Dr. Ng completed a BS Pharmacy in 1994 from Dalhousie University in Halifax (Canada), a PharmD in 1998 from Wayne State University (Detroit) and a Cardiovascular Pharmacotherapy Fellowship in 2000 from the University of Utah (Salt Lake City). He has been a board certified pharmacotherapy specialist since 2001. Prior to joining USC in March 2004, Dr. Ng was an assistant professor at the University of Nebraska Medical Center. He was the recipient of the Heart Failure Society of America Clinical/Integrative Physiology New Investigator Award in 2002.
Areas of Expertise (6)
Heart Failure Pathophysiology
Heart Failure Pharmacotherapy
Drug-induced QT Prolongation
Wayne State University: Pharm.D.
Dalhousie University: B.S.
Selected Articles (6)
Tien Ng et al.
2018 Hypoalbuminemia occurs in 25% to 76% of patients hospitalized for acute heart failure (HF) and is associated with increased mortality. Hypoalbuminemia may predispose patients to intravascular volume depletion, hypotension, and acute worsening of renal function; however, its association with treatment outcomes during hospitalization is unknown.
Tien Ng et al.
2017 Prevention of readmissions for heart failure (HF) is a distinct challenge, as up to 25% of patients require rehospitalization within 30 days.1 Although rates have fallen, progress has stalled.2 Currently, readmission prevention programs focus on patient education, self-care initiatives, telephonic follow-up, medication reconciliation, and weight monitoring,3 which are founded on behavior-modification, personnel-dependent models. However, consistent and reproducible improvements in 30-day readmission rates have not been demonstrated, and increasing the number of conventional interventions may not affect readmission rates to a degree that justifies added expenditures.4 Conversely, while lengths of stay are demonstrably longer in Europe, readmission rates are lower. Whether this reflects lower-intensity decongestion or simply prolongation of standard therapy is not known.
Tien Ng et al.
2016 For human monocyte studies, cells were isolated from 12 chronic heart failure (HF) (66 ± 12 years, New York Heart Association functional class III-IV, left ventricular ejection fraction 22% ± 9%) and 14 healthy subjects (66 ± 12 years). Monocytes (1 × 106/mL) were incubated with lipopolysaccharide (LPS) 100 ng/mL, LPS + norepinephrine (NE) 10-6 mol/L or neither (control) for 4 h. Tumor necrosis factor-alpha (TNFα) and interleukin-10 (IL-10) production were determined by ELISA. Relative contribution of α- and β-adrenergic receptor subtypes on immunomodulatory activity of NE was assessed in LPS-stimulated THP-1 cells incubated with NE, the α-selective agonist phenylephrine (PE), and the β-selective agonist isoproterenol (IPN). NE-pretreated THP-1 cells were also co-incubated with the β-selective antagonist propranolol (PROP), α2-selective antagonist yohimbine (YOH) or the α1-selective antagonist prazosin (PRAZ).
Tien Ng et al
2016 Acute heart failure remains a major cause of morbidity, and its treatment requires an increasing investment of the health care system. Whereas success in treating chronic heart failure has been achieved over the last decades, several pharmacological approaches for acute heart failure have been introduced but have failed to demonstrate any clinical benefit. Serelaxin is a recombinant human relaxin-2 vasoactive peptide that causes systemic and renal vasodilation. Data suggest that the clinical benefits may be attributable to a potential combination of multiple actions of serelaxin, including improving systemic, cardiac, and renal hemodynamics, and protecting cells and organs from damage via neurohormonal, anti-inflammatory, antiremodeling, antifibrotic, anti-ischemic, and proangiogenic effects. Recently, a number of clinical trials have demonstrated that serelaxin infusion over 48 hours improved dyspnea with more rapid relief of congestion during the first days after admission for heart failure. In addition, administration of serelaxin diminished cardiac, renal, and hepatic damage, which were associated with improved long-term mortality. Available data support substantial clinical benefits and significant promise for serelaxin as a treatment option for patients with acute heart failure. This review focuses on the pharmacology and mechanisms of action of serelaxin and provides a detailed discussion of the clinical evidence for this novel therapy in acute heart failure.
Tien Ng et al.
2015 Neurohormonal activation was first recognized as an important mediator of heart failure (HF) in the early 1990s. The neurohormonal model of HF helped to explain the hemodynamic alterations of the cardiorenal and cardiocirculatory models and built on them by providing a mechanism for the progressive nature of the syndrome.1 Since then, development of novel HF therapies has focused on antagonizing or counteracting the effects of so-called vasoconstrictive neurohormonal pathways.
2014 Although hyponatremia is a prognostic factor in acute heart failure (AHF), its influence on the acute clinical course of heart failure is unknown. Our objective was to evaluate the association of hyponatremia with diuretic response, renal function, and clinical outcomes in AHF.