Arterial dilators in mitral regurgitation

Effects on rest and exercise hemodynamics and long-term clinical follow-up

B. H. Greenberg, H. DeMots, Edward Murphy, S. H. Rahimtoola

    Research output: Contribution to journalArticle

    42 Citations (Scopus)

    Abstract

    The authors studied 16 patients with severe mitral regurgitation to determine the acute effects of hydralazine on cardiac performance at rest and during exercise and to assess the long-term clinical response to therapy. At rest, optimal-dose hydralazine (range 50-225 mg) reduced systemic vascular resistance from 1385 ± 88 to 964 ± 76 dyn-sec-cm-5 (mean ± SEM) (p <0.001). As a result, pulmonary artery wedge pressure decreased from 18 ± 2 to 15 ± 2 mm Hg (p <0.025), cardiac index increased from 2.5 ± 0.1 to 3.7 ± 0.2 l/min/m2 (p <0.001) and stroke volume index increased from 30 ± 2 to 39 ± 2 ml/m2 (p <0.001). The effects of hydralazine on exercise hemodynamics were evaluated in 12 patients. Before treatment, the patients exercised at increasing work loads until limited by symptoms. After hydralazine therapy, exercise was repeated at identical work loads. Although exercise alone resulted in a reduction in systemic vascular resistance, from 1385 ± 88 to 1111 ± 118 dyn-sec-cm-5, the addition of hydralazine caused a further reduction in resistance, from 1111 ± 118 to 755 ± 72 dyn-sec-cm-5 (p <0.005). Hydralazine reduced pulmonary artery wedge pressure during exercise from 27 ± 2 to 21 ± 1 mm Hg and increased cardiac index from 3.7 ± 0.3 to 4.9 ± 0.3 l/min/m2 (both p <0.001) and stroke volume index from 36 ± 3 to 45 ± 2 ml/m2 (p <0.005). All 16 patients were discharged on hydralazine therapy and their clinical course was followed. A marked improvement in symptoms from New York Heart Association functional class III-VI to class I-II, which was sustained for at least 6 months, occurred in 7 patients (44%). One patient improved from class IV to class III. The mean follow-up in these 8 patients has been 13 ± 4 months. In 4 of the 8 remaining patients, hydralazine was discontinued because of intolerable side effects. Mitral valve surgery was performed in 3 of these patients as well as in 4 patients who demonstrated an initial hemodynamic response to therapy but failed to experience symptomatic improvement. These data demonstrate that hydralazine therapy results in substantial improvement in cardiac performance in patients with mitral regurgitation. The beneficial effects seen at rest are maintained during exercise. The acute improvement in hemodynamics resulted in sustained clinical improvement in half the patients with mitral regurgitation; the other half needed valve surgery. Arterial dilator therapy is of benefit for some patients with severe mitral regurgitation.

    Original languageEnglish (US)
    Pages (from-to)181-187
    Number of pages7
    JournalCirculation
    Volume65
    Issue number1 I
    StatePublished - 1982

    Fingerprint

    Mitral Valve Insufficiency
    Hydralazine
    Hemodynamics
    Exercise
    Pulmonary Wedge Pressure
    Workload
    Vascular Resistance
    Stroke Volume
    Therapeutics
    Mitral Valve

    ASJC Scopus subject areas

    • Physiology
    • Cardiology and Cardiovascular Medicine

    Cite this

    Arterial dilators in mitral regurgitation : Effects on rest and exercise hemodynamics and long-term clinical follow-up. / Greenberg, B. H.; DeMots, H.; Murphy, Edward; Rahimtoola, S. H.

    In: Circulation, Vol. 65, No. 1 I, 1982, p. 181-187.

