Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the efficacy, plasma drug concentrations and adverse effects of a new sustained release preparation of procainamide, 33 patients with heart disease were studied in an acute dose-ranging protocol and a chronic treatment protocol. Patients initially received a daily dose of 3 g of sustained release procainamide; this dose was increased by 1.5 g daily until ventricular premature depolarizations were suppressed by 75 percent or more, adverse drug effects occurred or a total daily dose of 7.5 g of sustained-release procainamide was reached. Twenty-five patients (76 percent) had at least a 75 percent reduction (range 75 to 100percent [mean +/- standard deviation 91 +/- 8.2]) in ventricular permature depolarization frequency at a dosage of 4.8 +/- 1.46 g/day (range 3.0 to 7.5). Despite the 8 hour dosing interval, the variation between maximal and minimal plasma procainamide and N-acetylprocainamide concentrations under steady state conditions was very small. Mean maximal procainamide and N-acetylprocainamide plasma concentrations were 10.4 +/- 6.02 and 12.0 +/- 7.40 micrograms/ml, respectively. The respective mean minimal concentrations were 6.8 +/- 4.50 and 8.7 +/- 5.99 micrograms/ml. In nine patients (27 percent) treatment with sustained release procainamide resulted in conversion of the antinuclear antibody test from negative to positive. Adverse drug effects occurred in 17 (52 percent) of the subjects. In general, adverse effects were minor and abated within 24 hours after administration of the drug was stopped. One patient had the procainamide-induced systemic lupus erythematosus-like syndrome.
Am J Cardiol 1980 Nov
PMID:Efficacy, plasma concentrations and adverse effects of a new sustained release procainamide preparation. 615 83

Cardiovascular manifestations of Systemic Lupus Erythematosus (SLE) in 32 unselected patients, with active disease were reviewed. Primary cardiac disease manifested as pericarditis (22%), myocarditis (16%), and valvular disease (9%), was recognized along with secondary disease as heart failure with or without systemic hypertension. Comparison with previous work by others, suggest that our cases are more representative of actual clinical picture of cardiac SLE. It is interesting to notice tht 9% of our patients had valvular disease, and this alteration is only occasionally found in other Hospitals. Valvular disease is rarely noticed during life, although is highly prevalent in autopsy series. We stress the diagnosis and management of the cardiac manifestations of SLE, in order to lower the morbidity and mortality of this condition.
Arch Inst Cardiol Mex
PMID:[The heart in systemic lupus erythematosus. Study in 32 non-selected patients (author's transl)]. 621 24

Tocainide, an oral analog of lidocaine, was evaluated as a long-term antiarrhythmic agent in 21 patients with symptomatic complex ventricular ectopic activity (10 with hemodynamically significant ventricular tachycardia) refractory to currently available antiarrhythmics singly, and in combination for periods of 3 days to 35 months (mean 13.6 months). Tocainide appeared to be an effective and safe agent for the control of these refractory symptomatic ventricular arrhythmias in 14 of the 21 patients (66%). Minor central nervous system and gastrointestinal side effects were present in most of the patients, usually early on in therapy, and only precluded long-term use in 2 patients. Furthermore, lidocaine responsiveness was a good predictor of tocainide effectiveness in this group of patients. Tocainide precipitated atrioventricular (A-V) block in one patient with pre-existing A-V nodal disease; two patients developed a skin rash while on tocainide therapy. These two patients had previously developed lupus-like syndromes and skin rashes while on procainamide. The ANA titers had been falling in these two patients while on tocainide, and in one of these patients with true systemic lupus erythematosus, rechallenge with tocainide failed to produce skin rash. Tocainide's long plasma half-life and high oral bioavailability permit an 8-h regime. We conclude that tocainide is an effective, safe antiarrhythmic agent with tolerable side effects.
Clin Cardiol 1983 Feb
PMID:Chronic tocainide therapy for refractory high-grade ventricular arrhythmias. 640 67

