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Query: UMLS:C0151744 (myocardial ischemia)
31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ability to mechanically dilate and treat stenoses in the coronary arteries opened a new chapter in cardiovascular medicine. Percutaneous coronary intervention (PCI) has been shown to improve outcomes among patients with acute coronary syndromes as well as improve symptoms among patients with stable coronary artery disease. Adjunctive antiplatelet therapy plays a critical role both in the periprocedural setting as well as in the long-term management of atherothrombosis. Over the past several years, clinical trials of novel compounds and treatment strategies have further refined our pharmacotherapeutic approach. Aspirin remains the cornerstone for antiplatelet therapy across the spectrum of ischemic heart disease. In contrast, studies of glycoprotein IIb/IIIa inhibitors suggest a more limited role, particularly when used in addition to contemporary dual antiplatelet therapy. Clopidogrel, the most widely used P2Y(12) adenosine diphosphate receptor blocker--although having demonstrated efficacy in patients with ST-segment elevation myocardial infarction, non-ST-segment elevation acute coronary syndrome, and stable coronary artery disease undergoing PCI--has several limitations, including delay in onset, variability in response, and modest potency. The third-generation thienopyridine, prasugrel, as well as nonthienopyridine inhibitors of the P2Y(12) receptor such as ticagrelor and cangrelor address these shortcomings, offering more potent, consistent, and rapid platelet inhibition. Prasugrel and ticagrelor led to significant reductions in adverse cardiovascular events, including cardiovascular mortality for the latter, whereas cangrelor met noninferiority compared with 600 mg of clopidogrel in patients with ACS undergoing PCI. There are myriad novel compounds at varying stages of development, including thrombin receptor antagonists whose role in the periprocedural and long-term setting will be defined through further study. Significant questions regarding antiplatelet therapy remain unanswered, including the role of genetic and platelet function testing to "tailor therapy"; the optimal duration of therapy; and the optimal mechanism to deliver high-quality, cost-effective antiplatelet therapy to all patients.
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PMID:The state of periprocedural antiplatelet therapy after recent trials. 2063 Apr 50

Ischemic heart disease is a major cause of morbidity and mortality throughout the world. Percutaneous coronary intervention (PCI) has rapidly evolved from balloon angioplasty to drug-eluting stents over the past 25 years and has become an important treatment option for coronary heart disease. During PCI, atherosclerotic plaque disruption and the endothelium denudation stimulate both platelet aggregation and the thrombus generation. Therefore, pharmacological adjuvant therapies to protect the procedure-related thrombotic complication during PCI are indispensable. In addition to aspirin, whose benefit has been clearly shown in ischemic heart disease, clopidogrel and prasugrel have shown to dramatically reduce the rate of thrombosis after stent placement. The introduction of glycoprotein IIb/IIIa inhibitors has further improved the results of PCI especially in high-risk patients. In addition, several new drugs with antiplatelet or with antithrombin activities are currently under development.
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PMID:Adjunctive pharmacologic therapy in percutaneous coronary intervention: part I antiplatelet therapy. 2092 50

