Interview with Veterinary Cardiologist - Dr Christopher Lam

Interview with Dr Christopher Lam BA, BVSc (Hons), DACVIM

(Registered Specialist in Veterinary Cardiology at Veterinary Specialist Services (VSS) in Queensland, Australia)

Dr. Chris Lam graduated as a veterinarian from the University of Sydney in 2015 after previously obtaining a Bachelor of Arts in Biology and Japanese Studies from Middlebury College, Vermont in 2010 and working in cancer research in Hong Kong subsequently.

After obtaining his veterinary degree, he worked in a small animal practice in Ballarat for a brief period before commencing a 1-year small animal rotating internship at the Ontario Veterinary College (OVC) in Guelph, Canada where he also published his research on cardiac biomarkers.

After his internship, he started a mobile veterinary service in the High Western Arctic of Canada, where he was a part of the veterinary team for various international sled dog races including the 1000-mile Yukon Quest. Chris relocated back to Australia in 2018 where he practiced as a locum vet across various small animal practices in NSW and Victoria. In 2019, he commenced a 3-year American College of Veterinary Internal Medicine (ACVIM) clinical residency in cardiology under Veterinary Cardiologists Australia (VCA) at Veterinary Specialist Services (VSS) in Brisbane/Gold Coast, and in 2022, became a Diplomate of the ACVIM and registered specialist in veterinary cardiology. Chris now joins the rest of the VCA team to continue providing cardiac referral care for patients across southeast QLD from the two VSS hospitals at Underwood and Carrara. Chris has a special interest in both the medical and interventional managements of congenital cardiac diseases.

1. What inspired you to specialise in veterinary cardiology, and what did your journey look like to become fully qualified?

I’ve always had an interest in cardiology, even before I decided to become a vet. I think because it’s a discipline that is highly logical. In its essence, cardiology is all about plumbing and electricity, so if one has a good understanding of the physics that govern the system and where all the connections go, then you can start working through where the problem lies and how to fix it.

With that interest in mind, during my undergraduate degree as a biology student, I did an externship at the human cardiothoracic department, and after graduating from vet school, I spent a year completing a small animal rotating internship at Ontario Veterinary College (OVC) where they had a strong cardiology program. I attended weekly ECG rounds and cardiology journal club during my internship and spent my elective rotations either with the cardiology service at OVC or other cardiology services around the country. I also did research on cardiac biomarkers in dogs with acquired cardiac disease for my honors project during my vet degree as well as during my internship which allowed me to attend and present my findings at international conferences. After my internship, I moved to the Canadian arctic where I ran a mobile practice for two years then returned to Australia and completed a 3-year American College of Veterinary Internal Medicine clinical residency in veterinary cardiology at Veterinary Cardiologists Australia (VCA) in Queensland. After passing my general medicine and specialist exams and fulfilled the research/clinical requirements, I became board-certified as a specialist in veterinary cardiology.

Myxomatous mitral valve disease (MMVD) will be the majority of our daily case load, followed by a mix of dilated cardiomyopathy (DCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), patients with arrhythmia secondary to various systemic illnesses, then congenital diseases (pulmonic stenosis and patent ductus arteriosus being the most common).

Hypertrophic cardiomyopathy phenotypes (which includes various causes, eg. idiopathic, systemic hypertension, hyperthyroidism, pseudohypertrophy etc.), FATE (feline arterial thromboemboli), CHF (congestive heart failure), other cardiomyopathies (restrictive, dilated, non-specific), and congenital diseases (ventricular septal defect being the most common).

Echocardiography may often be perceived as a challenging skill to acquire as the theory itself is relatively straightforward, but it requires time to build the 3D brain map of the complex cardiovascular anatomy as well as the fine motor muscle memory in order to confidently examine and interpret the imaging results in different breeds, sizes and species of animals. I would suggest starting by reading through a textbook on veterinary echocardiography (which there are a few) to obtain a basic understanding of the theory, then attending an echocardiography course that ideally involves a lot of supervised hands-on practice opportunities and guidance on accurate interpretation of echo results by cardiologists. Then continue to follow through with a lot of practice during everyday practice.

If we are talking CHF in general, then diuretics remain the core therapy regardless of disease etiology. The underlying disease phenotype will then change the additional supportive therapy we would provide. For myxomatous mitral valve disease (MMVD), the concurrent therapy with pimobendan is well established by the QUEST study (Haggstrom et al., 2008, JVIM) in improving survival. The use of ACE-inhibitor (ACEi) has however come into question in recent years with the publication of the VALVE trial (Wess et al., 2020, JVIM) showing the addition of an ACEi to dual therapy (frusemide + pimobendan) did not show any significant improvement in survival than dual therapy alone. ACEi is therefore used less in CHF management for MMVD patients except in certain circumstances (eg. concurrent systemic hypertension, proteinuria, systolic dysfunction etc.).

With the introduction of interventional therapies such as Transapical Edge-to-Edge Repair (TEER) (or VClamp) and mitral valve repair, we may now also offer treatment modalities that may significantly reverse and alter disease progression and potentially a much better prognosis than conservative management alone.

Early detection of feline cardiomyopathy remains one of the trickiest things in veterinary medicine as there is no reliable way to accurately screen for early stages of cardiomyopathy except via echocardiography. Genetic testing is available for certain breeds (eg. Maine Coon, Ragdolls, Sphynx), however, due to the incomplete penetrance nature of inheritance, even if individual cats are positive for the genetic mutation, it does not mean they will definitely develop HCM. Cardiac biomarkers such as NTproBNP are unable to distinguish cats with mild-moderate disease from those that are healthy. Heart murmurs are unfortunately commonly found in normal cats, and lastly thoracic radiographs are poorly sensitive in detecting cardiomyopathy given that concentric hypertrophy found in HCM is the most common pathological changes in cats. Hence, the current recommendation remains that if a cat has suspected signs of cardiac disease (eg. gallop sound, heart murmur, tachypnoea/dyspnoea, neurological signs etc.), then an echocardiogram to assess for presence of cardiac disease is advised.

The detection of heart murmur on auscultation should always prompt further diagnostics. Echocardiogram remains the gold standard to assess for the underlying etiology, stratify disease severity and optimize individualized monitoring and therapy. Long gone are the days where heart murmur should just be “watched” given that therapy may be initiated months-years before actual clinical signs are evident (eg. pimobendan in MMVD dogs, clopidogrel in cats with left atrial enlargement etc.). If echocardiogram cannot be performed due to financial or geographical reasons, then thoracic radiographs should be performed in both dogs and cats to assess for presence of cardiomegaly/left atrial enlargement. Sleeping respiratory rates (SRR) should also be monitored to allow owners to detect tachypnoea promptly and advice should be given to owners to present patients for thoracic radiographs when SRR is persistently ≥30 breaths/min to assess for development of pulmonary infiltrates. It is important to note that coughing in dogs without an elevation in sleeping/resting respiratory rate, is unlikely secondary to cardiogenic pulmonary edema.

With the increase in accessibility to specialist cardiologists, any detection of abnormalities suspected of cardiac disease (eg. heart murmur, dysrhythmia, syncope, dyspnoea etc.) should prompt a discussion with pet owners for cardiologist referral. This is because accurate diagnosis allows us to provide an optimized approach to the ongoing monitoring, therapy and risk stratification for the patient and most importantly a sense of relief to the owners from the unknown. It also allows us to advise both the owners and primary care veterinarians on the appropriate management of any comorbidities, drug interactions, and anesthetic risk. We will often then work alongside the primary care GPs to continue manage their cardiac disease.