Treatment with anti-inflammatory drugs in community-acquired pneumonia.
J Intern …

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Von Willebrand factor predicts major bleeding and mortality during oral anticoagulant tre…

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Management of acute coronary syndrome: achievements and goals still to pursue. Novel deve…

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Stroke prevention in elderly patients with atrial fibrillation: challenges for anticoagul…

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Auto-antibodies against apolipoprotein A-1 and phosphorylcholine for diagnosis of non-ST-…

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Acute infections and venous thromboembolism.
J Intern Med. 2011 Oct 25;
Authors: Schmidt M, Horvath-Puho E, Thomsen RW, Smeeth L, Toft Sørensen H
Abstract
Objective:? The aim of the study was to examine whet…

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Combined clopidogrel and proton pump inhibitor therapy is associated with higher cardiovascular event rates after percutaneous coronary intervention: a report from the BASKET trial.
J Intern Med. 2011 Jul 5;
Authors: Burkard T…

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Patient-reported symptoms in acute myocardial infarction: differences related to ST-segment elevation. The MONICA/KORA Myocardial Infarction Registry.

J Intern Med. 2011 Feb 21;

Authors: Kirchberger I, Meisinger C, Heier M, Kling B, Wende R, Greschik C, von Scheidt W, Kuch B

Objectives:? The early recognition of symptoms of myocardial infarction (MI) is crucial for patients with both ST-segment elevation (STEMI) and non-ST-segment elevation MI (NSTEMI). However, to date only a few studies have examined the differences between patients with STEMI and NSTEMI with regard to the range of presenting MI symptoms. Design:? The study population comprised 889 individuals with STEMI and 1,268 with NSTEMI, aged 25-74 years, hospitalized with a first-time MI between January 2001 and December 2006 recruited from a population-based MI registry. The occurrence of 13 symptoms was recorded during a standardized patient interview. Results:? Patients with STEMI were significantly younger, more likely to be smokers and less likely to have a history of hypertension or sleep disturbances prior to the AMI event than those with NSTEMI. A total of 50% of the patients attributed their experienced symptoms to the heart. Logistic regression modelling revealed that patients with STEMI were significantly more likely than patients with NSTEMI to complain of vomiting (odds ratio [OR] 2.34, 95% confidence interval [CI] 1.76-3.05), dizziness (OR 1.63, 95% CI 1.30-2.03) and diaphoresis (OR 1.49, 95% CI 1.23-1.81). Furthermore, patients with STEMI were less likely to experience dyspnoea (OR 0.81, 95% CI 0.68-0.98) or pain in the throat/jaw (OR 0.80, 95% CI 0.66-0.98). Conclusions:? Only half of all patients correctly attributed their symptoms to the heart. Patients with STEMI and NSTEMI showed differences regarding several presenting symptoms. Further research is needed to replicate our results, and public awareness of AMI symptoms needs to be improved.

PMID: 21338424 [PubMed - as supplied by publisher]

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Antiphospholipid syndrome: laboratory detection, mechanisms of action and treatment.

J Intern Med. 2011 Feb 15;

Authors: Tripodi A, de Groot PG, Pengo V

The antiphospholipid syndrome (APS) identifies a condition at increased risk of vascular occlusion and/or pregnancy complications. Patients are defined as having APS if they have at least one clinical (vascular occlusion and/or pregnancy complications) and one laboratory criterion at the same time. The laboratory criteria that define APS are repeated positivity (confirmed 12 weeks apart) for lupus anticoagulants and/or antibodies targeted against cardiolipin or ?2-glycoprotein I immobilized on solid surfaces. Over the years APS has attracted the interest of many medical specialties. The aim of this review is to provide an update on: (i) the laboratory criteria that determine the presence of APS; (ii) how the antibodies increase the risk of vascular occlusion and fetal loss; and (iii) the treatment of the related clinical events.

PMID: 21323768 [PubMed - as supplied by publisher]

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Drug-drug interactions that reduce the formation of pharmacologically active metabolites: a poorly understood problem in clinical practice.

J Intern Med. 2010 Dec;268(6):540-8

Authors: Mannheimer B, Eliasson E

Abstract.? Mannheimer B, Eliasson E (Karolinska Institutet, Stockholm; Karolinska University Hospital Huddinge, Stockholm, Sweden) Drug-drug interactions that reduce the formation of pharmacologically active metabolites: a poorly understood problem in clinical practice (Review-Symposium). J Intern Med 2010; 268: 540-548. Drug-drug interactions can lead to reduced efficacy of medical treatment. Therapeutic failure may for instance result from combined treatment with an inhibitor of the specific pathway that is responsible for the generation of pharmacologically active drug metabolites. This problem may be overlooked in clinical practice. Several examples of drugs will be discussed -clopidogrel, losartan, tamoxifen and codeine – to illustrate differences in the potential impact on drug treatment in clinical practice. We conclude that the combined use of cytochrome P450-blocking serotonin reuptake inhibitors and tamoxifen or codeine should be avoided, whereas the situation is much more complex regarding the use of proton pump inhibitors together with clopidogrel, and the evidence regarding cytochrome P450 inhibitor-dependent activation of losartan is inconclusive.

