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

Striking variability has been observed in the presenting features in infancy of patients subsequently shown to have tetralogy of Fallot. Some patients presented with severe cyanosis in the neonatal period while others had a systolic murmur and cyanosis only on crying. In these latter patients cyanosis became present at rest over the subsequent months. Yet others presented with episodic attacks of unconsciousness, and a final group presented with dyspnoea and heart failure, accompanying a left-to-right shunt. Angiography demonstrates corresponding variations in the anatomy of the ventricular outflow tracts. In the severely cyanosed patients, the conus septum was deviated so as to obstruct the pulmonary outflow tract, and was best visualized in the lateral projection. In the patients with increasing cyanosis or episodic attacks of unconsciousness, the conus septum again obstructed the pulmonary infundibulum, but was obliquely orientated, not being seen clearly on either lateral or frontal projections. The episodic attacks were considered to be related to infundibular spasm, as previously shown to occur in Fallot's tetralogy. In contrast, increasing cyanosis was believed to be related to hypertrophy of infundibular musculature. In the patients with an initial left-to-right shunt, the arteries were orientated side-by-side so that the conus septum was observed in the frontal projection. Again, subsequent cyanosis was related to ventricular hypertrophy producing outflow tract obstruction. These findings are interpreted in the setting of a recent study, indicating that Fallot's tetralogy is produced by rotation of the embryonic conus together with sinistro-anterior deviation of the conus septum.
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PMID:Variations in clinical presentation of Fallot's tetralogy in infancy. Angiographic and pathogenetic implications. 119 55

Two patients, aged 8 weeks and 5 years, with D transposition of great arteries and large ventricular septal defect were treated by transection of both aorta and pulmonary arteries and reattaching them to the appropriate ventricles. This included the origins of the coronary arteries. The ventricular septal defect was closed through a transverse ventriculotomy using a Dacron patch. The younger child was operated on as an emergency because of cyanosis and severe heart failure resistant to intensive medical treatment. The older child had had previous banding of the pulmonary artery at the age of 1 year. In both patients pulmonary artery pressure dropped to below half systemic pressure immediately after the operation. Postoperative progress was satisfactory with relief of cyanosis and heart failure. Early anatomical correction of transposition of the great arteries and ventricular septal defect is feasible and should play an important part in the management of these patients.
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PMID:Anatomical correction of complete transposition of the great arteries and ventricular septal defect in infancy. 126 85

Heart failure in a 2-day-old infant was not readily explained by clinical examination. Cardiac catheterization suggested an intracranial arteriovenous (AV) fistula, and cerebral arteriography showed a malformation of the vein of Galen. The major feeding arteries were surgically obliterated. At age 27 months, the boy has normal mentation but moderate left hemiparesis. Review of the literature disclosed 39 other infants with AV malformations of the vein of Galen producing heart failure before age 3 months. Most of them were boys, and had cyanosis, a systolic murmer, cranial bruit, cardiomegaly, and right bentricular hypertrophy. Only three of the 13 who had surgery for their malformation survived. Removal of the malformation is difficult; obliteration of the nutrient vessels, using the operating microscope, is the currently accepted treatment.
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PMID:Arteriovenous malformation of the vein of Galen: treatment in a neonate. 127 3

Neonatal cardiac rhabdomyoma is the most frequent cardiac tumour in the newborn, and a classical way to diagnose tuberous sclerosis (Bourneville's disease). The authors report 4 cases, including 2 antenatal diagnosis: 2 of them had arrhythmia, one with asystolic cardiac failure and the other with cyanosis due to a right-left shunt; the tumour was asymptomatic in the 2 others. The 4 babies had clinical and radiological neurologic signs of tuberous sclerosis, initially or during the course of the disease. The authors discuss the polymorphism of the clinical presentation of tuberous sclerosis in the newborn. Although tuberous sclerosis is transmitted through a dominant gene, the expressivity and the penetrance are very variable. The authors discuss the examination and investigation of at risk family members. The genetic counsel is difficult but very important because of the poor neurologic prognosis of the disease.
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PMID:[Bourneville tuberous sclerosis manifested by prenatal finding of intracardiac tumors]. 132 12

Once the rules for understanding of complex congenital heart disease were reviewed in part I, the purpose in this second part is show how the clinical diagnosis is made. The first requirement is to separate patients into two groups: neonates and infants. A critical route based on five clue data: patient's age, presence or absence of cyanosis, presence or absence of myocardial failure, pulmonary blood flow estimated on x chest film, and presence of either right or left ventricular hypertrophy or both in ECG, is matched. This approach is helpful to reduce possibilities to diagnosis in congenital heart disease.
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PMID:[Understanding and diagnosis of complex congenital cardiopathies. II]. 141 55

A Japanese black calf with cyanosis, tachycardia, tachypnea and systolic murmur died of hypoxemia and cardiac insufficiency on the 38th day after birth. We could not establish the diagnosis during it's life. However, anatomically corrected malposition (ACM) with ventricular septal defect was confirmed at autopsy. There was situs solitus of the viscera and atria with atrio-ventricular discordance and ventriculo-arterial concordance. The ventricles demonstrated l-loop, i.e. on the right-sided ventricle there was a markedly enlarged morphologic left ventricle, and on the left-sided ventricle there was a hypoplastic morphologic right ventricle with a stenotic tricuspid valve and Ebstein-like deformity. The right posterior aorta originated from the left ventricle. The pulmonary artery arose from the left-sided right ventricle via infundibulum. There was a fibrous continuity between the aortic and mitral valve. We considered that this is the first reported case of bovine ACM.
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PMID:Anatomically corrected malposition (ACM) with subpulmonary infundibulum in a calf: clinico-morphologic case report. 142 May 62

