Showing papers by "Elliott M. Antman published in 2003"
TL;DR: The Clinical Efficacy Assessment Subcommittee of the American College of Physicians–American Society of Internal Medicine acknowledges the scientific validity of this product as a background paper and as a review that captures the levels of evidence in the management of patients with chronic stable angina as of November 17, 2002.
Abstract: The Clinical Efficacy Assessment Subcommittee of the American College of Physicians–American Society of Internal Medicine acknowledges the scientific validity of this product as a background paper and as a review that captures the levels of evidence in the management of patients with chronic stable angina as of November 17, 2002
The American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or a full revision is needed This process gives priority to areas in which major changes in text, and particularly recommendations, are merited on the basis of new understanding or evidence Minor changes in verbiage and references are discouraged
The ACC/AHA/American College of Physicians–American Society of Internal Medicine (ACP-ASIM) Guidelines for the Management of Patients With Chronic Stable Angina, which were published in June 1999, have now been updated The full-text guideline incorporating the updated material is available on the Internet (wwwaccorg or wwwamericanheartorg) in both a track-changes version showing the changes in the 1999 guideline in strike-out (deleted text) and highlighting …
1,796 citations
TL;DR: There are extensive revisions, especially of the sections on ischemic heart disease; congestive heart failure, cardiomyopathy, and assessment of left ventricular (LV) function; and screening and echocardiography in the critically ill.
1,523 citations
TL;DR: The American College of Cardiology/AHA Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or full revision is needed.
1,360 citations
TL;DR: New guidelines for the management of patients with supraventricular arrhythmias are introduced and recommended for use in combination with standard clinical practice.
Abstract: ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary : a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias).
966 citations
TL;DR: This document was approved by the American College of Cardiology Foundation Board of Trustees in May 2003, byThe American Heart Association Science Advisory and Coordinating Committee in May2003, and by theAmerican Society of Echocardiography Board of Directors in May 2002.
825 citations
01 Jan 2003
TL;DR: Blomstrom-Lundqvist et al. as discussed by the authors proposed the ESC guidelines for the management of patients with supraventricular arrhythmias, which are based on the guidelines of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.
Abstract: M This document does not cover atrial fibrillation; atrial fibrillation is covered in the ACC/AHA/ESC guidelines on the management of patients with atrial fibrillation found on the ACC, AHA, and ESC Web sites. † Former Task Force Member. ‡ Immediate Past Chair. This document was approved by the American College of Cardiology Foundation Board of Trustees in August 2003, by the American Heart Association Science Advisory and Coordinating Committee in July 2003, and by the European Society of Cardiology Committee for Practice Guidelines in July 2003. When citing this document, the American College of Cardiology Foundation, the American Heart Association, and the European Society of Cardiology request that the following citation format be used: Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, Alpert JS, Calkins H, Camm AJ, Campbell WB, Haines DE, Kuck KH, Lerman BB, Miller DD, Shaeffer CW, Stevenson WG, Tomaselli GF. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias.). Eur Heart J 2003;doi:10.1016/j.ehj.2003.08.002. This document is available on the World Wide Web sites of the American College of Cardiology (www.acc.org), the American Heart Association (www.americanheart.org), and the European Society of Cardiology (www.escardio.org), as well as published in the October 15, 2003, issue of the Journal of the American College of Cardiology, the October 14, 2003, issue of Circulation, and the 24/20 October 15, 2003, issue of the European Heart Journal. Single and bulk reprints of both the full-text guidelines and the executive summary are available from Elsevier Publishers by calling +44.207.424.4200 or +44.207.424.4389, faxing +44.207.424.4433, or writing to Elsevier Publishers Ltd, European Heart Journal, ESC Guidelines—Reprints, 32 Jamestown Road, London, NW1 7BY, UK; or E-mail gr.davies@elsevier.com. Single copies of executive summary and the full-text guidelines are also available by calling 800-253-4636 or writing the American College of Cardiology Foundation, Resource Center, at 9111 Old Georgetown Road, Bethesda, MD 20814-1699. To purchase bulk reprints (specify version and reprint number—executive summary 71-0261 and full-text guideline 71-0262): up to 999 copies, call 800-611-6083 (U.S. only) or fax 413-665-2671; 1000 or more copies, call 214-706-1789, fax 214-691-6342; or E-mail pubauth@heart.org. a American College of Cardiology b American Heart Association c European Society of Cardiology European Heart Journal (2003) ++, 1–41
599 citations
TL;DR: In this paper, the authors present a set of guidelines for the diagnosis and management of supraventricular arrhythmias, which are intended to assist physicians in clinical decision-making by describing a range of generally acceptable approaches.
