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

"Cardiomyopathy", a term formerly used for heart muscle disease of unknown aetiology, is at present applied to all myocardial diseases other than coronary-heart disease. This definition includes many different forms of metabolic disorders of heart muscle. Four manifestations of metabolic myocardial disease, differing in their aetiology and pathogenesis are distinguished: (1) "transport" myocardosis, (2) "arthrocytotic" myocardosis, (3) myocardia, and (4) idiopathic cardiomyopathy. They are differentiated by combined morphological and quantitative mineral examination. "Transport" myocardosis is the most common form and its particular aetiology can be further specified. Cause of death in patients with metabolic disorders often remains undiscovered even at autopsy. Combination of histological and quantitative mineral analysis of myocardium can further define the particular form.
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PMID:[Myocardosis - myocardia - cardiomyopathy (author's transl)]. 94 24

The purpose of this study was to clarify certain electrovectorcardiographic aspects suggestive of heart disease associated with W-P-W syndrome. Seventy-six vectorcardiograms with W-P-W features were analyzed. The curves were obtained by Grishman's cube system and in 8 cases by Frank's method, as well. In addition, the conventional electrocardiograms corresponding to 55 vectorcardiograms, were studied. Not all the electrocardiographic and vectorcardiographic tracings were recorded simultaneously. The W-P-W syndrome was classified as type A when the electrical records suggested a pre-excitation phenomenon in the left postero-superior septal mass, probably with a partial "wave jumping" toward the right anterior septal mass. The W-P-W syndrome was judged to be of type B when the electrical tracings showed a pre-excitation in the right anterior septal mass, probably with a partial "wave jumping" toward the left posterior septal mass. The results of this study permit the following conclusions: 1. It seems justified to assert that the calssification of the W-P-W syndrome must be realized deductively on the basis of the sequence of the ventricular activation and of the heart position. 2. An interval of 30 msec. or more between the end of initial slurring and the vertex or middle point of the R loop permits inferring the coexistence of left ventricle hypertrophy. 3. The presence of an inactivable zone due to myocardial infarction should be suspected on the basis of segmentary irregularities or distortions of the electrical curves, while extensive deformations are more suggestive of myocardiopathy. 4. The duration of terminal slurrings does not depend on that of the initial ones. However, when the initial slurrings are very prolonged, the terminal ones are relatively short. 5. In the presence of W-P-W syndrome, the primary ventricular repolarization changes cannot be considered as pathognomonic of any associated cardiopathy because they are often provoked by drugs.
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PMID:[Observations on varions electrovectocardiographic aspects of the W-P-W syndrome]. 98 54

This report details our total experience with documented chronic His bundle block in 24 patients. Ten patients had second-degree block (eight with 2:1 block and two with type-1 block), and 14 patients had complete heart block. There were 16 women (67 percent) and eight men (33 percent) with ages ranging from 17 to 87 years. Diagnoses were as follows: hypertensive cardiovascular disease, nine patients (38 percent); arteriosclerotic heart disease, six patients (25 percent); aortic valvular disease, three patients (13 percent); primary conduction disease, two patients (8 percent); primary myocardial disease, two patients (8 percent); congenital heart block, one patient (4 percent); and traumatic heart block, one patient (4 percent). Pacing was instituted in 20 patients because of the following; congestive heart failure, seven patients; syncope, seven patients; fatigue, four patients; and recurrent dizziness, two patients. Permanent pacing was indicated within ten days of initial diagnosis in 13 patients, from 20 to 80 days in four patients, and later than 100 days in three patients. An additional two asymptomatic patients were treated with prophylactic pacing.
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PMID:The clinical spectrum of chronic His bundle block. 100 Oct 51

Relative Cross-sectional area Differences (RCD) and Relative mean Velocity of Contraction (RVC) are easily, quickly and precisely determined by means of impulse-reflected ultrasound. They were recognized to be highly invariant under physiological conditions and thus were considered as sensitively regulated heart-dynamic-parameters. (his paper reports about a total of 395 examinations on patients with myocardial disease and on normal subjects. Various pathogenic factors are included excepting patients with myocardial infarction. In all subgroups there is a decrease of RCD and RVC with increasing degrees of cardiac disease. Correlating the angiocardiographically determined left-ventricular ejection fraction with both parameters, they show a significant linear relationship. Even in clinically latent myocardial disease the echocardiographic parameters are defnitely reduced. Small changes of myocardial function, e.g. under digoxin and in different degrees of uremic heart disease with uremic cardiomyopathy, can be recognized by RCD and RVC under exclusion of extracardiac factors. Physical tests during exercise confirm the observed trends. The typical changes of the echocardiographic parameters in myocardial disease, permitting a sharp discrimination of pathologic values with their small physiological variability, identify RCD and RVC as sensitive parameters of the mechanical function of the myocardium in the range of validity that was examined. The described properties and the lack of discomfort to the patient suggest a number of important indications of this method.
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PMID:[Heart diagnostics using M-mode echography. Continuing registration of transverse internal left ventricular diameters. II. Determination in patients with myocardial insufficiency with special reference to ischemic heart disease]. 100 90

