Pulse Pressure Relation to Aortic and Left Ventricular Structure in the Age, Gene/Environment Susceptibility (AGES)-Reykjavik Study

Abstract

High pulse pressure, a major cardiovascular risk factor, has been attributed to medial elastic fiber degeneration and aortic dilation, which transfers hemodynamic load to stiffer collagen. However, recent studies suggest higher pulse pressure is instead associated with smaller aortic diameter. Thus, we sought to elucidate relations of pulse pressure with aortic stiffness and aortic and cardiac dimensions. We used magnetic resonance imaging to examine relations of pulse pressure with lumen area and wall stiffness and thickness in the thoracic aorta and left ventricular structure in 526 participants (72 to 94 years of age, 295 women) in the community-based Age, Gene/Environment Susceptibility-Reykjavik Study. In a multivariable model that adjusted for age, sex, height, weight, and standard vascular risk factors, central pulse pressure had a negative relation with aortic lumen area (all effects expressed as mm Hg/SD; B=−8.1±1.2, P<0.001) and positive relations with left ventricular end-diastolic volume (B=3.8±1.0, P<0.001), carotid-femoral pulse wave velocity (B=3.6±1.0, P<0.001), and aortic wall area (B=3.0±1.2, P=0.015). Higher pulse pressure in older people is associated with smaller aortic lumen area and greater aortic wall stiffness and thickness and left ventricular volume. Relations of larger ventricular volume and smaller aortic lumen with higher pulse pressure suggest mismatch in hemodynamic load accommodation by the heart and aorta in older people.

Arterial Stiffness Measured with the Cuff Oscillometric Method Is Predictive of Exercise Capacity in Patients with Cardiac Diseases

“…Therefore, wave reflection might not be predictive of exercise capacity especially in patients with cardiac disease with reduced ejection fraction; however, it is reasonable to hypothesize that wave reflection, represented by AVI in our results, is correlated with exercise capacity in patients with preserved ejection fraction as well as in a population without known cardiac diseases (Vaitkevicius et al 1993;Jung et al 2014). Increased arterial stiffness causes decreased diastolic pressure and increased systolic pressure, which results in PP elevation (Mitchell et al 1997;Torjesen et al 2014). Increased PP causes decreased coronary perfusion because the coronary circulation is regulated by diastolic pressure (Anrep et al 1931).…”

Influence of Vascular Function and Pulsatile Hemodynamics on Cardiac Function

“…As a result, aortic diameter remodeling may be limited by the available pool of elastic fibers established early in life and may be exceeded in obese individuals, resulting in wide pulse pressure systolic hypertension. Because of the potentially greater ability of the heart to remodel in order to accommodate higher hemodynamic demand, LV remodeling may be seen as both a consequence of as well as a contributor to wide pulse pressure hypertension [27].…”

“…If the LV hypertrophies in response to this early systolic loading, the pressure-volume model suggests that the resulting increase in Ees would reduce the coupling ratio (Ea/Ees< 1) and increase stroke volume. The resulting increase in flow may contribute to chamber enlargement, resulting in observed mixed LV enlargement (higher volume, higher mass) often seen in hypertension [27]. In addition, proximal aortic stiffening will increase the amount of pulsatility that reaches the periphery and may contribute to microvascular remodeling [46], which could increase Ea and restore the Ea/Ees ratio to a value near unity but at values for Ea, Ees, and mean arterial pressure that are potentially much higher than normal.…”

Association of N-Terminal Pro B-Type Natriuretic Peptide With Blood Pressure and Pulse Pressure in Elderly People ― A Cross-Sectional Population Study ―

“…22 Therefore, the significant association between NT-proBNP and PP in the present study suggests that circulating NT-proBNP concentrations may show the effects of arterial stiffness in the left ventricle in the elderly population without CVD. Because circulating NT-proBNP concentrations increase with the severity of left ventricular dysfunction, 23 they have been widely used as a marker for the diagnosis and severity of heart failure.…”