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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ischemic cardiopathy in its various clinical manifestations, whether acute (angina pectoris or myocardial infarction) or chronic (chronic coronary insufficiency), has shown in recent years particular hemorheological characteristics of its own. The observation of patients with such diseases has allowed us to record the existence of modifications in the parameters indicative of rheological damage. Numerous studies have been made, many of which are still in progress, with the aim of clarifying the relationships between these data and the disease. In our experience an increase in blood and plasma viscosity and a decrease in red cell deformability are often present in a manner which is statistically significant, if these patients are compared with normal subjects. Hemorheological change is more evident in the acute forms of myocardial ischemia. In fact, in angina pectoris the occurrence of pain is always accompanied by an increase in blood viscosity and by a worsening of red cell deformability both during spontaneous crises and during provocative tests. The hemorheological damage tends to diminish fairly rapidly when the crisis is over, even if the level of stabilization proves to be still higher than normal. In myocardial infarction higher levels of viscosity appear for a brief period after the onset with a slight tendency to diminish up until the 30th day. With the aim of ascertaining whether the alteration is more evident precisely at the point where the ischemia occurs, we chose a necessarily limited number of subjects, undergoing coronarography and atrial pacing for diagnostic purposes, and decided to control the hemorheological data not only in the systemic venous blood but also in the blood taken from the coronary sinus. Our data has shown that the level of viscosity and of red cell filtrability, in the blood taken from the coronary sinus, is worse than those of the systemic venous blood and that, after atrial pacing, in negative pacing subjects the variations are of slight significance whilst in positive pacing subjects we observe a rapid increase in viscosity and a decrease in red cell filtrability. This seems to confirm what we have already observed in the limbs affected by peripheral ischemia, and to demonstrate the existence of a local hyperviscosity syndrome which, even in the myocardium, appears to be dependent on the tissue ischemia.
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PMID:[Hemorrheological changes in ischemic heart disease]. 667 96

The radiographic findings of a series of infants of diabetic mothers and a review of the literature are presented to illustrate the wide spectrum of abnormalities that may be seen with this condition. Congenital anomalies of the spine and skeletal, genitourinary, and cardiovascular systems and visceral situs inversus are significantly more frequent among infants of diabetic mothers than normal. The most specific anomaly is sacral agenesis. Renal vein thrombosis and adrenal hemorrhage are also more common and may be diagnosed by sonography. Over one-half of the cases of the small left colon are associated with maternal diabetes and may be diagnosed and treated with a contrast enema. The incidence of the respiratory distress syndrome is higher in infants of diabetic mothers than other premature infants, and the disease may occur in the presence of reliable indicators of lung maturity. Other common causes of dyspnea include cardiomyopathy, congenital heart disease, wet lung syndrome, hyperviscosity syndrome, and persistence of fetal circulation. Echocardiography is the most valuable adjunct in differentiating cardiac from pulmonary problems.
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PMID:Infants of diabetic mothers: radiographic manifestations. 678 62

For this article, the literature on the pathophysiology, clinical features, natural history, prognosis, and management of the Eisenmenger syndrome in adults was reviewed. English-language articles from 1966 to the present were identified through a search of the MEDLINE database by using the terms Eisenmenger, congenital heart disease, and pulmonary hypertension. Selected cross-referenced articles were also included. Articles on the pathophysiology, clinical presentation, evaluation, natural history, complications, and treatment of the Eisenmenger syndrome in adults were selected, and descriptive and analytical data relevant to the practicing physician were manually extracted. The Eisenmenger syndrome is characterized by elevated pulmonary vascular resistance and right-to-left shunting of blood through a systemic-to-pulmonary circulation connection. Most patients with the syndrome survive for 20 to 30 years. The hemostatic changes associated with the syndrome may lead to thromboembolic events, cerebrovascular complications, or the hyperviscosity syndrome. Erythrocytosis is present in most patients, but excessive phlebotomy may cause microcytosis and exacerbate the symptoms of hyperviscosity. Other complications associated with the Eisenmenger syndrome include hemoptysis, gout, cholelithiasis, hypertrophic osteoarthropathy, and decreased renal function. Pregnancy or noncardiac surgery is associated with a high mortality rate in patients with the Eisenmenger syndrome. Because most pediatric patients with the Eisenmenger syndrome survive to adulthood, primary care physicians should have a thorough understanding of the syndrome; its associated complications; and medical and surgical management, especially with regard to the appropriate timing of phlebotomy and lung or heart-lung transplantation. In addition, patients with the syndrome should undergo routine follow-up at a tertiary care center that has physicians and nurses with special expertise in congenital heart disease. In patients with the Eisenmenger syndrome who are pregnant or require noncardiac surgery, a multidisciplinary approach should be used to reduce the excessive mortality associated with these conditions.
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PMID:The Eisenmenger syndrome in adults. 955 69

Complications of chronic hypoxia, including erythrocytosis, hyperviscosity, abnormalities of hemostasis, cerebral abscesses, stroke, and endocarditis, are among the most common consequences of cyanotic heart disease in adults. The compensatory erythrocytosis of cyanotic heart disease can become pathologic by causing an increase in blood viscosity, thereby decreasing perfusion and resulting in decreased total oxygen delivery and increased risk of venoocclusive/hyperviscosity syndrome. Treatment of hyperviscosity secondary to erythrocytosis in cyanotic heart disease is controversial. Data is limited but suggest that phlebotomy has the potential to increase exercise capacity, reduce the symptoms of hyperviscosity, and reduce the potential risk of vasoocclusive disease in selected patients with polycythemia secondary to cyanotic heart disease. Unfortunately, repeated phlebotomy can quickly lead to iron deficiency, resulting in microcytic erythrocytes that induce higher viscosity than normocytic erythrocytes, which may increase the risk for venoocclusive events. There are limited data on the use of hydroxyurea to suppress erythrocytosis in this patient population. The authors conclude that until newer approaches to decreasing hematocrit without inducing iron deficiency are shown to be safe and efficacious, phlebotomy should only be used for the acute resolution of hyperviscosity symptoms. In addition, the use of hydroxyurea should be limited to patients with recurrent symptoms.
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PMID:Blood is thicker than water: the management of hyperviscosity in adults with cyanotic heart disease. 1717 81