Coupled systolic-ventricular and vascular stiffening with age
Implications for pressure regulation and cardiac reserve in the elderly
Chen-Huan Chen, MD*,
Masaru Nakayama, MD, PhD
,
Erez Nevo, MD, DSc
,
Barry J. Fetics, BE, MSE,
W. Lowell Maughan, MD and
David A. Kass, MD
* Veterans General Hospital-Taipei and National Yang-Ming University, Taipei, People’s Republic of China
Division of Cardiology, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
Division of Cardiology, St. Marianna University Hospital, Kawasaki, Japan
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Figure 1 (A) Pressure volume loops used to derive ventricular end systolic chamber stiffness (Ees) and end diastolic chamber stiffness (Ed). Multiple cardiac cycles measured at different levels of filling are recorded. The slope of the relation linking the upper left-hand corner of these beats (end systole) is Ees. The slope of the relation linking late diastolic points from these beats is Ed. (B) Relation between aortic arterial pulse pressure and the pulse pressure estimated from the ventricular pressure volume loop. For the loop, the pulse pressure is given by the difference between the pressure at the onset of ejection and the peak pressure (PPLV), and it somewhat underestimates the measured arterial pulse pressure (PPao). However, PPLV is highly correlated with PPao among individuals. (C) shows data from a separate group of 25 patients in which both ventricular pressure volume and aortic pressure data were recorded. This regression was  r = 0.91, p < 0.0001 (SEE = 8 mm Hg), and this relation was then used to predict PPao from PPLV.
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Figure 2 Effects of age on vascular stiffening and load. A shows pulse pressure versus age, and B shows arterial elastance, a measure of total (mean and pulsatile) arterial load, versus age. Both parameters significantly increased with age. Open circles = group 1 subjects with no demonstrable cardiovascular disease. Open triangles = those with coronary artery disease and no infarction or a history of systolic hypertension. Solid lines = linear regression for combined data.
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Figure 3 (A) Pressure volume loops and relations derived by preload reduction maneuver in a young and in an elderly patient. End systolic elastance (Ees) measures chamber systolic stiffness and is the slope of a line connecting the upper left-hand corners (end systole) from each pressure volume loop (dotted line). Arterial elastance (Ea) measures arterial load and stiffness and is depicted by the negative slope of the diagonal solid line shown in the figures. As noted in Figure 2, vascular stiffening was higher in the aged individual (Ea = 2.4 vs. 1.6 mm Hg/ml in these examples). This was accompanied by increases in ventricular stiffness (Ees = 3.6 vs. 2.1 mm Hg/ml, respectively). As a result, ventricular and vascular properties remained matched. (B) Group data showing positive correlation between ventricular systolic stiffness and arterial stiffness. See text for regression results. (C) Combined ventricular and vascular stiffening resulted in matching of the two systems (defined by the Ea/Ees ratio) that is independent of age. (D) Increased ventricular chamber systolic stiffness (Ees) also correlated with elevations in diastolic chamber stiffness (Ed). Both variables independently rise with age (data not shown).
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Figure 4 (A) Example of changes in systolic pressure to alterations in ventricular diastolic volume in a young and in an elderly patient. Data are derived from the same set of pressure volume loops shown in Figure 2. There is much greater sensitivity of systolic pressure to volume changes in the elderly patient, indicated by the steeper slope. (B) Group results showing effects of age on the slope of the systolic pressure LV end diastolic volume dependence (SBPEDV). This relation slope increased significantly with age.
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Copyright © 1998 by the American College of Cardiology Foundation.
