4.6 Article

Cerebral Microvascular Injury in Patients with Left Ventricular Assist Device: a Neuropathological Study

Journal

TRANSLATIONAL STROKE RESEARCH
Volume 13, Issue 2, Pages 257-264

Publisher

SPRINGER
DOI: 10.1007/s12975-021-00935-z

Keywords

Ventricular assist device; Autopsy; Cerebral infarction; Cerebral hemorrhage; Microvascular injury; Cerebral microbleeds

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The study examined post-mortem neuropathological findings of LVAD patients and found a high prevalence of cerebral injuries, with 90% of patients showing cerebral microvascular injuries. Multiple types of cerebral injuries coexisted, suggesting that subclinical microvascular injuries and cerebral microbleeds in LVAD patients may contribute to the frequent occurrence of cerebral injury.
Strokes are common among patients with left ventricular devices (LVAD). We hypothesize that there is ongoing cerebral microvascular injury with LVAD support and aim to describe this among LVAD-implanted patients through post-mortem neuropathologic evaluation. We identified and reviewed medical records of LVAD patients who underwent brain autopsy between January 2006 and December 2019 at a tertiary center. Cerebral injury was defined as both gross and microscopic injuries within the intracranial space including cerebral infarct (CI), hypoxic-ischemic brain injury (HIBI), intracranial hemorrhage (ICH), and cerebral microvascular injury. Cerebral microvascular injury was defined as microscopic brain intraparenchymal or perivascular hemorrhage, perivascular hemosiderin deposition, and perivascular inflammation. Twenty-one patients (median age = 57 years, 67% male) had autopsy after LVAD support (median LVAD support = 51 days). The median time from death to autopsy was 19 h. All 21 patients had cerebral injuries and 19 (90%) patients had cerebral microvascular injuries. Fourteen patients (78%) harbored more than one type of cerebral injury. On gross examination, 8 patients (38%) had CI, and 6 patients (29%) had ICH. On microscopic exam, 12 patients (57%) had microscopic intraparenchymal hemorrhage, 3 patients (14%) had perivascular hemorrhage, 11 patients (43%) had perivascular hemosiderin deposition, 5 patients (24%) had meningeal hemorrhage, 13 patients had chronic perivascular inflammation (62%), and 2 patients had diffuse HIBI (10%). Among patients with LVAD, there is a high prevalence of subclinical microvascular injuries and cerebral microbleeds (CMBs), which may provide some insights to the cause of frequent cerebral injury in LVAD population.

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