Intra-arterial Vasodilator Therapy Research Articles

Treatment of Refractory Vasospasm after Aneurysmal Subarachnoid Hemorrhage: What else could we do for our patients? A Case Report and Systemic Literature Review (P7-5.014)

<h3>Objective:</h3> Recognizing the treatment options for refractory vasospasm to recommended management protocols will allow clinicians to consider contingency treatments in the event of severe, refractory vasospasm. <h3>Background:</h3> Vasospasm is a known complication of aneurysmal subarachnoid hemorrhage and the leading cause of morbidity and mortality in these patients. Current guidelines recommend using nimodipine and maintaining euvolemia to prevent vasospasm, with hypertension induction and cerebral angioplasty and/or selective intra-arterial vasodilator therapy for its treatment. However, up to 10% of patients are refractory to current recommendations, and no systematic review has been published for many complementary therapies. <h3>Design/Methods:</h3> We present a case report of a patient treated at our institution who had severe diffuse refractory vasospasm with neuroimaging concerning for right medial cerebral artery (MCA) ischemic stroke. The patient fully recovered following treatment which included management recommendations per guidelines, milrinone for inducing hypertension, intrathecal nicardipine, and bilateral stellate ganglion block (SCG). Digital subtraction angiography before and after the right SGB showed improvement in vessel diameter in the right MCA, prompting us to perform a left SGB. The systematic review is being conducted according to established methodological standards following the Preferred Reporting Items for Systematic Reviews and Meta-analysis guidelines. The search strategy was created with input from a medical librarian. We searched the PubMed, Scopus, and Embase databases through the last search date of September 27, 2022. No restrictions were placed on date, language, or country of publication. <h3>Results:</h3> A total of 1460 references were identified, and 463 duplicates were removed, producing a final reference count of 997 studies to peruse. CT, RA, and CR are conducting ongoing study revisions. <h3>Conclusions:</h3> A variety of complementary therapies are available and could be used in the management of refractory vasospasm. Although these are alternative therapies, they are efficacious in managing this condition, and physicians should be aware of these options. <b>Disclosure:</b> Mr. Tiwari has nothing to disclose. Mr. Alghorazi has nothing to disclose. Mrs. Conklin has nothing to disclose. Dr. Mauck has received personal compensation in the range of $500-$4,999 for serving as an Expert Witness for North Carolina Industrial Commission. The institution of Dr. Mauck has received research support from NIH. Dr. Ho has nothing to disclose. Dr. McCullagh has nothing to disclose. Dr. Rubinos has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Qualtrics Inc. Dr. Rubinos has received personal compensation in the range of $5,000-$9,999 for serving on a Speakers Bureau for American Epilepsy Society . The institution of Dr. Rubinos has received research support from University of North Carolina .

Clazosentan for Improvement of Time to Peak Perfusion in Patients with Angiographically Confirmed Severe Vasospasm

Clazosentan, an endothelin-1 receptor antagonist, has been shown to prevent the development of large vessel angiographic vasospasm after aneurysmal subarachnoid hemorrhage. We hypothesized that clazosentan can improve cerebral perfusion for territories affected by angiographically confirmed vasospasm. The REVERSE study (REversal of Vasospasm with clazosEntan post-aneuRysmal Subarachnoid hEmorrhage) was a prospective multicenter open-label pilot study of adult patients with aneurysmal subarachnoid hemorrhage who received intravenous clazosentan after developing moderate to severe angiographic vasospasm. Using the radiographic data from the REVERSE study and additional retrospective radiographic data from our tertiary medical center, we compared the impact of intravenous clazosentan with intraarterial vasodilator therapy (medical standard of care) on vasospasm reversal using time to peak perfusion (TTPP; the time interval between the peak opacification of contrast dye in the main artery supplying an anatomically defined territory and the parenchymal phase when the dye is diffusely present in the brain parenchyma). Both intravenous clazosentan (n = 7 vessels) and intraarterial vasodilator therapy (n = 11 vessels) resulted in a statistically significant improvement in TTPP at 24h post intervention, when compared with the TTPP just prior to intervention for territories with angiographically confirmed severe vasospasm in the proximal arteries at baseline (linear mixed-effect model, p = 0.02). The clazosentan and intraarterial vasodilator therapy groups exhibited no statistically significant interaction term [time x treatment group (medical standard of care vs. clazosentan)] in our model (p = 0.71), suggesting similar temporal course of two therapies. In our small pilot study, intravenous clazosentan administered for at least 24h had an effect comparable with that of intraarterial vasodilator therapy in reversing angiographically confirmed severe vasospasm. Our results may indicate that clazosentan, in an appropriately selected patient cohort, could offer a noninvasive approach for alleviating vasospasm.