Invasive hemodynamic measurements were made in 10 supine patients with chronic refractory congestive heart failure (CHF) due to ischemic heart disease or cardiomyopathy before and after oral administration of a new arteriolar vasodilator, endralazine. In 9 patients, a 10 mg dose of endralazine produced maximal increases in cardiac and stroke volume indexes of 56 and 41%, respectively, with a 45% reduction in total systemic resistance. After a 5 mg dose of endralazine, cardiac index increased maximally by 38% and stroke volume index by 34%, with a 31% decrease in total systemic resistance. Mean arterial pressure decreased 11 +/- 4 mm Hg (mean +/- standard error of mean) with the 5 mg dose and 17 +/- 5 mm Hg after the 10 mg dose. There were no significant changes in the right atrial, pulmonary arterial, or pulmonary capillary wedge pressures. After administration of a single dose of endralazine, statistically significant hemodynamic changes were observed from 1 to 8 hours with peak responses at 3 to 4 hours. These observations suggest that endralazine has hemodynamic properties similar to those of its structural analog, hydralazine. However, endralazine metabolism is largely independent of the patients' acetylator status, and no cases of systemic lupus erythematosus have been reported after long-term oral administration. These findings suggest that endralazine may be an efficacious drug that is potentially safer than hydralazine in the treatment of chronic CHF.
Am J Cardiol 1983 May 01
PMID:Acute hemodynamic effects of endralazine: a new vasodilator for chronic refractory congestive heart failure. 684 62

To clarify the clinical spectrum of coronary arterial abnormalities in systemic lupus erythematosus, the data were reviewed on six patients who had a diagnosis of lupus at ages 15 to 29 years and who had ischemic heart disease before age 35. Two patients had coronary arteritis diagnosed on postmortem examination. In a third patient alterations in coronary arterial anatomy occurred with angiographic improvement temporally related to the initiation of steroid therapy. The other three patients had severe diffuse atherosclerotic coronary disease that was identified in two at postmortem examination. In the third patient the course of the disease strongly suggested coronary atherosclerosis, and eventually coronary bypass grafting was performed for relief of angina. In summary, clinically important extramural coronary arteritis and atherosclerosis both occur, although rarely, in young patients with lupus. Coronary artery disease may occur with or without coexisting active extracardiac lupus manifestations. Short-term steroid therapy and follow-up angiography for those with angina and in whom coronary arteritis is suspected warrant consideration. When stable coronary arterial anatomy is demonstrated on follow-up angiography, management is determined by the patient's symptoms irrespective of the prior history of lupus and, if indicated, cardiac surgery for symptomatic relief can be safely performed.
Am J Cardiol 1982 Feb 01
PMID:Ischemic heart disease in systemic lupus erythematosus in the young patient: report of six cases. 697 69

Chloroquine is a drug used mainly as an anti-malaria agent with many other pharmacological properties. It was given to a patient with chorea and disseminated lupus erytematosus seeking the anti-inflammatory effect of the drug. The unexpected result on chorea hastened its use in 7 other patients with the same success. Chloroquine seems to be an effective drug for the relief of chorea. The mechanism of action is unknown.
Arch Inst Cardiol Mex
PMID:[Chorea and chloroquine. A new treatment for an ancient malady]. 732 46

A case is reported of a 29-year-old woman with systemic lupus erythematosus (SLE) who developed clinical manifestations of pulmonary hypertension at a time when other manifestations of SLE were quiescent. She had a restrictive ventilatory defect but clear lung fields on chest x ray. Cardiac catheterization revealed severe pulmonary hypertension. Calculated pulmonary vascular resistance fell slightly after administration of oxygen and during infusion of vasodilators. Symptomatic improvement and a modest increase in right ventricular ejection fraction, as measured by radionuclide ventriculography, were noted following 1 week of oral hydralazine therapy. Clinically significant pulmonary hypertension is a rare complication of SLE and the increased pulmonary vascular resistance may not be entirely fixed. Cardiac catheterization and radionuclide ventriculography may be useful in assessing response to medical therapy.
Clin Cardiol 1980 Dec
PMID:Pulmonary hypertension in systemic lupus erythematosus: hemodynamics and effects of vasodilator therapy. 746 Apr 2