    Research output: Contribution to journalArticle

    @article{ecbc88d8293e425db5b8f901ecc9f4eb,
    title = "Arterial dilators in mitral regurgitation: Effects on rest and exercise hemodynamics and long-term clinical follow-up",
    abstract = "The authors studied 16 patients with severe mitral regurgitation to determine the acute effects of hydralazine on cardiac performance at rest and during exercise and to assess the long-term clinical response to therapy. At rest, optimal-dose hydralazine (range 50-225 mg) reduced systemic vascular resistance from 1385 ± 88 to 964 ± 76 dyn-sec-cm-5 (mean ± SEM) (p <0.001). As a result, pulmonary artery wedge pressure decreased from 18 ± 2 to 15 ± 2 mm Hg (p <0.025), cardiac index increased from 2.5 ± 0.1 to 3.7 ± 0.2 l/min/m2 (p <0.001) and stroke volume index increased from 30 ± 2 to 39 ± 2 ml/m2 (p <0.001). The effects of hydralazine on exercise hemodynamics were evaluated in 12 patients. Before treatment, the patients exercised at increasing work loads until limited by symptoms. After hydralazine therapy, exercise was repeated at identical work loads. Although exercise alone resulted in a reduction in systemic vascular resistance, from 1385 ± 88 to 1111 ± 118 dyn-sec-cm-5, the addition of hydralazine caused a further reduction in resistance, from 1111 ± 118 to 755 ± 72 dyn-sec-cm-5 (p <0.005). Hydralazine reduced pulmonary artery wedge pressure during exercise from 27 ± 2 to 21 ± 1 mm Hg and increased cardiac index from 3.7 ± 0.3 to 4.9 ± 0.3 l/min/m2 (both p <0.001) and stroke volume index from 36 ± 3 to 45 ± 2 ml/m2 (p <0.005). All 16 patients were discharged on hydralazine therapy and their clinical course was followed. A marked improvement in symptoms from New York Heart Association functional class III-VI to class I-II, which was sustained for at least 6 months, occurred in 7 patients (44{\%}). One patient improved from class IV to class III. The mean follow-up in these 8 patients has been 13 ± 4 months. In 4 of the 8 remaining patients, hydralazine was discontinued because of intolerable side effects. Mitral valve surgery was performed in 3 of these patients as well as in 4 patients who demonstrated an initial hemodynamic response to therapy but failed to experience symptomatic improvement. These data demonstrate that hydralazine therapy results in substantial improvement in cardiac performance in patients with mitral regurgitation. The beneficial effects seen at rest are maintained during exercise. The acute improvement in hemodynamics resulted in sustained clinical improvement in half the patients with mitral regurgitation; the other half needed valve surgery. Arterial dilator therapy is of benefit for some patients with severe mitral regurgitation.",
    author = "Greenberg, {B. H.} and H. DeMots and Edward Murphy and Rahimtoola, {S. H.}",
    year = "1982",
    language = "English (US)",
    volume = "65",
    pages = "181--187",
    journal = "Circulation",
    issn = "0009-7322",
    publisher = "Lippincott Williams and Wilkins",
    number = "1 I",

    }

    TY - JOUR

    T1 - Arterial dilators in mitral regurgitation

    T2 - Effects on rest and exercise hemodynamics and long-term clinical follow-up

    AU - Greenberg, B. H.

    AU - DeMots, H.

    AU - Murphy, Edward

    AU - Rahimtoola, S. H.

