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Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
Published on: April 17, 2021
The relationship between renal function and cardiac structure, function, and prognosis after myocardial infarction:
Anil Verma1, Nagesh S Anavekar, Alessandra Meris
1Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
Insights
Renal impairment after myocardial infarction (MI) is linked to cardiac structural changes, not reduced systolic function. Diastolic dysfunction may explain the increased risk in these patients.
Area of Science:
- Cardiology
- Nephrology
- Internal Medicine
Background:
- Renal impairment is a known risk factor for adverse cardiovascular outcomes following myocardial infarction (MI).
- Understanding the mechanisms linking renal function to cardiac health post-MI is crucial for risk stratification and management.
Purpose of the Study:
- To investigate whether cardiac structural or functional alterations mediate the heightened risk observed in patients with renal impairment after MI.
- To identify specific echocardiographic parameters associated with varying levels of renal function.
Main Methods:
- Echocardiography was performed on 603 post-MI patients with left ventricular (LV) dysfunction and/or heart failure (HF).
- Patients were stratified by estimated glomerular filtration rate (eGFR).
- Multivariable Cox regression analyzed the relationship between eGFR, cardiac parameters, and outcomes (death or HF).
Main Results:
- Reduced eGFR correlated with smaller LV volumes, larger left atrial (LA) volumes, and increased LV mass index (LVMI).
- LV hypertrophy was more prevalent in patients with reduced eGFR.
- While systolic function (ejection fraction, right ventricular function) was unaffected by renal function, diastolic parameters (mitral deceleration time) showed associations.
- LVMI and LA volume were significant independent predictors of adverse outcomes.
Conclusions:
- Renal impairment after MI is associated with adverse cardiac remodeling (smaller LV, larger LA, increased LVMI), but not with reduced systolic function.
- Diastolic dysfunction, suggested by altered mitral deceleration time and LA volume, may be a key mediator of the increased risk.
- These findings highlight the importance of assessing cardiac structure and diastolic function in patients with renal impairment post-MI.
Objectives:
The purpose of this study was to determine whether alterations in cardiac structure or function contribute to the increased risk associated with renal impairment after myocardial infarction (MI).
Background:
Renal impairment is associated with adverse cardiovascular outcomes after MI.
Methods:
Echocardiography was performed on 603 patients with left ventricular (LV) dysfunction, heart failure (HF), or both after MI. Patients were grouped according to their estimated glomerular filtration rate (eGFR), and measures of cardiac structure and function were related to baseline eGFR. The relationship between eGFR and cardiac structure and function and clinical outcomes of death or HF was assessed with multivariable Cox regression.
Results:
Ejection fraction, infarct segment length, right ventricular function, and mitral deceleration time were not influenced by renal function. Patients with reduced eGFR had smaller LV and larger left atrial (LA) volumes and higher left ventricular mass index (LVMI) and LV mass/LV volume ratio. A greater proportion of the patients with reduced eGFR had LV hypertrophy. The relationship between eGFR and the outcome of death or HF was attenuated by including baseline differences in LVMI, and both LVMI and LA volume conferred additional prognostic information in a multivariable model.
Conclusions:
Renal impairment was associated with smaller LV and larger LA volumes and increased LVMI. Systolic function was similar when compared with patients with normal renal function. Thus, reduced systolic function cannot account for worse outcomes in patients with renal impairment after MI. Indirect measures of diastolic function suggest that diastolic dysfunction might be an important mediator of increased risk in this population.
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