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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathological findings of six autopsy cases of dissecting intracranial aneurysm are studied. Clinically, all cases exhibited systemic hypertension or left ventricular hypertrophy. Macroscopically, all cases exhibited rupture of the vertebral artery and subarachnoid hemorrhage. Two types of lesion were present. First, all cases showed the formation of a dilatated pseudoaneurysm with widespread disruption of the entire arterial wall, which was composed of thin adventitia. Second, a medial disruption of the arterial wall and subadventitial dissecting hemorrhage, which formed a false lumen and stenosis of the 'true' lumen of the artery, was also found. However, these lesions were found to be connected to the site of rupture. The autopsy cases within 1 day of onset of intracranial dissecting aneurysm showed the formation of fibrin thrombus, a marked degree of leukocyte infiltration and necrosis of the arterial wall at the site of the lesion. The cases that survived more than 1 week showed smooth muscle cell proliferation, macrophage accumulation and lymphocytic infiltration. No arteriosclerosis was found in any lesion studied. These data suggest that the disruption of the entire arterial wall might initially occur and cause medial disruption and subadventitial hemorrhage. Hypertension and arteriosclerosis might function as causal and protective factors in the pathogenesis of dissecting intracranial aneurysms, respectively.
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PMID:Pathology of a dissecting intracranial aneurysm. 1093 47

Intracranial aneurysms (ICA) are a well-known feature of autosomal dominant polycystic kidney disease. There is only one report about ICA in an adult patient with autosomal recessive polycystic kidney disease (ARPKD). We observed a 2-year, 6-month old girl with ARPKD and multiple ICA. The family history is negative for kidney disease. The diagnosis of ARPKD was based on the typical findings in ultrasonography and computed tomography. Cystic ectasia of biliary ducts 6.3/4.8 cm in diameter was found in the liver. Arterial hypertension in a range of 140/100-170/120 mm Hg was registered. The child has polyuria, polydipsia and enuresis. Blood urea was 15 mmol/l, creatinine in a range of 120 to 75 micromol/l. One episode of vomiting, dizziness and lethargy was the reason for a brain magnetic resonance imaging. Multiple fusiform and saccular aneurysms in the branches of middle and posterior cerebral arteries were seen bilaterally. The girl is growing well without neurological symptoms during an observation period of 1.5 years. Blood pressure is well controlled with an ACE inhibitor (Enalapril 2.5 mg daily). It was concluded that ICA can be found in patients with ARPKD. Blood pressure control is essential to reduce the risk of intracranial hemorrhage.
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PMID:Intracranial aneurysms in a child with autosomal recessive polycystic kidney disease. 1179 94

Intra-aneurysmal embolization by Guglielmi detachable coil (GDC) is becoming an important method in treatment of intracranial aneurysm. However, intraoperative bleeding remains an essential problem. We reviewed our anesthesia records in patients treated with GDC embolization. Ninety four cases of ruptured cerebral aneurysms were treated with GDC embolization, including 59 females and 35 males. Their ages ranged from 21 to 88, with mean age of 67 years. Preoperative Hunt and Hess grading scales were 1 in 3 cases, 2 in 31, 3 in 40, 4 in 16 and 5 in 4. Intraoperative re-bleeding occurred in 3 cases. These were confirmed by extravasation in angiography or by increased HDA in CT. Each case has berry aneurysm. Acute hypertension at re-bleeding was treated with nicardipine as well as by increasing dose of anesthetic, and hemostasis was obtained by hypotension and reversal of heparin with protamine. After disappearance of extravasation, the procedures were continued. Anesthesia was maintained with fentanyl-propofol in 1 case and sevoflurane in 2 cases. Direct hemostasis is impossible during endovascular surgery and management of systemic circulation by an anesthesiologist is necessary.
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PMID:[Re-bleeding during embolization of ruptured cerebral aneurysms by Guglielmi detachable coil]. 1248 50

A 59-year-old man with abnormal vascular features (intracranial aneurysm, a cervical arteriovenous shunt, bilateral internal jugular vein occlusions, and left transverse sinus hypoplasia), as well as left optic atrophy was suspected to have familial polycystic kidney disease. The possibility of autosomal dominant polycystic kidney disease complicated by Ehlers-Danlos syndrome type IV due to the coexistence of vasculopathy and polycystic kidneys was considered. However, the negative results of a skin fibroblast culture rendered the diagnosis of Ehlers-Danlos syndrome type IV unlikely. The cause of left optic atrophy in our patient remains unclear although it was suspected to be a secondary consequence of papilledema, which was caused by intracranial hypertension.
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PMID:Polycystic kidney disease associated with cervical arteriovenous shunt and bilateral jugular vein occlusion. 1248 86

