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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A review of cerebral phlebothrombosis using material from the pathology departments of the National Institute of Cardiology and the General Hospital in Mexico City is presented. The most frequent causes found were: post partum. Secondary to congenital heart disease and associated with infections. In both institutions the most frequent anatomical find was thrombosis of the superior longitudinal sinus. Isolated venous thrombi in the brain probably takes place more frequently than reported. Hemorrhagic necrosis in brain tissue is the most frequent microscopic finding, associated in variable degrees with edema and anoxic encephalopathy. A description of clinical and angiographic findings is presented.
Arch Inst Cardiol Mex
PMID:[Cerebral venous thrombosis]. 66 32

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

A patent ductus venosus has been reported on only two previous occasions. Both involved adults who presented with recurrent bouts of encephalopathy. We present the case of an infant with complex congenital heart disease and multiple other abnormalities, in whom a patent ductus venosus was an incidental finding at necropsy. The etiology of this condition and the options for management are discussed.
Pediatr Cardiol 1991 Jul
PMID:Patent ductus venosus. 187 19

To determine whether the presence or absence of left ventricular (LV) intracavitary microbubbles during cardiac surgery predicts neurologic sequelae, 82 patients undergoing cardiac surgery were studied using transesophageal 2-dimensional (2-D) echocardiography. Cross-sectional images were recorded just before and immediately after cardiopulmonary bypass and stop frames were reviewed for the presence of microbubbles, rated as: 0 = absent, 1 = fewer than 5/frame, 2 = 10 to 25/frame, 3 = too numerous to count. Microbubbles were detected after cardiopulmonary bypass in 34 patients (41%) and found more often in valvular or other intracardiac manipulations than in coronary revascularization, 30 of 40 vs 4 of 42, respectively (p less than 0.001). When grade 2 or 3 microbubbles were identified (22 of 34 patients), mechanical attempts to eradicate them were not successful. Postoperative follow-up in all patients revealed no new focal neurologic deficits. Prolonged encephalopathy (confusional state more than 72 hours) occurred in 4 of 48 patients with no detectable microbubbles and in 3 of 34 patients with microbubbles (difference not significant). Thus, intracavitary left ventricular microbubbles are often detected during cardiac operations, particularly during valve replacement, but are not predictive of postoperative neurologic complications. This is true even if microbubbles are densely concentrated; attempts to eradicate microbubbles are unsuccessful and may be unnecessary.
Am J Cardiol 1985 Nov 01
PMID:Value of intraoperative left ventricular microbubbles detected by transesophageal two-dimensional echocardiography in predicting neurologic outcome after cardiac operations. 406

We describe a case of a 34-year-old male patient first hospitalized in February '93 for stroke (concomitant dilated-hypertrophic cardiomyopathy was noted), and then in April '93 for congestive heart failure. The presence of myopathy, encephalopathy, lactic acidosis and stroke episode allows for the diagnosis of MELAS syndrome, proven by a specific point mutation in mitochondrial DNA. In this case we were able to observe not only the electrocardiographic and echocardiographic features of hypertrophic cardiomyopathy, previously described in mitochondrial encephalomyopathies, but we were also able to monitor the rapid evolution of this cardiomyopathy towards the hypokinetic dilated form with severe impairment of systolic function; this transition was due to changes in the heart anatomy and structure with reduction in the left ventricular (LV) wall thickness and dilatation of all chambers. The remodeling of LV geometry seems to be not definite and capable of dynamic evolution, as suggested by clinical and echocardiographic findings evaluated six months after the hospitalization. In this patient, we obtained a mid-term favourable clinical outcome using inotropic drugs and Ubiquinone (coenzyme Q), an intermediate substrate of the energetic metabolism, which seems to be poorly synthetized because of the early enzymatic defects in the mitochondrial respiratory chain.
G Ital Cardiol 1995 Jan
PMID:[The MELAS syndrome and dilated-hypertrophic cardiomyopathy: a case report]. 764 13

Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) are known to be associated with cardiomyopathy. Systolic and diastolic left ventricular functions were assessed by M-mode and Doppler echocardiography in four patients with MELAS and in 14 normal controls. The interventricular septal thickness and left ventricular posterior wall thickness were greater (11.0 +/- 1.6 mm vs. 5.8 +/- 0.7 mm and 11.0 +/- 2.2 mm vs. 5.9 +/- 0.8 mm) in patients with MELAS than in a control group. Parameters of systolic left ventricular functions (ejection fraction, shortening fraction, systolic time intervals, and mean Vcf) and left ventricular dimensions were not significantly different between the two groups. To assess the diastolic function, blood flow velocity across the mitral valve was measured by Doppler echocardiography and various indexes were obtained. In patients with MELAS, the impairment of diastolic left ventricular filling was demonstrated by decrease in the following indexes: peak flow velocity in the early passive filling period (E) (0.76 +/- 0.10 m/s vs. 0.94 +/- 0.09 m/s), integrated velocity for total E (10.2 +/- 1.3 vs. 13.0 +/- 0.9), the ratio of E and late atrial filling integrated velocities (1.72 +/- 0.06 vs. 2.49 +/- 0.29).
Pediatr Cardiol 1993 Jul
PMID:Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) decrease in diastolic left ventricular function assessed by echocardiography. 841 19

