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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rupture of an intracranial aneurysm (IA) leads to a subarachnoid hemorrhage, a sudden onset disease that can lead to severe disability and death. Several risk factors such as smoking, hypertension and excessive alcohol intake are associated with subarachnoid hemorrhage. IAs, ruptured or unruptured, can be treated either surgically via a craniotomy (through an opening in the skull) or endovascularly by placing coils through a catheter in the femoral artery. Even though the etiology of IA formation is mostly unknown, several studies support a certain role of genetic factors. In reports so far, genome-wide linkage studies suggest several susceptibility loci that may contain one or more predisposing genes. Studies of several candidate genes report association with IAs. To date, no single gene has been identified as responsible for IA formation or rupture. The identification of susceptible genes may lead to the understanding of the mechanism of formation and rupture and possibly lead to the development of a pharmacological therapy.
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PMID:The genetics of intracranial aneurysms. 1673 93

Mutations in the PKD1 and PKD2 polycystin genes are responsible for autosomal dominant polycystic kidney disease (ADPKD), one of the most prevalent genetic kidney disorders. ADPKD is a multisystem disease characterized by the formation of numerous fluid-filled cysts in the kidneys, the pancreas, and the liver. Moreover, major cardiovascular manifestations are common complications in ADPKD. Intracranial aneurysms and arterial hypertension are among the leading causes of mortality in this disease. In the present review, we summarize our current understanding of the role of polycystins in the development, maintenance, and function of the cardiovascular system.
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PMID:Cardiovascular polycystins: insights from autosomal dominant polycystic kidney disease and transgenic animal models. 1705 86

Formation of cerebral de novo aneurysms (CDNA) is rare, and the pathogenesis remains obscure. In this study, we investigated the factors that contribute to the formation of CDNA and suggest guidelines for following patients treated for cerebral aneurysms. We retrospectively reviewed 2,887 patients treated for intracranial aneurysm at our institute from January of 1976 to December of 2005. Of those patients, 12 were readmitted due to recurrent rupture of CDNA, which was demonstrated by cerebral angiography. We assessed clinical characteristics, such as gender, size and site of rupture, past history, and the time to CDNA rupture. Of the 12 patients, 11 were female and 1 was male, with a mean age at rupture of the first aneurysm of 44.7 years (range: 30-69 years). The mean time between the first episode of subarachnoid hemorrhage (SAH) and the second was 8.9 years (range: 1.0-16.7 years). The most common site of ruptured CDNA was the internal carotid artery (5 patients, 41.7%), followed by basilar artery bifurcation (3 patients, 25.0%). In the remaining 4 patients, rupture occurred in the anterior communicating, middle cerebral, anterior cerebral (A1), or posterior cerebral (P1) arteries. In 5 cases (41.7%), the CDNA occurred contralateral to the initial aneurysm. Eleven patients (91.7%) had a past history of arterial hypertension. There was no history of habitual smoking or alcohol abuse in any of the patients. Eight patients underwent clipping for CDNA and three patients were treated with coiling. One patient who had multiple aneurysms was treated with clipping following intra-aneurysmal coiling. Assessment according to the Glasgow Outcome Scale (GOS) of the patients after the treatment was good in 10 cases (83.3%) and fair in 2 cases (16.7%). Although formation of CDNA after successful treatment of initial aneurysm is rare, several factors may contribute to recurrence. In our study, female patients with a history of arterial hypertension were at higher risk for ruptured CDNA. We recommend follow-up imaging studies every five years after treatment of the initial aneurysm, especially in women and those with a history of arterial hypertension.
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PMID:A clinical analysis of twelve cases of ruptured cerebral de novo aneurysms. 1732 42

The etiology of intracranial aneurysm formation and rupture remains mostly unknown, but lately several studies have increasingly supported the role of genetic factors. In reports so far, genome-wide linkage studies suggest several susceptibility loci that may contain one or more predisposing genes. Depending on the examined ethnic population, several different non-matching chromosomal regions have been found. Studies of several candidate genes report association with intracranial aneurysms. To date, no single gene has been identified as responsible for intracranial aneurysm formation or rupture. In addition to the well-published environmental factors, such as alcohol intake, hypertension and smoking, only the recent progress in molecular genetics enables us to investigate the possible genetic determinants of this disease. Although a familial predisposition is the strongest risk factor for the development of intracranial aneurysms, the mode of Mendelian inheritance is uncertain in most families. Therefore, multiple genetic susceptibilities in conjunction with the environmental factors are considered to act together in the disease's etiology. Accordingly, researchers performed linkage studies and case-control association studies for the genetic analysis and have identified several genes to be susceptible to intracranial aneurysms. The identification of susceptible genes may lead to the understanding of the mechanism of formation and rupture and possibly lead to the development of a pharmacological therapy. Furthermore, should it be possible to identify a genetic marker associated with an increased risk of formation and rupture of an intracranial aneurysm, the necessity for screening and urgency of treatment could be determined more easily. In this review we summarize the current knowledge of intracranial aneurysm genetics and also discuss the method to detect the causalities. In view of the recent advances made in this field, we also give an outlook on possible future genetically engineered therapies, whose development are well underway.
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PMID:The influence of genetics on intracranial aneurysm formation and rupture: current knowledge and its possible impact on future treatment. 1838 13

