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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nature of the changes occurring in the border zone of myocardial infarcts is uncertain. To study this question, the authors analyzed a number of morphologic features in hearts studied after postmortem arteriography and fixation in distention from 204 patients with single myocardial infarcts autopsied at The Johns Hopkins Hospital. Vacuolization of myocytes was observed in 53 (26%) cases, predominantly in surviving subendocardium and trabecular myocardium within the infarct. Lateral myocardium seldom and subepicardial myocardium almost never showed vacuolar change. Myocyte vacuolization progressively developed and then decreased with time: 1/20 (5%) hearts with infarcts less than 2 days old, 17/48 (35%) infarcts 2-14 days old, 13/27 (48%) infarcts 15-60 days old, 4/12 (33%) infarcts 61-365 days old, and 18/97 (19%) infarcts greater than 365 days old. Reduction in vacuolization with time was not explained by necrosis of vacuolated cells; rather, the myocardium showed normal morphology. Presence of vacuolization in old infarcts was associated with severe multivessel coronary artery disease and endocardial fibroelastosis. The results suggest that infarct border zone myocyte vacuolization may be correctable by reversal of regional ischemia; however, only a trivial amount of myocardium, relative to infarct size, undergoes vacuolar change.
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PMID:Myocyte vacuolization in infarct border zones is reversible. 407 19

The evaluation of prognostic factors in infants with critical stenosis of the aortic valve and intact ventricular septum is often misleading due to a complex interaction among lesions in the mitral and aortic valves, and the left ventricular myocardium. The clinical parameters on the left ventricular function, such as ejection fraction and left ventricular end-diastolic volume, are of particular interest as their effects on survival are very controversial. We performed a clinicopathologic analysis of two autopsied cases of this disease. Besides the morphological hallmarks of the aortic and mitral valves, these two cases showed two extreme types of pathology in the left ventricular myocardium, which might have significant impacts on the clinical evaluation of the left ventricular function. Case 1 showed endocardial fibroelastosis associated with abnormal intertrabecular spaces (so-called spongy myocardium), obscuring accurate estimation of the left ventricular end-diastolic volume. Case 2 showed ischemic necrosis of the apical part of the left ventricular myocardium. This infarct was associated with acute and chronic subendocardial ischemia and mild endocardial fibroelastosis. Aggravation of the left ventricular failure could be caused by the recent ischemic insult. The evaluation of the left ventricular function, therefore, should include the evaluation of the morphologic status of the myocardium as regards to whether there is ischemia, endocardial fibroelastosis or hypertrophied trabeculae in addition to stenotic lesions in the aortic and mitral valves.
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PMID:Abnormal morphological patterns of the left ventricular myocardium in the critical stenosis of the aortic valve and the intact ventricular septum. 914 60

A 3-month-old infant presented in extremis with a flail tricuspid valve. The authors theorized that the genesis of her papillary muscle rupture was perinatal ischemia compounded by worsening pulmonary valvular stenosis leading to excessive fiber tension. Her underlying diagnosis of autoimmune-mediated heart block with endocardial fibroelastosis and prenatal glucocorticoid steroid treatment represents potentiating factors.
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PMID:A case of an infant with flail tricuspid valve due to spontaneous papillary muscle rupture: was neonatal lupus the culprit? 1788 76

Patients who have pulmonary atresia with intact ventricular septum have been shown to have a number of various myocardium anomalies like ischemia, fibrosis, infarction, rupture, disarray, spongious myocardium and ventricular endocardial fibroelastosis. Multiple connections have been found between right ventricular myocardial sinusoids and small branches of intramural coronary arteries. Noncompation of ventricular myocardium has been shown to be the result of myocardial ischemia or excessive pressure preventing the reduction of embryonic sinusoids. The persistence of intertrabecular recesses that are connected to both the ventricular cavity and coronary circulation is the result of this process. In this text, we describe a PA-IVS patient who underwent patent ductus arteriosus stenting and pulmonary valve perforation to create antegrade flow and later developed left ventricular noncompaction. We posit that there is a connection between right ventricular coronary sinusoids and noncompaction sinusoids. As our patient's RV outflow tract stenosis and RV pressure increased, the coronary circulation connected to coronary sinuses became sufficient and LV function improved, which further supports our hypothesis.
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PMID:Possible link between right ventricular coronary sinusoids and noncompaction sinusoids in pulmonary atresia with intact ventricular septum patients that later develop left ventricular noncompaction. 2476 37