Advances in electrocardiography and enzymology in the 1940s and 1950s have provided better knowledge of the clinical evolution of myocardial infarction and recognition of the prognostic relevance of acute phase arrhythmias. This prompted the creation of intensive coronary care units in the subsequent decade. After the successful resolution of acute phase arrhythmias, it became clear that the myocardium necrotic area size was a determining factor in the long-term prognosis. The Killip-Kimball clinical classification in the 60s helped to clarify the role of infarct size on left ventricle (LV) dysfunction, from Class I for small infarcts to Class IV with major necrosis, (involving more than 30% of the LV free wall area, the majority of these being fatal). Along with these advances, a series of experimental studies have shown that myocardial ischemia depends on the oxygen supply-demand imbalance, highlighting the factors affecting oxygen consumption. The study of various physiological, pharmacological or mechanical interventions on these factors became the next step towards optimizing the supply-demand relation. Several animal experiments were conducted in the 1970s, followed by the first clinical studies to reduce infarct size, particularly by increasing the oxygen supply either with fibrinolytic agents or with mechanical coronary angioplasty. The clinical experience of coronary reperfusion showed that left ventricle function did not normalize in 30% of the patients. In spite of unblocking the epicardial vessel, demonstrated hemodynamically, no equivalent myocardial perfusion was observed in these studies. New concepts emerged such as reperfusion injury, microvascular dysfunction, "no-reflow" phenomenon, stunned myocardium, and hibernating myocardium, which have become the target of basic research and clinical investigation. The replication of these phenomena in experimental models has attempted on the one hand to improve characterization with the use of different technologies, e.g. contrast echocardiography, isotopic studies including positron tomography, and magnetic resonance. On the other hand it has tested new therapeutic approaches as adjuvants of coronary reperfusion. Reperfusion injury is responsible for 50% of infarct size, so it became the target of research on cardiac protection. Post-reperfusion arrhythmias, stunned myocardium, microvascular obstruction that translates into the "no-reflow" phenomenon, are reperfusion injury manifestations. Imaging technology developments made it possible to demonstrate that microvascular obstruction occurs in 40% of patients who underwent primary angioplasty. Several therapeutic approaches to prevent microembolization have been studied such as glycoprotein IIb/IIIa receptor blockers. Ischemic myocardium conditioning is one of the new strategies to reduce reperfusion injury. The concept of pre-conditioning, defined experimentally in 1986, establishes that multiple brief episodes of ischemia may protect the heart from a subsequent prolonged infarction. Several observations have proved that pre-conditioning occurs in cardiac patients, for example, during coronary angioplasty and coronary bypass graft surgery, and so it is regarded as a promising approach to reducing infarct size. The concept of pre-conditioning was then enlarged by the demonstration, experimentally, that producing ischemia in a vascular bed could induce pre-conditioning in another vascular bed. Ischemia resulting from repeated successive insufflations of a blood pressure cuff on a lim, reduces myocardial necrosis after coronary angioplasty or coronary bypass graft surgery. This remote pre-conditioning seems to be a safe and effective non-invasive way of reducing the reperfusion injury. In 2002 a hypothesis was tested in studies on dogs that multiple repeated episodes of ischemia, produced in the beginning of reperfusion, would attenuate the reperfusion injury. This technique, called post-conditioning, was first used in patients in 2005, in AMI reperfusion, with beneficial short and long-term results. In the last 15 years, a large number of clinical studies have been carried with different pharmacologic groups to explore association pre- and post-conditioning concepts. Four agents were studied in particular: adenosine, nicorandil, atrial natriuretic peptide, and statins. The most important studies are reviewed, calling attention to disparities in results and discussing possible causes of negative outcomes. Cyclosporine, recently tested, opens a new field of investigation since it inhibits mitochondrial permeability and may directly attenuate the reperfusion injury. Microvascular dysfunction occurs in many patients after coronary angioplasty and is caused, in the first place, by distal embolization. The purpose of thrombectomy is to reduce the probability of distal embolization during angioplasty and stent placement. Available devices for clinical use include thrombus aspiration and thrombectomy catheters. Initial studies did not have the expected impact, but the number of patients studied was limited. A recent series involving more than 1000 AMI patients undergoing coronary angioplasty and thrombus aspiration has shown an improvement of myocardial perfusion indices and a reduction of mortality at 30 days. Distal embolization protection systems aim to prevent the embolic material entering the circulation and causing macro-or microembolization. The present small and controversial experience does not yet recommend the routine use of this technique. Reduction of infarct size has been the main objective of research on ischemic myocardial disease during the last 40 years. Myocardial reperfusion is a major accomplishment in this field. But it is like a double-edged sword because reperfusion injury significantly reduces the potential benefits of reperfusion. The huge amount of research undertaken in the past 20 years constitutes a paradigm of the relationship between experimental work and clinical practice, and has improved the prospects for diminishing infarct size, in both the short and long-term.
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PMID:The reduction of infarct size--forty years of research. 2096 14

About 5% of patients undergoing coronary stenting need to undergo surgery within the next year. The risk of perioperative cardiac ischemic events, particularly stent thrombosis (ST), is high in these patients, because surgery has a prothrombotic effect and antiplatelet therapy is often withdrawn in order to avoid bleeding. The clinical and angiographic predictors of ST are well known, and the proximity to an acute coronary syndrome adds to the risk. The current guidelines recommend delaying non-urgent surgery for at least 6 weeks after the placement of a bare metal stent and for 6-12 months after the placement of a drug-eluting stent, when the risk of ST is reduced. However, in the absence of formal evidence, these recommendations provide little support with regard to managing urgent operations. When surgery cannot be postponed, stratifying the risk of surgical bleeding and cardiac ischemic events is crucial in order to manage perioperative antiplatelet therapy in individual cases. Dual antiplatelet therapy should not be withdrawn for minor surgery or most gastrointestinal endoscopic procedures. Aspirin can be safely continued perioperatively in the case of most major surgery, and provides coronary protection. In the case of interventions at high risk for both bleeding and ischemic events, when clopidogrel withdrawal is required in order to reduce perioperative bleeding, perioperative treatment with the short-acting intravenous glycoprotein IIb-IIIa inhibitor tirofiban is safe in terms of bleeding, and provides strong antithrombotic protection. Such surgical interventions should be performed at hospitals capable of performing an immediate percutaneous coronary intervention at any time in the case of acute myocardial ischemia.
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PMID:Management of patients with recently implanted coronary stents on dual antiplatelet therapy who need to undergo major surgery. 2181 37

