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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Activation of the sympathetic nervous system is an important factor in the genesis of ventricular arrhythmias in patients with impaired ventricular function. Such patients have an appropriate substrate that is capable of generating rhythm abnormalities, which may be related to enhanced automaticity, triggered automaticity, and reentrant mechanisms; all three mechanisms are markedly potentiated by the action of catecholamines. Additionally, the sympathetic nervous system can provoke the development of hypokalemia and ischemia (which can independently lead to the occurrence of rhythm disturbances), and catecholamines may negate the beneficial electrophysiological actions of antiarrhythmic drugs. A substantial amount of experimental data implicates the sympathetic nervous system as a potent stimulus for ventricular tachyarrhythmias and sudden cardiac death, especially in the setting of myocardial ischemia. Two important mechanisms that have been identified include 1) enhanced sympathetic outflow from the central nervous system and 2) nonuniform myocardial denervation resulting in beta-receptor up-regulation and catecholamine hypersensitivity in the infarct zone. Disruption of sympathetic neural innervation of the heart and the use of beta-blocking agents may reduce the occurrence of sudden death and improve survival in animal models of arrhythmias and in some subsets of patients, including those with the long QT syndrome, a recent myocardial infarction, and perhaps those with a cardiomyopathy. The mechanism of this beneficial effect remains to be defined.
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PMID:Role of the sympathetic nervous system in the genesis of ventricular arrhythmia. 1461 4

Beta-adrenoreceptor blocking agents have been used to relieve symptoms mainly in patients with ischemic heart disease. Prophylactic use of beta blockade in patients after acute myocardial infarction has shown a reduction in total mortality and also in sudden death. The overall total mortality reduction amounts to about 30%, whereas the reduction in the sudden death rate is 50%. The mechanisms behind this reduction in sudden death are probably manifold. Antiarrhythmic effects in ischemic myocardium, prevention of new ischemia, and also perhaps other factors may play a role. Apart from the prevention effect in chronic ischemic heart disease, beta blockers have also been able to reduce the sudden death rate in the long QT syndrome and are suggested for use in congestive cardiomyopathy.
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PMID:Prevention of sudden death by beta-blockade. 198 82

Nonsustained ventricular tachycardia, although usually asymptomatic, is associated with a high risk of sudden cardiac death in patients with depressed left ventricular function. To test the vulnerability of such patients to symptomatic and potentially life-threatening arrhythmias, complete electrophysiologic studies were performed in 58 patients with clinically documented nonsustained ventricular tachycardia (greater than or equal to three complexes but less than 15 seconds of self-terminating ventricular tachycardia by 24 hour ambulatory electrocardiographic [Holter] or telemetric monitoring) and abnormal left ventricular function (ejection fraction less than 50% by radionuclide angiography). All patients had nonsustained ventricular tachycardia in the absence of antiarrhythmic drugs, acute ischemia, long QT syndrome, recent infarction or electrolyte abnormalities. The stimulation protocol for each patient included the introduction of single, double and triple ventricular extrastimuli at three cycle lengths (sinus, 600 and 450 ms) and two right ventricular sites (apex and outflow tract). A sustained ventricular tachyarrhythmia was induced in 23 patients (40%) and a nonsustained ventricular tachycardia in 14 patients (24%). Induction of sustained tachycardia correlated with the presence of akinesia or aneurysm, or both, by radionuclide angiography, but not with ejection fraction or presence or absence of coronary artery disease. These results indicate that: 1) patients with clinical nonsustained ventricular tachycardia and chronic left ventricular dysfunction have a high incidence of inducible sustained ventricular tachycardia or ventricular fibrillation; and 2) electrophysiologic testing may allow further substratification of risk of sudden cardiac death in high risk patients with nonsustained ventricular tachycardia.
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PMID:Electrophysiologic testing in patients at high risk for sudden cardiac death. I. Nonsustained ventricular tachycardia and abnormal ventricular function. 400 86

