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Published on: March 1, 2022
Reversal of hypertensive heart disease: a multiple linear regression model
Shah Newaz Ahmed1, Ratinder Jhaj1, Balakrishnan Sadasivam1
1Department of Pharmacology, All India Institute of Medical Sciences, Bhopal, Madhya Pradesh, India.
Insights
Lower baseline Left Ventricular Mass Index and greater systolic blood pressure reduction are key to reversing left ventricular hypertrophy in hypertension. Diabetes may impede this regression, suggesting a need for further research into glycemic control.
Area of Science:
- Cardiology
- Hypertension Research
- Medical Research
Background:
- Left ventricular hypertrophy (LVH) in primary hypertension significantly elevates cardiovascular risks.
- Therapeutic blood pressure control is crucial for LVH regression and reducing adverse cardiovascular events.
Purpose of the Study:
- To identify the key determinants influencing the regression of left ventricular hypertrophy in patients with hypertension.
Main Methods:
- A cohort of 217 hypertensive patients with LVH was studied.
- Left Ventricular Mass Index (LVMI) was measured via echocardiography at baseline and after 24 weeks of pharmacotherapy.
- Multiple linear regression analysis modeled LVMI changes, incorporating baseline LVMI, blood pressure changes, and patient demographics.
Main Results:
- Baseline LVMI, reduction in systolic blood pressure, and diabetes were significant predictors of LVH regression.
- Higher baseline LVMI and greater systolic blood pressure reduction correlated with more significant LVH regression.
- Diabetic patients exhibited less LVH regression compared to non-diabetic individuals.
Conclusions:
- Pre-treatment LVMI and achieved systolic blood pressure reduction are primary drivers of LVH regression.
- Diabetes mellitus appears to be associated with diminished LVH regression, highlighting the potential role of glycemic control.
Background:
The development of left ventricular hypertrophy in primary hypertension increases cardiovascular mortality and morbidity. Reversal of left ventricular hypertrophy through therapeutic control of blood pressure reduces the risk of adverse cardiovascular incidents. Objective: In our study, we explored for the determinants of left ventricular hypertrophy regression. Methods: A cohort (n=217) of patients with hypertensive left ventricular hypertrophy was identified by screening consecutive patients in medical outpatient unit. The primary inclusion criteria were (i) Blood pressure more than140/90 mm of Hg (ii) Left Ventricular Mass Index more than 115 and 95 gm/m2 for males and females respectively. Left Ventricular Mass Index was determined by echocardiography at the time of recruitment and after 24 weeks of standard pharmacotherapy. The change in Left Ventricular Mass Index was modelled using multiple linear regression with both categorical and continuous explanatory variables. The effect of drug therapy on change in Left Ventricular Mass Index was tested in the model with dummy coded variables for the treatment categories. Results: In simple linear regression, the variables significantly correlating with change in Left Ventricular Mass Index were baseline Left Ventricular Mass Index (r=0.62, p<0.001), change in systolic blood pressure (r=0.22, p=0.001), change in mean blood pressure (r=0.16, p=0.02), baseline systolic blood pressure (r=0.15, p=0.02), age (r=0.12, p=0.09) and diabetes (r=0.12, p=0.09). The best fit model (r2=0.408) retained baseline Left Ventricular Mass Index (β=0.59, p<0.001), change in systolic blood pressure (β=0.14, p=0.01) and diabetes (β=-0.104, p=0.05) as the significant predictors. Introduction of treatment effect into the model non-significantly increased the fit of the model (r2=0.414, p=0.27-0.98). Conclusions: Pre-treatment Left Ventricular Mass Index and reduction in systolic blood pressure were the major determinants of left ventricular hypertrophy regression. We also observed that there is lesser left ventricular hypertrophy regression in diabetic patients, warranting future research to explore glycaemic control as a modifiable factor in left ventricular hypertrophy reversal.
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