Comorbidities are a hallmark of stroke that both increase the incidence of stroke and worsen outcome. Hypertension is prevalent in the stroke population and the most important modifiable risk factor ...for stroke. Hypertensive disorders promote stroke through increased shear stress, endothelial dysfunction, and large artery stiffness that transmits pulsatile flow to the cerebral microcirculation. Hypertension also promotes cerebral small vessel disease through several mechanisms, including hypoperfusion, diminished autoregulatory capacity and localized increase in blood–brain barrier permeability. Preeclampsia, a hypertensive disorder of pregnancy, also increases the risk of stroke 4–5-fold compared to normal pregnancy that predisposes women to early-onset cognitive impairment. In this review, we highlight how comorbidities and concomitant disorders are not only risk factors for ischemic stroke, but alter the response to acute ischemia. We focus on hypertension as a comorbidity and its effects on the cerebral circulation that alters the pathophysiology of ischemic stroke and should be considered in guiding future therapeutic strategies.
Summary Ischaemic stroke results from acute arterial occlusion leading to focal hypoperfusion. Thrombolysis is the only proven treatment. Advanced neuroimaging techniques allow a detailed assessment ...of the cerebral circulation in patients with acute stroke, and provide information about the status of collateral vessels and collateral blood flow, which could attenuate the effects of arterial occlusion. Imaging of the brain and vessels has shown that collateral flow can sustain brain tissue for hours after the occlusion of major arteries to the brain, and the augmentation or maintenance of collateral flow is therefore a potential therapeutic target. Several interventions that might augment collateral blood flow are being investigated.
Collateral Circulation Liebeskind, David S.
Stroke (1970),
2003-September-01, Letnik:
34, Številka:
9
Journal Article
Recenzirano
Odprti dostop
Background— The collateral circulation plays a pivotal role in the pathophysiology of cerebral ischemia. Current knowledge of the collateral circulation remains sparse, largely because of prior ...limitations in methods for evaluation of these diminutive routes of cerebral blood flow.Summary of Review— Anatomic descriptions of the collateral circulation often focus on more proximal anastomoses at the circle of Willis, neglecting secondary collateral pathways provided by leptomeningeal vessels. Pathophysiological recruitment of collateral vessels likely depends on the temporal course of numerous compensatory hemodynamic, metabolic, and neural mechanisms. Subsequent endurance of these protective vascular pathways may determine the severity of ischemic injury. Characterization of the collateral circulation with advanced neuroimaging modalities that provide angiographic information and perfusion data may elucidate critical determinants of collateral blood flow. Such information on the status of the collateral circulation may be used to guide therapeutic interventions. Prognostication and risk stratification may also be improved by routine evaluation of collateral blood flow.Conclusions— Contemporary understanding of the collateral circulation may be greatly enhanced through further refinement of neuroimaging modalities that correlate angiographic findings with perfusion status, providing the basis for future therapeutic and prognostic applications.
In a trial conducted in China, patients with large cerebral infarctions as determined by imaging criteria within 24 hours after onset had better outcomes with endovascular therapy than with medical ...therapy alone.
Precision cerebrovascular health or individualized long-term preservation of the brain and associated blood vessels, is predicated on understanding, diagnosing, and tailoring therapies for people at ...risk of ischemic injury associated with stroke and vascular dementia. The associated imaging patterns are sculpted by the protective effect of the collaterome, the innate compensatory ability of the brain and vasculature to offset hypoperfusion when antegrade or normal arterial inflow pathways are compromised. Theranostics or rational and synchronous use of diagnostic studies in tandem with specific therapies to optimally guide patient outcomes in ischemic brain disorders may capitalize on the pivotal role of the collaterome. Understanding the functional impact of the collaterome across populations of individuals would advance translational science on the brain, while questions with immediate clinical implications may be prioritized. Big data and systematic analyses are necessary to develop normative standards, multimodal imaging atlases, and delineation of specific patterns to guide clinical management. Large-scale, systematic imaging analyses of the collaterome provide a platform for translational work on cerebral collateral circulation and hemodynamics and a theranostic framework with direct clinical implications. This article frames incipient research objectives to guide precision stroke medicine in coming years, building upon the collaterome concept in brain health.
Background:
Chronic subdural hematoma (cSDH) is a debilitating condition with a high rate of recurrence after surgical evacuation.
Summary:
This review is focused on middle meningeal artery (MMA) ...embolization to treat cSDH. We discuss the underlying pathophysiology of chronic subdural hematoma and how cessation of arterial flow may resolve a venous hemorrhage. We also present the current evidence for MMA embolization and the roadmap for future trials.
Conclusion:
Frequent multimodal imaging and cSDH sampling would enable us to understand mechanisms of MMA embolization in cSDH treatment and therefore improve our ability to offer MMA embolization to the eligible population.
Summary Background The IMS III trial did not show a clinical benefit of endovascular treatment compared with intravenous alteplase (recombinant tissue plasminogen activator) alone for moderate or ...severe ischaemic strokes. Late reperfusion of tissue that was no longer salvageable could be one explanation, as suggested by previous exploratory studies that showed an association between time to reperfusion and good clinical outcome. We sought to validate this association in a preplanned analysis of data from the IMS III trial. Methods We used data for patients with complete proximal arterial occlusions in the anterior circulation who received endovascular treatment and achieved angiographic reperfusion (score on Thrombolysis in Cerebral Infarction scale of grade 2–3) during the endovascular procedure (within 7 h of symptom onset). We used logistic regression to model good clinical outcome (defined as a modified Rankin Scale score of 0–2 at 3 months) as a function of the time to reperfusion. We prespecified variables to be considered for adjustment, including age, baseline National Institutes of Health Stroke Scale score, sex, and baseline blood glucose concentration. Findings Of 240 patients who were otherwise eligible for inclusion in our analysis, 182 (76%) achieved angiographic reperfusion. Mean time from symptom onset to reperfusion (ie, procedure end) was 325 min (SD 52). Increased time to reperfusion was associated with a decreased likelihood of good clinical outcome (unadjusted relative risk for every 30-min delay 0·85 95% CI 0·77–0·94; adjusted relative risk 0·88 0·80–0·98). Interpretation Delays in time to angiographic reperfusion lead to a decreased likelihood of good clinical outcome in patients after moderate to severe stroke. Rapid reperfusion could be crucial for the success of future acute endovascular trials. Funding US National Institutes of Health and National Institute of Neurological Disorders and Stroke.
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