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

A study of cases and controls was performed to define the factors associated with nonembolic cerebral infarction and to compare the risk profiles of extensive cortical infarction (ECI) to those of lacunar infarction (LI). One hundred and four patients with ECI were matched with 71 patients with LI and with 90 controls. Although the initial analysis disclosed multiple factors associated with cerebral infarction, the analysis with control of the factors revealed that the only factors related with the occurrence of atherothrombotic infarction were: arterial hypertension [odds ratio (OR) = 6.8], diabetes mellitus (OR = 5.6), ischemic cardiac disease (OR = 5.5), increased hematocrit value (OR = 3.0), and atherogenic lipids in patients without arterial hypertension nor diabetes. Diabetes appeared as the only factor specifically associated with LI when compared with ECI (OR = 2.1). This study supports the following conclusions: 1) the risk profile of nonembolic cerebral infarction is concise and intelligible, 2) the possible role of arterial hypertension in the genesis of LI was not confirmed, and 3) diabetic microangiopathy may be implicated in the genesis of most of LI. Conclusions from this retrospective study should be taken as an interpretation of the results since some restriction in the sensitivity of the data analysis was deliberately introduced.
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PMID:[Risk factors in atherothrombotic cerebral infarct. Are there differential risk profiles in extensive cortical infarct and lacunar infarct? A case-control study]. 209 Aug 91

Thirteen (1.8%) of 708 patients with acute myocardial infarction treated with recombinant tissue-type plasminogen activator in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) I, II and III trials developed a stroke. Four strokes were hemorrhagic and nine were nonhemorrhagic. Of five prespecified risk factors for intracranial hemorrhage (age greater than 65 years, history of hypertension, history of prior cerebrovascular disease, aspirin use and acute hypertension), two patients had two risk factors and one patient had one risk factor. However, 80% of patients without intracranial hemorrhage had at least one risk factor and 31% had two risk factors. No patient with a prior stroke or transient ischemic attack (all greater than 6 months previously) had an intracranial hemorrhage. Of three prespecified risk factors for nonhemorrhagic stroke (atrial fibrillation, prior cerebrovascular disease and large anterior wall infarction), only the occurrence of a large anterior myocardial infarction (with ejection fraction less than 45%) was a predictor (p = 0.0015). The in-hospital death rate was 25% for patients with hemorrhagic stroke versus 11% for patients with a non-hemorrhagic stroke and 6% for those patients without a stroke. Furthermore, the hospital stay was greater than 50% longer in patients who had a stroke than in those who did not. Thus, intracranial hemorrhage remains an unpredictable risk in patients treated with thrombolytic therapy and cerebral infarction is related to anterior myocardial infarction and poor left ventricular function. Both types of stroke are associated with substantial morbidity and mortality.
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PMID:Stroke and acute myocardial infarction in the thrombolytic era: clinical correlates and long-term prognosis. 220 11

In summary, over a period of approximately four decades, an important new pathologic process was identified. There is no longer any doubt that the deposition of the subarachnoid clot in the basal cisterns can, over the course of a few days, lead to a progressive, severe vasoconstriction. This, in turn, can reduce cerebral blood flow to the distal brain, which, depending on a multitude of factors, can result in cerebral infarction. It is highly likely that the erythrocyte is the most important blood element in the pathophysiology of this process. The exact mechanism by which the blood vessel is forced into this destructive spasm remains to be elucidated. Significant steps have been taken to avoid the consequences of vasospasm by using hypertension and hypervolemia (or at the very least avoiding iatrogenic hypotension and hypovolemia). These measures have resulted in a reduced incidence of delayed ischemia. Because clot has been shown to cause vasospasm, it has seemed only logical that the early removal of clot would be efficacious in its prophylaxis. Experimental and clinical evidence to support this view has been gathered. Therapeutic measures based on it have been shown to be effective in the experimental situation but await controlled clinical evaluation. In the past decade, thanks to such trials, one of the calcium antagonist drugs has been shown to be effective in improving the outcome following subarachnoid hemorrhage, probably on the basis of reducing the frequency and extent of infarction by small vessel dilatation or neuronal protection. Although patients still die from this lethal complication of subarachnoid hemorrhage, it is difficult not to have some measure of optimism, based on the history just reviewed, that cerebral vasospasm will be a treatable disease within a few decades.
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PMID:The history of cerebral vasospasm. 213 40

