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

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

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

New cardiological techniques such as coronary sinus catheterization and selective catheterization of the cardiac veins permit the opening of new experimental and clinical fields, for instance in venous angiography and the reverse nourishment of myocardium which is endangered by ischemia,and also in the electrophysiological study of the components of the conduction system. New approaches in heart surgery, such as the removal of accessory pathways of the conduction system (as in WPW syndrome), necessitate the realization of the topographical relationships of the vessels in the various sections of the coronary sulci in a different way. The objective of this work is, therefore, to present comprehensive and almost new macro- and microanatomical data about the venous drainage of the myocardium via the coronary sinus and its related and unrelated (non-coronary) cardiac veins. Examination of meticulously dissected heart specimens (of individuals who had achieved old or extreme old age at the time of their death in Germany: n=250) as well as corrosion casts of adult cardiac vessels (of individuals of all ages, n=25) formed the basis for the exact description and documentation of the occurrence, frequency, origin, and courses of both the normal and anomalously developed human coronary sinus and cardiac veins. A wide range of morphological and experimental references was consulted in order to enable thorough discussion of the anatomical findings in the light of modern cardiological diagnostics and treatment. The anatomical and clinical nomenclature is presented and there is a brief comment on modern diagnostic techniques and their applications where the cardiac veins are concerned. The two principal and one compound cardiac venous system are defined and discussed with reference to the existence of both the normal and anomalous coronary sinus and cardiac vein. 1. The greater (major) cardiac venous system (2) The smaller (minor) cardiac venous system (3)The compound cardiac venous system. The microanatomy of the various proper cardiac veins is not very well explained and illustrated in old or new literature; therefore, special attention is paid in the present study to the detailed microanatomy of the cardiac venous drainage. This includes the topograpy and structural and surface anatomy of the coronary sinus (position, length and shape, diameters, area of cross-section, circumference and volume, curvature, elevation, ostial angle, enlargement, duplication, absence), and the exact enternal and internal morphological landmarks of the coronary sinus with reference to its myocardial cover, isolated myocardial belts, and "free" myocardial cords which connect the atrial and ventricular myocardium, and the atrial ostium of the coronary sinus. It is established that the frequency, distribution pattern, courses and mode of opening of the major ventricular and atrial cardiac veins and the occurrence, morphology, and efficiency of the ostial valves of the coronary sinus and its tributaries all influence the success of any selective catheter implantation and venous reperfusion technique to a great degree. There are many peculiarities of the cardiac veins which are worthy of consideration, for instance intramyocardial and aberrant courses of the anterior interventricular vein, the oblique vein of the left atrium, the posterior interventricular vein, the small cardiac vein, the posterior vein of the left ventricle, the left and right marginal veins, and the anterior cardiac veins. Various forms and courses of the intramural venous tunnel, sinus or channel of the right atrium were found and illustrated, and discussed in terms of developmental and comparative anatomy. This review incorporates a great variety of clinically significant, new morphological findings with regard to the coronary sinus and the cardiac venous system. The many anatomical peculiarities and hindrances to the catheterization of the coronary sinus and the reperfusion of (even selected) cardiac veins are documented and evaluated; the various problems which may arise in venous reperfusion due to the presence of anatomical anomalies of the coronary sinus, cardiac veins, and ostial valves (of greater or lesser efficiency) are addressed. The presentation narrows a gap in the rather incomplete knowledge of the venous drainage of the human myocardium.
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PMID:The venous drainage of the human myocardium. 1264 57

We studied myocardial biopsy specimens from the right atrium of cardiological patients with different degree of cardiac ischemia obtained during surgery. No inducible HSP70 stress proteins were detected in atrial cardiomyocytes of patients with the WPW syndrome without signs of ischemic injuries of the heart. These proteins were detected in the myocardium of coronary patients. Their expression was more intense in patients with coronary disease paralleled by the development of myocardial dyskinesia. Two-dimensional electrophoresis showed only acid HSP70 but no alkaline isoforms in coronary patients even with pronounced dyskinesia. Presumably, alkaline HSP70 isoforms are present in the myocardium directly involved in the dyskinesia zone.
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PMID:Initiation of stress protein synthesis in the myocardium of coronary patients. 1566 46

ECG changes during exercise stress testing, such as false-positive ST-segment depression and disappearance of the delta wave, are reported in patients with the Wolff-Parkinson-White (WPW) pattern. We present a case of exercise testing in a 53-year-old man with WPW syndrome with ischemic-appearing ECG changes and normal nuclear stress perfusion study findings who was thought to be at clinically low risk for having significant coronary disease. A literature review is discussed. Although ST-segment depression typical for ischemia occurs in half of the patients in whom WPW syndrome is reported, exercise testing is still an important tool in their evaluation. Data other than ECG response can be interpreted in the context of clinical history and physical examination findings to stratify the risk of coronary disease. Complete and sudden disappearance of the delta wave has been seen during exercise in 20% of patients with WPW syndrome and can identify those who are at low risk for sudden arrhythmic death.
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PMID:Exercise testing in Wolff-Parkinson-White syndrome: case report with ECG and literature review. 1582 Dec 31

AMP-activated protein kinase (AMPK) is activated during exercise and ischemia and is emerging as an important regulatory mechanism in the heart. AMPK promotes adenosine triphosphate-generating pathways, including glucose transport, glycolysis, and fatty acid oxidation, while inhibiting energy-consuming anabolic pathways. After ischemia-reperfusion, AMPK-deficient hearts from transgenic mice have severe left ventricular contractile dysfunction with increased apoptosis and necrosis. Mutations in the AMPKgamma(2) subunit lead to cardiac glycogen overload, Wolff-Parkinson-White syndrome, arrhythmias, and heart failure. This review focuses on the molecular mechanisms of activation and cardiovascular actions of AMPK in the heart.
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PMID:AMP-activated protein kinase: a key stress signaling pathway in the heart. 1603 71

