Meet The Author
June 2025
Joon Seo BVSc, MVetMed, DipACVIM (Cardiology)
Joon was born and raised in South Korea but moved to New Zealand at age of 11. He graduated with Bachelor of Veterinary Science from Massey University and completed his cardiology residency at The Royal Veterinary College. He is currently working at Animal Referral Centre (Auckland, New Zealand) while completing his PhD in feline cardiomyopathy. He lives with a 17 year old grumpy cat that he adopted during his residency training in the United Kingdom.
Joonbum Seo, José Novo Matos, John S. Munday, Hayley Hunt, David J. Connolly, Virginia Luis Fuentes
The Study Background
My fascination in feline hypertrophic cardiomyopathy (HCM) began during my residency training. I learned about many morphologic variations of HCM and found the heterogeneity of the disease process very interesting. My residency mentors were also passionate in unveiling many mysteries of feline HCM, and I think their passion naturally was passed down to me.
Systolic anterior motion of the mitral valve (SAM) is identified in approximately 30% of cats with HCM. Despite how common it is, we still do not know if SAM is harmful in cats with HCM or not. For example, previous studies showed that cats with HCM and SAM had a similar or longer lifespan than cats with HCM but without SAM. However, these studies were retrospective in design and cats with SAM were younger than those without, which suggested that cats with SAM potentially had an earlier disease process. Furthermore, the presence of SAM was assessed at a single timepoint, and the possibility of spontaneous gain or loss of SAM over time was not considered.
From a physiologic perspective, the presence of SAM is likely harmful as it increases the myocardial wall stress (force applied to cardiac myocytes) and myocardial injury. These were previously shown in studies of NT-proBNP (a biomarker of myocardial wall stress) and troponin I (a biomarker of myocardial injury). Additionally, studies involving human patients with HCM (who are excellent animal models for feline HCM) showed that the presence of SAM can increase the risk of cardiac symptoms and death.
It is understood that SAM is a labile process, and its presence is thought to be determined by the altered geometry of the left ventricle, hyperdynamic systolic function, and changes in the vascular tone. In cats with HCM, the left ventricular geometry and function can change over time. Overall, this means that some cats with HCM can spontaneously gain or lose SAM over time. We wanted to describe the incidence rate of spontaneous gain or loss of SAM over time, so we can better understand the results of the previous feline studies.
What is the primary knowledge gap your study aims to address?
In this study, we wanted to describe the incidence rate of spontaneous gain or loss of SAM in cats with HCM.
The Study Design
This was a retrospective study from two centres (The Royal Veterinary College (UK) and Animal Referral Centre (NZ)). The primary objective was to describe the incidence rate of spontaneous gain or loss of SAM in cats with HCM. The secondary objective was to assess clinical and echocardiographic variables associated with the gain or loss of SAM in cats with HCM.
The inclusion criteria were cats diagnosed with HCM and had at least 2 echocardiograms ≥12 months apart. The exclusion criteria from baseline (first time the cat was diagnosed with HCM) and the last recheck were incomplete clinical records, echocardiographic studies with low 2D temporal resolution (<60 frames per second), use of sedation, beta-blockers or pimobendan in between or during the 2 time points, and the presence of systemic diseases or conditions that can mimic HCM or change the cardiac function (dehydration, hyperthyroidism, diabetes mellitus, cardiac neoplasia, congenital heart disease, anaemia, and systemic hypertension).
Clinical and echocardiographic variables from two time points were recorded. To assess the geometry of the left ventricle, the left ventricular wall thickness from both interventricular septum and left ventricular free wall, and the interventricular wall to left ventricular free wall thickness ratio were measured.
What are the main study results?
The final sample size was 60 cats. At baseline, 38 had SAM and 22 did not have SAM. Over the median follow-up period of 2.1 years (minimum 1 year, maximum 5.9 years), 12 cats gained or lost SAM. The incidence rate for the gain or loss of SAM was 8 per 100 cat-years. This means that 8% of cats with HCM will gain or lose SAM in the first year, 16 out of 100 cats (16%) in 2 years, and so on.
The gain or loss of SAM was associated with the changes in the geometry of the left ventricle. Specifically, gaining SAM was associated with decreased interventricular septal to left ventricular free wall thickness ratio. The loss of SAM was associated with reduced left ventricular free wall thickness.
Were there any unexpected results or challenges during your research?
Similar to the previous studies, our study was retrospective in design, and cats with SAM were younger than those without. However, cats with SAM at baseline had faster disease progression than cats without SAM at baseline in our study. Specifically, cats with SAM at baseline developed left atrial enlargement and 4 of these cats developed congestive heart failure during the follow-up period. In comparison, none of the cats without SAM at baseline developed left heart enlargement or congestive heart failure during the study period (and both groups had a similar follow-up period). Further investigation of clinical significance of SAM in cats with HCM is needed.
Takeaways from this study
The main take home message should be that SAM is labile in cats with HCM, and some cats will gain or lose SAM over time. The labile nature of SAM needs to be considered in clinical research of feline HCM.
What future directions would you like to explore based on this study?
Our next step is to conduct a longitudinal study to investigate the clinical significance of SAM and the effects of therapeutic intervention (e.g., beta blockers).
