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Query: UMLS:C0232605 (regurgitation)
 8,217 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exercise intolerance, due to cardiovascular disease in horses, may be caused by cardiac arrhythmias, valvular regurgitation, congenital abnormalities, myocardial dysfunction, pericardial disease, and vascular thrombosis. The most common cardiovascular cause of exercise intolerance in horses is atrial fibrillation. Cardiovascular abnormalities such as cardiac arrhythmias or murmurs, however, are common in athletic horses and are not always associated with exercise intolerance. Use of an electrocardiography (during rest and exercise) and echocardiography may be necessary to better determine the significance of the cardiovascular abnormality.
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PMID:Cardiovascular causes of exercise intolerance. 893 57

Forty-three horses with mitral regurgitation (MR) and congestive heart failure were examined, using M-mode, 2-dimensional real-time and Doppler echocardiography. There was no breed or sex predisposition when compared to the general hospital population. The mean +/- s.d. age of affected horses was 7.6 +/- 8.1 years. Horses with MR and congestive heart failure had significant increases in mean values for left ventricular chamber size, left atrial size and heart rate and significant decreases in interventricular septal and left ventricular free wall thickness. Significant increases in pulmonary artery diameter were detected compared to aortic diameter. Mean values for fractional shortening were not significantly different from normal. All horses had a Grade 3-6/6 holosystolic or pansystolic murmur with its point of maximal intensity in the mitral to aortic valve area. Atrial fibrillation was found at presentation in 24 horses with MR and congestive heart failure. One horse presented with atrial tachycardia and subsequently developed atrial fibrillation. Seven horses had ventricular premature contractions. Exercise intolerance (n = 34), respiratory signs (n = 31), and fever (n = 21) were the most common presenting signs. Thickening of the left atrioventricular valve leaflets, endocarditis, flail valve leaflets, rupture of a chorda tendineae, and mitral valve prolapse were detected echocardiographically. Doppler echocardiography confirmed the presence of a large systolic regurgitant jet in the left atrium in all horses in which it was used, and in many horses, concurrent tricuspid and pulmonary regurgitation was detected. All horses died or were subjected to euthanasia due to the severity of their MR and/or lack of response to therapy. Post mortem examinations were performed in 35 horses and confirmed the echocardiographic findings. The echocardiographic detection of a flail mitral valve leaflet was significantly associated with the detection of a ruptured chorda tendineae at post mortem examination. There was a significant association between echocardiographic detection of a dilated pulmonary artery and its presence at post mortem examination. M-mode, 2-dimensional real-time, and Doppler echocardiography should be used to accurately characterise the valvular abnormalities and assess the severity of mitral regurgitation. Pulmonary artery dilatation, an echocardiographic indication of severe pulmonary hypertension, should be considered a grave prognostic indicator and may indicate impending pulmonary artery rupture.
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PMID:Severe mitral regurgitation in horses: clinical, echocardiographic and pathological findings. 945 95

Exercise intolerance in Ebstein's anomaly is usually attributed to desaturation secondary to right-to-left shunting as a result of a small or distorted left ventricle (LV), significant tricuspid valve regurgitation, right ventricular dysfunction, or a combination of these. We observed one boy (age 15 years) and two women (ages 20 and 29 years) with severe Ebstein's anomaly and strikingly abnormal LV myocardium resembling the features described for LV noncompaction. LV size and systolic function were normal in the two women; the boy had a dilated LV with severely diminished ejection fraction. The LV myocardium was found to be unusually coarse and hypertrabeculated, with small intertrabecular recesses and an irregular endocardial surface. The findings in these 3 patients represent the whole spectrum of mild to severe LV noncompaction. Diastolic dysfunction was present in 2 of the 3 patients. Exercise tolerance was diminished in all. There was no mitral or aortic valve disease. The 15-year-old boy underwent heart transplantation 6 months later for biventricular failure. Thus, Ebstein's anomaly does not seem to be a pathology confined to the right ventricle, but may rarely lead to LV noncompacted myocardium. This LV pathology may be an additional explanation for exercise intolerance or signs of left heart failure in patients with Ebstein's anomaly.
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PMID:Noncompacted myocardium in Ebstein's anomaly: initial description in three patients. 1516 43