Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac toxicity and hemodynamic alterations are frequently associated with high-dose interleukin-2 (IL-2) immunotherapy in cancer patients. Serious cardiac events including myocardial infarction, ischemia, and noninfectious myocarditis have been observed. We document two cases of unusually severe but reversible cardiac abnormalities related to IL-2 therapy: one patient with a profound form of global myocardial hypocontractility and a second patient with regional aneurysmal and dyskinetic changes of the left ventricle. These cases exhibit unique features not previously described in IL-2-treated patients. The possible pathophysiologic mechanisms underlying these global and regional forms of cardiomyopathy, including the production of secondary-messenger molecules such as nitric oxide and myocardial stunning, are discussed. Both patients remain disease free of their cancer (> 3 years since completing therapy), are without residual cardiac dysfunction or recurrent related symptoms, and have not experienced any additional cardiac events. The report demonstrates the complexity of the cardiac toxicities associated with IL-2-based immunotherapy and recognizes a need for treating physicians to be familiar with their management.
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PMID:Severe reversible global and regional ventricular dysfunction associated with high-dose interleukin-2 immunotherapy. 857 67

The two primary goals of mechanical circulatory support are to provide adequate perfusion of the vital organs and to decrease cardiac work. The support of the myocardium is in an effort to cause a reversal of cardiac damage. The recovery process apparently takes place in two stages. Initially, there is a rapid functional recovery of cells in marginally ischemia areas. Then there is a slower process of hypertrophy of normal and recovering myofibers. The process involves the reversal of interstitial and of intercellular myocardial edema in areas of viable myocardium while halting the extension of necrosis into reversibly ischemic areas. It appears that this process is extended from 3 to 5 days, and functional recovery can occur for up to 2 weeks. After a 2-week period, there appears to be little functional recovery of myocardial cells. In autopsy series of nonsurvivors, it appears that most of the patients had suffered from biventricular failure. Biventricular failure appears to be one of the more common complications of the support patient. Right ventricular failure will be attempted to be supported by right ventricular assist devices. The right ventricular assist device, unfortunately, adds a level of complication to the recovery process for the bridge-to-transplant or cardiomyopathy patient. The patients who are involved in support fall into three categories: (1) the bridge-to-transplant patient, (2) the patient recovering from postcardiotomy, and (3) the patient who recovers from an acute myocardial insult. It appears that after 2 weeks the recovery period for all of these groups demonstrates no further functional recovery. The bridge-to-transplant patients usually need to be supported until the transplant occurs. The postcardiotomy patient and the acute myocardial failure patient are the most disappointing support group, since they have a higher morbidity and mortality, and a lower chance of recovery. Salvage rates appear to be in approximately the 25% range in the acute insult category.
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PMID:Cardiac assist devices. 879 47

The mammalian heart is normally well oxygenated and anaerobic glycolysis is extremely rare except for the production of extra ATP during extreme exercise like a marathon race. Anaerobic glycolysis plays a role when there is a serious impairment in coronary blood flow such as during heart attack and open heart surgery. The control of glycolysis in ischemic myocardial tissue appears to be extremely complex. During aerobic glycolysis, phosphofructokinase is the most important regulatory enzyme that controls the energy requirements of the cell. Under anaerobic conditions, however, glyceraldehyde-3-phosphate dehydrogenase becomes the key enzyme because it responds promptly to any changes in the essential supply of co-factors for oxidation. The conversion of pyruvate to acetyl CoA (aerobic metabolism) involves a series of chain reactions primarily catalyzed by pyruvate dehydrogenase complex which is situated at the cross roads between both aerobic and anaerobic glycolysis. It is important to remember that substrate utilization is carefully controlled by substrate availability. During aerobic metabolism, control mechanisms using fatty acids, lactate and glucose as energy substrates regulate the rate of ATP production according to energy demand. This precise mechanism is upset during ischemia and post-ischemic reperfusion for reasons discussed in this review. The demand for ATP can no longer be met by its supply because of severely reduced anaerobic glycolysis and significantly inhibited beta-oxidation of fatty acids. The impairment of bioenergetics is discussed in the context of several diseases such as cardiomyopathy, heart failure, diabetes, arrhythmias, cardiac surgery, heart-lung transplantation, and also in aging and oxidative stress. The regulation of energy metabolism in preconditioned heart is also discussed. Finally, methods used to preserve energy in ischemic myocardium are summarized and quantitation of the high-energy phosphates is discussed. This review challenges scientists to discover drugs which will stimulate energy supply during myocardial ischemia.
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PMID:Bioenergetics, ischemic contracture and reperfusion injury. 880 94

