Isolated Dissection of the Ductus Arteriosus Associated with Sudden Unexpected Intrauterine Death

We report five cases of sudden intrauterine death due to premature closure of the ductus arteriosus. In four cases, this was caused by dissecting the hematoma of the ductus arteriosus with intimal flap and obliteration of the lumen. In one case, the ductus arteriosus was aneurysmatic, with lumen occlusion caused by thrombus stratification. No drug therapy or free medication consumption were reported during pregnancy. The time of stillbirth ranged between 26 and 33 gestational weeks. We performed TUNEL analysis for apoptosis quantification. The dissecting features were intimal tears with flap formation in four of the cases, just above the origin of the ductus arteriosus from the pulmonary artery. The dissecting hematoma of the ductus arteriosus extended downward to the descending aorta and backward to the aortic arch with involvement of the left carotid and left subclavian arteries. TUNEL analysis showed a high number of apoptotic smooth muscle cells in the media in two cases. Abnormal ductal remodeling with absence of subintimal cushions, lacunar spaces rich in glycosaminoglycans (cystic medial necrosis), and smooth muscle cell apoptosis were the pathological substrates accounting for failure of remodeling process and dissection.

Download Full-text

Smooth Muscle Cell Proliferation in the Ductus Arteriosus and the Descending Aorta, and Effects of Enalapril on SMC Proliferation in Perinatal Rats.

Journal of Veterinary Medical Science ◽

10.1292/jvms.61.1215 ◽

1999 ◽

Vol 61 (11) ◽

pp. 1215-1218 ◽

Cited By ~ 2

Author(s):

Tatsuya TAKIZAWA ◽

Mariko KAWAHATA ◽

Yoshinori IKEDA ◽

Masako YAMAMOTO ◽

Kazuyoshi ARISHIMA ◽

...

Keyword(s):

Cell Proliferation ◽

Smooth Muscle ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

Ductus Arteriosus ◽

Smooth Muscle Cell Proliferation ◽

Descending Aorta

Download Full-text

Pathology of Spontaneous Dissection of Intracranial Arteries

Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques ◽

10.1017/s0317167100026901 ◽

1987 ◽

Vol 14 (S1) ◽

pp. 88-91 ◽

Cited By ~ 24

Author(s):

John H.N. Deck

Keyword(s):

Internal Carotid ◽

Cerebral Arteries ◽

Internal Elastic Lamina ◽

Cystic Medial Necrosis ◽

Vertebrobasilar System ◽

Moya Moya Disease ◽

Medial Necrosis ◽

The Media ◽

And Control ◽

Spontaneous Dissection

ABSTRACT:Spontaneous dissection of a major subarachnoid artery is an uncommon cause of stroke in young and apparently healthy individuals. Such dissection does not correlate well with systemic conditions such as emboli, thrombotic or hemorrhagic tendencies or hypertension, nor with disease of blood vessels such as atherosclerosis, fibromuscular dysplasia, cystic medial necrosis or Moya-Moya disease. Unusual exertion has been implicated as a factor in some cases. Gap defects were found in the internal elastic lamina near the site of dissection in three of four cases of spontaneous dissection reported here. It is suggested that such defects, because of their unusual size or number, may be responsible for initiating dissection in susceptible individuals. A detailed study of the major cerebral arteries in cases of dissection and control cases to document the size and frequency of such defects could shed light on the pathogenesis of spontaneous dissection. The subsequent course of events tends to differ in the internal carotid and vertebro-basilar systems. In most cases, the dissection in the internal carotid system is sub-intimal leading to thrombosis and cerebral infarction, while in the vertebrobasilar system dissection lies between the media and adventitia leading to subarachnoid hemorrhage. It is not known what structural differences of the two arterial systems may underlie this difference in the pattern of arterial dissection.

Download Full-text

The JCR:LA-cp rat: a novel rodent model of cystic medial necrosis

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00653.2016 ◽

2017 ◽

Vol 312 (3) ◽

pp. H541-H545 ◽

Cited By ~ 1

Author(s):

Yuh Fen Pung ◽

William M. Chilian ◽

Martin R. Bennett ◽

Nichola Figg ◽

Mohd Hamzah Kamarulzaman

Keyword(s):

Metabolic Syndrome ◽

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Rodent Model ◽

Chow Diet ◽

Cystic Medial Necrosis ◽

Collagen Formation ◽

The Metabolic Syndrome ◽

Normal Chow ◽

Medial Necrosis

Although there are multiple rodent models of the metabolic syndrome, very few develop vascular complications. In contrast, the JCR:LA-cp rat develops both metabolic syndrome and early atherosclerosis in predisposed areas. However, the pathology of the normal vessel wall has not been described. We examined JCR:LA control (+/+) or cp/cp rats fed normal chow diet for 6 or 18 mo. JCR:LA-cp rats developed multiple features of advanced cystic medial necrosis including “cysts,” increased collagen formation and proteoglycan deposition around cysts, apoptosis of vascular smooth muscle cells, and spotty medial calcification. These appearances began within 6 mo and were extensive by 18 mo. JCR:LA-cp rats had reduced medial cellularity, increased medial thickness, and vessel hypoxia that was most marked in the adventitia. In conclusion, the normal chow-fed JCR:LA-cp rat represents a novel rodent model of cystic medial necrosis, associated with multiple metabolic abnormalities, vascular smooth muscle cell apoptosis, and vessel hypoxia. NEW & NOTEWORTHY Triggers for cystic medial necrosis (CMN) have been difficult to study due to lack of animal models to recapitulate the pathologies seen in humans. Our study is the first description of CMN in the rat. Thus the JCR:LA-cp rat represents a useful model to investigate the underlying molecular changes leading to the development of CMN.

Download Full-text