
Relations of Central Hemodynamics and Aortic Stiffness with Left Ventricular Structure and Function: The Framingham Heart Study
Author(s) -
Kaess Bernhard M.,
Rong Jian,
Larson Martin G.,
Hamburg Naomi M.,
Vita Joseph A.,
Cheng Susan,
Aragam Jayashree,
Levy Daniel,
Benjamin Emelia J.,
Vasan Ramachandran S.,
Mitchell Gary F.
Publication year - 2016
Publication title -
journal of the american heart association
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.494
H-Index - 85
ISSN - 2047-9980
DOI - 10.1161/jaha.115.002693
Subject(s) - medicine , cardiology , pulse pressure , pulse wave velocity , pulsatile flow , blood pressure , hemodynamics , arterial stiffness , framingham heart study , diastole , mean arterial pressure , framingham risk score , heart rate , disease
Background The differing relations of steady and pulsatile components of central hemodynamics and aortic stiffness with cardiac dimensions and function have not been fully elucidated. Methods and Results Central hemodynamics and carotid‐femoral pulse wave velocity ( CFPWV , a measure of aortic stiffness) were measured by arterial tonometry in 5799 participants of the Framingham Heart Study (mean age 51 years, 54% women) and related to echocardiographic left ventricular ( LV ) dimensions and systolic and diastolic function using multivariable‐adjusted partial Pearson correlations. Mean arterial pressure ( MAP , steady component of central blood pressure) was associated positively with LV wall thickness ( r =0.168; P <0.0001) but showed only a weak direct association with LV diastolic dimension ( r =0.035, P =0.006). Central pulse pressure (pulsatile component of central blood pressure) showed a direct correlation with both LV diastolic dimension and LV wall thickness ( r =0.08 and 0.044, both P <0.0001 in multivariable models that included MAP ). CFPWV was not associated with LV structure (all P ≥0.27) in MAP ‐adjusted models). Both MAP and CFPWV were associated inversely with LV diastolic function (E′; r =−0.140 and −0.153, respectively; both P <0.0001), and these associations persisted after additional adjustment for LV mass and central pulse pressure ( r =−0.142 and −0.108, both P <0.0001). MAP and CFPWV were not associated with LV fractional shortening ( P ≥0.10), whereas central pulse pressure was positively related ( r =0.064, P <0.0001). Conclusions Pulsatile and steady components of central pressure are conjointly yet variably related to LV structure. CFPWV is related to LV diastolic function but not to systolic function. Additional studies are warranted to confirm these observations.