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

Epidemiological studies have shown a consistent downward trend in the incidence and mortality of stroke in industrialized communities. There are however no reports on the pattern of stroke in Saudi nationals and expatriates in Saudi Arabia. The types and etiologies in 372 subjects (262 Saudis, 110 non-Saudis) are described. Males outnumbered females in the ratios of 2.2:1 and 8.2:1 for Saudis and non-Saudis, respectively. The frequency of stroke increased steadily with age until the 7th decade in Saudis but dropped sharply after the 6th in expatriates. The frequency of stroke types in Saudis was ischemic (61%), hemorrhagic (17%) and unspecified (22%) as against 46, 47, and 7% respectively in non-Saudis. Intracerebral hemorrhage was more frequent than subarachnoid hemorrhage (SAH) and was encountered more often in Saudis than in non-Saudis; SAH was 3 times more common in expatriates than in Saudis. The major predisposing factors for stroke were hypertension, diabetes mellitus, and cardiac disorders. Abnormal hemoglobinopathies, especially sickle cell anemia, were rare. The differences observed in the age and sex distribution and in the stroke pattern between Saudi nationals and expatriates most likely reflect the demographic structure existing in Saudi Arabia.
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PMID:Stroke in a tertiary hospital in Saudi Arabia: a study of 372 cases. 186 67

The known risk factors of atherosclerotic diseases may be involved in the development of a subarachnoid hemorrhage. We studied the morbidity and mortality due to subarachnoid hemorrhage among 42,862 men and women aged 20-69 years who had participated in a large health survey in Finland. During a mean follow-up of 12 years, 102 non-fatal and 85 fatal cases of subarachnoid hemorrhage were observed. The total incidence was 37 per 100,000 person-years. Smoking and hypertension were positively associated and body mass index was inversely associated with the risk of subarachnoid hemorrhage. These associations were not confounded by age or each other. No statistically significant association with risk was detected for serum cholesterol level, hematocrit content, known heart disease, or diabetes. The risk was especially elevated among lean hypertensive subjects and lean smoking subjects. The age-adjusted relative risks of subarachnoid hemorrhage for lean, hypertensive smokers were 18.3 (95% confidence interval (CI), 7.8-42.7) among women and 6.7 (95% CI, 2.3-19.7) among men as compared to the risk among subjects without these risk factors. We conclude that modifiable risk factors are predictive of subarachnoid hemorrhage, for which reason subarachnoid hemorrhage may in part be preventable. Leanness combined with arterial hypertension and/or smoking, in particular, poses a substantially elevated risk.
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PMID:Risk factors for subarachnoid hemorrhage in a longitudinal population study. 189 Apr 35

A model of rat arteriovenous fistula (AVF) was created using a proximal common carotid artery to distal external jugular vein anastomosis. Anatomical dissections revealed that the external jugular vein is the primary vessel draining intracranial venous blood. Physiological measurements were made with the AVF open and closed, and during venous outflow occlusion of the contralateral external jugular vein. Opening the AVF increased torcular pressure from 6.5 +/- 0.6 to 13.5 +/- 1.1 mm Hg and decreased mean arterial pressure from 82.7 +/- 1.8 to 62.8 +/- 1.8 mm Hg (both P less than .05), decreasing cerebral perfusion pressure from 76.2 +/- 1.7 to 49.3 +/- 2.2 mm Hg (P less than .05). Middle cerebral artery blood flow velocity (MCA BFV) decreased from 6.8 +/- 1.1 to 4.2 +/- 0.7 cm/s (P less than 0.05). In rats with an AVF, occlusion of venous outflow increased torcular pressure to 34.8 +/- 3.1 mm Hg (P less than 0.05), MCA BFV decreased to 1.8 +/- 0.5 cm/s (P less than 0.05), and severe ischemic changes were seen on the electroencephalogram. Under this condition, torcular pressure and systemic arterial pressure had a positive linear relationship (P less than 0.05), whereas in control rats torcular pressure and arterial pressure had no relationship. Restoration of cerebral perfusion pressure by release of venous outflow occlusion and AVF closure transiently increased MCA BFV to 69% above baseline (P less than 0.05). Histological examination 1 week after permanent venous outflow occlusion revealed venous infarction, subarachnoid hemorrhage, and severe brain edema in rats with an AVF but not in control rats without an AVF. This model of cerebrovascular steal with venous hypertension reproduces both hemodynamic and hemorrhagic complications of human AVF and emphasizes the importance of venous outflow obstruction and venous hypertension in the pathophysiology of these lesions.
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PMID:Intracranial venous hypertension and the effects of venous outflow obstruction in a rat model of arteriovenous fistula. 192