We describe the case of a patient with primary familiar antiphospholipid syndrome and acute myocardial infarction. A previously healthy 15-year-old adolescent was admitted with severe chest pain lasting from 1 hour associated with inferoposterolateral ST-segment elevation. The patient received intravenous thrombolysis. A 2-dimensional echocardiogram revealed an area localized in the basal posterolateral left ventricular myocardium, that was akinetic and abnormally thin throughout the cardiac cycle. Peak creatinine kinase level was 1461 U/I. Subsequent electrocardiogram revealed inferoposterior infarction. Plasma anticardiolipin (aCL) IgG antibodies resulted positive (24 U.GPL) in repeated determinations. A dypiridamole echocardiographic test resulted negative. The patient's parents refused cardiac catheterization. He continues to do well at home 28 months after discharge. The patient's sister is affected by primary antiphospholipid syndrome characterized by recurrent abortion, very low platelet count and lupus anticoagulant positivity. Plasma aCL antibodies resulted positive also in the mother who did not have clinical manifestations.
G Ital Cardiol 1995 Aug
PMID:[Primary antiphospholipid syndrome with a familial element and myocardial infarct in an adolescent]. 749 21

Cardiac adrenergic activity was investigated in 38 patients with systemic lupus erythematosus (SLE) who were not receiving cardiovascular agents using a new index of the adrenergic tone of the working left ventricular (LV) myocardium and using the heart rate to represent sinus node adrenergic tone. According to the active cross-bridge model employed in this study, the cross-bridge activation rate constant (Ka) of the LV myocardium, corresponding to the rate constant for the binding of Ca2+ to troponin C, can be approximately expressed as Ka = 3/electromechanical systole (sec-1). The Ka value corrected for heart rate (Kac) remains nearly constant in normal individuals, but is increased without change of the heart rate by dobutamine infusion. Fifty patients who fulfilled the American Rheumatism Association criteria for SLE underwent echocardiography, as well as simultaneous recording of the electrocardiogram, phonocardiogram, and carotid pulse wave tracing. Kac was calculated from the interval between the onset of the QRS complex to the second heart sound (QS2 interval) and the heart rate (HR) as follows: Kac = 3/QS2 + 0.0249 (66-HR). The 38 SLE patients were divided into a normal Kac group (n = 26, 6.9 < Kac < 8.3 sec-1) and a high Kac group (n = 12, Kac > or = 8.3 sec-1).(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiol 1995 Aug
PMID:Cross-bridge activation rate constant determined from systolic time intervals in patients with systemic lupus erythematosus. 767 48

We serially measured the plasma thrombomodulin (TM) levels in systemic lupus erythematosus (SLE) patients and assessed them clinically. The patients who responded to medical treatment experienced a decrease in plasma TM levels. Patients who developed exacerbations of SLE, thrombotic thrombocytopenic purpura or thrombosis, displayed increased plasma TM levels. There was no significant difference between the plasma TM levels of the lupus anticoagulant-positive (LAC-positive) patients and the LAC-negative patients or between the plasma TM levels of the anticardiolipin antibody-positive (aCL-positive) patients and the aCL-negative patients. While LAC and aCL titers did not always coincide with improvement in the patients' clinical course or with aggravation of the disease, the TM values correlated well with the patients' clinical condition. Plasma TM values may be used to evaluate disease activity and may predict the occurrence of thrombosis in SLE.
Int J Cardiol 1994 Dec
PMID:Plasma thrombomodulin as an indicator of thromboembolic disease in systemic lupus erythematosus. 773 45


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