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)

Traditionally, myocardial ischemia has been viewed as an imbalance in the supply and demand of myocardial oxygen. Stable angina is usually considered to involve a fixed lesion, whereas unstable angina involves a fixed lesion as well as such components as platelet aggregation, thrombotic processes, and vasospasm. Variant angina involves primarily vasospasm. A newer concept holds that most angina results from mixed mechanisms in which both fixed lesions and vasomotor alterations play a role. These mechanisms are responsible for mixed ischemic events, characterized by episodes at varying levels of exertion, with or without anginal pain. This concept would seem to be supported by the occurrence of silent ischemia in the setting of stable, unstable, or variant angina, despite differing pathophysiologic conditions. Ischemic events have important prognostic significance; unfortunately, many are unrecognized by patients. The question whether the treatment of ischemic events will improve prognosis remains a matter of debate.
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PMID:Mechanisms of myocardial ischemia. 144 93

A rational therapy of angina pectoris has to consider two recent pathophysiologic insights: 1. Not only in patients with instable but also with stable angina a dynamic, vasospastic component in addition to stenosis plays an important role. Stable angina is often a mixed form of disease. 2. In many patients stable angina is complicated by silent ischemia. Therapy of stable angina has 3 goals: 1. prevention or alleviation of angina; 2. reduction of silent ischemia episodes (number, extent); 3. cardioprotection i.e. prevention of instable angina, infarction and sudden death. The pharmacotherapeutic cornerstones are the nitrates, beta-blocking agents and calcium channel blockers. Their generally equivalent efficacy in short and longterm use is clinically and hemodynamically proven without doubt. Mode of action, pharmacokinetic aspects and recent as well as controversial questions regarding this group of drugs are reviewed. The pharmacotherapy of first choice should be determined for each patient individually and not according to schematic prescription. It should encompass pathogenesis of ischemia, specific indications for or adverse effects of the 3 drug classes, the question of induction of tolerance, possible cardioprotective benefit, side effects, compliance problems and finally cost of treatment. The rational aspects of combination therapy (nitrates and beta-blockers, beta-blockers and calcium antagonists) are explained and the therapeutic procedures for instable angina are outlined.
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PMID:[Therapy of angina pectoris--state of the art]. 196 77

The effect of stent coatings in preventing early thrombotic occlusion remains to be proved. The purpose of this study was to evaluate the safety and efficacy of the Carbostent, a new coronary stent with a nonthrombogenic coating (Carbofilm), in 110 consecutive patients (73.6% men, mean age 61 +/- 9 years) who met prespecified clinical and angiographic inclusion criteria and were treated with aspirin monotherapy after stenting. Stable angina (75.5%), unstable angina (18.2%), and silent ischemia (6.3%) were clinical indications for coronary revascularization. Patients received 10,000 U of heparin and no IIb/IIIa inhibitors or postprocedural heparin. Complex lesion characteristics (B2, C) were present in 39 out of 129 (30.2%) lesions. Mean lesion length was 15.6 +/- 7.4 mm, and 32% of the lesions were >15 mm (range 16-52 mm). Small coronary vessels (<3.0 mm) were treated in 28% of the cases. A total of 165 Carbostent were used in 129 coronary lesions of the 110 patients. Single-vessel stenting was performed in 97 (88%) patients and multivessel stent placement in 13 (12%) patients. The mean length of the stented segment was 21 +/- 13 mm (range 9-95 mm). Procedural and clinical success was achieved in all patients. At 1-month follow-up, there were no stent thrombosis or other major adverse cardiac events. We observed 2 (1.8%) non-Q-wave myocardial infarctions and 2 (1.8%) vascular complications. This study indicates that the Carbostent may prevent stent thrombosis in selected patients treated with aspirin only. A randomized study comparing aspirin alone versus combined ticlopidine and aspirin after Carbostent implantation will be needed to confirm these results.
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PMID:Aspirin alone antiplatelet regimen after intracoronary placement of the Carbostent: the ANTARES study. 1183 38