The case of a 21-year-old female patient with neck pain and brain stem symptomatology after appendectomy is reported. Duplex sonographic findings were compatible with right vertebral artery dissection and occlusion of the vessel. Angiography confirmed the diagnosis. The patient recovered within weeks and was free of symptoms 6 months after the acute episode. Dissection of the vertebral artery can occur with or without minor trauma. Associations with fibromuscular dysplasia, arterial hypertension and the use of oral contraceptives have been reported. As in our own patient, dissection can appear without any vessel pathology or risk situation. The most dangerous complication of the disease is rupture of the adventitia with subarachnoid hemorrhage. Without this complication, prognosis of vertebral artery dissection is favourable with complete recovery within weeks. Clinical findings, diagnostic procedure and therapy are discussed.
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PMID:[Spontaneous dissection and stenosis of the vertebral artery]. 192 54

We studied the pattern and outcome of strokes in 200 Saudi patients. Cerebral infarction constituted 87% of strokes, subarachnoid hemorrhage 4.5%, cerebral hemorrhage 6.5%, and venous infarction 2%. The vessel most commonly involved was part or all of the middle cerebral artery, constituting 52% (90) of the 174 arterial infarcts. Lacunar infarcts were seen in 21% (37) of the patients with arterial infarcts. Among all 200 patients, 8% died and 8% had secondary generalized seizures. Hypertension occurred in 41% of the 174 patients with arterial infarcts and 62% of the 13 with cerebral hemorrhages. The highest incidence of hypertension as a risk factor was among those with lacunar infarcts (81%), ganglionic cerebral hemorrhages (80%), and infarcts of deep branches of the middle cerebral artery (57%). Embolic infarcts due to rheumatic heart disease constituted 11% of all arterial infarcts. We conclude that our pattern of strokes is similar to that of the west rather than that of the Japanese, but with less frequent arteriovenous malformations and aneurysms.
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PMID:Cerebrovascular disease in Saudi Arabia. 192 60

Five autopsied cases of dissecting aneurysms of the intracranial vertebral artery are reported and the literature is reviewed to clarify the clinicopathological correlations. In an autopsy series of 110 patients with subarachnoid hemorrhage (SAH), the incidence of this entity was 4.5%, with all five cases progressing rapidly to death from massive SAH. Cases of intracranial vertebral dissection can be divided clearly into two groups based on the clinical and pathological features. In the first group, the dissection is confined to the vertebral artery and a massive SAH develops caused by the rupture of the arterial wall. The plane of dissection is mainly subadventitial. In the second group, brain-stem infarction develops resulting from luminal occlusion by intramural hematoma. The plane of dissection is mainly subintimal, with the dissection extending to the basilar artery. The condition in the second group affects patients at a younger age. If the lesion is localized within the vertebral artery and does not extend to the basilar artery, the disease seems not to be fatal. The clinical features of the vertebral dissection are largely determined by the plane and extension of dissection. Vertebral artery dissection is due to many causative factors including hypertension, congenital or degenerative changes in the arterial wall, and anatomical and pathological characteristics of the vertebral artery.
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PMID:A clinicopathological study of dissecting aneurysms of the intracranial vertebral artery. 194 Nov 16