We conducted a retrospective analysis on 311 patients with clinical diagnosis of pulmonary embolism (PE) in a period of 3 years. 163 patients were excluded based on clinical-laboratorial criteria. The remaining 146 patients had a median age of 69 years (range: 30-91 years). 54% of the patients were male. We found dyspnea (94%), abnormal cardiopulmonary observation (89%), risk factors for venous thromboembolism (74%), tachycardia (53%), cyanosis (49%), and neck vein distension (45%) to be the most frequent findings. 64% of the patients had heart failure, 32% had myocardial ischemia, 13% had cancer, and 11% had myocardial infarction. Lactic dehydrogenase (LDH) was higher than two-fold in 54% of the patients. There was severe hypoxemia in 55% of the cases and hypocapnia in 43% of the cases. Creatinine phosphokinase (CPK) was elevated in 16% of the cases. Electrocardiography was suggestive of PE in 37% of the cases. Echocardiography showed right heart dysfunction in 30% of the cases, 92% of the patients were treated with heparin, 37 patients (25%) died, 54% of which during the first 4 days after admittance. Trying to define an index of mortality in PE we evaluated all patients by discriminant analysis coming up with 14 items with good discriminative power. By approximation of their odds-ratios we determined how many points would correspond to each item in the total sum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pulmonary embolism--mortality risk]. 147 67

A male calf with ectopia cordis cervicalis inferior was investigated clinically, hemodynamically, and morphologically from the 3rd day of age until slaughter at the age of 22 months. Arterial hypertension (mean AOP 140 mm Hg), concentric myocardial hypertrophy and good ventricular contractility with normal valve function were found. Normal clinical condition at rest (cardiac output 48 l/min in the 600 kg bullock), but cyanosis and dyspnea during physical exercise were observed. Variations in the large vessels, such as persistence of the right cranial caval vein and one common pulmonary vein emptying into the left atrium, were found. Abrupt caliber differences of large arterial vessels together with a right angled aortic arch were observed, presumably contributing to increased afterload. The cytogenetic analysis showed the presence of a small marker chromosome leading to a chromosome number of 61 in a fraction of metaphases (mosaicism). Moreover, chromosome breakages were observed in many cells. From the 5 cows which were inseminated, 3 became pregnant. Ectopia cordis was not observed in any offspring. We conclude that in this animal compensated cardiac insufficiency with peripheral hypertension was established.
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PMID:Cardiac function, morphology and chromosomal aberrations in a calf with ectopia cordis cervicalis. 149 9

We present a case of the rare coincidence of three mechanisms leading to development of congenital heart disease in intrauterine life: intrinsic defect of the development of the cardiac loop (dextrocardia), failure of normal expansion of the subpulmonary infundibulum (Fallot syndrome) and endocardial cushion defect (common atrium and common atrioventricular valve ). It was associated with partial viscera inversion. A 31-year old man with congenital cyanotic heart disease, and Blalock-Taussig anastomosis was admitted to the hospital due to symptoms of severe cardiac failure. On physical examination: systolic murmur, hepatomegaly, ascites, leg's edema and cyanosis were found. In ECG--atrial fibrillation with 3-d degree a-v block. Standard echocardiography revealed: dextrocardia, a large single atrium with ostia of pulmonary and systemic veins, single atrio-ventricular valve , large ventricular, Fallot-like septal defect. The papillary muscles were not visible in the left ventricle. Aorta and pulmonary trunk arose from morphological right ventricle. The patient died on the 3-rd day of hospitalization in the course of cardiac and respiratory insufficiency. Postmorten examination confirmed the diagnosis.
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PMID:[Combined heart defects: tetralogy of Fallot, common atrium and a single atrioventricular valve diagnosed by echocardiography]. 164 Jun 69

Patients with congenital cyanotic heart disease may develop a glomerulopathy with proteinuria and impaired renal function. In order to investigate this problem we conducted a study on 27 patients with uncorrected cyanotic heart disease who were between 1 day and 25 years old. As a consequence of hypoxaemia haematocrit was elevated to 57%. Proteinuria was above 150 mg/day/1.73 m2 body surface in 12 patients. Only one of 9 children under 10 years of age had pathological proteinuria presenting as isolated albuminuria. Seven out of 10 patients between 11 and 20 years had an elevated proteinuria with a glomerular pattern. Creatinine clearance was normal in these patients. All four patients above 20 years of age had a considerable glomerular proteinuria with a mean excretion of 5.7 g/24 h/1.73 m2 body surface. These patients suffered additionally from chronic cardiac failure and creatinine clearance was below the normal range. There was a clear relationship between pathological proteinuria and age of the patients and thus duration of hypoxaemia. Patients with pathological proteinuria had a significant higher erythrocyte count (7.3 +/- 1.3 vs 5.6 +/- 1.4 10(12)/l p less than 0.01) and a lower mean corpuscular haemoglobin. In summary, children with persistent congenital cyanotic heart disease have substantial risk of developing a glomerulopathy if the cyanosis remains unchanged for more than ten years.
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PMID:Renal involvement in patients with congenital cyanotic heart disease. 178 94


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