Exercise-induced alterations in left ventricular volumes and the pressure-volume relationship: A sensitive indicator of left ventricular dysfunction in patients with coronary artery disease

G. J. Dehmer, S. E. Lewis, L. D. Hillis, J. Corbett, R. W. Parkey, J. T. Willerson

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Abstract

Thirty-three patients with coronary artery disease (CAD) and 13 subjects without demonstrable cardiac disease were studied with multigated equilibrium blood pool imaging to assess the diagnostic value of exercise-induced alterations in left ventricular (LV) volumes, segmental wall motion, ejection fraction (LVEF), and the end-systolic pressure-volume relationship. In subjects without cardiac disease, left ventricular end-diastolic volume (LVEDV) was 102 ± 7.2 ml (SEM) at rest and 125 ± 9.7 ml at peak exercise (PEx) (p <0.001). Left ventricular end-systolic volume (LVESV) was 35 ± 3.0 ml at rest 29 ± 3.4 ml at PEx (p <0.01). LVEF increased from 0.72 ± 0.02 at rest to 0.82 ± 0.02 at PEx (p <0.001). The nine patients with one-vessel CAD also had an increase in LVEDV (p <0.001) and LVEF (p <0.02) at PEx, but no significant change in LVESV. The 24 patients with significant two- or three-vessel CAD had increases in both LVEDV (196 ± 13.2 ml to 195 ± 13.7 ml, p <0.001) and LVESV (86 ± 12.0 ml to 102 ± 12.0 ml, p <0.01) at PEx and a decrease in LVEF (0.56 ± 0.03 to 0.52 ± 0.03, p <0.05). The relationship between cuff-determined peak systolic blood pressure and LVESV index (P/V index) was used to further characterize alterations in LV function at rest and during PEx. In subjects without cardiac disease, this index rose substantially during PEx (7.6 ± 0.73 at rest vs 14.9 ± 1.78 with PEx, p <0.001). This change was less dramatic in those with one-vessel disease and absent in patients with two- or three-vessel disease (4.2 ± 0.60 at rest vs 3.9 ± 0.50 at PEx, NS). The change in LVESV alone was different in each group. We conclude that the assessment of exercise-induced alterations in LVESV and the P/V index is useful for evaluating LV dysfunction associated with angiographically important coronary artery disease.

Original languageEnglish (US)
Pages (from-to)1008-1018
Number of pages11
JournalCirculation
Volume63
Issue number5
StatePublished - 1981
Externally publishedYes

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Left Ventricular Dysfunction
Ventricular Pressure
Coronary Artery Disease
Stroke Volume
Exercise
Blood Pressure
Heart Diseases
Left Ventricular Function

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Exercise-induced alterations in left ventricular volumes and the pressure-volume relationship : A sensitive indicator of left ventricular dysfunction in patients with coronary artery disease. / Dehmer, G. J.; Lewis, S. E.; Hillis, L. D.; Corbett, J.; Parkey, R. W.; Willerson, J. T.

In: Circulation, Vol. 63, No. 5, 1981, p. 1008-1018.

Research output: Contribution to journalArticle

Dehmer, G. J. ; Lewis, S. E. ; Hillis, L. D. ; Corbett, J. ; Parkey, R. W. ; Willerson, J. T. / Exercise-induced alterations in left ventricular volumes and the pressure-volume relationship : A sensitive indicator of left ventricular dysfunction in patients with coronary artery disease. In: Circulation. 1981 ; Vol. 63, No. 5. pp. 1008-1018.
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AU - Dehmer, G. J.

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AU - Hillis, L. D.

AU - Corbett, J.

AU - Parkey, R. W.

AU - Willerson, J. T.

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N2 - Thirty-three patients with coronary artery disease (CAD) and 13 subjects without demonstrable cardiac disease were studied with multigated equilibrium blood pool imaging to assess the diagnostic value of exercise-induced alterations in left ventricular (LV) volumes, segmental wall motion, ejection fraction (LVEF), and the end-systolic pressure-volume relationship. In subjects without cardiac disease, left ventricular end-diastolic volume (LVEDV) was 102 ± 7.2 ml (SEM) at rest and 125 ± 9.7 ml at peak exercise (PEx) (p <0.001). Left ventricular end-systolic volume (LVESV) was 35 ± 3.0 ml at rest 29 ± 3.4 ml at PEx (p <0.01). LVEF increased from 0.72 ± 0.02 at rest to 0.82 ± 0.02 at PEx (p <0.001). The nine patients with one-vessel CAD also had an increase in LVEDV (p <0.001) and LVEF (p <0.02) at PEx, but no significant change in LVESV. The 24 patients with significant two- or three-vessel CAD had increases in both LVEDV (196 ± 13.2 ml to 195 ± 13.7 ml, p <0.001) and LVESV (86 ± 12.0 ml to 102 ± 12.0 ml, p <0.01) at PEx and a decrease in LVEF (0.56 ± 0.03 to 0.52 ± 0.03, p <0.05). The relationship between cuff-determined peak systolic blood pressure and LVESV index (P/V index) was used to further characterize alterations in LV function at rest and during PEx. In subjects without cardiac disease, this index rose substantially during PEx (7.6 ± 0.73 at rest vs 14.9 ± 1.78 with PEx, p <0.001). This change was less dramatic in those with one-vessel disease and absent in patients with two- or three-vessel disease (4.2 ± 0.60 at rest vs 3.9 ± 0.50 at PEx, NS). The change in LVESV alone was different in each group. We conclude that the assessment of exercise-induced alterations in LVESV and the P/V index is useful for evaluating LV dysfunction associated with angiographically important coronary artery disease.

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