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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two young Black female patients with pulmonary valve stenosis and intact ventricular septa are presented in protracted congestive cardiac failure with severe tricuspid insufficiency and, in one, atrial fibrillation. Right ventricular systolic dysfunction was manifested by peak systolic pressures below systemic level, raised end-diastolic pressures and low cardiac output, but without right-to-left shunt. These findings are in strong contrast to those found in most patients with pulmonary stenosis of long standing, where persistent impairment of right ventricular function is diastolic with a high end-diastolic pressure and reversal of an interatrial shunt which result from poor right ventricular compliance. Evidence of left ventricular dysfunction was also present in both cases. Protracted heart failure in these patients is believed to have been the result of coincidental cardiomyopathy in a racial group highly predisposed to this disorder. A diagnostic appreciation of this phenomenon is important in the evaluation of heart disease in the Black, since cardiomyopathy may modify or even mask the features of the underlying disorder.
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PMID:Pulmonary stenosis and impaired myocardial function. 12 85

There has been many studies on myocardial catecholamine (CA) in congestive heart failure and ishemias heart disease. However, it has been mainly studied pharmacologically and biochemically and has not been elucidated completely the local change of CA of the myocardium. CA in sympathetic nerves was first stained fluorescence histochemically by Falck-Hillarp in 1962, and many observations were made on its distribution and morphologically concentration of CA in tissue was also observed. Furthermore, the fluorescence histochemical simplified method (cryostat method) by Laties and Jacobowitz was published in 1967. This cryostat method produced the same good preparation instead of the freezed dried method of Falck-Hillarp and could be used semi-quantitatively for the determination of CA concentration in tissue. The author examined fluorescent-histochemically the distribution of CA in sympathetic nerve endings of the myocardium of animals (mouses, rabbits and dogs). After the administration of several agents and in some pathologic conditions, those were in the hypertrophied heart and impending heart failure, in myocardial infarction and A-V block. Furthermore, the change of CA in the myocardium was examined biochemically by von Euler method and its results were compared with the results of fluorescence-histo chemical method.
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PMID:[Catecholamine in the myocardium; a fluorescence histochemical study]. 12 82

A study of 55 patients with heart disease suspected of being viral in origin was carried out a Medical College Hospital, Nagpur, over a period of 2 years. Virus studies as well as other routine tests were carried out on all patients. In 19 patients a virus aetiology of the heart disease was proved by isolation of one of the subtypes of Coxsackie B virus and/or on the basis of fourfold rise in neutralizing antibody titre in paired sera. Of these patients, 5 had acute myocarditis and 5 had acute myopericarditis; 3 had acute pericarditis; 3 had congestive cardiac failure of obscure aetiology; 2 had pleuropericarditis, and the remaining 1 developed post-partum heart failure with cardiogenic shock. All had electrocardiographic abnormalities. Thirteen had cardiomegaly; 1 had a right-sided pleural effusion and 2 had pericardial effusion. Virus could not be isolated from pericardial fluid or pleural fluid in these 3 patients. Follow-up studies up to 10 weeks from discharge revealed that 8 patients were clinically normal but 4 of these 8 had persisting ST-T wave changes, and in 4 the electrocardiogram had returned to normal. Of the remaining 11 patients, 3 had persistent chronic heart failure, 3 had vague symptoms of praecordial pain but no abnormal signs, and 5 patients were lost to follow-up.
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PMID:Heart disease caused by Coxsackie virus B infection. 12 98

To assess the relationship between diet and growth in congenital heart disease we studied nutrient intake, body measurements, and cardiac status in 568 affected ambulatory patients less than 11 years of age. Most had mild heart disease, 104 were cyanotic, and only 10 were in congestive heart failure. Major disturbances of growth were uncommon. For the entire group body weight was below normal but only in those studied before 2 years of age; rate of growth and weight gain were normal over the period preceding the dietary study. There was no statistically significant relationship between intake of calories, protein, or other nutrients and growth or gain, analyzing the entire group, or analyzing patients subgrouped according to age, severity of heart disease, or severity of growth retardation. Body size and growth were diminished in cyanosed compared with noncyanosed children but cardiac status had no effect on nutrient intake. We conclude that in children with growth failure associated with congenital heart disease, nutrient intake is not an important factor limiting their growth.
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PMID:Diet and growth in congenital heart disease. 12 32

