Differences in left ventricular functional adaptation to arterial stiffness and neurohormonal activation in patients...

Arterial stiffness increases pressure load to the left ventricle (LV), leading to LV hypertrophy and subendocardial ischemia. Neurohormones stimulate myocardial fibrosis and LV dysfunction. We aimed to explore the associations of arterial stiffness and plasma aldosterone with multi-directional, layer-specific LV, and left atrial (LA) mechanical function in hypertensive patients.

Layer-specific LV global longitudinal strain (GLS-trans, GLS-endo, GLS-epi), global circumferential strain (GCS-trans, GCS-endo, GCS-epi), LV torsional parameters, and LA global longitudinal strain (LA GLS) were analyzed by two-dimensional speckle tracking echocardiography in 195 hypertensive patients (110 men, mean age 55 years). Pulse wave velocity (PWV) was analyzed as a measure of arterial stiffness, and plasma aldosterone was measured for evaluation of neurohormonal activation.

In a simple correlation, PWV significantly correlated with LV GLS-endo and LA GLS. Log aldosterone correlated with both LV GCS-endo and LV GCS-trans. Multiple regression analysis revealed that LV GLS-endo (β = 0.223, p = 0.031) and LA GLS (β = -0.311, p = 0.002) were independently correlated with PWV even after controlling for confounding factors.

In hypertensive patients without clinically apparent target organ damage, LV GLS, especially endocardium, and LA GLS were more dominantly affected by arterial stiffness because, among the three myocardial layers, the endocardium is most susceptible to pressure overload. Two-dimensional layer-specific speckle-tracking echocardiography sensitively detects LV mechanical dysfunction and provides pathophysiologic insights into LV mechanical adaptations in hypertension.