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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship between the presence of silent cerebral infarcts (SCI) and etiology of an acute cerebral ischemia remains controversial. In a population of 306 patients with a first-ever stroke (225) or transient ischemic attack (TIA) (81), we studied the prevalence and associated risk factors of SCI as well as the presumed etiology of the qualifying event. Silent infarction was defined as a focal hypodensity on brain CT, not related to the recent ischemic event. The overall prevalence was 33% (102/306) with a higher rate in stroke patients (83/225, 37%) than in TIA patients (19/81, 23%; p = 0.028). Age (p < 0.01), smoking (p < 0.01), hypertension (p = 0.013), and leukoaraiosis (p = 0.05) were significantly associated with SCI, but only in some degree in TIA patients. Presence of SCI was statistically associated with a small-artery disease (p < 0.01) considered as the cause of the qualifying event. Emboligenic cardiopathy was significantly more frequent in patients without SCI (p < 0.05) in the TIA subgroup. Thus, in patients with silent cerebral infarcts, small-vessel disease may be in most cases the cause of the recent symptomatic cerebral ischemia.
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PMID:Stroke subtypes and risk factors associated with silent infarctions in patients with first-ever ischemic stroke or transient ischemic attack. 814 Aug 83

Possible intracardiac sources of emboli were looked for by transoesophageal echocardiography (TOE) in 271 patients (149 men, 122 women; mean age 60 +/- 11 years) a mean of 12 +/- 8 days after suffering an episode of cerebral ischaemia. Left atrial thrombi were revealed in 9 patients: they were more frequent in those with atrial fibrillation (odds ratio [OD] 25.2; P < 0.0001) or known cardiac disease (OD 3.5; P = 0.06). Using the two factors together, the 9 left atrial thrombi could be predicted in 96 patients, while in the remaining 175 patients without cardiac abnormalities no left atrial thrombi were found. Overall, TOE is not an essential investigation additional to transthoracic echocardiography to exclude left atrial thrombi in patients without heart disease who are in sinus rhythm. But in those with atrial fibrillation and/or organic heart disease, TOE can in many instances facilitate the indication for anticoagulation.
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PMID:[The indications for transesophageal echocardiography after cerebral ischemia]. 822 95

The pathogenic role of aortic arch atherosclerosis (AAA) in embolic stroke is not well understood. We investigated, prospectively, the prevalence and severity of AAA in patients with embolic stroke to ascertain its role as a risk factor for cerebral ischemia. We examined 100 consecutive patients who had experienced acute symptoms due to cerebral ischemia. Clinical examination, electrocardiogram, x-ray, ultrasound examination of craniocervical arteries, transesophageal echocardiography (TEE), cranial computerized tomography, and magnetic resonance imaging were undertaken. Seventy-five patients showed evidence of AAA; 34 patients had moderate to severe (> 5 mm thickening) AAA. Age was positively related to the severity of AAA, as were smoking, coronary heart disease, diabetes mellitus, internal carotid artery (ICA) occlusive disease, and embologenic heart disease. Hypertension, which was evident in 52 patients, did not distinguish those cases showing AAA. Twelve patients showed evidence of high-degree ICA stenosis on the symptomatic side, although the extent of ICA stenosis and AAA were unrelated. A cardiac source of emboli was found in 28 patients. AAA was found to be the probable source for embolic stroke in 14 patients. These data indicate that aortic arch atherosclerosis is an important source of cerebral emboli which may increase the risk for ischemic stroke. Furthermore, we suggest that TEE examination of the aortic arch may be important for the diagnosis of AAA and ultimately for the prophylactic treatment of severe cerebral ischemia.
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PMID:Embolism from the aortic arch in patients with cerebral ischemia. 891 14

The ischemic stroke syndrome is very broad and encompasses a wide range of underlying conditions. Its identification is of great importance in clinical routine, in particular in the management of young patients who have acute neurologic deficits. The introduction of CT, MR and ultra-sound demonstrating lesions of the brain and in certain degree of the cerebral arteries has in general eliminated the need for angiography as a first examination. The most common underlying anomaly found with thrombotic or embolic stroke is congenital or acquired heart disease. Thus, it is essential that patients with cerebral ischemia be submitted to a complete cardiac examination. Children tend to show more recovery after a stroke than adults do.
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PMID:Ischemic stroke syndromes in childhood. 922 89

