Vasospasm: does it cause infarction and poor outcome?
Risk of Rupture
The aspect ratio (dome/neck) of ruptured and unruptured aneurysms
Bryce Weir, Christina Amidei, Gail Kongable, J. Max Findlay, Neal F. Kassell, John Kelly, Lanting Dai, and Theodore G. Karrison
Object. In this retrospective study the authors examined the aspect ratio (AR; the maximum dimension of the dome/width of the neck of an aneurysm) and compared the distribution of this ratio in a group of ruptured and unruptured aneurysms. A similar comparison was performed in relation to the maximum dimension of the aneurysm alone. The authors sought to evaluate the utility of these measures for differentiating ruptured and unruptured aneurysms.
Methods. Measurements were made of 774 aneurysms in 532 patients at three medical centers. One hundred twenty-seven patients harbored only unruptured lesions, 290 only ruptured lesions, and 115 both ruptured and unruptured lesions. Cases were included if angiograms were available for measurement and the status of the individual patient's aneurysm(s) was known.
The odds of a lesion falling in the ruptured aneurysm group increased with both the lesion's maximum size and the AR. The odds ratio for rupture rose progressively only for the AR. The distribution curves showed that ruptured aneurysms were larger and had greater ARs. The mean size of unruptured aneurysms was 7 mm and that of ruptured ones was 8 mm; the corresponding mean ARs were 1.8 and 3.4, respectively. The odds of rupture were 20-fold greater when the AR was larger than 3.47 compared with an AR less than or equal to 1.38. Only 7% of ruptured aneurysms had an AR less than 1.38 compared with 45% of unruptured lesions.
Conclusions. The AR is probably a useful index to calculate. A high AR might reasonably influence the decision to treat actively an unruptured aneurysm independent of its maximum size. Prospective studies are warranted.
Sizes of ruptured and unruptured aneurysms in relation to their sites and the ages of patients
Bryce Weir, Lew Disney, and Theodore Karrison
Object. The authors explore the risk of rupture in aneurysms categorized by size.
Methods. A computerized database of 945 patients with aneurysms treated between 1967 and 1987 was retrospectively established. All available clinical and radiological studies were abstracted. Because of the recent interest in the size of intracranial aneurysms in relation to their likelihood of rupture, the database was searched with respect to this parameter. In 390 patients representing 41% of all cases, aneurysms were measured by neuroradiologists at the time of diagnosis. In 78% of the 945 patients there was only one aneurysm, and of the 507 aneurysms that were measured, 60% were solitary. Of all patients, 86% had ruptured aneurysms. The average age of all patients was 47 years, and for those with ruptured aneurysms it was 46 years. Of the ruptured aneurysms, 77% were 10 mm or smaller, compared with 85% of the unruptured aneurysms. It was found that 40.3% of the ruptured aneurysms were on the anterior cerebral artery or anterior communicating artery, compared with 13% of the unruptured aneurysms. None of the cavernous internal carotid artery (ICA) aneurysms were ruptured and 65% of the ophthalmic artery (OphA) aneurysms were. Of the unruptured aneurysms, 15% were located in the cavernous ICA or the OphA. Of the ruptured aneurysms, 29% were on the middle cerebral artery, compared with 36% of the unruptured aneurysms. The mean size of ruptured and unruptured aneurysms showed no statistically significant increase with patient age, although the difference in size between the ruptured and unruptured aneurysms decreased with increasing age. The mean size of all ruptured aneurysms (10.8 mm) was significantly larger than the mean size of all unruptured aneurysms (7.8 mm, p < 0.001); the median sizes were 10 mm and 5 mm, respectively. The size of ruptured aneurysms in patients who died in the hospital was significantly larger than those in the patients who survived (12 mm compared with 9.9 mm, p = 0.004). Symptomatic unruptured aneurysms were significantly larger than incidental unruptured aneurysms (14.6 mm compared with 6.9 mm, p = 0.032), which were, in turn, larger than aneurysms that were unruptured and part of a multiple aneurysm constellation. Both ruptured and unruptured aneurysms were larger in male than in female patients, but not significantly.
Conclusions. Site and patient age, as well as lesion size, may affect the chance of rupture.
Unruptured intracranial aneurysms: a review
Object. In this article, pathological, radiological, and clinical information regarding unruptured intracranial aneurysms is reviewed.
Methods. Treatment decisions require that surgeons and interventionists take into account information obtained in pathological, radiological, and clinical studies of unruptured aneurysms. The author has performed a detailed review of the literature and has compared, contrasted, and summarized his findings. Unruptured aneurysms may be classified as truly incidental, part of a multiple aneurysm constellation, or symptomatic by virtue of their mass, irritative, or embolic effects. Unruptured aneurysms with clinical pathological profiles resembling those of ruptured lesions should be considered for treatment at a smaller size than unruptured lesions with profiles typical of intact aneurysms, as has been determined at autopsy in patients who have died of other causes. The track record of the surgeon or interventionist and the institution in which treatment is to be performed should be considered while debating treatment options. In cases in which treatment is not performed immediately, ongoing periodic radiological assessment may be wise. Radiological investigations to detect unruptured aneurysms in asymptomatic patients should be restricted to high-prevalence groups such as adults with a strong family history of aneurysms or patients with autosomal dominant polycystic kidney disease. All patients with intact lesions should be strongly advised to discontinue cigarette smoking if they are addicted.