593 citations
TL;DR: The American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or full revision is needed as discussed by the authors.
Abstract: The American College of Cardiology (ACC)/American Heart Association (AHA) Task Force on Practice Guidelines regularly reviews existing guidelines to determine when an update or full revision is needed. Guidelines for the Clinical Use of Cardiac Radionuclide Imaging were originally published in 1986
564 citations
TL;DR: The most recent guideline for the use of transesophageal echocardiography (TEE) was published by the American Society of Anesthesiologists (ASAnet) and the Society of Cardiovascular Anetians (SCARA) as discussed by the authors.
Abstract: The previous guideline for the use of echocardiography was published in March 1997. Since that time, there have been significant advances in the technology of echocardiography and growth in its clinical use and in the scientific evidence leading to recommendations for its proper use.
Each section has been reviewed and updated in evidence tables, and where appropriate, changes have been made in recommendations. A new section on the use of intraoperative transesophageal echocardiography (TEE) is being added to update the guidelines published by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists. There are extensive revisions, especially of the sections on ischemic heart disease; congestive heart failure, cardiomyopathy, and assessment of left ventricular (LV) function; and screening and echocardiography in the critically ill. There are new tables of evidence and extensive revisions in the ischemic heart disease evidence tables.
Because of space limitations, only those sections and evidence tables with new recommendations will be printed in this summary article. Where there are minimal changes in a recommendation grouping, such as a change from Class IIa to Class I, only that change will be printed, not the entire set of recommendations. Advances for which the clinical applications are still being investigated, such as the use of myocardial contrast agents and three-dimensional echocardiography, will not be discussed.
The original recommendations of the 1997 guideline are based on a Medline search of the English literature from 1990 to May 1995. The original search yielded more than 3000 references, which the committee reviewed. For this guideline update, literature searching was conducted in Medline, EMBASE, Best Evidence, and the Cochrane Library for English-language meta-analyses and systematic reviews from 1995 through September 2001. Further searching was conducted for new clinical trials on the following topics: echocardiography in adult congenital heart disease, echocardiography for evaluation …
546 citations
TL;DR: In a large cohort of patients with acute coronary syndromes, an elevated baseline level of MCP-1 was associated both with traditional risk factors for atherosclerosis as well as an increased risk for death or myocardial infarction, independent of baseline variables.
Abstract: Background— Monocyte chemoattractant protein-1 (MCP-1) is a chemokine responsible for the recruitment of monocytes to sites of inflammation. MCP-1 appears to play a critical role at multiple stages in atherosclerosis, including the initiation of the fatty streak, promotion of plaque instability, and remodeling after myocardial infarction. Methods and Results— MCP-1 was measured from frozen plasma specimens in 279 healthy volunteers and 2270 patients with acute coronary syndromes enrolled in the Oral Glycoprotein IIb/IIIa Inhibition with Orbofiban in Patients with Unstable Coronary Syndromes (OPUS-TIMI) 16 trial. Median [25th, 75th percentiles] MCP-1 levels were 157 [124, 196] pg/mL in healthy volunteers and 178 [128, 238] pg/mL in the OPUS-TIMI 16 population (P<0.001). In OPUS-TIMI 16, baseline MCP-1 levels were associated with older age, female sex, hypertension, diabetes, prior coronary disease, and renal insufficiency (P<0.01 for each) but not with smoking status, body mass index, ejection fraction, tr...
455 citations
TL;DR: In the setting of STEMI, elevated Cr and/or impaired CrCl on presentation is associated with increased mortality, independent of other conventional risk factors and TRS, and does not appear to be mediated by reduced fibrinolytic efficacy among patients with impaired renal function.
TL;DR: A 65-year-old male presented for evaluation of chest pain this article, describing substernal chest pressure that comes on when he plays doubles tennis or walks up a hill on the golf course.
