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

Eight patients had cardiac manifestations that were life-threatening in five while taking psychotropic drugs, either phenothiazines or tricyclic antidepressants. Although most patients were receiving several drugs, Mellaril (thioridazine) appeared to be responsible for five cases of ventricular tachycardia, one of which was fatal in a 35 year old woman. Supraventricular tachycardia developed in one patient receiving Thorazine (chlorpromazine). Aventyl (nortriptyline) and Elavil (amitriptyline) each produced left bundle branch block in a 73 year old woman. Electrocardiographic T and U wave abnormalities were present in most patients. The ventricular arrhythmias responded to intravenous administration of lidocaine and to direct current electric shock; ventricular pacing was required in some instances and intravenous administration of propranolol combined with ventricular pacing in one. The tachyarrhythmias generally subsided within 48 hours after administration of the drugs was stopped. Five of the eight patients were 50 years of age or younger; only one clearly had antecedent heart disease. Major cardiac arrhythmias are a potential hazard in patients without heart disease who are receiving customary therapeutic doses of psychotropic drugs. A prospective clinical trial is suggested to quantify the risk of cardiac complications to patients receiving phenothiazines or tricyclic antidepressant drugs.
Am J Cardiol 1976 Feb
PMID:Electrocardiographic changes and cardiac arrhythmias in patients receiving psychotropic drugs. 0 4

Red cell volume reduction corrected the platelet aggregation abnormality and bleeding tendency in four boys, aged 5 to 16 years, with severe cyanotic congenital heart disease and polycythemia. Red cell volume was reduced by replacing 15 to 20 ml/kg body weight of the patient's blood with plasma in 50 ml increments over a 1 to 2 hour period. Within 3 days, platelet aggregation was restored essentially to normal, and previous bleeding symptoms disappeared. Platelet aggregation remained normal during 3 weeks of follow-up study and hematocrit values remained at palliative levels. The procedure was safe and simple, and it had beneficial effects not only on bleeding but also on other symptoms related to polycythemia. These preliminary observations suggest that red cell volume reduction may be useful preoperatively in patients with cyanotic heart disease and defects in platelet function to lessen the risk of serious bleeding during the early postoperative period. Palliation in severely cyanotic children whose condition is inoperable is another possible indication for this procedure.
Am J Cardiol 1975 Jun
PMID:Correction of platelet dysfunction and bleeding in cyanotic congenital heart disease by simple red cell volume reduction. 4 35

Ambulatory 24 hour electrocardiographic monitoring was performed in 124 patients before cardiac catheterization and coronary angiography. Ventricular premature beats were demonstrated in 83% of all patients. Ectopic activity persisted for at least 3 of the 24 hours in 75% of the 84 patients with coronary heart disease, 61% of 28 with other heart disease and in 24% of 12 normal subjects. The prevalence and grade of ventricular premature beats were increased in the 57 patients with multivessel disease compared with values in the 27 patients with one vessel disease (P less than 0.01). Findings in the latter group did not differ from those of normal subjects. The presence of elevated left ventricular end-diastolic pressure of asynergy was associated with increased ventricular ectopy. Of 15 patients having both asynergy and elevated left ventricular end=diastolic pressure (more than 19 mm Hg), 40% had paroxysms of ventricular tachycardia and 67% had coupled beats; these findings were present in 6 and 12%, respectively, of the 34 patients without asynergy or pressure abnormality (P less than 0.005). Repeat monitoring performed in 65 patients demonstrated greater reproducibility of advanced grades of ventricular premature beats among those with the most severe lesions. For the individual patient the prevalence and grade of ventricular ectopy may not always correlate with the severity of coronary artery disease or degree of left ventricular dysfunction.
Am J Cardiol 1977 May 04
PMID:Ventricular premature beats and anatomically defined coronary heart disease. 6 91