The purpose of this study was to determine the prevalence, clinical significance, and embolic potential of thoracic aortic plaque in patients with cerebral ischemia and to further study the correlation of aortic plaque with carotid or heart disease. We used transesophageal echography (TEE) to evaluate potential source of emboli in aortic arch and heart, and duplex in carotid artery. A atherosclerotic lesion of aortic arch was defined as normal (0), mild plaque (1), moderate plaque (2) and protruding plaque or mobile plaque (3). 75 of 100 patients were found to have atherosclerotic lesion in aortic arch. 16 of 75 patients over degree 2 exhibited no pathologic finding of heart or carotid and 4 of 16 patients were classified as degree 3. The pathologic findings of heart and carotid were significantly correlated with aortic plaque. Age, diabetes, CAD were also significantly correlated with aortic plaque. Aortic atherosclerosis was common in cerebral ischemia. Aortic plaque might be responsible for not only some unexplained embolic events, but also for some of the embolic stroke in patient who have carotid artery or heart disease. Age, diabetes, CAD might be important risk factors in the development of atherosclerotic lesion in the aortic arch.
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PMID:Aortic plaque as a potential cause for cerebral ischemia. 981 73

The endothelins (ETs) are regulatory peptides, distributed in many organ systems and producing potent physiological effects. They are the most powerful vasoconstrictive substances known today. They also act as promitogens. Many data supporting pathophysiological roles for ETs are reported, especially regarding diseases related to the vascular system, such as hypertension, pulmonary hypertension, preeclampsia, ischemic heart diseases, renal failure, subarachnoidal hemorrhage, and cerebral ischemia. The development of drugs blocking ET binding to its receptors (antagonists) and the biosynthesis of ETs (ECE inhibitors) presently attracts great interest in terms of establishing new treatments for diseases in which ETs are believed to be involved. Here we review the evidence supporting a role for ETs in the various etiologies related to ischemia-reperfusion injury, such as is found in heart disease, cerebral ischemia, and organ transplantation.
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PMID:The many aspects of endothelins in ischemia-reperfusion injury: emergence of a key mediator. 982 48

BACKGROUND: We investigated the association of cigarette smoking with high-grade carotid artery stenosis in patients with ischemic stroke and transient ischemic attacks. METHODS: Prospectively collected data from 404 patients with focal brain ischemia were used for a cross-sectional study estimating the association between cigarette smoking and high-grade carotid artery stenosis (diagnosed by Doppler-ultrasound and defined as a luminal narrowing of > or = 70%). Cerebral ischemia patients with normal sonographic findings served as a comparison group. Multivariate logistic regression models were used for statistical tests to determine the association between smoking and high-grade carotid stenosis. Age, gender, hypertension, diabetes mellitus, hypercholesterolemia and co-existing heart disease (myocardial infarction, angina, heart failure) were considered potential confounders. RESULTS: High-grade carotid stenoses were found in 25% (n = 101) of the patients; 39% (n = 156) were classified as smokers. Smoking (odds ratio 3.6, 95% confidence interval [CI] 2.2 to 5.8), hypercholesterolemia (odds ratio 1.8; CI 1.1 to 2.8) and preexisting heart disease (odds ratio 1.7; CI 1.1 to 2.7) were significantly associated with carotid stenosis > or = 70%. The impact of smoking augmented with increasing degree of stenosis (odds ratio for stenoses > or = 80%: 4.3, CI 2.3 to 7.7), whereas the association with hypercholesterolemia, and co-existing heart disease decreased in strength for stenoses greater than 80%. Hypertension and diabetes mellitus were not found to be significantly with high-grade carotid artery stenoses. CONCLUSION: Smoking is an independent determinant of severe carotid artery stenosis in patients with focal cerebral ischemia.
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PMID:[In Process Citation] 1059 30

