Changes in Pericardial Calcification Due to Antiplatelet Agents: In Vitro Studies

Abstract

To develop tissue valves for prolonged use in the cardiovascular system, the complicated process of surface induced calcification must be better understood. Calcification was examined for 60 days on glutaraldehyde treated bovine pericardium (GABP) and enzyme extracted tissues fixed in glutaraldehyde (GATBP) incubated in metastable solutions of calcium phosphate, and the roles of aspirin and persantine in conjunction with vitamins C, B, or E, gentamycin (antibiotic), or pentothal sodium (anesthetic) in the medium were examined. Further, the diffusion of calcium across the GATBP was evaluated using a diffusion cell with 2 compartments. Pericardial calcification was also observed using scanning electron microscopy (SEM) techniques. It seems that the examined antiplatelet agents can modify the pericardial surfaces and subsequently their mineralization processes (GATBP, 31.7 micrograms/mg tissue; in the presence of 5 mg% vitamin C, 13.1 micrograms/mg tissue; in 1.5 mg% aspirin, 17.2 micrograms/mg tissue; and 1 mg% gentamycin, 14.8 micrograms/mg tissue) on exposure with the metastable calcium phosphate solution for 60 days. In addition, these agents may modify calcium transport and interfere with the adsorption at the surface, hence reducing calcium nodulation on GATBP. Scanning electron micrographs also revealed a reduction in calcium deposition on the pericardium due to these antiplatelet agents. It may be hypothesized that the influx of calcium on GATBP may be due to the cellular components or the involvement of plasma proteins like the fibrinogen molecule. The exact mechanism of these changes in the calcification of the pericardium are still unknown. From these in vitro findings, it appears that a combined vitamin therapy with low doses of aspirin may be beneficial for platelet suppression and thereby for prevention of thrombosis and calcification. However, more in vivo studies are needed to develop applications.

Flow Velocity, Fluid Dynamics and Vascular Pathophysiology

“…As mentioned in an earlier paragraph, our studies at University of Minnesota were aimed at determining the extent of platelet activation during non-physiological blood flow over the mechanical heart valves. It is well known that abnormal flow patterns promote blood cell destruction and thus may initiate, thrombus formation as well as tissue calcification [27]. In a study conducted by Chandran et al, the peak turbulent shear stress measured along the centerline plane of the SJM valve at peak systole was in the order of 1500 dyn/cm 2 [28].…”

Cardiac calcification in acute intermittent porphyria

“…[13] Exact mechanism of the pericardial calcification is still not clear,[11] but is believed to be due to previous pericardial insult. [1] Pericardial calcification usually occurs over the posterior part, i.e., right atrium and anterior right ventricle, diaphragmatic surface, atrioventricular grooves because fluid preferentially gravitates toward the right side of the heart, where calcium and even bone are slowly deposited in the inspissated fluid.…”