Relationship Between Geometry and Ventricular Filling Pressures in Non-Diabetic Hypertensive Patients

Alejandro Suarez

doi:10.11648/j.ccr.20210503.12

Abstract

Hypertension and obesity make changes in the heart that are known as remodeling and diastolic dysfunction. These changes are the beginning of a later sistolic heart failure. Objectives Searching for the relation between geometry and ventricular function in hypertensive non diabetic and obese patients. 68 women and 20 men were evaluated by doppler- echocardiography. All patients had a normal ejection fraction. Results Ventricular geometry was altered in 53.4% of the subjects and diastolic function in 73.8% respectively. As body weight increased the ventricular mass, relative wall thickness, left atrial dimension and end diastolic volumes increased too. Overweight and obesity were found in 62.5% of the sample. A concentric left ventricular hypertrophy was present in 27.2% of the patients. An excentric left ventricular hypertrophy was found in 14.7% of them and 46.6% had a normal geometry. Eyection fraction values were lesser in the group with bigger ventricular mass and altered filling patterns. P=0.05, 0.1. Conclusion Arterial hypertension and obesity are risk factors for the development of cardiac abnormalities that lower systolic cardiac function in case of hypertrophy and dilatation are not resolved.

Highlights

IntroductionLeft ventricular hypertrophy is common. Grossman in 1975 pointed out that ventricular hypertrophy in response to overload pressure was initially produced to normalize parietal stress of ventricle [1].There is a stretch induced by high arterial pressure on the wall of the vessel and on the ventricular wall that leads to the generation of hypertrophy through angiotensin II and endotelin I and by the activation of the extracellular kinase protein regulated by signal. [2].This ventricular hypertrophy of hypertensive origin is associated with high mortality and an increased risk for developing myocardial infarction, stroke, and heart failure. [3].In line with this hypertrophy there is a remodeling that is defined as interstitial, cellular, molecular and genetic changes that alter the shape, volume and function of the heart.These changes involve myocytes, fibroblasts, colagen, and intramyocardic vessels
In hypertensive patients, left ventricular hypertrophy is common
This study considers an end-of-diastole volume value less than 97 ml/m2 which together with an ejection fraction (EF) of 50% or more are the criteria of the Echocardiography Association of the European Society of Cardiology. [9]

Summary

Introduction

Left ventricular hypertrophy is common. Grossman in 1975 pointed out that ventricular hypertrophy in response to overload pressure was initially produced to normalize parietal stress of ventricle [1].There is a stretch induced by high arterial pressure on the wall of the vessel and on the ventricular wall that leads to the generation of hypertrophy through angiotensin II and endotelin I and by the activation of the extracellular kinase protein regulated by signal. [2].This ventricular hypertrophy of hypertensive origin is associated with high mortality and an increased risk for developing myocardial infarction, stroke, and heart failure. [3].In line with this hypertrophy there is a remodeling that is defined as interstitial, cellular, molecular and genetic changes that alter the shape, volume and function of the heart.These changes involve myocytes, fibroblasts, colagen, and intramyocardic vessels. This ventricular hypertrophy of hypertensive origin is associated with high mortality and an increased risk for developing myocardial infarction, stroke, and heart failure. In line with this hypertrophy there is a remodeling that is defined as interstitial, cellular, molecular and genetic changes that alter the shape, volume and function of the heart. These changes involve myocytes, fibroblasts, colagen, and intramyocardic vessels. This remodeling can be evaluated by the measurement of cardiac dimensions and shape, the measurement of the ventricular mass, the relative parietal thickness, the ejection fraction, and the end volumes of sistole and diastole. This remodeling can be evaluated by the measurement of cardiac dimensions and shape, the measurement of the ventricular mass, the relative parietal thickness, the ejection fraction, and the end volumes of sistole and diastole. [4]

Objectives

Methods

Results

Discussion

Conclusion