A young woman who sustained severe head trauma presented to the operating room for emergent surgical intervention. Her electrocardiogram (ECG) exhibited signs of myocardial ischemia, which resolved several days postoperatively. ECG changes suggestive of cardiac pathology can be associated with intracranial pathology, most notably subarachnoid hemorrhage. Delay of operative therapy may have catastrophic results. Experimental data indicates massive sympathetic outflow results from stimulation of the lateral and posterior hypothalamic regions. Large amounts of norepinephrine are released into the systemic circulation, resulting in hypertension, tachycardia, dysrhythmias and ECG changes. Myocardial ischemia and injury can occur from the effects of this excessive sympathetic stimulation. In certain case reports, neurologic patients who experienced ECG changes had normal hearts on postmortem examination. This implies that myocardial recovery can occur despite the appearance of an abnormal ECG in the neurologic patient. Anesthetic management of these patients involves prevention of further increases in intracranial pressure and avoidance of hyperventilation in the presence of hypotension or vasospasm. Continuous ECG monitoring is essential. Ventricular dysrhythmias may prove resistant to conventional pharmaceutical management. Beta blockade may be indicated to prevent excessive cardiac stimulation by endogenous catecholamines, and, in addition, may prevent the formation of the microscopic cardiac lesions typical of this hyperstimulation.
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PMID:Electrocardiographic changes and intracranial pathology. 195 Apr 1

A prospective series of 265 patients with aneurysmal subarachnoid hemorrhage (SAH) of Grades I to III (Hunt and Hess classification) upon admission were evaluated as to neurological outcome and computerized tomography (CT) findings 1 to 3 years (mean 1.4 years) after the SAH and surgery. A total of 73 patients underwent acute surgery (within 72 hours after the bleed: Days 0 to 3), 86 were operated on subacutely (between Days 4 and 7), and 91 had late surgery (on Day 8 or later). Fifteen patients died before surgery was undertaken and another 20 patients died during the follow-up period. A total of 104 patients received nimodipine and the rest of the patients received either placebo (109 patients) or no medication (52 patients). A logistical regression analysis revealed the following prognostic factors for cerebral infarction, in order of importance: the amount of blood on the primary CT scan; postoperative angiographic vasospasm; the timing of the operation; and a history of hypertension. The use of nimodipine was associated with a significant reduction of cerebral infarcts visualized by CT scanning in patients who received intermediate or late surgery. In patients who underwent acute surgery no significant difference between the incidence of cerebral infarcts was observed.
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PMID:Risks factors for cerebral infarction in good-grade patients after aneurysmal subarachnoid hemorrhage and surgery: a prospective study. 186 62

Calcium channel blockers are effective antihypertensive agents, both as initial monotherapy and in combination with other antihypertensive agents. These drugs are also effective in the treatment of chronic, stable angina, variant angina and supraventricular arrhythmias. Drugs in this class have different affinities for calcium channels in vascular smooth muscle, cardiac muscle, cardiac sinus and atrioventricular node. They are all useful in hypertension and angina, but only verapamil and diltiazem are also useful in the control of heart rate and supraventricular arrhythmias. Nimodipine may control vascular spasm following subarachnoid hemorrhage. Calcium channel blockers have also been used in the treatment of migraine headache and Raynaud's phenomenon.
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PMID:Comparative clinical pharmacology of calcium channel blockers. 199 Jul 41

We studied the impairment of autoregulation of cerebral blood flow (CBF) and its effect on the electrical activity of the brain during the development of chronic cerebral vasospasm after subarachnoid hemorrhage, using a vasospasm model in primates. Fourteen animals were divided into two groups: a clot group (8) and a sham-operated group (6). To induce subarachnoid hemorrhage, all the animals underwent craniectomy, and in the clot group, the autologous blood clot was located around the arteries dissected free from the arachnoid membrane. Cerebral angiography was performed before subarachnoid hemorrhage and 7 days after (Day 7). On Day 7, regional CBF in the parietal lobe--measured by the hydrogen clearance method--and central conduction time were studied during either graded hypertension or hypotension. In the clot group, the mean vessel caliber of the cerebral arteries on the right side (clot side) of the circle of Willis showed significant (P less than 0.01) reduction (more than 40%) as compared with the values on the contralateral, non-clot side. The values for the bilateral parietal CBF in the sham-operated group and the left parietal CBF in the clot group were fairly constant when the mean arterial blood pressure (MABP) was in the range of 60 to 160 mm Hg. In the clot group, right parietal CBF was significantly (P less than 0.05) smaller than that on the left side at an MABP level of 40 to 100 mm Hg, and increased at an MABP level of 180 mm Hg. The right parietal CBF increased as the arterial blood pressure increased, showing impairment of autoregulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impairment of cerebral autoregulation during the development of chronic cerebral vasospasm after subarachnoid hemorrhage in primates. 199 80


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