BACKGROUND: Clinical and experimental studies have suggested that brain death may cause hemodynamic, electrocardiographic, functional or histopathologic changes of the heart. METHODS: Brain death was induced by increasing intracranial pressure(ICP) abruptly by intermittent bolus injection of saline(model ) or gradually by continuous infusion of saline(model ) to the epidural catheter in 5 mongrel dogs, respectively. Hemodynamic and biochemical changes during the process of brain death and histopathologic changes of the myocardium were analyzed and compared in two brain death models, and the association of apoptosis was also evaluated. RESULTS: 1) Two predominant subsets of acute contraction band lesion were produced in both brain death models : paradiscal and holocystic contraction band lesions. Both contraction band lesions were more prevalent in brain death model . 2) The frequency of both contraction band lesions was lowest in the epicardial layer and highest in the endocardial layer in both models, but no correlation was observed between the degree of contraction band lesions and ICP, LV maximum +dp/dt or catecholamine levels. There was no statistical difference between any of the LV circumferential blocks and either type of contraction band lesion, and transaxial distribution was not also different in both models. 3) There was no remarkable histopathologic changes in the analysis of major epicardial coronary arteries. Apoptotic cells were suggested in the scattered myocytes in the light microscopy and apoptosis was detected by in situ nick end labeling method. Electron microscopy revealed a condensation of nuclear chromatin and convolution of nuclear membrane in those myocytes. CONCLUSIONS: Myocardial changes due to brain were observed frequently, and few apoptotic cells were found in the brain death heart. Studies on the treatment strategy to minimize damages of myocardial structure and function caused by brain death should be followed in the near future.
Animals ; Apoptosis ; Brain Death* ; Brain* ; Catheters ; Chromatin ; Coronary Vessels ; Dogs ; Electrocardiography ; Heart ; Hemodynamics ; In Situ Nick-End Labeling ; Microscopy ; Microscopy, Electron ; Muscle Cells ; Myocardium* ; Nuclear Envelope

BACKGROUND: The cardiac electrophysiological characteristics differ significantly among mammalian species or among various disease processes. However, difficulties in the procedures for harvesting and isolating tissue have precluded studies using human cardiac specimens. METHODS: The outward K+ -currents were recorded in human atrial myocytes isolated from patients undergoing open heart surgery. The electrophysiological characteristics of the voltage-dependent outward currents were investigated using a whole-cell patchclamp technique. RESULTS: Using depolarizing step pulses, the transient outward currents were activated within 10 msec, which slowly inactivated thereafter. After inactivation, the sustained components of the outward currents remained for up to 5.0 seconds of depolarizing step pulses. While the inactivating component was almost completely inactivated at potentials >+30 mV, the non-inactivating component showed only 10-15% inactivation. The non-inactivating component was highly sensitive to 4-AP and was inhibited by >80% at a concentration of 0.2 mM, while the inactivating component was inhibited by only 25%. The delayed rectifier potassium currents were not recorded. The ratios of the amplitudes of the inactivating and non-inactivating components varied. CONCLUSION: Two components of the voltage dependent outward K+ currents in human cardiac tissue were identified, which could be separated according to their kinetic and pharmacologic properties.
Atrial Appendage ; Humans* ; Muscle Cells* ; Patch-Clamp Techniques ; Potassium ; Potassium Channels ; Thoracic Surgery

No abstract available.
Bias (Epidemiology) ; Interpersonal Relations ; Stereotyping

