Details
| Original language | English |
|---|---|
| Pages (from-to) | 786- 793 |
| Number of pages | 8 |
| Journal | Journal of Heart and Lung Transplantation |
| Volume | 40 |
| Issue number | 8 |
| Early online date | 21 May 2021 |
| Publication status | Published - Aug 2021 |
| Externally published | Yes |
Abstract
Background: While rates of stroke have declined with the HeartMate3 (HM3) continuous- flow (CF) left ventricular assist device (LVAD), the impact of non-pulsatile flow and artificial pulse physiology on cerebrovascular function is not known. We hypothesized that improved hemodynamics and artificial pulse physiology of HM3 patients would augment cerebrovascular metabolic reactivity (CVR) compared with HeartMate II (HMII) CF-LVAD and heart failure (HF) patients. Methods: Mean, peak systolic and diastolic flow velocities (MFV, PSV, MinFV, respectively) and cerebral pulsatility index were determined in the middle cerebral artery (MCA) before and after a 30 sec breath-hold challenge in 90 participants: 24 healthy controls; 30 HF, 15 HMII, and 21 HM3 patients. Results: In HM3 patients, breath-holding increased MFV (Δ8 ± 10 cm/sec, p < .0001 vs baseline) to levels similar to HF patients (Δ9 ± 8 cm/sec, p > .05), higher than HMII patients (Δ2 ± 8 cm/sec, p < .01) but lower than healthy controls (Δ13 ± 7 cm/sec, p < .05). CF-LVAD altered the proportion of systolic and diastolic flow responses as reflected by a differential cerebral pulsatility index (p = .03). Baseline MFV was not related to CVR (r 2 = 0.0008, p = .81). However, CF-LVAD pump speed was strongly inversely associated with CVR in HM II (r 2 = 0.51, p = .003) but not HM3 patients (r 2 = 0.01, p = .65). Conclusions: Compared with HMII, HM3 patients have a significantly improved CVR. However, CVR remains lower in HM3 and HF patients than in healthy controls, therefore suggesting that changes in cerebral hemodynamics are not reversed by CF-LVAD therapy. Further research on the mechanisms and the long-term impact of altered cerebral hemodynamics in this unique patient population are warranted.
Keywords
- cerebral autoregulation, heart failure, HM3, LVAD, pulsatility
ASJC Scopus subject areas
- Medicine(all)
- Cardiology and Cardiovascular Medicine
- Medicine(all)
- Transplantation
- Medicine(all)
- Pulmonary and Respiratory Medicine
- Medicine(all)
- Surgery
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In: Journal of Heart and Lung Transplantation, Vol. 40, No. 8, 08.2021, p. 786- 793.
Research output: Contribution to journal › Article › Research › peer review
}
TY - JOUR
T1 - Cerebral vasoreactivity in HeartMate 3 patients
AU - Stöhr, Eric Jean
AU - Ji, Ruiping
AU - Akiyama, Koichi
AU - Mondellini , Giulio M.
AU - Braghieri, Lorenzo
AU - Pinsino , Alberto
AU - Cockroft, John R.
AU - Yuzefpolskaya, Melana
AU - Amlani, Amrin
AU - Topkara, Veli K.
AU - Takayama, Hiroo
AU - Naka, Yoshifumi
AU - Uriel, Nir
AU - Takeda, Koji
AU - Colombo, Paolo C.
AU - McDonnell, Barry J.
AU - Willey, Joshua Z.
N1 - Funding information: This project has received funding from the European Union's Horizon 2020 research and innovation program under the Marie Sk?odowska-Curie grant agreement No 705219 , and from the Lisa and Mark Schwartz Program to Reverse Heart Failure at New York – Presbyterian Hospital/Columbia University.