Abstract: Case Presentation : A 65-year-old male presents for evaluation of chest pain. He describes substernal chest pressure that comes on when he plays doubles tennis or walks up a hill on the golf course. His discomfort is associated with dyspnea and is relieved within a few minutes by rest. On one occasion, a golfing partner gave him one of his sublingual nitroglycerin tablets. This brought prompt relief of the discomfort. He denies any chest pain at rest or at night. He has a history of hypertension, for which he is taking a diuretic. On a routine physical examination last year, his cholesterol was 240, with low-density lipoprotein (LDL) cholesterol of 150. He is trying to follow a low-fat diet and lose weight to reduce this. He has smoked 1 pack of cigarettes a day most of his adult life, although he did quit for a year or 2 on 2 separate occasions in the past. He has no history of diabetes. Both his mother and father lived into their late eighties and died of cancer. He is an only child.
On physical examination, his blood pressure is 145/95 mm Hg. His heart rate is 72 beats per minute and regular. His cardiac examination is normal. His resting ECG is normal.
The patient undergoes a treadmill exercise test. He completes 6 minutes of exercise according to a Bruce protocol. He stops because of fatigue but does note some mild chest pressure at peak exercise. Peak exercise heart rate is 135 beats per minute, and the peak exercise blood pressure is 190/100 mm Hg. Exercise electrocardiography shows 0.5 mm of up-sloping ST depression measured 80 seconds after the J point at peak exercise.
To better define the patient’s diagnosis and prognosis, he then undergoes exercise myocardial perfusion imaging with sestamibi. He again …
TL;DR: Obesity did not impact clinical outcomes in the combined analysis of ESSENCE and TIMI 11B and patients without renal insufficiency have a higher risk of clinical events and major and any hemorrhages than patients without severe renal impairment, whether they are treated with UFH or enoxaparin.
TL;DR: Early recurrent MI is associated with increased mortality up to two years, however, most deaths occur early, and the risk of additional deaths between the index hospital period and two years was not significantly increased among patients with recurrent MI.
TL;DR: The ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, and the European Society of Cardiologist Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias).
Abstract: These practice guidelines are intended to assist physicians in clinical decision making by describing a range of generally acceptable approaches for the diagnosis and management of supraventricular arrhythmias. These guidelines attempt to define practices that meet the needs of most patients in most
TL;DR: The NICE-3 study was an open-label observational study of enoxaparin in combination with any 1 of 3 available GP IIb/IIIa antagonists in patients presenting with non-ST-elevation acute coronary syndromes.
TL;DR: The LMWHs could potentially replace unfractionated heparin as the antithrombotic agent of choice across the spectrum of acute coronary syndromes (ACSs) and as an adjunct to percutaneous coronary intervention (PCI).
Abstract: ContextLow-molecular-weight heparins (LMWHs) possess several potential pharmacological
advantages over unfractionated heparin as an antithrombotic agent.ObjectiveTo systematically summarize the clinical data on the efficacy and safety
of LMWHs compared with unfractionated heparin across the spectrum of acute
coronary syndromes (ACSs), and as an adjunct to percutaneous coronary intervention
(PCI).Data SourcesWe searched MEDLINE for articles from 1990 to 2002 using the index terms heparin, enoxaparin, dalteparin, nadroparin, tinzaparin, low molecular
weight heparin, myocardial infarction, unstable angina, coronary angiography,
coronary angioplasty, thrombolytic therapy, reperfusion, and drug therapy, combination. Additional data sources included
bibliographies of articles identified on MEDLINE, inquiry of experts and pharmaceutical
companies, and data presented at recent national and international cardiology
conferences.Study SelectionWe selected for review randomized trials comparing LMWHs against either
unfractionated heparin or placebo for treatment of ACS, as well as trials
and registries examining clinical outcomes, pharmacokinetics, and/or phamacodynamics
of LMWHs in the setting of PCI. Of 39 studies identified, 31 fulfilled criteria
for analysis.Data ExtractionData quality was determined by publication in the peer-reviewed literature
or presentation at an official cardiology society–sponsored meeting.Data SynthesisThe LMWHs are recommended by the American Heart Association and the
American College of Cardiology for treatment of unstable angina/non–ST-elevation
myocardial infarction. Clinical trials have demonstrated similar safety with
LMWHs compared with unfractionated heparin in the setting of PCI and in conjunction
with glycoprotein IIb/IIIa inhibitors. Finally, LMWHs show promise as an antithrombotic
agent for the treatment of ST-elevation myocardial infarction.ConclusionsThe LMWHs could potentially replace unfractionated heparin as the antithrombotic
agent of choice across the spectrum of ACSs. In addition, they show promise
as a safe and efficacious antithrombotic agent for PCI. However, further study
is warranted to define the benefit of LMWHs in certain high-risk subgroups
before their use can be universally recommended.
