Background and Aim: Pulmonic stenosis (PS) is the most common congenital heart disease in dogs. This condition causes right ventricle (RV) overload and disrupts overall systolic function. The aim of this study was to examine the alterations of cardiac electrical activity and mechanical function in dogs with PS compared to normal healthy dogs. Materials and Methods: The ventricular systolic function of dogs with PS was studied. Dogs were divided into two groups, PS (n=13) and control (CONT) (n=12). Measurements of blood pressure, electrocardiography (ECG), and echocardiography were performed. Results: PS dogs had exercise intolerance, with six experiencing syncope. ECG of PS dogs showed higher amplitudes of P, S, and T waves (p<0.01), and a lower R:S ratio (p<0.001) with longer QRS duration (p<0.001) compared to CONT dogs. Echocardiography demonstrated that the pulmonic flow velocity and pressure gradient (PG) between the RV and the pulmonary artery of PS dogs were significantly higher than CONT dogs (p<0.001). The RV free wall thickness to the left ventricular posterior wall thickness ratio and the right atrium to the left atrium diameter ratio was higher (p<0.001), while interventricular septum (IVS) was thicker (p<0.01) in PS dogs compared with CONT dogs (p<0.001). The systolic function in PS dogs showed higher pulmonic valve velocity time integral (PVVTI) value (p<0.001) and longer pulmonic valve ejection time (ET) (p<0.05) than CONT dogs. However, aortic valve VTI (AVVTI) value and aortic valve ET were not significantly different between the groups, although fractional shortening in PS dogs was higher. In PS dogs, PG showed a significant positive correlation with PVVTI:AVVTI ratio (p<0.05). Conclusion: PS had prolonged pulmonic valve opening. The thickening of the RV wall and IVS can cause a detrimental reduction of the left ventricular preload in PS dogs.

Pulmonic valvular stenosis (PS) is one of the most common congenital heart diseases in dogs that can lead to the cardiac maladaptation. Also, PS can affect the cardiac autonomic nervous system (ANS). However, clinical information regarding to systolic function and cardiac ANS alteration in PS dogs had not been fully elucidated. The objectives of this study were to evaluate cardiac electrical property, left ventricular (LV) function, and to assess cardiac ANS from heart rate variability (HRV) analysis in PS dogs compared with healthy dogs. The dogs in this study were divided into 2 groups, PS dogs (n=13) and healthy control dogs (CONT) (n=12). Physical examination, oscillometric blood pressure measurement and assessments of cardiac function including electrocardiography (ECG), echocardiography and 30-min heart rate variability (HRV) were performed. The blood sample were collected for determination of complete blood count and blood chemistries. The results showed that all PS dogs had exercise intolerance while 6 developed syncope. ECG findings indicated that PS dogs had higher amplitudes of P, and T waves (P<0.01), deeper S wave, lower R:S ratio (P<0.001) with longer QRS duration than CONT dogs (P<0.001). For cardiac structural and functional studies, the pulmonic flow velocity (PV) and pressure gradient (PG) between the right ventricle (RV) and the pulmonary artery (PA) of PS dogs were significantly higher than CONT dogs (P<0.001). PS dogs had thicker RV free wall (P<0.001) and interventricular septum (IVS) (P<0.01), bigger right atrium (RA) (P<0.001) with smaller LV chamber during diastole and systole compared with CONT dogs (P<0.001). The RV systolic function in PS dogs showed higher pulmonic valve velocity time integral (PVVTI) value (P<0.001) and longer pulmonic valve ejection time (PVET) (P<0.01). However, there was no significantly difference in HRV parameters between groups. PG had positive correlations with amplitudes of P (r=0.597, P<0.01), S (r=0.569, P<0.01) and T waves (r=0.423, P<0.05) and negative correlations with amplitude of R wave (r=-0.599, P<0.01), R:S ratio (r=-0.677, P<0.001) and QRS duration (r=-0.423, P<0.05). Also, PG had positive correlations with IVS during diastole normalized by body weight (IVSdN) (r=0.560, P<0.01), IVS during systole normalized by body weight (IVSsN) (r=0.538, P<0.01), PVVTI (r=0.812, P<0.001), PVET (r=0.408, P<0.05), right ventricular free wall thickness to left ventricular posterior wall thickness (RVFW:LVPW) ratio (r=0.688, P<0.001) and right atrium to left atrium diameter (RA:LA) ratio (r=0.802, P<0.001). In conclusion, RV hypertrophy induced by PS may lead to reduction of LV preload and function. The increased PVET in PS dogs may be one of the cardiac compensations to maintain pulmonary blood flow. However, the unremarkable cardiac ANS changes in PS dogs may not play a crucial role in chronic pathophysiological alteration of the hemodynamics.