In the present article the authors describe a case of a twenty-one year-old patient with a mitochondrial encephalomyopathy presenting cardiac changes. Mitochondrial encephalomyopathy a multisystemic disease is described in various publications having cardiac involvement although there are sparse references about cardiomyopathy in this same disease. In the present case, the patient had a syndrome of both Mitochondrial Encephalopathy, Lactic Acidosis and Stroke like episodes (MELAS) and Myoclonic Epilepsy and Ragged Red Fibers (MERRF). There were no significant changes in the cardiac conductivity studied by ECG but an echocardiographic pattern of hypertrophic cardiomyopathy was found.
Rev Port Cardiol 1993 Mar
PMID:[Cardiac changes in a case of mitochondrial encephalomyopathy]. 851 18

The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Study is a randomized evaluation of treatment of atrial fibrillation by 1 of 2 strategies: ventricular rate control and anticoagulation versus rhythm control and anticoagulation. The primary end point is total mortality, analyzed by intention-to-treat. Secondary end points are composite end points (total mortality, disabling intracranial bleed [subdural and/or subarachnoid hemorrhage], stroke [embolus, thrombosis, hemorrhage], disabling anoxic encephalopathy, cardiac arrest, major noncentral nervous system bleed), cost of therapy, and quality of life. AFFIRM will randomize therapy and follow 5,300 patients for an average of 3.5 years (minimum 2 years) at 200 sites in the United States and Canada.
Am J Cardiol 1997 May 01
PMID:Atrial fibrillation follow-up investigation of rhythm management -- the AFFIRM study design. The Planning and Steering Committees of the AFFIRM study for the NHLBI AFFIRM investigators. 916 85

We reviewed the timing and mechanism of death in 1,184 consecutive patients with acute myocardial infarction (AMI) treated with primary angioplasty from 1984 to 1995. Of 98 deaths, 48 (49%) occurred early on day 0 or 1. The mechanisms of death were pump failure in 60 patients (61%), reinfarction in 7 patients (7.1%), left ventricular rupture in 5 patients (5.1%), arrhythmia in 3 patients (3.1%), other cardiac causes in 5 patients (5.1%), stroke in 6 patients (6.1%), anoxic encephalopathy in 7 patients (7.1%), and procedure-related deaths in 5 patients (5.1%). The strongest predictors of mortality were cardiogenic shock and unsuccessful reperfusion. Our data indicate that mortality after primary angioplasty, like thrombolytic therapy, is highest in the early hours and is usually due to pump failure. In contrast to thrombolytic therapy, the incidence of death from myocardial rupture and bleeding complications is low. Future treatment strategies will need to focus on the large number of patients with early death due to pump failure, especially patients with cardiogenic shock.
Am J Cardiol 1997 Jun 15
PMID:Timing and mechanism of death determined clinically after primary angioplasty for acute myocardial infarction. 920 45

Visual interpretation of iodine-123-beta-15-(p-iodophenyl)-3(R,S)-methyl-pentadecanoic acid (123I-BMIPP) myocardial images cannot easily detect mild reduction in tracer uptake. Objective assessment of myocardial 123I-BMIPP maldistributions at rest was attempted using a bull's-eye map and its normal data file for detecting myocardial damage in patients with mitochondrial encephalomyopathy. Six patients, two with Kearns-Sayre syndrome and four with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), and 10 normal subjects were studied. Fractional myocardial uptake of 123I-BMIPP was also measured by dynamic static imaging to assess the global myocardial free fatty acid. These data were compared with the cardiothoracic ratio measured by chest radiography and left ventricular ejection fraction assessed by echocardiography. Abnormal cardiothoracic ratio and lower ejection fraction were detected in only one patient with Kearns-Sayre syndrome. Abnormal fractional myocardial uptake was detected in two patients (1.61%, 1.91%), whereas abnormal regional 123I-BMIPP uptake assessed by the bull's-eye map was detected in five patients (83%). All patients showed abnormal uptake in the anterior portion, and one showed progressive atrioventricular conduction abnormality and systolic dysfunction with extended 123I-BMIPP abnormal uptake. The results suggest that assessment based on the normal data file in a bull's-eye polar map is clinically useful for detection of myocardial damage in patients with mitochondrial encephalomyopathy.
J Cardiol 1998 Jan
PMID:[Clinical usefulness of myocardial iodine-123-15-(p-iodophenyl)-3(R,S)-methyl-pentadecanoic acid distribution abnormality in patients with mitochondrial encephalomyopathy based on normal data file in bull's-eye polar map]. 948 45


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