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)

The combination of calcium overload and oxidative stress opens a non-specific pore in the inner mitochondrial membrane known as the mitochondrial permeability transition pore (MPTP). This uncouples oxidative phosphorylation and compromises intracellular ATP levels eventually leading to necrotic cell death. In cardiac ischemia and reperfusion, as during treatment of a coronary thrombosis or cardiac surgery, the extent of MPTP opening determines the amount of irreversible damage (infarct size). Furthermore, cardioprotection can be achieved by inhibiting MPTP opening either directly with cyclosporin A analogues, or indirectly by reducing oxidative stress. The detailed molecular mechanism of the MPTP remains uncertain. Knockout studies have confirmed important regulatory roles for cyclophilin-D (CyP-D) and the adenine nucleotide translocase (ANT) but not the voltage dependent anion channel. Our own studies have implicated a calcium-triggered conformational change of the mitochondrial phosphate carrier that is facilitated by CyP-D and modulated by the conformation of the ANT.
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PMID:Mitochondria and reperfusion injury of the heart--a holey death but not beyond salvation. 1935 38

Owing to their higher risk for cardiac death or ischemic complications, patients with acute coronary syndrome (ACS) must be identified from other causes of chest pain. Patients with acute coronary syndrome are divided into categories based on their electrocardiogram; those with new ST-segment elevation and those who present with ST-segment depression. The subgroups of patients with ST-segment elevation are candidates for immediate reperfusion, while fibrinolysis appears harmful for those with non-ST elevation myocardial infarction. There is increasing evidence to encourage appropriate risk stratification before deciding on a management strategy (invasive or conservative) for each patient. The TIMI, GRACE or PURSUIT risk models are recommended as useful for decisions regarding therapeutic options. Cardiac biomarkers are useful additions to these clinical tools to correctly risk stratify ACS patients. Cardiac troponin is the biomarker of choice to detect myocardial necrosis and is central to the universal definition of myocardial infarction. The introduction of troponin assays with a lower limit of detection will allow for earlier diagnosis of patients who present with chest pain. Analytical and clinical validations of these new assays are currently in progress. The question is whether the lower detection limit of the troponin assays will be able to indicate myocardial ischemia in the absence of myocardial necrosis. Previous to the development of ultrasensitive cardiac troponin assays free fatty acids unbound to albumin and ischemia modified albumin were proposed as biochemical markers of ischemia. Advances in our knowledge of the pathogenesis of acute coronary thrombosis have stimulated the development of new biomarkers. Markers of left ventricular performance (N-terminal pro-brain natriuretic peptide) and inflammation (e.g. C-reactive protein) are generally recognized as risk indicators. Studies suggest that using a number of biomarkers clinicians can risk stratify patients over a broad range of short and long term cardiac events. Nevertheless, it is still under debate as to which biomarker combination is best preferred for risk prediction. This review will focus on recent practice guidelines for the management of patients with ACS as well as current advances in cardiac biomarkers, their integration into clinical care and their diagnostic, prognostic and therapeutic utility.
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PMID:Biochemical markers in acute coronary syndrome. 2150 3

Sudden cardiac death remains one of the most prevalent modes of death and is mainly caused by ventricular fibrillation (VF) in the setting of acute ischemia resulting from coronary thrombi. Animal experiments have shown that platelet activation may increase susceptibility of ischemic myocardium to VF, but the mechanism is unknown. In the present study, we evaluated the effects of activated blood platelet products (ABPPs) on electrophysiological properties and intracellular Ca(2+) (Ca(2+)(i)) homeostasis. Platelets were collected from healthy volunteers. After activation, their secreted ABPPs were added to superfusion solutions. Rabbit ventricular myocytes were freshly isolated, and membrane potentials and Ca(2+)(i) were recorded using patch-clamp methodology and indo-1 fluorescence measurements, respectively. ABPPs prolonged action potential duration and induced early and delayed afterdepolarizations. ABPPs increased L-type Ca(2+) current (I(Ca,L)) density, but left densities of sodium current, inward rectifier K(+) current, transient outward K(+) current, and rapid component of the delayed rectifier K(+) current unchanged. ABPPs did not affect kinetics or (in)activation properties of membrane currents. ABPPs increased systolic Ca(2+)(i), Ca(2+)(i) transient amplitude, and sarcoplasmic reticulum Ca(2+) content. ABPPs did not affect the Na(+)-Ca(2+) exchange current (I(NCX)) in Ca(2+)-buffered conditions. Products secreted from activated human platelets induce changes in I(Ca,L) and Ca(2+)(i), which result in action potential prolongation and the occurrence of early and delayed afterdepolarizations in rabbit myocytes. These changes may trigger and support reentrant arrhythmias in ischemia models of coronary thrombosis.
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PMID:Activated human platelet products induce proarrhythmic effects in ventricular myocytes. 2165 13