PMID: 21091806 [PubMed - in process]

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Antiplatelet drug interactions.

J Intern Med. 2010 Nov 14;

Authors: Mackenzie IS, Coughtrie MW, Macdonald TM, Wei L

Abstract.? Mackenzie IS, Coughtrie MWH, MacDonald TM, Wei L. (Medicines Monitoring Unit (MEMO); and Centre for Oncology & Molecular Medicine, Division of Medical Sciences, University of Dundee, Ninewells Hospital & Medical School; Dundee, UK). Antiplatelet drug interactions (Review-Symposium). J Intern Med 2010; 268: 516-529. Both laboratory studies in healthy volunteers and clinical studies have suggested adverse interactions between antiplatelet drugs and other commonly used medications. Interactions described include those between aspirin and ibuprofen, aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), and the thienopyridine, clopidogrel, and drugs inhibiting CYP2C19, notably the proton pump inhibitors (PPI) omeprazole and esomeprazole. Other interactions between thienopyridines and CYP3A4/5 have also been reported for statins and calcium channel blockers. The ibuprofen/aspirin interaction is thought to be caused by ibuprofen blocking the access of aspirin to platelet cyclo-oxygenase. The thienopyridine interactions are caused by inhibition of microsomal enzymes that metabolize these pro-drugs to their active metabolites. We review the evidence for these interactions, assess their clinical importance and suggest strategies of how to deal with them in clinical practice. We conclude that ibuprofen is likely to interact with aspirin and reduce its anti-platelet action particularly in those patients who take ibuprofen chronically. This interaction is of greater relevance to those patients at high cardiovascular risk. A sensible strategy is to advise users of aspirin to avoid chronic ibuprofen or to ingest aspirin at least 2?h prior to ibuprofen. Clearly the use of NSAIDs that do not interact in this way is preferred. For the clopidogrel CYP2C19 and CYP3A4/5 interactions, there is good evidence that these interactions occur. However, there is less good evidence to support the clinical importance of these interactions. Again, a reasonable strategy is to avoid the chronic use of drugs that inhibit CYP2C19, notably PPIs, in subjects taking clopidogrel and use high dose H2 antagonists instead. Finally, anti-platelet agents probably interact with other drugs that affect platelet function such as selective serotonin reuptake inhibitors, and clinicians should probably judge patients taking such combination therapies as at high risk for bleeding.

PMID: 21073556 [PubMed - as supplied by publisher]

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Interleukin family member ST2 and mortality in acute dyspnoea.

J Intern Med. 2010 Jul 15;

Authors: Socrates T, Defilippi C, Reichlin T, Twerenbold R, Breidhardt T, Noveanu M, Potocki M, Reiter M, Arenja N, Heinisch C, Meissner J, Jaeger C, Christenson R, Mueller C

Abstract. Socrates T, deFilippi C, Reichlin T, Twerenbold R, Breidhardt T, Noveanu M, Potocki M, Reiter M, Arenja N, Heinisch C, Meissner J, Jaeger C, Christenson R, Mueller C. (Department of Internal Medicine, University Hospital Basel, Basel, Switzerland; University of Maryland, School of Medicine, Baltimore, MD, USA). Interleukin family member ST2 and mortality in acute dyspnoea. J Intern Med 2010; doi: 10.1111/j.1365-2796.2010.02263.x. Objectives. The study objective was to investigate the prognostic utility and patient-specific characteristics of ST2 (suppression of tumorigenicity 2), assessed with a novel sensitive assay. Background. Suppression of tumorigenicity 2 signalling has been shown to be associated with death in cardiac and pulmonary diseases. Design/Subjects. In an international multicentre cohort design, we prospectively enrolled 1091 patients presenting with acute dyspnoea to the emergency department (ED). ST2 was measured in a blinded fashion using a novel assay and compared to B-type natriuretic peptide (BNP) and NT-proBNP. The primary end-point was mortality within 30 days and 1 year. The prognostic value of ST2 was evaluated in comparison and in addition to BNP and NT-proBNP. Results. Suppression of tumorigenicity 2 concentrations was higher amongst decedents than among survivors (median 85 vs. 43 U mL(-1), P < 0.001) and also higher in patients with impaired left ventricular ejection fraction (LVEF) when compared with preserved LVEF (P < 0.001). In receiver operator characteristics analysis, the area under the curve (AUC) for ST2, BNP and NT-proBNP to predict 30-day and 1-year mortality were 0.76, 0.63 and 0.71, and 0.72, 0.71 and 0.73, respectively. The combinations of ST2 with BNP or NT-proBNP improved prediction of mortality provided by BNP or NT-proBNP alone. After multivariable adjustment, ST2 values above the median (50 U mL(-1)) significantly predicted 1-year mortality (HR 2.3, P < 0.001). Conclusion. In patients presenting to the ED with acute dyspnoea, ST2 is a strong and independent predictor of 30-day and 1-year mortality and might improve risk stratification already provided by BNP or NT-proBNP.

