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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

208 hospitalized patients, nearly 80 years old, were investigated because of risk factors and complicating diseases. Hypertension (58.2%), typical myocardial infarctions (37.2%) and diabetes (45.2%) were twice often as in our comparable cases without stroke. Corresponding we found signs of left ventricular hypertrophy in more than 50% post mortem. The dimensions of heart failure by hypertension are visible in ECG indicating LVH with many dysrhythmias. Early mortality (40%) as survival time are dependent on the size of the stroke. Cardiovascular causes of death were found mainly. The differences to younger patients with brain infarction seem to be only of gradually nature and especially to refer to the more intensive damaged heart.
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PMID:[Survived brain infarction in old age - clinical and morphological findings. II. Risk factors (author's transl)]. 3 Mar 24

The heart of the old hemiplegic patient is examined as follows: 1. The preapoplectic situation of the heart which often induces in a conclusive manner the beginning of a stroke, 2. the occurrence of heart troubles with the stroke itself and 3. the influence of rehabilitation measures and the heart function. Preexistent heart troubles are very frequent (in ca. 80%). Thereby the hypertension with a left ventricular hypertrophy and later with heart failure play an important role. The stroke itself especially in subarachnoidal bleedings can cause severe electrocardiographic anomalies. The telemetric controlled heart shows specially while rehabilitation more extrasystoles and alterations of repolarisation but usually do not impair the rehabilitation. With a systematic rehabilitation (training) the heart is most favourably influenced.
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PMID:[The heart of the old hemiplegic patient (author's transl)]. 3 57

A model for high output heart failure (HCO) was developed in male, Sprague-Dawley rats using an abdominal aortocaval shunt equal to 50% of total cardiac output (CO) with 2 mo of postsurgical recovery. The model was evaluated by analysis of hemodynamics, peripheral blood flows (BF) (radioactive microspheres), and plasma catecholamine levels as well as mass and fluid content of organs. In HCO, CO and left ventricular end-diastolic pressure were increased with significant left and right ventricular hypertrophy. Mean blood pressure (BP) was unchanged, but pulse BP was increased in HCO. BF to skeletal muscle, cutaneous, and some splanchnic regions was reduced to HCO, whereas BF to the cerebral, coronary, and renal beds was protected. Plasma epinephrine and norepinephrine levels were significantly elevated in HCO suggesting enhanced sympathetic as well as adrenal catecholamine release. Tissue analysis indicated altered circulatory status secondary to HCO in liver, kidney, spleen, and lung. The results indicate that this model will be a relevant tool for studies of the circulatory effects of heart failure.
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PMID:Chronic arteriovenous shunt: evaluation of a model for heart failure in rat. 3 84

Cases of acute cardiac failure which are apparently primary, and occurring in babies or young children have one characteristics clinical picture. There are three etiological agents, which cannot be differentiated clinically: myocarditis, fibroelastosis, and primary non-obstructive cardiomyopathies. When the critical early period, which still carries a high mortality, has been passed, the outlook is relatively favourable. 61 babies or infants of less than 30 months with acute primary cardiac failure were followed up for a period of between 5 and 20 years. 33 of them were considered cured; 22 have minor sequelae (most frequently) left ventricular hypertrophy on X-ray or ECG); 3 have persistent cardiac failure despite treatment; 3 have died after a period of more than 5 years. There is no clinical, X-ray or ECG finding which can predict the longterm outlook in this condition. It is virtually impossible to differentiate between myocarditis and firboelastosis; it seems likely in the majority of cases that we are dealing with different modes of development in the same condition.
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PMID:[Apparently primary acute heart failure in infants. Long-term outcome]. 9 60

The case of a girl who presented with gastrointestinal upsets with nausea, vomiting and occasional hypoglycaemic attacks during childhood is reported. At about 5 years of age generalised muscular weakness with severe amyotrophy, cardiomegaly with a cardiothoracic ratio of 0,63, left ventricular hypertrophy on electrocardiography and left ventricular dilatation with hypokinesis on echocardiography were observed. A few weeks later she developed severe cardiac failure. Muscle biopsy showed muscular dystrophy with lipid infiltration due to carnitine deficiency )serum carnitine 9 nmoles/ml, normal values: 46 +/- 6,9 nmoles/ml; muscle carnitine 0,27 nmoles/mg, normal values: 3,0 +/- 0,79 nmoles/mg fresh frozen weight). She improved rapidly with carnitine chlorhydrate and a diet low in lipids and high in medium chain triglycerides. Regression of muscular symptoms and cardiac failure was observed. After 13 months follow-up with no tonicardiac therapy she is much improved; the signs of heart failure have disappeared, the cardiothoracic ratio is now 0,55 and the electrocardiogramme and echocardiogramme are normal.
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PMID:[Lipidic myopathy with severe cardiomyopathy caused by a generalized carnitine deficiency. Favourable course during carnitine hydrochloride treatment]. 11 7

Nine cases of the combination of coarctation of the aorta and mitral stenosis were evaluated over a seven-year period. Symptoms did not usually cause distress in infancy, but began subtly with pneumonia or cardiac failure at about 2 years of age. Important clues were differences in blood pressure between the arms and legs, paroxysmal dyspnea, congestive heart failure, right ventricular hypertrophy, and left atrial enlargement. Cardiac catheterization studies showed elevated right ventricular and main pulmonary artery wedge pressures. These features in patients with coarctation of the aorta should suggest associated mitral valve disease. The importance of demonstrating associated valvular lesions, particularly mitral stenosis, is emphasized. Two of our children had successful repair of the coarctation of the aorta and mitral stenosis simultaneously. In a third child, resection of the coarctation was followed in six years by mitral valve replacement.
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PMID:Associated coarctation of the aorta and mitral valve disease: nine cases with surgical correction of both lesions in three. 12 22