A 53-year-old man is treated by L-asparaginase for an acute lymphoblastic leukaemia. He received anti thrombin infusions. A systematic electrocardiogram showed an asymptomatic subepicardium ischemia without troponin elevation. Echocardiography and heart magnetic resonance imaging showed an apical thrombus facing a zone of myocardial necrosis. A thrombus regression was observed under anticoagulation. Atypical and asymptomatic coronary thrombosis may occur following L-asparaginase treatment. Regular electrocardiogram monitoring is proposed along this treatment. Arterial thrombosis associated with anti tumor chemotherapies are reviewed.
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PMID:[Distal coronary thrombosis during L-asparaginase treatment for an acute lymphoblastic leukaemia]. 2166 90

The introduction of drug-eluting stents (DES) to interventional cardiology has been a breakthrough in the treatment of in-stent restenosis. However, the downside of reduced restenosis is a significantly prolonged and practically incalculable time to reendothelialization of thrombogenic stent-surfaces with an increased risk for coronary thrombosis. As the use of DES in non-coronary arteries (e.g. carotid, renal, infrainguinal and even cerebral arteries) is increasing, new vascular beds might be put at risk of ischemia. The practice of stopping antiplatelet drugs in a perioperative setting is highly problematic and contemporary guidelines released by scientific societies from different medical specialties have recently addressed this problem. While many case reports have reported alarming incidents of stent thrombosis, prospective clinical data are scarcely available to guide anticoagulation during the perioperative phase. This review summarizes information on the vascular biology of DES and associated adverse events based on a systematic search of the available literature in public data bases. An emphasis is put on the growing use of DES in non-coronary vessels and the associated danger of putting new vascular beds at risk of thrombotic complications.
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PMID:Drug-eluting stents and perioperative risk - more than matters of the heart? 2312 36

Perioperative myocardial ischemia is rare but serious complication of CABG. Graft dysfunction, coronary artery thrombosis and incomplete revascularization are main causes. Pharmacological treatment, intra aortic counter pulsation and immediate additional grafting have limited results. Treatment strategy based on coronary angiography findings could lessen the burden of high mortality rate in these patients. The purpose of this study was to analyze the causes of perioperative ischemia and angiography based treatment strategy including percutaneous intervention. We enrolled all 55 consecutive patients that went early coronary angiography for perioperative myocardial ischemia in a prospective longitudinal study. Incorrect graft anastomosis, graft spasm, displacement and dissection were found in 49%, 7%, 5% and 4% of patients, respectively. Acute coronary artery thrombotic occlusion was found in 5% of patients and ischemia due to incomplete revascularization in 6% of patients. In 22% of patients no cause of myocardial ischemia could be detected. There were no complications of coronary angiography. Based on coronary angiography findings percutaneous intervention was performed in 30 patients, additional grafting in 8 patients and no action was taken in 17 patients. Percutaneous intervention with stenting was performed on coronary arteries (78%) and graft anastomosis (22%) with primary success 97%. One anastomosis rupture with treatable tamponade and one lethal stent thrombosis were complications of percutaneous treatment. Overall in hospital mortality was 30%. We concluded that graft dysfunction is usual cause of myocardial ischemia due to incorrect anastomosis and that percutaneous intervention on bypass graft or coronary artery can lessen high mortality rate in these patients.
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PMID:Angiographic control and percutaneous treatment of myocardial ischemia immediately after CABG. 2339 Aug 39

