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Published on: April 13, 2015
Relations of left ventricular mass and systolic function to endothelial function and coronary flow reserve in
V Palmieri1, G Storto, E Arezzi
1Department of Clinical and Experimental Medicine, Federico II University School of Medicine, Naples, Italy. vpalmier@med.cornell.edu
Insights
Left ventricular hypertrophy (LVH) in early hypertension is linked to endothelial dysfunction. However, impaired myocardial contractility, not LVH itself, correlated with reduced coronary flow reserve (CFR) in this study.
Area of Science:
- Cardiology
- Hypertension Research
- Vascular Biology
Background:
- Left ventricular hypertrophy (LVH) is a known cardiovascular risk factor.
- The independent association between LVH, coronary flow reserve (CFR), and endothelial dysfunction in early hypertension remains unclear.
Purpose of the Study:
- To investigate the relationship between left ventricular mass and systolic function with CFR and endothelial function in newly diagnosed, untreated essential arterial hypertension patients.
Main Methods:
- Echocardiography assessed LVH, ejection fraction (EF), and stress-corrected midwall shortening (MWS).
- Coronary flow reserve (CFR) was measured using single-photon emission computed tomography with dipyridamole infusion.
- Endothelial function was evaluated via flow-mediated dilatation (FMD) and nitroglycerine-mediated dilatation (NMD) of the brachial artery.
Main Results:
- LV mass index negatively correlated with FMD (P<0.05), indicating endothelial dysfunction, but not with NMD or CFR.
- Stress-corrected MWS independently correlated with CFR (P<0.05).
- Five of 21 subjects had LVH; no significant association was found between LVH and CFR.
Conclusions:
- In early-stage, untreated hypertension, LVH may be associated with endothelial dysfunction.
- Impaired myocardial contractility, assessed by MWS, is linked to reduced CFR, suggesting a distinct early cardiovascular phenotype.
Abstract:
Left ventricular hypertrophy (LVH) is prognostically relevant, associated with major cardiovascular risk factors and with atherosclerosis. However, whether LVH is independently associated with impaired coronary flow reserve (CFR) and with endothelial dysfunction is disputed. We assessed the relationship of LV mass and systolic function to CFR and endothelial function in new discovered never treated subjects with essential arterial hypertension, but without coronary artery disease or microalbuminuria. LVH, ejection fraction (EF) and stress-corrected midwall shortening (MWS, a measure of myocardial contractility) were assessed by echocardiography. CFR was assessed by single-photon emission computed tomography and dipyridamole infusion. Endothelial function was evaluated by assessing 1-min postischaemic flow-mediated dilatation of the brachial artery (FMD); nitroglycerine-mediated dilatation (NMD) of the same brachial artery was used as measure of nonendothelium-dependent vasodilatation. In approximately 1 year, we enrolled 21 subjects who met stringent inclusion criteria (47+/-10 years old, 26.6+/-2.8 kg/m2, 78% men). Five patients showed LVH. Multivariate analyses showed a significant negative correlation of LV mass index with FMD (beta=-0.61, P<0.05) but not with NMD, neither with CFR. Stress-corrected MWS showed independent correlation with CFR (beta=0.51, P<0.05). Thus, in clinically healthy, new discovered hypertensive subjects, never treated and mostly in the early stage of arterial hypertension, LVH can be associated with endothelial dysfunction while maximal dipyridamole- dependent CFR may be preserved; nevertheless, a cardiac phenotype presenting with tendency to impaired myocardial contractility, assessed by stress-corrected MWS, showed association with lower CFR in the early stage of arterial hypertension.
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