About

Sarah Ho is the CVM Director of Student Engagement at the College of Veterinary Medicine at NC State University. Her role involves overseeing student development and engagement initiatives, fostering a supportive and collaborative campus community, and promoting opportunities for students to enrich their academic and personal growth. She is actively involved in creating a welcoming environment that encourages students to build lifelong friendships, explore extracurricular passions, and participate in international study programs. Her focus is on supporting students' success and well-being throughout their veterinary education.

Research topics

• Medicine
• Internal medicine
• Cardiology
• Biology
• Genetics
• Gastroenterology
• Pharmacology
• Endocrinology

Selected publications

• Effect of trazodone on heart rate, heart rate variability, and QT-intervals in dogs

  Journal of Veterinary Cardiology · 2025-06-12

  articleOpen accessSenior author

  INTRODUCTION/OBJECTIVES: To determine the effect of trazodone and placebo on heart rate (HR), heart rate variability, and QT intervals in dogs after oral administration of trazodone or placebo. ANIMALS, MATERIALS AND METHODS: Twenty healthy adult client-owned dogs were included in the study. Dogs were randomized in a double-blind, placebo-controlled crossover trial. Dogs received trazodone (6 mg/kg q 8 h) or placebo for 24 h, during which a 24-h ambulatory electrocardiogram (ECG) (Holter) was recorded. Diagnostic ECGs and clinician-assessed behavior scores were obtained before and after the 24-h study period. Owners also scored the dog's behavior changes during each of the 24-h study periods. Following a minimum one-week washout period, dogs received the alternate study drug, and all procedures were repeated. Linear and mixed models were used for statistical analyses. RESULTS: Dogs receiving trazodone had higher average HRs (P=0.035), higher minimum HRs (P<0.001), and reduced HR variability parameters (P<0.001) on the Holter recordings. Electrocardiogram-derived QT interval was not different between groups. Dogs receiving trazodone appeared calmer based on owner assessments (P<0.001) and behavior scores (P=0.006). STUDY LIMITATIONS: Blood pressure and trazodone blood levels were not measured, making it impossible to determine the effect of these variables on the HR and ECG findings. CONCLUSIONS: Trazodone increased HR and decreased HRV. Possible explanations include a previously described anticholinergic effect or a possible decrease in blood pressure causing a reflex response. No demonstrable effect on QTi was identified in this cohort of healthy dogs using standard trazodone dosing.

  PublisherDOI

• Myocardial Enhancement Following Agitated Saline Contrast Study in a Boxer Dog

  CASE · 2023-04-30

  articleOpen access

  •Myocardial enhancement after agitated saline contrast study in a dog is described.•Suspect air microemboli can inadvertently be introduced into coronary vasculature.•Air microemboli are a theoretic risk of saline contrast echocardiography.

  PublisherOA PDFDOI

• What Is Your Diagnosis?

  Journal of Avian Medicine and Surgery · 2022-01-28

  articleCorresponding
  PublisherDOI

• Letter to the editor regarding “Efficacy of adding ramipril (VAsotop) to the combination of furosemide (Lasix) and pimobendan (VEtmedin) in dogs with mitral valve degeneration: The VALVE trial”

