Objective—To compare echocardiographic indices of myocardial strain with invasive measurements of left ventricular (LV) systolic function in anesthetized healthy dogs.
Animals—7 healthy dogs.
Procedures—In each anesthetized dog, preload and inotropic conditions were manipulated sequentially to induce 6 hemodynamic states; in each state, longitudinal, radial, and global strains and strain rate (SR), derived via 2-D speckle-tracking echocardiography, were evaluated along with conventional echocardiographic indices of LV function and maximum rate of rise (first derivative) of LV systolic pressure (LV+dp/dtmax). Catheter-derived and echocardiographic data were acquired simultaneously. Partial and semipartial correlation coefficients were calculated to determine the correlation between LV+dp/dtmax and each echocardiographic variable. Global longitudinal strain was compared with conventional echocardiographic indices via partial correlation analysis.
Results—All myocardial segments could be analyzed in all dogs. Significant semipartial correlations were identified between conventional echocardiographic strain indices and LV+dp/dtmax. Correlation coefficients for longitudinal deformation and global strain, segmental longitudinal strain, and segmental SR were −0.773, −0.562 to −0.786, and −0.777 to −0.875, respectively. Correlation coefficients for radial segments and strain or SR were 0.654 to 0.811 and 0.748 to 0.775, respectively. Correlation coefficients for traditional echocardiographic indices and LV+dp/dtmax (−0.586 to 0.821) and semipartial correlation coefficients for global strain and echocardiographic indices of LV systolic function (−0.656 [shortening fraction], −0.726 [shortening area], and −0.744 [ejection fraction]) were also significant.
Conclusions and Clinical Relevance—Results indicated that LV systolic function can be predicted by myocardial strain and SR derived via 2-D speckle-tracking echocardiographic analysis in anesthetized healthy dogs.
Objective—To identify Doppler echocardiographic (DE) variables that correlate with left ventricular filling pressure (LVFP).
Animals—7 healthy dogs (1 to 3 years old).
Procedures—Dogs were anesthetized and instrumented to measure left atrial pressure (LAP), left ventricular pressures, and cardiac output. Nine DE variables of LVFP derived from diastolic time intervals, transmitral and pulmonary venous flow, and tissue Doppler images were measured over a range of hemodynamic states induced by volume loading and right atrial pacing. Associations between simultaneous invasive measures of LVFP and DE measures of LVFP were determined by use of regression analysis. Receiver operating characteristic analysis was used to predict increases in mean LAP on the basis of DE variables.
Results—Mean LAP was correlated with several DE variables: the ratio between peak velocity during early diastolic transmitral flow and left ventricular isovolumic relaxation time (peak E:IVRT) during sinus rhythm and during right atrial pacing, IVRT, the ratio between late diastolic transmitral flow velocity and pulmonary venous flow duration, and the interval between onset of early diastolic mitral annulus motion and onset of early diastolic transmitral flow. Cutoff values of 2.20 and 2.17, for peak E:IVRT in dogs with sinus rhythm and atrial pacing predicted increases in mean LAP (≥ 15 mm Hg) with sensitivities of 90% and 100% and specificities of 92% and 100%, respectively.
Conclusions and Clinical Relevance—Doppler echocardiography can be used to predict an increase in LVFP in healthy anesthetized dogs subjected to volume loading.
Objective—To evaluate the effects of the pacemaker funny current (If) inhibitor ivabradine on heart rate (HR), left ventricular (LV) systolic and diastolic function, and left atrial performance in healthy cats and cats with hypertrophic cardiomyopathy (HCM).
Animals—6 healthy cats and 6 cats with subclinical HCM.
Procedures—Anesthetized cats underwent cardiac catheterization and were studied over a range of hemodynamic states induced by treatment with esmolol (200 to 400 μg/kg/min, IV), esmolol and dobutamine (5 μg/kg/min, IV), ivabradine (0.3 mg/kg, IV), and ivabradine and dobutamine. Left ventricular systolic and diastolic function, cardiac output, and left atrial function were studied via catheter-based methods and echocardiography.
Results—Treatment with ivabradine resulted in a significant reduction of HR, rate-pressure product, and LV contractile function and a significant increase in LV end-diastolic pressure, LV end-diastolic wall stress, and LV relaxation time constant (tau) in cats with HCM. Concurrent administration of ivabradine and dobutamine resulted in a significant increase of LV contractility and lusitropy, with blunted chronotropic effects of the catecholamine. Left atrial performance was not significantly altered by ivabradine in cats with HCM. Regression analysis revealed an association between maximum rate of LV pressure rise and tau in cats with HCM.
Conclusions and Clinical Relevance—Ivabradine had significant effects on several cardiovascular variables in anesthetized cats with HCM. Studies in awake cats with HCM are needed to clinically validate these findings.
Objective—To evaluate the accuracy of a commercial ultrasonographic cardiac output (CO) monitoring system (UCOMS) in anesthetized Beagles as assessed by comparison with thermodilution CO (TDCO).
Animals—8 healthy anesthetized Beagles.
Procedures—Simultaneous UCOMS and TDCO measurements of CO were obtained during 4 hemodynamic states: baseline anesthesia (0.5% to 1.5% isoflurane), a higher depth of anesthesia (2% to 3.5% isoflurane) to yield a ≥ 15% reduction in systolic arterial blood pressure, IV infusion of colloidal solution to a mean right atrial pressure of ≥ 15 mm Hg, and IV infusion of dobutamine at 5 μg/kg/min. Measurements were obtained at 2 probe positions: the subxiphoid region and the right thoracic inlet. Correlation and agreement of results between methods were determined via linear regression analysis and Bland-Altman plots.
Results—A significant positive correlation was detected between UCOMS andTDCO measurements obtained at the subxiphoid (R = 0.86) and thoracic inlet (R = 0.83) positions. Bland-Altman plots revealed minimal bias between methods (bias ± SD, −0.03 ± 0.73 L/min and −0.20 ± 0.80 L/min for subxiphoid and thoracic inlet measurements, respectively). However, the percentage error associated with UCOMS measurements made at the 2 positions was > 45%.
Conclusions and Clinical Relevance—When compared with the results of TDCO, CO measured with the UCOMS exceeded commonly accepted limits of error in healthy dogs. The UCOMS was, however, able to track changes in CO across hemodynamic states. Additional research is needed to assess the usefulness of the UCOMS for monitoring CO in critically ill dogs.