Abstract 38: Soluble ST2 Predicts Delayed Cerebral Ischemia and Outcome After Subarachnoid Hemorrhage

Introduction: Soluble ST2 (sST2) is a member of the Toll-like receptor superfamily implicated in pro-inflammatory signaling. We investigated whether sST2 predicts delayed cerebral ischemia (DCI) and 90-day clinical outcome in patients with aneurysmal subarachnoid hemorrhage (SAH). Methods: Soluble ST2 was measured in plasma samples from 182 patients who presented to a single institution with SAH. Blood samples were collected between days 1 and 5 after onset of SAH, and prior to the onset of DCI. Functional outcome was assessed at 3 months using the modified Rankin Scale (mRS) with good and poor outcome defined as mRS 0-2 and 3-6, respectively. Using a consensus definition, DCI was defined as a 2-point drop in GCS over a sustained period in patients whose clinical deterioration could not be explained by another cause. The relationships between sST2 level, DCI and outcome were assessed in univariable analysis. Multivariable logistic regression, Kaplan-Meier survival analysis, and receiver operating characteristic curves were used to determine the ability of sST2 to predict outcome and mortality. These findings were tested for replication in an independent cohort of 51 SAH patients recruited from a separate institution. Results: The discovery cohort consisted of 182 subjects (mean age 56±12 years, 61% women). Elevated plasma sST2 predicted the development of DCI (OR 2.10, 95% 1.06-4.18 CI, P=0.0295), which remained an independent predictor after adjustment for age, World Federation of Neurological Surgeons (WFNS) grading score, modified Fisher score, intra-arterial vasodilator therapy and hydrocephalus (OR 2.78, 95% CI 1.00-7.97, p=0.0453). Elevated sST2 was also independently associated with poor 90-day functional outcome (OR 2.65, 95%CI 1.07-6.59, P =0.0304), and mortality (OR 5.36, 95% CI 1.48-19.39, p=0.0039) when adjusted for age, WFNS score, modified Fisher score and hydrocephalus. In the replication cohort (N=51, 88% women), sST2 level was an independent predictor of DCI (OR 5.02, 95% CI 1.46-17.20, p=0.0034) and outcome at 90 days (OR 4.24, 95% CI 1.31-13.74, p=0.0072). Conclusion: Plasma sST2 level predicted risk of DCI, outcome, and mortality after SAH. Further study of the potential link between sST2 and brain injury after SAH is warranted.

Feasibility of Real-Time Angiographic Perfusion Imaging in the Treatment of Cerebral Vasospasm

Background: Objective assessment and quantification of the severity of cerebral vasospasm following aneurysmal subarachnoid hemorrhage is not routinely utilized. We investigated the feasibility of angiographic perfusion imaging derived from digital subtraction angiography (DSA) following endovascular vasospasm treatment procedures. Methodology: Real-time blood flow analysis was performed using parametric color coding on pre- and postintervention DSA. Semiquantitative parenchymal perfusion parameters (arrival time [AT] of contrast, time to peak [TTP] opacification, and mean transit time [MTT] of contrast) were calculated across 3 vascular territories (anterior cerebral artery [ACA], middle cerebral artery [MCA], and lenticulostriate arteries) using standard 2-D angiographic perfusion software. The pre- and postintervention arterial vessel diameters were compared. Results: Twelve endovascular vasospasm treatments in 6 patients were performed. All patients received intra-arterial vasodilator therapy with either nimodipine, milrinone, or both. Following intra-arterial intervention, parenchymal flow analysis showed improvement in TTP and MTT across all vascular territories (p < 0.002) and improvement in AT in the ACA and MCA territories (p < 0.03). Improvement in parenchymal perfusion parameters was associated with improvement in vessel diameters in all territories following treatment (p < 0.05). Conclusion: Real-time parenchymal perfusion imaging during endovascular vasospasm treatment procedures is feasible and provides reliable semiquantitative measurement of angiographic treatment response.

