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

Idiopathic or unexplained VT occurs in a small but important subset of patients without clinically evident heart disease. The majority of these patients appear to have a structurally normal heart. The cause of the arrhythmias in these individuals is unclear and may never be recognized. Other patients with this condition may have minor abnormalities not sufficient to impair overall cardiac function. The significance of these abnormalities to the genesis of the arrhythmia is uncertain. Whether patients with minor abnormalities are more likely to harbor covert heart disease such as myocarditis or a focal defect is not known, nor is it resolved whether such patients warrant a more aggressive search for a structural cause. The question that remains in any patient not subjected to surgical or pathological exploration is whether undetermined heart disease is responsible for the arrhythmia. Continued correlation between functional (electrophysiological) and structural (pathological) data will provide meaningful information concerning the pathophysiology (substrate) of these arrhythmias. Because of the preservation of normal cardiac function, these arrhythmias are generally well-tolerated. Although the condition is usually associated with a favorable prognosis, the occasional deaths reported in patients with apparently idiopathic ventricular arrhythmias may not permit calling this condition benign. It would be important to know the extent to which unrecognized abnormalities play a role in the genesis of these tachycardias, and whether such patients are more predisposed to fatal arrhythmias or have a different natural history. If cases involving undetermined or covert heart disease were excluded from consideration, then a relatively homogeneous disease-free group may be identified with a truly benign condition and a uniformly favorable prognosis. In these cases, a primary electrical abnormality may prove to be the basis for the arrhythmia. These issues remain to be elucidated in future studies.
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PMID:Idiopathic ventricular tachycardia. A review. 304 77

The diagnosis of "viral myocarditis" remains uncertain in most cases, despite varied efforts to obtain diagnostic criteria and techniques. The combination of virological, histological and immunohistological data may offer an opportunity to improve diagnosis. The pathophysiological processes which are involved in the transition from myocarditis into dilated cardiomyopathy are still unclear. A variety of new data point out that viral infection induces a loss of self-tolerance and subsequent autoaggression towards myocardial structures. The management of viral myocarditis remains problematic and a specific form of therapy still does not exist. Studies on immune suppressive therapy are contradictory. Moreover, in these studies the diagnostic criteria were non-uniform and the number of patients was low. Nevertheless, immune suppressive therapy can be very effective in individual cases. But until now, a clear decision cannot be made on the selection of those patients who would respond favourably to immune suppressive therapy. Only controlled studies which consider the aetiology, the grade of clinical severity, the duration of clinical symptoms, the degree of cellular infiltration, and the histological alterations may answer the questions concerning the benefit of immune suppressive therapy for viral myocarditis and its sequelae. Until these studies are available, the general implementation of immune suppressive therapy in viral heart disease should not be recommended, especially in view of the incidence of side effects.
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PMID:[Viral myocarditis--new aspects of pathomechanisms, diagnosis and therapy]. 307 Sep 64

Our experience with the use of five new antiarrhythmic drugs for treating life-threatening arrhythmias in children will be briefly reviewed. Prevention of recurrent episodes of atrial flutter with digoxin and local anesthetic antiarrhythmic drugs often is only moderately successful, benefiting 65% of patients. Amiodarone is particularly useful for those patients who cannot be controlled on this regimen. We caution that the heart rate be monitored carefully when therapy with amiodarone is initiated in patients likely to have sick sinus syndrome. We have found mexiletine useful for controlling significant ventricular arrhythmias in patients with congenital heart disease. Likewise, 79% (11 of 14) of patients with ventricular tachycardia treated with amiodarone were well controlled. However, the range of disease categories (congenital heart disease, myocarditis, cardiomyopathy) in which amiodarone is effective is much broader than for mexiletine. Although other investigators have used amiodarone successfully for controlling supraventricular tachycardia in the Wolff-Parkinson-White syndrome or secondary to concealed accessory AV connections, we recommend surgical ablation. Propafenone has significantly improved our ability to control postoperative JET. Although JET is self-limited in duration and spontaneously remits, it frequently produces life-threatening hemodynamic compromise in the postoperative setting. Propafenone slows the ventricular rate into a range in which AV sequential pacing may be instituted. Generally, after 24 to 72 hours, the patient may be quickly weaned from propafenone. Chronic incessant supraventricular tachycardia (SVT) is frequently associated with a dilated cardiomyopathy. The two most common mechanisms of incessant SVT are PJRT and AET. We have found encainide and ethmozine extremely effective in suppressing tachycardia episodes in PJRT and AET, respectively. Medical therapy has been associated with few side effects.
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PMID:Newer antiarrhythmic drugs in children. 309 60

