Left ventricular systolic function in dogs with pulmonic stenosis

Abstract

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.

Propofol‐dexmedetomidine continuous infusion in a dog with pulmonic stenosis undergoing balloon valvuloplasty

“…Depending on the severity of the PS, concentric RV hypertrophy develops to normalise the increased systolic wall stress. 22,[29][30][31] Reducing the RV volume, the concentric hypertrophy and the thickening of the interventricular septum might impair diastolic function, decreasing RV output further and leading to right congestive heart failure. 29,31,32 The low RV output together with the cardiac remodelling will also affect the venous return to the left atrium and ventricle, thus reducing cardiac output.…”

“…Consequently, systemic hypoperfusion and myocardial ischaemia might develop. 29,31 To retard the development of RV hypertrophy, to improve the coronary blood flow and to reduce the myocardial oxygen consumption and the risk of ventricular arrhythmias, atenolol, a β-blocker, is generally administrated to dogs with PS. 9,30 Haemodynamically, as PS represents a fixed obstruction, it is essential to preserve RV output by maintaining RV preload and contractility, while avoiding excessive fluid administration.…”

“…The low RV output together with the cardiac remodelling will also affect the venous return to the left atrium and ventricle, thus reducing cardiac output. Consequently, systemic hypoperfusion and myocardial ischaemia might develop 29,31 . To retard the development of RV hypertrophy, to improve the coronary blood flow and to reduce the myocardial oxygen consumption and the risk of ventricular arrhythmias, atenolol, a β‐blocker, is generally administrated to dogs with PS 9,30 …”

“…Consequently, both RV work and myocardial oxygen consumption increase. Depending on the severity of the PS, concentric RV hypertrophy develops to normalise the increased systolic wall stress 22,29–31 . Reducing the RV volume, the concentric hypertrophy and the thickening of the interventricular septum might impair diastolic function, decreasing RV output further and leading to right congestive heart failure 29,31,32 .…”

“…22,[29][30][31] Reducing the RV volume, the concentric hypertrophy and the thickening of the interventricular septum might impair diastolic function, decreasing RV output further and leading to right congestive heart failure. 29,31,32 The low RV output together with the cardiac remodelling will also affect the venous return to the left atrium and ventricle, thus reducing cardiac output. Consequently, systemic hypoperfusion and myocardial ischaemia might develop.…”