Acute and chronic ventricular-arterial coupling in systole and diastole: Insights from an elderly hypertensive model

Brian P Shapiro, Carolyn S P Lam, Jeetendra B. Patel, Selma F. Mohammed, Martina Kruger, Donna M. Meyer, Wolfgang A. Linke, Margaret May Redfield

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

Aging and hypertension lead to arterial remodeling and tandem increases in arterial (Ea) and ventricular (LV) systolic stiffness (ventricular-arterial [VA] coupling). Age and hypertension also predispose to heart failure with normal ejection fraction (HFnlEF), where symptoms during hypertensive urgencies or exercise are common. We hypothesized that: (1) chronic VA coupling also occurs in diastole, (2) acute changes in Ea are coupled with shifts in the diastolic and systolic pressure-volume relationships (PVR), and (3) diastolic VA coupling reflects changes in LV diastolic stiffness rather than external forces or relaxation. Old chronically hypertensive (OHT, n=8) and young normal (YNL, n=7) dogs underwent assessment of PVR (caval occlusion) and of aortic pressure, dimension, and flow, at baseline and during changes in afterload and preload. Concomitant changes in the slope/position of PVR were accounted for by calculating systolic (ESV200) and diastolic (EDV20) volumes at common pressures (capacitance). OHT displayed marked vascular remodeling. Indices reflecting the pulsatile component of Ea (aortic stiffness and systemic arterial compliance) were more impaired in OHT at any distending pressure. In both groups, acute increases in Ea were associated with decreases in ESV200 and EDV20. However, at any load, OHT had lower ESV200 and EDV20, associated with LV remodeling and myocardial endothelin activation. Acute changes in EDV20 were not mediated by changes in relaxation or external forces. These observations provide insight into the mechanisms whereby arterial remodeling and acute and chronic VA coupling in both systole and diastole may predispose to and interact with increases in load to cause HFnlEF.

Original languageEnglish (US)
Pages (from-to)503-511
Number of pages9
JournalHypertension
Volume50
Issue number3
DOIs
StatePublished - Sep 2007

Fingerprint

Diastole
Systole
Pressure
Vascular Stiffness
Heart Failure
Blood Pressure
Hypertension
Venae Cavae
Endothelins
Compliance
Arterial Pressure
Dogs
Exercise

Keywords

  • Diastole
  • Endothelin
  • Heart failure
  • Hypertension, elderly
  • Hypertension, experimental
  • Vasculature
  • Ventricular function, left

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Acute and chronic ventricular-arterial coupling in systole and diastole : Insights from an elderly hypertensive model. / Shapiro, Brian P; Lam, Carolyn S P; Patel, Jeetendra B.; Mohammed, Selma F.; Kruger, Martina; Meyer, Donna M.; Linke, Wolfgang A.; Redfield, Margaret May.

In: Hypertension, Vol. 50, No. 3, 09.2007, p. 503-511.

Research output: Contribution to journalArticle

Shapiro, Brian P ; Lam, Carolyn S P ; Patel, Jeetendra B. ; Mohammed, Selma F. ; Kruger, Martina ; Meyer, Donna M. ; Linke, Wolfgang A. ; Redfield, Margaret May. / Acute and chronic ventricular-arterial coupling in systole and diastole : Insights from an elderly hypertensive model. In: Hypertension. 2007 ; Vol. 50, No. 3. pp. 503-511.
@article{4bcbd19fd26b43d89f3c91cddd69d9c0,
title = "Acute and chronic ventricular-arterial coupling in systole and diastole: Insights from an elderly hypertensive model",
abstract = "Aging and hypertension lead to arterial remodeling and tandem increases in arterial (Ea) and ventricular (LV) systolic stiffness (ventricular-arterial [VA] coupling). Age and hypertension also predispose to heart failure with normal ejection fraction (HFnlEF), where symptoms during hypertensive urgencies or exercise are common. We hypothesized that: (1) chronic VA coupling also occurs in diastole, (2) acute changes in Ea are coupled with shifts in the diastolic and systolic pressure-volume relationships (PVR), and (3) diastolic VA coupling reflects changes in LV diastolic stiffness rather than external forces or relaxation. Old chronically hypertensive (OHT, n=8) and young normal (YNL, n=7) dogs underwent assessment of PVR (caval occlusion) and of aortic pressure, dimension, and flow, at baseline and during changes in afterload and preload. Concomitant changes in the slope/position of PVR were accounted for by calculating systolic (ESV200) and diastolic (EDV20) volumes at common pressures (capacitance). OHT displayed marked vascular remodeling. Indices reflecting the pulsatile component of Ea (aortic stiffness and systemic arterial compliance) were more impaired in OHT at any distending pressure. In both groups, acute increases in Ea were associated with decreases in ESV200 and EDV20. However, at any load, OHT had lower ESV200 and EDV20, associated with LV remodeling and myocardial endothelin activation. Acute changes in EDV20 were not mediated by changes in relaxation or external forces. These observations provide insight into the mechanisms whereby arterial remodeling and acute and chronic VA coupling in both systole and diastole may predispose to and interact with increases in load to cause HFnlEF.",
keywords = "Diastole, Endothelin, Heart failure, Hypertension, elderly, Hypertension, experimental, Vasculature, Ventricular function, left",
author = "Shapiro, {Brian P} and Lam, {Carolyn S P} and Patel, {Jeetendra B.} and Mohammed, {Selma F.} and Martina Kruger and Meyer, {Donna M.} and Linke, {Wolfgang A.} and Redfield, {Margaret May}",
year = "2007",
month = "9",
doi = "10.1161/HYPERTENSIONAHA.107.090092",
language = "English (US)",
volume = "50",
pages = "503--511",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - Acute and chronic ventricular-arterial coupling in systole and diastole