Twenty-seven patients (15 men, 12 women; mean age 48.9 years) suffering from ventricular tachycardia (VT) (n = 30) were studied by radionuclide angiocardiography with Fourier phase analysis, both in sinus rhythm and during tachycardia. VT was spontaneous, electrically inducible, sustained, haemodynamically stable and monomorphous, with a mean rate of 174 beats/min (range: 115-260 beats). Heart diseases responsible for VT were: non-obstructive cardiomyopathy (n = 7), hypertrophic cardiomyopathy (n = 1), ischaemic heart disease (n = 5), probable right ventricular arrhythmogenic dysplasia (n = 4), congenital left ventricular aneurysm (n = 2), sequela of myocarditis (n = 2) and aortic valve regurgitation (n = 1); no heart disease was detectable in 5 patients. On surface electrocardiogram there was good concordance between the initial radionuclide site of VT activation and the configuration and electrical axis of QRS. At Fourier phase analysis all 17 VT of the right lag type originated in the left ventricle, arising from the apical septum (n = 7) or lateral segment (n = 2) in case of left axis, from the basal segment (n = 6) or the lateral segment (n = 1) in case of vertical or right axis, and from the middle left septum (n = 1) in case of normal axis. Nine VT of the left lag type originated in the right ventricle, arising from the basal septum or the latero-basal region in case of vertical or right axis (n = 6), from the apical septum or the inferior-apical region in case of left axis (n = 2) and from the middle septum in case of normal axis (n = 1). Four of our patients (3 with coronary disease and 1 with congenital left ventricular aneurysm) had VT of the left lag type and an initial radionuclide site of activation in the middle part of the left septum in case of left axis (n = 2) and in the basal part of that septum in case of right axis (n = 2). Seven patients were operated upon for recurrent VT: 4 had intra-operative mapping which in every case confirmed the results of radionuclide angiocardiography, a method which in the other 3 patients was the only surgeon's guide. Correlations between the site of origin of VT at radionuclide mapping and kinetic abnormalities visualized at radiological angiography and gamma-ray angiocardiography were common in our study. In one of our patients the same lesion gave birth to 2 VT of different morphologies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Isotope angiocardiographic study of 30 cases of ventricular tachycardia with Fourier phase analysis]. 313 7

The indications for endomyocardial biopsy were evaluated from 116 consecutive cases. The diagnostic value of this invasive but well tolerated procedure was in agreement with data from the literature. An accurate diagnosis, unforseeable in 8% of the patients, was established in 12%. The diagnosis of apparently primary myocardiopathy with ventricular dilatation was confirmed in 45 out of 59 cases; there were 3 cases of myocarditis, 3 cases of restrictive cardiopathy (haemochromatosis, fibroplastic endocarditis) and 1 case of hypertrophic cardiopathy. No tissue abnormality was noted in 6 cases. An accurate diagnosis was obtained by biopsy in 1 case of "eosinophilic lung" without overt cardiac involvement. In malignant diseases treated with anthracyclines in doses reaching maximal theoretical total dosage (30 patients), severe tissue lesions were present in 10% of the cases, incipient haemochromatosis in 16.6% and subendocardial fibrosis in 3.3%. However, total doses of up to 600 mg/m2 could be administered to 90% of the patients. Myocardial lesions could be demonstrated in 1 of 2 patients with collagen disease. Endomyocardial biopsy therefore seems to be justified in myocardiopathies with ventricular dilatation, in some collagen diseases with a tendency to cardiac involvement and to monitor treatment with anthracyclines in total doses higher than the theoretical maximum dosage.
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PMID:[Right intraventricular biopsy. Indications and results. 116 cases]. 315 91

In order to study the etiologies and mechanisms in sports-related sudden death, the author selected 198 cases from the world literature which met the following criteria: subjects were less than 40 years of age and in good physical condition, death occurred at the latest 1 hour after the physical activity, there was no known heart disease, and an autopsy had been performed. In spite of the heterogeneous character of those subjects included in this study and numerous biases, the following results were obtained: in some cases, the mechanism underlying the sudden death could be confirmed by autopsy (massive myocardial infarction, rupture of the aorta, cerebral hemorrhage), and in others it appeared highly probable (atheromatous or congenital coronary artery lesions, hypertrophic cardiomyopathies). Finally, in a certain number of cases, the observed abnormalities could only be seen as presumptive evidence (mitral prolapse, sequelae of myocarditis, or the presence of toxic agents). Failure to establish a precise diagnosis at autopsy occurred in only 22 cases (11%), however, amphetamine drug presence was discovered in 7 of these cases. Approximately one-half of the group studied revealed atheromatous coronary artery lesions (29% of cases) or congenital lesions (17.5%) especially involving the origin of the left coronary artery. These were followed in frequency by the hypertrophic cardiomyopathies. Mitral valve prolapse and WPW syndrome were rarely encountered. Extracardiac causes included rupture of the aorta (4.5%) and cerebral vascular accidents (5%).
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PMID:[Sudden death in athletes]. 315 27

