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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-seven cases of ruptured chordae tendineae have been discovered during surgery for mitral regurgitation (9,3 %) : the highest incidence of ruptured chordae tendineae has been found among pure mitral insufficiency (36 %). In thirteen cases, the rupture was isolated, without any other valvular lesion. The syndrome described as characteristic of rupture was present in one third of our patients : isolated cases do not differ clinically from the others but for a more frequent acute evolution. In pure or predominant mitral regurgitation, surgery seems needed when clinical aggravation, acute or progressive, cannot be explained by arrhythmia, anaemia, pulmonary embolism, hyperthyroidism.
Acta Cardiol 1975
PMID:[Rupture of the mitral chordae tendinae]. 13 12

Clinical studies have long suggested the presence of a specific cardiomyopathy in sickle cell anemia secondary to intracoronary thrombosis and subsequent infarction. Fifty-two autopsy patients were studied (48 with SS hemoglobin, 4 with S-C or S-Thal hemoglobin) to ascertain the range of cardiac pathologic abnormalities associated with this disease. The average age was 17 years (range 1 month to 48 years). Renal failure and infection were the most common causes of death; the former was a more common cause in adults than in children. Right and left ventricular hypertrophy and dilatation were the most common abnormal pathologic findings. No evidence of recent or remote myocardial infarction, coronary thrombosis or arteritis was noted in any patient. Eight patients who were studied with postmortem coronary arteriograms exhibited markedly increased coronary arterial caliber with no evidence of atherosclerosis. Seventeen of the 52 patients studied had clinical evidence of congestive heart failure before death. Of these 17 patients, 7 had moderate to severe left ventricular hypertrophy associated with chronic renal failure and hypertension, 2 had right ventricular hypertrophy with organized pulmonary thrombosis, 2 had rheumatic mitral valve disease and 2 died during the second trimester of pregnancy. Two of the 17 patients thought to have pulmonary edema before death in fact had aspiration pneumonia and hemorrhagic pneumonitis, respectively. The data suggest that cardiac dysfunction in sickle cell anemia can usually be explained by the adverse effect of coexisting disease on the diminished cardiac reserve of chronic anemia. The data do not support the concept of a specific "sickle cell cardiomyopathy".
Am J Cardiol 1978 Aug
PMID:Clinicopathologic analysis of cardiac dysfunction in 52 patients with sickle cell anemia. 15 Jul 86

Circulatory behavior in chronic, severely anaemic patients on volume loading is not precisely known. Twenty young male subjets with hook-worm anaemia, (Hb 2 to 5 gm %), without any complications were transfused with 300 or 600 ml of whole blood at 3 6 or ml/mt. Haemodynamic study was done before and immediately after. Blood volume was low, intracardiac pressures normal or minimally abnormal, cardiac output raised and vascular resistances low. After transfusion, there was a small but significant rise in arterial and mixed venous oxygen content, oxygen transport, heart rate, pulmonary wedge and mean polmonary arterial pressures and fall in % coeffcient of oxygen utilisation. Central venous pressures rose only with bigger transfusion. Change in cardiac output was related to the output before transfusion. Three subjects with cardiac index above 7 1/min had a fall and 6 of 7 below 7 1/min. a rise. Fall is perhaps related to the rise in blood oxygen content. It is argued that it is not an index of cardiac failure, as is often believed. Changes in pulmonary pressures are more sensitive than central venous pressure. One of our subjects died suddenly a day after uneventful study. Existing knowledge of haemodynamic status in severe anaemia and the change on transfusion helps little in explaining such deaths and others due to pulmonary oedema during or shortly after small to large transfusions. Further work in this field aiming to study changes in myocardial function and dynamic pressure volume relation in the vascular system is required.
Acta Cardiol 1977
PMID:Haemodynamic changes with blood transfusion in chronic severe anaemia. 30 Sep 64

