Role of microcirculatory impairment in delayed cerebral ischemia and outcome after aneurysmal subarachnoid hemorrhage

Abstract

Early brain injury (EBI) is considered an important cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage (aSAH). As a factor in EBI, microcirculatory dysfunction has become a focus of interest, but whether microcirculatory dysfunction is more important than angiographic vasospasm (aVS) remains unclear. Using data from 128 cases, we measured the time to peak (TTP) in several regions of interest on digital subtraction angiography. The intracerebral circulation time (iCCT) was obtained between the TTP in the ultra-early phase (the baseline iCCT) and in the subacute phase and/or at delayed cerebral ischemia (DCI) onset (the follow-up iCCT). In addition, the difference in the iCCT was calculated by subtracting the baseline iCCT from the follow-up iCCT. Univariate analysis showed that DCI was significantly increased in those patients with a prolonged baseline iCCT, prolonged follow-up iCCT, increased differences in the iCCT, and with severe aVS. Poor outcome was significantly increased in patients with prolonged follow-up iCCT and increased differences in the iCCT. Multivariate analysis revealed that increased differences in the iCCT were a significant risk factor that increased DCI and poor outcome. The results suggest that the increasing microcirculatory dysfunction over time, not aVS, causes DCI and poor outcome after aneurysmal aSAH.

Effect of prolonged microcirculation time after thrombectomy on the outcome of acute stroke

“…Recently, Philipp Gölitz et al showed that the microcirculatory transit time has more advantages than the other periods of CCT 8. Thus, we used post-processing software that subdivided the different measurement points of TTP and different stages of CCT 7 18. We found that TTP VR , CCT C5-VR , and mCCT were all factors independently associated with 90-day functional independence.…”

“…18 The regions of interest (ROIs) were placed in the intravenous vertical portion of the internal carotid artery (ROI C5 ), the cortical segment of the rolandic artery (ROI M4 ), and the rolandic vein (ROI VR ) to calculate the time-density profile. 7 The time to peak (TTP) on the time-density curve for each region of interest was recorded as TTP C5 , TTP M4 , and TTP VR . CCT is defined as the difference in the time to peak intensity between ROIs.…”

“…The microvascular CCT (mCCT) is the time for blood flow to pass through the microvasculature during the entire CCT. Several studies have shown that prolonged mCCT can reflect microcirculatory dysfunction in aneurysmal subarachnoid hemorrhage by different measurement methods 7 8. This may be caused by microvascular spasm and microvascular obstruction 9 10.…”

Rethinking the initial changes in subarachnoid haemorrhage: Focusing on real-time metabolism during early brain injury

“…During aneurysm clipping surgery, Uhl et al observed monosegmental and pearl-string multisegmental microvasospasms in arterioles for the first time, with a 75% reduction in cortical microcirculation after SAH. 12 A recent digital subtraction angiography (DSA) study found that the intracerebral circulation time within 24 hrs after ictus was significantly correlated with the occurrence of delayed cerebral ischaemia in SAH patients as an independent factor in addition to angiographic vasospasm in traditional understanding, 13 which suggests that microcirculatory dysfunction in the ultra-early and subacute phases can be a causative factor for delayed cerebral ischaemia development and poor outcome.…”

Role of hydrogen sulfide in subarachnoid hemorrhage

“…Cerebral vasospasm after aneurysmal SAH (aSAH) is defined as large and medium intracranial artery stenosis. Cerebral vasospasm can lead to local cerebral hypoperfusion and DCI and is one of the major causes of death and disability in patients with aSAH 106 . The exact mechanism of vasospasm after SAH is not fully understood, but many mechanisms have been proposed, such as endothelial injury and microthrombi formation; smooth muscle contraction, resulting from the lysis of subarachnoid blood clots and blood degradation products and hemoglobin released into the subarachnoid space; decreased NO production leading to prolonged vasoconstriction; increased production and release of the potent vasoconstrictor endothelin‐1; cortical spreading depolarization; inflammation‐mediated oxidative stress and free radical damage to smooth muscle cells; and upregulation of apoptotic pathways 12,107 …”