Six patients with intracavernous carotid artery aneurysms (ICCAAns) were seen at our department from 1998 to 2002. All patients had only one intracranial aneurysm and their ages at diagnosis ranged from 36 to 72 years (median 56). Five were women and four had a history of hypertension. One patient was pregnant. All of the ICCAAns were symptomatic at diagnosis. Duration of symptoms was 2-30 days. On admission to our department, initial symptom was headache in four patients, visual loss in two, eye pain in one, third nerve paresis in two and subarachnoid hemorrhage (SAH) in one. Spontaneous thrombosis was present in two patients. All of the ICCAAns were saccular. Computed tomography (CT) was superior when compared with magnetic resonance imaging (MRI) for diagnosis of ICCAAns on admission. Angiography remains the gold standard for diagnosis and determination of specific anatomical details, which are necessary to plan treatment.
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PMID:Intracavernous carotid artery aneurysms. 1551 63

The advent of non-invasive methods of imaging intracranial blood vessels has facilitated screening for intracranial aneurysms in people who are at risk. A strong risk factor for intracranial aneurysm, which causes subarachnoid haemorrhage, is a positive family history, defined as two or more first-degree relatives with subarachnoid haemorrhages (relative risk [RR]=6.6). The greatest familial risk is associated with an affected sibling. Another strong risk factor is polycystic kidney disease (RR=4.4). People who have these risk factors are potential candidates for screening. Even if screening does not find abnormality, there is a high risk of new aneurysms 5 years later. Repeated screening might be done, although the optimum interval between screening assessments and the duration of repeated screening is unclear. Patients who have survived a subarachnoid haemorrhage are at increased risk of another from a newly developed aneurysm, but whether screening is beneficial in such patients is not clear. Most occurrences of subarachnoid haemorrhage in the general population are related to the more common risk factors of hypertension (RR=2.8) and smoking (RR=1.9). Therefore, screening of individuals who have a family history of subarachnoid haemorrhage or polycystic kidney disease will have little effect on the incidence of subarachnoid haemorrhage in the general population. When patients present for screening, the construction of a family tree and discussion of the history of relatives with stroke can be revealing. Before referring a patient for non-invasive imaging of the circle of Willis, the physician should discuss the risks and benefits of screening, the implications for holding a licence to drive or fly and for life insurance, and whether or not the patient wants to be informed about other incidental findings.
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PMID:Intracranial aneurysm screening: indications and advice for practice. 1566 44

Many risk factors for subarachnoid hemorrhage (SAH), such as hypertension and recent infection, have already been established. Chlamydia pneumoniae is a common respiratory pathogen that has been implicated as a potential risk factor for hypertension and atherosclerotic diseases. The purpose of the case-control study presented here was to examine the causative relationship between C. pneumoniae infection and SAH. Serum C. pneumoniae IgG and IgA antibodies were measured using an enzyme-linked immunosorbent assay in 52 patients with SAH and in 104 healthy age-matched control subjects. Multivariate analysis revealed a significant association between SAH and both a strong seropositivity for IgG and/or IgA antibodies against C. pneumoniae (odds ratio, OR, 3.62; 95% confidence intervals, CI, 1.06-12.39; p = 0.040), which indicates the presence of acute C. pneumoniae infection, and hypertension (OR, 2.91; 95% CI, 1.42-5.96; p = 0.0035). These results provide evidence that infection with C. pneumoniae may be a risk factor for SAH from a ruptured intracranial aneurysm.
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PMID:Chlamydia pneumoniae infection as a risk factor for subarachnoid hemorrhage. 1570 63

Intracranial aneurysms have long been considered a once in a lifetime event. Nevertheless, patients who survive after subarachnoid haemorrhage (SAH) may be at risk for new aneurysms. In a cohort of patients with clipped aneurysms, we studied the yield of screening in the years after the SAH and we tried to identify risk factors for formation of new aneurysms as well as for enlargement of aneurysms that were already present at the time of the SAH. We screened 610 patients who had been admitted between 1985 and 2001 for SAH by means of CT-angiography. Risk factors were evaluated by Cox regression analyses. With screening we detected 129 aneurysms in 96 (16%) patients, after a mean interval of 8.9 years. Of these, 24 (19%) were located at the site of the previously ruptured and clipped aneurysm and 105 (81%) at a site remote from the clip site. Of the aneurysms at a remote site 59 could be compared with the initial (CT)-angiogram. Of these, 19 were truly de novo (32%) and 40 (68%) were already visible in retrospect. Of the 53 aneurysms that were followed over time 13 (25%) had enlarged. Risk factors for aneurysm formation and growth were presence of multiple aneurysms at time of SAH (HR 3.2, 95% CI 1.2-8.6), current smoking (HR 3.8, 95% CI 1.5-9.4) and hypertension (HR 2.3, 95% CI 1.1-4.9). These results suggest that intracranial aneurysms should not be considered as a single event in a lifetime but rather as a continuous process. Patients with a previous SAH have a substantial risk for new aneurysm formation and enlargement of untreated aneurysms. Screening these patients might be beneficial, especially in patients with multiple aneurysms, hypertension and a history of smoking. The risks and benefits of screening, however, should be carefully weighed, for example, in a decision model.
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PMID:Follow-up screening after subarachnoid haemorrhage: frequency and determinants of new aneurysms and enlargement of existing aneurysms. 1693 47