Lyme disease has been recognized in humans since 1975 when it was associated with an outbreak of oligoarthritis in children in Lyme, Connecticut. Erythema chronicum migrans (ECM) is a clinical marker for the human disease, which usually appears within 3 to 32 days after an infected tick bite. Lyme disease is caused by spirochete, Borrelia burgdorferi, which is vectored by the hard ticks Ixodes dammini or Ixodes pacificus in the United States. In humans, Lyme disease has been found to cause a variety of clinical syndromes including cardiopathy, neuropathy, dermatopathy, and arthropathy. Human Lyme carditis is characterized by varying degrees of atrioventricular (AV) heart block that usually resolve regardless of therapy. Lyme disease has been reported in the dog as an arthropathy. This article reports a case of complete heart block and myocarditis in a dog with a positive titer for B burgdorferi, in which clinical and pathologic findings were similar to those seen in human Lyme myocarditis.
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PMID:Complete heart block in a dog seropositive for Borrelia burgdorferi. Similarity to human Lyme carditis. 322 8

From 1969 to 1973, 68 patients were admitted to the 4th Division of Medicine of the Brescia Civil Hospital with the diagnosis of viral myocarditis. The patients were divided into two groups according to the results of the Coxsackie virus complement fixing antibodies test: Group 1 (42 patients) with a fourfold or greater rising antibody titre; Group 2 (26 patients) with a negative serum test. Both groups were examined after a follow-up period of 15 years. Ten patients from Group 1 died. The diagnoses were chronic myocarditis (three cases); chronic cardiomyopathy-pulmonary embolism (one case); chronic cardiomyopathy-liver cirrhosis (one case); dilated cardiomyopathy-sudden death (two cases); congestive cardiomyopathy (three cases). No Group 2 patients died. The 15-year mortality rate of Group 1 was significantly higher than that of Group 2 (Fisher Test: p less than 0.005). In conclusion, the natural history of Coxsackie virus heart disease is characterized by two possibilities: a complete recovery from a clinical point of view, in some cases with only minor T wave abnormalities, or evolution into a chronic disease (dilated cardiomyopathy) having a high mortality rate within 10 years of the onset of the acute disease.
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PMID:Coxsackie virus heart disease: 15 years after. 322 24

Prevention of sudden arrhythmic cardiac death must be preceded by identification of the high-risk patient to whom appropriate therapy can be given. The most common disease state associated with sudden cardiac death is coronary artery disease. Factors which identify a high-risk subset include: left ventricular dysfunction; frequent and complex arrhythmias on Holter monitoring; abnormal signal-averaged electrocardiograms; angina, ST depression, and exertional hypotension or ventricular arrthythmias on exercise testing; inducible sustained arrhythmias at electrophysiologic testing, or a combination of these factors. Other conditions which are known to be associated with sudden death include: dilated or congestive cardiomyopathy, hypertrophic cardiomyopathy, mitral valve prolapse, valvular heart disease, Wolff-Parkinson-White syndrome, myocarditis, congenital heart disease, electrolyte abnormalities, long QT syndromes, proarrhythmic effects of drugs, and less common conditions such as myocardial tumors and pulmonary hypertension. If the primary abnormality responsible for the tendency toward arrhythmias cannot be corrected, appropriate therapy should be administered to attempt to reduce the patient's risk of sudden arrhythmic cardiac death.
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PMID:Definition of patients at high risk of sudden arrhythmic cardiac death. 327 Nov 94

Cardiac transplantation offers an excellent chance of long-term survival and functional rehabilitation for the carefully selected patient with end-stage heart disease. The part played by the pathologist in the care of these patients is crucial. It is vital to make the diagnosis of acute rejection before it becomes irreversible and also before it causes chronic damage to the coronary arteries. It is also vital that the pathologist does not either miss the diagnosis of an infectious myocarditis in the immunosuppressed patient or misdiagnose myocarditis as rejection, because the treatments for each one of these conditions are diametrically opposed. The role of the pathologist has become one of an important clinical colleague in the management and survival of patients with cardiac allografts.
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PMID:Cardiac transplantation. 327 11


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