This review describes the evolving concepts of diagnosis and management of patients with cyanotic congenital heart disease. Early palliative surgical procedures were followed by reparative operations and are now to a large extent replaced by these operations which are designed to relieve the problem. Collaboration of the team of cardiologists, surgeons, radiologists, anesthesiologists and nurses has made the many developments possible. The teamwork has not only widened the scope of what can be accomplished but has also extended the opportunities for beneficial reparative surgery down to the first weeks and months of life. Precise diagnosis and meticulous operative and perioperative care by the team are essential elements of success. Long-term follow-up and regular analyses of results have led to continuing improvements. Although these patients were born to be blue, their color and their outlook have been changed during these last 3 decades to something close to rosy.
Am J Cardiol 1976 Feb
PMID:Cyanotic congenital heart disease. 12

The extent and rate of left ventricular wall thickening during systole has previously been shown to be a useful measure of regional ventricular function and to play an important role in the ejection of blood from the left ventricle. The relation among systolic wall thickening, the directional components of contraction, ejection fraction and force velocity measurements is therefore of interest in understanding the dynamics of contraction of the intact ventricle. This report describes a theoretical basis and method for using ventricular angiograms to quantify the separate contributions of longitudinal shortening, circumferential shortening and systolic wall thickening to overall ventricular performance in man. One hundred twenty-two patients with valvular, coronary or myocardial heart disease were studied with biplane angiocardiography during diagnostic cardiac catheterizations. The percent contribution of directional components to total work or power developed by a mid-wall equatorial element of myocardium was shown to be: longitudinal, 14 percent in normal and diseased ventricles; circumferential, 45 percent in normal, increasing to 55 percent in dilated ventricles (P less than 0.005); wall thickening, 40 percent in normal, decreasing to 31 percent in dilated ventricles (P less than 0.001). Thus, left ventricular contraction, which is expressed as systolic wall thickening, quantified separately from inward wall displacement due to mid-wall circumferential shortening, accounts for nearly half of segmental left ventricular work and power. The rate and extent of ventricular wall thickening correlated closely with ejection fraction (r = 0.92 and 0.95, respectively) and with velocity of circumferential shortening (r = 0.90 and 0.80, respectively). Previous models of ventricular and myocardial mechanics that include computations of mid-wall longitudinal and circumferential stress and strain do not appear to account for the large contribution of systolic wall thickening to the performance of the intact heart. Force-velocity relations as heretofore described may therefore be partial descriptors of myocardial function in the intact ventricle.
Am J Cardiol 1976 Sep
PMID:Analysis of wall dynamics and directional components of left ventricular contraction in man. 13 32

Left ventricular diastolic compliance is determined by the level of operating pressure and the diastolic pressure-volume relation. This relation is curvillinear and the slope of a tangent (operative chamber stiffness) to the pressure-volume curve increases as the chamber progressively fills. Such preload-dependent changes in compliance occur during any acute alteration in ventricular volume. At a given diastolic pressure, operative chamber stiffness (or its reciprocal, operative chamber compliance) is determined by the relative values for ventricular volume and muscle mass and by the stiffness of a unit of myocardium. Thus, there may be a leftward shift of the diastolic pressure-volume curve (increase in the modulus of chamber stiffness) as a consequence of ventricular hypertrophy or an increase in the stiffness of heart muscle itself (increase in modulus of muscle stiffness). To distinguish between hypertrophy and stiff muscle, it is useful to examine the modulus of chamber stiffness, derived from pressure-volume data, together with the volume/mass ratio of the ventricle. In this fashion, changes in the modulus of chamber stiffness that are inappropriate for a given volume/mass ratio may be attributed to changes in the material properties of the heart muscle. Examples of clinical and experimental pressure-volume studies are presented to illustrate the variety of mechanisms by which acute and chronic changes in ventricular chamber compliance evolve during the course of clinical heart disease. The pathophysiology of pulmonary congestion is best understood by considering the factors responsible for producing changes in chamber stiffness of the ventricle, whereas an examination of muscle stiffness is likely to provide more insight into the extent of irreversible functional and structural defects of the myocardium.
Am J Cardiol 1976 Nov 04
PMID:Left ventricular compliance: mechanisms and clinical implications. 13 86