The aim of this multicenter, prospective, non-randomized study was to examine the procedural, in-hospital, and mid-term clinical and angiographic outcome of patients undergoing coronary angioplasty with the Tecnic Carbostent system. Between October 2001 and March 2002, 123 consecutive patients were treated with coronary implantation of the Tecnic Carbostent. Stable angina (54%), unstable angina (37%) and silent ischemia (9%) were clinical indications for revascularisation. The baseline lesion morphology was complex (Type B2 or C) in 59% of the cases, and the mean lesion length was 15+/-8 mm. A total of 179 stents were implanted in 149 lesions. The procedural success rate was 100%. Mean percent diameter of the stenosis decreased after the intervention from 75%+/-11% to 8%+/-4%. The mean cross-sectional area stent recoil was 8.8%+/-7.3%. No in-hospital or 30-day major adverse cardiac events were observed. During the 6-month follow-up period, there were no deaths or myocardial infarctions, whereas the incidence of target lesion revascularisation was 12.7%. The angiographic restenosis rate was 14.1%: a focal or limited pattern (class I or II) was found in 83% of cases, whereas the remaining 17% had a proliferative morphology (class III or IV). In conclusion, this study indicates that a good clinical and angiographic outcome may be obtained with the Tecnic Carbostent coronary system in consecutive patients with de novo coronary lesions.
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PMID:Six-month clinical and angiographic outcomes of the Tecnic Carbostent coronary system: the phantom IV study. 1555 Jul 35

Stable angina (SA) pectoris is a common and disabling disorder in patients with coronary artery disease (CAD), with increasing epidemiology and is associated with myocardial infarction and increased mortality. However, within the population of SA patients, an individual's prognosis can vary considerably. Except from conventional risk factors a variety of biomarkers have been evaluated for their prognostic significance in the settings of SA. Novel biomarkers associated with inflammatory status, such as C reactive protein and tumor necrosis factor alpha, with myocardial performance, such as B-type natriuretic peptide, with extracellular matrix remodeling, with vascular calcification such as osteoprotogerin and osteopontin, with myocardial ischemia, such as ischemia modified albumin have been associated with the progression of CAD and with the prognosis of SA patients. Despite the multiplicity of novel biomarkers there is lack of a clinical useful, highly specific for CAD biomarker with the ability to guide treatment decisions. In the context of this evidence in this review article we summarize the so far acquired knowledge of the most promising biomarkers and we discuss the major clinical correlations of novel risk factors with SA physical history, their predictive value for future cardiovascular events and their use in the treatment monitoring of this population.
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PMID:Novel risk factors related to stable angina. 2301 18

Ischemic heart disease, the leading cause of death worldwide, may result in devastating perioperative ischemia and infarction. The underlying pathophysiology, precipitating factors, and approach to prevention differ between patients presenting for noncardiac surgery, developing acute coronary syndrome versus stable angina. The first half of this article reviews the pathophysiology of acute coronary syndrome and stable angina. Acute coronary syndrome, otherwise known as Type 1 myocardial infarction, includes unstable angina, non-ST segment elevated myocardial infarction and ST segment elevated myocardial infarction. Acute coronary syndrome occurs as a result of vulnerable plaque rupture with subsequent varying degrees of thrombus formation, arterial spasm, and thus coronary occlusion. Stable angina, on the other hand, results from a myocardial oxygen delivery and demand mismatch in the setting of fixed coronary stenosis. After this discussion, the review article considers how both apply to perioperative myocardial infarctions and myocardial injury after noncardiac surgery. This article furthermore argues why myocardial oxygen delivery demand mismatch (Type 2) myocardial infarction is the most likely underlying pathophysiology responsible for perioperative myocardial infarctions. Being aware of this and knowledgeable about Type 2 infarctions may enable anesthetic providers to better predict the majority of triggers contributing to, and thus decreasing the incidence of, perioperative myocardial infarctions.
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PMID:The Pathophysiology of Myocardial Ischemia and Perioperative Myocardial Infarction. 3168 19