Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the case of a six-day-old male infant exposed in utero to a prostaglandin synthetase inhibitor, who presented pulmonary arterial hypertension, tricuspid insufficiency, and electrocardiographic signs of diffuse myocardial ischemia. The necropsy showed organizing infarction of the anterior and posterior right papillary muscles (probably occurred in utero) with complete rupture of the former, besides abnormal muscularization of the intraacinar pulmonary arterioles (persistent fetal circulation of the newborn). The authors suggest a possible relation between the myocardial ischemic and pulmonary hypertensive lesions since the prostaglandin synthetase inhibitor can induce precocious pulmonary arteriolar muscularization and constriction of the arterial duct, leading to right ventricular overload, thus facilitating the occurrence of papillary and subendocardial ischemia.
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PMID:Post-ischemic rupture of the anterior papillary muscle of the right ventricle associated with persistent pulmonary hypertension of the newborn: a case report. 162 31

To determine the sequelae of transient myocardial ischemia (TMI) in term infants, we reviewed clinical and investigative data in 59 infants (37 male, 22 female) with structurally normal hearts admitted over the 2-year period of 1983-1985. Twenty-three were diagnosed prior to admission as cases of birth asphyxia (5-min Apgar score less than 6), and 36 had signs of persistent fetal circulation with electrocardiographic (ECG) changes of ischemia greater than 24 h after birth. Murmurs of atrioventricular valve regurgitation (AVVR), detected in 28 patients, were confirmed in 23 of the 24 patients investigated. The murmurs resolved over a 2-day to 6-month period (median 6 days). In three patients, AVVR, left ventricular dyskinesia, and ECG anomalies persisted for 2 months (until death), 4 months, and 48 months. Initial ECGs were abnormal in 57 patients, and (of those reviewed) 60% returned to normal over a 6-day to 7-month period (median 2 months). Residual ECG anomalies included second-degree AV block and persistent ST-T wave changes. Ten patients died from noncardiac causes. Neither the presence nor resolution of AVVR correlated significantly with the severity of birth asphyxia using the Apgar score, nor with the severity of the ischemic changes on the ECG. Although the cardiovascular sequelae of myocardial ischemia are usually transient, the data should prompt the need for careful review after the initial admission.
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PMID:Persistence of atrioventricular valve regurgitation and electrocardiographic abnormalities following transient myocardial ischemia of the newborn. 259 71

Clinicopathological features were examined in 65 neonates and 8 stillborn infants with pontosubicular necrosis (PSN) compared to 57 neonates and 19 stillborn infants without PSN. Twelve out of 65 neonates with PSN had congenital heart disease and 3 out of 65 neonates showed persistent fetal circulation. On neuropathological examination, the frequency of neonates with PSN who also showed karyorrhetic/eosinophilic neurons in other regions of the brain stem, basal ganglia and thalamus was higher than in controls. The results of this study suggest that acute ischemia is an important underlying pathogenetic factor and PSN occurs in the prenatal as well as postnatal period.
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PMID:Clinicopathological study of pontosubicular necrosis. 823 77

Persistent fetal circulation (PFC), also known as persistent pulmonary hypertension of the newborn, is defined as postnatal persistence of right-to-left ductal or atrial shunting, or both in the presence of elevated right ventricular pressure. It is a relatively rare condition that is usually seen in newborns with respiratory distress syndrome, overwhelming sepsis, meconium and other aspiration syndromes, intrauterine hypoxia and ischemia, and/or neonatal hypoxia and ischemia. This condition causes severe hypoxemia, and, as a result, has significant morbidity and mortality. Improved antenatal and neonatal care; the use of surfactant; continuous monitoring of oxygenation, blood pressure and other vital functions; and early recognition and intervention have made this condition even more rare. In modern neonatal intensive care units, anticipation and early treatment of PFC and its complications in sick newborns are commonplace. Thus, severe forms of PFC are only seen on isolated occasions. Consequently, it is even more imperative to revisit PFC compared with the time when there were occasional cases of PFC seen in neonatal intensive care units, and to discuss evolving treatment and management issues that pertain to this syndrome.
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PMID:Persistent fetal circulation. 2008 50

Persistent pulmonary hypertension of the newborn may occur with perinatal asphyxia, either because of direct effects of hypoxia/ischemia on pulmonary arterial function or indirectly because both are associated with meconium aspiration syndrome or perinatal sepsis/pneumonia. Therapies for persistent pulmonary hypertension of the newborn have the potential to affect cerebral function and cerebral perfusion in infants with hypoxic ischemic encephalopathy. Our literature review concludes that hyperventilation should be avoided, bicarbonate therapy is unproven, and hypoxia and hyperoxia should both be avoided. Nitric oxide improves pulmonary artery pressure and systemic perfusion. The effects of inotropic agents on cerebral perfusion or outcomes are uncertain.
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PMID:Pulmonary hypertension and the asphyxiated newborn. 2123 1