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Morphological and Functional Assessment of the Right Ventricle Using 3D Echocardiography
Published on: October 28, 2020
Significance of left ventricular hypertrophy in cardiovascular morbidity and mortality
1Heart Institute, Sheba Medical Center, Tel-Hashomer, Israel.
Insights
Left ventricular hypertrophy (LVH) independently increases mortality risk after myocardial infarction. Patients with LVH experienced doubled 1- and 5-year mortality rates, highlighting its prognostic significance.
Area of Science:
- Cardiology
- Internal Medicine
- Pathophysiology
Background:
- Left ventricular hypertrophy (LVH) is traditionally linked to hemodynamic factors.
- LVH is an independent risk factor for adverse cardiovascular outcomes.
- Its presence in various conditions, including obesity and aging, underscores its prognostic importance.
Purpose of the Study:
- To investigate the long-term impact of LVH on mortality in myocardial infarction survivors.
- To assess LVH as an independent prognostic indicator in post-myocardial infarction patients.
Main Methods:
- Analysis of patients surviving myocardial infarction from the SPRINT database.
- Evaluation of long-term mortality (mean 5.5 years) in relation to electrocardiogram-detected LVH (ECG-LVH).
Main Results:
- Patients with ECG-LVH were older and had more in-hospital complications.
- The 1- and 5-year mortality rates were doubled in patients with ECG-LVH compared to those without.
- LVH is associated with significant increases in risk for patients with hypertensive or coronary artery disease.
Conclusions:
- LVH is a significant independent predictor of long-term mortality post-myocardial infarction.
- Mechanisms include cardiac fibrosis, impaired function, and abnormal electrophysiology.
- Regression of LVH through treatment may improve prognosis, requiring further investigation.
Abstract:
Being a "classical" sequel of hemodynamic burdens (pressure and/or volume), the untoward results of left ventricular hypertrophy (LVH) were traditionally related to its underlying causes. The Framingham study was the first to demonstrate the increased independent risk associated with LVH detected by ECG and/or by echocardiography. The presence of LVH in "nonhypertensive" individuals (e.g., obese), the association of LVH with age and gender, and the possibility of genetic control of left ventricular size via "nonhemodynamic" mechanisms had underscored the importance of LVH per se as a prognostic indicator. The presence of LVH in patients with hypertensive or coronary artery disease results in a severalfold increase in risk compared to similar patients without LVH. Early studies have indicated that the presence of LVH is associated with a significantly worse prognosis in patients recovering from myocardial infarction. We have studied the effect of LVH on long-term (mean 5.5 years) mortality in patients surviving myocardial infarction registered in the SPRINT database. The LVH patients were older and had more complications during hospitalization. The 1- and 5-year mortality rates were doubled in patients with ECG-LVH. Review of the mechanisms operating in LVH reveals important changes in the anatomy and physiology of hypertrophied heart, leading to increased fibrosis, inadequate vascular growth, impaired myocardial function (systolic and diastolic), reduced coronary reserve, and abnormal electrophysiological properties. Regression of LVH by proper treatment (achieved mainly by calcium antagonists and ACE inhibitors) may correct many of the above-mentioned adverse phenomena. Whether the regression of LVH per se will lead to improved prognosis remains to be answered in the future.
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