TL;DR: In the ideal circumstance, physicians could reliably identify patients with definite ACS and begin appropriate therapy as early as possible, as well as distinguish those without acute coronary ischemia who may be candidates for early discharge without extended observation in the emergency department, chest pain unit, or inpatient wards.
Abstract: With ∼8 million patients arriving with nontraumatic chest pain to emergency departments in the US each year, the clinical evaluation, triage, and management of patients with possible acute coronary syndromes (ACS) presents a substantial medical and fiscal challenge (1). Although 2–5% of patients with myocardial infarction (MI) are inadvertently discharged from the emergency department and are a leading reason for malpractice claims, more than 50% of patients hospitalized for evaluation of chest pain are discharged with diagnoses other than ACS (1). Among those patients with definite ACS, early treatment may reduce the extent of myocardial injury, and thus rapid diagnosis and initiation of therapy is a central tenet of management (2). In addition, given the increasing array of treatments for the heterogeneous population of patients admitted with definite ACS, effective risk stratification and targeting of therapy have become a focus of contemporary management of ACS (2)(3). As such, the objectives of the initial assessment are twofold: (a) to assess the probability that the patient’s symptoms are related to acute coronary ischemia; and (b) to assess the patient’s risk of recurrent cardiac events, including death and recurrent ischemia (2). In the ideal circumstance, physicians could reliably identify patients with definite ACS and begin appropriate therapy as early as possible, as well as distinguish those without acute coronary ischemia who may be candidates for early discharge without extended observation in the emergency department, chest pain unit, or inpatient wards.
Unfortunately, other than in the ∼15% of patients with ACS who present with diagnostic ST-segment elevation, our basic clinical tools (history, physical exam, and electrocardiogram) for making the diagnosis of ACS offer limited sensitivity and specificity. Biomarkers of myocardial necrosis add importantly to these other clinical tools and are a critical component of the assessment of suspected ACS (4). In particular, …
TL;DR: In this article, a 50-year-old male presented to his office for evaluation of a recent episode of atrial fibrillation, where he was working in a woodworking shop on a large cabinet and fell on his right great toe.
Abstract: Case Presentation: A 50-year-old male presents to your office for evaluation of a recent episode of atrial fibrillation. The patient had no prior history of atrial fibrillation until 3 days ago. At that time, he was working in his home woodworking shop on a large cabinet. The cabinet slipped out of the clamps holding it and fell on his right great toe. The patient was having moderate to severe toe pain when he noticed that his heart was beating rapidly and irregularly. His palpitations were not associated with any chest pain, shortness of breath, or lightheadedness. He went to his local emergency room. His blood pressure was 135/80, and his pulse was rapid and irregularly irregular. An ECG showed that he was in atrial fibrillation with a ventricular response rate of 160. There were no ST segment changes. Before the patient received any therapy, he converted to normal sinus rhythm. The total duration of his episode of atrial fibrillation was 2 hours. A subsequent ECG was entirely normal. X-rays of his right foot did not show any fracture. He was discharged from the local emergency room and advised to see you. The patient is physically active. He denies any history of chest pain or chest pressure. He has no history of hypertension, diabetes, or tobacco use. His only other medical problem is mild asthma, treated with occasional inhalers. Both his mother and father lived into their late 80s and died of cancer. His two siblings are both alive and well without any cardiovascular disease. On physical examination, his blood pressure is 120/ 80 mm Hg. His heart rate is 70 bpm and regular. His cardiac examination is normal. On lung examination, there are rare wheezes over both lung fields. His right great toe is badly bruised. His ECG from the local emergency room is available and is normal. What are the appropriate next steps in the evaluation of this patient, as outlined in the American College of Cardiology (ACC)/American Heart Association (AHA)/European Society of Cardiology (ESC) Guidelines for the Management of Patients With Atrial Fibrillation?1 Appropriate clinical evaluation is shown in Table 1. This patient merits a chest x-ray (to evaluate his rare wheezes), a transthoracic echocardiogram, and blood tests of thyroid function. None of the additional tests listed, ie, exercise testing, Holter monitoring, transesophageal echocardiography, or electrophysiological study, are appropriate at this time.
