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

A 40-year-old woman was admitted because of increasing exertional dyspnea. Right heart failure was suggested by the presence of hepatomegaly, pretibial edema and also echocardiographic findings. Physical examination and echocardiography showed no evidence of valvular disease or congenital heart disease except for right ventricular dilatation and tricuspid regurgitation. The ventricular septum deviated toward the left ventricle throughout the cardiac cycle, but left ventricular function was preserved. Severe pulmonary hypertension averaging 44 mmHg was revealed by cardiac catheterization. Digital subtraction angiography and pulmonary blood flow scintigraphy showed no evidence of pulmonary artery embolism, and no interstitial pulmonary lesions that might have caused pulmonary hypertension were recognized. Hypergammaglobulinemia suggested an autoimmune disorder, and signs of systemic lupus erythematosus (SLE), such as pleural effusion, proteinuria, lymphocytopenia, LE cell phenomenon and antinuclear antibodies were present. Several autoimmune diseases are known to be causative factors of pulmonary hypertension. However, only ten cases of SLE complicated by pulmonary hypertension have been reported the present one. These cases were characterized by a high incidence of Raynaud's phenomenon and positivity for anti-RNP antibody. In our present case, SLE activity was suppressed using prednisolone, but pulmonary hypertension persisted and the patient eventually died due to right cardiac failure. Judging from the clinical course of the ten reported cases of SLE-pulmonary hypertension, there seems to be no hope of improving the pulmonary hypertension once it has become established. Therefore it is important to detect and cure pulmonary hypertension as early as possible.
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PMID:[A case of lupus erythematosus preceded by right heart failure due to pulmonary hypertension]. 174 69

Between 1972 and 1987, 43 patients underwent isolated mitral valve replacement with mean pulmonary arterial pressures greater than 50 mmHg. The valve disease was stenosis in 13 cases, regurgitation in 15 cases and mixed mitral valve disease in 15 cases. Forty-one patients (95 %) had invalidating cardiac failure (Stages III and IV of the NYHA Classification). The hospital mortality was 2.3%. Thirteen patients died during follow-up, 8 of cardiac failure, 3 of sudden death and 2 died of non-cardiac causes. The 8 year actuarial survival was 82 +/- 7% with an average postoperative follow-up of 96 +/- 41 months. No patients were lost to follow-up. Eighty six per cent of survivors (25/29) are asymptomatic or paucisymptomatic. Doppler studies were performed in 22 patients, showing normal prosthetic function in 18 cases and an obstructive prosthesis in 4 cases. Seventeen patients had tricuspid regurgitation showing normal pulmonary artery systolic pressures in 9 cases and less than 55 mmHg in 5 cases. On average, systolic pulmonary artery pressure fell from 88 +/- 11 mmHg before to 33 +/- 9 mmHg after surgery (p = 0.01). These results show that severe pulmonary hypertension is not prohibitive for mitral valve replacement. The long-term results are good with functional improvement and reduction of pulmonary hypertension.
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PMID:[Mitral valve replacement in severe pulmonary hypertension. Long-term results]. 195 13

Afterload reduction therapy can acutely improve hemodynamic function in patients with advanced heart failure; however, it is unknown if initial reductions in mitral and tricuspid regurgitation and atrial volumes can be sustained with oral therapy. Atrial volumes and atrioventricular valve regurgitation were measured using 2-dimensional and Doppler echocardiography with color-flow imaging in 14 patients with dilated heart failure (ejection fraction 17 +/- 4%) before and after 3 +/- 1 days of intensive vasodilator and diuretic therapy tailored to hemodynamic goals. Echocardiography was repeated again after 6 +/- 2 months on oral vasodilators and a flexible diuretic regimen. Acute therapy reduced systemic vascular resistance from 1,760 +/- 460 to 1,010 +/- 310 dynes.s.cm-5, pulmonary artery wedge pressure from 30 +/- 5 to 17 +/- 4 mm Hg, and right atrial pressure from 13 +/- 5 to 7 +/- 3 mm Hg, and led to a 61% increase in stroke volume (from 36 +/- 10 to 58 +/- 14 ml) (p less than 0.01). Mitral and tricuspid regurgitation, determined by color-flow fraction, initially decreased from 0.34 +/- 0.17 to 0.20 +/- 0.20 and from 0.33 +/- 0.15 to 0.13 +/- 0.13, respectively (p less than 0.001). This reduction was sustained at 6 months. Significant decreases occurred with acute therapy, with further reductions at 6 months in both mean left atrial volume (from 100 +/- 25 to 80 +/- 19 to 65 +/- 15 cm3) and right atrial volume (from 85 +/- 23 to 64 +/- 23 to 52 +/- 14 cm3) (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sustained reduction in valvular regurgitation and atrial volumes with tailored vasodilator therapy in advanced congestive heart failure secondary to dilated (ischemic or idiopathic) cardiomyopathy. 199 Jul 89

