Predictors of left ventricular dysfunction in patients with Takayasu's or giant cell aortitis

The aim of this study was to determine the clinical and angiographic predictors of left ventricular systolic dysfunction (LVSD) from a relatively large and angiographically characterized Takayasu's or Giant Cell aortitis (TA/GCA) population. LVSD in patients with TA/GCA has been described in ca...

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Veröffentlicht in:Clinical and experimental rheumatology 2004, Vol.22 (6 Suppl 36), p.S41-S45
Hauptverfasser: Pfizenmaier, D H, Al Atawi, F O, Castillo, Y, Chandrasekaran, K, Cooper, L T
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container_end_page S45
container_issue 6 Suppl 36
container_start_page S41
container_title Clinical and experimental rheumatology
container_volume 22
creator Pfizenmaier, D H
Al Atawi, F O
Castillo, Y
Chandrasekaran, K
Cooper, L T
description The aim of this study was to determine the clinical and angiographic predictors of left ventricular systolic dysfunction (LVSD) from a relatively large and angiographically characterized Takayasu's or Giant Cell aortitis (TA/GCA) population. LVSD in patients with TA/GCA has been described in case reports and attributed variously to hemodynamic and immunologic factors. The predictors of LVSD in patients with angiographically confirmed TA/GCA are not known. We identified 78 patients with angiographically confirmed TA/ GCA that underwent transthoracic echocardiography (TTE) at Mayo Clinic. Echocardiograms were then reviewed independently by reviewers blinded to clinical and angiographic data. LVSD was defined as an ejection fraction (LVEF) less than 50%. The study population was 84% Caucasian (54/78), 91% female (58/78), and had a mean age of disease onset of 30 years (+/- 15 years). LVSD was present in 14 of 78 patients (18%) with TA/GCA. The mean LVEF in the LVSD group (n = 14) was 37% +/- 7%, compared to an LVEF of 62% +/- 6% (p < 0.0001) in those without LVSD (n = 64). LVSD was not associated with hypertension or aortic regurgitation (p > 0.5). However, LVSD was found in 43% (9/21) of patients with aortic arch involvement, versus only 9% (5/57) of patients without aortic arch involvement (p = 0.0013). Patients with LVSD had a median of 2 (range 1-4) involved aortic segments compared to a median of 1 (range 1-4) among those without LVSD (p = 0.013). In TA/GCA aortitis, LVSD is associated with involvement of the aortic arch and with the greater extent of aortic involvement. The hemodynamic variables, aortic regurgitation and systemic hypertension, were not associated with LVSD, consistent with reports that cardiac inflammation is responsible for LVSD in a majority of cases. Ours is the first study to estimate an incidence of LVSD in patients with TA/GCA aortitis, which was 18%.
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LVSD in patients with TA/GCA has been described in case reports and attributed variously to hemodynamic and immunologic factors. The predictors of LVSD in patients with angiographically confirmed TA/GCA are not known. We identified 78 patients with angiographically confirmed TA/ GCA that underwent transthoracic echocardiography (TTE) at Mayo Clinic. Echocardiograms were then reviewed independently by reviewers blinded to clinical and angiographic data. LVSD was defined as an ejection fraction (LVEF) less than 50%. The study population was 84% Caucasian (54/78), 91% female (58/78), and had a mean age of disease onset of 30 years (+/- 15 years). LVSD was present in 14 of 78 patients (18%) with TA/GCA. The mean LVEF in the LVSD group (n = 14) was 37% +/- 7%, compared to an LVEF of 62% +/- 6% (p &lt; 0.0001) in those without LVSD (n = 64). LVSD was not associated with hypertension or aortic regurgitation (p &gt; 0.5). 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LVSD in patients with TA/GCA has been described in case reports and attributed variously to hemodynamic and immunologic factors. The predictors of LVSD in patients with angiographically confirmed TA/GCA are not known. We identified 78 patients with angiographically confirmed TA/ GCA that underwent transthoracic echocardiography (TTE) at Mayo Clinic. Echocardiograms were then reviewed independently by reviewers blinded to clinical and angiographic data. LVSD was defined as an ejection fraction (LVEF) less than 50%. The study population was 84% Caucasian (54/78), 91% female (58/78), and had a mean age of disease onset of 30 years (+/- 15 years). LVSD was present in 14 of 78 patients (18%) with TA/GCA. The mean LVEF in the LVSD group (n = 14) was 37% +/- 7%, compared to an LVEF of 62% +/- 6% (p &lt; 0.0001) in those without LVSD (n = 64). LVSD was not associated with hypertension or aortic regurgitation (p &gt; 0.5). However, LVSD was found in 43% (9/21) of patients with aortic arch involvement, versus only 9% (5/57) of patients without aortic arch involvement (p = 0.0013). Patients with LVSD had a median of 2 (range 1-4) involved aortic segments compared to a median of 1 (range 1-4) among those without LVSD (p = 0.013). In TA/GCA aortitis, LVSD is associated with involvement of the aortic arch and with the greater extent of aortic involvement. The hemodynamic variables, aortic regurgitation and systemic hypertension, were not associated with LVSD, consistent with reports that cardiac inflammation is responsible for LVSD in a majority of cases. Ours is the first study to estimate an incidence of LVSD in patients with TA/GCA aortitis, which was 18%.</abstract><cop>Italy</cop><pmid>15675134</pmid></addata></record>
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source MEDLINE; Alma/SFX Local Collection
subjects Adult
Comorbidity
Echocardiography
Female
Giant Cell Arteritis - complications
Giant Cell Arteritis - pathology
Giant Cell Arteritis - physiopathology
Humans
Incidence
Male
Minnesota - epidemiology
Retrospective Studies
Single-Blind Method
Takayasu Arteritis - complications
Takayasu Arteritis - pathology
Takayasu Arteritis - physiopathology
Ventricular Dysfunction, Left - epidemiology
Ventricular Dysfunction, Left - etiology
Ventricular Dysfunction, Left - pathology
title Predictors of left ventricular dysfunction in patients with Takayasu's or giant cell aortitis
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