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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is sometimes very difficult to diagnose dissecting aortic aneurysms (DAA), particularly in its early stage, due to manifold signs and symptoms. The purpose of this study is to clarify the reasons for such erroneous diagnoses. A total of 41 patients with DAA were referred to our hospitals for further examination and/or surgery from April 1986 to August 1989. In 18 of these patients, the diagnostic possibility of an underlying DAA was overlooked by the referring physicians. Among these 18 patients, 2 were mistakenly diagnosed as uncomplicated myocardial infarction (MI), one as pneumonia, 2 as cerebral infarction, 6 as acute abdominal disease, one as cholelithiasis, 5 as thrombosis of the lower extremities, and one as malignant metastasis to the pericardium. The following is the detail: In 2 cases thought to be uncomplicated MI, an expanding dissecting ascending aorta had crushed the lumen of the left coronary artery, causing MI, in turn, wasting clinical treatment and consuming precious time. In one case, enlargement of the descending aorta on the chest radiography was overlooked and the patient's symptoms were mistakenly attributed to pneumonia. In 2 cases in which symptoms of cerebral ischemia were thought to be attributed to cerebral thrombosis, the real cause turned out to be occlusion of the brachiocephalic artery following aortic dissection. Among 6 cases which were initially considered to have only acute abdominal disease, 3 presented with symptoms and signs of ileus, and their exploratory laparotomies yielded no positive findings.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiol 1992
PMID:[The pitfalls in the clinical diagnosis of dissecting aortic aneurysm]. 133 5

To evaluate the prevalence and prognostic role of silent coronary artery disease (CAD) in patients with symptomatic high-grade carotid stenosis (70 to 99%) undergoing carotid endarterectomy, and with neither history nor symptoms of CAD, 106 patients (76 men, 30 women, mean age 58.7 years [range 42 to 71]) with recent cerebral ischemia were prospectively studied. Patients were stratified as to the presence (n = 27, 25%) or absence (n = 79, 75%) of silent CAD defined by concordant abnormal exercise electrocardiographic testing and thallium-201 myocardial scintigraphy. The male sex, the severity of the symptomatic carotid lesion (greater than 90%), and the coexistence of contralateral carotid disease identified patients with higher probability of coexisting CAD. The 106 patients underwent 121 operations (bilateral in 15). In the perioperative period, no deaths or cardiac events occurred, 1 patient suffered a recurrent stroke and 3 had a transient ischemic attack. During a mean follow-up period of 5.4 years, 9 patients died (1.7%/year): fatal myocardial infarction occurred in 5 (all in the silent CAD group), cancer in 3 and vertebrobasilar stroke in 1. Nonfatal events occurred in 9 patients: myocardial infarction in 1 (without silent CAD), unstable angina in 3 (with silent CAD), and cerebral ischemic attacks in 5. After 7 years, the Kaplan-Meier estimated survival free from coronary events was 51% in patients with silent CAD, and 98% in patients without CAD (p less than 0.01). In conclusion, among patients with symptomatic high-grade carotid stenosis undergoing carotid endarterectomy, even in absence of history or symptoms of CAD, a silent CAD is detectable in one fourth of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1992 May 01
PMID:Frequency and prognostic significance of silent coronary artery disease in patients with cerebral ischemia undergoing carotid endarterectomy. 843 Jun 60

We describe a case of fatal hypoxic-ischemic encephalopathy, leading to brain death following the modified Fontan procedure in a child with asymptomatic subclavian steal syndrome (SSS). This patient's brain death was most likely multifactorial in view of his postoperative course. However, we believe that the presence of the SSS contributed to the abnormal cerebral circulation during surgery and postoperatively, leading to brain death. The presence of SSS in patients undergoing an open-heart procedure may be a risk factor for cerebral ischemia or brain death.
Pediatr Cardiol 1992 Apr
PMID:Asymptomatic subclavian steal syndrome in children following cardiac surgery: a potential hazard with re-operation? 161 13

The prevalence and clinical significance of left atrial (LA) spontaneous echo contrast were investigated in 103 consecutive patients with chronic nonrheumatic atrial fibrillation (AF) using transesophageal echocardiography. LA spontaneous echo contrast was visualized in 25 of 103 patients (24.3%). Age, sex, LA diameter, left ventricular diastolic and systolic dimensions, left ventricular ejection fraction, and the percentage of lone AF were not significantly different between patients with and without LA spontaneous echo contrast; however, those with LA spontaneous echo contrast were less likely to have moderate or severe mitral regurgitation. LA thrombi were observed in 7 patients (6.8%), and all 7 thrombi were found in the atria with spontaneous echo contrast. History of cerebral ischemia or peripheral embolism, or both, was significantly more frequent in patients with than without LA spontaneous echo contrast (84 vs 18%; p less than 0.001). The presence of LA spontaneous echo contrast was highly specific (94%) and predictive for thromboembolic events (positive and negative predictive values of 84 and 82%, respectively). Thus, transesophageal echo-detected LA spontaneous echo contrast is frequently found in patients with chronic nonrheumatic AF. This phenomenon may represent a precursor of thrombus formation, and its presence is associated with an increased thromboembolic risk.
Am J Cardiol 1992 Aug 01
PMID:Clinical implications of left atrial spontaneous echo contrast in nonrheumatic atrial fibrillation. 163 97

