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Biomedical subjects

Tien M H Ng

Publications and source records attributed to Tien M H Ng.

8 recordsLinked to original sources
PubMed2006

Contemporary issues in the pharmacologic management of acute heart failure.

Acute heart failure is an evolving syndrome that continues to be defined by ongoing studies and registries. It is associated with significant morbidity and mortality and places a huge economic burden on health care systems. Improved understanding of the underlying pathophysiologic processes has prompted interest into understanding the implications of current and future pharmacologic management strategies beyond hemodynamics. Diuretics, vasodilators, and inotropes remain the mainstays of therapy with several new classes of agents on the horizon. Clinicians should understand the rationale for use and limitations of each therapy to maximize benefit and cost-effectiveness, while minimizing the potential for adverse outcomes.

Aged↗
PubMed2005

Comparison of N-acetylcysteine and fenoldopam for preventing contrast-induced nephropathy (CAFCIN).

BACKGROUND: N-acetylcysteine and fenoldopam are commonly prescribed for prevention of contrast mediated nephropathy, however, comparative superiority of either agent is unknown. METHODS: In a prospective, randomized, parallel-group trial, adult cardiac catheterization patients at the university and veterans' hospitals with pre-existing stable renal insufficiency were randomized to N-acetylcysteine 600 mg orally twice daily for 4 doses or fenoldopam 0.1 mcg/kg/min intravenously for a minimum of 8 h. All patients received intravenous hydration with normal saline (5% dextrose in normal saline for diabetics on insulin). Randomization was stratified for diabetes. The primary endpoint was mean change in Scr at 72 h. Secondary endpoint was the incidence of contrast-induced nephropathy (25% increase above baseline Scr or absolute increase of 0.5 mg/dL). RESULTS: Study termination occurred after ninety-five patients (mean age 68+/-10 years, female 25%, diabetic 42%, mean baseline Scr 1.5+/-0.4 mg/dL) were randomized, with 84 completing follow-up (44 N-acetylcysteine, 40 fenoldopam). Overall, there were no significant differences in mean change in Scr at 72 h (N-acetylcysteine 0.20+/-0.72 vs. fenoldopam 0.08+/-0.48 mg/dL, p=0.4) or incidence of contrast-induced nephropathy (N-acetylcysteine 5 vs fenoldopam 8, p=0.4). No differences were detected in subgroup analyses for diabetes, baseline Scr >1.7 or 2.0 mg/dL, gender, age >70 years, or contrast volume >150 mL. Results were similar after multivariate adjustment for diabetes, contrast volume, heart failure and gender. CONCLUSIONS: Our randomized comparison failed to demonstrate a significant difference in the abilities of N-acetylcysteine and fenoldopam to prevent the decline in renal function or the incidence of contrast-induced nephropathy during cardiac catheterization.

Acetylcysteine↗
PubMed2005

Moxifloxacin and warfarin: additional evidence for a clinically relevant interaction.

Several case reports have been published regarding an interaction between fluoroquinolones and warfarin; however, the exact mechanism of the interaction has yet to be established. We describe three patients who were receiving warfarin and experienced increases in international normalized ratio (INR) when moxifloxacin was added. Two of the patients had stable anticoagulation regimens and then experienced persistent elevations in their INRs shortly after therapy with moxifloxacin was started. The third patient experienced a dramatic rise in INR after the first dose of moxifloxacin was administered. These cases strengthen the evidence that an interaction does exist despite manufacturer-generated statements to the contrary. Increased awareness of this potential interaction is necessary to ensure appropriate monitoring and improve therapeutic decision making.

Aged↗
PubMed2004

Levosimendan, a new calcium-sensitizing inotrope for heart failure.

Calcium sensitizers are a new class of inotropes that share the in vitro properties of calcium sensitization and phosphodiesterase inhibition. Levosimendan is a distinct calcium sensitizer, as it stabilizes the interaction between calcium and troponin C by binding to troponin C in a calcium-dependent manner, improving inotropy without adversely affecting lusitropy. It does not exhibit clinically relevant phosphodiesterase inhibition at therapeutic concentrations. It also exerts vasodilatory effects, possibly through activation of several potassium channels and other less well characterized mechanisms. The pharmacokinetics of levosimendan are similar in healthy subjects and patients with heart failure and remain relatively unaltered by age, sex, and organ dysfunction. In preclinical and clinical studies, levosimendan exerted potent dose-dependent positive inotropic and vasodilatory activity. Unlike conventional inotropes, levosimendan is not associated with significant increases in myocardial oxygen consumption, proarrhythmia, or neurohormonal activation. The most common adverse effects are attributable to the vasodilation. Two large, double-blind, randomized trials demonstrated favorable hemodynamic effects, improved tolerability, and a possible mortality benefit over dobutamine and placebo in patients who had acute symptoms of failure and required inotropic therapy. The long-term effect on patient outcomes is being confirmed in ongoing placebo- and inotrope-controlled trials. Levosimendan appears to be an effective inodilator devoid of the detrimental effects of conventional inotropes. In the future, levosimendan may provide a promising alternative to conventional inotropes for patients with acutely decompensated heart failure.

