Restenosis was studied histopathologically by serial step sectioning of 22 coronary arteries from 21 patients in whom percutaneous transluminal coronary angioplasty (PTCA) had been performed (9 arteries from patients who had died shortly after PTCA and 1 3 from those who had died considerably later). Nine of the 13 arteries from the patients who had died long after PTCA were immunohistochemically stained using anti-actin antibody for examination of spindle-shaped cells proliferating in the intima. In the patients who had died shortly after PTCA, all 9 arteries showed fresh thrombus formation. In the patients who had died considerably later after PTCA, however, there was fragmentation of the internal elastic lamina (IEL) in 9 arteries. In each of these 9 arteries, a remarkable proliferation of intimal cells was observed on the intimal side, mainly at the site of the IEL fragmentation. These spindle-shaped cells were identified as smooth muscle cells (SMC) because they stained reddish-brown with Masson's trichrome, and because immunohistochemical staining with anti-actin antibody was also positive. In 2 arteries, proliferation of SMC and elastic fibers was observed on the luminal side of the intima, despite absence of fragmentation in the IEL. Proliferation of SMC in false lumens was identified in 2 patients with medial dissection . From the above findings, the following 4 forms of restenosis after PTCA have been identified: l. thrombus formation; 2. proliferation of SMC on the intimal side, mainly around fragmentation in the IEL; 3. proliferation of SMC on the luminal side of the intima where there was no fragmentation of the IEL ; and 4. proliferation of SMC in dissected false lumen. The proliferation of SMC on the intimal side of the disrupted IEL was thought to have been a result of migration of SMC from the media to the intima, because SMC proliferation was seen around the disrupted region.
The present study was designed to determine whether the wall thickening seen in acute myocarditis is caused by interstitial edema. The study group comprised 25 patients (idiopathic myocarditis, 17; eosinophilic myocarditis, 8) in whom acute myocarditis was diagnosed histologically and who underwent echocardiography and endomyocardial biopsy during both the acute and convalescent phases. The following echocardiographic parameters were measured: interventricular septum and left ventricular posterior wall thickness, left ventricular end-diastolic dimension, and left ventricular ejection fraction. Based on the myocardial biopsy specimens, the degree of interstitial edema was classified into 3 grades [(-), 1(+), 2(+)] and the transverse diameter of cardiac myocytes was measured using light microscopy. The thickness of both the interventricular septum and left ventricular wall decreased from 14.3±3.7 mm and 13.3±2.4 mm in the acute phase to 9.7±1.7 mm (p<0.001) and 10.2±1.7 mm (p<0.0001), respectively, in the convalescent phase. Edema was present in 22 patients (88.0%) in the acute phase, but in the convalescent phase, edema was present in only 7 patients (28.0%), indicating a significant reduction in the degree of edema (p<0.0001). Cardiac myocyte diameter did not differ significantly between the acute (13.6±1.1 μm) and convalescent (13.8±1.8 μm) phases. (Jpn Circ J 2001; 65: 863 - 866)