    PY - 1982

    Y1 - 1982

    N2 - The authors studied 16 patients with severe mitral regurgitation to determine the acute effects of hydralazine on cardiac performance at rest and during exercise and to assess the long-term clinical response to therapy. At rest, optimal-dose hydralazine (range 50-225 mg) reduced systemic vascular resistance from 1385 ± 88 to 964 ± 76 dyn-sec-cm-5 (mean ± SEM) (p <0.001). As a result, pulmonary artery wedge pressure decreased from 18 ± 2 to 15 ± 2 mm Hg (p <0.025), cardiac index increased from 2.5 ± 0.1 to 3.7 ± 0.2 l/min/m2 (p <0.001) and stroke volume index increased from 30 ± 2 to 39 ± 2 ml/m2 (p <0.001). The effects of hydralazine on exercise hemodynamics were evaluated in 12 patients. Before treatment, the patients exercised at increasing work loads until limited by symptoms. After hydralazine therapy, exercise was repeated at identical work loads. Although exercise alone resulted in a reduction in systemic vascular resistance, from 1385 ± 88 to 1111 ± 118 dyn-sec-cm-5, the addition of hydralazine caused a further reduction in resistance, from 1111 ± 118 to 755 ± 72 dyn-sec-cm-5 (p <0.005). Hydralazine reduced pulmonary artery wedge pressure during exercise from 27 ± 2 to 21 ± 1 mm Hg and increased cardiac index from 3.7 ± 0.3 to 4.9 ± 0.3 l/min/m2 (both p <0.001) and stroke volume index from 36 ± 3 to 45 ± 2 ml/m2 (p <0.005). All 16 patients were discharged on hydralazine therapy and their clinical course was followed. A marked improvement in symptoms from New York Heart Association functional class III-VI to class I-II, which was sustained for at least 6 months, occurred in 7 patients (44%). One patient improved from class IV to class III. The mean follow-up in these 8 patients has been 13 ± 4 months. In 4 of the 8 remaining patients, hydralazine was discontinued because of intolerable side effects. Mitral valve surgery was performed in 3 of these patients as well as in 4 patients who demonstrated an initial hemodynamic response to therapy but failed to experience symptomatic improvement. These data demonstrate that hydralazine therapy results in substantial improvement in cardiac performance in patients with mitral regurgitation. The beneficial effects seen at rest are maintained during exercise. The acute improvement in hemodynamics resulted in sustained clinical improvement in half the patients with mitral regurgitation; the other half needed valve surgery. Arterial dilator therapy is of benefit for some patients with severe mitral regurgitation.

    AB - The authors studied 16 patients with severe mitral regurgitation to determine the acute effects of hydralazine on cardiac performance at rest and during exercise and to assess the long-term clinical response to therapy. At rest, optimal-dose hydralazine (range 50-225 mg) reduced systemic vascular resistance from 1385 ± 88 to 964 ± 76 dyn-sec-cm-5 (mean ± SEM) (p <0.001). As a result, pulmonary artery wedge pressure decreased from 18 ± 2 to 15 ± 2 mm Hg (p <0.025), cardiac index increased from 2.5 ± 0.1 to 3.7 ± 0.2 l/min/m2 (p <0.001) and stroke volume index increased from 30 ± 2 to 39 ± 2 ml/m2 (p <0.001). The effects of hydralazine on exercise hemodynamics were evaluated in 12 patients. Before treatment, the patients exercised at increasing work loads until limited by symptoms. After hydralazine therapy, exercise was repeated at identical work loads. Although exercise alone resulted in a reduction in systemic vascular resistance, from 1385 ± 88 to 1111 ± 118 dyn-sec-cm-5, the addition of hydralazine caused a further reduction in resistance, from 1111 ± 118 to 755 ± 72 dyn-sec-cm-5 (p <0.005). Hydralazine reduced pulmonary artery wedge pressure during exercise from 27 ± 2 to 21 ± 1 mm Hg and increased cardiac index from 3.7 ± 0.3 to 4.9 ± 0.3 l/min/m2 (both p <0.001) and stroke volume index from 36 ± 3 to 45 ± 2 ml/m2 (p <0.005). All 16 patients were discharged on hydralazine therapy and their clinical course was followed. A marked improvement in symptoms from New York Heart Association functional class III-VI to class I-II, which was sustained for at least 6 months, occurred in 7 patients (44%). One patient improved from class IV to class III. The mean follow-up in these 8 patients has been 13 ± 4 months. In 4 of the 8 remaining patients, hydralazine was discontinued because of intolerable side effects. Mitral valve surgery was performed in 3 of these patients as well as in 4 patients who demonstrated an initial hemodynamic response to therapy but failed to experience symptomatic improvement. These data demonstrate that hydralazine therapy results in substantial improvement in cardiac performance in patients with mitral regurgitation. The beneficial effects seen at rest are maintained during exercise. The acute improvement in hemodynamics resulted in sustained clinical improvement in half the patients with mitral regurgitation; the other half needed valve surgery. Arterial dilator therapy is of benefit for some patients with severe mitral regurgitation.

    UR - http://www.scopus.com/inward/record.url?scp=0020062394&partnerID=8YFLogxK

    UR - http://www.scopus.com/inward/citedby.url?scp=0020062394&partnerID=8YFLogxK

    M3 - Article

    VL - 65

    SP - 181

    EP - 187

    JO - Circulation

    JF - Circulation

    SN - 0009-7322

    IS - 1 I

    ER -