PY - 2021/8
Y1 - 2021/8
N2 - Background: While rates of stroke have declined with the HeartMate3 (HM3) continuous- flow (CF) left ventricular assist device (LVAD), the impact of non-pulsatile flow and artificial pulse physiology on cerebrovascular function is not known. We hypothesized that improved hemodynamics and artificial pulse physiology of HM3 patients would augment cerebrovascular metabolic reactivity (CVR) compared with HeartMate II (HMII) CF-LVAD and heart failure (HF) patients. Methods: Mean, peak systolic and diastolic flow velocities (MFV, PSV, MinFV, respectively) and cerebral pulsatility index were determined in the middle cerebral artery (MCA) before and after a 30 sec breath-hold challenge in 90 participants: 24 healthy controls; 30 HF, 15 HMII, and 21 HM3 patients. Results: In HM3 patients, breath-holding increased MFV (Δ8 ± 10 cm/sec, p < .0001 vs baseline) to levels similar to HF patients (Δ9 ± 8 cm/sec, p > .05), higher than HMII patients (Δ2 ± 8 cm/sec, p < .01) but lower than healthy controls (Δ13 ± 7 cm/sec, p < .05). CF-LVAD altered the proportion of systolic and diastolic flow responses as reflected by a differential cerebral pulsatility index (p = .03). Baseline MFV was not related to CVR (r 2 = 0.0008, p = .81). However, CF-LVAD pump speed was strongly inversely associated with CVR in HM II (r 2 = 0.51, p = .003) but not HM3 patients (r 2 = 0.01, p = .65). Conclusions: Compared with HMII, HM3 patients have a significantly improved CVR. However, CVR remains lower in HM3 and HF patients than in healthy controls, therefore suggesting that changes in cerebral hemodynamics are not reversed by CF-LVAD therapy. Further research on the mechanisms and the long-term impact of altered cerebral hemodynamics in this unique patient population are warranted.
AB - Background: While rates of stroke have declined with the HeartMate3 (HM3) continuous- flow (CF) left ventricular assist device (LVAD), the impact of non-pulsatile flow and artificial pulse physiology on cerebrovascular function is not known. We hypothesized that improved hemodynamics and artificial pulse physiology of HM3 patients would augment cerebrovascular metabolic reactivity (CVR) compared with HeartMate II (HMII) CF-LVAD and heart failure (HF) patients. Methods: Mean, peak systolic and diastolic flow velocities (MFV, PSV, MinFV, respectively) and cerebral pulsatility index were determined in the middle cerebral artery (MCA) before and after a 30 sec breath-hold challenge in 90 participants: 24 healthy controls; 30 HF, 15 HMII, and 21 HM3 patients. Results: In HM3 patients, breath-holding increased MFV (Δ8 ± 10 cm/sec, p < .0001 vs baseline) to levels similar to HF patients (Δ9 ± 8 cm/sec, p > .05), higher than HMII patients (Δ2 ± 8 cm/sec, p < .01) but lower than healthy controls (Δ13 ± 7 cm/sec, p < .05). CF-LVAD altered the proportion of systolic and diastolic flow responses as reflected by a differential cerebral pulsatility index (p = .03). Baseline MFV was not related to CVR (r 2 = 0.0008, p = .81). However, CF-LVAD pump speed was strongly inversely associated with CVR in HM II (r 2 = 0.51, p = .003) but not HM3 patients (r 2 = 0.01, p = .65). Conclusions: Compared with HMII, HM3 patients have a significantly improved CVR. However, CVR remains lower in HM3 and HF patients than in healthy controls, therefore suggesting that changes in cerebral hemodynamics are not reversed by CF-LVAD therapy. Further research on the mechanisms and the long-term impact of altered cerebral hemodynamics in this unique patient population are warranted.
KW - cerebral autoregulation
KW - heart failure
KW - HM3
KW - LVAD
KW - pulsatility
UR - http://www.scopus.com/inward/record.url?scp=85107912878&partnerID=8YFLogxK
U2 - 10.1016/j.healun.2021.05.005
DO - 10.1016/j.healun.2021.05.005
M3 - Article
VL - 40
SP - 786
EP - 793
JO - Journal of Heart and Lung Transplantation
JF - Journal of Heart and Lung Transplantation
SN - 1053-2498
IS - 8
ER -