Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined specimens from explanted human hearts by two-dimensional electrophoresis. The protocol selected includes: (a) solubilization of the sample in a urea-detergent mix; (b) charge fractionation in the presence of urea and nonionic detergent on a pH 4-10 immobilized pH gradient; (c) size fractionation on a polyacrylamide concentration gradient in the presence of sodium dodecyl sulfate; and (d) staining with silver nitrate. The method is sensitive enough for analysis of biopsies in the 1-3 mg range (wet tissue). We saw, for explanted hearts, variations in the protein pattern with the site of sample dissection. Results are presented for 11 explanted human hearts: one control organ and 10 pathological samples. The recorded pathologies included dilatative cardiomyopathy (six cases), valvulopathy (one case), ischemic cardiopathy (two cases), and graft rejection (one case). The patterns for whole extracts as well as for cytoplasmic proteins and myofibril components are compared. Extensive individual variability was observed both between control and pathological cases and among the abnormal samples.
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PMID:An examination of heart proteins by two-dimensional electrophoresis. 331 3

Parenteral magnesium has been used for several decades in the empiric treatment of various arrhythmias, but the data on its electrophysiologic effects in man are limited. We evaluated the electrophysiologic effects of magnesium sulfate (MgSO4) administration in eight normomagnesemic patients with normal mononuclear cell magnesium content, who had no clinically significant heart disease and had normal baseline electrophysiologic properties. After administration of intravenous MgSO4, serum magnesium rose significantly from 1.9 +/- 0.1 to 4.4 +/- 1.7 mg/dl (p less than 0.02). During a maintenance magnesium infusion, we observed significant prolongation of the ECG PR interval (145 +/- 18 to 155 +/- 26 msec, p less than 0.05), AH interval (77 +/- 27 to 83 +/- 26 msec, p less than 0.002), antegrade atrioventricular (AV) nodal effective refractory period (278 +/- 67 to 293 +/- 67 msec, p less than 0.05), and sinoatrial conduction time (60 +/- 34 to 76 +/- 32 msec, p less than 0.02). No significant effect was observed on sinus cycle length, sinus node recovery time, intra-atrial or intraventricular conduction times, QRS duration (during both sinus rhythm and ventricular pacing), QT interval, HV interval, paced cycle length resulting in AV nodal Wenckebach block, AV nodal functional refractory period, retrograde ventriculoatrial (VA) effective refractory period, or atrial and ventricular refractory periods. These findings, in conjunction with the demonstrated ability of magnesium to block slow channels for sodium movement, may provide an explanation of the mechanism by which magnesium exerts its effect in the treatment of atrial and junctional arrhythmias.
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PMID:Electrophysiologic effects of intravenous magnesium in patients with normal conduction systems and no clinical evidence of significant cardiac disease. 334 Nov 71

Programmed ventricular stimulation was used to test oral bethanidine sulfate in 10 patients with life-threatening ventricular arrhythmias. These patients had previously documented, recurrent, sustained ventricular tachycardia (VT) and/or ventricular fibrillation (VF) complicating stable heart disease. During control electrophysiologic studies, VT could be induced in all 10 patients: 6 with nonsustained VT, 3 with sustained VT, and 1 with VT/VF. After control, bethanidine 20-30 mg/kg was administered orally and beginning 60 minutes later, programmed ventricular stimulation was repeated. After bethanidine administration, VT could be induced in nine patients; in four, the VT was essentially unchanged from that induced during control studies. In four others, worse VT was induced after bethanidine. The remaining two patients had a potentially beneficial response to the drug. Bethanidine was poorly tolerated: seven patients had symptomatic orthostatic hypotension that persisted for several days despite concurrent protriptyline therapy. Furthermore, in four patients, spontaneous VT or VT/VF occurred 3-8 hours after the last dose. Nausea, vomiting, flushing, and blood pressure elevation were also noted. Bethanidine sulfate in the dosages used usually does not prevent the induction of VT by programmed ventricular stimulation and frequently causes serious toxicity. These findings suggest that the drug would be ineffective and poorly tolerated for long-term therapy in patients with serious ventricular arrhythmias.
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PMID:Bethanidine sulfate in paroxysmal ventricular tachycardia: toxicity and antifibrillatory actions. 377 63

