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

Clinical studies were carried out during digoxin maintenance therapy to clarify three questions concerning digitalis therapy: optimal time for blood sample collection for serum digoxin concentration (SDC), the overlapping range of SDC levels in which some patients may be intoxicated while others are not, and both resistance and sensitivity of atrial fibrillation (AF) to digitalis. The SDC curve after a single dose of digoxin or beta-methyldigoxin shows the appropriate sampling time to be at least 12 hours after the administration. The optimal time is 24 hours. The overlapping SDC range was 1.7-2.7 ng/ml. There were significant differences in CTR and ventricular rates in AF between intoxicated and non-intoxicated groups. This suggests that susceptibility to digitalis increases with the severity of underlying heart disease. Precipitating factors such as CTR should be taken into consideration, if the SDC is in the overlapping level. Digitalis resistance occurs in 6.7% of 105 patients with AF, and more frequently in hypertensive heart disease than others. Digitalis sensitivity occurs more often in the elderly and in patients with dilated cardiomyopathy. But it is not necessary to attain higher therapeutic levels for AF than for sinus rhythm. Clearly optimal digitalis therapy for AF can be best accomplished when precise clinical findings, SDC and EKG recordings are carefully monitored and used to correct treatment.
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PMID:The problems of digitalis therapy from the viewpoint of serum concentration with special reference to the sampling time, to the overlapping range of serum concentration where intoxicated and non-intoxicated patients are located and to atrial fibrillation. 377 29

The clinical diagnosis of tricuspid regurgitation (TR) is often difficult. Two-dimensional pulsed Doppler echocardiography offers a sensitive and specific method for detecting and semi-quantitating tricuspid regurgitation. The clinical, radiographic, radionuclide, echocardiographic, and when available, the right cardiac catheterization findings were evaluated in 36 patients with a diagnosis of tricuspid regurgitation by pulsed Doppler. Ten healthy subjects served as controls. The underlying cardiac cause was rheumatic heart disease in 7 (20%), ischemic heart disease in 12 (33%), dilated cardiomyopathy in 5 (14%), hypertensive heart disease in 2 (5%), aortic valve stenosis and/or regurgitation in 3 (8%), mitral valve prolapse with mitral regurgitation in 1 (3%), and congenital heart disease in 6 (17%). Seven patients (19%) had a temporary or permanent transvenous right ventricular pacing wire. A systolic murmur was heard in 29 patients (81%) with 16 (46%) having an elevated jugular venous pressure. Tricuspid regurgitation was clinically suspected in only 2 patients (6%). Isolated tricuspid regurgitation was uncommon, seen in 6 patients (17%), and usually secondary to congenital heart disease, ischemic heart disease, with the use of a transvenous pacing wire and following mitral valve replacement. Right cardiac catheterization was performed in 10 patients, of which 7 demonstrated elevated right atrial and pulmonary artery pressure. Pulsed Doppler echocardiography offers a practical and accurate method of detecting and evaluating the severity of tricuspid regurgitation. Tricuspid regurgitation is generally a functional disorder, and frequently occurs in association with left sided valvular heart disease, cardiomyopathy or congenital heart disease.
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PMID:The clinical spectrum of tricuspid regurgitation detected by pulsed Doppler echocardiography. 390 35

Incidence and prognostic significance of repetitive ventricular premature contractions in various cardiac diseases were evaluated retrospectively with 593 consecutive patients referred for the 24-hour continuous electrocardiographic monitoring (Holter monitoring). Primary cardiac diagnoses for 308 patients with structural heart diseases included previous myocardial infarction (MI) in 151 patients, angina pectoris in 34, congestive cardiomyopathy (COCM) in 21, valvular heart disease in 29, hypertensive heart disease (HHD) in 18, conduction disturbance in 28, and other cardiovascular abnormalities in 17 patients. Other 285 patients (48%) had no known structural heart disease. Repetitive ventricular premature contractions (VPCs) was defined as the occurrence of self-terminating two (couplet), three (triplet) or more consecutive VPCs without associated hemodynamic sequelae. Holter monitoring was done with simultaneous two-channel recordings. Repetitive VPCs were seen in 96 patients; 17% of patients with MI, 52% of COCM and 7% of no structural hart disease. Among 308 patients with structural heart disease, 91 had congestive heart failure and 42% of these had repetitive VPCs, whereas only 17% of patients without congestive heart failure had repetitive VPCs. Coronary arteriographic and ventriculographic findings were reviewed in 91 patients with previous MI. Neither the degree of coronary artery involvements nor left ventricular ejection fraction had influence on the occurrence of repetitive VPCs. Four hundreds and sixty-nine patients under the age of 69 years were followed from 6 to 36 months (mean 19 months). Thirteen patients including 5 cases with MI (4% of the cases with MI), 4 with COCM (21% of COCM) and 4 with other structural heart disease (4% of other disease) died suddenly in the follow-up period. In the patients followed, 72 had repetitive VPCs and 9 of them died suddenly. These 9 patients consisted of 4 patients with MI (25% of the cases with MI having repetitive VPCs), 4 with COCM (40% of COCM) and 1 with other structural heart disease (3% of other disease). Thus, patients with MI or COCM had higher incidence of repetitive VPCs and they are at a high risk for sudden cardiac death.
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PMID:[Incidence and prognostic implication of repetitive ventricular premature contractions detected by Holter monitoring (author's transl)]. 617 83