It is generally accepted that increased blood pressure, especially high systolic blood pressure, is a major risk indicator in people over 60 years of age. Retrospective analyses of published trials show that when the elevation in arterial pressure has been firmly established by repeated blood pressure measurements, antihypertensive treatment should be considered for the following subgroups. (1) All elderly hypertensive patients with grade III or IV retinopathy, congestive heart failure or cerebral infarction or hemorrhage should be treated regardless of age or degree of blood pressure elevation. (2) In elderly patients with established mild hypertension and no symptoms or complications, non-pharmacological treatment should be started in patients less than 80 years of age, with antihypertensive drugs prescribed if diastolic pressure reaches 100 mmHg or more over 3 months or 95 mmHg or more over 6 months of follow-up. The therapeutic benefit of pharmacologic antihypertensive treatment has not yet been established in hypertensive patients over 80 years of age or in those with isolated systolic hypertension. All things considered, the indication to intervene pharmacologically should be viewed as becoming gradually more compelling as blood pressure rises. The more closely a patient's characteristics match those of a subset of elderly hypertensive patients in whom therapeutic benefit has been proven, the greater the need for pharmacologic treatment.
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PMID:Treatment of the elderly hypertensive patient. 214 7

Hypertension and serum cholesterol levels are strongly interrelated as cardiovascular risk factors. The Framingham study showed that the risk of both ischaemic heart disease and brain infarction doubles in presence of mild hypertensive status and triplicates in presence of a definitive hypertension. The systolic pressure showed to be the best predictor of both ischaemic heart disease and cerebral infarction particularly in persons aged more than 65 years. In terms of physiopathology we point out several mechanisms by which hypertension could interact with hypercholesterolemia on the arterial wall causing endothelial lesion, enhancing the penetration of arterial wall by lipoproteins, calcium accumulation on smooth subendothelial muscle and suppression of the relaxation factor produced by endothelial cells. In relation to the dietetic treatment, we must restrict more rigorously the ingestion of salt, saturated fatty acids, and total calories. In terms of anti-hypertensive drugs, we should: Avoid thiazide diuretics in case of cholesterol levels of moderate to high risk. Avoid beta blockers in patients with high levels of triglycerides, low HDL and low ratio total cholesterol/HDL. Consider to choose a calcium antagonist, a converting enzyme or an alpha blocker.
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PMID:[Arterial hypertension associated with hyperlipoproteinemia]. 218 49

Normal sleep provides a period of physiologically reduced workload for the cardiovascular system for almost one third of the human life span. Snoring, the most common disorder of sleep, heralds the presence of an unstable upper airway and alerts perceptive clinicians to the possibility of OSA. Epidemiologic evidence has implicated snoring as an independent risk factor for the development of hypertension, ischemic heart disease, and cerebral infarction. However, many investigators would attribute these adverse cardiovascular effects to the substantial prevalence of OSA in habitual snorers. The detrimental effects of OSA on hemodynamics and cardiac rhythm have been well documented, and recent data have linked OSA with increased cardiovascular mortality. Worsening hypoxemia during sleep likely contributes to the nocturnal mortality observed in patients with severe COPD. Effective treatment to prevent nocturnal hypoxemia is available for OSA and COPD, with current evidence supporting beneficial effects on survival.
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PMID:Cardiovascular effects of sleep disorders. 218 99

To assess the impact of cigarette smoking on stroke in young adults (15 to 45 years old), we compared smoking data from 181 patients with cerebral infarction with that of 307 control subjects matched for age, gender, geographic location, and hospital admission dates. While controlling for these matching variables and hypertension, an analysis based on a conditional logistic regression model indicated that a smoker was 1.6 times more likely to have a cerebral infarction than a non-smoker (95% confidence interval, 1.07 to 2.42). There was a cumulative dose effect with each additional pack-year causing a greater risk of having a cerebral infarction. In fact, after adjusting for all other risk factors, there was a significant quadratic component to the dose-response relationships, with the result that individuals with a larger number of pack-years were invariably the stroke patients. There was no significant difference in smoking status among the various subtypes of cerebral infarction (atherosclerotic, nonatherosclerotic vasculopathy, cardioembolic, hematologic related, undetermined). These data indicate that cigarette smoking is an important risk factor for cerebral infarction in young adults. Risk factor modification through cessation of smoking may reduce the risk of ischemic stroke in young adults.
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PMID:Cigarette smoking. A risk factor for cerebral infarction in young adults. 218 78

