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

One-third of 327 newborn infants referred to the perinatal service of the Hospital for Sick Children during 1975 with suspected cardiopulmonary disorders proved to have nonstructural heart disease. Most of these were term infants with transient tachypnoea or cyanosis who recovered. A history of fetal distress or difficult delivery was commonly associated. The haemodynamic disorder for most was a delay in the normal progress of the transitional circulation. Evidence of myocardial ischaemia was present in 40%, and about half of these developed congestive heart failure. Aids to diagnosis of the ischaemic complication included echocardiography and myocardial perfusion scanning. For a small proportion specific metabolic disturbances, myocarditis, or dysrhythmia seemed the primary cause but even for these there were reasonable grounds to suspect a prenatal origin. Current general supportive measures were of value in treatment.
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PMID:Nonstructural heart disease in the newborn. Observations during one year in a perinatal service. 71 41

Five term and two premature newborn infants were referred for respiratory distress and congestive heart failure, and were found to have electrocardiographic Q or ST-T abnormalities suggesting ischemia. Echocardiographic and/or hemodynamic assessment excluded anatomic heart disease in six infants. In three infants, moderate or severe hemodynamic impairment within 36 hours of age was suggested by these studies. Myocardial perfusion images in all patients showed very poor myocardial uptake of thallium 201, compatible with global myocardial ischemia. Infants of similar age with myocarditis, or with congenital heart disease and congestive failure, had normal myocardial uptake. Rapid clinical improvement occurred within three to seven days. Two to five months later, all infants were well. Two had persistent electrocardiographic abnormalities but repeat thallium 201 imaging in six demonstrated almost normal myocardial uptake. These data provide further evidence that perinatal respiratory distress may be associated with myocardial dysfunction and congestive heart failure in some infants without anatomic heart disease, and suggest that myocardial dysfunction in these infants is associated with global myocardial ischemia, most of which is transient. The timing and nature of the insult causing the ischemia are unclear.
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PMID:Transient myocardial ischemia of the newborn infant demonstrated by thallium myocardial imaging. 76 22

Twenty-two cases of Coxsackie virus heart disease diagnosed from November, 1969, to December, 1971, were re-examined after a period of 42 to 68 months from the acute illness. The patients with hypertension, diabetes, chronic alcohol intake, or aged over 35 were eliminated from the trial. With the purpose of assessing myocardial function, the systolic time intervals were recorded by a noninvasive standard technique. The differences in systolic time intervals between the group of patients with previous viral myocarditis and a group of normal control subjects were not statistically significant. However, the pre-ejection period was clearly prolonged in three patients out of 10, a modification consistent with a depressed myocardial function, as in patients with cardiomyopathy.
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PMID:Coxsackie virus heart disease and cardiomyopathy. 84 36

Twenty-nine young men with AV block I (P-R interval greater than 0.22 sec), without any history of heart disease, have been compared with 112 randomly selected healthy men of the same age. In 24 subjects who were free from concomitant ECG changes the P-R interval was normalized during orthostatic test and/or physical exercise. This group did not differ from the controls regarding anthropometric data and physical work capacity except for a higher heart rate at rest, thus suggesting that in these subjects an occurrence of AV block I has no pathological significance. However, it cannot be excluded that the block is a sequela, for instance, to myocarditis. Three subjects with AV block I and inverted T waves in the precordial leads and two subjects with unchanged P-R intervals to increased sympathetic tone had on average a smaller body size, a higher HR and systolic BP in recumbent position and smaller blood volumes.
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PMID:The significance of AV block I in asymptomatic young men. Variability, some anthropometric data, orthostatic test reaction and physical work capacity. 85 Oct 46

Clinical and pathologic changes in 87 patients who could not be resuscitated from an episode of sudden cardiovascular collapse are described and compared with observations from patients in the same community who were successfully resuscitated from ventricular fibrillation. Findings in patients who died suddenly generally did not differ when the patients were groups by electrocardiographic rhythm on arrival of the mobile coronary aid unit. The pathologic changes of acute thrombosis and recent myocardial infarction did not occur with sufficient frequency in the entire group to be considered causally related to the sudden collapse, occurring in 10 and 5 percent of cases, respectively. Although most patients had evidence of obstructive coronary disease and old myocardial infarction, 8 percent had no significant vascular disease, acute thrombosis, myocarditis or valve disease that might be implicated as a factor in sudden death. There was no relation between age and severity of obstructive coronary disease or frequency of old myocardial infarction in patients who died suddenly. Complete atherosclerotic occlusion in one or more coronary vessels occurred in 51 of 87 (59 percent) and old myocardial infarction in 48 of 87 (55 percent). Although the mean age of this autopsy population was similar to that of all patients in the community who have had ventricular fibrillation on arrival of the aid unit, the nonsurvivors had a greater incidence of myocardial infarction and symptomatic heart disease (73 of 87) than did survivors. Comparison of this autopsy group with persons from the community who were resuscitated from ventricular fibrillation and subsequently had coronary angiograms indicates that the severity of coronary stenosis does not distinguish between survivors and nonsurvivors of an episode of ventricular fibrillation and suggests that other factors influence the outcome of an episode of ventricular fibrillation.
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PMID:Pathology of the heart in sudden cardiac death. 87 Nov 13

