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[The influence of left systolic ventricular function on right ventricular function after an acute myocardial infarct]
A Izzo1, M Galderisi, O de Divitiis
1Laboratorio di Ecocardiografia, Cattedra di Medicina d'Urgenza, Università degli Studi Federico II, Napoli.
Insights
Right ventricular systolic function is impaired after acute myocardial infarction (AMI), especially with inferior AMI. This impairment correlates with left ventricular dysfunction and infarct severity, highlighting the interconnectedness of heart chambers post-MI.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Echocardiography
Background:
- Acute myocardial infarction (AMI) can affect both left and right ventricular function.
- Understanding the interaction between ventricular systolic function post-AMI is crucial for patient outcomes.
- Previous studies have focused on left ventricular (LV) function, with less emphasis on right ventricular (RV) interactions.
Purpose of the Study:
- To assess the interaction between left ventricular (LV) and right ventricular (RV) systolic function following acute myocardial infarction (AMI).
- To investigate how AMI location (inferior vs. non-inferior) influences RV and LV systolic function.
- To identify factors associated with RV systolic impairment after AMI.
Main Methods:
- Echocardiographic assessment of RV function using tricuspid annular plane systolic excursion (TAPSE) and Doppler analysis of RV outflow tract.
- Echocardiographic assessment of LV systolic function using ejection fraction (LVEF) and wall motion score index.
- Comparison of RV and LV function between normal subjects, inferior AMI patients, and non-inferior AMI patients.
Main Results:
- Overall AMI population showed reduced RV function (TAPSE, outflow tract velocity-time integral, peak velocity) and LV dysfunction (decreased LVEF, increased wall motion score index).
- Inferior AMI patients exhibited more pronounced RV and LV systolic impairment compared to non-inferior AMI patients.
- Significant correlations were found between LV and RV functional parameters, particularly in inferior AMI patients, with infarct size (creatine kinase peak) related to RV function.
Conclusions:
- Right ventricular systolic impairment after LV AMI is dependent on the degree of LV dysfunction and hemodynamic load.
- AMI location and infarct extension are key determinants of RV systolic dysfunction post-MI.
- The findings underscore the significant interaction between RV and LV systolic function following acute myocardial infarction.
Abstract:
The aim of this study was to assess the interaction between left ventricular and right ventricular systolic function after acute myocardial infarction (AMI). The study population comprises 27 normal subjects and 71 patients assessed at predischarge (12 +/- 7 days) after AMI and divided into two subgroups, 24 with inferior AMI and 47 with non inferior AMI. The three groups were comparable for sex, age, heart rate and blood pressure. Right ventricular function was evaluated by two-dimensional assessment of tricuspid annular plane systolic excursion (TAPSE) and by Doppler analysis of right ventricular outflow tract. Left ventricular systolic function was evaluated by two-dimensional determination of ejection fraction and wall motion score index, and by Doppler analysis of left ventricular outflow tract. The overall AMI population showed reduced TAPSE, velocity-time integral (both p < 0.05) and peak velocity (p < 0.005) of right ventricular outflow tract, prolongation of Q-S2 interval and increase of pre-ejection period/acceleration time ratio (both p < 0.05) in comparison with normals. These alterations were accompanied by a decrease of left ventricular ejection fraction and increase of wall motion score index. (p < 0.0001) The changes of right ventricular indexes were confirmed in patients with inferior AMI who had also lower left ventricular ejection fraction (46 +/- 9%). Functional parameters of the right ventricle were not significantly modified in patients with non inferior AMI who had greater left ventricular ejection fraction (53 +/- 8.6%). In the overall AMI population, and in particular in inferior AMI, we found univariate relations between time-velocity integrals of left ventricular and right ventricular outflow tract and between left ventricular ejection fraction and TAPSE. Only in inferior AMI creatinkinase peak was related to time-velocity integral of right ventricular outflow tract (r = -0.59, p < 0.01). In conclusion, the magnitude of right ventricular systolic impairment developing after left ventricular AMI depends on the degree of left ventricular dysfunction, likewise by changes of hemodynamic load imposed to the right ventricle. AMI location and, only in inferior AMI, infarct extension participate in determining this dysfunction.