The heart is capable of utilizing a variety of substrates to produce the necessary ATP for cardiac function. AMP-activated protein kinase (AMPK) has emerged as a key regulator of cellular energy homeostasis and coordinates multiple catabolic and anabolic pathways in the heart. During times of acute metabolic stresses, cardiac AMPK activation seems to be primarily involved in increasing energy-generating pathways to maintain or restore intracellular ATP levels. In acute situations such as mild ischemia or short durations of severe ischemia, activation of cardiac AMPK appears to be necessary for cardiac myocyte function and survival by stimulating ATP generation via increased glycolysis and accelerated fatty acid oxidation. Whereas AMPK activation may be essential for adaptation of cardiac energy metabolism to acute and/or minor metabolic stresses, it is unknown whether AMPK activation becomes maladaptive in certain chronic disease states and/or extreme energetic stresses. However, alterations in cardiac AMPK activity are associated with a number of cardiovascular-related diseases such as pathological cardiac hypertrophy, myocardial ischemia, glycogen storage cardiomyopathy, and Wolff-Parkinson-White syndrome, suggesting the possibility of a maladaptive role. Although the precise role AMPK plays in the diseased heart is still in question, it is clear that AMPK is a major regulator of cardiac energy metabolism. The consequences of alterations in AMPK activity and subsequent cardiac energy metabolism in the healthy and the diseased heart will be discussed.
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PMID:Role of AMP-activated protein kinase in healthy and diseased hearts. 1684 22

TGF-beta-activated kinase-1 (TAK1), also known as MAPKK kinase-7 (MAP3K7), is a candidate effector of multiple circuits in cardiac biology and disease. Here, we show that inhibition of TAK1 in mice by a cardiac-specific dominant-negative mutation evokes electrophysiological and biochemical properties reminiscent of human Wolff-Parkinson-White syndrome, arising from mutations in AMP-activated protein kinase (AMPK), most notably, accelerated atrioventricular conduction and impaired AMPK activation. To test conclusively the biochemical connection from TAK1 to AMPK suggested by this phenotype, we disrupted TAK1 in mouse embryos and embryonic fibroblasts by Cre-mediated recombination. In TAK1-null embryos, the activating phosphorylation of AMPK at T172 was blocked, accompanied by defective AMPK activity. However, loss of endogenous TAK1 causes midgestation lethality, with defective yolk sac and intraembryonic vasculature. To preclude confounding lethal defects, we acutely ablated floxed TAK1 in culture by viral delivery of Cre. In culture, endogenous TAK1 was activated by oligomycin, the antidiabetic drug metformin, 5-aminoimidazole-4-carboxamide riboside (AICAR), and ischemia, well established triggers of AMPK activity. Loss of TAK1 in culture blocked T172 phosphorylation induced by all three agents, interfered with AMPK activation, impaired phosphorylation of the endogenous AMPK substrate acetyl CoA carboxylase, and also interfered with activation of the AMPK kinase LKB1. Thus, by disrupting the endogenous TAK1 locus, we prove a pivotal role for TAK1 in the LKB1/AMPK signaling axis, an essential governor of cell metabolism.
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PMID:A pivotal role for endogenous TGF-beta-activated kinase-1 in the LKB1/AMP-activated protein kinase energy-sensor pathway. 1708 80

A 60-year-old woman was admitted to cardiology clinic because of typical chest pain. The presenting electrocardiography (ECG) revealed sinus rhythm and T wave inversion on inferolateral wall. Her chest pain relapsed at second day of admission and electrocardiogram recorded during chest pain had ECG changes consistent with Wolf Parkinson White (WPW) syndrome. She underwent cardiac catheterization and borderline lesion was detected in proximal of left anterior descending artery and direct stent implantation was performed. This is the first case report in which acute ischemia may induce typical ECG changes of WPW in a patient with concealed WPW syndrome. We concluded that acute coronary ischemia may manifest concealed WPW syndrome.
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PMID:Coronary ischemia induced Wolf Parkinson White syndrome. 1769 40

Mutation in PRKAG2 encoding the gamma2 subunit of the AMP activated protein kinase (AMPK) cause human cardiomyopathy characterized by hypertrophy, Wolff-Parkinson-White syndrome, conduction system disease and glycogen storage in the myocardium. AMPK is a master metabolic regulator activated by hormones and energy deficient states. A heterotrimer enzyme comprising the catalytic alpha- and regulatory beta-and gamma-subunits was preserved through evolution and is ubiquitously expressed among mammalian tissues. AMPK is activated by AMP and inhibited by ATP that competes for binding to the regulatory sites on the gamma-subunit. Upstream kinases which phosphorylate Thr172 on the catalytic subunit activate the enzyme during exercise, ischemia, in response to sympathetic stimulation and hormones such as leptin and adiponectin. AMPK operates by phosphorylating its target proteins such as Acetyl CoA Carboxylase. Its classic functions include decreased fat synthesis in liver and adipose tissues, increased fatty acid oxidation, stimulating muscle glucose uptake and glycolysis. Altogether, these activities serve to restore the cellular and whole body energy balance. Human mutations which disrupt the nucleotide-binding affinity of the gamma2 subunit lead to loss of inhibition by ATP and inappropriate activate AMPK under resting conditions. As a result, myocytes recruit energy metabolites in excess of demand, causing storage of glycogen. Will AMPK ever emerge as a therapeutic target? Bench experiments suggest its potential in treating diabetes, ischemia and cell cycle regulation but much work is needed until these developments reach the bedside.
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PMID:[AMP-activated protein kinase: how a mistake in energy gauge causes glycogen storage]. 1799 Mar 92


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