Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Catecholamine-induced polymorphic ventricular tachycardia (CPVT), a rare disease that occurs in subjects without obvious organic heart disease, is characterized by episodes of syncope, seizures, or sudden death in response to physiologic or emotional stress. This report reviews evidence that a missense mutation in the CASQ2 gene is associated with autosomal-recessive CPVT.
Trends Cardiovasc Med 2003 May
PMID:A missense mutation in the CASQ2 gene is associated with autosomal-recessive catecholamine-induced polymorphic ventricular tachycardia. 1273 48

Because of its wide range of presentations, its highly variable mode of onset, its numerous causes, and its unpredictable outcome, cerebral venous thrombosis (CVT) remains a diagnostic and therapeutic challenge. Treatment of CVT consists primarily of symptomatic treatment of seizures and intracranial hypertension, antithrombotics, and etiologic treatment whenever possible. Heparin remains the first line of treatment for CVT; although its systematic use remains debated, recent studies have confirmed its safety even in patients with large hemorrhagic infarctions. The addition of local thrombolysis is indicated for patients with clinical worsening related to extension of the venous thrombosis, despite adequate anticoagulation and optimal symptomatic and etiologic treatment. In contrast to arterial stroke, complete recovery of prolonged or severe neurologic deficit is possible, justifying initiation of anticoagulation and eventually thrombolysis, even when the clinical situation seems desperate. New techniques using mechanical devices disrupting the clot may be used in addition to thrombolysis in rare cases. Ventricular drainage is indicated in cases of cerebellar infarction or deep venous thrombosis associated with hydrocephalus. Decompressive craniotomy may be performed acutely in patients with untractable intracranial hypertension and herniation.
Curr Treat Options Cardiovasc Med 2003 Jul
PMID:Cerebral Venous Thrombosis. 1277 96

Syncope is a complex symptom with multiple potential etiologies that can be difficult to establish. The major obstacles to diagnosis are the periodic and unpredictable nature of events and the high spontaneous remission rate. Short-term ECG monitoring often is unproductive when initial noninvasive testing is negative due to the low probability of recurrence during the brief monitoring period. Implantable loop recorders extend the ability to monitor cardiac patients, enhancing the diagnostic yield to as high as 85% in difficult to diagnose syncope. Several recent studies suggest that prolonged monitoring with an implantable loop recorder has a role in patients with syncope and conduction disturbances, negative tilt testing, and unexplained seizures, and may be superior to conventional testing with tilt and electrophysiologic studies.
J Cardiovasc Electrophysiol 2003 Sep
PMID:Use of the implantable loop recorder in evaluation of patients with unexplained syncope. 1295 May 23

A precise balance of ionic currents underlies normal cardiac excitation and relaxation. Disruption of this equilibrium by genetic defects, polymorphisms, therapeutic intervention, and structural abnormalities can cause arrhythmogenic phenotypes leading to syncope, seizures, and sudden cardiac death. Congenital defects result in an unpredictable expression of phenotypes with variable penetrance, even within single families. Additionally, phenotypically opposite and overlapping cardiac arrhythmogenic syndromes can even stem from the same mutation. Accordingly, the relationship between genetic mutations and clinical syndromes is becoming increasingly complex.
Prog Cardiovasc Dis
PMID:Mechanisms of genetic arrhythmias: from DNA to ECG. 1468 43

Tissue-type plasmingen activator (tPA) is a highly specific serine proteinase that activates the zymogen plasminogen to the broad-specificity proteinase plasmin. tPA is found in the blood, where its primary function is as a thrombolytic enzyme, as well as in the central nervous system (CNS), where it promotes events associated with synaptic plasticity and cell death in a number of settings, such as cerebral ischemia and seizures. Neuroserpin is a fully inhibitory serine proteinase inhibitor (serpin) that reacts preferentially with tPA, and is located in regions of the brain where either tPA message or tPA protein are also found, suggesting that neuroserpin is the selective inhibitor of tPA in the CNS. There is a growing body of evidence demonstrating the participation of tPA in a number of physiologic and pathologic events in the CNS, and the role of neuroserpin as the natural regulator of tPA's activity in these processes.
Trends Cardiovasc Med 2004 Jul
PMID:Tissue-type plasminogen activator and neuroserpin: a well-balanced act in the nervous system? 1526 88

The recent developments in the management of spinal cord injury (SCI) have led to a reduction in mortality and in the consequences, resulting from incomplete spinal cord damage in those who survive. In this respect, it is noteworthy that SCI not only results in paraplegia or tetraplegia, but also in systemic, cardiovascular and metabolic alterations secondary to autonomic dysfunction. After SCI there is a decrease in sympathetic discharge and an increase in parasympathetic drive, resulting in profound changes in arterial blood pressure and heart rate. When SCI is induced in experimental animals, an immediate hypotension occurs (acute phase) which has been attributed to an autonomic imbalance involving a predominance of parasympathetic activity. Subsequently, an episodic hypertension may develop (chronic phase) as a part of a condition denominated autonomic dysreflexia. This hypertension is caused by afferent stimulation below the level of injury and can be so severe that sometimes may lead to cerebral haemorrhage, seizures, and death. In the light of the above lines of evidence, experimental SCI may provide an ideal model to study the nature of cardiovascular mechanisms following traumatic injury. Thus, the present review will deal with an update of the possible cardiovascular complications associated to SCI (including spinal shock, autonomic dysreflexia, deep venous thrombosis, and risk for coronary heart disease). This will be discussed within the context of the development of drugs with potential therapeutic usefulness in the acute and chronic stages of SCI.
Curr Med Chem Cardiovasc Hematol Agents 2004 Apr
PMID:Cardiovascular alterations after spinal cord injury: an overview. 1532 Jul 96

