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Ventricular-arterial uncoupling in heart failure with preserved ejection fraction after myocardial infarction in dogs - invasive versus echocardiographic evaluation.

Mathieu M, El Oumeiri B, Touihri K, Hadad I, Mahmoudabady M, Thoma P, Metens T, Bartunek J, Heyndrickx GR, Brimioulle S, Naeije R, Mc Entee K - BMC Cardiovasc Disord (2010)

Bottom Line: Healed myocardial infarction was associated with preserved echocardiographic left ventricular ejection fraction (0.57 +/- 0.01, mean +/- SEM) and altered Doppler mitral indices of diastolic function.NT-proBNP was increased, aldosterone was decreased, and norepinephrine was unchanged.Invasive measurements showed a markedly decreased end-systolic elastance (2.1 +/- 0.2 vs 6.1 +/- 0.8, mmHg/ml, p < 0.001) and end-systolic elastance to effective arterial elastance ratio (0.6 +/- 0.1 vs 1.4 +/- 0.2, p < 0.001), with altered active relaxation (dP/dtmin -1992 +/- 71 vs -2821 +/- 305, mmHg/s, p < 0.01) but preserved left ventricular capacitance (70 +/- 6 vs 61 +/- 3, ml at 20 mmHg, p = NS) and stiffness constant.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Physiology and Pathophysiology, ULB, Brussels, Belgium. myrielle.mathieu@ulb.ac.be

ABSTRACT

Background: Heart failure with preserved left ventricular ejection fraction and abnormal diastolic function is commonly observed after recovery from an acute myocardial infarction. The aim of this study was to investigate the physiopathology of heart failure with preserved ejection fraction in a model of healed myocardial infarction in dogs.

Methods: Echocardiography, levels of neurohormones and conductance catheter measurements of left ventricular pressure-volume relationships were obtained in 17 beagle dogs 2 months after a coronary artery ligation, and in 6 controls.

Results: Healed myocardial infarction was associated with preserved echocardiographic left ventricular ejection fraction (0.57 +/- 0.01, mean +/- SEM) and altered Doppler mitral indices of diastolic function. NT-proBNP was increased, aldosterone was decreased, and norepinephrine was unchanged. Invasive measurements showed a markedly decreased end-systolic elastance (2.1 +/- 0.2 vs 6.1 +/- 0.8, mmHg/ml, p < 0.001) and end-systolic elastance to effective arterial elastance ratio (0.6 +/- 0.1 vs 1.4 +/- 0.2, p < 0.001), with altered active relaxation (dP/dtmin -1992 +/- 71 vs -2821 +/- 305, mmHg/s, p < 0.01) but preserved left ventricular capacitance (70 +/- 6 vs 61 +/- 3, ml at 20 mmHg, p = NS) and stiffness constant. Among echocardiographic variables, the wall motion score index was the most reliable indicator of cardiac contractility while E', E/A and E'/A' were correlated to dP/dtmin.

Conclusions: In the canine model of healed myocardial infarction induced by coronary ligation, heart failure is essentially characterized by an altered contractility with left ventricular-arterial uncoupling despite vascular compensation rather than by abnormal diastolic function.

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Correlations between hemodynamic and echocardiographic data: systolic function. A: Scatterplot of Ees as a function of WMSI. B: Scatterplot of Ees/Ea as a function of S'. Ees: left ventricular end-systolic elastance; WMSI: wall motion score index; Ea: arterial elastance; S': Tissue Doppler mitral annulus S wave.
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Figure 2: Correlations between hemodynamic and echocardiographic data: systolic function. A: Scatterplot of Ees as a function of WMSI. B: Scatterplot of Ees/Ea as a function of S'. Ees: left ventricular end-systolic elastance; WMSI: wall motion score index; Ea: arterial elastance; S': Tissue Doppler mitral annulus S wave.

Mentions: The echocardiographic indices of systolic function WMSI, LVEF, S' and LVESV were correlated to Ees (r = 0.73, p < 0.001 for WMSI, r = 0.71, p < 0.001 for LVEF, r = 0.71, p < 0.01 for S' and r = 0.59, p < 0.01 for LVESV) and to Ees/Ea (r = 0.61, p < 0.01 for WMSI, r = 0.60, p < 0.01 for S' and r = 0.58, p < 0.01 for LVEF) while FS was not correlated to Ees (r = 0.25, p = NS) and FS and LVESV were not correlated to Ees/Ea (r = 0.33, p = NS for FS and r = 0.29, p = NS for LVESV). Forward stepwise regression analyses showed that the best predictors of Ees and Ees/Ea were respectively WMSI (r = 0.74, p < 0.001) and S' (r = 0.60, p = 0.024) (Figure 2). NT-proBNP was correlated to Ees (r = 0.46, p < 0.05) but not to Ees/Ea (r = 0.34, p = NS).