Regular physical activity provides a variety of health benefits, including improvement in cardiopulmonary or metabolic status, reduction of the risk of coronary artery disease or stroke, prevention of cancer, and decrease in total mortality. Exercise-related cardiac events are occasionally reported during highly competitive sports activity or vigorous exercises. However, the risk of sudden death is extremely low during vigorous exercise, and habitual vigorous exercise actually decreases the risk of sudden death during exercise. The cause of sudden death is ischemic in older subjects (> or =35 years old), while cardiomyopathies or genetic ion channel diseases are important underlying pathology in younger (<35 years old) victims. The subgroup of patients who are particularly at higher risk of exercise-related sudden death may be identified in different ways, such as pre-participation history taking, physical examination and/or supplementary cardiac evaluation. Limitations exist because current diagnostic tools are not sufficient to predict a coronary artery plaque with potential risk of disruption and/or an acute thrombotic occlusion. Proper and cost-effective methods for identification of younger subjects with cardiac structural problems or genetic ion channel diseases are still controversial.
Cardiomyopathies ; Coronary Artery Disease ; Coronary Vessels ; Death, Sudden ; Death, Sudden, Cardiac ; Exercise ; Heart ; Humans ; Insurance Benefits ; Ion Channels ; Motor Activity ; Physical Examination ; Sports ; Stroke

Management of cardiac arrhythmias involves antiarrhythmic drugs (AADs), catheter ablation, pacemakers, and implantable defibrillators. The effects of AADs are mediated by blocking various cardiac ion channels, mostly the cardiac sodium, calcium, or potassium channels. A simple classification of AADs based upon the target sites of drug action is useful for clinical application of AADs for common cardiac arrhythmias. Atrioventricular nodal blocking agents are useful for management of tachycardias with the atrioventricular node as a part of the reentrant circuit. Membrane active AADs are used for tachycardias occurring within the atrium or ventricle. Recent large randomized clinical trials have failed to show any beneficial effects of AADs for reducing cardiac mortality in patients with heart failure and at risk of sudden cardiac death or in patients with atrial fibrillation. In spite of these limitations, AAD medication remains an important initial or adjunctive therapy in the management of cardiac arrhythmias.
Anti-Arrhythmia Agents ; Arrhythmias, Cardiac ; Atrial Fibrillation ; Atrioventricular Node ; Calcium ; Catheter Ablation ; Death, Sudden, Cardiac ; Defibrillators, Implantable ; Heart Failure ; Humans ; Ion Channels ; Membranes ; Potassium Channels ; Sodium ; Tachycardia

The aconite root has been used in oriental medicine to improve metabolism of debilitated patient and to cure acute dysuria, cardiac weakness, gout, neuralgias and rheumatism. The crude drug "bu-shi" or "cho-oh", which is obtained from the Aconitum roots, contains the potent poisons aconitine, mesaconitine, jesaconitine, and hypaconitine, which are C
Aconitine ; Aconitum* ; Adult ; Alkaloids ; Animal Experimentation ; Arrhythmias, Cardiac* ; Dizziness ; Dysuria ; Gout ; Hemodynamics ; Humans ; Medicine, East Asian Traditional ; Metabolism ; Nausea ; Neuralgia ; Poisons ; Rheumatic Diseases ; Shock* ; Tachycardia ; Tachycardia, Ventricular ; Torsades de Pointes ; Ventricular Fibrillation ; Vomiting

The hypokalemic periodic paralysis is characterized by intermittent falccid paralysis of extremities with spontaneous recovery. It is rarely accompanied by cardiac arrhythmia, especially fatal ventricular tachycardia or torsades de pointes. We observed a 29 year old man, who had suffered from intermittent periodic paralysis and fatal ventricular tachyarrhythmia. He had the first episode of muscle weakness in his low grade of elementary school, which lasted for 20 -30 hours. Similar episodes of muscle weakness occurred 1 -7 times per year, especially after carbohydrate rich food. On admission to emergency room, his chief complaints were generalized weakness and chest tightness, serum potassium level was 1.6mEq/l, and four extremities showed Grade 0 motor weakness. His electrocardiography(ECG) showed Atrioventricular dissociation due to sinus tachycardia and accelerated junctional rhythm, intraventricular conduction distrubance. During intravenous potassium administration, ECG showed sustained ventricular tachycardia and cardiovascular collapse occurred. So we carried out resuscitation and cardioversion. After resuscitation, he recovered from cardovascular collapse and ECG showed sinus tachycardia. But during continuous monitoring ECG showed torsades de pointes with cardiovascular collapse. We carried out resuscitation and defibrillation repeatedly. Serum potassium level was 1.7 - 1.8mEq/L at that time. After successful resuscitation, ECG showed sinus rhythm, and his mental status was fully recovered. After he admitted to intensive care unit, paralytic attack and cardiac arrhythmia did not occurred any more. Serum potassium level was maintained between 3.9 -6.1lmEq/L during his hospital days. He was fully recovered but could not take any medications(e.g. acetazolamide, potassium supplying agent and antiarrhythmic drugs) due to severe gastrointestinal disturbances. During the 30 months of postdischarge period, he experienced three mild paralysis attacks, but they were not accompanied by chest tightness, palpitation or syncope.
Acetazolamide ; Adult ; Arrhythmias, Cardiac* ; Electric Countershock ; Electrocardiography ; Emergency Service, Hospital ; Extremities ; Heart Block ; Humans ; Hypokalemia ; Hypokalemic Periodic Paralysis* ; Intensive Care Units ; Muscle Weakness ; Paralysis ; Potassium ; Resuscitation ; Syncope ; Tachycardia ; Tachycardia, Sinus ; Tachycardia, Ventricular ; Thorax ; Torsades de Pointes