Animals↗
PubMed2004

High-impact articles related to the pharmacotherapeutic management of systolic heart failure.

This compilation is part of a series of five articles identifying important literature in cardiovascular pharmacotherapy. This list focuses on pharmacotherapeutic management of acute decompensated and chronic heart failure. Most of the cited works present the results of landmark clinical studies that have shaped the management of patients with left ventricular systolic dysfunction. Limited primary literature is available for some topics; thus, pertinent review articles also are listed. In addition, consensus documents formed by expert panels in the United States and Europe are reviewed. This compilation may serve as a teaching tool, reference resource, or update of the literature for pharmacy clinicians, physicians, and students.

Heart Failure↗
PubMed2003

Effects of subclinical hypothyroidism and its treatment on serum lipids.

OBJECTIVE: To determine whether the literature supports an effect of subclinical hypothyroidism on serum lipids and, if so, what are the effects of thyroxine replacement therapy. DATA SOURCES: Articles were identified on MEDLINE using the MeSH terms hypothyroidism, lipids, or cholesterol. DATA SYNTHESIS: The majority of studies that determined the prevalence of lipid abnormalities in subclinical hypothyroidism and studies that evaluated the effects of thyroxine replacement on lipids were small, uncontrolled, and varied in inclusion criteria. Six randomized, placebo-controlled trials were identified that evaluated the effect of levothyroxine on lipids in subclinically hypothyroid patients. CONCLUSIONS: Subclinical hypothyroidism can potentially contribute to a pro-atherogenic lipid profile, with effects being greater at higher thyroid-stimulating hormone levels. Thyroxine replacement reduces total cholesterol and low-density lipoprotein cholesterol, with no effect on triglycerides. Effects on high-density lipoprotein, lipoprotein (a), and apolipoproteins A1 and B require further study. Larger prospective studies are needed to clarify many issues.

Humans↗
PubMed2002

Chronically inhaled salmeterol improves pulmonary function in heart failure.

Inhaled beta-agonists are commonly prescribed for the symptoms of exercise intolerance in heart failure despite a paucity of data regarding their safety and efficacy. This was a prospective, randomized, double-blind, double-dummy, placebo-controlled 14-day cross-over study to determine if chronic inhaled salmeterol therapy 84 microg every 12 hours improved pulmonary function without augmentation of neurohormonal systems or ventricular ectopy in 8 symptomatic heart failure subjects with left ventricular ejection fraction (LVEF) <40% and FEV1 <or=80%. The primary endpoint was FEV1, and the secondary endpoints were forced vital capacity (FVC), forced expiratory flow (FEF25-75), peak expiratory flow rate (PEFR), blood pressure, heart rate, rate-pressure product, plasma norepinephrine, plasma epinephrine, plasma renin activity, percent ventricular ectopy, and salmeterol pharmacokinetics. Salmeterol was associated with a significant 6% improvement in FEV1 compared with placebo (salmeterol 2.46 +/- 0.73 vs. placebo 2.33 +/- 0.73 L, p = 0.01). There was no significant difference in FVC, FEF25-75, and PEFR. Salmeterol increased mean rate-pressure product by 5% (salmeterol 8878 +/- 1560 vs. placebo 8414 +/- 1440 bpm x mm Hg, p = 0.04), although no increase in plasma norepinephrine, epinephrine, plasma renin activity or ventricular ectopy was detected. The Tmax, Cmax, and half-life of salmeterol at steady-state were 5 min, 715 pg/ml and 11.4 hours, respectively. Inhaled salmeterol significantly improves FEV1 without producing measurable effects on neuroactivation or ventricular ectopy. Inhaled salmeterol causes minor increases in rate-pressure product, whose clinical significance remains to be determined. The plasma half-life of salmeterol may be prolonged in heart failure patients, thus leading to accumulation at steady-state.

Administration, Inhalation↗