The effects of normal respiration on echocardiographic right and left ventricular dimensions were studied in 8 normal subjects (group 1) and in 10 patients with ventricular volume overload due to anaemia (group 2). Right ventricular internal diameter (RVID) increased on inspiration in both groups of patients (group 1, 0.3 +/- 0.1 cm; group 2, 0.6 +/- 0.4 cm), while left ventricular internal diameter (LVID) decreased (group 1, 0.3 +/- 0.2 cm; group 2, 0.4 +/- 0.3 cm). The changes in echocardiographic diameter were related to the duration of electromechanical systole and to the changes in the splitting of the second heart sound; there was a linear relationship between RVID and Q--P2 (P less than 0.001) and A2--P2 (P less than 0.001). Echocardiographic measurements of cardiac chamber size should take into account the changes which occur during respiration.
Eur J Cardiol 1979 Aug
PMID:Effect of respiration on echocardiographic ventricular dimensions and relationship to the second heart sound. 47 5

Echocardiographic aortic root motion in systole was studied in 57 patients: 13 normal subjects, 4 patients with left ventricular (LV) volume overload due to anaemia, 16 patients with mitral incompetence, 13 with aortic incompetence and 11 with mitral stenosis. In normal subjects, patients with mitral stenosis and in patients with LV volume overload, in whom the increased stroke volume was ejected forwards into the ascending aorta (anaemia, aortic incompetence) the amplitude of motion of the posterior aortic wall (vp), the aortic widening fraction (AWF) and total aortic motion (TAM) were increased. In mitral incompetence, however, despite the large increase in total LV stroke index, there was a decrease in vp (P less than 0.01), AWF (P less than 0.001) and TAM (P less than 0.001), and the decrease in aortic motion for a given stroke index was related to the mitral regurgitant fraction, indicating that aortic wall movement in systole depended predominantly on forward ejection of the LV stroke volume. Reduced echocardiographic aortic root motion and widening during systole are useful echocardiographic signs of mitral regurgitation.
Eur J Cardiol 1979 Nov
PMID:Echocardiographic aortic root motion in ventricular volume overload and the effect of mitral incompetence. 51 Mar 47

Twenty-one patients with polymyositis were prospectively examined with echocardiography, phonocardiography and electrocardiography. Cardiac performance, estimated with echocardiography, was enhanced as shown by a significant (P less than 0.01) increase in ejection phase indexes of left ventricular function compared with values in a matched control group. Known causes of the high output state, such as anemia or thyrotoxicosis, were not clinically evident. There was no evidence of left ventricular enlargement, left ventricular wall hypertrophy, or left atrial enlargement in the echocardiogram or chest X-ray film. The echocardiogram showed systolic mitral valve prolapse in 11 of 17 patients (65 percent) with an adequately imaged mitral valve; midsystolic clicks were present in 7 of these. One patient, who did not have prolapse, had echocardiographic evidence of a small pericardial effusion. Electrocardiographic abnormalities were present in 11 of 21 patients (52 percent) and included evidence of atrioventricular conduction disturbances, atrial and ventricular arrhythmias and left atrial abnormality. The pathophysiology of mitral valve prolapse and increased systolic left ventricular function in polymyositis remains uncertain; however, the spectrum of cardiac abnormalities, detected noninvasively in 16 of 21 of our patients (76 percent) may represent a high frequency rate of cardiac involvement in this disease.
Am J Cardiol 1978 Jun
PMID:Cardiac manifestations in polymyositis. 66 23

Computerized axial tomography of the brain is a revolutionary noninvasive technique that has provided remarkable resolution of intracerebral structures. This study was undertaken to determine the potential of computerized tomography for defining the anatomy of 40 arrested and 9 beating (ejecting left heart preparation) canine hearts. Using an EMI cranial unit, scanning was performed in hearts under in vitro conditions with a lactated Ringer's interface. The tomographic scans obtained were later compared with comparable 8 mm thick sections of the heart. At physiologic levels of hematocrit (range 36 to 45%) external structures were well defined, but because of the lack of a differential between cavitary and myocardial densities, it was not possible to distinguish intracardiac structures. With very small amounts of iodinated contrast material (remotely administered in the case of the beating hearts) or with anemia (hematocrit less than 33%), the right and left ventricular cavities became clearly visible in both horizontal and longitudinal tomographic scans. It was possible to distinguish readily the boundaries of the ventricular and atrial cavities, the papillary muscles, the major trabeculae and the aorta. Rhythmic motion of the beating heart, suspended in its pericardium, did not eliminate structural definition. Thus, computerized tomography provides a new approach to the definition of cardiac structure with a relatively high degree of resolution. These observations point to the potential usefulness of this noninvasive technique for the evluation of both cardiac function and ventricular wall abnormalities.
Am J Cardiol 1977 May 04
PMID:Definition of cardiac structures using computerized tomography in isolated arrested and beating canine hearts. 85 96

