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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ruptured aortic arch aneurysm with cardiac tamponade is rare and has severely high mortality. We report a case of ruptured aortic arch aneurysm with cardiac tamponade. A 66-year-old man who had syncope attack was transferred to city hospital. Brain computed tomography (CT) showed no significant lesion and he admitted to our hospital for suspecting of aortic dissection. Chest CT showed ruptured aortic arch aneurysm and pericardial effusion. Emergent operation was done on the same day. It was found that the hematoma beneath the tunica adventitia existed at the distal arch and extended to the ascending aorta. Cardiac tamponade was caused by rupture of subadventitial hematoma in pericardial space. Aortic arch replacement was performed using selective cerebral perfusion under deep hypothermia. Postoperatively, he had no cerebral complication and was discharged uneventfully.
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PMID:[Ruptured aortic arch aneurysm with hemorrhagic cardiac tamponade; report of a case]. 1279 57

We present an unusual case of a young Thai immigrant, symptomatic, who had suffered prior episodes of syncope with strong family background: male, first-degree relatives, younger than 45 years old who had died suddenly. The rest ECG, with the patient asymptomatic at the time, showed persistent ST-segment elevation, in inferior leads and "mirror" image in the anterior wall, which were not modified with sublingual nitrates, in absence of demonstrable structural heart disease by chest X-rays and echocardiogram, hypothermia, ischemia, or electrolytic disorders. Holter monitoring revealed at dawn, a short episode of polymorphic ventricular tachycardia of short onset extrasystole coupling, which evolved into asystole and sudden cardiac death. We believe this is a sudden unexplained death syndrome, although we did not have a chance to conduct a genetic study.
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PMID:Brugada syndrome with atypical ECG: downsloping ST-segment elevation in inferior leads. 1512 75

Exposure to stressors that elicit fear and feelings of hopelessness can cause severe vagal activation leading to bradycardia, syncope, and sudden death. These phenomena though documented, are difficult to diagnose, treat clinically, and prevent. Therefore, an animal model incorporating these cardiovascular conditions could be useful. The present study examined 'sinking' during a 2-h swim stress, a phenomenon that occurs in 50% of rats during 25 degrees C water exposure. Concurrent measurements of body temperature, immobility, heart rate (HR), and PR interval (a measure of vagal activity) were made. Neither decreases in immobility nor variations in hypothermia during swim were correlated with sinking. Bradycardia was more severe in sinking rats (average minimum HR+/-SEM; 143+/-13 vs 247+/-14; p<0.01), and PR interval was elevated (p<0.0001). To examine potential modulation of vagal activity during stress, corticotropin-relasing factor (CRF) receptor antagonists (antalarmin, R121919 and astressin B), a glucocorticoid receptor antagonist (RU486), and a peripherally acting cholinergic antagonist (methylatropine nitrate) were administered. The centrally acting CRF antagonist, antalarmin (32 mg/kg), produced elongation of the PR interval (p<0.0001), robust bradycardia (135+/-18; p<0.001), and increased sinking (92%; p<0.05), and methylatropine nitrate (3.2 mg/kg) blocked these effects. Corroborating these data, two different CRF antagonists, R121919 (30 mg/kg) and astressin B (intracerebroventricular (i.c.v.), 0.03 mug/rat) increased sinking to 100%. RU486 (20 mg/kg) blocked HPA axis negative feedback and decreased percent sinking to 25%. From these studies, we concluded that sinking during a 2-h water exposure was a result of extreme vagal hyperactivity. Furthermore, stress-induced CRF release may serve to protect against elevated cardiac vagal activity.
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PMID:Facilitation of cardiac vagal activity by CRF-R1 antagonists during swim stress in rats. 1671 Mar 22

Dopamine beta-hydroxylase (DbetaH) deficiency is a very rare form of primary autonomic failure characterized by a complete absence of noradrenaline and adrenaline in plasma together with increased dopamine plasma levels. The prevalence of DbetaH deficiency is unknown. Only a limited number of cases with this disease have been reported. DbetaH deficiency is mainly characterized by cardiovascular disorders and severe orthostatic hypotension. First symptoms often start during a complicated perinatal period with hypotension, muscle hypotonia, hypothermia and hypoglycemia. Children with DbetaH deficiency exhibit reduced ability to exercise because of blood pressure inadaptation with exertion and syncope. Symptoms usually worsen progressively during late adolescence and early adulthood with severe orthostatic hypotension, eyelid ptosis, nasal stuffiness and sexual disorders. Limitation in standing tolerance, limited ability to exercise and traumatic morbidity related to falls and syncope may represent later evolution. The syndrome is caused by heterogeneous molecular alterations of the DBH gene and is inherited in an autosomal recessive manner. Restoration of plasma noradrenaline to the normal range can be achieved by therapy with the synthetic precursor of noradrenaline, L-threo-dihydroxyphenylserine (DOPS). Oral administration of 100 to 500 mg DOPS, twice or three times daily, increases blood pressure and reverses the orthostatic intolerance.
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PMID:Dopamine beta-hydroxylase deficiency. 1672 95