The purpose of this study was to determine whether prior transient cerebral ischemia, in conscious mice, would alter the biological responses resulting from excessive activation of N-methyl-D-aspartate (NMDA) receptors, in an early stage. The responses to the activation of NMDA receptors by an intracerebroventricular injection of NMDA, such as wild running, tonic and clonic convulsions, absence of the visual placing reflex, loss of the righting reflex, impaired motor function and a high mortality rate, were to a large extent prevented if 30 min before treatment, either a 10-min period of global cerebral ischemia was induced or a 1 nmol intraventricular injection of NMDA was given but not if either of the above procedures was done one day before the test dose of NMDA. In contrast, behavioral symptoms, in response to activation of non-NMDA-type glutamate receptors elicited by intraventricular injection of either kainic acid or AMPA, were not clearly affected. Transient systemic hypercapnic anoxia (22-sec exposure to 100% CO2 gas), before treatment with NMDA did not significantly reduce the NMDA-induced behavior. The severity of these behavioral responses and high mortality rate observed after intraventricular injection of pentylenetetrazole (PTZ, 30 mumol) were not altered by either prior global ischemic insult or by a preexposure to NMDA given intraventricularly. The NMDA antagonist, MK801 (0.1 and 0.3 mg/kg i.p.) greatly reduced the behavioral effects and mortality rate, resulting from the intraventricular injection of NMDA and somewhat reduced the effects of the intraventricular injection of PTZ.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral ischemia decreases the behavioral effects and mortality rate elicited by activation of NMDA receptors in mice. 183 47

Although indapamide has been used for many years as a first-line treatment of hypertension, it is only recently that some of its activities on the changes of the cardiovascular system, brought on by age and high blood pressure, have been studied. Indapamide appears to reduce blood pressure by a combined diuretic and direct vascular activity reducing vascular reactivity and total peripheral resistance. In addition, it has discrete effects on a number of interrelated systems that may protect the cardiovascular system. Indapamide reduces intracellular calcium levels, maintains magnesium ions, but reduces phosphate ions that may be involved in arterial rigidity. Circulating catecholamines remain unchanged but there is a reduction in normetanephrine, suggesting a reduction in sympathetic tone. It stimulates prostacyclin synthesis, increases levels of circulating prostacyclin, reduces platelet aggregation and stimulates the vasodilation elicited by endothelium-derived relaxing factor in the presence of bradykinin. In addition, it inhibits the formation of the vasoconstrictor prostanoid, thromboxane A2. The free radical scavenging activity of indapamide could also protect the vascular smooth muscle from the reperfusion injury of cerebral and myocardial ischemia. Indapamide induces a reduction in cerebral ischemia after carotid ligation. Unlike some other antihypertensives, it does not upset the high-density/low-density lipoprotein-cholesterol balance, reducing the possible risk of atherosclerosis. Moreover, the combination of binding to elastin and reduction in uptake of calcium and phosphate into the smooth muscle could be a mechanism for reducing arterial rigidity seen in the elderly and hypertensive patient. In hypertensive patients, these properties induce an improvement in arterial compliance, and in the long term a reduction in left ventricular hypertrophy. These pharmacologic and clinical results, together with a good antihypertensive efficacy and acceptability, suggest that indapamide may be a preferential agent in the long-term cardiovascular protection of the hypertensive patient.
Am J Cardiol 1990 May 02
PMID:Cardiovascular protective properties of indapamide. 218 50