PMID: 20804518 [PubMed - as supplied by publisher]

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Contemporary management of pulmonary embolism: the answers to ten questions.

J Intern Med. 2010 Jun 14;

Authors: Bounameaux H

Abstract. Bounameaux H (Division of Angiology and Hemostasis, Department of Internal Medicine, University Hospitals of Geneva and Faculty of Medicine, Geneva, Switzerland). Contemporary management of pulmonary embolism: the answers to ten questions (Review). J Intern Med 2010; doi: 10.1111/j.1365-2796.2010.02254.x. Pulmonary embolism (PE) cannot be diagnosed solely on a clinical basis, because of the lack of sensitivity and specificity of clinical signs and symptoms. Pulmonary angiography is invasive and resource demanding. Because the prevalence of PE is relatively low (20% or less) amongst individuals who are clinically suspected of having the disease, submitting all of them to imaging (multi-detector CT angiography or ventilation/perfusion lung scintigraphy) would not be cost-effective. Therefore, diagnostic algorithms have been developed that include clinical probability assessment and D-dimer measurement to select the patients who require noninvasive imaging. Once the diagnosis is suspected or confirmed, therapy must be started to avoid potentially fatal recurrence. Treatment starts for an initial 3-month period with a 5-day course of parenteral unfractionated or low-molecular-weight heparin or fondaparinux overlapping with and followed by oral vitamin K antagonists monitored to maintain an international normalized ratio of 2-3. This initial period of 3 months may then be followed by a long-term secondary prevention period in patients who experience an idiopathic thromboembolic event and are at low risk of bleeding. New oral anticoagulants that do require patient monitoring and might exhibit a more favourable benefit-risk balance are currently under extensive clinical testing and might change the situation in the near future. A critical appraisal of the contemporary management of suspected PE is given in this overview with the discussion of 10 practical questions.

PMID: 20626551 [PubMed - as supplied by publisher]

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New features of troponin testing in different clinical settings.

J Intern Med. 2010 Jun 8;

Authors: Omland T

Abstract. Omland T. (Institute of Clinical Medicine, University of Oslo, Oslo and Division of Medicine, Akershus University Hospital, Lørenskog, Norway) New features of troponin testing in different clinical settings (Review). J Intern Med 2010. doi: 10.1111/j.1365-2796.2010.02253.x. Cardiac troponin levels are routinely measured for diagnosing acute myocardial infarction. Cardiac troponin measurements also provide information concerning prognosis and the effect of early intervention in patients with acute coronary syndromes. The recent development of highly sensitive cardiac troponin assays permits detection of very low circulating levels. Use of sensitive troponin assays improves overall diagnostic accuracy in patients with suspected acute coronary syndromes, and these assays provide strong prognostic information in stable coronary artery disease and chronic heart failure. However, increased sensitivity comes with a cost of decreased specificity, and serial testing, as well as clinical context and judgment, is likely to become increasingly important in the interpretation of troponin assay results.

PMID: 20626552 [PubMed - as supplied by publisher]

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Vitamin D deficiency and frailty in older Americans.

J Intern Med. 2010 Apr 28;

Authors: Wilhelm-Leen ER, Hall YN, Deboer IH, Chertow GM

Abstract. Wilhelm-Leen ER, Hall YN, deBoer IH, Chertow GM. (Stanford University School of Medicine; University of Washington; Stanford University School of Medicine, Palo Alto, CA, USA). Vitamin D deficiency and frailty in older Americans. J Intern Med 2010; doi: 10.1111/j.1365-2796.2010.02248.x. Objective. To explore the relation between 25-hydroxyvitamin D deficiency and frailty. Frailty is a multidimensional phenotype that describes declining physical function and a vulnerability to adverse outcomes in the setting of physical stress such as illness or hospitalization. Low serum concentrations of 25-hydroxyvitamin D are known to be associated with multiple chronic diseases such as cardiovascular disease and diabetes, in addition to all cause mortality. Design. Using data from the Third National Health and Nutrition Survey (NHANES III), we evaluated the association between low serum 25-hydroxyvitamin D concentration and frailty, defined according to a set of criteria derived from a definition previously described and validated. Subjects. Nationally representative survey of noninstitutionalized US residents collected between 1988 and 1994. Results. 25-Hydroxyvitamin D deficiency, defined as a serum concentration <15 ng mL(-1), was associated with a 3.7-fold increase in the odds of frailty amongst whites and a fourfold increase in the odds of frailty amongst non-whites. This association persisted after sensitivity analyses adjusting for season of the year and latitude of residence, intended to reduce misclassification of persons as 25-hydroxyvitamin D deficient or insufficient. Conclusion. Low serum 25-hydroxyvitamin D concentrations are associated with frailty amongst older adults.

PMID: 20528970 [PubMed - as supplied by publisher]

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