Inflammatory mediators are implicated in the pathogenesis of ischemic injury in immature brain. The phosphodiesterase inhibitor pentoxifylline inhibits production of tumor necrosis factor-alpha and platelet-activating factor. We hypothesized that pentoxifylline treatment would attenuate hypoxic-ischemic brain injury in immature rats. Seven-day-old rats (n = 79) underwent right carotid ligation, followed by hypoxia (FiO2 = 0.08). Rats received pentoxifylline immediately before and again after hypoxia (two doses, 25-150 mg/kg/dose, n = 34), or vehicle (n = 27). In separate experiments, rats received pentoxifylline treatment (40 mg/kg/dose, n = 8), or vehicle (n = 10) immediately and again 3 h after hypoxia-ischemia. Severity of injury was assessed 5 d later by visual evaluation of ipsilateral hemisphere infarction and by measurement of bilateral hemispheric cross-sectional areas. Pentoxifylline pretreatment reduced the incidence of liquefactive cerebral infarction, from 75% in controls to 10% with pentoxifylline, 40 mg/kg/dose (p<0.001, chi2 trend test). Quantification of hemispheric areas confirmed these findings. In contrast, posthypoxic-ischemic treatment with pentoxifylline resulted in only a modest reduction in cortical damage, without an overall reduction in incidence of infarction. Phosphodiesterase inhibition may be an effective strategy to use to decrease the severity of neonatal hypoxic-ischemic brain injury. Pretreatment regimens could be clinically relevant in settings in which an increased risk of cerebral ischemia can be anticipated, such as in infants undergoing surgery to correct congenital heart disease.
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PMID:Pentoxifylline attenuates hypoxic-ischemic brain injury in immature rats. 1062 85

Heart and brain vascular diseases are the leading causes of mortality in the world. Cardiac complications can frequently occur during the development of cerebral ischemia. The aim of this study was to establish the possible changes in fractions of creatinine-phosphokinase as the sensitive laboratory index of parenchymal lesion of brain parenchyma and the presence/absence of risk factors for ischemic brain and heart disease. The study comprised 80 patients with acute ischemic brain disease (AIBD), without the history of previous coronary disease. Blood samples were taken in all patients within the first 48 hours from AIBD onset aiming to determine a total (muscular MM) and heart fraction of creatinine-phosphokinase (MB), and brain parenchyma ischemia was confirmed by CT or MR scan of the head. A detailed history of the risk factors for ischemic brain disease (IBD) and ischemic heart disease was taken from all patients with AIBD, and the profile of glycemia and lipid status were determined, and blood pressure was measured 6 times a day. Independent variables in statistical analysis were: age, degree of severity and the side of neurologic event, size of ischemic lesion and maximal values of systolic and dyastolic pressure. Dependent variables were the values of fractions of creatinine-phosphokinase (CPK). Control group (n = 40) comprised patients with neurologic diseases of non-vascular origin. All parameters as well as their interrelations were statistically analyzed. The results revealed significant correlation of the increased levels of CPK of MM and MB fraction with the size and place of ischemic lesion in the right cerebral hemisphere, which was highly significant for MB fraction in the total group of patients with AIBD, and for MM fraction, only for cases of more severe IBD. Highly significant increased values of those fractions were also observed compared to the control group of patients.
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PMID:The significance of determination of the fraction of creatinine-phosphokinase in patients with acute ischemic brain disease. 1093 26

Diseases of the heart are the No. 1 killer in industrialized countries. Brain injury can develop as a result of cerebral ischemia-reperfusion due to stroke (brain attack) and other cardiovascular diseases. Learning about the disease is the best way to reduce disability and death. We present here whether gene repair activities are associated with neuronal death in an ischemia-reperfusion model that simulates stroke in male Long-Evans rats. This experimental stroke model is known to induce necrosis in the ischemic cortex. Cerebral ischemia causes overactivation of membrane receptors and accumulation of extracellur glutamate and intracellular calcium, which activates neuronal nitric oxide synthase, causing damage to lipids, proteins, and nucleic acids, and reduces energy sources with consequent functional deterioration, leading to cell death. Restoration processes normally repair genes with few errors. However, ischemia elevates oxidative DNA lesions despite these repair mechanisms. These episodes concurrently occur with the induction of immediate-early genes that critically activate other late genes in the signal transduction pathway. Damage, repair, and transcription of the c-FOS gene are presented here as examples, because Fos peptide, one of the components of activator protein 1, activates nerve growth factor and repair mechanisms. The results of our studies show that treatments with 7-nitroindazole, a specific inhibitor of nitric oxide synthase known to attenuate nitric oxide, oxidative DNA lesions, and necrosis, increase intact c-fos mRNA levels after stroke. This suggests that the accuracy of gene expression could be accounted for the recovery of cellular function after cerebral injury.
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PMID:Ischemia-reperfusion-related repair deficit after oxidative stress: implications of faulty transcripts in neuronal sensitivity after brain injury. 1256 81


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