A detailed review was made of 180 patients with severe aortic regurgitation of rheumatic origin. Of these patients, 110 underwent aortic valve replacement. Thirty-nine clinical and haemodynamic factors were studied in an attempt to define those associated with (1) death before surgery, (2) a higher incidence of complications and hospital mortality after surgery, and (3) an unsatisfactory longer-term result of surgery. Only heart failure, radiographic heart size, left ventricular hypertrophy, and ventricular premature beats were associated with death before surgery. No factor predisposed to surgical complications and only preoperative factors associated with an unfavourable result after surgery were advanced heart failure, cardiomyopathy, extreme cardiomegaly, and ventricular premature beats. It is concluded that the indications for operation are: a cardiothoracic ratio of greater than 0-60, or a history of heart failure combined with electrocardiographic evidence of extreme left ventricular hypertrophy. Operation may be safely postponed if these indications are not met, though the presence of ventricular extrasystoles or evidence of independent myocardial disease are further factors which should influence the decision.
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PMID:The natural history of rheumatic aortic regurgitation and the indications for surgery. 13 Sep 16

Cardiac hypertrophy in weaning beagle dogs was obtained by a loose aortic banding with a 10-mm Dacron-Teflon band, positioned 1 cm distal from the aortic valve 9 months later all animals developed left ventricular hypertrophy without signs of heart failure. Sarcoplasmic reticulum proteins as well as their calcium-exchanging properties were measured in hypertrophic heart and in those from sham-operated control animals. The calcium exchangeable fraction for hypertrophic heart was found to the higher than for controls, while sarcoplasmic reticulum proteins obtained from hypertrophic hearts were lower than those obtained from control animals. It is probable that the increase in the calcium exchangeable fraction could represent a mechanism of compensation in an early stage of the development of the hypertrophic heart whose sarcoplasmic reticulum fraction is not adequately developed.
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PMID:Calcium exchangeable fraction of sarcoplasmic reticulum in hypertrophic dog heart. 13 82

The magnitude of ventricular hypertrophy in response to afterloading is determined by wall stress, with wall thickness increasing in proportion to ventricular load until systolic wall stress is normalized. With use of echocardiographic measurements of left ventricular end-systolic wall thickness (Ws) and cavity transverse dimension (Ds), the pressure constant k was calculated in 16 patients without left heart obstruction according to the formula k = P-Ds/Ws. The mean value for k was 225 +/- 6.7 (standard deviation) mm Hg. From this value, left ventricular pressure was estimated in 13 patients with aortic stenosis aged 4 to 17 years using the formula P = k-Ws/Ds. No subject had evidence of cardiac failure. Peak systolic aortic pressure difference (delta P) was calculated by subtracting cuff-measured brachial arterial peak systolic pressure from the estimated left ventricular pressure. Excellent correlation was obtained between the estimated delta P and that found at cardiac catheterization (r = 0.89). In two patients, echocardiographic data predicted significant obstruction in the presence of normal electrocardiographic, vectorcardiographic and vector lead tracings. Echocardiography offers a noninvasive method for estimating the severity of aortic stenosis, in the absence of myocardial failure; it appears to be more sensitive than other currently employed techniques.
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PMID:Echocardiographic assessment of the severity of aortic stenosis in children and adolescents. 13 84

This study examined the recuperative potential of cat hearts subjected to experimental right ventricular pressure overload (for a 10- to 14-day period) which provoked hypertrophy with and without congestive heart failure. Five groups of cats were studied: normal controls; one group with 70% pulmonary artery constriction which produced right ventricular hypertrophy (RVH); one group with an 87% constriction which also produced right ventricular hypertrophy but with congestive heart failure (CHF); and two groups which had been similarly subjected to pressure overload but which had been allowed a recovery period of 30 days after relief of the pressure overload. Both the 70% and 87% pulmonic constrictions were associated with extensive right ventricular hypertrophy, depression of myocardial contractile function, and severe redlction of cardiac norepinephrine stores (normal, 1.42 mug/g: RVH, 0.11 mug/g; CHF, 0.01 mug/g). After a 30-day period of relief from the pulmonic constriction normal hemodynamic function returned. In cats in which RVH had been relieved, right ventricular weight and contractile function were normal but catecholamine depletion persisted. Cats with relieved CHF showed depressed contractile function and depleted myocardial norepinephrine, and the right ventricular weight did not return to normal. Cardiac muscle of all pressure-overloaded nonrelieved hearts showed depressed velocity of shortening and depressed ability to sustain load. Cats with RVH alone regained normal muscle shortening velocity and load-bearing ability after relief. However, cardiac muscle from the CHF-relieved group recovered only unloaded shortening velocity while the ability to sustain load remained depressed. We conclude that the recuperative potential of myocardium damaged by pressure overload is adequate provided congestive heart failure has not occurred. Heart failure produces a persistent reduction in force-generating ability of the myocardium. Hypertrophy due to pressure overload, with or without CHF, leads to cardiac catecholamine depletion which is not readily reversed by relief of the overload.
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PMID:Recuperative potential of cardiac muscle following relief of pressure overload hypertrophy and right ventricular failure in the cat. 13 86


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