In a consecutive series of 1,225 routine echocardiograms, a pericardial effusion (PE) was present in 15% and was considered substantial in 10%. Sixty-one percent (68/111) of the latter were clinically unsuspected. A retrospective analysis of these patients showed that 60% (41/68) had underlying heart disease such as congestive heart failure, left ventricular hypertrophy, or asymmetric septal hypertrophy without other discernible causes for PE. In patients referred specifically for suspected pericardial effusion, 67% (29/43) had diseases recognized as causes of pericardial effusion. Unsuspected substantial PE are commonly detected by echocardiography, especially in patients with underlying heart disease.
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PMID:Unsuspected substantial pericardial effusions detected by echocardiography. 13 24

Fourteen term newborn infants have been recognized as having transient tricuspid insufficiency associated with significant perinatal stress. Five of these infants underwent cardiac catheterization for presumed congenital heart disease, but had only massive tricuspid valve insufficiency. The other nine infants were diagnosed on the basis of a murmur characteristic of tricuspid valve insufficiency and on other clinical grounds. All had a history of significant perinatal stress in the form of asphyxia with or without hypoglycemia. Frequently, congestive heart failure, persistent cyanosis, and ECG evidence of myocardial ischemia were present. Twelve of the 14 survived, and in each of them all cardiac signs and symptoms, including the murmur, spontaneously resolved. The two patients who died had histopathologic evidence of necrosis in the anterior papillary muscle of the tricuspid valve. The constant features of perinatal stress, ST-T wave abnormalities on the ECG, and spontaneous resolution of the transient tricuspid insufficiency strongly suggest that this syndrome is secondary to a reversible form of myocardial dysfunction, perhaps by affecting papillary muscle specifically. We believe that hypoxia with or without hypoglycemia precipitates the events leading to this clinical syndrome which is distinguishable from other cardiac abnormalities in the newborn by the history, distinctive murmur, and the ECG abnormalities.
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PMID:Transient tricuspid insufficiency of the newborn: a form of myocardial dysfunction in stressed newborns. 13 40

A comparative histochemical and clinical study concerning the state of the intrinsic adrenergic innervation of the human atrial myocardium was carried out, using the glyoxylic acid-induced fluorescence histochemical method. Specimens from the right auricular appendage were obtained during open-heart surgery from patients suffering from 1. ischaemic heart disease (IHD), 2. atrial septal defect of the secundum type (ASD), and 3. left-sided univalvular or multivalvular heart disease (VHD) with or without congestive heart failure (CHF) experienced prior to surgery. In the IHD group the densities of both the perivascular and the "free" myocardial adrenergic nerve net were greater than in the ASD group and especially in the VHD/CHF group. Secondly, the intensity of fluorescence of the adrenergic structures was generally higher in the IHD group than that in the VDH/CHF group. Further, the average size of the varicosities, the number of varicosities per given length of axon, and the proportional share of the large varicosities were greater in the IHD group than in the ASD and VHD/CHF groups. The difference between the IHD and ASD groups was not great but was obvious in any case. In some patients with VHD/CHF fluorescing axons were observed only occasionally, and the tiny varicosities exhibited a hardly discernible fluorescence. Thus the amount of noradrenaline (NA) in the adrenergic fibres in the IHD group seems to be higher than in the ASD and especially VHD/CHF groups. The level of NA in the IHD group is assumed to constitute a contributory factor in both intracellular metabolic changes and the systemic changes typical of myocardial ischaemia and infarction. In one patient with IHD and in six patients with VHD/CHF with significantly higher heart volume (mean+/-SD) compared with the rest of the patients (P less than 0.001), huge local axonal accumulations of NA in the form of "droplet fibres" were found. These enlarged, bulging adrenergic axons are assumed to be a consequence of mechanical trauma with stretching or disruption of the axons due to myodegenerative processes. It is further assumed that these "droplet fibres" are relatively common in those patients with diseased myocardium. They may constitute an extra contributory factor to the tendency to arrhythmiility of non-atuomatic tissue.
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PMID:Studies of auricular catecholamines by fluorescence histochemistry in various heart diseases of man. 14 May 8