Mechanical complications of acute myocardial infarction which may lead to heart failure or shock include ruptute of left ventricular free wall, ventricular septum and papillary muscle. The clinical characteristics of these lesions vary conservative management alone has high mortality rate, for which reason surgical repair of these defects are essential. Structural defects including rupture of the left ventricular free wall, ventricular septum, and papillary muscle, accout for 5% to 20% of all deaths from acute myocardial infarction. Among these, ventricular septal defects occur in approximately 1% of all myocardial infarction, and account for up to 2% of deaths subsequent to myocardial infarction. Rupture of the ventricular septum following acute myocardial infarction(AMI) is associated with high mortality rate, as 54% of the patients succumb within two weeks, 87% within two months and 92.5% during the first year. We experienced two cases of postinfarct ventricular septal defects(VSD) which had been repaired within 1 week after AMI due to progressive deterioration of patients` conditions, and were to be reoperated because of repeated septal ruptures in postoperation period and development of cardiogenic shock.
Heart Failure ; Heart Septal Defects, Ventricular ; Humans ; Infarction* ; Mortality ; Myocardial Infarction ; Papillary Muscles ; Rupture ; Shock ; Shock, Cardiogenic ; Ventricular Septum

BACKGROUND AND OBJECTIVES: The mechanism responsible for the generation of ectopic beats in pulmonary veins (PVs) remains to be well defined. The present study examines the electrophysiological characteristics of the PVs and other regions of the canine left atrium (LA) under low dose (300 micrometer) caffeine condition. MATERIALS AND METHODS: Transmembrane action potentials were recorded from the left superior PVs, PV-LA junctions (PLJ, atrium <5 mm from the PV ostium), LA appendage (LAA) or Bachmann's bundle (BB) in arterially perfused canine LA-PV preparations, using floating glass microelectrodes. Rapid atrial pacing (cycle lengths 140-300 ms, 10 sec) was used to induce delayed afterdepolarizations (DAD) at the baseline and under low dose (300 micrometer) caffeine conditions. RESULTS: Spontaneous diastolic depolarization or triggered activity (TA) was not observed in any of the recording area under the baseline condition. DAD and TA were induced by caffeine in 4/8 PVs and in 3/8 PLJs, but in no LAA (0/6) or BB (0/5). These TA and DAD were also observed after termination of pacing-induced atrial tachyarrhythmia. DAD was abolished by pretreatment of the atria with verapamil or propranolol (1.0 micrometer). CONCLUSION: Spontaneous diastolic depolarization was not present in perfused canine left atria or proximal PV. Pulmonary veins and adjacent areas displayed an increased susceptibility to develop DAD-induced TA under low dose caffeine condition. This distinctive electrophysiological property of the PV and PLJ area may contribute to the arrhythmogenic substrate responsible for the ectopic activity that initiates atrial fibrillation.
Action Potentials ; Atrial Fibrillation ; Caffeine ; Calcium ; Glass ; Heart Atria ; Microelectrodes ; Propranolol ; Pulmonary Veins* ; Tachycardia ; Verapamil