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Published on: June 27, 2025
The cardiovascular risk factor, left ventricular hypertrophy, is highly prevalent in stable, treated angina pectoris
Donald Swee Cheng Ang1, Stuart D Pringle, Allan D Struthers
1Division of Medicine and Therapeutics, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK. d.s.c.ang@dundee.ac.uk
Insights
Left ventricular hypertrophy (LVH) affects 73% of patients with stable angina. Many with LVH have normal blood pressure, indicating LVH is a key factor in coronary artery disease (CAD) risk.
Area of Science:
- Cardiology
- Cardiovascular Disease
- Hypertension Research
Background:
- Left ventricular hypertrophy (LVH) is a reversible factor in cardiac death for coronary artery disease (CAD) patients.
- The overall impact of LVH in CAD depends on its prevalence.
- Assessing LVH prevalence in stable, treated angina patients and its relation to blood pressure (BP) is crucial.
Purpose of the Study:
- To determine the prevalence of left ventricular hypertrophy (LVH) in patients with stable, treated angina.
- To investigate the relationship between LVH and blood pressure (BP) in this patient group.
Main Methods:
- Recruited 322 consecutive patients with confirmed coronary artery disease (CAD).
- Performed echocardiographic LV mass measurements.
- Correlated LV mass with both office and 24-h ambulatory blood pressure (BP).
Main Results:
- Of 267 patients with LV mass data, 195 (73%) exhibited LVH.
- The LVH group had a mean 24-h ambulatory BP of 125/68 mm Hg.
- 62% of LVH patients had nonhypertensive 24-h BP readings.
- Independent predictors of LVH included hypertension history, BMI, and age.
Conclusions:
- Echocardiographic LVH is highly prevalent in stable, treated angina patients.
- A majority of these patients with LVH had nonhypertensive BP readings during the study.
- Further research is needed to evaluate if treating LVH reduces premature death risk in CAD.
Background:
In coronary artery disease (CAD), a potentially reversible factor leading to cardiac death is left ventricular hypertrophy (LVH). However, LVH will only have a large impact overall in CAD if it is highly prevalent. Therefore we aimed to assess the prevalence of LVH in patients with stable, treated angina and its relationship with blood pressure (BP).
Methods:
Three hundred twenty-two consecutive patients with angiographically confirmed coronary artery disease were recruited. Echocardiographic LV mass was performed and correlated with both office and 24-h ambulatory BP.
Results:
Of the 267 patients with LV mass measurements, 195 (73%) had LVH. The mean 24-h ambulatory BP reading was systolic 125 +/- 12 mm Hg and diastolic 68 +/- 8 mm Hg in the LVH group. Of the LVH patients 62% had a nonhypertensive 24-h BP reading. On multivariate logistic regression analysis, factors independently related to LVH were history of hypertension (odds ratio [OR] 1.848, 95% confidence interval [CI] 1.051-3.248), body mass index (OR 1.085, 95% CI 1.011-1.165), and age (OR 1.039, 95% CI 1.004-1.076).
Conclusions:
We conclude that echo LVH is very common in patients with stable, treated angina and the majority of these patients had a nonhypertensive BP at the time of study. Studies are now required to determine whether identifying and vigorously treating LVH in CAD would reduce the risk of premature death in these patients.
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