Comparative study of myocardial function in cases of feline hypertrophic cardiomyopathy with and without dynamic left-ventricular outflow-tract obstruction

Abstract

In recent years, hypertrophic cardiomyopathy (HCM) in cats has become much more common in clinical practice due to improvements in diagnostic techniques and equipment performance. One phenotype is obstructive HCM with left ventricular (LV) outflow tract obstruction (DLVOTO). It has been reported that the presence or absence of DLVOTO does not affect long-term prognosis in cats with HCM. In this study, we evaluated and compared myocardial function in HCM-affected cats with and without DLVOTO using the two-dimensional speckle-tracking echocardiography. LV longitudinal strain of the endocardial, epicardial, and whole layer and LV circumferential strain of the epicardium were significantly decreased in all HCM-affected cats compared to healthy cats. However, these values were not significantly different between those with and without DLVOTO. In contrast, the endocardial and whole layers of LV circumferential strain were only significantly decreased in HCM-affected cats with DLVOTO compared to healthy cats. This could be attributed to the fact that the LV pressure load associated with DLVOTO affected the endocardial myocardium more in the LV endocardial layer, and that lower values of LV endocardial strain lowered the values of LV strain in the whole layer. In conclusion, our results suggest that LV myocardial function may have been more compromised in the HCM-affected cats with DLVOTO.

Rivaroxaban versus enoxaparin plus clopidogrel therapy for hypertrophic cardiomyopathy-associated thromboembolism in cats

“…Myocardial wall stress abnormalities in HCM lead to mortality and scarring of the myocardium, eventually resulting in stiffening of the heart muscle, diastolic dysfunction, increased susceptibility to unstable electricity, and sudden death [ 22 , 23 ]. Cardiogenic embolism is the most common complication in cats with cardiomyopathy and can lead to thromboembolism.…”

Cardiac myosin inhibitor, CK-586, minimally reduces systolic function and ameliorates obstruction in feline hypertrophic cardiomyopathy

“…Like humans, the etiology of the disease has a genetic basis; however, all previously reported feline HCM-causing mutations remain breed-specific (i.e., Maine Coons, Ragdolls, and Sphynx) and explain only a small portion of total feline HCM cases 15 – 17 . Left ventricular outflow tract obstruction (LVOTO) is observed in ~ 33–63% of HCM-affected cats; yet, unlike oHCM-affected human patients, the presence of LVOTO has not yet been linked to increased disease morbidity in cats 13 , 14 , 18 , 19 . Despite the aforementioned clinical differences in disease manifestations, cats closely recapitulate the genetic, pathophysiologic, and hemodynamic aspects of human HCM.…”