TL;DR: In patients with a LAD culprit lesion, proximal lesion location is a multivariate correlate of adverse outcomes even after adjustment for coronary blood flow and other covariates, which is likely due to a larger area of subtended myocardium.
Abstract: Impaired coronary artery blood flow and left anterior descending (LAD) artery culprit location are angiographic variables that have been associated with poorer outcomes after fibrinolytic administration in patients with acute myocardial infarction (AMI). We hypothesized that culprit lesion location in the proximal portion of the culprit artery would also be associated with poorer clinical outcomes compared with a mid or distal location. Lesion location and clinical outcomes were evaluated in 2,488 patients from the Thrombolysis In Myocardial Infarction (TIMI) 4, 10A, 10B, and 14 trials. Proximal lesions were located before or at the first major branch of the parent artery, mid lesions were between the first and the second major branches, and all other lesions were classified as distal. Proximal lesions were associated with a higher incidence of in-hospital death or recurrent AMI compared with mid or distal lesions (10.5% [n = 478] vs 6.1% [n = 1,498] vs 3.7% [n = 511], p <0.001), and they were associated with a higher rate of in-hospital death (6.7% [n = 478] vs 3.2% [n = 1,498] vs 2.5% [n = 511], p = 0.001). In a multiple logistic regression model adjusting for TIMI flow grade, age, gender, and pulse, the planimetered distance from the ostium to the LAD culprit lesion was associated with 30-day death or recurrent AMI (odds ratio 0.79 per centimeter increase in distance down the artery, p = 0.01). Proximal culprit lesion location is associated with an increased risk of adverse outcomes after fibrinolytic administration, which is likely due to a larger area of subtended myocardium. In patients with a LAD culprit lesion, proximal lesion location is a multivariate correlate of adverse outcomes even after adjustment for coronary blood flow and other covariates.
TL;DR: Using the TIMI risk score to categorize patients also effectively defines a gradient for benefit with specific treatments such as low-molecular-weight heparins, glycoprotein IIb/IIIa inhibitors, and an early invasive strategy.
TL;DR: The increase in systemic bleeding and apparent excess of intracranial hemorrhage among STEMI patients over 75 years has led to reassessment of the suitability of combination reperfusion with IV GP IIb/IIIa inhibitors and reduced dose fibrinolysis.
Abstract: “The reports of my death are greatly exaggerated.” — —Mark Twain, 1897, cable from London to the Associated Press
Pharmacological reperfusion therapy for acute myocardial infarction was incorporated into the armamentarium of clinicians over 15 years ago and has had an extraordinarily beneficial impact on outcome of patients with ST-elevation myocardial infarction (STEMI). There are 3 fundamental components to pharmacological reperfusion; these consist of the core fibrinolytic agent as well as the accompanying antithrombotic and antiplatelet conjunctive therapies. No contemporary therapy in cardiovascular medicine has been as carefully and critically examined in multiple large randomized trials. These have comprehensively examined the efficacy, safety, and impact of novel therapeutic third-generation fibrinolytics and advances in conjunctive therapies aimed at enhancing restoration of myocardial flow in the epicardial infarct-related coronary artery.1–3
The tissue plasminogen activator (tPA) congeners tenecteplase (TNK-tPA) and reteplase (rPA) that possess initial plasma half-lives of 15 to 30 minutes constitute the newest, most conveniently administered bolus fibrinolytics. They not only reduce the potential for medication errors but also greatly simplify the prospects of prehospital fibrinolysis.2–4 Although these newer agents do not confer additional mortality reduction over that achieved by the 90-minute weight-adjusted accelerated t-PA regimen, the enhanced fibrin specificity of TNK-tPA results in a significant reduction in systemic bleeding.4 Whereas conjunctive therapy with intravenous glycoprotein IIb/IIIa (IV GP IIb/IIIa) inhibitors enhances epicardial flow and myocardial perfusion and reduces reinfarction, these advantages have not resulted in the expected improvement in survival.5,6 Indeed, the increase in systemic bleeding and apparent excess of intracranial hemorrhage among STEMI patients over 75 years has led to reassessment of the suitability of combination reperfusion with IV GP IIb/IIIa inhibitors and reduced dose fibrinolysis.7,8 Currently, the combination of full dose fibrinolysis and low molecular weight heparin or a direct antithrombin appears to …
TL;DR: In this prospective registry, patients not enrolled in a clinical trial had higher risk characteristics and worse outcomes; however, they also were treated less frequently with guideline-recommended medications, which may have contributed to their higher mortality rates.
