scholarly journals Spironolactone Reduces Aortic Stiffness in Patients With Resistant Hypertension Independent of Blood Pressure Change

Author(s):  
Sudeep R. Aryal ◽  
Mohammed Siddiqui ◽  
Oleg F. Sharifov ◽  
Megan D. Coffin ◽  
Bin Zhang ◽  
...  

Background Aortic stiffness is an independent predictor of cardiovascular events in patients with arterial hypertension. Resistant hypertension is often linked to hyperaldosteronism and associated with adverse outcomes. Spironolactone, a mineralocorticoid receptor antagonist, has been shown to reduce both the arterial blood pressure (BP) and aortic stiffness in resistant hypertension. However, the mechanism of aortic stiffness reduction by spironolactone is not well understood. We hypothesized that spironolactone reduces aortic stiffness in resistant hypertension independently of BP change. Methods and Results Patients with uncontrolled BP (≥140/90 mm Hg) despite use of ≥3 antihypertensive medications (including diuretics) were prospectively recruited. Participants were started on spironolactone at 25 mg/d, and increased to 50 mg/d at 4 weeks while other antihypertensive medications were withdrawn to maintain constant mean BP. Phase‐contrast cardiac magnetic resonance imaging of the ascending aorta was performed in 30 participants at baseline and after 6 months of spironolactone treatment to measure aortic pulsatility, distensibility, and pulse wave velocity. Pulse wave velocity decreased (6.3±2.3 m/s to 4.5±1.8 m/s, P <0.001) and pulsatility and distensibility increased (15.9%±5.3% to 22.1%±7.9%, P <0.001; and 0.28%±0.10%/mm Hg to 0.40%±0.14%/mm Hg, P <0.001, respectively) following 6 months of spironolactone. Conclusions Our results suggest that spironolactone improves aortic properties in resistant hypertension independently of BP, which may support the hypothesis of an effect of aldosterone on the arterial wall. A larger prospective study is needed to confirm our findings.

2020 ◽  
Vol 25 (12) ◽  
pp. 4036
Author(s):  
H. Yilmaz Ak ◽  
Y. Ozsahin ◽  
N. Baskurt Aladag ◽  
F. Gencoglu ◽  
B. Sahin Yildiz ◽  
...  

Aim. Patients with chronic inflammatory diseases (CID), such as rheumatoid arthritis (RA) and familial Mediterranean fever (FMF) are more likely to have higher risk of cardiac events. Pulse wave velocity (PWV) can be used to measure the aortic dis-tensibility and it is known as inversely related to the arterial compliance. Increased aortic stiffness which is assessed by PWV, is seem to be associated with arterial blood pressure. In this study, we investigated the arterial compliance by PWV in patients with CID including RA and FMF.Material and methods. We studied 25 patients with RA, 33 patients with FMF and 31 healthy subjects without a history of any cardiovascular risk factors such as hypertension, diabetes mellitus, hyperlipidaemia (89 subjects in total). We measured the arterial compliance by automatic carotid-femoral (aortic) PWV using Complior Colson (France) device. PWV (m/s) = distance (m)/transit time(s).Results. It is seen that, patients with CID have higher carotid-femoral (aortic) PWV (8,76±2,09 vs 8,07±0,94 m/s) compared to control groups (p=0,03). There were significant correlations between PWV and age, body-mass index, systolic blood pressure, diastolic blood pressure and mean blood pressure. (p<0,001, r=0,65; p<0,001, r=0,36; p<0,001, r=0,42; p<0,001, r=0,46; p<0,001, r=0,48, respectively).Conclusion. Arterial compliance, which is assessed by carotid-femoral (aortic) PWV, is decreased in patients with CID such as RA and FMF when it is compared to healthy control group.


Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Mircea Anghelescu ◽  
Keith J Gooch ◽  
Aaron J Trask