Hemodilution decreases blood viscosity and circulatory input impedance and thus reduces afterload. Its use in treatment of LV power failure has been advocated, but the safe limits of isovolemic hemodilution are not known. Compensation of the reduced O2-capacity of the blood was therefore studied with normal and impaired coronary reserve. In 20 dogs the LAD was stenosed to a degree just not affecting the supplied region and central and coronary hemodynamics were studied. Regional myocardial function was assessed by ultrasound transit time between transducers implanted in the LV wall. Lowering the hematocrit to 15% by isovolumic exchange of blood for Dextran 60 increased CVP (18%), PAP (47%), LAP (64%), LVedP (46%), CO (67%), and flow to the intact area (LCA: 211%). Flow in the stenosed LAD increased slightly. Enddiastolic length (EDL) of LAD dependent muscle segments rose to 120% and their contraction amplitude deltaL was decreased by 46%. Whereas non-ischemic segments showed compensatory rise in deltaL (38%) at almost constant EDL (+9%). After release of the LAD stenosis EDL and deltaL returned to normal. During progressive anemia myocardial O2-demand is not adequately met if coronary reserve capacity is depleted. Reversion of hypokinesia after removal of the stenosis shows unimpaired myocardial function at a hematocrit as low as 15% provided the coronary circulation is intact.
Basic Res Cardiol
PMID:The effect of hemodilution on regional myocardial function in the presence of coronary stenosis. 90 78

To elucidate the genesis of normal ejection systolic murmurs, we performed phono and Doppler echocardiography in 42 normal subjects. Individuals with hypertension, ST.T changes on ECG, anemia or other cases with definite cardiovascular findings were excluded from the study. Their ages ranged from 22 to 61 years with an average of 48.1 years. They were classified in 2 groups; 9 with Levine 2/6 systolic murmur and 33 without murmur or with 1/6 murmur. Fifteen patients with pure aortic regurgitation or with aortic prosthesis but without significant stenosis, and 7 patients with pulmonic valvular stenosis were served as control. We correlated the intensity and timing of murmur with maximal flow velocity, acceleration time and other parameters. All systolic murmurs were early systolic. Mid-systolic murmur was not noted. Peak of flow velocity increased at the aortic orifice than at the left ventricular outflow tract or pulmonary orifice. Left-sided peak flow velocity occurred earlier than the right-sided peak flow velocity. Early systolic maximal flow velocity of the aorta significantly increased in 9 subjects with murmur than in the remaining 33 without significant murmur. Ejection fraction, hematocrit and body surface area did not differ between the groups with and without significant murmur. Systolic blood pressure and age, however, were higher in subjects with murmur. In aortic valvular disease, systolic murmurs and peak flow signals were early systolic, but in pulmonary stenosis these were mid-systolic in timing. In conclusion, normal ejection systolic murmurs were early systolic and originated at the aortic orifice. Mid-systolic murmurs were unlikely as left-sided murmur in origin. Flow velocity was the most important determinant of the intensity of ejection murmur.
J Cardiol Suppl 1992
PMID:[Doppler and echocardiographic study of normal systolic murmurs]. 141 82

Anaemia is common in children following cardiac transplantation. In a series of 5 children with anaemia beyond the immediate post-operative period one had a hypochromic, microcytic anaemia which corrected with oral iron. The other four had normochromic, normocytic anaemias unresponsive to iron or folate supplementation and associated with inappropriately low levels of erythropoietin. Subcutaneous administration of low dose human recombinant erythropoietin to these four patients resulted in correction of their anaemia. Our findings suggest that erythropoietin deficiency is an important cause of anaemia in transplant recipients and should be sought in cases of anaemia refractory to conventional haematinic therapy. In cases of proven erythropoietin deficiency, treatment with erythropoietin is effective, acceptable to patients and preferable to repeated blood transfusion.
Int J Cardiol 1992 Sep
PMID:Anaemia in children following cardiac transplantation: treatment with low dose human recombinant erythropoietin. 142 59


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