Coupled systolic-ventricular and vascular stiffening with age: Implications for pressure regulation and cardiac reserve in the elderly

Chen Huan Chen, Masaru Nakayama, Erez Nevo, Barry J. Fetics, William L Maughan, David A Kass

Research output: Contribution to journalArticle

Abstract

Objectives. We tested the hypothesis that age-related arterial stiffening is matched by ventricular systolic stiffening, and that both enhance systolic pressure sensitivity to altered cardiac preload. Background. Arterial rigidity with age likely enhances blood pressure sensitivity to ventricular filling volume shifts. Tandem increases in ventricular systolic stiffness may also occur and could potentially enhance this sensitivity. Methods. Invasive left ventricular pressure- volume relations were measured by conductance catheter in 57 adults aged 19 to 93 years. Patients had normal heart function and no cardiac hypertrophy and were referred for catheterization to evaluate chest pain. Twenty-eight subjects had normal coronary angiography and hemodynamics, and the remaining had either systolic hypertension or coronary artery disease without infarction. Data recorded at rest and during transient preload reduction by inferior vena caval obstruction yielded systolic and diastolic left ventricular chamber and effective arterial stiffness and pulse pressure. Results. Left ventricular volumes, ejection fraction and heart rate were unaltered by age, whereas vascular load and stiffening increased (p <0.008). Arterial stiffening (E(a)) was matched by increased ventricular systolic stiffness (E(es)): E(es) = 0.91·E(a) + 0.53, (r = 0.50, p <0.0001), maintaining arterial-heart interaction (E(a)/E(es) ratio) age- independent. Ventricular systolic and diastolic stiffnesses correlated (r = 0.51, p <0.0001) and increased with age (p <0.03). Both ventricular and vascular stiffening significantly increased systolic pressure sensitivity to cardiac preload (p <0.006). Conclusions. Arterial stiffening with age is matched by ventricular systolic stiffening even without hypertrophy. The two effects contribute to elevating systolic pressure sensitivity to altered chamber filling. In addition to recognized baroreflex and autonomic dysfunction with age, combined stiffening could further enhance pressure lability with diuretics and postural shifts in the elderly.

Original languageEnglish (US)
Pages (from-to)1221-1227
Number of pages7
JournalJournal of the American College of Cardiology
Volume32
Issue number5
DOIs
StatePublished - Nov 1 1998

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Blood Vessels
Blood Pressure
Pressure
Venae Cavae
Vascular Stiffness
Baroreflex
Cardiomegaly
Ventricular Pressure
Coronary Angiography
Chest Pain
Diuretics
Catheterization
Stroke Volume
Infarction
Hypertrophy
Coronary Artery Disease
Arterial Pressure
Catheters
Heart Rate
Hemodynamics

ASJC Scopus subject areas

  • Nursing(all)

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Coupled systolic-ventricular and vascular stiffening with age : Implications for pressure regulation and cardiac reserve in the elderly. / Chen, Chen Huan; Nakayama, Masaru; Nevo, Erez; Fetics, Barry J.; Maughan, William L; Kass, David A.

In: Journal of the American College of Cardiology, Vol. 32, No. 5, 01.11.1998, p. 1221-1227.

Research output: Contribution to journalArticle

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abstract = "Objectives. We tested the hypothesis that age-related arterial stiffening is matched by ventricular systolic stiffening, and that both enhance systolic pressure sensitivity to altered cardiac preload. Background. Arterial rigidity with age likely enhances blood pressure sensitivity to ventricular filling volume shifts. Tandem increases in ventricular systolic stiffness may also occur and could potentially enhance this sensitivity. Methods. Invasive left ventricular pressure- volume relations were measured by conductance catheter in 57 adults aged 19 to 93 years. Patients had normal heart function and no cardiac hypertrophy and were referred for catheterization to evaluate chest pain. Twenty-eight subjects had normal coronary angiography and hemodynamics, and the remaining had either systolic hypertension or coronary artery disease without infarction. Data recorded at rest and during transient preload reduction by inferior vena caval obstruction yielded systolic and diastolic left ventricular chamber and effective arterial stiffness and pulse pressure. Results. Left ventricular volumes, ejection fraction and heart rate were unaltered by age, whereas vascular load and stiffening increased (p <0.008). Arterial stiffening (E(a)) was matched by increased ventricular systolic stiffness (E(es)): E(es) = 0.91·E(a) + 0.53, (r = 0.50, p <0.0001), maintaining arterial-heart interaction (E(a)/E(es) ratio) age- independent. Ventricular systolic and diastolic stiffnesses correlated (r = 0.51, p <0.0001) and increased with age (p <0.03). Both ventricular and vascular stiffening significantly increased systolic pressure sensitivity to cardiac preload (p <0.006). Conclusions. Arterial stiffening with age is matched by ventricular systolic stiffening even without hypertrophy. The two effects contribute to elevating systolic pressure sensitivity to altered chamber filling. In addition to recognized baroreflex and autonomic dysfunction with age, combined stiffening could further enhance pressure lability with diuretics and postural shifts in the elderly.",
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AB - Objectives. We tested the hypothesis that age-related arterial stiffening is matched by ventricular systolic stiffening, and that both enhance systolic pressure sensitivity to altered cardiac preload. Background. Arterial rigidity with age likely enhances blood pressure sensitivity to ventricular filling volume shifts. Tandem increases in ventricular systolic stiffness may also occur and could potentially enhance this sensitivity. Methods. Invasive left ventricular pressure- volume relations were measured by conductance catheter in 57 adults aged 19 to 93 years. Patients had normal heart function and no cardiac hypertrophy and were referred for catheterization to evaluate chest pain. Twenty-eight subjects had normal coronary angiography and hemodynamics, and the remaining had either systolic hypertension or coronary artery disease without infarction. Data recorded at rest and during transient preload reduction by inferior vena caval obstruction yielded systolic and diastolic left ventricular chamber and effective arterial stiffness and pulse pressure. Results. Left ventricular volumes, ejection fraction and heart rate were unaltered by age, whereas vascular load and stiffening increased (p <0.008). Arterial stiffening (E(a)) was matched by increased ventricular systolic stiffness (E(es)): E(es) = 0.91·E(a) + 0.53, (r = 0.50, p <0.0001), maintaining arterial-heart interaction (E(a)/E(es) ratio) age- independent. Ventricular systolic and diastolic stiffnesses correlated (r = 0.51, p <0.0001) and increased with age (p <0.03). Both ventricular and vascular stiffening significantly increased systolic pressure sensitivity to cardiac preload (p <0.006). Conclusions. Arterial stiffening with age is matched by ventricular systolic stiffening even without hypertrophy. The two effects contribute to elevating systolic pressure sensitivity to altered chamber filling. In addition to recognized baroreflex and autonomic dysfunction with age, combined stiffening could further enhance pressure lability with diuretics and postural shifts in the elderly.

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