Journal Article•
TL;DR: A mathematical model is developed to estimate how far down the coronary artery a drug-eluting stent would have to be placed to theoretically mitigate the risk of proximal plaque rupture, and the majority of culprit lesions in STEMI are contained within the proximal 30% of the major epicardial coronary arteries.
Abstract: Background: Shorter distances from the coronary ostia to culprit lesions have been associated with a higher incidence of adverse outcomes in ST elevation acute myocardial infarction (STEMI). As drug-eluting stents are associated with low rates of restenosis and formation of a stable intima, we sought to develop a mathematical model to estimate how far down the coronary artery a drug-eluting stent would have to be placed to theoretically mitigate the risk of proximal plaque rupture.
TL;DR: Evidence supporting the use of glycoprotein IIb/IIIa inhibitors in unstable angina and non-ST-segment elevation myocardial infarction is reviewed.
TL;DR: Enoxaparin clearance depends on body weight, and, therefore, weight-adjusted dosing is recommended to minimize interpatient variability in drug exposure and the risk of haemorrhage.
Abstract: Aims A major concern with any antithrombotic therapy is an increase in the risk of haemorrhage. The aim of this study was to analyse population pharmacokinetics and pharmacokinetic/pharmacodynamic (PK/PD) relationships for enoxaparin in patients with unstable angina (UA) and non-ST-segment elevation myocardial infarction (NSTEMI), which may help predict risk of haemorrhage.
Methods Anti-factor Xa (anti-Xa) activity was measured as marker of enoxaparin concentration in 448 patients receiving the drug as a single 30-mg intravenous bolus followed by 1.0 or 1.25 mg kg−1 subcutaneously twice a day. A population pharmacokinetic analysis was conducted and individual estimates of enoxaparin clearance and area under the curve were tested as prognostic factors for the occurrence of haemorrhagic episodes.
Results Basic population PK parameters were an enoxaparin clearance of 0.733 l h−1[95% confidence interval (CI) 0.698, 0.738], a distribution volume of 5.24 l (95% CI 4.20, 6.28) and an elimination half-life of 5.0 h. Enoxaparin clearance was significantly related to patient weight and creatinine clearance, and was the only independent predictor of experiencing both all (10.7%, P = 0.0013) and major (2.2%, P = 0.0004) haemorrhagic events. A creatinine clearance of 30 ml min−1 was associated with a decrease in enoxaparin clearance of 27% compared with that in a patient with a median creatinine clearance of 88 ml min−1, and was related to a 1.5- and 3.8-fold increase in the risk of ‘all’ and ‘major’ haemorrhagic episodes, respectively.
Conclusions Enoxaparin clearance depends on body weight, and, therefore, weight-adjusted dosing is recommended to minimize interpatient variability in drug exposure and the risk of haemorrhage. The importance of an increased risk of haemorrhage with decreasing renal function must be weighed against the benefit of treatment with enoxaparin in patients with UA and NSTEMI.
TL;DR: A 47-year-old man with no history of cardiac disease presented to a hospital, reporting severe substernal chest pressure associated with bilateral arm weakness, and was treated with fibrinolytic therapy and transferred to another hospital for catheterization.
Abstract: A 47-year-old man with no history of cardiac disease presented to a hospital, reporting severe substernal chest pressure associated with bilateral arm weakness. A standard 12-lead electrocardiogram (Panel A) showed marked ST-segment elevation in leads V1, V2, and V3 and slight ST-segment elevation in leads II, III, and aVF. The patient was treated with fibrinolytic therapy and transferred to another hospital for catheterization. Angiography showed severe proximal stenosis of a small, nondominant right coronary artery and no clinically significant disease in the left coronary artery. Contrast-enhanced magnetic resonance imaging 48 hours after presentation (Panel B) . . .