Patients with acute alcohol intoxication often present with pathological electrocardiographic (ECG) changes. The changes are more frequent and prognostically more significant in chronic alcoholics, in patients with ischaemic heart disease (IHD), in alcohol cardiomyopathy or another organic heart disease, but they can also occur in young and healthy individuals. The typical ECG changes in inebriety are disturbances of heart rate having the nature of electric impulse generation disorder or of impulse conduction pathology. In persons without clinical evidence of heart disease, they are classified as 'holiday heart syndrome'. The most frequent tachyarrhythmia is atrial fibrillation; less frequent but prognostically much more significant is torsades de pointes (TdP) polymorphous ventricular tachycardia. Among bradyarrhythmias, the most significant is alcohol-induced sinus bradycardia which may be manifested by recurrent syncope. The higher the blood alcohol concentration, the higher the occurrence of a significant extension of ECG intervals with possible manifestation of latent conduction disturbance or even sudden cardiac death. Apart from heart rate disturbances, ECG picture very often shows non-specific repolarisation changes. Ischaemia, which is mostly asymptomatic in the form of silent myocardial ischaemia, is worsened in alcohol-intoxicated IHD patients. The resulting ECG may be to a large extent influenced by states which often associate with inebriety, such as hypothermia, hypoglycaemia or electrolyte imbalance. ECG changes similar to those due to acute alcohol intoxication are also present in acute abstinence syndrome, especially in delirium tremens. There is convincing evidence that not only chronic alcoholism, but also single episodes of excessive alcohol consumption are associated with increased cardiovascular mortality.
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PMID:[ECG changes in alcoholic intoxication]. 1863 Jun 9

Melatonin, a major photoperiod-dependent hormone, regulates circadian rhythms and biological rhythms and acts as a prominent sleep promoter. Symptoms related to hypermelatoninemia have been reported in individuals supplemented with melatonin. However, spontaneous endogenous hypermelatoninemia has not been reported previously. A 6-year-old girl previously diagnosed with Shapiro's syndrome was admitted to our hospital on several occasions during a 1-year period with complaints of altered consciousness, syncope, hypothermia and episodes of sweating. The episodes occurred daily and during sleep and lasted for 1-6 h. During these episodes, she sweated profusely and felt faint and her skin was pale and cool. Other complaints included recurrent abdominal pain, urge incontinence and myopia. She was shown to have hypermelatoninemia (>1,000 pg/ml, normal range 0-150 pg/ml) during these episodes. The duration of her attacks decreased with phototherapy and she was successfully treated with propranolol. To our knowledge, this is the first case of hypermelatoninemia without any detectable organic pathology. We did not determine the exact mechanism of hypermelatoninemia in this patient; however, it might have been related to irregular control of pinealocytes by the suprachiasmatic nucleus or related pathways. Hypermelatoninemia should be considered in patients with spontaneous periodic hypothermia and hyperhidrosis, and also in patients with Shapiro's syndrome.
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PMID:Spontaneous endogenous hypermelatoninemia: a new disease? 2104 95