Ventricular-arterial uncoupling in heart failure with preserved ejection fraction after myocardial infarction in dogs - invasive versus echocardiographic evaluation.

Mathieu M, El Oumeiri B, Touihri K, Hadad I, Mahmoudabady M, Thoma P, Metens T, Bartunek J, Heyndrickx GR, Brimioulle S, Naeije R, Mc Entee K - BMC Cardiovasc Disord (2010)

Correlations between hemodynamic and echocardiographic data: systolic function. A: Scatterplot of Ees as a function of WMSI. B: Scatterplot of Ees/Ea as a function of S'. Ees: left ventricular end-systolic elastance; WMSI: wall motion score index; Ea: arterial elastance; S': Tissue Doppler mitral annulus S wave.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2902405&req=5

Figure 2: Correlations between hemodynamic and echocardiographic data: systolic function. A: Scatterplot of Ees as a function of WMSI. B: Scatterplot of Ees/Ea as a function of S'. Ees: left ventricular end-systolic elastance; WMSI: wall motion score index; Ea: arterial elastance; S': Tissue Doppler mitral annulus S wave.
Mentions: The echocardiographic indices of systolic function WMSI, LVEF, S' and LVESV were correlated to Ees (r = 0.73, p < 0.001 for WMSI, r = 0.71, p < 0.001 for LVEF, r = 0.71, p < 0.01 for S' and r = 0.59, p < 0.01 for LVESV) and to Ees/Ea (r = 0.61, p < 0.01 for WMSI, r = 0.60, p < 0.01 for S' and r = 0.58, p < 0.01 for LVEF) while FS was not correlated to Ees (r = 0.25, p = NS) and FS and LVESV were not correlated to Ees/Ea (r = 0.33, p = NS for FS and r = 0.29, p = NS for LVESV). Forward stepwise regression analyses showed that the best predictors of Ees and Ees/Ea were respectively WMSI (r = 0.74, p < 0.001) and S' (r = 0.60, p = 0.024) (Figure 2). NT-proBNP was correlated to Ees (r = 0.46, p < 0.05) but not to Ees/Ea (r = 0.34, p = NS).

Bottom Line: Healed myocardial infarction was associated with preserved echocardiographic left ventricular ejection fraction (0.57 +/- 0.01, mean +/- SEM) and altered Doppler mitral indices of diastolic function.NT-proBNP was increased, aldosterone was decreased, and norepinephrine was unchanged.Invasive measurements showed a markedly decreased end-systolic elastance (2.1 +/- 0.2 vs 6.1 +/- 0.8, mmHg/ml, p < 0.001) and end-systolic elastance to effective arterial elastance ratio (0.6 +/- 0.1 vs 1.4 +/- 0.2, p < 0.001), with altered active relaxation (dP/dtmin -1992 +/- 71 vs -2821 +/- 305, mmHg/s, p < 0.01) but preserved left ventricular capacitance (70 +/- 6 vs 61 +/- 3, ml at 20 mmHg, p = NS) and stiffness constant.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Physiology and Pathophysiology, ULB, Brussels, Belgium. myrielle.mathieu@ulb.ac.be

ABSTRACT

Background: Heart failure with preserved left ventricular ejection fraction and abnormal diastolic function is commonly observed after recovery from an acute myocardial infarction. The aim of this study was to investigate the physiopathology of heart failure with preserved ejection fraction in a model of healed myocardial infarction in dogs.

Methods: Echocardiography, levels of neurohormones and conductance catheter measurements of left ventricular pressure-volume relationships were obtained in 17 beagle dogs 2 months after a coronary artery ligation, and in 6 controls.

Results: Healed myocardial infarction was associated with preserved echocardiographic left ventricular ejection fraction (0.57 +/- 0.01, mean +/- SEM) and altered Doppler mitral indices of diastolic function. NT-proBNP was increased, aldosterone was decreased, and norepinephrine was unchanged. Invasive measurements showed a markedly decreased end-systolic elastance (2.1 +/- 0.2 vs 6.1 +/- 0.8, mmHg/ml, p < 0.001) and end-systolic elastance to effective arterial elastance ratio (0.6 +/- 0.1 vs 1.4 +/- 0.2, p < 0.001), with altered active relaxation (dP/dtmin -1992 +/- 71 vs -2821 +/- 305, mmHg/s, p < 0.01) but preserved left ventricular capacitance (70 +/- 6 vs 61 +/- 3, ml at 20 mmHg, p = NS) and stiffness constant. Among echocardiographic variables, the wall motion score index was the most reliable indicator of cardiac contractility while E', E/A and E'/A' were correlated to dP/dtmin.

Conclusions: In the canine model of healed myocardial infarction induced by coronary ligation, heart failure is essentially characterized by an altered contractility with left ventricular-arterial uncoupling despite vascular compensation rather than by abnormal diastolic function.

Show MeSH
Related in: MedlinePlus