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Left ventricular hypertrophy in young hypertensives: the possible crosstalk of mTOR and angiotensin-II -a

Busayo Onafowoke Oguntola1,2, Stephen Olawale Oguntola3, Opeyemi Ezekiel Ojo4

  • 1Department of Internal Medicine, ABUAD Multisystem Hospital, Afe Babalola University, Ado- Ekiti, 360101, Nigeria. busayoonafeso@gmail.com.

BMC Cardiovascular Disorders
|January 8, 2025
PubMed

Insights

Hypertension can cause early heart changes like left ventricular hypertrophy (LVH) in young adults. The study found mTOR and Angiotensin-II may interact in LVH development, linked to inflammation and fibrosis.

Area of Science:

  • Cardiology
  • Hypertension Research
  • Molecular Medicine

Background:

  • Hypertension is a primary driver of cardiac dysfunction, with left ventricular hypertrophy (LVH) as an early indicator.
  • Adverse cardiac remodeling in hypertension affects all age groups, particularly in Black populations.
  • This study investigated LVH prevalence and the roles of mTOR and Angiotensin-II in young hypertensives.

Purpose of the Study:

  • To estimate the prevalence of left ventricular hypertrophy (LVH) in young hypertensive individuals.
  • To assess the involvement of mammalian target of rapamycin (mTOR) and Angiotensin-II (Ang II) in the pathogenesis of LVH.
  • To explore potential biomarkers for LVH in young adults with hypertension.

Main Methods:

  • A prospective case-control study included 110 hypertensive and 60 normotensive participants aged 18-45.
  • Echocardiography, ECG, and enzyme-linked immunosorbent assays were used to measure LVH, blood pressure, and serum markers.
  • Key markers assessed included mTOR, Ang II, chemerin, lipids, troponin-T, NF-Kβ, and Galectin-3.

Main Results:

  • LVH prevalence varied from 11.01% to 39% based on echocardiographic and ECG criteria among hypertensives.
  • Hypertensives with LVH exhibited significantly higher blood pressure, BMI, triglycerides, and markers of inflammation and fibrosis (chemerin, troponin T, Galectin-3).
  • Serum levels of mTOR were positively correlated with Angiotensin-II, suggesting a potential interaction in LVH development.

Conclusions:

  • The findings suggest a significant interaction between mTOR and Angiotensin-II in the development of LVH.
  • Left ventricular hypertrophy in young hypertensives is associated with dyslipidemia, inflammation, and fibrosis.
  • mTOR and Ang II may serve as pathogenic markers for LVH in young hypertensive patients.
Abstract

Keywords:
Angiotensin IIEchocardiographyHypertensionLeft ventricular hypertrophyMammalian target organ of rapamycin

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