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Left ventricular hypertrophy contributes to Myocardial Ischemia in Non-obstructive Coronary Artery Disease (the
Ingeborg Eskerud1, Eva Gerdts2, Terje H Larsen3
1Department of Clinical Science, University of Bergen, PO box 7804, N-5020 Bergen, Norway.
Insights
Left ventricular hypertrophy (LVH) is linked to myocardial ischemia in patients with non-obstructive coronary artery disease (CAD). This finding suggests LVH may independently contribute to ischemia in this patient group.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Medical Diagnostics
Background:
- Mechanisms of myocardial ischemia in non-obstructive coronary artery disease (CAD) remain unclear.
- Investigating the association between left ventricular hypertrophy (LVH) and myocardial ischemia in patients with stable angina and non-obstructive CAD.
Purpose of the Study:
- To determine if left ventricular hypertrophy (LVH) is associated with myocardial ischemia in patients diagnosed with stable angina and non-obstructive coronary artery disease (CAD).
Main Methods:
- 132 patients with stable angina and non-obstructive CAD (<50% stenosis via CCTA) underwent myocardial contrast stress echocardiography.
- LVH was defined by LV mass index; myocardial ischemia was assessed by echocardiography.
- Patients were categorized based on the presence and extent of ischemia.
Main Results:
- Myocardial ischemia was detected in 52% of patients.
- Patients with ischemia showed a higher prevalence of LVH (23% vs. 10%, p=0.035).
- LVH independently correlated with the presence (OR 3.27, p=0.031) and extent (β=0.22, p=0.012) of myocardial ischemia.
Conclusions:
- Left ventricular hypertrophy (LVH) is an independent predictor of myocardial ischemia in patients with stable angina and non-obstructive CAD.
- LVH contributes to both the occurrence and severity of myocardial ischemia in this population.
- These findings highlight LVH as a significant factor in non-obstructive CAD-related ischemia.
Background:
The underlying mechanisms causing myocardial ischemia in non-obstructive coronary artery disease (CAD) are still unclear. We explored whether left ventricular hypertrophy (LVH) was associated with myocardial ischemia in patients with stable angina and non-obstructive CAD.
Methods:
132 patients (mean age 63 ± 8 years, 56% women) with stable angina and non-obstructive CAD diagnosed as <50% stenosis by coronary computed tomography angiography (CCTA) underwent myocardial contrast stress echocardiography. Left ventricular (LV) hypertrophy (LVH) was identified by LV mass index >46.7 g/m2.7 in women and >49.2 g/m2.7 in men. Patients were grouped according to presence or absence of myocardial ischemia by myocardial contrast stress echocardiography. The number of LV segments with ischemia at peak stress was taken as a measure of the extent of myocardial ischemia.
Results:
Myocardial ischemia was found in 52% of patients, with on average 5 ± 3 ischemic LV segments per patient. The group with myocardial ischemia had higher prevalence of LVH (23 vs. 10%, p = 0.035), while age, sex and prevalence of hypertension did not differ between groups (all p > 0.05). In multivariable regression analyses, LVH was associated with presence of myocardial ischemia (odds ratio 3.27, 95% confidence interval [1.11-9.60], p = 0.031), and larger extent of myocardial ischemia (β = 0.22, p = 0.012), independent of confounders including age, hypertension, obesity, hypercholesterolemia, calcium score and segment involvement score by CCTA.
Conclusions:
LVH was independently associated with both presence and extent of myocardial ischemia in patients with stable angina and non-obstructive CAD by CCTA. These results suggest LVH as an independent contributor to myocardial ischemia in non-obstructive CAD.
Clinical Trial Registration Number:
ClinicalTrials.gov, identifier NCT018535271.
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