Temporal evolution of vasospasm and clinical outcome after intra-arterial vasodilator therapy in patients with aneurysmal subarachnoid hemorrhage.

Intra-arterial (IA) vasodilator therapy is one of the recommended treatments to minimize the impact of aneurysmal subarachnoid hemorrhage-induced cerebral vasospasm refractory to standard management. However, its usefulness and efficacy is not well established. We evaluated the effect IA vasodilator therapy on middle cerebral artery blood flow and on discharge outcome. We reviewed records for 115 adults admitted to Neurointensive Care Unit to test whether there was a difference in clinical outcome (discharge mRS) in those who received IA infusions. In a subset of 19 patients (33 vessels) treated using IA therapy, we tested whether therapy was effective in reversing the trends in blood flow. All measures of MCA blood flow increased from day -2 to -1 before infusion (maximum Peak Systolic Velocity (PSV) 232.2±9.4 to 262.4±12.5 cm/s [p = 0.02]; average PSV 202.1±8.5 to 229.9±10.9 [p = 0.02]; highest Mean Flow Velocity (MFV) 154.3±8.3 to 172.9±10.5 [p = 0.10]; average MFV 125.5±6.3 to 147.8±9.5 cm/s, [p = 0.02]) but not post-infusion (maximum PSV 261.2±14.6 cm/s [p = .89]; average PSV 223.4±11.4 [p = 0.56]; highest MFV 182.9±12.4 cm/s [p = 0.38]; average MFV 153.0±10.2 cm/s [p = 0.54]). After IA therapy, flow velocities were consistently reduced (day X infusion interaction p<0.01 for all measures). However, discharge mRS was higher in IA infusion group, even after adjusting for sex, age, and admission grades. Thus, while IA vasodilator therapy was effective in reversing the vasospasm-mediated deterioration in blood flow, clinical outcomes in the treated group were worse than the untreated group. There is need for a prospective randomized controlled trial to avoid potential confounding effect of selection bias.

Abstract 64: Glucocorticoid-associated Worsening in Reversible Cerebral Vasoconstriction Syndrome (RCVS): primum non nocere!

Objective: Factors predicting poor outcome in RCVS are not fully identified. Methods: We retrospectively analyzed clinical, imaging and angiography data in 162 RCVS patients. Uni- and multi-variable analysis were performed to identify predictors of persistent (non-transient) clinical worsening, radiological worsening, early angiographic progression, and poor discharge outcome (modified Rankin Scale score 4-6). Results: The mean age was 44±13 years, 78% women. Persistent clinical worsening occurred in 14% at 6.6±4.1 days after symptom onset; radiological worsening in 27% (mainly new infarcts), and angiographic progression in 15%. Clinical worsening correlated with angiographic progression and new non-hemorrhagic lesions. Age and gender did not independently predict any type of worsening. Infarction on baseline imaging predicted poor outcome. Prior serotonergic antidepressant use predicted clinical and angiographic worsening but not poor outcome. Intra-arterial vasodilator therapy independently predicted clinical worsening and poor discharge outcome but was offered to more severe cases. Glucocorticoid treatment was an independent predictor of clinical worsening (OR 10.2, 95% CI 3.3-31.6) as well as imaging and angiographic worsening and poor discharge outcome. Of N=23 with clinical worsening, 17 received glucocorticoids (15 within prior 2 days - FIGURE). There were no significant differences in baseline brain lesions and angiographic abnormalities between glucocorticoid-treated and untreated patients. Clinical worsening occurred in 37% of 46 treated vs. 5% of 116 not treated (p&lt;0.001); discharge mRS 4-6 occurred in 47% treated vs. 17% not-treated, and 61% of treated patients developed new brain lesions. Conclusion: Worsening in RCVS can be predicted from certain baseline features. Empiric glucocorticoids " until vasculitis is ruled out " is best avoided esp. since RCVS can be accurately diagnosed upon admission using our recent criteria.

Glucocorticoid-associated worsening in reversible cerebral vasoconstriction syndrome.

