Melanie Leguizamon, Caleb Han, Maria Garza, Mackenzie Horne, Wesley T Richerson, L Taylor Davis, Dann Martin, Matthew Fusco, Rohan Chitale, Lori C Jordan, Manus J Donahue
{"title":"诊断性高碳酸血症脑血管反应性影像学对限流颅内动脉狭窄患者生命体征及急性及随访缺血性不良事件的影响。","authors":"Melanie Leguizamon, Caleb Han, Maria Garza, Mackenzie Horne, Wesley T Richerson, L Taylor Davis, Dann Martin, Matthew Fusco, Rohan Chitale, Lori C Jordan, Manus J Donahue","doi":"10.3174/ajnr.A8714","DOIUrl":null,"url":null,"abstract":"<p><strong>Background and purpose: </strong>Anatomical imaging is a hallmark for visualizing chronic and acute infarcts but provides incomplete information on stroke risk. Respiratory hypercapnic gas challenges show promise for non-invasively assessing hemodynamic function and mapping cerebrovascular reserve capacity, an indicator of how near parenchyma is to exhausting autoregulatory capacity. However, limited safety information exists for this method in high-risk patients with flow-limiting stenosis. This study reports on the physiological changes and adverse events (AEs) following diagnostic hypercapnic cerebrovascular reactivity imaging assessments.</p><p><strong>Materials and methods: </strong>Between January 2011 and May 2024, reactivity scans were performed on 262 patients. In patients with flow-limiting intracranial arterial steno-occlusion (>70%), vital signs were assessed during a twice-repeated three-minute fixed-inspired 5%CO2/95%O2 stimulus, and acute (0-24 hours), sub-acute (24 hours - 2 months), and longer-term (2 - 12 months) AEs were recorded.</p><p><strong>Results: </strong>129 patients met criteria for flow-limiting arterial steno-occlusion. Blood pressure did not change (p>0.40) with hypercapnia. EtCO<sub>2</sub> (baseline:36.5±4.5 mmHg, hypercapnia:42.5±3.8 mmHg) and SaO<sub>2</sub> (baseline:97.5±1.8%, hypercapnia:99.4±0.8%) increased (p<0.001), paralleling hypercapnic-hyperoxic physiology. No acute ischemic adverse events were noted. One sub-acute and four long-term neurological events were noted, within expected range for this population.</p><p><strong>Conclusions: </strong>Findings support using hypercapnic reactivity mapping in the setting of flow-limiting cerebrovascular disease.</p><p><strong>Abbreviations: </strong>CVR = cerebrovascular reactivity, MRI = magnetic resonance imaging, EtCO<sub>2</sub> = end-tidal carbon dioxide, SaO<sub>2</sub> = arterial oxygen saturation, BOLD = blood oxygenation level-dependent, AE = adverse event, SAE = serious adverse event.</p>","PeriodicalId":93863,"journal":{"name":"AJNR. American journal of neuroradiology","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The effect of diagnostic hypercapnic cerebrovascular reactivity imaging on vital signs and acute and follow-up ischemic adverse events in patients with flow-limiting intracranial arterial stenosis.\",\"authors\":\"Melanie Leguizamon, Caleb Han, Maria Garza, Mackenzie Horne, Wesley T Richerson, L Taylor Davis, Dann Martin, Matthew Fusco, Rohan Chitale, Lori C Jordan, Manus J Donahue\",\"doi\":\"10.3174/ajnr.A8714\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background and purpose: </strong>Anatomical imaging is a hallmark for visualizing chronic and acute infarcts but provides incomplete information on stroke risk. Respiratory hypercapnic gas challenges show promise for non-invasively assessing hemodynamic function and mapping cerebrovascular reserve capacity, an indicator of how near parenchyma is to exhausting autoregulatory capacity. However, limited safety information exists for this method in high-risk patients with flow-limiting stenosis. This study reports on the physiological changes and adverse events (AEs) following diagnostic hypercapnic cerebrovascular reactivity imaging assessments.</p><p><strong>Materials and methods: </strong>Between January 2011 and May 2024, reactivity scans were performed on 262 patients. In patients with flow-limiting intracranial arterial steno-occlusion (>70%), vital signs were assessed during a twice-repeated three-minute fixed-inspired 5%CO2/95%O2 stimulus, and acute (0-24 hours), sub-acute (24 hours - 2 months), and longer-term (2 - 12 months) AEs were recorded.</p><p><strong>Results: </strong>129 patients met criteria for flow-limiting arterial steno-occlusion. Blood pressure did not change (p>0.40) with hypercapnia. EtCO<sub>2</sub> (baseline:36.5±4.5 mmHg, hypercapnia:42.5±3.8 mmHg) and SaO<sub>2</sub> (baseline:97.5±1.8%, hypercapnia:99.4±0.8%) increased (p<0.001), paralleling hypercapnic-hyperoxic physiology. No acute ischemic adverse events were noted. One sub-acute and four long-term neurological events were noted, within expected range for this population.</p><p><strong>Conclusions: </strong>Findings support using hypercapnic reactivity mapping in the setting of flow-limiting cerebrovascular disease.</p><p><strong>Abbreviations: </strong>CVR = cerebrovascular reactivity, MRI = magnetic resonance imaging, EtCO<sub>2</sub> = end-tidal carbon dioxide, SaO<sub>2</sub> = arterial oxygen saturation, BOLD = blood oxygenation level-dependent, AE = adverse event, SAE = serious adverse event.</p>\",\"PeriodicalId\":93863,\"journal\":{\"name\":\"AJNR. American journal of neuroradiology\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-02-24\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"AJNR. American journal of neuroradiology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3174/ajnr.A8714\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"AJNR. American journal of neuroradiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3174/ajnr.A8714","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The effect of diagnostic hypercapnic cerebrovascular reactivity imaging on vital signs and acute and follow-up ischemic adverse events in patients with flow-limiting intracranial arterial stenosis.
Background and purpose: Anatomical imaging is a hallmark for visualizing chronic and acute infarcts but provides incomplete information on stroke risk. Respiratory hypercapnic gas challenges show promise for non-invasively assessing hemodynamic function and mapping cerebrovascular reserve capacity, an indicator of how near parenchyma is to exhausting autoregulatory capacity. However, limited safety information exists for this method in high-risk patients with flow-limiting stenosis. This study reports on the physiological changes and adverse events (AEs) following diagnostic hypercapnic cerebrovascular reactivity imaging assessments.
Materials and methods: Between January 2011 and May 2024, reactivity scans were performed on 262 patients. In patients with flow-limiting intracranial arterial steno-occlusion (>70%), vital signs were assessed during a twice-repeated three-minute fixed-inspired 5%CO2/95%O2 stimulus, and acute (0-24 hours), sub-acute (24 hours - 2 months), and longer-term (2 - 12 months) AEs were recorded.
Results: 129 patients met criteria for flow-limiting arterial steno-occlusion. Blood pressure did not change (p>0.40) with hypercapnia. EtCO2 (baseline:36.5±4.5 mmHg, hypercapnia:42.5±3.8 mmHg) and SaO2 (baseline:97.5±1.8%, hypercapnia:99.4±0.8%) increased (p<0.001), paralleling hypercapnic-hyperoxic physiology. No acute ischemic adverse events were noted. One sub-acute and four long-term neurological events were noted, within expected range for this population.
Conclusions: Findings support using hypercapnic reactivity mapping in the setting of flow-limiting cerebrovascular disease.
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