Advances in antiplatelet therapy have significantly improved outcomes in patients with ischemic heart disease. Thienopyridines remain a cornerstone of therapy along with aspirin. Recently, concerns have been raised about the use of clopidogrel due to its pharmacokinetic and pharmacogenetic interpatient variability. A third-generation thienopyridine, prasugrel, overcomes some of these problems by improving inhibition of platelet aggregation, but increasing the risk of peri-procedural bleeding. Other novel antiplatelet agents, such as ticagrelor, have shown improved efficacy in recent trials and require further investigations. The field of pharmacotherapy continues to rapidly evolve as newer agents, such as thrombin receptor antagonists, along with older agents, such as cilostazol and glycoprotein IIb/IIIa inhibitors, are being explored.
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PMID:Novel antiplatelet therapies. 2210 61

Ischemic heart disease shows gender differences, both in terms of clinical characteristics and pathophysiological mechanisms. It is still debated whether these characteristics influence the diagnostic and therapeutic approach and the outcomes in female patients treated with percutaneous coronary intervention. Percutaneous coronary intervention in women has been shown to be feasible, safe and effective as it is in men throughout the whole clinical spectrum of ischemic syndromes. There is a solid scientific evidence of a different diagnostic and therapeutic approach to women suffering from ischemic heart disease compared to men, with a tendency to undertreat female patients, despite the worst risk profile at presentation. Women, in fact, less frequently undergo coronary angiography and receive antiplatelet, antithrombotic or anti-ischemic drugs. They experience more bleedings than men after administration of glycoprotein IIb/IIIa inhibitors. Gender differences, therefore, affect more the clinical than the interventional approach. At least in part, this is due to the fact that current guidelines are based on a male model of diagnostics. It would be desirable to analyze cohorts of patients in whom the percentage of individuals of both sexes will be equally represented, or rather, exclusively female cohorts in order to formulate more targeted diagnostic and therapeutic indications.
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PMID:[Does percutaneous coronary intervention in women provide the same results as in men?]. 2262 20

The Third Universal Definition of Myocardial Infarction (MI) requires cardiac myocyte necrosis with an increase and/or a decrease in a patient's plasma of cardiac troponin (cTn) with at least one cTn measurement greater than the 99(th) percentile of the upper normal reference limit during: (1) symptoms of myocardial ischemia; (2) new significant electrocardiogram (ECG) ST-segment/T-wave changes or left bundle branch block; (3) the development of pathological ECG Q waves; (4) new loss of viable myocardium or regional wall motion abnormality identified by an imaging procedure; or (5) identification of intracoronary thrombus by angiography or autopsy. Myocardial infarction, when diagnosed, is now classified into five types. Detection of a rise and a fall of troponin are essential to the diagnosis of acute MI. However, high sensitivity troponin assays can increase the sensitivity but decrease the specificity of MI diagnosis. The ECG remains a cornerstone in the diagnosis of MI and should be frequently repeated, especially if the initial ECG is not diagnostic of MI. There have been significant advances in adjunctive pharmacotherapy, procedural techniques and stent technology in the treatment of patients with MIs. The routine use of antiplatelet agents such as clopidogrel, prasugrel or ticagrelor, in addition to aspirin, reduces patient morbidity and mortality. Percutaneous coronary intervention (PCI) in a timely manner is the primary treatment of patients with acute ST segment elevation MI. Drug eluting coronary stents are safe and beneficial with primary coronary intervention. Treatment with direct thrombin inhibitors during PCI is non-inferior to unfractionated heparin and glycoprotein IIb/IIIa receptor antagonists and is associated with a significant reduction in bleeding. The intra-coronary use of a glycoprotein IIb/IIIa antagonist can reduce infarct size. Pre- and post-conditioning techniques can provide additional cardioprotection. However, the incidence and mortality due to MI continues to be high despite all these recent advances. The initial ten year experience with autologous human bone marrow mononuclear cells (BMCs) in patients with MI showed modest but significant increases in left ventricular (LV) ejection fraction, decreases in LV end-systolic volume and reductions in MI size. These studies established that the intramyocardial or intracoronary administration of stem cells is safe. However, many of these studies consisted of small numbers of patients who were not randomized to BMCs or placebo. The recent LateTime, Time, and Swiss Multicenter Trials in patients with MI did not demonstrate significant improvement in patient LV ejection fraction with BMCs in comparison with placebo. Possible explanations include the early use of PCI in these patients, heterogeneous BMC populations which died prematurely from patients with chronic ischemic disease, red blood cell contamination which decreases BMC renewal, and heparin which decreases BMC migration. In contrast, cardiac stem cells from the right atrial appendage and ventricular septum and apex in the SCIPIO and CADUCEUS Trials appear to reduce patient MI size and increase viable myocardium. Additional clinical studies with cardiac stem cells are in progress.
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PMID:Recent advances in the diagnosis and treatment of acute myocardial infarction. 2601 57


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