Validation of a combined comorbidity index.

https://www.medpagetoday.com/upload/2014/3/3/02536-1.pdf

2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease

Preamble and Transition to ACC/AHA Guidelines to Reduce Cardiovascular Risk S50

The goals of the American College of Cardiology (ACC) and the American Heart Association (AHA) are to prevent cardiovascular diseases (CVD); improve the management of people who have these diseases through professional education and research; and develop guidelines, standards, and policies that promote optimal patient care and cardiovascular health. Toward these objectives, the ACC and AHA have collaborated with the National Heart, Lung, and Blood Institute (NHLBI) and stakeholder and professional organizations to develop …

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2013 ACC/AHA Guideline on the Assessment of Cardiovascular Risk

Medical practice is constantly changing. The rate of change is accelerating, and physicians can be forgiven if they often find it dizzying. How can physicians learn about new information and innovations, and decide how (if at all) they should modify their practice? Possible sources include summaries from the medical literature (review articles, practice guidelines, consensus statements, editorials, and summary articles in "throwaway" journals); consultation with colleagues who have special expertise; lectures; seminars; advertisements in medical journals; conversations with representatives from pharmaceutical companies; and original articles in journals and journal supplements. Each of these sources of information might be valuable, though each is subject to its own particular biases. 1,2 Problems arise when, as is often the case, these sources of information provide different suggestions about patient care. See also p 2093. Without a way of critically appraising the information they receive, clinicians are relatively helpless in deciding what new information

https://hopkinsmedicine.org/gim/_pdf/jama/17-screening.pdf

Users' Guides to the Medical Literature

2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines

Clinical isolates of enterococci (Streptococcus faecalis) with high-level resistance to both streptomycin and kanamycin (minimal inhibitory concentration >2,000 mug/ml), and resistant to synergism with penicillin and streptomycin or kanamycin were examined for aminoglycoside-inactivating enzymes. All of the 10 strains studied had streptomycin adenylyltransferase and neomycin phosphotransferase activities; the latter enzyme phosphorylated amikacin as well as its normal substrates, such as kanamycin. Substrate profiles of the neomycin phosphotransferase activity suggested that phosphorylation occurred at the 3'-hydroxyl position, i.e., aminoglycoside 3'-phosphotransferase. A transconjugant strain, which acquired high-level aminoglycoside resistance and resistance to antibiotic synergism after mating with a resistant clinical isolate, also acquired both enzyme activities. Quantitative phosphorylation of amikacin in vitro by a sonicate of the transconjugant strain inactivated the antibiotic, as measured by bioassay, and the phosphorylated drug failed to produce synergism when combined with penicillin against a strain sensitive to penicillin-amikacin synergism.No differences were found in the sensitivity of ribosomes from a sensitive and resistant strain when examined in vitro using polyuridylic acid directed [(14)C]-phenylalanine incorporation in the presence of streptomycin, kanamycin, or amikacin. Therefore, we conclude that aminoglycoside-inactivating enzymes are responsible for the aminoglycoside resistance, and resistance to antibiotic synergism observed in these strains.

/pdf/aminoglycoside-inactivating-enzymes-in-clinical-isolates-of-jsa6c0abf9.pdf

Aminoglycoside-Inactivating Enzymes in Clinical Isolates of Streptococcus Faecalis: AN EXPLANATION FOR RESISTANCE TO ANTIBIOTIC SYNERGISM

Two hundred and three recent clinical isolates of enterococci were tested for susceptibility to streptomycin, kanamycin, amikacin, gentamicin, sisomicin, and tobramycin. Depending upon the source of the isolate, 36 to 54% of the enterococci demonstrated high-level resistance (minimal inhibitory concentration, >2,000 μg/ml) to streptomycin, 16 to 49% to kanamycin, and 0 to 14% to amikacin. None of the strains was highly resistant to gentamicin, sisomicin, or tobramycin. A comparison with isolates of enterococci obtained in 1968 revealed that there has been a decrease in prevalence of high-level resistance among organisms isolated from wound cultures in 1976. However, no decrease in resistance to streptomycin or kanamycin was demonstrated among blood or urine isolates. Penicillin, combined with gentamicin, sisomicin, or tobramycin, was synergistic against all 10 strains of Streptococcus faecalis subjected to formal testing. For streptomycin and kanamycin, the presence or absence of synergism with penicillin correlated with the absence or presence of high-level aminoglycoside resistance. High-level resistance to amikacin was seen in only 1 of the 10 strains. Nonetheless, combinations of penicillin plus amikacin failed to produce synergistic killing against 6 of the 10 strains. Indeed, the combination was synergistic only against those four strains that were susceptible to high levels of kanamycin.

Resistance to Six Aminoglycosidic Aminocyclitol Antibiotics Among Enterococci: Prevalence, Evolution, and Relationship to Synergism with Penicillin

Recent novel clinical applications of vancomycin have stimulated reinvestigations of the pharmacologic properties of this drug. Absorption from the gastrointestinal tract is negligible, and oral administration is appropriate only for patients with certain staphylococcal and clostridial diarrheas. After intravenous administration (the intramuscular route being painful), vancomycin is excreted by glomerular filtration, with virtually total recovery in the urine. Distribution is consistent with a three-compartment open pharmacokinetic model. Serum half-life values are usually greater than 8 min in the distribution phase, 30 min to 1.5 hr in the intermediate phase, and between 5 and 11 hr in the elimination phase. The level of binding to human serum proteins is 55%. Since the relation between the vancomycin clearance and the creatinine clearance (but not the level of creatinine in serum) is linear in both normal and impaired renal function, a nomogram has been prepared that delineates dosages that will produce a mean steady-state concentration in serum of 15 micrograms/ml. Vancomycin penetrates well into pericardial, pleural, synovial, and ascitic fluid in humans, but concentrations in cerebrospinal fluid after parenteral administration may be insufficient for the successful treatment of certain cases of meningitis.

Pharmacokinetics of Vancomycin in Normal Subjects and in Patients with Reduced Renal Function

MULTIFACTORIAL INDEX OF CARDIAC RISK IN NONCARDIAC SURGICAL PROCEDURES L. Goldman;D. Caldera;S. Nussbaum;F. Southwick;D. Krogstad;B. Murray;D. Burke;T. O'Malley;A. Goroll;C. Caplan;J. Nolan;B. Carabello;E. Slater; Survey of Anesthesiology

Donald J. Krogstad

Papers

Aminoglycoside-Inactivating Enzymes in Clinical Isolates of Streptococcus Faecalis: AN EXPLANATION FOR RESISTANCE TO ANTIBIOTIC SYNERGISM

Resistance to Six Aminoglycosidic Aminocyclitol Antibiotics Among Enterococci: Prevalence, Evolution, and Relationship to Synergism with Penicillin

Pharmacokinetics of Vancomycin in Normal Subjects and in Patients with Reduced Renal Function

Multifactorial index of cardiac risk in noncardiac surgical procedures

Current concepts in parasitology. Amebiasis.