Although unruptured intracranial aneurysm (UIA) is becoming a more common finding nowadays, determining the optimal treatment strategy is difficult because the risk of rupture is poorly understood and surgery is not without its own hazards. As the mortality rate after rupture is estimated to range from 56 to 83%, the final therapeutic decision is the result of an analysis of rupture risk and the risks related to surgical exclusion, which may be determined by consideration of the risk factors. We considered the UIA to have a high risk of rupture if it was located on the vertebrobasilar arterial system (RR: 4.4; CI 95%, 2.7-6.8), between 7 and 12 mm in size (RR: 3.3; CI 95%, 1.3-8.2) or larger (RR: 17; CI 95%, 8-36.1), multilobular and had a ratio of depth to width greater than 3.4 (risk x 20). A family history of UIA would constitute a major rupture risk (two to seven times that of spontaneous UIA). Other factors related to UIA rupture include arterial hypertension (RR: 1.46; CI 95%, 1.01-2.11) and smoking (RR: 3.04; CI 95%, 1.21-7.66). After microsurgical exclusion, the morbidity and mortality rates were calculated as 9 and 1.5%, respectively. Microsurgical risk factors were age (32% > 65 years), and factors related to the UIA itself and surgery, such as size (14% > 15 mm), location, presence of atherosclerosis and difficulty of surgical clip application. The incidence of rupture after microsurgical exclusion was estimated to be 0.2% per year, and complete microsurgical exclusion was achieved in 90% of patients. A randomised study of microsurgical exclusion of UIA would offer further proof of our therapeutic hypotheses.
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PMID:[Unruptured intracranial aneurysm and microsurgical exclusion: the need of a randomized study of surgery versus natural history]. 1841 19

Systematic reviews of systematic reviews identify good quality reviews of earlier studies of medical conditions. This article describes a systematic review of systematic reviews performed to investigate factors that might influence the risk of rupture of an intracranial aneurysm. It exemplifies the technique of this type of research and reports the finding of a specific study. The annual incidence of subarachnoid haemorrhage resulting from the rupture of intracranial aneurysms is estimated to be nine per 100,000. A large proportion of people who have this bleed, will die or remain dependent on the care of others for some time. Reliable knowledge about the risks of subarachnoid haemorrhage in different populations will help in planning, screening and prevention strategies and in predicting the prognosis of individual patients. If the necessary data were available in the identified reviews, an estimate for the numerical relationship between a particular characteristic and the risk of subarachnoid haemorrhage was included in this report. The identification of eligible systematic reviews relied mainly on the two major bibliographic databases of the biomedical literature: PubMed and EMBASE. These were searched in 2006, using specially designed search strategies. Approximately 2,000 records were retrieved and each of these was checked carefully against the eligibility criteria for this systematic review. These criteria required that the report be a systematic review of studies assessing the risk of subarachnoid haemorrhage in patients known to have an unruptured intracranial aneurysm or of studies that had investigated the characteristics of people who experienced a subarachnoid haemorrhage without previously being known to have an unruptured aneurysm. Reports which included more than one systematic review were eligible and each of these reviews was potentially eligible. The quality of each systematic review was assessed. In this review, 16 separate reports were identified, including a total of 46 eligible systematic reviews. These brought together research studies for 24 different risk factors. This has shown that the following factors appear to be associated with a higher risk of subarachnoid haemorrhage: being a woman, older age, posterior circulation aneurysms, larger aneurysms, previous symptoms, "non-white" ethnicity, hypertension, low body mass index, smoking and alcohol consumption of more than 150 g per week. The following factors appear to be associated with a lower risk of subarachnoid haemorrhage: high cholesterol, diabetes and use of hormone replacement therapy.
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PMID:Systematic review of reviews of risk factors for intracranial aneurysms. 1856 Aug 19