Eight families were identified in which premature cardiac death due to hypertrophic cardiomyopathy occurred with unusual frequency. A total of 69 first degree relatives in the eight families were studied; 41 relatives had evidence of hypertrophic cardiomyopathy and 31 (75 per cent) died of their heart disease. Eighteen of these 31 patients were less than 25 years of age at the time of death. Death was sudden and unexpected in 23 of the 31 patients; in 15 of these 23 patients sudden death was the initial manifestation of cardiac disease. The remaining eight patients (seven were from two families) died after a chronic cardiac illness characterized by congestive heart failure, atrial fibrillation or thromboembolic events. Hence, premature cardiac death occurs frequently in certain families with hypertrophic cardiomyopathy. Such deaths are usually sudden, often occur in previously asymptomatic subjects and are common in children and young adults. These findings suggest that some families may manifest an unusually virulent expression of hypertrophic cardiomyopathy. Although this study cannot establish the precise prevalence with which "malignant" hypertrophic cardiomyopathy occurs, such families appear to be uncommon.
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PMID:"Malignant" hypertrophic cardiomyopathy: identification of a subgroup of families with unusually frequent premature death. 14 94

Clinical and necropsy findings in 10 dogs with a spontaneous primary hypertrophic cardiomyopathy are described. Each dog had marked cardiac hypertrophy, and 8 dogs had disproportionate thickening of the ventricular septum with respect to the left ventricular free wall (compared with dogs with normal hearts or with cardiac hypertrophy due to acquired or congenital heart disease). Septal:free wall thickness ratios in the 10 dogs ranged from 1.1 to 1.5; 6 had ratios greater than or equal to 1.3. However, marked cardiac muscle cell disorganization in the ventricular septum, characteristic of patients with hypertrophic cardiomyopathy, was present in only 2 of the 10 dogs. Death occurred most commonly while the dogs were under anesthesia during the course of operative procedures (5 dogs) or suddenly and unexpectedly in animals without previous symptomatic manifestations of cardiac disease (3 dogs). Four dogs had clinical signs of congestive heart failure, including 2 with marked cardiac decompensation. In addition, 2 of these 4 dogs with heart failure and 1 dog without previous symptoms (that died during a noncardiac operation) manifested complete heart block. It is conceivable that dogs with spontaneous hypertrophic cardiomyopathy may prove useful in the future investigations of the clinical, hemodynamic, and pathologic features of this disease in humans.
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PMID:Hypertrophic cardiomyopathy in the dog. 15 45

Six examples of intrauterine supraventricular tachycardia together with 31 previously reported cases are described and analyzed. Among the 37 infants, structural heart disease was present in only four (11%), three of whom died. Males comprised 68% of the group without identifiable heart disease or pre-excitation. Congestive heart failure was evident in 62% of the infants at birth or shortly thereafter; ascites was the predominant finding in three (8%). Neither the duration of SVT nor heart rate was predictive of the clinical status at birth. Infants without underlying heart disease or conduction abnormalities had a benign course after the neonatal period. Thirty-eight percent of the babies converted to sinus rhythm during or shortly after delivery without medication, and most of the others converted after digitalization. The failure of maternal digitalization to convert SVT to sinus rhythm in two of our infants was perhaps related to subtherapeutic maternal and fetal digoxin levels. Newborn infants presenting with unexplained ascites or congestive heart failure should have an ECG to determine whether pre-excitation is present, and their cardiac rhythm should be monitored for several days.
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PMID:Intrauterine supraventricular tachycardia. 15 40


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