patients, 47% in group A and 3% in group B. While in group A the abnormal pattern of contractility was segmental in all, but one patient, in group B it was diffuse in the large majority (93%).
Conclusion:
Initially LV abnormality in CCM is segmental. Beyond the apex, other regions of the LV are involved, the postero-inferior wall and basal septum for instance, even with aneurysm morphology. The CCM seems to evolve from an stage with essentially segmental wall motion abnormalities and normal LVDD to LV dilatation and diffuse hypocontractility.