Conclusions. The current state of knowledge about unruptured aneurysms does not support the use of the largest diameter of the lesion as the sole criterion on which to base treatment decisions, although it is of undoubted importance.
Extradural posterior inferior cerebellar artery aneurysm
Marcus A. Stoodley, Cornelia Hermann, and Bryce Weir
Subarachnoid hemorrhage as a cause of an adaptive response in cerebral arteries
Marcus Stoodley, R. Loch Macdonald, Bryce Weir, Linda S. Marton, Lydia Johns, Zhen Du Zhang, and Andrew Kowalczuk
Object. It is not known whether the factors responsible for vasospasm after subarachnoid hemorrhage (SAH) cause the cerebral arteries to be narrowed independent of the subarachnoid blood clot or whether the continued presence of clot is required for the entire time of vasospasm. The authors undertook the present study to investigate this issue.
Methods. To distinguish between these possibilities, bilateral SAH was induced in monkeys. The diameters of the monkeys' cerebral arteries were measured on angiograms obtained on Days 0 (the day of SAH), 1, 3, 5, 7, and 9. The subarachnoid blood clot was removed surgically on Day 1, 3, or 5 or, in control animals, was not removed until the animals were killed on Day 7 or 9. The concentrations of hemoglobins and adenosine triphosphate (ATP), substances believed to cause vasospasm, were measured in the removed clots and the contractile activity of the clots was measured in monkey basilar arteries in vitro. If the clot was removed 1 or 3 days after placement, vasospasm was significantly diminished 4 days after clot removal. Clot removal on Day 5 had no marked effect on vasospasm. There was a significant decrease over time in hemoglobin and ATP concentrations and in the contractile activity of the clots, although substantial hemoglobin and contractile activity was still present on Day 7.
Conclusions. The authors infer from these results that vasospasm requires the presence of subarachnoid blood for at least 3 days, whereas by Day 5 vasospasm is less dependent on subarachnoid blood clot. Because the clot still contains substantial amounts of hemoglobin and contractile activity after 5 days, there may be an adaptive response in the cerebral arteries that allows them to relax in the presence of the stimulus that earlier caused contraction.
Adenosine triphosphate and hemoglobin in vasospastic monkeys
R. Loch Macdonald, Bryce Weir, John Zhang, Linda S. Marton, Michael Sajdak, and Lydia M. Johns
Adenosine triphosphate (ATP) is a vasoactive compound found in high levels inside erythrocytes that may contribute to vasospasm occurring after subarachnoid hemorrhage (SAH). This study was instituted to test whether ATP causes vasospasm in a monkey model.
Thirty-two monkeys were randomized to four groups of eight monkeys each to undergo cerebral angiography at baseline (Day 0) and then at Day 7 after subarachnoid placement of: 1) agarose, 2) ATP in agarose, 3) autologous hemolysate in agarose, or 4) purified human hemoglobin A0 in agarose. Vasospasm was assessed by comparison of Day 0 and Day 7 angiograms between and within groups and by pathological examination of a subset of perfusion-fixed monkeys. Levels of adenine nucleotides were measured on Day 7 in subarachnoid agarose by high-pressure liquid chromatography.
There was significant vasospasm of the right middle cerebral artery in groups given ATP (-28 ± 7% reduction, paired t-test, p < 0.05), hemolysate (-23 ± 7%, p < 0.05), or pure hemoglobin (-15 ± 2%, p < 0.005). Analysis of variance revealed no significant differences between groups in diameters of cerebral arteries on Day 7. Pathological examination showed mild inflammation in the subarachnoid spaces of animals exposed to hemolysate or hemoglobin and less inflammation in those given ATP or agarose. There were no pathological changes in the cerebral arteries of animals in any group. Most of the ATP diffused out of the subarachnoid agarose by Day 7, and levels of adenine nucleotides in subarachnoid agarose were higher on Day 7 in animals exposed to hemoglobin or hemolysate.
It is concluded that ATP could contribute to vasospasm occurring after SAH but that further investigations are necessary to determine if levels of ATP adjacent to vasospastic arteries are sufficient to contribute to vasospasm. In addition, no observation was made of severe vasospasm with histopathological changes in the arteries equivalent to that produced by whole blood clot in the subarachnoid space of monkeys. It should be determined whether this is because a single compound, such as ATP or hemoglobin, causes vasospasm, but that placing the compound in agarose alters its delivery and decreases the amount of vasospasm produced, or whether vasospasm is a more complex, multifactorial process.