With rapid advances occurring in both basic and clinical electrophysiology, the gap between the two disciplines appears to be widening rather than narrowing. In most instances, we cannot apply the knowledge derived from cellular studies directly to clinical practice. Monophasic action potential (MAP) recording by contact electrode technique allows us to measure basic electrophysiological phenomena in the human heart and thus provides an important bridge between basic and clinical electrophysiology. MAP recordings produce the time course of cellular repolarization during cycle length changes and antiarrhythmic drug administration, lending insights into use dependency and reverse use dependency of antiarrhythmic drug effects in the clinical electrophysiology laboratory. The ability to deliver electrical stimuli at the MAP recording site further allows one to investigate drug-induced postrepolarization refractoriness. MAP recordings provide precise local activation times, important for mapping of abnormal ventricular activation, and detect areas of abnormal repolarization due to ischemia or scarring. MAP recordings are uniquely suited to detect early and delayed afterdepolarizations in the human heart, thereby helping to unravel the arrhythmia mechanisms in the long QT syndrome. By embedding the MAP electrode in a radiofrequency electrode, arrhythmogenic foci may be both detected and ablated. In many instances, MAP recordings are more accurate than ECG tracings in defining and distinguishing ventricular fibrillation and ventricular tachycardia. This can be of clinical importance during testing of the implantable cardioverter/defibrillator. An area of growing interest is stretch-activated arrhythmias. Here, MAP recordings are of particular value because no other method is available to record mechanically induced electrophysiological changes in the vigorously beating heart. It can be expected that MAP recordings will, in the future, provide this important bridge between "cell and bedside" also in atrial tachyarrhythmias, such as in atrial fibrillation and flutter.
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PMID:Bridging the gap between basic and clinical electrophysiology: what can be learned from monophasic action potential recordings? 780 22

Sinus nodes of five symptomatic patients with the long QT syndrome were surgically excised and followed by permanent electronic pacing as part of a new surgical treatment. We examined those sinus nodes by light and electron microscopy with tissue that was promptly fixed at the time of surgery. All five sinus nodes were similarly abnormal. By light microscopy we found distinctive focal fibrosis, some degenerating myocytes and neural elements, and numerous narrowed small vessels. Except in the nerves there was no evidence of inflammation. In electron micrographs the mitochondria within nodal myocytes were abnormally abundant, remarkably pleomorphic, and smaller than those in normal human sinus nodal cells. The ultrastructural features of the degenerated nodal cells were typical of apoptosis, characterized by the absence of inflammation, well-preserved mitochondria, the presence of apoptotic bodies, phagocytosis of these cells by neighboring myocytes, and especially in smooth muscle cells of arterioles, nuclear chromatin margination and nucleolar disintegration. Apoptotic degeneration of nodal myocytes was stochastic, with adjacent cells appearing unaffected. Focal ischemia caused by narrowed vessels may be a contributory factor, and the nerves may harbor some viral infection, but for the nodal myocytes the abnormality appears to be primarily apoptosis, sometimes called programmed cell death. Both the typically episodic clinical features and the terminal event in fatal cases of the long QT syndrome may be due to apoptosis.
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PMID:Apoptosis and pleomorphic micromitochondriosis in the sinus nodes surgically excised from five patients with the long QT syndrome. 840 7

The efficacy of antitachycardia pacing (ATP) incorporated into implantable cardioverter defibrillators (ICDs) was assessed in 29 consecutive survivors of cardiac arrest, not attributable to acute myocardial infarction, ischemia, or drug and electrolyte effects. The cohort included 25 men and 4 women with a mean age of 65 years and a mean left ventricular ejection fraction of 29%. Seventeen patients had coronary artery disease, 11 had nonischemic dilated cardiomyopathy, and 1 had long QT syndrome. Programmed stimulation yielded monomorphic ventricular tachycardia (VT) in 17 patients, polymorphic VT in 6, and no inducible VT in 6. During a mean follow-up of 22 months, a total of 91 episodes of monomorphic VT occurred, 73 of which were successfully pace terminated (83%). Monomorphic VT amenable to pace termination recurred only in the group that had this arrhythmia inducible. The recurrent arrhythmias in the 12 patients having either no inducible VT or polymorphic VT were all rapid VTs, having a cycle length < 220 ms; and therefore, not amenable to pace termination. These results suggest that ATP incorporated into ICDs is useful in survivors of cardiac arrest and may significantly reduce the number of shocks that these patients would otherwise receive. Programmed stimulation may also help to define those patients who would receive the maximum benefit from ATP.
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PMID:Efficacy of antitachycardia pacing in patients presenting with cardiac arrest. 855 18

About 10-20% of patients dying suddenly and unexpectedly do not have structural heart disease. The major causes of sudden death in this population are acute ischemia, the syndrome of right bundle branch block, and ST-elevation from V1 to V3, the long QT-syndrome, and the Wolff-Parkinson-While syndrome. In some patients, none of these syndromes can be recognized and ventricular fibrillation is classified as idiopathic. There are good preventive and therapeutic methods against acute ischemia and there are also curative treatments for the Wolff-Parkinson-White syndrome. Patients with idiopathic ventricular fibrillation cannot be recognized beforehand. However, there are electrocardiographic and genetic markers for the Brugada syndrome and the long QT syndrome. It is, therefore, justified to discuss the possible role of the prophylactic defibrillator to prevent sudden death in these 2 syndromes for which no effective treatment exists. Patients with Brugada syndrome have a high incidence of sudden death, and prophylactic defibrillators are indicated in patients with inducible arrhythmias at electrophysiologic study, irrespective of symptoms. On the contrary, the incidence of sudden death in the long QT syndrome is very low, making prophylactic defibrillator implantation not cost-effective.
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PMID:Use of the prophylactic implantable cardioverter defibrillator for patients with normal hearts. 1008 49