The benefits of early perfusion in ST elevation myocardial infarctions (STEMI) are established; however, early perfusion of non-ST elevation myocardial infarctions has not been shown to be beneficial. In addition, ST elevation (STE) caused by conditions other than acute ischemia is common. Non-ischemic STE may be confused as STEMI, but can also mask STEMI on electrocardiogram (ECG). As a result, activating the primary percutaneous coronary intervention (pPCI) protocol often depends on determining which ST elevation patterns reflect transmural infarction due to acute coronary artery thrombosis. Coordination of interpreting the ECG in its clinical context and appropriately activating the pPCI protocol has proved a difficult task in borderline cases. But its importance cannot be ignored, as reflected in the 2013 American College of Cardiology Foundation/American Heart Association guidelines concerning the treatment of ST elevation myocardial infarction. Multiples strategies have been tested and studied, and are currently being further perfected. No matter the strategy, at the heart of delivering the best care lies rapid and accurate interpretation of the ECG. Here, we present the different patterns of non-ischemic STE and methods of distinguishing between them. In writing this paper, we hope for quicker and better stratification of patients with STE on ECG, which will lead to be better outcomes.
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PMID:ST-segment elevation: Distinguishing ST elevation myocardial infarction from ST elevation secondary to nonischemic etiologies. 2534 51

Patients with coronary artery aneurysms caused by Kawasaki disease are at increased risk of coronary thrombosis and ischemia. To prevent coronary thrombosis, long term thromboprophylaxis using anti-platelet drugs, such as aspirin, dipyridamole, ticlopidine, clopidogrel, and abciximab, with or without warfarin is recommended by official guidelines. In fact, aspirin or aspirin with warfarin are the most frequently administered regimen in these patients with coronary aneurysms. However, still there has been paucity of data and no randomized controlled study to determine the efficacy of these drugs. This short article describes the currently accepted practice of thromboprophylaxis in patients with coronary aneurysms caused by Kawasaki disease.
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PMID:[Thromboprophylaxis in patients with coronary aneurysms caused by Kawasaki disease]. 2551 19

All patients with stable ischemic heart disease (SIHD) should be managed with guideline-directed medical therapy (GDMT), which reduces progression of atherosclerosis and prevents coronary thrombosis. Revascularization is also indicated in patients with SIHD and progressive or refractory symptoms, despite medical management. Whether a strategy of routine revascularization (with percutaneous coronary intervention or coronary artery bypass graft surgery as appropriate) plus GDMT reduces rates of death or myocardial infarction, or improves quality of life compared to an initial approach of GDMT alone in patients with substantial ischemia is uncertain. Opinions run strongly on both sides, and evidence may be used to support either approach. Careful review of the data demonstrates the limitations of our current knowledge, resulting in a state of community equipoise. The ongoing ISCHEMIA trial (International Study of Comparative Health Effectiveness With Medical and Invasive Approaches) is being performed to determine the optimal approach to managing patients with SIHD, moderate-to-severe ischemia, and symptoms that can be controlled medically. (International Study of Comparative Health Effectiveness With Medical and Invasive Approaches [ISCHEMIA]; NCT01471522).
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PMID:Medical Therapy With Versus Without Revascularization in Stable Patients With Moderate and Severe Ischemia: The Case for Community Equipoise. 2661 30

We present a 65-year-old male who received rivaroxaban therapy prior to and after left knee replacement surgery. The patient developed generalized weakness soon after stopping rivaroxaban. An electrocardiogram showed acute infero-lateral ischemia and an echocardiogram reported an akinetic antero-apical wall segment, an apical clot and a reduced systolic function. A subsequent coronary angiogram revealed two-vessel coronary artery thrombosis. The case illustrates a temporal relationship of coronary thrombosis following rivaroxaban cessation.
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PMID:Rivaroxaban Rebound Acute Coronary Event: A Post Marketing Experience. 2835 47


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