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Aim: As acute short-lived increase in afterload may be a contributory mechanism to sudden death, we studied an acute 30% systolic pressure increase (SBPI) in a closed chest, closed pericardium porcine model, closed pericardium being essential to the model clinical applicability. Methods: 7 pigs were studied. All had an acute 5 beat 30% SBPI induced by a non-occlusive mid-descending aortic balloon inflation and release. Each challenge was continuously monitored for changes in cardiac morphology and function by cardiac ultrasound (2D, Doppler and Doppler Myocardial Imaging) and changes were correlated with pressure data from 3 Millar catheters (LV/Ao; LA; RV/RA). Continuous 12 lead ECG and intracardiac electrograms were also recorded. Results: Balloon inflation caused an acute diastolic pressure increase in all cavities (except pulmonary artery) with early diastolic preceding late changes and a corresponding systolic increase in LV, LA and RA pressures. Acute LV dilatation resulted in pericardial flattening (which is a visualization of the effects of pericardial constraint), a septal shift towards the RV and a decrease in RV size with a 30% reduction in LVEF % (Figure 1a). During inflation, pericardial excursion flattened >40% in basal, mid and apical LV segments, mostly mid wall (from 3.4 ±1.4 mm to 1.6 ±0.7 mm, p<0.05) (Figure 1b). With balloon deflation, the above rap- idly returned to baseline. Conclusion: Acute afterload increase induced immediate, profound and consistent changes in LV dimensions and function. Pericardial constraint caused a marked rightward septal shift which altered right heart diastolic function and reduced filling. Acute loading markedly altered both systolic and diastolic function for both the right and the left heart. It remains to be evaluated how these changes affect the mechano-electric coupling and as such could play a role in fatal arrhythmias. [ABSTRACT FROM AUTHOR]

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. 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. [ABSTRACT FROM AUTHOR]