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)

The electrophysiological criteria for diagnosing right ventricular hypertrophy, characteristic of chronic cor pulmonale, are described. Right ventricular hypertrophy due to a sustained systolic overload can be global or regional. In the first situation, as for example, an idiopathic pulmonary hypertension, the magnitude and manifestation of all the main vectors resulting from the depolarization of this ventricle are increased: Ils (septal), llr (parietal), and Illr (basal). When the right ventricular hypertrophy is of the segmental (regional) type, as for example, that due to a chronic bronchial obstruction, the magnitude and manifestation of only some right vectors are increased. In this condition, only the magnitude of the right basal vector (Illr) is augmented. In the presence of subepicardial or transmural ischemia of the right ventricle, negative T waves of primary type are recorded in right precordial and transitional leads, where the Q-Tc interval is prolonged in the absence of digitalis effect. Two demonstrative examples of the correlations existing between the electrocardiographic and anatomical findings in global and regional hypertrophies, respectively, of the right ventricle are presented.
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PMID:[Electrocardiographic features of right ventricular hypertrophy in chronic cor pulmonale]. 1674 5

Erythropoietin (EPO), already known as the stimulating hormone for erythropoiesis, has shown different and interesting pleiotropic actions. It does not only affect erythroid cells, but also myeloid cells, lymphocytes and megakaryocytes. This hormone can also enhance phagocytic function of the polymorphonuclear cells and reduce the activation of macrophages, thus modulating the inflammatory process.Moreover, hematopoietic and endothelial cells probably have the same cellular origin, and the discovery of erythropoietin receptors (EPO-R) also on mesangial and myocardial cells, smooth muscle fibrocells and neurons has prompted the study of the non-erythropoietic functions of this hormone.The interaction between EPO and VEGF may be of particular importance in neovascularization and wound healing. Different studies have demonstrated that EPO has an important direct hemodynamic and vasoactive action, which does not depend exclusively on any increase in hematocrit and viscosity. Moreover EPO showed protective effects on myocardial cells against apoptosis induced by ischemia/repefusion injury, but it could negatively affect pulmonary hypertension in patient with chronic cor pulmonale.This review aims to stress the importance of the increasing interest in EPO applications and the necessity of further studies to gain a deeper knowledge of this hormone and its pleiotropic and complex actions.
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PMID:From the oxygen to the organ protection: erythropoietin as protagonist in internal medicine. 1707 7

The purpose of the study was to assess the influence of structural and functional changes in the myocardium of the right and left ventricle (RVand LV) on the development of ischemia and arrhythmia in chronic obstructive pulmonary disease (COPD) and bronchial asthma (BA). The subjects of the study were 156 patients with either persistent BA (81 patients) or COPD (75 patients). Patients with decompensated cor pulmonale were excluded. ECG, 24-hour ECG monitoring, and echocardioscopy were performed. The study found that the occurrence of supraventricular and ventricular extrasystoles (SVES and VES) in patients with mild COPD or BA depended on the condition of RV diastolic function and on LV diastolic function and myocardial ischemia as well in COPD. In moderate BA the processes of myocardial remodeling correlate with myocardial ischemia, RV dysfunction and increased pulmonary arterial pressure (PAP), as well as with lipid dismetabolism. The appearance of SVES in patients with severe BA is connected with interventricular septal hypertrophy, LV dysfunction, and increased PAP, while VEC appear due to myocardial ischemia and hypercholesterolemia. In severe COPD the occurrence of SVES and VES does not depend on structural and functional changes in the myocardium, while myocardial ischemia is connected with LV hypertrophy. In BA ischemia depends on the development of RV and LV diastolic dysfunction, as well as hypercholesterolemia.
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PMID:[The myocardial condition in chronic obstructive pulmonary disease and bronchial asthma]. 1752 Aug 83

In 1991, Frostell and colleagues reported that breathing low concentrations of nitric oxide (NO) decreased pulmonary artery pressure (PAP) in awake lambs with experimental pulmonary hypertension (PH) [Frostell C, Fratacci MD, Wain JC, Jones R, Zapol WM. Inhaled nitric oxide. A selective pulmonary vasodilator reversing hypoxic pulmonary vasoconstriction. Circulation 1991;83:2038-47]. Subsequently, efforts of multiple research groups studying animals and patients led to approval of inhaled NO by the US Food and Drug Administration in 1999 and the European Medicine Evaluation Agency and European Commission in 2001. Inhaled NO is currently indicated for the treatment of term and near-term neonates with hypoxemia and PH. Since regulatory approval, several studies have suggested that NO inhalation can prevent chronic lung disease in premature infants. In addition, unanticipated systemic effects of inhaled NO may lead to treatments for a variety of disorders including ischemia-reperfusion injury. This review summarizes the pharmacology and physiological effects of breathing NO. The application of inhaled NO to hypoxemic neonates with PH is discussed including recent studies exploring the use of inhaled NO to prevent bronchopulmonary dysplasia in premature infants. This review also highlights the application of inhaled NO to treat adults with cardiopulmonary disease, strategies to augment the efficacy of inhaled NO, and potential applications of the systemic effects of the gas.
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PMID:Inhaled NO as a therapeutic agent. 1754 87

Sarcoidosis is a multisystem disease of uncertain etiology characterized by multifocal areas of discrete and confluent granulomatous inflammation that may rarely be responsible for sudden and unexpected death. Two cases are reported to demonstrate disparate pathological features in fatal cases, one involving cardiac sarcoidosis, and the other neurosarcoidosis with hypothalamic infiltration. Sarcoidosis in individuals dying suddenly may be completely unrelated to the death, contributory or causal. Cardiovascular causes of sudden death in sarcoidosis include arrhythmias associated with cardiomyopathy and ischemia, ventricular rupture, and cor pulmonale due to pulmonary hypertension; respiratory causes include hemorrhage and upper airway obstruction; central nervous system causes include arrhythmias from infiltration of autonomic centers, epilepsy, and obstructive hydrocephalus from brainstem involvement; and gastrointestinal deaths may be due to hemorrhage from esophageal varices associated with portal hypertension. The diagnosis relies on the demonstration of typical noncaseating granulomas and the exclusion of other infective and environmental diseases with similar histopathological findings.
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PMID:Sarcoidosis and mechanisms of unexpected death. 1836 80

Central alveolar hypoventilation (CAH) syndrome is a clinical condition that is characterized by the loss of automatic breathing, particularly during sleep. Most forms in adults are caused by brainstem ischemia, mass, infection, demyelinating disease, or anoxic-ischemic damage. We present a case of a fatal symptomatic acquired CAH syndrome caused by megadolichobasilar artery. A 62-year-old man with pre-existing vascular dementia suffered an acute posterior stroke. During stroke care, long episodes of hypopnea and apnea were observed which responded well to verbal reminders. During an unobserved episode, the patient was found unresponsive, with chemical signs of prolonged hypoventilation not explainable by cardiopulmonary disease. A diaphragmatic pacemaker, assisted ventilation, and repeated resuscitation were refused by the patient, who died some days later. CAH is a rare complication that can occur in patients with megadolichobasilar artery.
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PMID:Central alveolar hypoventilation (Ondine's curse) caused by megadolichobasilar artery. 2346 43


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