Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

In 31 patients who had undergone cardiac orthotopic transplantation, valvular regurgitation was studied by echocardiographic and pulsed Doppler over 2 years. The first week after cardiac transplantation, transplant recipients had an increase in the severity of tricuspid, mitral (group II), and aortic regurgitation, as well as a greater number of simultaneously regurgitating valves when compared with those in a group of 60 normal subjects of similar age to heart donors: transplant recipients, trivalvular regurgitation 48% (95% confidence interval [CI] 30 to 66) vs control group, 5% (CI 1 to 13; p < 0.001). Moderate-severe tricuspid regurgitation (TR) was the most frequent occurrence (55%, CI 36 to 73) followed by pulmonary (PR) (42%, CI 25 to 61), moderate mitral (MR) (32%, CI 15 to 51), and mild aortic (AR) (23%, CI 10 to 43) regurgitation. These regurgitations were asymptomatic at rest except for TR. TR was associated with right-sided heart failure in 76% of patients in the early postoperative period and controlled with diuretic drugs. This regurgitation correlated with persistence of post-transplant pulmonary hypertension (r = 0.6) and was not related to pulmonary hypertension before cardiac transplant. There was also no relation found between donor ischemia time or episodes of cardiac rejection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantitative assessment of valvular function after cardiac transplantation by pulsed Doppler echocardiography. 820 38

Mitral valve regurgitation affects heart ventricle volumes, which can be accurately measured by electron beam tomography (EBT). Most studies have focused on the left ventricle, but findings have failed to resolve some crucial clinical issues. We reviewed EBT studies of 35 patients with moderate mitral valve regurgitation but no ischemia, aortic valve regurgitation, or left ventricular failure to investigate the relationship between right ventricle volumes and ejection fraction and extent of mitral regurgitation. EBT in cine mode was performed during exercise and at rest in 839 patients from 1990-1994. Sixty-one of these showed evidence of significant mitral regurgitation, 35 of whom met the criteria for inclusion in this study. Left and right end-diastolic and end-systolic volumes were computed from the scans, and ventricular stroke volumes, ejection fractions, regurgitant stroke volume, and regurgitant fraction were computed from these values. Correlation coefficients between ventricular values and regurgitant fraction were computed. Regurgitant fraction was significantly and negatively associated with the ejection fraction in the right ventricle (r = -0.55, p < 0.001) but not in the left. Ten of the 35 patients studied had right ventricular ejection fractions of less than 45%. In addition, there was evidence for a subgroup of cases with moderate amounts of regurgitation and dilation of the right ventricle. It is concluded that reduced right ventricular ejection fraction is a common finding in patients with mitral regurgitation without left ventricular failure. It is most commonly observed in cases with large regurgitant fraction and/or with a large right ventricular end-diastolic volume/left ventricular end-diastolic volume ratio. Identification of mitral regurgitation patients with reduced right ventricular ejection fraction may have clinical significance, indicating a sub-group of patients with more severe disease prior to the development of left ventricular dysfunction.
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PMID:The right ventricle in mitral regurgitation: evaluation by electron beam tomography. 858 Nov 91

Orthotopic liver transplantation is an established therapy for end-stage liver disease. This study evaluated the range of cardiovascular abnormalities in patients undergoing evaluation for orthotopic liver transplantation and determined the prognostic implications of abnormal echocardiographic features, including ischemia during dobutamine stress echocardiography, in predicting postoperative cardiac events. Two-dimensional echocardiography was performed in 190 patients for assessment of left ventricular function, valvular pathology, and pulmonary hypertension. Dobutamine stress echocardiography was performed in 165 patients for evaluation of inducible ischemia. Contrast echocardiography for detection of intrapulmonary shunting was performed in 125 patients at rest and in 99 during dobutamine stress. Left ventricular dysfunction, significant valvular regurgitation, and inducible ischemia were identified in <1O% of patients. Pulmonary hypertension, left ventricular hypertrophy and > or = moderate intrapulmonary shunting were present in 12%, 16%, and 26% of patients, respectively. Severe intrapulmonary shunting predicted death prior to transplantation (P=0.01). Of the 71 transplanted patients, major perioperative events included global left ventricular dysfunction in four patients and myocardial infarction in one patient with normal coronary arteries. No preoperative echocardiographic parameters, including ischemia on dobutamine echocardiography, predicted these perioperative events. No cardiac events related to obstructive coronary artery disease occurred in the 154 patients without ischemia on dobutamine stress echocardiography. The majority of patients with end-stage liver disease, including those with alcoholic cirrhosis, have normal cardiac function on two-dimensional echocardiography. Severe intrapulmonary shunting portends a poor prognosis in patients awaiting transplantation. A negative dobutamine stress echocardiogram appears useful in excluding patients at risk for perioperative cardiac events related to obstructive coronary artery disease.
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PMID:Two-dimensional and dobutamine stress echocardiography in the preoperative assessment of patients with end-stage liver disease prior to orthotopic liver transplantation. 861 Apr 15

