Guidelines for Complications of Cancer Treatment Vol VIII Part B

Acute fibrinous pericarditis can present with classic signs andsymptoms identical to other forms of acute pericarditis. Twotemporal patterns have been observed, firstly early acutepericarditis occurring during treatment (likely caused by tumorlysis) and secondly, delayed onset acute pericarditis. Chronicfibrosing pericarditis with constrictive physiology can developmonths, years, or decades following therapy. Unlike otherforms of the disease, fibrous bands or adhesions between theparietal and visceral layers are uncommon. Instead, there iscollagenous thickening of both layers, usually with apredominance of changes in the parietal pericardium.Thickening varies from 1 to 7 mm with disproportionateinvolvement of the anterior pericardial region.Microscopically, dense eosinophilic cicatricial collagen bandscontaining altered vessels are seen. The small arteries displayfibrointimal proliferation and medial muscular hypertrophy.Radiation damages the myocardium by injuring capillaryendothelial cells, which causes the obstruction of the capillarylumen and the formation of fibrin and platelet thrombi. Thisprocess leads to ischemia and then to myocardial cell deathand fibrosis. Damaged myocardium is characterized by nonspecific,diffuse interstitial fibrosis, but it rarely encompassesthe entire myocardium. The severity of fibrosis can differmarkedly from one region to another. Another pattern is thecardiomyopathic type of RIHD. The morphological changesin this group include marked thickening of the endocardiumby increased numbers of collagen and to a lesser extent elastinfibers.The incidence of clinically significant radiation inducedvalvular disease is unknown. The microscopic findings ofvalvular tissues examined at the time of valve replacement ornecropsy are nonspecific and include diffuse fibrosis with or300