Five patients suffering from transient myocardial ischemia of the newborn are discussed. The role of two-dimensional doppler-echocardiography is emphasized in establishing the diagnosis. Tricuspid insufficiency due to perinatal asphyxia can be detected easier by ultrasound than by any other cardiac examination. Cardiac failure as a result of hypoxic myocardial ischemia is usually reversible and responds well to anticongestive treatment and administration of oxygen. On the other hand some cases can be fatal, histopathologic examination on the heart shows similarity to myocardial infarction.
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PMID:[Neonatal hypoxic myocardial lesion]. 199 10

A-59-year old woman died from heart failure associated with tricuspid regurgitation and pulmonary hypertension. Necropsy revealed that her tricuspid valve was composed of six leaflets. We found no previous report of this type of tricuspid valve abnormality.
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PMID:A case of congenital tricuspid valve abnormality showing six leaflets. 200 1

This paper reports a retrospective study of 21 children with atrioventricular and ventriculo-arterial discordance, or double discordance, associated with a large ventricular septal defect responsible for pulmonary hypertension. Other associated congenital defects were: atrioventricular block (5 cases), coarctation of the aorta with neonatal cardiac failure (6 cases), tricuspid valve malformations responsible for significant tricuspid regurgitation (11 cases) and right ventricular hypoplasia (1 case). Two children died before any therapeutic intervention, one from syncope related to atrioventricular block and the other after a decision of therapeutic abstention. Three children underwent total correction with one good result (the only case of situs inversus), one late death and one lost to follow-up. The majority of patients (n = 16) underwent initial palliative surgery consisting in pulmonary artery banding occasionally associated with reconstruction of the aortic arch: there was no early mortality but there were 2 late deaths. Of the 14 survivors, 6 are well after a mean follow-up period of 31 months. Eight underwent open heart surgery with 1 operative death, 6 post-operative complete atrioventricular blocks requiring cardiac pacing and 5 poor results due to aggravation or secondary tricuspid regurgitation leading to 1 cardiac transplantation (death) and 2 reoperations for valvular surgery (1 plasty and 1 tricuspid valve replacement). The overall results of this series are poor: high mortality (33 per cent) and equally high morbidity when direct surgery is undertaken. Two major complications are observed: complete atrioventricular block (55 per cent) and regurgitation of the systemic atrioventricular valve (45 per cent), both of which often necessitate invalidating complementary procedures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Double discordance with ventricular septal defect and pulmonary artery hypertension. A study of 21 cases]. 211 74

Doppler echocardiography, providing objective data on heart anatomy and cardiac function, is a diagnostic method of unquestionable value in the acute phase of myocardial infarction. In what concerns myocardial infarction complications; echocardiography permits: a) evaluation of ventricular function, by quantifying heart failure and establishing the diagnosis of ventricular aneurysm; b) it is the most reliable method in the diagnosis of thrombi, and c) it constitutes a fundamental diagnostic tool in mechanical complications: rupture of the heart structures and evaluation of valvular competence. a) Evaluation of ventricular function. The analysis of ventricular dimensions and segmentary wall motion abnormalities permits the quantification of the infarct size and its repercussion upon the cardiac function. Otherwise, left ventricular proto and end diastolic filling rates give an idea about ventricular diastolic function alterations. b) Ventricular thrombi. The incidence of ventricular thrombi in AMI is variable, depending on the site of infarction and the number of segments with wall motion abnormalities. By echocardiography it has been demonstrated that 40% of the anterior transmural myocardial infarctions and 10% of the inferior ones disclosed thrombi, although the incidence of systemic embolism is scarce and similar on both anterior and inferior infarctions: nearly 2% during the first month after infarction. The criteria that identify the embolic risk include: thrombus size over 2 x 2 x 2 cm, pediculated and mobile thrombi. On the other hand, right intraventricular thrombi incidence is rare nearly 5% of right ventricular infarctions and post-infarction pulmonary embolism is probably more related to peripheral venous thrombus than to an intraventricular one. c) Mechanical complications. Echocardiography enables the direct diagnosis of interventricular septum and papillary muscles rupture in about 80% of the cases and although ordinary does not provide direct data on free ventricular wall rupture, the detection of pericardial effusion with high density echoes, together with finding of free right ventricular and atrial wall collapse, gives 80% of sensibility and over 90% of specificity in the diagnosis of free ventricular wall rupture. Finally, Doppler echocardiography permits the diagnosis and quantification of mitral and tricuspid regurgitation secondary to a rupture of even a simple disfunction of the atrioventricular subvalvular apparatus.
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PMID:[Usefulness of Doppler echocardiography in the diagnosis of complications in the acute phase of myocardial infarct]. 220 45

