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Published on: May 13, 2019
Relationship between left ventricular mass and endothelium-dependent vasodilation in never-treated hypertensive
F Perticone1, R Maio, R Ceravolo
1Department of Medicina Sperimentale e Clinica "G. Salvatore" University of Catanzaro, Italy.perticone@unicz.it
Insights
Hypertension damages blood vessels and the heart. In hypertensive patients, increased left ventricular mass (LVM) is linked to poorer endothelium-dependent vasodilation, suggesting dual damage from hypertension.
Area of Science:
- Cardiology
- Vascular Biology
- Hypertension Research
Background:
- Hypertension is associated with left ventricular hypertrophy (LVH) and endothelial dysfunction.
- Assessing the interplay between cardiac structure and vascular function in hypertension is crucial.
Purpose of the Study:
- To investigate the relationship between echocardiographic left ventricular mass (LVM) and endothelium-dependent vasodilation in never-treated hypertensive patients.
Main Methods:
- Echocardiography was used to measure LVM in 65 hypertensive patients.
- Endothelial function was assessed by forearm blood flow (FBF) responses to acetylcholine (ACh) and sodium nitroprusside (SNP) infusions.
- LVM was indexed by body surface area and height to the 2.7th power.
Main Results:
- A significant inverse relationship was observed between indexed LVM and FBF response to ACh (r=-0.554; P<0.0001).
- Patients with LVH showed significantly lower FBF responses to ACh compared to those without LVH (9.9+/-3.7 vs. 16.1+/-8.1 mL/100 mL/min; P<0.0001).
- No significant correlation was found between LVM and FBF response to SNP.
Conclusions:
- Echocardiographic LVM is inversely related to endothelium-dependent vasodilation in hypertensive patients.
- Hypertension likely contributes to damage in both the left ventricle and the endothelium.
Background:
Hypertensive patients are characterized by development of both left ventricular hypertrophy (LVH) and endothelial dysfunction
Methods And Results:
We enrolled 65 never-treated hypertensive patients (36 men and 29 women aged 45.6+/-6.0 years) to assess the possible relationship between echocardiographic left ventricular mass (LVM) and endothelium-dependent vasodilation. Left ventricular measurements were performed at end diastole and end systole according to the recommendations of the American Society of Echocardiography and the Penn Convention. LVM was calculated with the Devereux formula and indexed by body surface area and height raised to the 2.7th power. The endothelial function was tested as responses of forearm vasculature to acetylcholine (ACh), an endothelium-dependent vasodilator (7.5, 15, and 30 microg. mL-1. min-1, each for 5 minutes), and sodium nitroprusside (SNP), an endothelium-independent vasodilator (0.8, 1.6, and 3.2 microg. mL-1. min-1, each for 5 minutes). Drugs were infused into the brachial artery, and forearm blood flow (FBF) was measured by strain-gauge plethysmography. A negative significant relationship between indexed LVM and peak of increase in FBF was found during ACh infusions (r=-0. 554; P<0.0001). In addition, hypertrophic patients had a significantly lower responsive to ACh than patients without LVH (the peak increase in FBF was 9.9+/-3.7 versus 16.1+/-8.1 mL per 100 mL of tissue per minute; P<0.0001). No significant correlation was observed between LVM and FBF during SNP infusion.
Conclusions:
Our data provide the first evidence that echocardiographic LVM in hypertensive patients is inversely related to FBF responses to the endothelium-dependent vasodilating agent ACh, but it is likely that both endothelium and LVM are damaged by hypertension.
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