The burden of ischemic heart disease is high in dialysis patients. Ischemia may result from atherosclerotic and nonatherosclerotic disease and may cause myocardial infarction and angina. The impact of diminished perfusion is intricately associated with the underlying cardiomyopathy, both of which predispose to heart failure. The etiology of ischemia is complex and associated with the underlying cardiomyopathy, whether it be concentric left ventricular hypertrophy, left ventricular dilatation, or systolic dysfunction. Hypertension, diabetes, dyslipidemia, abnormalities of divalent ion metabolism, hypoalbuminemia, and left ventricular hypertrophy are probably adverse risk factors for ischemia, but the relative importance of each is unknown.
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PMID:Ischemic heart disease in chronic uremia. 887 58

Sudden cardiac death is the leading cause of death in industrialized countries. It is most frequently due to ventricular tachyarrhythmias occurring in the presence of coronary heart disease, but mechanisms linking sudden death to coronary atherosclerosis are still unclear. In autopsy studies of sudden death patients, the incidence of acute thrombotic coronary occlusions has varied between 4 and 74%. In over 600 consecutive patients with implantable cardioverter-defibrillators, we observed that appropriate shocks for electrogram-verified ventricular tachyarrhythmias was only very rarely followed by signs of acute myocardial infarction (< 3% of cases), not supporting the coronary occlusion theory of fatal arrhythmias. Cellular hypertrophy compensating for cell loss due to ischemia, intraventricular hypertension, cardiomyopathy, and myocarditis might play a role in arrhythmogenesis as evidenced by the fact that experimental induction and regression of hypertrophy are paralleled by changes in the inducibility of ventricular tachyarrhythmias. Atherogenic hyperlipidemias are associated with a systemic inflammatory response manifested by leukocytosis (lymphocytosis) and complex upregulations of proinflammatory-prothrombotic mediators, such as platelet-activating factor, cytokines, and hemostasis factors. The diurnal regulation of these mediators parallels circadian rhythms of coronary morbidity and mortality. Some upregulated mediators have been shown to exert direct arrhythmogenic effects. The potential contribution of hyperlipidemia-associated inflammatory factors to arrhythmogenesis is important, because it opens new molecular targets for antiarrhythmic drug design.
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PMID:Sudden cardiac death: still more questions than answers. 947 68

L-Carnitine can affect cardiac function principally by improving fatty acid and/or glucose metabolism, by increasing perfusion due to modulation of the deformability of erythrocytes and/or vasodilatation, and by stabilising mitochondrial and plasma membranes of cardiomyocytes. While short-term administration of L-carnitine in vivo does not increase the muscular and probably also not the cardiac L-carnitine content, it improves the function of perfused rat or pig hearts in the reperfusion phase after ischemia. Long-term administration of L-carnitine increases the cardiac L-carnitine content in mice and has been shown to improve surrogate markers of coronary heart disease such as arrhythmias, nitrate consumption, and left ventricular dilatation and infarct size in patients after myocardial infarction. The only clear indication for L-carnitine in cardiology is to date cardiomyopathy associated with primary L-carnitine deficiency.
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PMID:[Physiologic bases for the use of L-carnitine in cardiology]. 952 39

