TY - JOUR
T1 - Essential hypertension worsens left ventricular contractility in systemic sclerosis
AU - Mercurio, Valentina
AU - Hinze, Alicia M.
AU - Hummers, Laura K.
AU - Wigley, Fredrick M.
AU - Shah, Ami A.
AU - Mukherjee, Monica
N1 - Publisher Copyright:
© 2021 The Journal of Rheumatology
PY - 2021/8/1
Y1 - 2021/8/1
N2 - Objective. Primary cardiac involvement in systemic sclerosis (SSc) is prevalent and morbid; however, the influence of traditional cardiovascular (CV) risk factors, such as essential hypertension (HTN), are unclear. In the present study, we sought to understand the effects of HTN on left ventricular (LV) contractility in patients with SSc using echocardiographic speckle-derived global longitudinal strain (GLS). Methods. Fifty-six SSc patients with HTN (SSc+HTN+) and 82 SSc patients without HTN (SSc+ HTN-) were compared with 40 non-SSc controls with HTN (SSc-HTN+) and 40 non-SSc controls without HTN (SSc-HTN-), matched by age and sex. All HTN patients were on stable antihypertensive therapies. Echocardiographic measures included LV (LV) ejection fraction (LVEF), left atrial volume index (LAVI), and LV diastolic function. LV contractility was assessed by GLS, averaged across the 18 LV segments. Results. Patients with SSc had diminished GLS regardless of HTN status when compared to both control groups, despite normal LVEF (P < 0.001). SSc+HTN+ had the highest prevalence of diastolic dysfunction, with significantly higher septal E/e, a marker of LV filling pressures (P < 0.05), as well as the largest reduction in GLS compared to SSc+HTN- and both control groups. Conclusion. Speckle-derived strain revealed diminished LV contractility in patients with SSc, despite normal LVEF. SSc+HTN+ had more prominent reductions in GLS associated with evidence of LV remodeling and worsened diastolic function. Our findings demonstrate the presence of subclinical LV contractile dysfunction in SSc that is further exacerbated by concomitant HTN, thereby identifying HTN as an important modifiable CV risk factor that should be managed aggressively in this at-risk population.
AB - Objective. Primary cardiac involvement in systemic sclerosis (SSc) is prevalent and morbid; however, the influence of traditional cardiovascular (CV) risk factors, such as essential hypertension (HTN), are unclear. In the present study, we sought to understand the effects of HTN on left ventricular (LV) contractility in patients with SSc using echocardiographic speckle-derived global longitudinal strain (GLS). Methods. Fifty-six SSc patients with HTN (SSc+HTN+) and 82 SSc patients without HTN (SSc+ HTN-) were compared with 40 non-SSc controls with HTN (SSc-HTN+) and 40 non-SSc controls without HTN (SSc-HTN-), matched by age and sex. All HTN patients were on stable antihypertensive therapies. Echocardiographic measures included LV (LV) ejection fraction (LVEF), left atrial volume index (LAVI), and LV diastolic function. LV contractility was assessed by GLS, averaged across the 18 LV segments. Results. Patients with SSc had diminished GLS regardless of HTN status when compared to both control groups, despite normal LVEF (P < 0.001). SSc+HTN+ had the highest prevalence of diastolic dysfunction, with significantly higher septal E/e, a marker of LV filling pressures (P < 0.05), as well as the largest reduction in GLS compared to SSc+HTN- and both control groups. Conclusion. Speckle-derived strain revealed diminished LV contractility in patients with SSc, despite normal LVEF. SSc+HTN+ had more prominent reductions in GLS associated with evidence of LV remodeling and worsened diastolic function. Our findings demonstrate the presence of subclinical LV contractile dysfunction in SSc that is further exacerbated by concomitant HTN, thereby identifying HTN as an important modifiable CV risk factor that should be managed aggressively in this at-risk population.
KW - Echocardiography
KW - Essential hypertension
KW - Global longitudinal strain
KW - Systemic sclerosis
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U2 - 10.3899/jrheum.200873
DO - 10.3899/jrheum.200873
M3 - Article
C2 - 33452172
AN - SCOPUS:85112323641
SN - 0315-162X
VL - 48
SP - 1299
EP - 1306
JO - Journal of Rheumatology
JF - Journal of Rheumatology
IS - 8
ER -