When an ECG shows (or is suspicious for) a Brugada pattern, i.e., the association of a positive terminal deflection and ST segment elevation in the right precordial leads, the cardiologist often faces several problems. Three important questions are raised by this ECG pattern: (1) is this really a Brugada ECG pattern? (2) How can be determined whether this patient is at risk for sudden death? and (3) Should this patient receive an implantable cardioverter-defibrillator (ICD)? The term "Brugada syndrome" should be restricted to patients who have diagnostic ECG changes, as well as a history of symptoms. Asymptomatic subjects, in contrast, should be categorized as having a "Brugada ECG pattern" rather than the syndrome. Diagnostic ECG (type 1) is characterized by a J wave (a terminal positive wave) whose amplitude is > or =2 mm, and a "coved" type ST segment elevation located in the right precordial leads. These signs are usually present in leads V1 and/or V2 (lead V3 is more rarely involved, and is never the only affected one), but occasionally also can be observed in some of the limb leads. Types 2 and 3 ECGs, which are not truly diagnostic of Brugada pattern, are characterized by a "saddle back" ST segment elevation, that is > or =1 mm in type 2 and <1 mm in type 3. In Brugada ECG pattern, the QRS complex characteristically shows a positive terminal deflection that mimics an r' prime wave (the wave occurring in right bundle branch block), in the right precordial leads. Actually, it is a J wave that is very similar to the "Osborn" one observed during hypothermia. The J wave of Brugada ECG pattern is generated by a voltage gradient across the myocardial wall of the right ventricular outflow tract. This abnormal potential can be recorded only by electrodes located very close to the site where that phenomenon is originating. Displacement of the right precordial leads electrodes one or two intercostal spaces above their normal positions may, at times, disclose the diagnostic pattern when conventional leads, recorded at the fourth intercostal space, are non-diagnostic or even normal. High right precordial leads should be recorded whenever standard V1-V3 leads raise the suspicion of Brugada pattern. For example, when a relatively large positive terminal wave, even of low amplitude, is recorded, placing high right precordial leads is an option that should be considered. The ECG may show a marked variation over time, ranging from the typical pattern to a completely normal ECG and back again. In subjects with a non-diagnostic ECG, a pharmacological test with sodium channel blockers may disclose the typical Brugada pattern. In order to establish the diagnosis, several conditions that can mimic Brugada pattern must be excluded. These include right bundle branch block, early repolarization, acute myocardial ischemia, pericarditis, hypercalcemia, hyperkalemia, hypothermia and primary right ventricular diseases, particularly arrhythmogenic right ventricular dysplasia. Some drugs (e.g., some antiarrhythmic drugs, psychotropic agents or antihistamines), hyperthermia and enhanced vagal tone, as it occurs after a full meal, may render Brugada pattern more evident on the ECG. Typical ventricular arrhythmia in Brugada syndrome is a polymorphic ventricular tachycardia, that can evolve into ventricular fibrillation; its mechanism is assumed to be phase 2 reentry. Monomorphic ventricular tachycardia is rarely seen. Atrial fibrillation occurs more frequently in patients with the Brugada ECG pattern than in the general population. A mutation in the SCN5A gene, which encodes the alpha subunit of the cardiac sodium channel, is found in about 20% of the subjects with Brugada pattern; mutations in other genes have less frequently been described. Genetic testing is not very helpful in formulating the diagnosis, but when a mutation is found it could be useful to extend testing to first degree relatives, enabling early detection of abnormal gene carriers. Patients who have experienced an aborted sudden death have a high risk of recurrence and should receive an ICD. A history of syncope, spontaneous type 1 ECG and male sex, not family history of sudden death, are independent risk factors. The role of programmed ventricular stimulation in risk stratification remains the subject of debate. Asymptomatic patients with a Brugada ECG pattern should: (1) receive adequate information on current knowledge concerning this topic, (2) be given the list of forbidden drugs, (3) be informed to promptly treat hyperthermia, (4) be informed that clinical evaluation should be extended to their first degree relatives, 5) undergo regular cardiology follow-up. Also in this group the role of programmed ventricular stimulation in risk stratification is debated. Subjects showing a Brugada pattern after a pharmacological challenge should be followed-up with ECG and 12-lead Holter monitoring, if available, to identify the appearance of spontaneous type 1 ECG. Symptoms should be promptly reported.
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PMID:[Doubts of the cardiologist regarding an electrocardiogram presenting QRS V1-V2 complexes with positive terminal wave and ST segment elevation. Consensus Conference promoted by the Italian Cardiology Society]. 2156 Apr 82