Ventricular arrhythmias detected in the late-hospital phase of myocardial infarction have been identified as a risk factor for sudden death, being their prognostic value independent of ventricular function. However, relations between both factors are not clarified. In order to study hypothetic associations between ventricular arrhythmias and some clinical, hemodynamic and angiographic variables, 60 patients (52 males, 8 females) underwent 24-hour Holter recordings and cardiac catheterization with left ventricular and coronary angiographies, 3-5 weeks after hospital admission. Past history data, acute phase complications and hemodynamic and angiographic results were compared between patients with and without significant ventricular arrhythmias during Holter monitoring (10 or more PVC's/hour and/or repetitive forms). No significant differences were found between both groups neither in mean age nor in the incidence of previous angina or infarction, cerebral ischemia, diabetes, lipid disorders or subjective feeling of being under psychological stress. Prior history of arterial hypertension was, however, significantly more frequent in patients with ventricular arrhythmias (53.3% vs 17.8%; p = 0.0183). No differences were observed in the localization of the infarct or in the complications during the acute phase (CPK peak, Killip's score, angina after 24 hours of evolution, intraventricular or A-V conduction disorders and supraventricular and ventricular arrhythmias). Among hemodynamic data, only left ventricular and aortic systolic pressures were different in both groups, being significantly higher in patients with ventricular arrhythmias. There were not differences in left ventricular segmentary contraction and in number of coronary vessels involved. To conclude, significant ventricular arrhythmias were recorded in 25% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Rev Esp Cardiol 1990 May
PMID:[Anatomo-functional substrate of high risk arrhythmia after myocardial infarct]. 239 9

Current research suggests that cerebral ischemia induces a cascade of pathophysiologic reactions. A massive influx of calcium into the neuron constitutes the "final common pathway," resulting in catabolism and cell necrosis due to calcium overload. Treatment with calcium antagonists may offer a means of arresting and possibly preventing the destruction of cerebral tissue in patients with stroke. One such drug, nimodipine, selectively inhibits spasm of isolated cerebral arteries induced by either depolarization or receptor stimulation. In vivo experiments have shown that nimodipine prevents the postischemic impairment of cerebral blood flow that may be a major contributor to neuronal damage. After encouraging although not conclusive results of a single-blind pilot study, a double-blind, placebo-controlled, multicenter clinical investigation of nimodipine was undertaken. Some benefit was strongly suggested in patients with acute ischemic stroke who were treated with 120 mg of nimodipine, begun within 24 hours after the onset of the event, combined with "standard" treatment (i.e., hemodilution using low molecular dextran). Calcium antagonists such as nimodipine may be useful in the treatment of stroke due to acute cerebral ischemia.
Am J Cardiol 1987 Jan 30
PMID:Effect of calcium antagonists on the cerebral circulation. 243 32

Nicardipine has high affinity for the dihydropyridine-binding site and has been shown to inhibit the influx of extracellular calcium through membrane slow channels. The calcium antagonist activity of nicardipine is greater in vascular smooth muscle than in cardiac muscle. Nicardipine has also been shown to possess greater activity in coronary than in peripheral vascular smooth muscle. This in vitro profile accounts for the decreased blood pressure and increased coronary blood flow in animal models in vivo. These pharmacologic properties are the basis for nicardipine's clinical utility in essential hypertension and acute myocardial ischemia. Nicardipine has been shown to be more vascular selective than other calcium antagonists and, therefore, possibly less inclined to produce negative inotropicity. This latter property has been confirmed in human hemodynamic studies. Nicardipine is effective in models of acute myocardial ischemia and hypertension. These results have been confirmed in antianginal and antihypertensive studies in humans. This new calcium antagonist has been shown to limit myocardial infarct size in both dogs and baboons subject to left anterior descending coronary artery ligation and to reduce the extent of ischemia-induced cerebral neuronal death in rats. Other protective effects of nicardipine have been demonstrated in paracetamol overdose in mice, chloroform-induced hepatotoxicity in rats and cerebral ischemia in gerbils and baboons. The mechanism of this cell protection of nicardipine may be related to physicochemical effects.
Am J Cardiol 1987 Jun 30
PMID:Animal pharmacology of nicardipine and its clinical relevance. 244 Feb 94

Acquired calcified aortic stenosis in elderly patients successfully resolved after percutaneous aortic valvuloplasty (PAV) using the antegrade or retrograde method. The effectiveness and complications of these two methods were compared. A 79-year-old man who had acute myocardial infarction and pulmonary emphysema underwent aortic valvuloplasty using Medi-Tech balloons, 15 mm and 20 mm in diameter, via the brachial artery route. This caused a reduction of the peak and mean aortic valve pressure gradients, from 56 to 30 and from 59 to 35 mmHg, respectively and an increase in the valve area from 0.6 to 0.8 cm2. However, cardiac tamponade developed due to penetration of the left ventricular wall by the guide wire. A 73-year-old man who had transient cerebral ischemia and pulmonary emphysema underwent valvuloplasty by the Inoue's balloon technique (inflated up to 19 mm) via the saphenous vein. This resulted in a reduction of the peak and mean pressure gradients from 35 to 15 and from 39 to 15 mmHg respectively, a month thereafter. There were no complications. To our knowledge, these are the first two reported cases of acquired aortic stenosis which were relieved by percutaneous aortic valvuloplasty in Japan.
J Cardiol 1989 Jun
PMID:[Percutaneous aortic valvuloplasty in the aged using the antegrade or retrograde method: a report of two cases]. 263 37


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