  Journal of Veterinary Internal Medicine · 2021-01-27 · 1 citations

  letterOpen access

  The manuscript entitled Efficacy of adding ramipril (VAsotop) to the combination of furosemide (Lasix) and pimobendan (VEtmedin) in dogs with mitral valve degeneration: The VALVE trial1 reports a study which sought to answer the question “could pimobendan be all that is needed beyond loop diuretics to manage congestive heart failure (CHF) in myxomatous mitral valve disease (MMVD)?” This was done by prospectively comparing the efficacy of pimobendan + ramipril + furosemide (triple treatment) to pimobendan + furosemide (double treatment) to treat new-onset CHF caused by MMVD. While agreeing with the authors that this question has merit, we share several comments and questions regarding applicability of their study results to current practice. During the VALVE trial, worsening signs of CHF were primarily managed with progressively larger diuretic dosages, as opposed to other potential pharmacological interventions such as greater renin-angiotensin-aldosterone system (RAAS) suppression, alternative diuretic use, higher pimobendan dosing, and arterial vasodilator treatment. While the angiotensin-converting enzyme inhibitor (ACEI) ramipril (VASOTOP) was begun at a once daily dosage according to label recommendation, the initial furosemide dosage (median, 8 mg/kg/d), high by current clinical standards, was increased to as much as 15 mg/kg/d, before predefined treatment failure was reached; ramipril dosage was increased (doubled) in only 3 dogs. Spironolactone dosing was left to the clinicians' discretion (added to baseline treatment in only 13 dogs, 8 in the triple treatment group, and 5 dogs in the double treatment group). The VALVE trial did not assess the efficacy of RAAS suppression using biomarkers. Therefore, the question of whether ramipril adequately or optimally suppressed RAAS, while failing to improve survival in the face of these diuretic dosages, remains unanswered. We are also concerned that dogs in both treatment groups received ACEI for an average of 9 months before entering the study (44% of triple treatment group vs 26% of double treatment group; P = .02), indicating that over one-quarter of the double treatment group (the no ACEI group) previously had received an ACEI—and for a duration longer than the median 7.6 months that these dogs remained in the study. This is important because it is known that RAAS suppression before the onset of CHF has favorable effects on cardiac remodeling.2 Although unknowable by the authors at the time of the VALVE trial design, other studies completed during the 10-year duration of the VALVE trial have demonstrated significant benefit from greater, longer, and more broad-spectrum RAAS suppression (eg, higher or q12h ACEI dosing and mineralocorticoid antagonist [MRA] inclusion) in treating proteinuria and CHF.3-5 Because the VALVE trial was performed under Good Clinical Practice guidelines, owner adherence to the trial protocol was quantified. It would be useful to know whether those measurements identified “adherence parity” between the 2 treatment groups, thus eliminating 1 potential source of unintentional bias. Ramipril, a narrow-spectrum RAAS suppressant (ie, it causes no direct MRA effect), was tested as an “add-on” to drugs providing symptomatic relief (pimobendan and furosemide). Although the absence of an MRA as part of the test article is understandable because of the timing of the VALVE study design, its absence impairs our understanding of the potential role that true RAAS suppression (ie, more RAAS suppression than ACE inhibition alone) might play in managing CHF caused by MMVD. It is now known that incomplete RAAS suppression (aldosterone breakthrough) is common with either ACEI or angiotensin II receptor blockers (ARB) in normal dogs challenged with furosemide or amlodipine5, 6; with ACEI in natural MMVD before CHF (without furosemide)5, 7; and in MMVD with CHF in dogs receiving ACEI and furosemide.5, 7 Furthermore, inclusion of MRAs in therapeutic protocols has improved survival in CHF caused by MMVD.3, 5 Although it has not been directly investigated, it is likely that the high doses of furosemide used in the VALVE Trial, with greater RAAS stimulatory potential, enhanced the propensity for aldosterone breakthrough.8 In dogs treated with ACEI and ARBs, there is an estimated 30% to 40% incidence of aldosterone breakthrough at conventional furosemide dosages, and a proportional clinical benefit is seen with broad-spectrum RAAS suppression.3, 5-7, 9 For this reason, it would be important to know the average maximum furosemide dosage received, as well as the number of dogs that experienced renal compromise, were euthanized, or exited the study for polyuria and polydipsia or worsening renal dysfunction. It would also be relevant to know the number of cases accrued from each institution, as well as the average furosemide dosage, number of dogs receiving spironolactone or doubled ramipril dosage, and how these potential institutional differences were accounted for during data analysis. A large number of cases from a single center may diminish the benefits of a multicenter study design or raise the possibility of unintentional institutional acquisition bias. Although the VALVE results are surprising and interesting, a conclusion that they obviate the need for ACEI treatment in the management of CHF from MMVD is not justified. We believe this study to be hypothesis generating, rather than pivotal. A larger study, employing methodology that provides evidence of more complete RAAS inhibition with contemporary adjunctive heart failure treatment is needed to provide pivotal data upon which to guide practice. Programmatic or institutional grant support, consultant/speaker for pharmaceutical companies marketing veterinary cardiovascular drugs are as follows: Clarke Atkins: Boehringer-Ingelheim, CEVA Sant Animalé, Vetoquinol, Virbac; Bruce Keene: Boehringer-Ingelheim, CEVA Santa Animalé; Teresa C. DeFrancesco: Boehringer-Ingelheim, CEVA Santé Animale; Sandra Tou: Boehringer-Ingelheim, CEVA Santé Animale; Valérie Chetboul: Boehringer-Ingelheim, CEVA Santé Animale, Vetoquinol; Étienne Côté, Boehringer-Ingelheim, CEVA Santé Animale; Stephen Ettinger: Purina-Nestle; Philip R. Fox: Boehringer-Ingelheim; Robert L. Hamlin: none; Jonathan P. Mochel: Boehringer-Ingelheim, Ceva Santé Animale, Ethos, LEAH Labs, 3D Health Solutions; Jean-Louis Pouchelon: Boehringer-Ingelheim, CEVA Santé Animale, Vetoquinol; Rebecca L. Stepien: Boehringer-Ingelheim, CEVA Santé Animale.

