Hemodynamic and clinical significance of the pulmonary vascular response to long-term captopril therapy in patients with severe chronic heart failure

M. Packer, W. H. Lee, N. Medina, M. Yushak

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Exercise capacity in patients with left heart failure is closely related to the performance of the right ventricle and the pulmonary circulation. To determine the significance of changes in pulmonary resistance during long-term vasodilator therapy, hemodynamic studies were performed before and after 1 to 3 months of treatment with captopril in 75 patients with severe chronic left heart failure. Patients were grouped according to the relative changes in pulmonary and systemic resistances during long-term therapy: patients in Group I (n = 24) showed greater decreases in pulmonary artriolar resistance (PAR) than in systemic vascular resistance (SVR) (% Δ PAR/% Δ SVR > 1.0), whereas patients in Group II showed predominant systemic vasodilation (% Δ PAR/% Δ SVR < 1.0). Despite similar changes in systemic resistance, patients in Group I showed greater increases in cardiac index, stroke volume index and left ventricular stroke work index (p < 0.01 to 0.001) but less dramatic decreases in mean systemic arterial pressure (p < 0.02) than did patients in Group II. Despite similar changes in left ventricular filling pressure, patients in Group I showed greater decreases in mean pulmonary artery and mean right atrial pressures (p < 0.02 to 0.01) than did patients in Group II. Pretreatment variables in Groups I and II were similar, except that plasma renin activity were higher (8.7 ± 2.1 versus 3.0 ± 0.6 ng/ml per h) and serum sodium concentration was lower (133.1 ± 0.9 versus 137.1 ± 0.6 mEq/liter) in Group II than in Group I (both p < 0.05). Both groups improved clinically after 1 to 3 months, but symptomatic hypotension occurred more frequently in Group II than in Group I (36 versus 8%) (p < 0.005). These findings indicate that changes in the pulmonary circulation modulate alterations in both right and left ventricular performance during the treatment of patients with left heart failure. Hyponatremic patients are likely to experience symptomatic hypotension with captopril because they are limited in their ability to increase cardiac output as a result of an inadequate pulmonary vasodilator response to the drug.

Original languageEnglish (US)
Pages (from-to)635-645
Number of pages11
JournalJournal of the American College of Cardiology
Volume6
Issue number3
StatePublished - 1985

Fingerprint

Captopril
Blood Vessels
Heart Failure
Hemodynamics
Lung
Therapeutics
Vascular Resistance
Pulmonary Circulation
Vasodilator Agents
Hypotension
Atrial Pressure
Ventricular Pressure
Renin
Vasodilation
Cardiac Output
Stroke Volume
Pulmonary Artery
Heart Ventricles
Arterial Pressure
Sodium

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Hemodynamic and clinical significance of the pulmonary vascular response to long-term captopril therapy in patients with severe chronic heart failure. / Packer, M.; Lee, W. H.; Medina, N.; Yushak, M.

In: Journal of the American College of Cardiology, Vol. 6, No. 3, 1985, p. 635-645.

Research output: Contribution to journalArticle

@article{66cd068ff622486e9fb820496f106848,
title = "Hemodynamic and clinical significance of the pulmonary vascular response to long-term captopril therapy in patients with severe chronic heart failure",
abstract = "Exercise capacity in patients with left heart failure is closely related to the performance of the right ventricle and the pulmonary circulation. To determine the significance of changes in pulmonary resistance during long-term vasodilator therapy, hemodynamic studies were performed before and after 1 to 3 months of treatment with captopril in 75 patients with severe chronic left heart failure. Patients were grouped according to the relative changes in pulmonary and systemic resistances during long-term therapy: patients in Group I (n = 24) showed greater decreases in pulmonary artriolar resistance (PAR) than in systemic vascular resistance (SVR) ({\%} Δ PAR/{\%} Δ SVR > 1.0), whereas patients in Group II showed predominant systemic vasodilation ({\%} Δ PAR/{\%} Δ SVR < 1.0). Despite similar changes in systemic resistance, patients in Group I showed greater increases in cardiac index, stroke volume index and left ventricular stroke work index (p < 0.01 to 0.001) but less dramatic decreases in mean systemic arterial pressure (p < 0.02) than did patients in Group II. Despite similar changes in left ventricular filling pressure, patients in Group I showed greater decreases in mean pulmonary artery and mean right atrial pressures (p < 0.02 to 0.01) than did patients in Group II. Pretreatment variables in Groups I and II were similar, except that plasma renin activity were higher (8.7 ± 2.1 versus 3.0 ± 0.6 ng/ml per h) and serum sodium concentration was lower (133.1 ± 0.9 versus 137.1 ± 0.6 mEq/liter) in Group II than in Group I (both p < 0.05). Both groups improved clinically after 1 to 3 months, but symptomatic hypotension occurred more frequently in Group II than in Group I (36 versus 8{\%}) (p < 0.005). These findings indicate that changes in the pulmonary circulation modulate alterations in both right and left ventricular performance during the treatment of patients with left heart failure. Hyponatremic patients are likely to experience symptomatic hypotension with captopril because they are limited in their ability to increase cardiac output as a result of an inadequate pulmonary vasodilator response to the drug.",
author = "M. Packer and Lee, {W. H.} and N. Medina and M. Yushak",
year = "1985",
language = "English (US)",
volume = "6",
pages = "635--645",
journal = "Journal of the American College of Cardiology",
issn = "0735-1097",
publisher = "Elsevier USA",
number = "3",

}

TY - JOUR

T1 - Hemodynamic and clinical significance of the pulmonary vascular response to long-term captopril therapy in patients with severe chronic heart failure

AU - Packer, M.