T2 - Insights from an elderly hypertensive model

AU - Shapiro, Brian P

AU - Lam, Carolyn S P

AU - Patel, Jeetendra B.

AU - Mohammed, Selma F.

AU - Kruger, Martina

AU - Meyer, Donna M.

AU - Linke, Wolfgang A.

AU - Redfield, Margaret May

PY - 2007/9

Y1 - 2007/9

N2 - Aging and hypertension lead to arterial remodeling and tandem increases in arterial (Ea) and ventricular (LV) systolic stiffness (ventricular-arterial [VA] coupling). Age and hypertension also predispose to heart failure with normal ejection fraction (HFnlEF), where symptoms during hypertensive urgencies or exercise are common. We hypothesized that: (1) chronic VA coupling also occurs in diastole, (2) acute changes in Ea are coupled with shifts in the diastolic and systolic pressure-volume relationships (PVR), and (3) diastolic VA coupling reflects changes in LV diastolic stiffness rather than external forces or relaxation. Old chronically hypertensive (OHT, n=8) and young normal (YNL, n=7) dogs underwent assessment of PVR (caval occlusion) and of aortic pressure, dimension, and flow, at baseline and during changes in afterload and preload. Concomitant changes in the slope/position of PVR were accounted for by calculating systolic (ESV200) and diastolic (EDV20) volumes at common pressures (capacitance). OHT displayed marked vascular remodeling. Indices reflecting the pulsatile component of Ea (aortic stiffness and systemic arterial compliance) were more impaired in OHT at any distending pressure. In both groups, acute increases in Ea were associated with decreases in ESV200 and EDV20. However, at any load, OHT had lower ESV200 and EDV20, associated with LV remodeling and myocardial endothelin activation. Acute changes in EDV20 were not mediated by changes in relaxation or external forces. These observations provide insight into the mechanisms whereby arterial remodeling and acute and chronic VA coupling in both systole and diastole may predispose to and interact with increases in load to cause HFnlEF.

AB - Aging and hypertension lead to arterial remodeling and tandem increases in arterial (Ea) and ventricular (LV) systolic stiffness (ventricular-arterial [VA] coupling). Age and hypertension also predispose to heart failure with normal ejection fraction (HFnlEF), where symptoms during hypertensive urgencies or exercise are common. We hypothesized that: (1) chronic VA coupling also occurs in diastole, (2) acute changes in Ea are coupled with shifts in the diastolic and systolic pressure-volume relationships (PVR), and (3) diastolic VA coupling reflects changes in LV diastolic stiffness rather than external forces or relaxation. Old chronically hypertensive (OHT, n=8) and young normal (YNL, n=7) dogs underwent assessment of PVR (caval occlusion) and of aortic pressure, dimension, and flow, at baseline and during changes in afterload and preload. Concomitant changes in the slope/position of PVR were accounted for by calculating systolic (ESV200) and diastolic (EDV20) volumes at common pressures (capacitance). OHT displayed marked vascular remodeling. Indices reflecting the pulsatile component of Ea (aortic stiffness and systemic arterial compliance) were more impaired in OHT at any distending pressure. In both groups, acute increases in Ea were associated with decreases in ESV200 and EDV20. However, at any load, OHT had lower ESV200 and EDV20, associated with LV remodeling and myocardial endothelin activation. Acute changes in EDV20 were not mediated by changes in relaxation or external forces. These observations provide insight into the mechanisms whereby arterial remodeling and acute and chronic VA coupling in both systole and diastole may predispose to and interact with increases in load to cause HFnlEF.

KW - Diastole

KW - Endothelin

KW - Heart failure

KW - Hypertension, elderly

KW - Hypertension, experimental

KW - Vasculature

KW - Ventricular function, left

UR - http://www.scopus.com/inward/record.url?scp=34548185475&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34548185475&partnerID=8YFLogxK

U2 - 10.1161/HYPERTENSIONAHA.107.090092

DO - 10.1161/HYPERTENSIONAHA.107.090092

M3 - Article

C2 - 17620524

AN - SCOPUS:34548185475

VL - 50

SP - 503

EP - 511

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 3

ER -