  PublisherOA PDFDOI

• Additional file 1 of A deleterious mutation in the ALMS1 gene in a naturally occurring model of hypertrophic cardiomyopathy in the Sphynx cat

  Open MIND · 2021-01-01

  dataset

  Additional file 1: Supplemental Table 1. Variants pursued by Sanger Sequencing.

  DOI

• Myxomatous mitral valve disease in Miniature Schnauzers and Yorkshire Terriers: 134 cases (2007–2016)

  Journal of the American Veterinary Medical Association · 2021-11-10 · 23 citations

  article

  OBJECTIVE: To characterize features of myxomatous mitral valve disease (MMVD) in Miniature Schnauzers and Yorkshire Terriers. ANIMALS: 69 Miniature Schnauzers and 65 Yorkshire Terriers, each with MMVD. PROCEDURES: Medical record data for each dog were collected; the study period was January 2007 through December 2016. If available, radiographic data were evaluated, and a vertebral heart scale score was assigned for each dog. Statistical analysis was performed with Student t and Fisher exact tests. RESULTS: Compared with Yorkshire Terriers, the prevalence of MMVD was significantly higher in Miniature Schnauzers and affected dogs were significantly younger at the time of diagnosis. Miniature Schnauzers were significantly more likely to have mitral valve prolapse and syncope, compared with Yorkshire Terriers. Yorkshire Terriers were significantly more likely to have coughing and have had previous or current treatment with cardiac medications, compared with Miniature Schnauzers. There was no statistical difference between breeds with regard to abnormally high vertebral heart scale scores or radiographic evidence of congestive heart failure. CONCLUSIONS AND CLINICAL RELEVANCE: With regard to MMVD, features of the disease among Miniature Schnauzers and Yorkshire Terriers were similar, but there were also a few discernable differences between these 2 breeds and from historical findings for dogs with MMVD of other breeds. Clinical signs at the time of diagnosis differed between the 2 breeds, which may have reflected concurrent breed-specific conditions (sick sinus syndrome or airway disease [eg, tracheal collapse]). Future work should include prospective studies to provide additional information regarding the natural progression of MMVD in these dog breeds.

  PublisherDOI

• A deleterious mutation in the ALMS1 gene in a naturally occurring model of hypertrophic cardiomyopathy in the Sphynx cat