Vascular diseases are multifactorial, and several risk factors, such as increasing age, male sex, hypertension, diabetes, dyslipidemias and smoking, are well-known. In recent studies, associations have also been found between preceding infections and development of myocardial or cerebral infarction. Preceding acute respiratory infections are reported to be more common in patients with myocardial or cerebral infarction. Cerebral infarction may follow infective endocarditis, bacterial meningitis or any other bacteremic infection. Oral infections are common chronic bacterial infections. Although oral infections are local, they may lead to systemic infectious complications via stransient bacteremias, and there may also be other systemic effects, for instance, via immunologic or toxic mechanisms. Association between oral infections and vascular diseases has been studied in 2 Finnish case-control studies concerning myocardial and cerebral infarction. In these case-control studies, it was found that oral infections were more common in patients with myocardial or cerebral infarction than in their age- and sex-matched community controls. There are many factors, such as diabetes, smoking and alcohol abuse, which may predispose to both development of infarction and oral infections. Therefore, the observed association between oral infections and vascular diseases may result from these common predisposing factors, and causality between them cannot be inferred. There are, however, several possible links between oral infections and infarction. Although causality between oral infections and infarction cannot be proven, patients who have poor oral health need health education, paying attention to those common risk factors of oral infections and vascular diseases. Furthermore, their oral infections should be treated, because they may predispose to infectious complications, which may lead to infarction.
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PMID:Vascular diseases and oral infections. 220 46

We investigated the clinical and pathologic characteristics of stroke in 234 patients with systemic lupus erythematosus. Thirteen patients (5.6%) developed cerebrovascular disease. Cerebral infarction was noted in eight, cerebral hemorrhage in two, and subarachnoid hemorrhage in three. In seven (54%) of these 13 patients, stroke occurred less than or equal to 5 years after systemic lupus erythematosus was diagnosed. Among the predisposing risk factors for stroke, hypertension was the most important. Lupus anticoagulant was detected in three (38%) and anticardiolipin antibody in three (43% of seven investigated) of the patients with infarction. Evaluation of the clinical manifestations and autoantibodies indicated that renal involvement and high titers of anti-deoxyribonucleic acid antibody were more frequent in the stroke group than in the non-stroke group. Autopsy studies on six of the patients with stroke revealed small infarcts and hemorrhages in all, but in no case was true angiitis observed. Libman-Sacks endocarditis was found in two of the three patients with infarction. In conclusion, the important contributory factor to the development of stroke in patients with systemic lupus erythematosus is considered to be hypertension mediated by immunologic abnormalities. Antiphospholipid antibodies and Libman-Sacks endocarditis are closely associated with occlusive cerebrovascular disease.
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PMID:Stroke in systemic lupus erythematosus. 223 45

We performed unenhanced computed tomographic scans on 141 asymptomatic patients with nonvalvular atrial fibrillation. Thirty-six patients (26%) had hypodense areas consistent with cerebral infarction. The majority of these were small deep infarcts, seen in 29 patients (21%), but 13 patients (9%) had cortical or large deep infarctions. Twelve patients had more than one infarct on computed tomographic scan. Increasing age and increased left atrial diameter were the only clinical features associated with asymptomatic infarction. Patients older than 65 years with a left atrial diameter greater than 5.0 cm (n = 23) had a 52% prevalence of asymptomatic infarction. Patients younger than 65 years with a left atrial diameter less than 5.0 cm (n = 38) had an 11% prevalence of silent infarction. Patients with only one of these risk factors (n = 72) had a 24% prevalence of silent infarction. Infarction was more common in those with chronic (34%) as opposed to intermittent (22%) nonvalvular atrial fibrillation, but this difference was not significant. Hypertension, diabetes, duration of atrial fibrillation, congestive heart failure, history of myocardial infarction, and echocardiographic evidence of left ventricular dysfunction were not associated with asymptomatic infarction. A history of hypertension was present in only 35% of our patients with small-deep asymptomatic infarction, similar to the percentage in patients without stroke. Asymptomatic cerebral infarction is common in nonvalvular atrial fibrillation. The association with enlarged left atria and the lack of correlation with major cerebrovascular risk factors suggests a cardioembolic mechanism. Further study is needed to determine the functional and prognostic significance of these strokes.
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PMID:Epidemiologic features of asymptomatic cerebral infarction in patients with nonvalvular atrial fibrillation. 224 43


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