Early repolarization (ER) pattern has been recognized for several decades and was interpreted as a variant of the normal electrocardiogram (ECG) as it was frequently observed in young healthy subjects or athletes. It is characterized by a J point elevation and ST-segment elevation inscribed as a QRS slurring or a notch of the S wave in the inferior leads or/and the lateral leads. The ER pattern has been the subject of increased interest since the report of its higher prevalence in subjects resuscitated from cardiac arrest related to idiopathic ventricular fibrillation (VF). Furthermore, population-based studies showed in healthy young adults that ER pattern was associated with an increased cardiovascular mortality and total mortality. A relationship between ER pattern and malignant arrhythmias is also supported by the experimental work of Antzelevitch et al. which provided the cellular and ionic basis for the J point elevation and its arrhythmogenic potential. The ER pattern may coexist with a number of cardiac or extracardiac conditions such as hypothermia. But this review will focus attention on the "isolated ER pattern" in healthy individuals. Antzelevitch and Yan proposed because of a number of similarities between the "ER syndrome" and the Brugada syndrome to group both syndromes under the heading of "J wave syndromes". The management of ER syndrome (associated with idiopathic VF) is clearly the insertion of an implantable cardioverter defibrillator (ICD). The ER pattern associated with symptoms such as syncope or a familial history of sudden cardiac death requires a complete work-up. Caution should be raised not to generate anxiety in the subject with asymptomatic "isolated ER pattern" as the odds of developing malignant ventricular arrhythmias or to suffer sudden death in this case are extremely low.
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PMID:ECG repolarization syndrome abnormalities (J wave syndromes) and idiopathic ventricular fibrillation: diagnostic and management. 2183 14

Anomalous origin of the coronary artery from the opposite sinus of Valsalva and a course of that artery between the ascending aorta and the pulmonary artery is a rare congenital anomaly. It can cause myocardial ischemia, syncope, and sudden cardiac death in young people. Herein, we report the case of a 24-year-old man who was brought to our hospital after cardiac arrest due to ventricular fibrillation. Emergent coronary angiography revealed that the left coronary artery was normal; however, the right coronary artery originated at the left sinus of Valsalva. After admission, the patient was treated with mild therapeutic hypothermia for 48 hours and had a favorable neurologic recovery. Subsequent 16-slice multidetector computed tomography revealed that the right coronary artery arose from the left main coronary artery, took an intramural course, and was severely compressed between the ascending aorta and the pulmonary artery. The patient underwent direct implantation of the anomalous artery into the correct aortic sinus. Histologic specimens from the proximal end of the right coronary artery showed an intramural segment with intimal fibrous thickening, fragmentation and random arrangement of the elastic fiber, degeneration of the medial smooth-muscle cells, and an increase in the medial stromal substance. Postoperatively, repeat coronary angiography with provocation testing for coronary spasm revealed no myocardial ischemic change. The patient recovered uneventfully. We found that cardiac multidetector computed tomography was useful in evaluating the cause of the sudden cardiac arrest, identifying the anomalous coronary artery, and helping to guide the surgical decisions.
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PMID:Sudden cardiac arrest: associated with anomalous origin of the right coronary artery from the left main coronary artery. 2216 30

Herein, we report the findings of 2 forensic autopsy cases, in which unexpected pituitary lesions were the underlying cause of death. Case 1: A 56-year-old woman was found dead at her home during a cold winter spell. Macroscopic autopsy findings included a difference in the color of blood that filled her left and right cardiac chambers (deep red and dark red, respectively), collapse of both lungs, atrophy of the thyroid gland, and a large tumor arising from the sella turcica. Microscopic examination revealed a pituitary adenoma along with extensive bleeding. The cause of death was considered to be hypothermia, resulting from dysregulation of thermogenesis due to the pituitary adenoma. Case 2: An 86-year-old man with a history of pollakiuria was found dead in a bathtub, with his face and chest submerged in bathwater and his legs positioned outside the bathtub. The macroscopic findings of the autopsy included hyper-inflated lungs, fluid collection in the thoracic cavity, and aspiration of gastric contents in the bronchi. The atherosclerotic changes of the man's coronary and cerebral arteries were considered mild for his age. Microscopic examination showed a marked infiltration of lymphocytes and plasma cells in the posterior pituitary gland, as well as in the liver, pancreas, and submandibular gland. Considering the results of the autopsy and the findings from the investigation conducted at the death scene, we concluded that the man probably lost consciousness following a neurally mediated syncope, which was induced by diabetes insipidus (lymphocytic hypophysitis). After losing consciousness, the man likely fell in the filled bathtub and then drowned. These 2 cases highlight the need for a thorough post-mortem investigation, including a microscopic examination of the pituitary gland. In addition, forensic pathologists should carefully study the pituitary gland in cases where the cause of death is thought to be related to dysfunction of thermoregulation or osmoregulation.
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PMID:Two forensic autopsy cases of death from unexpected lesions of the pituitary gland. 2426 73


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