Longitudinal changes in left ventricular stiffness a community-based study

Barry A Borlaug, Margaret May Redfield, Vojtech Melenovsky, Garvan M Kane, Barry L. Karon, Steven J. Jacobsen, Richard J. Rodeheffer

Research output: Contribution to journalArticle

88 Citations (Scopus)

Abstract

Background-Cross-sectional studies suggest that left ventricular (LV) and arterial elastance (stiffness) increase with age, but data examining longitudinal changes within human subjects are lacking. In addition, it remains unknown whether age-related LV stiffening is merely a reaction to arterial stiffening or caused by other processes. Methods and Results-Comprehensive echo-Doppler cardiography was performed in 1402 subjects participating in a randomly selected community-based study at 2 examinations separated by 4 years. From this population, 788 subjects had adequate paired data to determine LV end-systolic elastance (Ees), end-diastolic elastance (Eed), and effective arterial elastance. Throughout 4 years, blood pressure, arterial elastance, and LV mass decreased, coupled with significantly greater use of antihypertensive medications. However, despite reductions in arterial load, Ees increased by 14% (2.10±0.67-2.26±0.70 mm Hg/mL; P<0.0001) and Eed increased by 8% (0.13±0.03-0.14±0.04 mm Hg/mL; P<0.0001). Increases in Eed were greater in women than men, whereas Ees changes were similar. Age-related increases in Ees and Eed were correlated with changes in body weight, but were similar in subjects with or without cardiovascular disease. Changes in Ees were correlated with Eed (r=0.5; P<0.0001), but not with other measures of contractility, indicating that the increase in Ees was reflective of passive stiffening rather than enhanced systolic function. Conclusions-Despite reductions in arterial load with medical therapy, LV systolic and diastolic stiffness increase over time in humans, particularly in women. In addition to blood pressure control, therapies targeting load-independent ventricular stiffening may be effective to treat and prevent age-associated cardiovascular diseases, such as heart failure.

Original languageEnglish (US)
Pages (from-to)944-952
Number of pages9
JournalCirculation: Heart Failure
Volume6
Issue number5
DOIs
StatePublished - Sep 2013

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Cardiovascular Diseases
Vascular Stiffness
Body Weight Changes
Antihypertensive Agents
Arterial Pressure
Heart Failure
Cross-Sectional Studies
Blood Pressure
Therapeutics
Population

Keywords

  • Aging
  • Arterial stiffness
  • Heart failure
  • Hemodynamics
  • Ventricular function

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Longitudinal changes in left ventricular stiffness a community-based study. / Borlaug, Barry A; Redfield, Margaret May; Melenovsky, Vojtech; Kane, Garvan M; Karon, Barry L.; Jacobsen, Steven J.; Rodeheffer, Richard J.

In: Circulation: Heart Failure, Vol. 6, No. 5, 09.2013, p. 944-952.

Research output: Contribution to journalArticle

Borlaug, Barry A ; Redfield, Margaret May ; Melenovsky, Vojtech ; Kane, Garvan M ; Karon, Barry L. ; Jacobsen, Steven J. ; Rodeheffer, Richard J. / Longitudinal changes in left ventricular stiffness a community-based study. In: Circulation: Heart Failure. 2013 ; Vol. 6, No. 5. pp. 944-952.
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AU - Jacobsen, Steven J.

AU - Rodeheffer, Richard J.

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AB - Background-Cross-sectional studies suggest that left ventricular (LV) and arterial elastance (stiffness) increase with age, but data examining longitudinal changes within human subjects are lacking. In addition, it remains unknown whether age-related LV stiffening is merely a reaction to arterial stiffening or caused by other processes. Methods and Results-Comprehensive echo-Doppler cardiography was performed in 1402 subjects participating in a randomly selected community-based study at 2 examinations separated by 4 years. From this population, 788 subjects had adequate paired data to determine LV end-systolic elastance (Ees), end-diastolic elastance (Eed), and effective arterial elastance. Throughout 4 years, blood pressure, arterial elastance, and LV mass decreased, coupled with significantly greater use of antihypertensive medications. However, despite reductions in arterial load, Ees increased by 14% (2.10±0.67-2.26±0.70 mm Hg/mL; P<0.0001) and Eed increased by 8% (0.13±0.03-0.14±0.04 mm Hg/mL; P<0.0001). Increases in Eed were greater in women than men, whereas Ees changes were similar. Age-related increases in Ees and Eed were correlated with changes in body weight, but were similar in subjects with or without cardiovascular disease. Changes in Ees were correlated with Eed (r=0.5; P<0.0001), but not with other measures of contractility, indicating that the increase in Ees was reflective of passive stiffening rather than enhanced systolic function. Conclusions-Despite reductions in arterial load with medical therapy, LV systolic and diastolic stiffness increase over time in humans, particularly in women. In addition to blood pressure control, therapies targeting load-independent ventricular stiffening may be effective to treat and prevent age-associated cardiovascular diseases, such as heart failure.

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KW - Arterial stiffness

KW - Heart failure

KW - Hemodynamics

KW - Ventricular function

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