Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Five hundred and eighty-eight patients with mitral valve disease were studied. The incidence of systemic emboli was found to be higher in patients with pure mitral stenosis (16.6%) and mixed mitral stenosis and incompetence (19.4%) than in patients with mitral incompetence (3.1%). The patients with mitral stenosis who had episodes of systemic emboli tended to be older than 40 years, with moderate or severe valve lesions, atrial fibrillation and moderate or gross enlargement of the left atrial appendage or left atrium. The following factors were found to be unrelated to systemic embolism---associated aortic valve disease, sex, smoking habit, history of rheumatism, parity, haemoglobin, blood urea, pulmonary hypertension, duration of antifailure treatment, presence of heart failure, and cardiothoracic ratio.
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PMID:Thromboembolic complications of mitral valve disease. 28 50

Mitral commissurotomy is the treatment of choice for mitral stenosis. If this is not feasible, replacement of the valve becomes necessary. Open commissurotomy has been performed at Loyola University Medical Center, Maywood, Ill, in 105 patients since 1970. The mean age was 45 years. The indication for surgery was heart failure in 92 of the cases. Sixty of the patients were in class 3 of the New York Heart Association (NYHA) classification. Eighty-five underwent open mitral commissurotomy alone. This was not feasible in 42 patients scheduled for it who required valvular replacement. Twenty-five patients had a left atrial thrombus. Two patients died, one from aortic dissection and the other from acute infarction in the perioperative period. Ninety-eight patients are NYHA class 1 or 2 at present. Two patients required valvular replacement following the commissurotomy. The low mobidity and mortality with excellent long-term results support our contention that open mitral commissurotomy is the treatment of choice for mitral stenosis.
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PMID:The advantages of open mitral commissurotomy for mitral stenosis. 42 47

Left atrial myxomas are extremely difficult to diagnose since their variable manifestations mimic a host of clinical entities more commonly seen, e.g. mitral stenosis, endocarditis, rheumatic fever, cardiomyopathy or mesenchymosis. At the same time, early diagnosis followed by prompt surgical removal are mandatory to prevent mutilating or lethal complications of the tumor. Six cases of left atrial myxoma were diagnosed in our hospital during 2 1/2 years. We present the case histories, diagnostic procedures and surgical findings, consolidating the unique role of echocardiography in detecting left atrial myxomas. We propose the use of echocardiography as a screening examination for atrial myxomas in the following settings: suspected mitral obstructive disease, suspected endocarditis with negative blood cultures, peripheral embolism or thrombosis in young patients, unexplained cardiac failure and mesenchymosis with uncharacteristic presentation.
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PMID:The diagnostic challenge of left atrial myxoma. Importance of echocardiographic screening. 48 52

Hemodynamic response to exercise before and 10 minutes after propranolol (5 mg intravenously) was studied in 10 young patients with pure mitral stenosis who had normal sinus rhythm and no cardiac failure. After propranolol the mean heart rate and cardiac index at rest were lower than during the control state (respectively, 95 +/- 4 versus 82 +/- 3 beats/min, P less than 0.005; 3.4 +/- 0.2 versus 2.8 +/- 0.1 liters/min per m2, P less than 0.025). As a result, the mean pulmonary wedge pressure and mean mitral valve gradient at rest were lower (respectively, 22 +/- 2 versus 18 +/- 2 mm Hg, P less than 0.005; 24 +/- 2 versus 17 +/- 2 mm Hg, P less than 0.001). During exercise after propranolol the values of pulmonary wedge pressure and mitral valve gradient were lower than control values during exercise (respectively, 39 +/- 3 versus 30 +/- 2 mm Hg, P less than 0.005; 44 +/- 3 versus 32 +/- 3 mm Hg, P less than 0.005), again because of the lower heart rate and cardiac index (130 +/- 6 versus 104 +/- 6 beats/min, P less than 0.001; 4.6 +/- 3 versus 3.7 +/- 2 liters/min per m2, P less than 0.01). Left ventricular end-diastolic pressure and stroke index showed no significant changes. Thus, propranolol may benefit patients with pure mitral stenosis with sinus rhythm and no cardiac failure whose symptoms occur during those reversible conditions characterized by an increase in heart rate or cardiac output, or both.
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PMID:Hemodynamic response to exercise after propranolol in patients with mitral stenosis. 49 1

A patient who had aortic and mitral valves replaced by Carpentier porcine heterografts for bacterial endocarditis developed severe heart failure 18 days after operation. A second emergency operation revealed that the mitral prosthesis had become severely stenosed and calcified. A loud Graham Steell murmur had developed during the 12 hours before reoperation but no distinct murmurs of mitral stenosis had been detected.
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PMID:Severe and early stenosis of porcine heterograft mitral valve. 56 77