Factors predicting poor outcome in patients with the reversible cerebral vasoconstriction syndrome (RCVS) have not been identified. In this single-center retrospective study, we analyzed the clinical, brain imaging, and angiography data in 162 patients with RCVS. Univariable and multivariable regression analysis were performed to identify predictors of persistent (nontransient) clinical worsening, radiologic worsening, early angiographic progression, and poor discharge outcome (modified Rankin Scale score 4-6). The mean age was 44 ± 13 years; 78% of patients were women. Persistent clinical worsening occurred in 14% at 6.6 ± 4.1 days after symptom onset, radiologic worsening in 27% (mainly new infarcts), and angiographic progression in 15%. Clinical worsening correlated with angiographic progression and new nonhemorrhagic lesions. Age and sex did not independently predict any type of worsening. Infarction on baseline imaging predicted poor outcome. Prior serotonergic antidepressant use predicted clinical and angiographic worsening but not poor outcome. Intra-arterial vasodilator therapy independently predicted clinical worsening and poor discharge outcome but was offered to more severe cases. Glucocorticoid treatment proved to be an independent predictor of clinical, imaging, and angiographic worsening and poor outcome. Of the 23 patients with clinical worsening, 17 received glucocorticoids (15 within the preceding 2 days). There were no significant differences in baseline brain lesions and angiographic abnormalities between glucocorticoid-treated and untreated patients. Patients with RCVS at risk for worsening can be identified on basis of baseline features. Iatrogenic factors such as glucocorticoid exposure may contribute to worsening.

Decreased Flow Velocity with Transcranial Color-Coded Duplex Sonography Correlates with Delayed Cerebral Ischemia due to Peripheral Vasospasm of the Middle Cerebral Artery

Despite intensive therapy, vasospasm remains a major cause of delayed cerebral ischemia (DCI) in worsening patient outcome after aneurysmal subarachnoid hemorrhage (aSAH). Transcranial Doppler (TCD) and transcranial color-coded duplex sonography (TCCS) are noninvasive modalities that can be used to assess vasospasm. However, high flow velocity does not always reflect DCI. The purpose of this study was to investigate the utility of TCD/TCCS in decreasing permanent neurological deficits. We retrospectively enrolled patients with aSAH who were treated within 72 hours after onset. TCCS was performed every day from days 4 to 14. Peak systolic velocity (PSV), mean velocity (MV), and pulsatility index were recorded and compared between DCI and non-DCI patients. In patients with DCI, endovascular therapy was administered to improve vasospasm, which led to a documented change in velocity. Of the 73 patients, 7 (9.6%) exhibited DCI. In 5 of the 7 patients, DCI was caused by vasospasm of M2 or the more peripheral middle cerebral artery (MCA), and the PSV and MV of the DCI group were lower than those of the non-DCI group after day 7. Intra-arterial vasodilator therapy (IAVT) was performed for all patients with DCI immediately to increase the flow volume by the next day. Increasing flow velocity cannot always reveal vasospasm excluding M1. In patients with vasospasm of M2 or more distal arteries, decreasing flow velocity might be suggestive of DCI. IAVT led to increases in the flow velocity through expansion of the peripheral MCA.

Endovascular therapy for vasospasm after aneurysmatic subarachnoid hemorrhage

Introduction: Balloon angioplasty and/or selective intra-arterial vasodilator therapies are treatment options in patients with vasospasm after subarachnoid hemorrhage (SAH). We analyzed the effect of balloon angioplasty and/or selective intra-arterial vasodilator therapy in our patients.Methods: Twenty-six patients (vasodilation group, VDT) were treated with intra-arterial nimodipine. The balloon angioplasty with nimodiopine-group (BAP-N group) comprised 21 patients. The primary endpoint of this study was successful angiographic vessel dilation in vasospastic vessels after balloon angioplasty, together with nimodipine (BAP-N group), compared to intra-arterial vasodilator therapy (VDT group) with nimodipine alone.Results: A significant effect of angioplasty plus nimodipine was found in the central arteries (composite endpoint) with an OR of 2.4 (95% CI: 1.4–4.2], p = 0.002), indicating a chance of improvement of the BAP-N group of more than twice compared to nimodipine infusions alone. Significant advantages for BAP-N-therapy were also encountered in the internal carotid artery (OR 5.4, p < 0.001) and basilar artery (OR 29.7, p = 0.003). A joint analysis of all arteries combined failed to show significant benefit of BAP-N therapy (OR 1.5, p = 0.079), which was also true for cerebral peripheral arteries (OR 0.77, p = 0.367). There was no difference in clinical outcome between both groups.Conclusions: In SAH patients with vasospasm, a combination therapy of balloon angioplasty and intra-arterial nimodipine resulted in a more than doubled vasodilative effect in the central cerebral arteries compared to the sole infusion of nimodipine. Regarding the ICA and BA arteries, this beneficial effect was even more pronounced. Although there was a tendency of better effects of the BAP-N group, regarding the overall effect in all territories combined, this failed to reach statistical evidence. In cerebral peripheral arteries, no differences were observed, and there was no difference in clinical outcome, too.