In this report, we evaluated the cardiac findings of 15 children with polyarteritis nodosa. The age range of the patients was 4-14 years; with a mean of 10 years. All have had systemic involvement of the disease. The most common findings in cardiac evaluation were diminished left ventricular systolic functions and mild mitral and/or tricuspid valve regurgitation. One patient had pericardial thickening with no effusion. One had sinus tachycardia. There were no signs of myocardial infarction or ischemia clinically or electro-cardiographically. In conclusion, we did not find cardiac complications, such as pericarditis or myocardial infarction, to be as frequent as in previous reports. However, even in asymptomatic patients, systolic dysfunction or valvular involvement were common findings in patients with polyarteritis nodosa, which were not reported previously. These findings may be due to the histological changes of the myocardium or atrioventricular valves. Although these were not severe and fatal lesions, long-term follow-up of these patients with echocardiography may help to determine the course of cardiac involvement.
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PMID:Cardiac involvement in childhood polyarteritis nodosa. 926 36

Most patients with advanced congestive heart failure have altered thyroid hormone metabolism. A low triiodothyronine level is associated with impaired hemodynamics and is an independent predictor of poor survival. This study sought to evaluate safety and hemodynamic effects of short-term intravenous administration of triiodothyronine in patients with advanced heart failure. An intravenous bolus dose of triiodothyronine, with or without a 6- to 12-hour infusion (cumulative dose 0. 1 5 to 2.7 microg/kg), was administered to 23 patients with advanced heart failure (mean left ventricular ejection fraction 0.22 +/- 0.01). Cardiac rhythm and hemodynamic status were monitored for 12 hours, and basal metabolic rate by indirect calorimetry, echocardiographic parameters of systolic function and valvular regurgitation, thyroid hormone, and catecholamine levels were measured at baseline and at 4 to 6 hours. Triiodothyronine was well tolerated without episodes of ischemia or clinical arrhythmia. There was no significant change in heart rate or metabolic rate and there was minimal increase in core temperature. Cardiac output increased with a reduction in systemic vascular resistance in patients receiving the largest dose, consistent with a peripheral vasodilatory effect. Acute intravenous administration of triiodothyronine is well tolerated in patients with advanced heart failure, establishing the basis for further investigation into the safety and potential hemodynamic benefits of longer infusions, combined infusion with inotropic agents, oral triiodothyronine replacement therapy, and new triiodothyronine analogs.
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PMID:Safety and hemodynamic effects of intravenous triiodothyronine in advanced congestive heart failure. 948 41

Dynamic mitral regurgitation (MR) is typically associated with either severe systolic left ventricular dysfunction or episodes of acute myocardial ischemia. We report three patients with mild combined mitral stenosis and regurgitation and normal global left ventricular systolic function who presented with severe exertional dyspnea. Upright bicycle exercise echocardiography revealed development of severe dynamic MR in all three cases with Doppler evidence of severe pulmonary hypertension. There was no echocardiographic or electrocardiographic evidence of ischemia. Exercise echocardiography is an established tool for assessing dynamic changes in transvalvar pressure gradients. These results suggest that exercise echocardiography may also be useful for evaluating changes in severity of MR and for the assessment of dynamic changes in pulmonary artery systolic pressures.
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PMID:Exercise echocardiography in combined mild mitral valve stenosis and regurgitation. 1014 21

A gene therapy strategy involving direct myocardial administration of an adenovirus (Ad) vector encoding the vascular endothelial growth factor 121 cDNA (Ad(GV)VEGF121.10) has been shown to be capable of "biological revascularization" of ischemic myocardium in an established porcine model [Mack, C.A. (1998). J. Thorac. Cardiovasc. Surg. 115, 168-177]. The present study evaluates the local and systemic safety of this therapy in this porcine ischemia model and in normal mice. Myocardial ischemia was induced in Yorkshire swine with an ameroid constrictor 21 days prior to vector administration. Ad(GV)VEGF121.10 (10(9) or 10(10) PFU), Ad5 wild type (10(9) PFU), AdNull (control vector with no transgene; 10(9) PFU), saline, or no injection (naive) was administered in 10 sites in the ischemic, circumflex distribution of the myocardium. Toxicity was assessed by survival, serial echocardiography, blood analyses, and myocardial and liver histology at 3 and 28 days after vector administration. All pigs survived to sacrifice, except for one animal in the Ad(GV)VEGF121.10 (10(10) PFU) group, which died as a result of oversedation. Echocardiograms of Ad(GV)VEGF121.10-treated pigs demonstrated no differences in pericardial effusion, mitral valve regurgitation, or regional wall motion compared with control pigs. Intramyocardial administration of Ad(GV)VEGF121.10 included only minimal myocardial inflammation and necrosis, and no hepatic inflammation or necrosis. Only a mild elevation of the white blood cell count was encountered on day 3, which was transient and self-limited in the Ad(GV)VEGF121.10 group as compared with the saline-treated animals. As a measure of inadvertent intravascular administration of vector, normal C57/BL6 mice received intravenous Ad(GV)VEGF121.10 (10(4), 10(6), 5 x 10(7), or 10(9) PFU), AdNull (5 x 10(7) or 10(9) PFU), or saline. Toxicity was assessed by survival, blood analyses, and organ histology at 3 and 7 days after vector administration. A separate group of C57/BL6 mice received intravenous AdmVEGF164 (Ad vector encoding the murine VEGF164 cDNA), Ad(GV)VEGF121.10, AdNull (10(8) PFU each group), or saline to assess duration of expression and safety of a homologous transgene. All mice survived to sacrifice except for 40% of the mice in the highest (10(9) PFU; a dose more than 10(3)-fold higher by body weight than the efficacious dose in pigs) Ad(GV)VEGF121.10 dose group, which died on days 5-6 after vector administration. The only differences seen in the blood analyses between treated and control mice were in the very high Ad(GV)VEGF121.10 dose group (10(9) PFU), which demonstrated an anemia as well as an increase in alkaline phosphatase when compared with all other treatment groups. Hepatic VEGF levels by ELISA in AdmVEGF164-treated mice did not persist beyond 14 days after vector administration, suggesting that persistent expression of a homologous VEGF gene transferred with an Ad vector is not a significant safety risk. Although this is not a chronic toxicity study, these data demonstrate the safety of direct myocardial administration of Ad(GV)VEGF121.10, and support the potential use of this strategy to treat human myocardial ischemia.
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PMID:Safety of direct myocardial administration of an adenovirus vector encoding vascular endothelial growth factor 121. 1036 64