Hemodynamics was studied in different trimesters of pregnancy in 94 women with mitral stenosis and in 32 healthy women with pregnancy following a normal course. Each trimester in women with mitral stenosis was marked by different changes in hemodynamics. Study of the state of hemodynamics allows preclinical signs of cardiac insufficiency to be already detected in the early periods. This makes it possible to assess the risk of pregnancy and delivery in women with mitral stenosis at the right time and more correctly. The disclosure of unfavourable signs of changes in hemodynamics in conjunction with the clinical signs of cardiac insufficiency aids in the choice of the therapeutic and obstetrical tactics.
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PMID:[State of the hemodynamics in pregnant women suffering from mitral stenosis]. 63 14

Left ventricular myocardial stiffness was calculated in clinical cases. Thirty patients who underwent diagnostic cardiac catheterization were studied. Left ventricular cineangiograms and simultaneously recorded left ventricular pressure tracings were analyzed. The left ventricular stiffness constant k, was computed by substituting the left ventricular myocardial stress (sigma) and strain (epsilon) throughout the period between the end of rapid ventricular filling and the beginning of atrial contraction, in the equation sigma = b.ek.epsilon. Left ventricular myocardial stiffness was measured as follows: Group I (normal): 9.6 +/- 4.3, Group II (mitral stenosis): 10.7 +/- 4.0, Group III (left ventricular volume overload): 12.1 +/- 4.2, Group IV (coronary artery disease without myocardial infarction): 8.6 +/- 2.5, and Group V (myocardial infarction): 23.6 +/- 7.4. All of the normal cases showed stiffness constants of less than 15 and maxVcf of more than 2.0 circ/sec, and all the patients with histories of heart failure in Groups III to V showed stiffness constants of more than 15 and maxVcf of less than 1.0 circ/sec. For the rest of the patients, measurements of the stiffness constant were valuable for the assessment of patients' clinical status, especially when combined with contractility.
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PMID:Clinical evaluation of left ventricular myocardial stiffness. 65 Sep 1

In 53 patients with mitral- or aortic-mitral valve disease, the content of ATP and lactate of the papillary muscles resected at the time of valve replacement was investigated at the beginning of ischemic arrest and at the time of reperfusion. Profound body hypothermia (25 degrees C) and injection cardioplegia using magnesium-aspartate-procaine were applied for myocardial protection. In hypertrophic papillary muscles the myocardial ATP content decreased at a slower rate (ATP decay 12% of the initial value after 60 minutes of ischemia) than in normal papillary muscles obtained from patients with isolated mitral stenosis (ATP decay 33% of the initial value after 40 minutes of ischemia). 20% of the patients required temporary inotropic circulatory support postoperatively for 12 to 88 hours. The ATP content of the papillary muscles of these patients differed only little from those, in who no myocardial failure occurred. However the myocardial lactate levels were higher in patients in whom a low cardiac output state evolved.
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PMID:[Behaviour of ATP and lactate in human papillary muscle during profound hypothermia and injection cardioplegia with magnesium-asparatate-procaine (author's transl)]. 75 Dec 88

Patients with cardiac disorders have defective parasympathetic control of heart rate. To evaluate the possibility of similar changes in sympathetic control of heart rate, we compared reflex chronotropic responses to 80 degree upright tilt and nitroglycerin-induced hypotension in 31 cardiac patients and 7 normal individuals before and after partial parasympathetic blockade with atropine. Tilting revealed an attenuation of the normal heart rate increase in patients; the magnitude of this defect was greatest in patients with more severe symptoms (class III) and evidence of left ventricular dysfunction (the heart rate increase averaged 25 plus or minus 3 beats/min in normal subjects, 12 plus or minus 2 beats/min in class I-II patients, and 7 plus or minus 1 beats/min in class III patients). Class III symptoms due to mechanical causes (mitral stenosis), however, were not associated with this defect. A marked reduction in heart rate rise with hypotension was seen only in those class III patients without mitral stenosis (0.4 plus or minus 0.1 beats min-minus 1 mm Hg-minus 1 vs. 3.0 plus or minus 0.5 beats min-minus 1 mm Hg-minus 1 in normal subjects). This abnormality also persisted after atropine administration, thus confirming a defect in the sympathetic as well as the parasympathetic component of baroreceptor-mediated reflex heart rate control in patients with cardiac dysfunction. Infusions of isoproterenol produced equivalent rises in heart rate in patients and normal individuals, excluding a reduction in beta-receptor responsiveness as a cause of impaired sympathetic influence. Norepinephrine depletion, however, is a well-recognized concomitant of cardiac failure. It is possible that the reduction in sympathetically mediated heart rate responses results in part from depletion of the sympathetic neurotransmitter.
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PMID:Impairment of autonomically mediated heart rate control in patients with cardiac dysfunction. 80 57


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