Can ventricular function be assessed by echocardiography in chronic canine mitral valve disease?

Abstract

Mitral regurgitation (MR) related to chronic degenerative valvular disease is the most important cause of heart failure in dogs. Ultrasound examination of the heart can identify valve lesions, confirm the presence of valvular regurgitation, document cardiac remodeling, estimate intracardiac pressures, and quantify systolic ventricular function. These findings can influence prognosis or selection of medical therapy. Reductions in ventricular systolic function may be detected on serial echocardiographic examinations in some dogs with MR. However the changes in ventricular loading that accompany MR often complicate these measurements. For example, shortening and ejection fractions are often increased in severe MR, even in the setting of congestive heart failure. Echocardiography with Doppler is also used to assess ventricular diastolic function and filling pressures. This information helps predict the risk of congestive heart failure. However these findings are often rendered ambiguous by age-related impairment of ventricular relaxation, elevations in left atrial pressure due to MR, and effects of volume overload on myocardial tissue velocities. These factors limit the usefulness of ventricular filling and tissue velocities, as well as derived ratios such as the E/E' ratio, for predicting congestive heart failure in MR. More advanced Doppler and tissue echocardiographic methods, as well as prospective clinical studies, are needed to reduce the ambiguity involved with assessment of ventricular function and filling pressures in the setting of MR.

Pathologic Manifestations on Surgical Biopsy and Their Correlation with Clinical Indices in Dogs with Degenerative Mitral Valve Disease

“…Myocardial systolic or diastolic dysfunction accrues from histopathologic changes that cause myocardial decompensation, which in turn induces clinical signs such as cough, dyspnea, and exercise intolerance 3, 4, 8, 9, 10. However, knowledge is incomplete regarding the pathologic progression of myocardial degeneration and attendant difficulties in evaluating myocardial dysfunction in DMVD.…”

“…Particularly, LVEDd was strongly correlated with the pathologic variables of the LA, such as fatty replacement and vacuolization, suggesting that increase in LVEDd may imply progression to myocardial degeneration in the LA. Increased LVEDd can be useful for identifying volume overload and increased ventricular filling pressure, which also is evidence of the increased pressure in the LA 3, 4. Hence, the association of LVEDd and the degeneration of the LA may be a result of the increased LA filling pressure because of mitral regurgitation.…”

“…In chronic heart diseases, accurate evaluation of myocardial function is important, because it aids clinicians in planning medical treatment and formulating a prognosis 3, 4. However, assessment of myocardial function is challenging in DMVD because mitral insufficiency induces hemodynamic changes of high volume and low pressure 3, 4.…”

“…However, assessment of myocardial function is challenging in DMVD because mitral insufficiency induces hemodynamic changes of high volume and low pressure 3, 4. These alterations result in hyperdynamic ventricular wall motion, which can result in misleading echocardiographic measurements 3, 4. Thus, in the presence of DMVD, cardiac function is likely to seem normal, even in the setting of intrinsic myocardial dysfunction that has resulted from pathologic degeneration.…”

Dobutamine Stress Echocardiography for Assessment of Systolic Function in Dogs with Experimentally Induced Mitral Regurgitation

“…However, identification of systolic dysfunction is challenging in dogs with MMVD22; EF, FS, and PEP/ET at rest and dobutamine infusion could not detect systolic dysfunction. In addition to being dependent on intrinsic contractility, these parameters are also known to be influenced by hemodynamic load and sympathetic tone, which may mask significant myocardial dysfunction in dogs with MR 22.…”