Recently disorders of sinus node function have found increasing interest in clinical medicine thanks to new diagnostic and therapeutic developments. This paper represents a comprehensive review of these conditions, combined under the name "Sick Sinus Syndrome" (SSS). Besides a detailed analysis of 63 cases seen at our institution, the results of other groups are compared and extensively discussed. The clinical picture of the SSS is characterized by a wide variety of bradycardiac and tachycardic atrial arrhythmias, occurring separately or in combination. These can be classified in three subgroups: Patients with exclusive sinus bradycardia; patients with sinoatrial exit block or transient episodes of sinus arrest with or without AV escape rhythms; and finally patients with the bradycardia/tachycardia-syndrome, which are complicated by additional atrial tachyarrhythmias. The symptomatology of the SSS is multiform and extends from symptomless cases and those with only general signs of reduced cardiac function to patients with recurrent severe syncopal attacks which may lead to cerebral damage and even death. Besides the typical history, the diagnosis of the SSS primarily rests upon the ECG, especially the long term ECG recorded continuously on a 24 hrs. tape (Holter technique). Also the exercise ECG is of some value, characteristically showing an inadequate increase in the sinus rate, sometimes with AV escape systoles and -rhythms. In addition various provocative tests have been devised which are of help to differentiate between a pathologic and a normal sinus node function. Among these the determination of the sinus node recovery time following overdrive atrial pacing has gained wide acceptance. In most cases the exact etiology of the SSS is not known. In addition to coronary and inflammatory heart diseases a primarily degenerative lesion of the sinus node, comparable to cases with "primary heart block" are discussed. There is also a remarkably frequent past history diththeria. Rarer causes of the condition represent cases with cardiomyopathy, thyreotoxic heart disease, collagen and other disorders and also a familial manifestation of the SSS has been described. Therapeutically, pharmacologic treatment with vagolytic, beta-adrenergic or the common antiarrhythmic drugs is often unsuccessful, especially in the treatment of the Brady-Tachy-Syndrome. Digitalis glycosides, however, are frequently of some value, as they represent an effective prophylactic agent against atrial tachyarrhythmias without prolonging the sinus node recovery time or reducing significantly the sinus rate. While a few patients do not require any treatment, an artificial cardiac pacemaker has to be inserted in most cases. Atrial stimulation may be superior to ventricular on-demand pacing in some patients, and also a special system for the treatment of the SSS combined with significant AV block (binodal disease) has been designed, the bifocal sequential pacemaker.
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PMID:[Sinus node syndrome]. 109 30

Bipolar electrode catheter recordings of His bundle electrograms with three simultaneously recorded surface electrocardiographic leads were obtained from 30 pediatric and adolescent patients (aged 3 to 18 years). In 14 patients, cardiac murmurs were proved to be innocent by cardiac catheterization. The control conduction intervals were compared to those of 13 patients with congenital heart disease, and three with acquired heart disease (myocardiopathy, rheumatic valvular disease, and Friedreich's ataxia). P-R, intra-atrial (P-A), A-V nodal (A-H), and intraventricular (H-V) conduction intervals were measured to the nearest 5 msec. Conduction delays were analyzed in each of the three components of the P-R interval. These delays occurred both in single components of the system as well as in combined conduction delays and were not always demonstrable by surface electrocardiograms. The Wenckebach phenomenon induced by atrial pacing was localized to the A-V node as well as the His-Purkinje system. This technique of intracardiac electrogram recordings is safe, does not significantly prolong cardiac atheterization time, and often yields unique and useful data concerning A-V conduction.
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PMID:A His bundle electrocardiographic analysis of cardiac conduction in the pediatric and adolescent patient. 111 61