The preimplantation arrhythmias, coexistent medical conditions, the causes of death, and survival course are described for 399 patients who received their initial ventricular pacemaker implantation for a bradyarrhythmia (AV block, sinus node disease, and hypersensitive carotid sinus syndrome) at the University of Michigan from 1961 to 1979. Factors which correlated with a poor survival are elucidated. Survival for those with sinus node disease was virtually identical to those with AV block, with only 63% surviving over five years. Advanced age and congestive heart failure prior to implantation, and underlying ischemic or hypertensive heart disease portended a poorer survival in both groups. Patients with hypersensitive carotid sinus syndrome had a distinctly better prognosis--no deaths occurred until the eight year after pacing. Patients with no underlying heart disease and those with valvular disease did remarkably better than those with an ischemic or myopathic etiology. Apparent progression or complications of the underlying heart disease was the major cause of mortality. Sudden death, congestive heart failure, myocardial infarction, and major arrhythmias were the causes of death in 48% of those who died. Implications of improved pacing modalities on late complications and death are discussed.
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PMID:Symptomatic bradyarrhythmias in the adult: natural history following ventricular pacemaker implantation. 617 56

Massive cardiomegaly (heart weight above 400 g in females and 450 g in males) was studied in 26 Zambians examined post mortem. The aetiologies found were: hypertensive heart disease alone in six cases; hypertensive and alcoholic heart disease in two cases; alcoholic heart disease alone in five; alcoholic and pulmonary heart disease in one; alcohol with possible hypertensive heart disease in one. Eleven cases were classified as being idiopathic mainly due to lack of data and in five of these hypertension was suspected as being the cause. The series qualitatively represented the spectrum of non-rheumatic heart disease seen in patients admitted to the Central Hospital, Ndola, Zambia. Hypertension had a central role in the causation of massive cardiomegaly. Follow-up of several patients enabled observations on the cardiac effects of hypertension and alcoholism operating simultaneously and on the relationship between hypertension and congestive cardiomyopathy.
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PMID:Cardiomegaly in Northern Zambia: clinico-pathological observations. 622 32

The effects of long-term (mean 3.9 months) pharmacotherapy of hypertensive and normotensive hypertrophy (hypertensive heart disease, hypertrophic non-obstructive cardiomyopathy) as well as of advanced cardiac disease due to coronary artery disease and dilatative cardiomyopathy by large doses of nifedipine (mean 120 mg/day-1) were analyzed with regard to systolic blood pressure, to left ventricular function and to the hypertrophy degree of the ventricle. Nifedipine, in addition to conventional and maintained antihypertensive and cardiac therapy, lowers blood pressure in hypertensive patients, whereas hypotensive effects in the normotensive patients were absent. Nifedipine enhances left ventricular function in all patient groups significantly, i.e. in normotensive hypertrophic non-obstructive cardiomyopathy, in hypertensive heart disease and especially in heart disease due to coronary artery disease and dilatative cardiomyopathy. Significant regression of septal and of global hypertrophy was found in hypertrophic non-obstructive cardiomyopathy and in hypertensive heart disease. These results indicate, that long-term nifedipine treatment may be beneficial for left ventricular function in all patient groups and for hypertrophy regression in established left ventricular hypertrophy due to hypertrophic, non-obstructive cardiomyopathy and due to hypertensive left ventricular hypertrophy. It is concluded that long-term nifedipine treatment improves left ventricular function and leads to regression of established ventricular wall hypertrophy in hypertrophic non-obstructive cardiomyopathy and in hypertensive heart disease.
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PMID:Reversal of left ventricular hypertrophy and improvement of cardiac function in man by nifedipine. 624 3