The case of surgical treatment of a 44-years old female with a double atrio-ventricular accessory pathway and mitral stenosis was described. Fast ventricular rates due to conduction through the accessory pathways during atrial fibrillation in course of mitral stenosis caused severe heart failure, occasionally with deep hypotonia. Combined treatment with prajmaline and propafenone blocked conduction through accessory pathways. The ventricular rate slowed from approx. 200/min to 150/min. Addition of digoxin slowed the ventricular rate down to approx 80-100/min. There were no signs of preexcitation. Treatment with diuretics and vasodilators was continued. The state of patient improved. Echocardiographic and hemodynamic evaluation revealed: mitral stenosis (orifice - 75 mm2) with moderate regurgitation, small aortic and tricuspid regurgitation. The coronary arteries were normal. On the base of the ECG recordings during atrial fibrillation both accessory pathways were localized on lateral and posterior parts of the left free wall. The patient was operated on. Both atrio-ventricular by-pass tracts were dissected using Sealy's method in Cox modification and then mitral valve prosthesis Medtronic-Hall 27 mm was implanted. Prajmaline and propafenone were discontinued and preexcitation did not recovered. The sinus rhythm was restored by electroversion. The patient had no overt heart failure on discharge from the Institute.
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PMID:[Dissection of the accessory conduction pathways with simultaneous mitral valve surgery]. 227 77

A 63-year-old female of two-chambered right ventricle (TCRV) associated with tricuspid regurgitation (TR), patent foramen ovale (PFO) and small ventricular septal defect (VSD) underwent corrective surgery successfully. She suffered severe heart failure and cyanosis with 47.7% of right-to-left shunt through PFO. The VSD was so small that no significant shunt was shown in catheterization data. Operative findings suggested that TR was caused by elongation of the chorda as a consequence of long-term pressure load of right ventricular inflow chamber. Among reported cases of TCRV, the present case is the oldest one who underwent corrective surgery successfully.
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PMID:[A case of two-chambered right ventricle complicating severe cyanosis due to tricuspid regurgitation and patent foramen ovale]. 231 27

Dextro-Transposition of Great Arteries (d-TGA) was repaired by Mustard's operation in 69 patients during a 10 year period (1973-1982) in our institution. Ages at the time of surgery ranged from 3 months to 18 years, with a median age of 18 months. Factors that most affected mortality and morbidity were associated cardiac defect, the year of the operation and the age of the patient. Of the 69 patients, 26 (38%) had complex d-TGA. Early post-operative mortality was 2.38% for patients with simple transposition and 22% for the complex group. All early deaths occurred in the early part of series. Ten consecutive cases with complex transpositions in the late part of the series have done well. There were 5 late deaths--4 from the early series and these had complex transposition. Postoperative non-fatal complications included arrhythmia which occurred in 6 patients (9%). The rhythm abnormality was temporary in 2 and permanent pacing was required in 2 other patients (2.9%). There were 3 cases of late caval obstruction and 4 cases of late pulmonary venous obstruction--six of these seven patients were less then 12 months of age. Postoperative renal failure occurred in patients in the early series but was not seen in the late series. Three children developed postoperative pulmonary edema due to large bronchial collateral arteries and underwent successful collateral vessel ligation subsequent to the Mustard operation. Two patients have demonstrated late tricuspid regurgitation, are presently in heart failure and may need valve replacement.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Results of Mustard's repair for dextro-transposition of the great arteries. 232 86


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