Curative treatment of both supraventricular and ventricular tachyarrhythmias started with the introduction of surgical therapy. Surgical treatment modalities were often very successful and associated with low mortality and morbidity, especially in patients with various supraventricular tachyarrhythmias. However, results were acceptable in patients with ventricular tachyarrhythmias, with often a very complex and extended arrhythmogenic area associated with structural heart disease. Because of the development and proven effectiveness of catheter ablation and defibrillator implantation, the role of surgical therapy became limited. In the treatment of supraventricular arrhythmias, surgical therapy is an option after failure of catheter ablation. Since His-bundle catheter ablation is only a palliative treatment for atrial fibrillation, the potentially curative Maze operation may be an acceptable alternative. However, its potential against formation of intracavitary thrombi has not yet been proven. In the treatment of ventricular tachyarrhythmias, ischemia related polymorphic ventricular tachycardia and ventricular fibrillation can be treated very effectively by revascularization. Map-guided surgery is an appropriate treatment modality for patients with monomorphic ventricular tachycardia and an extended arrhythmogenic area. However, patients with very poor left ventricular function may have an unacceptable perioperative risk. In patients with congenital long QT syndrome who are refractory to beta blocking agents, left-sided sympathectomy is the most appropriate choice.
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PMID:Is there space for surgery in the treatment of tachyarrhythmias? 1015 78

It has been suggested that patients be admitted for the initiation of Class I and Class III antiarrhythmic drugs to avoid serious proarrhythmic consequences. The most clinically significant proarrhythmic response to Class IC agents is likely due to an interaction with acute ischemia, and hospitalization for initiation of drug therapy has little predictive or preventive value. Amiodarone has a low risk of proarrhythmia, and any proarrhythmic reactions are generally delayed. Class IA and Class III antiarrhythmic drugs cause acquired long QT syndrome arrhythmias, which can occur soon after initiation of therapy; however, only about half of the arrhythmic events occur within 3 days of initiation of therapy. It could be argued that all patients should be hospitalized to begin Class IA or Class III drugs; however, this approach has a low yield and is extremely expensive. An alternative is to use Class IA and Class III drugs for patients at low risk of torsades de pointes (e.g., males without heart failure, ventricular tachyarrhythmias, or active coronary disease), in whom hospitalization for drug initiation is not warranted. Higher risk patients are probably better treated with other agents, such as Class IC drugs or amiodarone for women without organic heart disease and amiodarone for patients with heart failure, a history of ventricular tachycardia, or active coronary disease. When a Class IA or Class III drug is required for patient with an increased risk of torsades de pointes, hospital admission for drug initiation may be indicated.
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PMID:Optimal management with Class I and Class III antiarrhythmic drugs should be done in the outpatient setting: protagonist. 1021 May 15

Sudden cardiac death due to ventricular arrhythmias remains a significant problem. In most studies about 50% of all death related to coronary artery disease and heart failure are sudden and unexpected and are caused by acute fatal ventricular tachycardia and fibrillation. Most of the patients suffering sudden cardiac death have some kind of structural heart disease but 80% of SCD events are associated with coronary artery disease, 10-15% with dilated and hypertrophic cardiomyopathy, and only small fraction with the less common disorders as valvular heart disease, ventricular dysplasia and cardiac involvement in sarcoidosis or amyloidosis. In some patients the anomaly responsible for sudden cardiac death is not structural but mainly electrical as in patients with the long QT syndrome, WPW syndrome or in patients with a proarrhythmic effect from antiarrhythmic drugs. In this review, data from clinical trials and other studies on on antiarrhythmic therapies have been evaluated in order to determine effective strategies for the prevention sudden cardiac death in high risk patients. Taken together with the mortality data routine prophylactic use of class I antiarrhythmic drugs in the patients survivors of acute myocardial infarction and patients with heart failure is associated with increased risk of death. Conversely beta-blockers are associated with significant reduction in nonfatal cardiac arrest in the short term trials and sudden cardiac death in long term trials. These benefits are likely due to relief ischemia, reduction of heart rate and maintenance favourable autonomic nervous system balance. Overall trial data on amiodarone suggests that this agent is effective in reducing the risk of death in survivors of cardiac arrest, post infarction patients, and patients with heart failure but the routine prophylactic use of amiodarone remains of uncertain efficacy. The physician who considers the use of antiarrhythmic medications in patients with ventricular arrhythmias must be aware of which arrhythmias are malignant or potentially malignant and which are benign and the decision to initiate antiarrhythmic therapy should be based on consideration of the patients absolute mortality risk.
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PMID:[Antiarrhythmic agents in the prevention of sudden cardiac death]. 1036 92


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