  Orphanet Journal of Rare Diseases · 2021-02-27 · 31 citations

  articleOpen access

  BACKGROUND: Familial hypertrophic cardiomyopathy is a common inherited cardiovascular disorder in people. Many causal mutations have been identified, but about 40% of cases do not have a known causative mutation. Mutations in the ALMS1 gene are associated with the development of Alstrom syndrome, a multisystem familial disease that can include cardiomyopathy (dilated, restrictive). Hypertrophic cardiomyopathy has not been described. The ALMS1 gene is a large gene that encodes for a ubiquitously expressed protein. The function of the protein is not well understood although it is believed to be associated with energy metabolism and homeostasis, cell differentiation and cell cycle control. The ALMS1 protein has also been shown to be involved in the regulation of cell cycle proliferation in perinatal cardiomyocytes. Although cardiomyocyte cell division and replication in mammals generally declines soon after birth, inhibition of ALMS1 expression in mice lead to increased cardiomyocyte proliferation, and deficiency of Alstrom protein has been suggested to impair post-natal cardiomyocyte cell cycle arrest. Here we describe the association of familial hypertrophic cardiomyopathy in Sphynx cats with a novel ALMS1 mutation. RESULTS: A G/C variant was identified in exon 12 (human exon 13) of the ALMS1 gene in affected cats and was positively associated with the presence of hypertrophic cardiomyopathy in the feline population (p < 0.0001). The variant was predicted to change a highly conserved nonpolar Glycine to a positively charged Arginine. This was predicted to be a deleterious change by three in silico programs. Protein prediction programs indicated that the variant changed the protein structure in this region from a coil to a helix. Light microscopy findings included myofiber disarray with interstitial fibrosis with significantly more nuclear proliferative activity in the affected cats than controls (p < 0.0001). CONCLUSION: This study demonstrates a novel form of cardiomyopathy associated with ALMS1 in the cat. Familial hypertrophic cardiomyopathy is a disease of genetic heterogeneity; many of the known causative genes encoding for sarcomeric proteins. Our findings suggest that variants in genes involved with cardiac development and cell regulation, like the ALMS1 gene, may deserve further consideration for association with familial hypertrophic cardiomyopathy.

  PublisherOA PDFDOI

• Absence of known feline <i>MYH7</i> and <i>MYBPC3</i> variants in a diverse cohort of cats with hypertrophic cardiomyopathy

  Animal Genetics · 2021-05-10 · 9 citations

  article

  Hypertrophic cardiomyopathy (HCM) is the most common cause of heart disease in the domestic cat with a genetic predisposition in a few breeds. In the Maine Coon and Ragdoll breeds, two variants associated with the HCM phenotype have been identified in the cardiac myosin binding protein C gene (MYBPC3; p.Ala31Pro and p.Arg820Trp respectively), and a single variant has been identified in the myosin heavy chain gene (MYH7; p.Glu1883Lys) in one domestic cat with HCM. It is not known if these variants influence the development of HCM in other cohorts of the feline population. The objective of this study was to evaluate the presence of the known MYBPC3 and MYH7 variants in a population of cats with HCM. DNA was isolated from samples collected from non-Ragdoll and non-Maine Coon domestic cats diagnosed with HCM through the North Carolina State University College of Veterinary Medicine and genotyped for the three variants. One-hundred and three DNA samples from cats with HCM were evaluated from domestic shorthair, domestic longhair and purebred cats. All samples were wt for the MYBPC3 and MYH7 variants. Although this study was limited by its inclusion of cats from one tertiary hospital, the lack of these MYBPC3 and MYH7 variants in this feline HCM population indicates that the clinical utility of genetic testing for these variants may be isolated to the two cat breeds in which these variants have been identified. Further studies to identify the causative variants for the feline HCM population are warranted.

  PublisherDOI

• Association of diet with clinical outcomes in dogs with dilated cardiomyopathy and congestive heart failure

  Journal of Veterinary Cardiology · 2021 · 41 citations

  • Medicine
  • Internal medicine
  • Cardiology
  PublisherDOI

• Use of whole genome analysis to identify shared genomic variants across breeds in canine mitral valve disease

  Human Genetics · 2021-06-27 · 6 citations

  article
  PublisherDOI

Frequent coauthors

• Clarke E. Atkins

  North Carolina State University

  122 shared

• Teresa C. DeFrancesco

  North Carolina State University

  98 shared

• Kathryn M. Meurs

  North Carolina State University

  75 shared

• John E. Rush

  Tufts University

  55 shared

• W Ruehl

  Urbana University

  50 shared

• Philip R. Fox

  The Schwarzman Animal Medical Center

  34 shared

• Jens Häggström

  33 shared

• Paul D. Pion

  31 shared

Education

• Ph.D., Animal Science

  North Carolina State University

  1990

• M.S., Animal Science

  University of California, Davis

  1985

• B.S., Animal Science

  University of California, Davis

  1983

Awards & honors

• Diplomate, American College of Veterinary Internal Medicine…
• American College of Veterinary Internal Medicine
• American Society of Echocardiography