AU - Lee, W. H.

AU - Medina, N.

AU - Yushak, M.

PY - 1985

Y1 - 1985

N2 - Exercise capacity in patients with left heart failure is closely related to the performance of the right ventricle and the pulmonary circulation. To determine the significance of changes in pulmonary resistance during long-term vasodilator therapy, hemodynamic studies were performed before and after 1 to 3 months of treatment with captopril in 75 patients with severe chronic left heart failure. Patients were grouped according to the relative changes in pulmonary and systemic resistances during long-term therapy: patients in Group I (n = 24) showed greater decreases in pulmonary artriolar resistance (PAR) than in systemic vascular resistance (SVR) (% Δ PAR/% Δ SVR > 1.0), whereas patients in Group II showed predominant systemic vasodilation (% Δ PAR/% Δ SVR < 1.0). Despite similar changes in systemic resistance, patients in Group I showed greater increases in cardiac index, stroke volume index and left ventricular stroke work index (p < 0.01 to 0.001) but less dramatic decreases in mean systemic arterial pressure (p < 0.02) than did patients in Group II. Despite similar changes in left ventricular filling pressure, patients in Group I showed greater decreases in mean pulmonary artery and mean right atrial pressures (p < 0.02 to 0.01) than did patients in Group II. Pretreatment variables in Groups I and II were similar, except that plasma renin activity were higher (8.7 ± 2.1 versus 3.0 ± 0.6 ng/ml per h) and serum sodium concentration was lower (133.1 ± 0.9 versus 137.1 ± 0.6 mEq/liter) in Group II than in Group I (both p < 0.05). Both groups improved clinically after 1 to 3 months, but symptomatic hypotension occurred more frequently in Group II than in Group I (36 versus 8%) (p < 0.005). These findings indicate that changes in the pulmonary circulation modulate alterations in both right and left ventricular performance during the treatment of patients with left heart failure. Hyponatremic patients are likely to experience symptomatic hypotension with captopril because they are limited in their ability to increase cardiac output as a result of an inadequate pulmonary vasodilator response to the drug.

AB - Exercise capacity in patients with left heart failure is closely related to the performance of the right ventricle and the pulmonary circulation. To determine the significance of changes in pulmonary resistance during long-term vasodilator therapy, hemodynamic studies were performed before and after 1 to 3 months of treatment with captopril in 75 patients with severe chronic left heart failure. Patients were grouped according to the relative changes in pulmonary and systemic resistances during long-term therapy: patients in Group I (n = 24) showed greater decreases in pulmonary artriolar resistance (PAR) than in systemic vascular resistance (SVR) (% Δ PAR/% Δ SVR > 1.0), whereas patients in Group II showed predominant systemic vasodilation (% Δ PAR/% Δ SVR < 1.0). Despite similar changes in systemic resistance, patients in Group I showed greater increases in cardiac index, stroke volume index and left ventricular stroke work index (p < 0.01 to 0.001) but less dramatic decreases in mean systemic arterial pressure (p < 0.02) than did patients in Group II. Despite similar changes in left ventricular filling pressure, patients in Group I showed greater decreases in mean pulmonary artery and mean right atrial pressures (p < 0.02 to 0.01) than did patients in Group II. Pretreatment variables in Groups I and II were similar, except that plasma renin activity were higher (8.7 ± 2.1 versus 3.0 ± 0.6 ng/ml per h) and serum sodium concentration was lower (133.1 ± 0.9 versus 137.1 ± 0.6 mEq/liter) in Group II than in Group I (both p < 0.05). Both groups improved clinically after 1 to 3 months, but symptomatic hypotension occurred more frequently in Group II than in Group I (36 versus 8%) (p < 0.005). These findings indicate that changes in the pulmonary circulation modulate alterations in both right and left ventricular performance during the treatment of patients with left heart failure. Hyponatremic patients are likely to experience symptomatic hypotension with captopril because they are limited in their ability to increase cardiac output as a result of an inadequate pulmonary vasodilator response to the drug.

UR - http://www.scopus.com/inward/record.url?scp=0022372020&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0022372020&partnerID=8YFLogxK

M3 - Article

VL - 6

SP - 635

EP - 645

JO - Journal of the American College of Cardiology

JF - Journal of the American College of Cardiology

SN - 0735-1097

IS - 3

ER -