https://caltcm.memberclicks.net/assets/documents/acc_aha_chf_2013_guidelines.pdf

2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines

https://vascular.stanford.edu/content/dam/sm/vascular/documents/endovasc/guidelines/PIIS0741521406022968.pdf

Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II)

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/pdf/acc-aha-2005-guideline-update-for-the-diagnosis-and-4hik65ngbe.pdf

ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult

ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure).

Mariell Jessup, MD, FACC, FAHA, Chair [*][1]

William T. Abraham, MD, FACC, FAHA[†][2]

Donald E. Casey, MD, MPH, MBA[‡][3]

Arthur M. Feldman, MD, PhD, FACC, FAHA[§][4]

Gary S. Francis, MD, FACC, FAHA[§][4]

Theodore G. Ganiats, MD[∥][5]

Marvin A. Konstam, MD, FACC[¶][6]

Donna M.

/pdf/2009-focused-update-incorporated-into-the-acc-aha-2005-3z9lhvyqwq.pdf

2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: Developed in Collaboration With the International Society for Heart and Lung Transplantation

https://www.amjmed.com/article/S0002-9343(99)00369-1/pdf

Effects of nonsteroidal anti-inflammatory drugs on renal function: focus on cyclooxygenase -2–selective inhibition

The bioavailability, pharmacokinetics, and pharmacodynamics of torsemide (10 mg orally and intravenously) and furosemide (40 mg orally and 20 mg intravenously) were determined in a randomized crossover clinical trial in 16 patients with compensated congestive heart failure. Torsemide (time to reach maximum concentration [tmax], 1.1 +/- 0.9 hour) was more rapidly absorbed than furosemide (tmax, 2.4 +/- 2.5 hours), the absorption of which was delayed compared with that in healthy volunteers. Bioavailability of torsemide was also greater and less variable than that of furosemide. All four treatments yielded comparable changes from baseline in 24-hour electrolyte excretion. Based on the relationships between sodium excretion rate and fractional sodium and urinary drug excretion rate, response to both diuretic agents at the level of the nephron was decreased compared with previous studies with healthy subjects. Assessment of the clinical relevance, if any, of the difference in the variability of absorption warrants further study.

Bioavailability, pharmacokinetics, and pharmacodynamics of torsemide and furosemide in patients with congestive heart failure

Background
Lovastatin is oxidized by cytochrome P4503A to active metabolites but pravastatin is active alone and is not metabolized by cytochrome P450. Diltiazem, a substrate and a potent inhibitor of cytochrome P4503A enzymes, is commonly coadministered with cholesterol-lowering agents.

Methods
This was a balanced, randomized, open-label, 4-way crossover study in 10 healthy volunteers, with a 2-week washout period between the phases. Study arms were (1) administration of a single dose of 20 mg lovastatin, (2) administration of a single dose of 20 mg pravastatin, (3) administration of a single dose of lovastatin after administration of 120 mg diltiazem twice a day for 2 weeks, and (4) administration of a single dose of pravastatin after administration of 120 mg diltiazem twice a day for 2 weeks.

Results
Diltiazem significantly (P < .05) increased the oral area under the serum concentration-time curve (AUC) of lovastatin from 3607 ± 1525 ng/ml/min (mean ± SD) to 12886 ± 6558 ng/ml/min and maximum serum concentration (Cmax) from 6 ± 2 to 26 ± 9 ng/ml but did not influence the elimination half-life. Diltiazem did not affect the oral AUC, Cmax, or half-life of pravastatin. The average steady-state serum concentrations of diltiazem were not significantly different between the lovastatin (130 ± 58 ng/ml) and pravastatin (110 ± 30 ng/ml) study arms.

Conclusion
Diltiazem greatly increased the plasma concentration of lovastatin, but the magnitude of this effect was much greater than that predicted by the systemic serum concentration, suggesting that this interaction is a first-pass rather than a systemic event. The magnitude of this effect and the frequency of coadministration suggest that caution is necessary when administering diltiazem and lovastatin together. Further studies should explore whether this interaction abrogates the efficacy of lovastatin or enhances toxicity and whether it occurs with other cytochrome P4503A4-metabolized 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, such as simvastatin, fluvastatin, and atorvastatin.

Clinical Pharmacology & Therapeutics (1998) 64, 369–377; doi:

The interaction of diltiazem with lovastatin and pravastatin.

The diuretic response to loop diuretics in various disease states has consistently been found to be subnormal. One of the key determinants of the degree of diuretic response is the functional integrity of the sodium-potassium-chloride transporter in the loop of Henle. Studies in animal models suggest that expression/activity of the transporter may be affected by factors such as altered natural splicing events of NKCC2 (the gene encoding for the renal transporter), renal prostanoids, vasopressin, and other autacoids. We have reviewed the pharmacokinetics and pharmacodynamics of loop diuretics in health and in edematous disorders for which they are used. On the basis of evidence reviewed in this paper, we propose that altered expression or activity of the sodium-potassium-chloride transporter in the loop of Henle, in conjunction with events occurring in other segments of the nephron, possibly accounts for the altered diuretic response to these agents. Thus the modulators of this altered expression/activity could serve as important therapeutic targets for alternative diuretic regimens in these conditions.

Loop diuretics: from the Na-K-2Cl transporter to clinical use

All nonsteroidal anti inflammatory drugs (NSAIDs) are characterized by a high degree of protein binding and small volumes of distribution. Differences in clearance account for the variability in half-life among these drugs. The majority are metabolized by the liver through a variety of pathways. These drugs are subject to drug interactions of several mechanisms, including protein-binding-displacement interactions, induction or inhibition of hepatic drug metabolism, and competition for active renal tubular secretion with other organic acids. NSAIDs are also subject to special pharmacokinetic considerations about which a great deal has been learned recently. These include data demonstrating that assessment of disposition of these drugs using only total drug concentrations can be misleading and that one must instead assess the disposition of unbound, pharmacologically active drug. Second, it appears that only one enantiomer of the propionic acid NSAIDs is active; studies of the pharmacokinetics of this class of NSAID should include assessment of the active stereoisomer. Finally, the propionic acid NSAIDs are metabolized to acyl-glucuronide conjugates, which are unstable and can cleave back to the parent drug. This feature allows the paradox of a drug that is metabolized by the liver being able to accumulate in patients who have renal insufficiency. Because of these newer pharmacokinetic considerations, much of the old data concerning the clinical pharmacology of NSAIDs are obsolete. More precise new information is needed in this area.

D. Craig Brater

Papers

Effects of nonsteroidal anti-inflammatory drugs on renal function: focus on cyclooxygenase -2–selective inhibition

Bioavailability, pharmacokinetics, and pharmacodynamics of torsemide and furosemide in patients with congestive heart failure

The interaction of diltiazem with lovastatin and pravastatin.

Loop diuretics: from the Na-K-2Cl transporter to clinical use

Clinical Pharmacology of NSAIDs