Mitral regurgitation is a common valvular abnormality that can result in substantial morbidity. Primary care physicians should maintain a high index of suspicion for this disorder, especially in patients with symptoms of heart failure. The paramount concern is early identification of patients with mitral regurgitation and prompt referral to a cardiologist when symptoms occur or if evidence of ventricular enlargement or reduction in ejection fraction is found. Echocardiography is an invaluable tool in determining the severity of regurgitation, the integrity of the mitral valve apparatus, the extent of left ventricular enlargement, and the ejection fraction. Although no standard medical treatment has been established for mitral regurgitation, use of ACE inhibitors is appropriate. Patients presenting with severe, acute mitral regurgitation from papillary muscle rupture should be evaluated for ischemia and treated expediently. The preferred operative procedure in patients with severe mitral regurgitation and left ventricular dysfunction is mitral valve repair, if possible, or mitral valve replacement with posterior chordal preservation, if feasible.
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PMID:Native mitral valve regurgitation. Proactive management can improve outlook. 1178 16

Celiac axis compression syndrome has generated much controversy since its original description in 1963. The main symptoms are postprandial epigastric abdominal pain, regurgitation of undigested food, and weight loss, all of which are caused by gastric ischemia from impingement of the celiac axis by the median arcuate ligament of the diaphragm. These symptoms are seen in other common disorders such as chronic mesenteric ischemia and gastroparesis. This makes the diagnosis of celiac axis compression syndrome a true challenge for the clinician. We present data on three patients successfully treated. The pre- and postoperative studies clearly demonstrate a resolution of the condition. The duplex ultrasound images clearly show variable compression on the celiac axis. The angiogram presented shows a classic image of the disease. A review of the data has enabled us to develop an algorithm for the diagnosis of this disease.
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PMID:Reversible gastroparesis: functional documentation of celiac axis compression syndrome and postoperative improvement. 1667 60

Cholestatic disorders may arise from liver ischemia (e.g., in liver transplantation) through various mechanisms. We have examined the potential of hypoxia to induce changes in the expression of hepatobiliary transporter genes. In a model of arterial liver ischemia subsequent to complete arterial deprivation of the rat liver, the mRNA levels of VEGF, a hypoxia-inducible gene, were increased fivefold after 24 h. The pattern of VEGF-induced expression and ultrastructural changes, including swelling of the endoplasmic reticulum, indicated that hypoxia affected primarily cholangiocytes, but also hepatocytes, predominantly in the periportal area. Serum and bile analyses demonstrated liver dysfunction of cholestatic type with reduced bile acid biliary excretion. Fluorescence-labeled ursodeoxycholic acid used as a tracer displayed no regurgitation, eliminating bile leakage as a significant mechanism of cholestasis in this model. In liver tissue, a marked reduction in the mRNA levels of Na(+)-taurocholate-cotransporting polypeptide (Ntcp), bile salt export protein (Bsep), and multidrug resistance-associated protein 2 (Mrp2) and an increase in those of Cftr were detected before bile duct proliferation occurred. In cultured hepatocytes, a nontoxic hypoxic treatment caused a decrease in the mRNA and protein expression of Ntcp, Bsep, and Mrp2 and in the mRNA levels of nuclear factors involved in the transactivation of these genes, i.e., HNF4alpha, RXRalpha, and FXR. In bile duct preparations, hypoxic treatment elicited an increase in Cftr transcripts, along with a rise in cAMP, a major regulator of Cftr expression and function. In conclusion, hypoxia triggers a downregulation of hepatocellular transporters, which may contribute to cholestasis, whereas Cftr, which drives secretion in cholangiocytes, is upregulated.
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PMID:Hypoxia-induced changes in the expression of rat hepatobiliary transporter genes. 1761 79


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