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Published on: February 20, 2017
Predictors of left ventricular dysfunction in patients with Takayasu's or giant cell aortitis
D H Pfizenmaier1, F O Al Atawi, Y Castillo
1Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota 55905, USA.
Insights
Left ventricular systolic dysfunction (LVSD) affects 18% of patients with Takayasu
Area of Science:
- Cardiology
- Rheumatology
- Vascular Inflammation
Background:
- Left ventricular systolic dysfunction (LVSD) in Takayasu's or Giant Cell aortitis (TA/GCA) is rarely reported.
- Potential causes include hemodynamic and immunologic factors, but predictors remain unknown.
- This study investigates predictors in a large, angiographically characterized TA/GCA cohort.
Purpose of the Study:
- To identify clinical and angiographic predictors of LVSD in patients with TA/GCA.
- To estimate the incidence of LVSD in this population.
- To differentiate between hemodynamic and inflammatory causes of LVSD.
Main Methods:
- Retrospective analysis of 78 patients with angiographically confirmed TA/GCA.
- Transthoracic echocardiography (TTE) was used to assess LVSD (defined as LVEF < 50%).
- Reviewers blinded to clinical and angiographic data evaluated echocardiograms.
Main Results:
- 18% (14/78) of patients had LVSD, with a mean LVEF of 37%.
- LVSD was significantly associated with aortic arch involvement (43% vs 9%) and greater extent of aortic disease (median 2 vs 1 segment).
- Hypertension and aortic regurgitation were not associated with LVSD.
Conclusions:
- LVSD in TA/GCA is linked to aortic arch involvement and disease extent.
- Hemodynamic factors like hypertension and aortic regurgitation do not predict LVSD.
- Cardiac inflammation is likely the primary cause of LVSD in TA/GCA.
Objectives:
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.
Background:
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.
Methods:
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%.
Results:
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).
Conclusions:
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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