Echocardiography was used to evaluate the heart in 19 patients with one of various systemic diseases known to be associated with infiltrative cardiomyopathy. Four patients had systemic amyloidosis, 10 had idiopathic hypereosinophilia and 5 had iron overload caused by multiple blood transfusions. Although 10 patients (53 percent) had no clinical evidence of cardiac disease, all 19 had echocardiographic abnormalities; the left ventricle was symmetrically thickened (more than 11 mm) and left ventricular mass was increased (more than 275 g) in all; the left ventricular transverse dimension was modestly increased (more than 52 mm) in 5 patients (26 percent) and the velocity of mitral valve closure in early diastole was reduced (less that 60 mm/sec) in 5 patients. Systolic function, as evidenced by ejection fraction, was well maintained (greater than 60 percent) in 18 of 19 patients. Thus, it appears that echocardiographic abnormalities can be detected in many patients with a systemic disease associated with infiltrative cardiomyopathy even before clinically evident heart disease develops.
Am J Cardiol 1977 Feb
PMID:Echocardiographic observations in patients with systemic infiltrative disease involving the heart. 13 57

The mechanism of the electrocardiographic pattern termed left atrial enlargement was evaluated in 21 patients. Left atrial size and pressure as well as interatrial conduction were correlated with electrocardiographic left atrial enlargement using echocardiography, mean pulmonary capillary wedge pressure and activation time from the P wave to the coronary sinus. In the group as a whole only prolongation of interatrial conduction time was consistently related to the electrocardiographic pattern of left atrial enlargement; left atrial size or pressure was not predictably abnormal in patients with this pattern. Five patients had neither elevation of pulmonary capillary wedge pressure nor echocardiographic evidence of an enlarged left atrium. When the etiologic type of heart disease was analyzed, an enlarged left atrium correlated with electrocardiographic left atrial enlargement only in patients with rheumatic mitral valve disease (eight of nine patients). Elevated pulmonary capillary wedge pressure correlated with electrocardiographic left atrial enlargement in all four patients with cardiomyopathy. In patients with coronary artery disease the electrocardiographic pattern was unrelated to either left atrial pressure or volume overload. Thus, the electrocardiographic pattern termed left atrial enlargement appears to represent an interatrial conduction defect that can be produced by a variety of factors.
Am J Cardiol 1977 Jun
PMID:Electrocardiographic left atrial enlargement. Electrophysiologic, echocardiographic and hemodynamic correlates. 14 Dec 2

Electric and mechanical atrial paralysis is a condition usually associated with a primitive or secondary cardiopathy. Only extremely rare cases are characterized by early appearance in young subjects without evidence of cardiac disease of any kind whatever, without character of familiarity, with atrial paralysis being the only abnormality, and are thus defined as idiopathic atrial paralysis. One of these cases (the eighth in the literature, to our knowledge), presented with a complete study and the hypothesis that "chronic idiopathic atrial paralysis" and "idiopathic right atrial enlargement" (sometimes associated, as in this case) may be different manifestations of the same chronic myocardial disease.
G Ital Cardiol 1977
PMID:["Idiopathic" chronic paralysis and dilatation of the right atrium]. 14 89

This report reviews morphologic aspects of pericardial heart disease. A morphologic classification for this condition is presented. An ideal classification of pericardial heart disease obviously would take into account clinical, etiologic and morphologic features of this condition but a single classification combining these 3 components is lacking. Pericardial heart disease is relatively uncommon clinically and when present at necropsy it usually had not been recognized during life. The term "pericarditis" is inaccurate because most pericardial diseases are noninflammatory in nature. Morphologically chronic pericardial heart disease may present clinically as an acut eillness. Even when clinical symptoms are present, however, fewpatients develop evidence of cardiac dysfunction (constriction). When pericardial "constriction" occurs, it is the result of increased pericardial fluid or increased pericardial tissue or both. Increased fluid is treated by drainage; increased tissue is treated by excision. In most patients with chronic constrictive "pericarditis," the etiology is not apparent even after histologic examination of pericardia.
Curr Probl Cardiol 1977 Jun
PMID:Pericardial heart disease. 14 12


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