Association of Arterial Stiffness and Electrocardiography-Determined Left Ventricular Hypertrophy with Left Ventricular Diastolic Dysfunction

Abstract

ObjectivesIncreased arterial stiffness is associated with left ventricular diastolic dysfunction (LVDD), but this association may be influenced by left ventricular (LV) performance. Left ventricular hypertrophy (LVH) is not only a significant determinant of LV performance, but is also correlated with LVDD. This study is designed to compare LV diastolic function among patients divided by brachial-ankle pulse wave velocity (baPWV) and electrocardiography (ECG)-determined LVH and to assess whether increased baPWV and ECG-determined LVH are independently associated with LVDD.MethodsThis cross-sectional study enrolled 270 patients and classified them into four groups according to the median value of baPWV and with/without ECG-determined LVH. The baPWV was measured using an ABI-form device. ECG-determined LVH was defined by Sokolow-Lyon criterion. LVDD was defined as impaired relaxation, pseudonormal, and restrictive mitral inflow patterns. Groups 1, 2, 3, and 4 were patients with lower baPWV and without ECG-determined LVH, lower baPWV but with ECG-determined LVH, higher baPWV but without ECG-determined LVH, and higher baPWV and with ECG-determined LVH respectively.ResultsEarly diastolic mitral velocity (Ea) was gradually decreased from group 1 to group 4 (p≦0.027). Patients in group 4 had the highest prevalence of LVDD (all p<0.001). After multivariate analysis, both baPWV and ECG-determined LVH were independent determinants of Ea (β = −0.02, P<0.001; β = −1.77, P<0.001 respectively) and LVDD (odds ratio = 1.02, P = 0.011 and odds ratio = 3.53, P = 0.013 respectively).ConclusionOur study showed the group with higher baPWV and ECG-determined LVH had the lowest Ea and highest prevalence of LVDD. In addition, both baPWV and ECG-determined LVH were independently associated with Ea and LVDD. Hence, assessment of arterial stiffness by baPWV and LVH by ECG may be useful in identifying the high risk group of LVDD.

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“…Although the physiology of diastolic function is complex, the intrinsic LV abnormalities contributing to LVDD are impaired in LV relaxation, increased LV asynchrony, and the complex of LVH [39]. LVH increases the ratio of myocardial mass to volume, and the degree of hypertrophy is the main determinant of chamber stiffness.…”

“…LVH increases the ratio of myocardial mass to volume, and the degree of hypertrophy is the main determinant of chamber stiffness. LVH often leads to poor LV compliance and a vicious cycle of greater LV filling pressures and hypertrophy [39]. Furthermore, LVDD in hypertrophied hearts contributes to HF with preserved ejection, which consists of prolonged isovolumic LV relaxation, slow LV filling, and increased diastolic LV stiffness [40].…”

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“…This cardiac abnormality includes prolonged isovolumic LV relaxation, slow LV filling, and increased diastolic LV stiffness [14, 15]. One factor that may be involved in DD pathology is LV hypertrophy (LVH) which increases the ratio of myocardial mass to volume, and the hypertrophy level is a critical determinant of chamber stiffness.…”

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“…Although the physiology of diastolic function is complex, the intrinsic left ventricular (LV) abnormalities contributing to LV diastolic dysfunction (LVDD) are impaired LV relaxation, increased LV asynchrony, and hypertrophy [49]. Compared to individuals without diabetes, diabetic patients had higher left ventricle mass and greater wall thickness [52]. Furthermore, LVDD in hypertrophied hearts contributes to heart failure with preserved ejection, consisting of prolonged isovolumic LV relaxation, slow LV filling, and increased LV stiffness [53].…”