Serial Quantitative Computed Tomography Perfusion in Aneurysmal Subarachnoid Hemorrhage.

Computed tomography perfusion (CTP) has been performed to predict which patients with aneurysmal subarachnoid hemorrhage are at risk of developing delayed cerebral ischemia (DCI). Patients with severe arterial narrowing may have significant reduction in perfusion. However, many patients have less severe arterial narrowing. There is a paucity of literature evaluating perfusion changes which occur with mild to moderate narrowing. The purpose of our study was to investigate serial whole-brain CTP/computed tomography angiography in aneurysm-related subarachnoid hemorrhage (aSAH) patients with mild to moderate angiographic narrowing. We retrospectively studied 18 aSAH patients who had baseline and follow-up whole-brain CTP/computed tomography angiography. Thirty-one regions of interest/hemisphere at six levels were grouped by vascular territory. Arterial diameters were measured at the circle of Willis. The correlation between arterial diameter and change in CTP values, change in CTP in with and without DCI, and response to intra-arterial vasodilator therapy in DCI patients was evaluated. There was correlation among the overall average cerebral blood flow (CBF; R=0.49, p<0.04), mean transit time (R=-0.48, p=0.04), and angiographic narrowing. In individual arterial territories, there was correlation between changes in CBF and arterial diameter in the middle cerebral artery (R=0.53, p=0.03), posterior cerebral artery (R=0.5, p=0.03), and anterior cerebral artery (R=0.54, p=0.02) territories. Prolonged mean transit time was correlated with arterial diameter narrowing in the middle cerebral artery territory (R=0.52, p=0.03). Patients with DCI tended to have serial worsening of CBF compared with those without DCI (p=0.055). Our preliminary study demonstrates there is a correlation between mild to moderate angiographic narrowing and serial changes in perfusion in patients with aSAH. Patients developing DCI tended to have progressively worsening CBF compared with those not developing DCI.

Prevention and treatment of cerebral vasospasm after aneurysmalsubarachnoid hemorrhage

Background. Cerebral vasospasm is the most serious complication of subarachnoid hemorrhage. It can be defined as deferred and self-limited condition whose severity is linked to the volume, solidity, prolonged presence and location of subarachnoid blood. Almost 70% of these patients have angiographic manifestation of vasospasm, and circa 50% of these patients experience neurological deficits. The purpose of this article is to concentrate on the current progress and prospective approaches in the prevention and treatment of cerebral vasospasm after aneurismal subarachnoid hemorrhage. Materials and methods. A thorough literature search through the Medline and Ebscodatabases was performed. Original investigations, meta-analyses and reviews from the past 10 years, with accessible full-texts, in the English language, were selected. Prevention and treatment. The main medical approach for prevention of vasospasm includes upkeep of normal blood circulation level and oral Nimodipine. The only type of treatment for cerebral vasospasm, which is recognized at present, is induced hypertension with the maintenance of euvolemia. Percutaneous transluminal angioplasty and/or selective intra-arterial vasodilator therapy are recommended in patients with symptomatic cerebral vasospasm, especially in those without quick response to hypertensive therapy. Conclusion. Novel approaches with immunomodulators, anesthetics, hypothermia, acupuncture, neuroprotective agents and multimodal treatment regimens are under active development and hold promise in the treatment of vasospasm in the coming years.