After heart transplantation a number of factors such as pre- and postoperative hypoxia of the myocardium, myocardial failure of the early postoperative period, acute rejection episodes, cytomegalovirus infection, and finally the progressive atherosclerosis of the coronary arteries lead to the development of transplanted heart failure. Severe alterations of the myocardial function at this end stage of the process correspond to incurable cardiomyopathy. The target of plasmapheresis in this case is to decrease the extent of the disturbances in the lipoprotein contents and blood rheology for the improvement of the coronary perfusion of the transplanted heart. Nine patients with 3-7 year survival periods after heart transplantations underwent plasmapheresis twice a year using the Haemonetics PCS-plus machine. 2,100-2,700 ml of plasma was removed. Biochemical data, rheology and coagulation, and the concentration of Sandimmune (Sandoz Pharma Ltd., Basel, Switzerland) were controlled, and radionuclide scintigraphy of the myocardium, coronarographia, and transesophageal ultrasound investigations were completed for these patients. The result was the significant improvement of the coronary perfusion of the myocardium. The level of immunosuppression after the plasmapheresis procedures did not change and therefore did not demand any correction. Thus, we think that plasmapheresis can be an effective method of treatment of posttransplantation cardiomyopathy; the improvement of coronary perfusion decreases the extent of chronic ischemia. Further studies are necessary to answer the question as to whether it is possible to prolong the time before retransplantation with the help of plasmapheresis.
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PMID:Plasmapheresis in the treatment of posttransplant cardiomyopathy. 952 79

Antimyosin monoclonal antibody is a specific marker of impaired sarcolemmal integrity resulting not only from ischemia but also from non-ischemic myocardial injury, such as infection, inflammatory, or immunologic reactions, and alcohol or drug intoxication. In addition, antimyosin accumulation has been demonstrated in some forms of cardiomyopathy with unknown as well as known etiologies. Antimyosin positivity appears to indicate precisely the extent of myocardial necrosis and to reflect cardiac dysfunction in an acute stage of active myocardial damage caused by ischemia and inflammation. However, the correlation is not necessarily good in the chronic stages of the disease or in idiopathic cardiomyopathic hearts; in other words, cardiac antimyosin uptake can be detected even in myocardial tissue with a normal histologic appearance independent of the presence of inflammatory responses, myocyte necrosis, or functional or morphologic deterioration. Thus, antimyosin is useful not only for detecting and quantifying acute myocardial necrosis but also for specifically identifying ongoing or latently progressing myocardial degeneration and sarcolemmal disruption, which will certainly lead to myocardial necrosis. These characteristics may contribute to the early detection of myocardial damage and lead to the investigation of pathophysiologic mechanisms. Further progress in immunologic and radiolabeling techniques is necessary for better specificity and less antigenicity against humans in antimyosin monoclonal antibody imaging.
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PMID:Ischemic and non-ischemic myocyte damage and antimyosin monoclonal imaging. 955 23

The protein composition of human myocardium at some cardiovascular pathologies was studied by use of 2D electrophoresis. It was found that dilitation(al) cardiomyopathy and ischemia are both characterized by transferrin accumulation in myocardium and by enhanced expression of a protein with Mm 3 kD/pI 5. Besides that, at ischemic disease there was seen an elevation of the fetal isoform in the light chain of myosin. For one of the polymorphous protein systems, the occurrence rate changes were also recorded.
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PMID:[Two-dimensional electrophoresis of myocardial proteins in human cardio-vascular diseases]. 957 20

Dilated Cardiomyopathy (DCM) is associated with many diseases. By means of epidemiologic, clinical and invasive diagnostic techniques, the etiology of DCM is identified almost in 50% of the cases. Chronic infection with Trypanosoma cruzi is recognized as a cause of DCM in Latin America. A blind study of 40 cases of DCM explores the electrovectorcardiographic data obtained in chronic chagasic cardiomyopathy (CCC). Twenty one of 40 patients fulfilled epidemiologic and seroimmunologic criteria for CCC, 19 had DCM. There were not differences between these groups in regard to sex or age. Patients suffering DCM had in addition diabetes mellitus, systemic hypertension or ischemic heart disease. Those with CCC had not comorbid diseases in 50% of the cases. Arrhythmias and conduction blocks were equally recognized in both groups, as well as ECG evidence of injury or necrosis (p > 0.05). However, ECG signs of subepicardial ischemia were a dominant feature in patients with CCC and normal epicardial coronary arteries (p < 0.05). Probably this finding is due to a small vessels damage, a pathogenic mechanism proposed in CCC.
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PMID:[Vector electrocardiographic findings in chronic Chagas cardiomyopathy]. 965 83


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