We investigated smooth muscle cell proliferation associated with restenosis after percutaneous transluminal coronary angioplasty (PTCA) in 8 arteries with fragmented internal elastic lamina obtained at autopsy in 7 patients who died between 2 months to 2 years 11 months after coronary angioplasty. The internal elastic lamina fragmentation, measured longitudinally along the blood vessels, measured 6.6 +/- 6.9 mm. Smooth muscle cell proliferation was concentrated around the fragmented internal elastic lamina, extending longitudinally even to unfragmented areas. The proliferation of smooth muscle cells extended for 1.8 +/- 2.2 mm in the proximal portion of the fragmentation, and for 2.0 +/- 2.9 mm in the distal portion. The possibility of new stenoses resulting from smooth muscle cell proliferation at sites adjacent to those subjected to PTCA should be borne in mind when PTCA of the proximal segments of the left anterior descending coronary artery is contemplated.

Aged↗

PubMed1993

[Histopathologic observations of restenosis following coronary angioplasty].

Explore the source record for details and available documents.

Angioplasty, Balloon, Coronary↗

PubMed1992

Clinical and pathologic features of chronic myocarditis: four autopsy cases presenting as dilated cardiomyopathy in life.

Four patients who appeared to suffer from dilated cardiomyopathy in life were found at autopsy to have had chronic myocarditis (two males and two females, aged 7 to 42 years). Before the appearance of cardiac symptoms, a flu-like illness was observed in two cases and fever in two others. The duration of illness was from 7 months to 10 years and 11 months (mean: 3 years and 8 months) and the heart weight in three adult patients varied from 510 to 940 g (mean: 720 g). Histologic observation of a transverse ventricular section in each patient showed 10 to 187 clusters of small round cells, and massive fibrosis was also found at these sites. The mean percent area of interstitial fibrosis was 26.3% in the ventricular septum, 31.2% in the left ventricular free wall, and 21.6% in the right ventricular free wall. These histologic findings indicated the presence of myocarditis, which was presumably chronic. Our findings suggest that some of the patients diagnosed as having dilated cardiomyopathy may in fact have chronic myocarditis.

Adult↗

PubMed1992

[A case of brain stem encephalitis complicated with bifascicular block caused by rubella virus].

We reported a case of a 29-year-old man who had been in good health until contracting brain stem encephalitis due to a rubella virus 5 years previously, at which time the ECG revealed complete right bundle branch block and right axis deviation. An ECG obtained 6 months earlier had been within normal limits. Since yearly health checkups continued to show the same abnormalities, the patient was admitted for closer examination. At the time of admission, physical findings and blood tests revealed no abnormalities. No cardiomegaly nor pulmonary congestion was observed on chest X-rays either at the time of the original illness or at this time. An endomyocardial biopsy specimen obtained from the right ventricle revealed size variation of cardiac myocytes, moderate disarrangement, and mild myocardial interstitial fibrosis, indicative of post-myocarditic changes. The above findings suggest that bifascicular block (right bundle branch and posterior fascicle) appeared at the time of the rubella virus infection, in the pathogenesis of which the involvement of myocarditis was strongly suspected. Some patients developing myocarditis do not manifest cardiac symptoms such as heart failure. In these cases, conduction disturbances are the sole sequelae. To differentiate pathogenesis in such cases, endomyocardial biopsy was thought to be of value.

Adult↗

PubMed1990

Lesions in side branches of arteries having undergone percutaneous transluminal coronary angioplasty: a histopathologic study.

Percutaneous transluminal coronary angioplasty (PTCA) may cause occlusion in side branches. No histologic studies, however, have been made on side branches of the arteries in which PTCA has been performed. A histologic study was therefore made to explain the effect of PTCA on side branches. Histologic specimens were prepared by serial step sectioning from 15 side branches of 10 autopsied cases that had undergone PTCA. The results of examination by light microscope were as follows: (1) Stenoses due to PTCA were seen in seven branches (46.7%). (2) The stenoses were classified into three types: (a) stenosis due to blocking of the orifice of a side branch by the disrupted portion of the intima of the main artery (one branch); (b) stenosis due to medial dissection of the main artery or further dissection occurring even in the side branches (three branches); and (c) stenosis due to fragmentation of the internal elastic lamina of the main artery accompanied by proliferation of smooth muscle cells even in the side branch (three branches). It is now clear that stenosis is caused in side branches long after PTCA. Extra care is required when major side branches exist in the portion where this procedure is to be performed.

Adult↗

PubMed1990

Restenosis after percutaneous transluminal coronary angioplasty--a histopathological study using autopsied hearts.

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 13 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: 1. 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.

Adult↗

PubMed1990

[Two autopsied cases of arrhythmogenic right ventricular dysplasia].

Autopsy studies of arrhythmogenic right ventricular dysplasia (ARVD) have rarely been reported, and its etiology remains unknown. The present report describes a detailed histopathological study of two autopsied cases of ARVD. Case 1: This 21-year-old man experienced palpitation accompanied by syncope. He died after ventricular tachycardia of right ventricular origin. The heart weighed 365 g and the right ventricular cavity was markedly dilated. The distribution of fatty tissue was roughly limited to the middle layer of the free wall, replacing the myocardium with fatty degeneration. Medial hyperplasia of the small arteries within the fatty tissue was also observed. Fibroelastosis was observed in the left ventricular endocardium. In the conduction system, fatty tissue was found in the sinus node. In addition, medial hypoplasia was observed in the pulmonary arteries. Case 2: This 32-year-old man who had had an arrhythmia for 10 years died of ventricular tachycardia of right ventricular origin. His older brother also died of heart disease. His heart weighed 515 g and both the right and left ventricles were dilated. Fatty tissue, unlike that in Case 1, was shown to markedly infiltrate from the epicardium into both the right and left ventricular walls. In the right ventricular wall, muscle layers disappeared in some portions. In the conduction system, fatty tissue was observed in the sinus node. Although ARVD may be considered a syndromic entity, individual cases are different in terms of pathological morphology, with possible variations in the etiology and pathogenesis.

Adipose Tissue↗

PubMed1988

Plaque rupture possibly induced by coronary spasm--an autopsy case of acute myocardial infarction.

The histological picture of sites of coronary spasms has not yet been made sufficiently clear. A histopathological examination was performed on the coronary artery of a patient who died of acute myocardial infarction after a refractory coronary spasm was identified by coronary arteriography. In the site of the coronary spasm, intimal bleeding as well as infiltration by lymphocytes and plasma cells in the adventitia were seen. In the same region, fracture of intimal collagen fibers and rupture of atheromatous plaque were observed. Although it is very difficult to prove in individual cases of acute myocardial infarction that spasms played a part, some cases involving spasms may possibly exist among the cases of acute myocardial infarction showing atheromatous plaque rupture--thrombus formation.

Coronary Angiography↗

PubMedDate not supplied

The evaluation of corticosteroid therapy in conjunction with plasma exchange in the treatment of renal cholesterol embolic disease. A report of 5 cases.

In this report, we describe 5 patients with cholesterol atheroembolic renal failure. In 3 of the 5 patients, combined therapy with corticosteroids and plasma exchange was performed. These 3 patients survived, with 2 showing an improvement in renal function. The 2 remaining patients died of multifactorial causes. The literature on therapy for cholesterol atheroembolic renal failure is reviewed and the efficacy of combined therapy by use of corticosteroids and plasma exchange is evaluated.

Acute Kidney Injury↗