A Case Report of Non-Occlusive Mesenteric Ischemia in a Patient with Multiple Risk Factors

Non-occlusive mesenteric ischemia (NOMI) refers to all types of mesenteric ischemia without any organic blockage of blood vessels. It is usually seen in elderly age group with risk factors of previous myocardial infarction, congestive cardiac failure, aortic insufficiency, renal or liver impairment and post-cardiac surgery. Amongst all the cases of acute mesenteric ischemia, NOMI constitutes 20-30%. The mortality is generally high, at least 50% because it usually presents late and the bowel is already gangrenous. Common presentations include nausea, vomiting and acute abdominal pain. Selective angiography is the gold standard to exclude obstructive mesenteric ischemia, for which the diagnosis of NOMI could be made, but one can use other non-invasive modalities such as CT, MRI or ultrasound. Colonoscopy, lactate, arterial blood gas can be used to investigate for bowel ischemia. In the early stages, there is no need for surgery. Surgical intervention is generally limited unless there is a need to excise away the gangrenous bowel. The only effective treatment is by administering intra-arterial vasodilator therapy and it should be done as early as possible to improve prognosis. We describe a case of large bowel ischemia likely secondary to non-occlusive mesenteric ischemia.

E-024 Intra-arterial Vasodilator Therapy for Severe Vasospasm in Acute Bacterial Meningitis

Introduction and PurposeCerebrovascular complications of acute bacterial meningitis may include vasculitis, vasospasm, venous and arterial thrombosis, intracranial aneurysm formation and others. These complications have been shown to be important predictors...

E-002 Reversible cerebral vasoconstriction syndrome treated with intra-arterial vasodilator therapy: a case report

BackgroundReversible vasoconstriction syndrome has been described as an important cause of cerebral arteriopathy and/or vasoconstriction, with non-aneurysmal SAH recently being noted as a more common presentation that previously recognized. No...

E-008 Intra-arterial treatment of cerebral vasospasm

IntroductionAneurysmal subarachnoid hemorrhage (SAH) is associated with high morbidity and mortality primarily attributed to the delayed onset of cerebral vasospasm. Patient outcomes after aneurysmal SAH have considerably improved largely due...

A novel approach for percutaneous treatment of massive nonocclusive mesenteric ischemia: Tolazoline and glycerol trinitrate as effective local vasodilators

Nonocclusive mesenteric ischemia (NOMI) generally affects patients with low cardiac output, resulting in splanchnic hypoperfusion. It includes all forms of mesenteric ischemia without vessel occlusion and makes up between 20 and 30% of all cases of acute mesenteric ischemia. We present the case of a 84-year-old man with a history of total atrioventricular block developing NOMI. This was diagnosed by percutaneous selective catheter arteriography (PSCA), which demonstrated remarkable abrupt termination of the jejunal vasculature and multiple severe spasms of the colonic arteries. Control PSCA after local intraarterial vasodilator therapy (LIVT) with tolazoline and glycerol trinitrate documented an excellent therapeutic result with a completely unremarkable vasculature. Although LIVT was complicated by severe cardiovascular complications inclusive of cardiac arrest with the need of cardiopulmonary resuscitation, the patient fully recovered and was discharged after implantation of a cardiac pacemaker in good clinical condition 7 days later.

The acute cerebrovascular effects of intracarotid adenosine in nonhuman primates.

In this study we sought to determine the acute cerebrovascular effects of intracarotid adenosine by using real-time cerebral blood flow (CBF) measurements in nonhuman primates. The internal carotid arteries of healthy anesthetized baboons were transfemorally cannulated. Changes in CBF were continuously measured at baseline and with 6 increasing doses of adenosine (0.002 to 1.5 mg/min) by use of an intraparenchymal thermal diffusion (TD) probe. Each infusion lasted 5 min. At baseline and at the largest dose of adenosine, CBF was also determined by the intraarterial (133)Xe technique. TD measurements revealed a dose-dependent increase in CBF from 32 +/- 6 mL x l00 g(-1) x min(-1) at baseline to 90 +/- 38 mL x l00 g(-1) x min(-1) with the largest dose of adenosine (n = 5; P < 0.0001). A similar magnitude of increase in CBF was also observed with (133)Xe CBF measurements. No significant increases in intracranial pressure or adverse systemic hemodynamic side effects were observed during adenosine infusion. The increase in CBF after adenosine lasted only for the duration of drug infusion. In conclusion, the transient cerebrovascular effects of intracarotid adenosine make it suitable for a trial of intraarterial vasodilator therapy and for controlled manipulation of cerebrovascular resistance. Using a real-time cerebral blood flow (CBF) measurement technique, we evaluated the acute cerebrovascular effects of intracarotid adenosine in anesthetized baboons. The increase in CBF lasted only for the duration of the adenosine infusion. Adenosine might be a suitable drug for trial as an intraarterial vasodilator for the treatment of cerebral vasospasm.