Diagnostic separation of infants with signs of cardiac failure (hypoglycemia, sepsis, myocarditis, hypoxemia) but no congenital cardiocirculatory malformation from those with a large left to right shunt is crucial in newborn management. Echocardiographic studies of 218 infants and children allowed group separation and distinction from normal by the assessment of mean velocity of circumferential fiber shortening (Vcf) and the ratio of left atrial to aortic root diameter at end-systole (LA/Ao). In normal premature and full-term infants, Vcf (1.51 +/- 0.04 [mean +/- standard error]) was significantly lower than in infants with a large shunt (2.12 +/- 0.08, P less than 0.01) and higher than in infants with nonstructural heart disease (1.18 +/- 0.06, P less than 0.001). LA/Ao ratios were comparable in the groups with a large shunt and nonstructural heart disease (1.14 +/- 0.1 and 1.26 +/- 0.2, respectively) and were significantly higher in both groups than in normal subjects (0.77 +/- 0.01, P less than 0.001). Similar echocardiographic distinctions could be made when 10 older children (aged 2 to 10 years) with cardiomyopathy were compared with 45 normal older children. Serial determination of these variables was of major assistance in patient management.
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PMID:Echocardiographic detection of large left to right shunts and cardiomyopathies in infants and children. 93 2

A case of aneurism of the left ventricle, confirmed by ventriculogram, associated to an inactive rheumatic cardiopathy with a pure mitral stenosis is presented. Since none of the usual causes that have been reported were found to explain the aneurism of the left ventricle; the possibility of the aneurism resulting from residual myocardiac fibrosis produced by the rheumatic myocarditis is suggested.
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PMID:[Aneurysm of the left ventricle associated with inactive rheumatic heart disease. Report of a case]. 115 9

In 20 children needing treatment for symptomatic sick sinus syndrome, the average age at presentation was 7.1 years and ranged from 9 months to 18 years. Symptoms were never precise but, in retrospect, 5 children had syncope, 7 had a rapid heart action, 6 had dyspnoea or tachypnoea, 2 had nonspecific chest pains, 2 had pale spells, and 1 had a sudden hemiplegia. Symptoms followed cardiac surgery in 15 cases and were related to unoperated congenital heart disease in 2 and to myocarditis in 2. The aetiology was unknown in 1 case. The type of cardiac surgery resulting in the development of the sick sinus syndrome was predominantly related to atrial suturing. Both tachy- and bradydysrhythmias were found, including wandering atrial pacemaker (9 cases), junctional rhythm (19 cases), supraventricular tachycardia (9 cases), atrial flutter (11 cases), and atrial fibrillation (2 cases). Both atrial (8 cases) and ventricular (7 cases) premature beats were seen. All patients were given trials of drug therapy but difficulties were encountered. Cardioversion was used for tachyarrhythmias in 11 cases without serious problems. Six children had permanent cardiac pacemakers inserted with good results. Recognition of the sick sinus syndrome in childhood is important and treatment must be regulated by the severity of symptoms.
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PMID:Sick sinus syndrome. Symptomatic cases in children. 121 60

Coxsackievirus B3-induced myocarditis in different immunocompetent mouse strains was used as a model to investigate interrelationships between virus replication and development of chronic enteroviral heart disease. Using in situ hybridization to detect enteroviral RNA, we show that heart muscle infection is not only detected in acute myocarditis but is also detected during the chronic phase of the disease. Coxsackievirus B3 could evade immunological surveillance in a host-dependent fashion, thus inducing a persistent infection of the myocardium in association with ongoing inflammation. Patterns of acute and persistent myocardial infection were quantitatively assessed in one representative mouse strain (A.CA/SnJ, H-2f) by applying computer-assisted digital image processing; these patterns were then related to the extent of myocardial tissue damage as well as to inflammation. We observed a strong correlation, both spatial and temporal, between viral replication and development of myocardial lesions, indicating that acute and chronic myocardial injuries are a consequence of multifocal organ infection. Analysis of strand-specific in situ hybridization revealed that viral replication in persistent infection is restricted at the level of RNA synthesis. The described procedure for quantitating organ infection provides a powerful tool for evaluating virus-host interactions and will be of particular interest to those studying human enterovirus-induced cardiomyopathies.
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PMID:Ongoing enterovirus-induced myocarditis is associated with persistent heart muscle infection: quantitative analysis of virus replication, tissue damage, and inflammation. 130 11

It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.
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PMID:The effects of acute and chronic cocaine use on the heart. 134 9


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