Out of a pacemaker population of 392 patients, 90 (23%) have been found to have sinoatrial syndrome. Their ages ranged from 22 to 86 years, and averaged 66 for men and 70 for women. The male-to-female ratio was 1:1.6. Before pacemaker implantation, syncopal attacks had occurred in 54%, dizziness without syncope in 31% and tachyarrhythmias in 57%. Atrial or paroxysmal supraventricular tachycardia had been recorded in 33%, atrial fibrillation or flutter in 28%, and ventricular tachycardia in 11%. First and/or second degree AV block was found in 36%. Coronary heart disease was present in 61% and 20% had had myocardial infarction. Cardiomyopathy and previous carditis were other associated heart diseases. Sinoatrial syndrome was the only manifestation of heart disease in 20%. Follow-up time after pacemaker implantation ranged from 3 months to 7 years, mean 23 months. Syncopal attacks were stopped in 48 of 49 patients, dizziness was relieved in all 28 patients and tachyarrhythmias were controlled by combined drug treatment in 43 of 51 patients. Nineteen patients died during the follow-up, most of them of cerebrovascular events or myocardial infarction. Associated coronary heart disease was especially frequent in this group. The death of one patient was caused by a run-away pacemaker. Other pacing failures were due to electrode movement or premature battery exhaustion. There was no mortality associated with pacemaker implantations or replacements. These results strongly support the view that pacemaker treatment most effectively controls symptoms of sinoatrial syndrome when drug treatment fails.
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PMID:Treatment of sinoatrial syndrome with permanent cardiac pacing in 90 patients. 119 8

Furazolidone (FZ) at 700 ppm was added to feed mixtures fed turkey poults two weeks posthatching to induce acute experimental cardiomyopathy. Poults in the control pen received the same ration but without FZ. Four of the control poults developed spontaneous round heart disease. From EKG data and blood samples obtained at weekly intervals, poults were selected for sacrifice at 5 weeks of age. Tissue samples from the left myocardial wall, liver, and pectoralis major and tibialis anterior muscles were analyzed for glycogen by biochemical assay. Blood glucose was determined with the Technicon autoanalyzer. Deposition of glycogen increased significantly (p less than 0.05) in the myocardium of all affected poults and in the liver of all FZ-treated poults. Glycogen levels of the pectoralis major and tibialis anterior muscles were not affected by FZ, but a significant increase (p less than 0.05) was apparent in the pectoralis major muscle of spontaneous round heart poults. It was concluded that FZ influences glycogen metabolism, probably by enzyme inhibition, and that it tends to magnify effects seen in the spontaneous round heart syndrome. Glycogen infiltration of tissues such as the heart and white skeletal muscle suggests that the round heart syndrome may be a manifestation of the glycogen storage disease, idiopathic generalized glycogenosis. Lack of significant differences in the blood serum glucose levels of all poults indicates that these levels are not a reliable clinical parameter for monitoring development of the round heart syndrome.
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PMID:Blood glucose and tissue glycogen levels in turkey poults with spontaneous round heart disease and furazolidone-induced cardiomyopathy. 120 Sep 48

Alcoholic subjects differ in the incidence of cardiomyopathy. Of potential variables, sex may be important since few females are seen with cardiomyopathy, even adjusting for the lower incidence of alcoholism. To examine this question, noninvasive systolic time intervals were measured in 22 males and 14 females of similar age, heart rate, and arterial pressure, without clinical evidence of heart disease or hypertrophy. Duration and intensity of ethanol intake and the interval from last drinking episode were apparently equivalent. In male alcoholics, the left ventricular preejection period and ejection time (PEP/LVET) ratio of 0.410 +/- 0.020 was significantly higher than in the 11 normal males (0.316 +/- 0.007) (P less than 0.001). In female alcoholics, the ratio was 0.322 +/- 0.015, compared to 0.310 +/- 0.01 for 11 normal females, and was significantly less than in the male patients (P +/- 0.001). In addition prolonged intraventricular conduction by high-frequency ECG was more prevalent in the male group. To further ensure equivalency of alcoholism, patients with biopsy-proved cirrhosis were selected. In nine males, PEP/LVET was significantly higher than in the 10 females. Thus, abnormal myocardial function was evident in males but not in females, suggesting that sex is a determinant of the toxic effects of ethanol on myocardium.
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PMID:Preclinical cardiomyopathy in chronic alcoholics: a sex difference. 125 24

In this review, the coronary haemodynamics of hypertrophic heart disease are discussed with reference to data published over the last 15 years. Coronary reserve is reduced in the presence of concentric cardiac hypertrophy, but is similar to normal in hypertrophic obstructive cardiomyopathy and aortic stenosis, despite marked left ventricular hypertrophy. A moderate decrease in coronary reserve is found in aortic incompetence and in dilated essential hypertension. In hypertensive heart disease, improvement in coronary reserve can be achieved by long-term vasodilator therapy.
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PMID:Left ventricular hypertrophy, myocardial blood flow and coronary flow reserve. 130 Dec 55


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