CCCardiol CroatCardiologia CroaticaCardiol. Croat.1848-543X1848-5448Croatian Cardiac SocietyCC 2013_8_5-6_19110.15836/ccar.2013.191Extended AbstractHow rapidly can diastolic function alter with acute afterloading: insights from a closed chest/closed pericardium acute afterload porcine modelJakusNina1SutherlandGeorge R.2CikesMaja1HaemersPeter1VoigtJens-Uwe1RademakersFrank1D’hoogeJan1ClausPiet1Catholic University of Leuven, Leuven, BelgiumUniversity Hospital Brussels, Brussels, BelgiumCorrespondence to Piet Claus, KU Leuven, Cardiovascular Imaging and Dynamics, UZ Herestraat 49 - box 7003, 3000 Leuven, Belgium; Phone: +32-16-3-49017; E-mail: Piet.Claus@med.kuleuven.be05201305201385-6191191Croatian Cardiac Society2013Croatian Cardiac SocietyKEYWORDS: acute ventricular afterloadpericardial constraintseptal shiftdiastolic pressurepulsed Doppler echocardiography
Background: The speed and timing of changes in diastolic function parameters during acute LV loading and unloading is unknown.
Methods: In a closed chest, closed pericardium porcine model, LV systolic pressure was increased by 30% using a transient descending aortic partial balloon inflation. Morphology and mechanical changes were monitored in real time by echocardiography, as were changes in left and right heart diastolic pressures by 3 Millar catheters. Simultaneous blood pool and tissue Doppler data (radial and long axis) were acquired during afterload changes.
Results: In 7 animals, acute loading consistently induced LV dilatation and a rightwards ventricular septal shift due to lateral LV pericardial restraint. This reduced RV volume. Afterload increase caused an immediate decrease in early diastolic filling wave (E) and lateral wall velocity (E’). This was mirrored by an immediate increase in both early diastolic LV (LVDPmin) and LA (LADPmin) pressure (Figure 1). Pulmonary vein flow gradually reduced with decreased late flow. The rightwards septal shift induced a small but significant increase in RVDPmin and an increase in mean RA pressure, but failed to increase pulmonary artery pressure. Acute afterload release immediately returned E values to baseline, but E’ showed a transient further 3 to 5 beat increase before it normalized.
Left panel: Early diastolic filling wave (E) and lateral wall velocity (E’) before, during and after acute pressure increase. Right panel: Left ventricular and atrial early diastolic pressure and transmitral pressure gradient before, during and after acute pressure increase.
Conclusion: Acute afterloading variably elevates all cardiac diastolic pressures and reduces LV relaxation. These early changes in myocardial mechanics occur simultaneously with changes in LVDPmin. Right heart diastolic pressures increase due to the septal shift which both reduced RV volume and decreased LV compliance but did not elevate pulmonary pressure. E’/E recovery differed which could be attributed to transient preload changes (Figure 1). (1-4)
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