This report describes a fatal case of left atrial-esophageal fistula occurring in a 72-year-old man after a radiofrequency catheter ablation of paroxysmal atrial fibrillation. Catheter ablation was performed around the pulmonary vein using an 8-mm-tip electrode (60 W or 55 degrees C) guided by a 25-mm circular catheter. On day 22 of follow-up, the patient presented with seizures followed by hematemesis due to left atrial-esophageal fistula. His clinical condition deteriorated, and he died of speticemia. Thus, left atrial-esophageal fistula is a sever complication of radiofrequency catheter ablation of the left atrial posterior wall.
J Cardiovasc Electrophysiol 2004 Aug
PMID:Left atrial-esophageal fistula following radiofrequency catheter ablation of atrial fibrillation. 1533 97

Preeclampsia has been suggested to be a two-stage disorder of an alteration in placental perfusion (stage 1) leading to generalized vascular endothelial damage (stage 2). Because the mechanism linking the two stages remains unclear, effective primary prevention is still impossible. However, advances made in our understanding of the pathophysiology of preeclampsia have paved the way for secondary and tertiary prevention approaches. Platelets are known to be activated in early pregnancy. They also play a pivotal role in the process of inflammation, as demonstrated by the finding that CD40 ligand is shed from activated platelets to directly initiate inflammation of the vessel wall. According to the Cochrane Library Update summarizing data from over 30,000 women, secondary prevention with antiplatelet drugs is associated with a 19% decrease in the risk of preeclampsia. Additional randomized controlled trials are needed to establish the association between preeclampsia and thrombophilia. The effect of the antithrombotic agent heparin on pregnancy outcome in preeclampsia and its potential preventive action in high-risk patients need to be elucidated. One of the several hypotheses of the pathogenesis of preeclampsia focuses on the oxidative stress caused by the imbalance in prooxidant and antioxidant forces. Preliminary findings on vitamin E and vitamin C supplementation in preeclamptic women are encouraging, and suggest a rationale for larger clinical trials. Although there is currently no explanation for the positive effect of magnesium sulfate on eclamptic seizures, studies have provided enough evidence to encourage its worldwide use as the primary anticonvulsant of choice in the tertiary prevention of maternal and perinatal death in severe preeclampsia/eclampsia. In conclusion, secondary and tertiary prevention of preeclampsia is possible when targeted at reducing maternal and neonatal morbidity and mortality.
Curr Med Chem Cardiovasc Hematol Agents 2005 Jul
PMID:The pharmacologic approach to the prevention of preeclampsia: from antiplatelet, antithrombosis and antioxidant therapy to anticonvulsants. 1597 82

Benign cerebral angiopathy and postpartum cerebral angiopathy are reversible cerebral arterial vasoconstriction syndromes. Presentation includes recurrent severe headaches, altered consciousness, and focal neurologic deficits; ischemic and/or hemorrhagic strokes can occur. No standard management has been established, but most authors agree that 1) acute-phase treatment includes cessation of vasoconstrictors, treatment of associated conditions, vasospasm treatment (calcium channel antagonists), and corticosteroids; 2) other measures include headache relief, blood pressure control, and stroke, cerebral edema, and seizure treatment; 3) definitive diagnosis requires conventional angiography and exclusion of alternative diagnosis; 4) a second arterial examination after 4 to 6 weeks is mandatory to confirm reversibility of vasoconstriction; 5) brain biopsy is indicated to rule out cerebral vasculitis in severe cases with clinical deterioration under steroid treatment or atypical findings; 6) immunosuppression should be reserved for patients with brain-leptomeningeal biopsy-proven vasculitis or used while waiting for a brain biopsy result; and 7) long-term measures include secondary stroke prevention and treatment of complications.
Curr Treat Options Cardiovasc Med 2006 May
PMID:Benign cerebral angiopathy; postpartum cerebral angiopathy: characteristics and treatment. 1663 39

Long QT syndrome (LQTS) can be asymptomatic-identifiable as an incidental finding on electrocardiogram-or it can present with palpitation, syncope, seizures, or sudden cardiac death. LQTS is characterized by a prolonged QT interval, which can be associated with a specific form of polymorphic ventricular tachycardia known as torsade de pointes. Other electrocardiogram changes in LQTS include T-wave abnormalities, particularly bifid T waves, U waves, and T-wave alternans. The precipitating factors of LQTS include electrolyte abnormalities, bradyarrhythmias, medications (such as antiarrhythmic drugs, antibiotics, antipsychotics, and antihistamines), and myocardial ischemia. The authors report a case of LQTS in a 47-year-old woman with no other significant cardiac history.
Rev Cardiovasc Med 2006
PMID:Congenital long QT syndrome. 1709 73


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