Non-occlusive mesenteric ischemia: etiology, diagnosis, and interventional therapy.

Non-occlusive mesenteric ischemia (NOMI) compromises all forms of mesenteric ischemia with patent mesenteric arteries. It generally affects patients over 50 years of age suffering from myocardial infarction, congestive heart failure, aortic insufficiency, renal or hepatic disease and patients following cardiac surgery. Non-occlusive disease accounts for 20-30% of all cases of acute mesenteric ischemia with a mortality rate of the order of 50%. Acute abdominal pain may be the only early presenting symptom of mesenteric ischemia. Non-invasive imaging modalities, such as CT, MRI, and ultrasound, are able to evaluate the aorta and the origins of splanchnic arteries. Despite the technical evolution of those methods, selective angiography of mesenteric arteries is still the gold standard in diagnosing peripheral splanchnic vessel disease. In early non-occlusive mesenteric ischemia, as opposed to occlusive disease, there is no surgical therapy. It is known that mesenteric vasospasm persists even after correction of the precipitating event. Vasospasm frequently responds to direct intra-arterial vasodilator therapy, which is the only treatment that has been shown to be effective.

Effect of prolonged selective intramesenteric arterial vasodilator therapy on intestinal viability after acute segmental mesenteric vascular occlusion.

To evaluate the effect of selective intramesenteric artery vasodilator infusion on intestinal viability in a rat model of acute segmental mesenteric vascular occlusion. Although intramesenteric arterial vasodilator infusion may be an effective treatment for nonocclusive mesenteric ischemia, it has also been advocated to increase collateral blood flow after mesenteric vascular occlusion. However, the authors have previously found that intraarterial vasodilators actually reduce collateral blood flow acutely, by preferentially dilating the vasculature of adjacent, nonischemic mesenteric vascular beds, a phenomenon well established in other organs. A segment of rat ileum was acutely devascularized, with blood flow provided only by collateral arterial vessels from adjacent, nonischemic bowel. Papaverine (30 or 40 microg/kg/min), isoproterenol (0.06 microg/kg/min), norepinephrine (0.1 or 0.2 microg/kg/min), or vehicle saline was continuously infused into the cranial (superior) mesenteric artery for 48 hours. Viability was then assessed using previously established, objective gross and microscopic criteria. Although papaverine increased total mesenteric blood flow in normally vascularized rats, it not only failed to improve but actually significantly reduced the length of the devascularized segment maintained viable by collateral blood flow after 48 hours. Isoproterenol had a similar effect. Norepinephrine infusion decreased both normal mesenteric blood flow and viable segment length. These findings suggest that intraarterial vasodilator therapy fails to improve intestinal viability after segmental mesenteric vascular occlusion.

Acute mesenteric ischemia: angiographic spectrum.

Fifty-six patients, selected by clinical criteria, underwent angiography for suspected acute mesenteric ischemia. Twenty-nine patients subsequently did not have mesenteric ischemia and had negative arteriograms. Twenty-seven patients had mesenteric ischemia: arterial thrombosis (three), arterial embolus (seven), venous thrombosis (five), vasculitis with thrombosis (one), and nonocclusive ischemia (11). Of these 27 patients, 12 (44%) received intraarterial vasodilator infusions. Overall, 13 (48%) of the 27 patients survived their hospitalization, including five (45%) of 11 with nonocclusive ischemia. This experience confirms that nonocclusive ischemia is the most common form of the disorder diagnosed by angiography. Most patients with mesenteric ischemia are candidates for intraarterial vasodilator therapy. Early angiography in patients with suspected acute mesenteric ischemia permits early diagnosis and differentiation between occlusive and nonocclusive types. Interventional infusion therapy may improve survival.