Despite the catastrophic consequence of ruptured intracranial aneurysms, very little is understood regarding their pathogenesis, and there are no reliable predictive markers for identifying at-risk individuals. Few studies have addressed the molecular pathological basis and mechanisms of intracranial aneurysm formation, growth, and rupture. The pathogenesis and rupture of cerebral aneurysms have been associated with inflammatory processes, and these have been implicated in the digestion and breakdown of vascular wall matrix. Epidemiological data indicate that the risk of cerebral aneurysm pathogenesis and rupture in women rises during and after menopause as compared to premenopausal women, and has been attributed to hormonal factors. Moreover, experimental evidence supports a role for estrogen in the modulation of each phase of the inflammatory response implicated in cerebral aneurysm pathogenesis and rupture. While the risk of aneurysm rupture in men also increases with age, this increased risk has been attributed to other recognized risk factors including cigarette smoking, use of alcohol, and history of hypertension, all of which are more common in men than women. We hypothesize, therefore, that decreases in both circulating estrogen levels and cerebrovascular estrogen receptor density may contribute to an increased risk of cerebral aneurysm pathogenesis and rupture in women during and after menopause. To test our hypothesis, experiments are needed to identify genes regulated by estrogen and to evaluate gene expression and intracellular mechanisms in cells/tissues exposed to varying concentrations and duration of treatment with estrogen, metabolites of estrogen, and selective estrogen receptor modulators (SERMs). Furthermore, it is not likely that the regulation of cerebrovascular homeostasis is due to the actions of estrogen alone, but rather the interplay of estrogen and other hormones and their associated receptor expression. The potential interactions of these hormones in the maintenance of normal cerebrovascular tone need to be elucidated. Additional studies are needed to define the role that estrogen and other sex hormones may play in the cerebrovascular circulation and the pathogenesis and rupture of cerebral aneurysms. Efforts directed at understanding the basic pathophysiological mechanisms of aneurysm pathogenesis and rupture promise to yield dividends that may have important therapeutic and clinical implications. The development of non-invasive tools such as molecular MRI for the detection of specific cells, molecular markers, and tissues may facilitate early diagnosis of initial pathophysiological changes that are undetectable by clinical examination or other diagnostic tools, and can also be used to evaluate the state of activity of cerebral aneurysm pathogenesis before, during, and after treatment.
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PMID:Deficiencies in estrogen-mediated regulation of cerebrovascular homeostasis may contribute to an increased risk of cerebral aneurysm pathogenesis and rupture in menopausal and postmenopausal women. 1635 55

The objective of the present study was to determine the frequency of the most common clinical features in patients with autosomal dominant polycystic kidney disease in a sample of the Brazilian population. The medical records of 92 patients with autosomal dominant polycystic kidney disease attended during the period from 1985 to 2003 were reviewed. The following data were recorded: age at diagnosis, gender, associated clinical manifestations, occurrence of stroke, age at loss of renal function (beginning of dialysis), and presence of a family history. The involvement of abdominal viscera was investigated by ultrasonography. Intracranial alterations were prospectively investigated by magnetic resonance angiography in 42 asymptomatic patients, and complemented with digital subtraction arteriography when indicated. Mean age at diagnosis was 35.1 +/- 14.9 years, and mean serum creatinine at referral was 2.4 +/- 2.8 mg/dL. The most frequent clinical manifestations during the disease were arterial hypertension (63.3%), lumbar pain (55.4%), an abdominal mass (47.8%), and urinary infection (35.8%). Loss of renal function occurred in 27 patients (mean age: 45.4 +/- 9.5 years). The liver was the second organ most frequently affected (39.1%). Stroke occurred in 7.6% of the patients. Asymptomatic intracranial aneurysm was detected in 3 patients and arachnoid cysts in 3 other patients. In conclusion, the most common clinical features were lumbar pain, arterial hypertension, abdominal mass, and urinary infection, and the most serious complications were chronic renal failure and stroke. Both intracranial aneurysms and arachnoid cysts occurred in asymptomatic patients at a frequency of 7.14%.
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PMID:Renal and extrarenal manifestations of autosomal dominant polycystic kidney disease. 1661 77


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