Arterial stiffness and left-ventricular diastolic dysfunction: Guangzhou Biobank Cohort Study-CVD

Abstract

Brachial-ankle pulse wave velocity (baPWV), a marker of arterial stiffness, is an established cardiovascular risk factor of ventricular stiffening. We studied the association of baPWV with left-ventricular (LV) diastolic function in a sub-study of the Guangzhou Biobank Cohort Study. In all, 378 Chinese subjects with a normal ejection fraction (450%) had baPWV measurement by a noninvasive automatic waveform analyser, carotid intima-medial thickness (IMT) measurement by B-mode ultrasonography and cardiac diastolic function assessment by echocardiography. After adjusting for age, both baPWV and IMT were associated with LV mass index, posterior wall end-diastolic thickness and inter-ventricular end-diastolic thickness, but only baPWV was associated with deceleration time, atrial flow velocity and E/A ratio. Multivariable linear regression model showed that baPWV and mean arterial pressure, but not IMT, were significantly associated with E/A ratio (b ¼ À0.02, P ¼ 0.03 and b ¼ À0.36, P ¼ 0.02, respectively). The receiver operator characteristic curve showed that baPWV was better than pulse pressure or mean arterial pressure to detect LV diastolic dysfunction (E/Ao1.0). Our study suggested that increased baPWV might be an independent risk factor or marker for diastolic dysfunction. Early detection of an intervention on increased baPWV may be important for prevention of cardiac diastolic dysfunction.

Differential relationships of systolic and diastolic blood pressure with components of left ventricular diastolic dysfunction

“…However, the relationships between indices of aortic stiffness and mild diastolic dysfunction, as defined by abnormalities in E/A (relaxation abnormalities), are less clear, with associations noted in some [15,23,26], but not other studies [19,21,27,29,30]. Moreover, the BP most strongly related to E/A or LVDD in some large studies is DBP rather than SBP [12,13,31,32].…”

“…Indeed, a number of studies have demonstrated that increases in aortic stiffness, which are thought to mediate vascular-ventricular interactions, are associated with LVDD [15][16][17][18][19][20][21][22][23][24][25][26][27][28]. It is therefore possible that increases in SBP, which more closely reflect aortic stiffness changes, are more important in mediating LVDD than increases in DBP.…”

Correlation of Arterial Stiffness to Left Ventricular Function in Patients with Reduced Ejection Fraction

“…The most striking result in our analysis was that hypertensive patients with reduced EF showed a closer relationship between arterial stiffness and LV function than hypertensive patients with preserved EF. Previous studies (Miyoshi et al 2011;Xu et al 2011) have demonstrated an association between arterial stiffness and LV diastolic dysfunction in patients with preserved EF, and suggested that increased arterial stiffness may be a causative factor of heart failure produced by LV diastolic dysfunction. Our data is in agreement with the association between arterial stiffness and LV diastolic dysfunction in hypertensives with preserved EF.…”

Brachial-Ankle PWV: Current Status and Future Directions as a Useful Marker in the Management of Cardiovascular Disease and/or Cardiovascular Risk Factors

“…Sympathetic nervous activation induced by hypoxia resulting from apnea may be one of the mechanisms underlying the accelerated increase of the arterial stiffness in subjects with sleep apnea 34) . Although several cross- 46) , subclinical cerebral damage 47) , cognitive dysfunction 48) , renal dysfunction 49,50) , cardiac diastolic dysfunction 51) , left ventricular hypertrophy 52) , and/or increased carotid intima-media thickness 53) ].…”