While the current literature contains numerous studies and even more numerous assumptions linking aspects of the work setting, stress, and mortality; no systematic investigation has been made of possible patterns of stress-induced self-destructive behaviors among the work settings per se. This research paper attempts to help fill that gap by reporting on an analysis of data on industry, age and mortality rates for seven stress-related causes of death (suicide, homocide, hypertensive heart disease, cirrhosis of the liver, arteriosclerotic heart disease, ulcer of the stomach, and hypertension). Using available United States' mortality statistics, a consistent pattern is found for all of the stress-related types of deaths by industry and age. A suggested explanation of this pattern is based on status integration theory.
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PMID:Is work conducive to self-destruction? 717 4

Chronic atrial fibrillation is a very common arrhythmia affecting 2 to 4% of the population older than 60 years of age. Atrial fibrillation may cause disabling symptoms and serious adverse effects, such as impairment of cardiac function or thromboembolic events. It is also associated with an increased risk of death. In the past, the most common underlying heart disease related to chronic atrial fibrillation was rheumatic heart disease. Today, this disease occurs relatively rarely. Nevertheless, the incidence of atrial fibrillation is likely to increase in the future due to the aging of the population, since its prevalence increases with age. In most patients with chronic atrial fibrillation, the arrhythmia can be attributed to organic heart disease or metabolic disorders. In western countries ischemic and hypertensive heart disease (including sick sinus syndrome) and alcohol (holiday heart syndrome) are numerically more important than the classical causes of atrial fibrillation--rheumatic heart disease and thyrotoxicosis--which are declining in incidence. Overall, atrial fibrillation is associated with an increased mortality. In about 15% of patients with chronic atrial fibrillation, no underlying cardiac or metabolic abnormality can be found, also the arrhythmia can itself give right to atrial dilatation. Atrial fibrillation consists most probably of several coexisting reentrant wave fronts of activation within the atria. Atrial activation and atrial fibrillation is as follows: multiple wavelets sweep round the atria in irregular, shifting patterns; completed reentrant circuits are the exception. Atrial flutter in its common form is characterized by evidence of atrial activity at a rate of 250-350 bpm, and usually almost exactly 300 bpm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Atrial fibrillation and atrial flutter: pathophysiology and pathogenesis]. 784 37

In order to determine whether changes in myocardial perfusion can be assessed by myocardial contrast echocardiography, intracoronary injections of 2 ml of sonicated iopromid were performed before and 30 to 45 s after application of papaverine in 31 patients (mean age 58 years). 13 patients showed coronary artery disease (KHE), 6 patients hypertensive heart disease (HHE), and 12 patients had no proven heart disease (KTR). Contrast decay-halftime (T/2), maximal video-intensity (Imax) and area under the curve (Area) were derived by computer-assisted videodensitometry. After papaverine KTR showed a significant increase of T/2 (from 5.1 +/- 1.5 to 6.8 +/- 3.2 s, p < 0.05), of Imax (from 36 +/- 13 to 52 +/- 16 E, p < 0.002) and of Area (from 203 +/- 95 to 379 +/- 188 E*s, p < 0.002) compared to baseline values. In this group the ratios of hyperemia to baseline flow conditions were 1.5 +/- 0.4 (from 1.0 to 2.4) for Imax and 1.9 +/- 0.9 (from 1.1 to 3.9) for Area. In HHE and KHE, hyperemia induced no significant changes of T/2, Imax and Area. Heart rate was increased by 4.3% and mean aortic pressure was decreased by 6.2% in all groups after papaverine. Double-product was not altered significantly in any group. Myocardial contrast echocardiography revealed a significant increase in variables of contrast wash-out curves only in patients without proven heart disease. In contrast, no relevant changes of T/2, Imax and Area on average were observed in patients with coronary and hypertensive heart disease. Thus, myocardial contrast echocardiography seems to be suitable to document a reduced papaverine vasodilator response in these patients.
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PMID:[Contrast echocardiography in the evaluation of myocardial flow reserve]. 814 54

The heart is of great importance in systemic hypertension; it has a role in its pathogenesis but also suffers its consequences. Heart disease is, therefore, often found in hypertensive patients. Patients with hypertension may develop left ventricular hypertrophy, cardiac failure and atherosclerotic vascular problems, such as coronary artery disease, as well as strokes and peripheral vascular disease. There have been a great many advances in our understanding of the pathogenesis of hypertensive heart disease as well as its epidemiology over the last decade and these are reviewed briefly here.
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PMID:Hypertension and the heart. 820 60


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