Pulse wave velocity (PWV) is the gold standard for in vivo aortic stiffness measurements but can be dependent upon blood pressure and/or heart rate. Previous studies from our and other labs have shown increased aortic PWV in type 2 diabetic db/db mice. Moreover, preliminary ex vivo pressure myography data from our lab has also shown a lack of increase in passive aortic stiffness, suggesting that increased PWV in vivo , and therefore, increased stiffness in db/db mice may be dependent upon other mechanisms. In this study, we tested the hypothesis that increased aortic pulse wave velocity measured in db/db mice in vivo is blood pressure dependent under anesthesia. 16-wk old normal Db/db (n=9) and type 2 diabetic db/db (n=5) mice were anesthetized with 2% isoflurane and instrumented with two 1.2F pressure-tip catheters: one inserted in the left carotid artery and advanced to the thoracic aorta, the other inserted into the left femoral artery and advanced into the abdominal aorta. Blood pressure was continuously recorded and PWV was calculated using the foot-to-foot method. A microcannula was inserted into the right jugular vein for the administration of drugs. After a stabilization period of 25-30 mins, baseline BPs and PWVs were measured, after which mice were infused with increasing doses of phenylephrine (Phe, 100-500 nmol/kg/min) and sodium nitroprusside (SNP, 100-500 nmol/kg/min) to increase and decrease blood pressure, respectively. At baseline (prior to the infusion of any drugs), mean arterial pressure and aortic PWV were significantly elevated in db/db mice under anesthesia (MAP; Db/db: 77±5 vs. db/db: 100±4 mmHg, p <0.05; PWV; Db/db: 0.31±0.01 vs. db/db: 0.35±0.01 cm/ms, p <0.05). The increase in aortic PWV in db/db mice at baseline was completely abrogated when measured at equivalent MAPs ranging from 40-120 mmHg during the Phe and SNP infusions ( p >0.05). In both Db/db and db/db mice, aortic PWV was significantly correlated with MAP (Db/db: r=0.94, p <0.001; db/db: r=0.97, p <0.0001). These data show that increased aortic PWV, and therefore increased aortic stiffness in db/db mice in vivo is dependent upon blood pressure.


2016 ◽  
Vol 34 (4) ◽  
pp. 666-675 ◽  
Author(s):  
Marc Isabelle ◽  
Stefano Chimenti ◽  
Hélène Beaussier ◽  
Denis Gransagne ◽  
Nicole Villeneuve ◽  
...  

2018 ◽  
Vol 24 (C) ◽  
pp. 124
Author(s):  
Jose Mesquita Bastos ◽  
Susana Lopes ◽  
Catarina Garcia ◽  
Verónica Ribau ◽  
Susana Bertoquini ◽  
...  

Hypertension ◽  
2020 ◽  
Vol 76 (6) ◽  
pp. 1800-1807 ◽  
Author(s):  
Virginia R. Nuckols ◽  
Seth W. Holwerda ◽  
Rachel E. Luehrs ◽  
Lyndsey E. DuBose ◽  
Amy K. Stroud ◽  
...  

Women with preeclampsia, a hypertensive disorder of pregnancy, exhibit greater beat-to-beat blood pressure variability (BPV) in the third trimester after clinical onset of the disorder. However, it remains unknown whether elevated BPV precedes the development of preeclampsia. A prospective study cohort of 139 women (age 30.2±4.0 years) were enrolled in early pregnancy (<14 weeks gestation). BPV was quantified by time domain analyses of 10-minute continuous beat-to-beat blood pressure recordings via finger photoplethysmography in the first, second, and third trimesters. Aortic stiffness (carotid-femoral pulse wave velocity) and spontaneous cardiovagal baroreflex sensitivity were also measured each trimester. Eighteen women (13%) developed preeclampsia. Systolic BPV was higher in all trimesters among women who developed versus did not develop preeclampsia (first: 4.8±1.3 versus 3.7±1.2, P =0.001; second: 5.1±1.8 versus 3.8±1.1, P =0.02; third: 5.2±0.8 versus 4.0±1.1 mm Hg, P =0.002). Elevated first trimester systolic BPV was associated with preeclampsia (odds ratio, 1.94 [95% CI, 1.27–2.99]), even after adjusting for risk factors (age, body mass index, systolic blood pressure, history of preeclampsia, and diabetes mellitus) and was a significant predictor of preeclampsia (area under the receiver operator characteristic curve=0.75±0.07; P =0.002). Carotid-femoral pulse wave velocity was elevated in the first trimester among women who developed preeclampsia (5.9±0.8 versus 5.2±0.8 m/s; P =0.002) and was associated with BPV after adjustment for mean blood pressure ( r =0.26; P =0.005). First trimester baroreflex sensitivity did not differ between groups ( P =0.23) and was not related to BPV ( P =0.36). Elevated systolic BPV is independently associated with the development of preeclampsia as early as the first trimester, possibly mediated in part by higher aortic stiffness.


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