Some suggest that cerebral aneurysms form and then grow at a constant rate, others that growth alternates stochastically between periods of stability and instability or growth, during which they are prone to rupture. This would, in part help to understand discrepancy between the low risk of rupture of small, incidentally detected aneurysms and the high proportion of small aneurysms in patients with SAH. Obtaining more understanding about formation and natural history of cerebral aneurysms is of great significance given fatality rate of ruptured aneurysm of 35%.
In this very elegantly designed study, the authors used radiocarbon birth dating of collagen type I to estimate its chronological development and turnover to investigate chronological development of cerebral aneurysms. Collagen type I is the most common collagen type in cerebral aneurysms. Between 1955 and 1963 after above ground nuclear bomb tests, sharp increase and subsequent slow attenuation of atmospheric 14CO2 concentrations occurred. This allows measurement precision in radiocarbon birth dating with temporal resolution of 1 to 3 years.
36 ruptured and 10 unruptured aneurysms harvested during surgical clipping had sufficient amounts of collagen for further analysis. This collagen was compared with extracts from ten samples from human cerebral as well as two samples from extra-cerebral arteries from five cadavers and five collagen samples of known age from newborn mouse tendons, however cerebral aneurysms and controls did not share a dominant structural protein which could be used for comparison of collagen dynamics.
Except in 3 samples, all collagen samples were 5 years or less old. The age of collagen was independent of aneurysm clinical and morphological presentation such as: ruptured and unruptured, largest aneurysmal diameter and irregularity. It was also independent of patients age. Mean collagen age was 1.6 ± 1.2 years for patients with risk factors such as hypertension, cigarette smoking or cocaine use, comparing with 3.9 ± 3.3 years for patients without risk factors.
Inability to compare collagen turnover in control sites with harvested aneurysms, limited authors of reaching the conclusion that the age of collagen in the cerebral aneurysms is different than control. Their findings, however indicate that there is ongoing collagen type I biosynthesis in cerebral aneurysms due to dynamic remodeling, and that this remodeling seems to be significantly accelerated in patients with listed risk factors. By tightly controlling hypertension, cigarette smoking and cocaine use in patients with incidentally diagnosed cerebral aneurysms, not fulfilling criteria for surgical clipping or endovascular coiling, perhaps we can halt their progression.