Presence Of Pericardium Research Articles

Revisiting Methods for Assessing and Comparing Left Ventricular Diastolic Stiffness

Background: Controversies over the pathophysiology of heart failure with preserved EF have renewed interest in characterization and comparison of LV diastolic stiffness, best assessed using the LV end-diastolic (ED) pressure (P)-volume (V) relationship obtained from multiple beats (MB) during rapid preload reduction. As the MB method is difficult, the diastolic P-V over a single beat with P corrected for effect of ongoing relaxation (RCSB) has been used in human studies but not validated against MB method. Further, the LV stiffness coefficient β in the relation EDP = αeβ∗EDV has been used to compare stiffness, but β covaries with α. This covariance is accounted for by comparing derived EDV at similar EDP, calculated from α, β and EDP of 10, 20 or 30 mmHg (EDV10-30). Objective: Determine if the RCSB method of assessing diastolic stiffness (as quantified by β or EDV10-30) shows good correlation and agreement with the MB method. Methods: P, V were invasively measured and the RCSB followed by MB methods performed in 26 young normal or elderly hypertensive dogs before and during phenylephrine (to vary afterload) or acute volume expansion. In the RCSB method, diastolic P was corrected by subtracting the P due to relaxation, monoexponentially extrapolated from isovolumic relaxation. Correlation was assessed by linear regression. Agreement was expressed as the mean ± SD of the paired difference between MB and RCSB values for β or EDV10-30, expressed as percentages of their mean values; p is for paired t-test. Results: Over widely varying afterloads (LV systolic P 95 to 236 mmHg), EDV10-30 derived from RCSB and MB methods showed excellent correlation (r = 0.98, p < 0.0001) and agreement (0.6 ± 5%, p = 0.6). Correlation (r = 0.62, p = 0.002) and agreement (4.2 ± 45%, p = 0.7) between β from SB and MB was poorer. Use of a limited number of P and V points for the RCSB method (at minimum LV P, pre-atrial contraction, and ED) resulted in less agreement between the methods in assessing EDV10-30 (4.4 ± 9%, p = 0.0003) or β (21 ± 40%, p = 0.025). Neither β (12.5 ± 55%, p = 0.5) nor EDV10-30 (10 ± 10%, p < 0.0001) derived from RCSB agreed with MB after marked volume expansion in presence of pericardium. Conclusion: Clinical studies seeking to compare diastolic stiffness between groups can use the clinically more feasible RCSB to substitute for the complex MB technique under a wide range of afterload. Accuracy will be influenced by the number of P and V points used and by presence of acute volume overload. Comparison of stiffness between groups will be enhanced by methods which account for the covariance between α and β.

Load dependence of left ventricular diastolic pressure-volume relations during short-term coronary artery occlusion.

We evaluated the effect of altered loading conditions on left ventricular (LV) diastolic pressure-volume relations during acute coronary artery occlusion that was produced by inflation of an intracoronary balloon. Open-chest anesthetized dogs (n = 18) were instrumented so that LV pressure (micromanometer) and LV volume (conductance) could be measured without disturbing the pericardium. The effects of brief periods of occlusion (1-2 minutes) were assessed under steady-state conditions before and after dextran infusion with the pericardium present and absent and during vena caval occlusion. Under steady-state conditions before dextran infusion with the pericardium removed, at an LV end-diastolic pressure (EDP) of 8.4 +/- 1.4 mm Hg, occlusion resulted in a rightward shift in the diastolic portion of the LV pressure-volume loop (delta LVEDP, 2.7 +/- 2.3 mm Hg; delta LVEDV, 6.3 +/- 4.7 ml, both p less than 0.05 versus control). After dextran infusion (LVEDP, 20.9 +/- 6.0 mm Hg), occlusion resulted in a rightward and upward shift in the diastolic portion of the LV pressure-volume loop (delta LVEDP, 5.8 +/- 4.4 mm Hg; delta LVEDV, 4.2 +/- 3.0 ml, both p less than 0.05 versus control). At low cardiac volumes before dextran infusion, the intact pericardium did not affect the response to occlusion. By contrast, after dextran infusion in the presence of an intact pericardium, LVEDP significantly increased (delta, 6.4 +/- 3.6 mm Hg, p less than 0.05) but LVDEV did not (delta, 0.7 +/- 1.5 ml, p = NS). There was a parallel upward shift in the diastolic portion of the LV pressure-volume loop that was eliminated by removal of the pericardium. Thus, the change in LV diastolic pressure and volume during occlusion varied and depended on the baseline cardiac volume and presence of the pericardium. Before dextran infusion with the pericardium present and absent, coronary artery occlusion did not alter the LV diastolic chamber stiffness parameter, which was calculated from the diastolic interval of an averaged steady-state beat (0.040 +/- 0.019 versus 0.036 +/- 0.015 mm Hg/ml, p = NS). After dextran infusion with the pericardium present and absent, coronary artery occlusion increased the LV diastolic chamber stiffness parameter (0.057 +/- 0.034 and 0.074 +/- 0.034 mm Hg/ml, both p less than 0.05 versus controls, respectively). Vena caval occlusion eliminated the shifts in the diastolic portion of the LV pressure-volume loop with the pericardium present and absent.(ABSTRACT TRUNCATED AT 400 WORDS)

Reduced tracheal growth after reconstruction with pericardium

Four groups of piglets were used to test the use of pericardium and periosteum as free grafts in the repair of full thickness cervical tracheal defects. Pericardium provided an airtight, rapidly healing graft, but did not give sufficient structural rigidity to prevent narrowing and growth failure at the graft site. Composite grafts of pericardium and periosteum were also unsatisfactory, in that the periosteum failed to produce enough bone to prevent collapse of the graft. Since previous studies have shown that periosteal grafts result in good bone formation when applied alone or as an extramucosal support, it is concluded that the osteogenic potential is dependent on the available blood supply and speed of revascularization. It appears that the presence of pericardium in the composite grafts may have inhibited this property.