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Glucose intolerance exaggerates left ventricular hypertrophy and dysfunction in essential hypertension

N Hara-Nakamura1, K Kohara, T Sumimoto

  • 1Second Department of Internal Medicine, Ehime University School of Medicine, Japan.

American Journal of Hypertension
|December 1, 1994
PubMed
Summary

Glucose intolerance, a precursor to diabetes, worsens heart problems in essential hypertension. It accelerates left ventricular hypertrophy and impairs heart muscle function, impacting both diastolic and systolic performance.

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Area of Science:

  • Cardiology
  • Metabolic Disorders
  • Hypertension Research

Background:

  • Essential hypertension is a major risk factor for cardiovascular disease.
  • Glucose intolerance, a pre-diabetic state, is increasingly recognized as a significant comorbidity.
  • The impact of glucose intolerance on cardiac structure and function in hypertensive individuals requires further elucidation.

Purpose of the Study:

  • To investigate the influence of glucose intolerance on left ventricular hypertrophy (LVH) and left ventricular dysfunction in patients with essential hypertension.
  • To compare cardiac parameters between hypertensive patients with and without glucose intolerance, and normotensive controls.

Main Methods:

  • Two-dimensional M-mode echocardiography was utilized to assess cardiac parameters.

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  • Study included three groups: essential hypertensive patients with glucose intolerance (n=28), essential hypertensive patients without glucose intolerance (n=44), and normotensive controls (n=29).
  • Age- and sex-matched participants were selected for comparative analysis.

    • Main Results:

    • Hypertensive patients with glucose intolerance exhibited significantly higher left ventricular mass index (LVMI) compared to those without (115.6 +/- 28.2 vs 102.1 +/- 22.1 g/m2; P < .05).
    • Left ventricular diastolic function, indicated by peak lengthening rate, was reduced in glucose-intolerant hypertensive patients (2.68 +/- 0.71/sec) versus non-intolerant hypertensive patients (3.16 +/- 0.82/sec; P < .05).
    • Left ventricular contractility, assessed by end-systolic wall stress/LV end-systolic volume index, was more diminished in glucose-intolerant hypertensive patients (2.75 +/- 0.55 x 10(3) dyn.m2/cm2.mL-1) compared to their non-intolerant counterparts (3.13 +/- 0.55 x 10(3) dyn.m2/cm2.mL-1; P < .01).

    Conclusions:

    • Glucose intolerance accelerates the progression of left ventricular hypertrophy in essential hypertension.
    • The preclinical stage of diabetes mellitus significantly deteriorates both diastolic and systolic left ventricular function in hypertensive individuals.
    • Early identification and management of glucose intolerance may be crucial for preventing cardiac remodeling and dysfunction in essential hypertension.