An aim of the study was to compare by the analysis of pedigrees the frequency of vascular pathology in first-degree relatives (FDR) of patients with intracranial aneurysms (IA) and controls. Pedigrees were selected by interviewing 194 patients with IA (94 men and 100 women) and 193 age- and sex-matched control patients. Only FDR with complete information about their health status were included: 1011 FDR of patients with IA and 812 FDR of controls. The results of the study revealed that the frequency of strokes was 2.5 times higher in FDR of patients with IA than in those of controls: 6.5% and 2.6%, respectively (RR = 2.52, 95% CI = 1.56-4.09). Hemorrhages occurred 3.7 times more often in FDR of patients with IA than in FDR of controls: 3.4% versus 0.9% (RR = 3.90, 95% CI = 1.74-8.75). Only 0.9% of FDR of patients with IA had the rupture of intracranial aneurysm compared with nobody in FDR of controls. The frequency of headaches was 2.8 times greater in FDR of patients with IA than in those of controls: 19.6% versus 7.1% (RR = 2.74, 95% CI = 2.08-3.62). FDR of patients with IA suffered from arterial hypertension 2 times more often than FDR of controls: 24.9% and 11.6%, respectively (RR = 2.15, 95% CI = 1.73-2.68). Coronary heart disease was 2.7 times more frequent in FDR of patients with IA than in controls: 8.9% and 3.3%, respectively (RR = 2.68, 95% CI = 1.76-4.07). Sudden death occurred in FDR of patients with IA 5.8 times more often than FDR of controls: 11.1% and 1.9%, respectively (RR = 5.68, 95% CI = 1.37-23.39). Thus, vascular pathology occurs relatively often in FDR of patients with IA implying that vascular defects which cause the development of IA may be, at least in part, genetically determined. Prevention of stroke and cardiovascular disease is necessary for FDR of patients with IA.
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PMID:[Vascular pathology in first-degree relatives of patients with intracranial aneurysms]. 1892 79

A 55-year-old man developed hypertension and acute epigastric pain during dobutamine-atropine stress echocardiography (DASE). Evaluation-including a helical computed tomography (CT) scan of the abdomen and pelvis, as well as surgical exploration-revealed a ruptured splenic artery aneurysm. The patient died, despite multiple surgical interventions and a massive blood product transfusion. Impressively, no deaths from DASE have been previously reported. Additionally, no adverse sequelae during DASE have been reported in patients with an unruptured abdominal aortic aneurysm >or=4 cm in diameter or with an unruptured intracranial aneurysm. We report the first case, to our knowledge, of death caused by splenic artery aneurysm rupture during DASE. Splenic artery aneurysm rupture during DASE, though rare, can lead to death.
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PMID:Death caused by splenic artery aneurysm rupture during dobutamine-atropine stress echocardiography: case report and literature review. 1912 12

The coexistence of internal carotid artery (ICA) stenosis and intracranial aneurysm, although uncommon, can be a therapeutic dilemma. We present a case of a 73-year-old woman with a history of arterial hypertension and diabetes who had a severe symptomatic ICA stenosis (>90%) and an incidental ipsilateral cerebral aneurysm. The carotid stenosis was treated with angioplasty and stenting using a distal cerebral protection system. The patient was anticoagulated and maintained on antiplatelet therapy according to a standard protocol. Microcoil embolization of the aneurysm was performed 5 months after an intracranial stent was implanted. No growth has been observed in the aneurysm of the arterial lumen since the carotid intervention. There were no complications after the procedures during the postoperative period. This case shows that the incidental presence of an ipsilateral intracranial aneurysm does not appear to be a contraindication for the endovascular treatment of a carotid artery stenosis.
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PMID:Endovascular treatment of carotid stenosis associated with incidental intracranial aneurysm. 1954 89

Mechanisms of formation and growth of intracranial aneurysms are poorly understood. To investigate the pathophysiology of intracranial aneurysms, an animal model of intracranial aneurysm yielding a high incidence of large aneurysm formation within a short incubation period is needed. We combined two well-known clinical factors associated with human intracranial aneurysms, hypertension and the degeneration of elastic lamina, to induce intracranial aneurysm formation in mice. Roles of matrix metalloproteinases (MMPs) in this model were investigated using doxycycline, a broad-spectrum MMP inhibitor, and MMP knockout mice. Hypertension was induced by continuous infusion of angiotensin II for 2 weeks. The disruption of elastic lamina was achieved by a single stereotaxic injection of elastase into the cerebrospinal fluid at the right basal cistern. A total of 77% of the mice that received 35 milliunits of elastase and 1000 ng/kg per minute of angiotensin II developed intracranial aneurysms in 2 weeks. There were dose-dependent effects of elastase and angiotensin II on the incidence of aneurysms. Histologically, intracranial aneurysms observed in this model closely resembled human intracranial aneurysms. Doxycycline, a broad-spectrum MMP inhibitor, reduced the incidence of aneurysm to 10%. MMP-9 knockout mice, but not MMP-2 knockout mice, had reduced the incidence of intracranial aneurysms. In summary, a stereotaxic injection of elastase into the basal cistern in hypertensive mice resulted in intracranial aneurysms that closely resembled human intracranial aneurysms. The intracranial aneurysm formation in this model appeared to depend on MMP activation.
Hypertension 2009 Dec
PMID:Elastase-induced intracranial aneurysms in hypertensive mice. 1988 66


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