Improvement of afterload mismatch of left atrial booster pump function with positive inotropic agent
ABSTRACT The objective of this study was to examine the hypothesis that a positive inotropic agent improves left ventricular (LV) filling during left atrial (LA) contraction in the presence of markedly elevated LV filling pressure.
In patients with old myocardial infarction (MI), an increase in the operational LV chamber stiffness reduces LV filling during the LA contraction, resulting from an "afterload mismatch" of the LA booster pump function.
We investigated the effect of dobutamine infusion (3 microg/kg/min) on the LA pump function in the presence of elevated LV filling pressure induced by aortic constriction (Aoc) during acute MI in 10 dogs. Transmitral flow velocity was determined by transesophageal echocardiography, LV pressure by a micromanometer and LV volume by a conductance catheter. We measured the early (E) and late (A) diastolic peak transmitral flow velocities (cm/s) and LV chamber stiffness (deltaP/deltaV: mm Hg/ml; where deltaP is developed pressure and deltaV is the absolute filling volume during LA contraction).
When the deltaP/deltaV was increased by Aoc during MI (from 1.1 +/- 0.8 to 3.1 +/- 2.6 mm Hg/ml, p < 0.01), A decreased significantly (from 30 +/- 5 to 22 +/- 8 cm/s, p < 0.01), and the ratio of E to A increased (from 1.0 +/- 0.3 to 1.4 +/- 0.8, p < 0.05) compared with MI without Aoc, showing the pseudonormal transmitral flow pattern, the so called "LA afterload mismatch." Dobutamine under this condition significantly reduced the deltaP/deltaV (to 1.7 +/- 1.2 mm Hg/ml, p < 0.05), resulting in an increase in A (to 31 +/- 8 cm/s, p < 0.01) and a decrease in E/A (to 1.0 +/- 0.3, p < 0.05), and the transmitral flow became a prolonged relaxation pattern as in MI without Aoc in all dogs. There was an inverse correlation between the deltaP/deltaV and the time-velocity integral of A (r = -0.70, p < 0.01).
Dobutamine improved the afterload mismatch of the LA booster pump function. This effect may have been due to the reduction in LV operational chamber stiffness, resulting in an increase in the LA forward ejection into the LV.
Full-textDOI: · Available from: Toshiro Miura, Dec 26, 2013
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ABSTRACT: To evaluate left ventricular (LV) diastolic function in boxer dogs with aortic stenosis (AS). LV relaxation, elastic recoil, filling and stiffness have been found to be abnormal in people with AS and were related to disease severity, clinical signs and prognosis. 2-D, M-mode and Doppler echocardiography was done in 74 boxers with AS (55 with mild AS, 7 with moderate AS and 12 with severe AS) and compared with reference values from 66 normal boxers. Measurements included isovolumic relaxation time (IVRT), peak early (E) and late (A) transmitral filling velocities, mitral E wave deceleration time, peak systolic, and early and late (AR) diastolic pulmonary wenous flow velocities and related variables. In addition, left atrial (LA) function, LV dimensions and hypertrophy and LV systolic performance were assessed. Eight dogs (15%) with mild AS had abnormal LV diastolic function, compared with 16 dogs (84%) with moderate or severe AS. Two dogs (3%) had also systolic abnormalities. The flow pattern of delayed relaxation, pseudonormal mitral inflow and restrictive flow were found in 10, 11 and 3 dogs, respectively. IVRT and E:A were heterogeneous in dogs with moderate or severe AS, being either high, normal, or low. Peak AR velocity was significantly higher (p </= 0.05) in dogs with severe AS, and the A duration:AR duration ratio was significantly lower (p </= 0.05) in dogs with moderate and severe AS compared with the other dogs, suggesting decreased LV compliance, increased LV end-diastolic pressure, and normal or increased LA systolic function. Bivariate linear regression analysis revealed significant correlations between the severity of AS based on Doppler and LV hypertrophy (IVSd: r = 0.61, p </= 0.001 and LVPWd: r = 0.46, p </= 0.001) and AS severity and A duration: AR duration (r = -0.64, p </= 0.001). CONCLUTION: In most boxer dogs with moderate or severe AS, LV diastolic function is abnormal even in the presence of normal systolic performance.Journal of veterinary cardiology: the official journal of the European Society of Veterinary Cardiology 05/2002; 4(1):7-16. DOI:10.1016/S1760-2734(06)70018-2
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ABSTRACT: To analyze clinical, electrocardiographic and echocardiographic characteristics, survival, cause of death and possible modes of inheritance of dilated cardiomyopathy (DCM) in Doberman pinschers (DP) and to compare the occurrence and survival with dogs of other breeds. Dogs - Two cohorts of dogs were studied: 1. A consecutive series of 52 dogs of different breeds with DCM were included, 21 were Doberman pinschers and 31 dogs belonged to other breeds: 2. 28 asymptomatic Doberman pinschers, who were screened for DCM. Methods - Medical records of dogs with DCM were reviewed. Physical, electrocardiographic and echocardiographic examinations were performed on asymptomatic Doberman pinschers. Their pedigrees were reviewed. Doberman pinschers survived on average 52 days (range <1-180), while dogs of other breeds survived significantly longer, i.e. 240 days (<1-1230). Survival of Doberman pinschers in congestive heart failure (mean 62, range <1-180) was not different from survival of Doberman pinschers with sudden death (mean 33, range <1-105). High prevalence, short survival time and the clinical course of DCM in Doberman pinschers showed similarities to previous studies. Twenty-one percent of asymptomatic Doberman pinschers had increased left ventricular end-systolic diameter and 14% developed DCM within a year. A line of Doberman pinschers with multiple members affected with DCM was identified by the review of their pedigrees. Exact mode of inheritance could not be established. The prognosis of Doberman pinschers with DCM is poor. Further molecular genetic studies, which would enable detection and exclusion of disease carriers from the breeding, are necessary.Journal of veterinary cardiology: the official journal of the European Society of Veterinary Cardiology 05/2002; 4(1):17-24. DOI:10.1016/S1760-2734(06)70019-4
- Anesthesiology 05/2003; 98(4):975-94. · 6.17 Impact Factor