Twelve cardiac electrophysiology centers conducted an open label prospective trial of bethanidine sulfate, an oral bretylium analog, for the prevention of ventricular tachyarrhythmias during programmed electrical stimulation. The study group included 56 patients (44 men, 12 women; mean age 60 years; 55 with structural heart disease). Sixteen patients had both ventricular tachycardia and fibrillation, 30 had ventricular tachycardia alone and 10 had ventricular fibrillation alone. Programmed stimulation on no antiarrhythmic drugs induced sustained ventricular tachycardia in 46 patients, nonsustained ventricular tachycardia in 4 patients and ventricular fibrillation in 6 patients. During programmed ventricular stimulation after 59 trials of 20 to 30 mg/kg body weight of oral bethanidine (acute dosing in 40 patients, and divided dosing over 24 hours in 19 patients), no ventricular tachyarrhythmias were inducible in 6 patients (11%), sustained ventricular tachycardia was converted to nonsustained ventricular tachycardia in 3 patients (5%), ventricular tachyarrhythmias remained inducible in 39 patients (70%) and spontaneous ventricular tachyarrhythmias occurred more frequently in 4 patients (7%). Side effects prevented repeat testing in four patients. The 10 patients presenting with only ventricular fibrillation appeared to have a higher response rate: no ventricular tachyarrhythmias were inducible in 2 patients and sustained ventricular tachycardia was converted to nonsustained ventricular tachycardia in 2 patients. Despite protriptyline administration in 54 of 59 bethanidine trials, symptomatic hypotension occurred in 30 trials (51%). In conclusion, the efficacy of bethanidine for preventing ventricular tachyarrhythmias as assessed by programmed stimulation is low. Patients presenting with only ventricular fibrillation may have a more favorable response to bethanidine sulfate. Symptomatic hypotension occurs frequently despite concomitant use of protriptyline.
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PMID:Bethanidine sulfate: efficacy in prevention of ventricular tachyarrhythmias during programmed stimulation. Report of a multicenter study of 56 patients. 389 40

Endocarditis and unilateral endophthalmitis due to Actinobacillus actinomycetemcomitans heart disease. The ocular infection was notable for its localized presentation and slow evolution. Treatment with systemic, subconjunctival, and topical gentamicin sulfate and ampicillin sodium achieved 20/20 acuity with a residual chorioretinal scar in the nasal periphery. Intravitreal injection of the organism into a rabbit confirmed its minimal pathogenicity within the eye. This organism must now be considered in patients with differential diagnosis of endogenous endophthalmitis complicating endocarditis and septicemia.
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PMID:Actinobacillus actinomycetemcomitans endophthalmitis with subacute endocarditis. 660 7

Pregnancy causes substantial changes in the cardiovascular system: cardiac output (40%-50%) and blood volume (40%) increase whereas systemic peripheral resistance and arterial pressure decrease. The rise in progesterone and estrogen levels accompanying pregnancy stimulates the renin-angiotensin-aldosterone system. Increased prostaglandin production follows renin activation; simultaneously, the arterial vessels show diminished angiotensin sensitivity. The result is pronounced vasodilatation. Cardiovascular diseases remain the most important nonobstetric cause of maternal death. The physiological changes in the cardiovascular system during pregnancy influence cardiac diseases in different ways. Pregnancy, labor, and delivery appear to be well tolerated in gravidae with an atrial septal defect, ventricular septal defect, and patent ductus arteriosus. Sometimes congestive heart failure occurs and appropriate medical therapy is necessary. Pregnant women with uncorrected cyanotic congenital heart disease (Eisenmenger's syndrome, tetralogy of Fallot) constitute a high-risk group because of right ventricular insufficiency and hypoxic attacks. The consequences for anaesthesia in parturients with congenital heart disease are discussed. The symptoms of acquired mitral or aortic stenosis are aggravated by the physiological changes in the cardiovascular system during pregnancy; the clinical symptoms of valve insufficiency are ameliorated by vasodilatation. Peripartum cardiomyopathy clinically shows similar features to idiopathic dilated cardiomyopathy. The basis of treatment is the same as that of congestive heart failure, with the therapeutic spectrum ranging from diet to heart transplantation. Women with hypertrophic cardiomyopathy tolerate pregnancy, labor, and delivery surprisingly well. Vaginal delivery is possible, but epidural anaesthesia is contraindicated. Hypertensive disorders associated with pregnancy are classified into three groups: chronic, transient, and pre-eclamptic hypertension. Whereas chronic and transient hypertension do not affect the outcome of pregnancy appreciably, pre-eclampsia presents a potential danger to mother and fetus. Pre-eclamptic hypertension is accompanied by low cardiac output and plasma volume. An upregulation of angiotensin receptors enhances vascular reactivity, with the consequence of high peripheral resistance. For antihypertensive therapy hydralazine, alpha-methyldopa, and magnesium sulfate are the drugs of choice. A generalised recommendation of anaesthesia for the pre-eclamptic gravida cannot be made because both general and epidural anaesthesia have risks of severe side effects.
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PMID:[Cardiovascular diseases during pregnancy. Considerations for the anesthesiologist]. 765 90

A controlled study was carried out to evaluate the effects of postoperative iron therapy on iron status in anemic children after cardiopulmonary bypass. The patients were 8 boys and 9 girls (mean age 6.5 years) who underwent elective closure of atrial septal defect, secundum type. On postoperative day 9, patients were randomly assigned to either iron supplementation with iron sulfate 5 mg/kg until day 56 or to a control group. Hemoglobin, reticulocytes, transferrin saturation, free erythrocyte protoporphyrin, and ferritin were measured, the final outcome measure being postoperative iron status on day 56. The treatment group showed higher transferrin saturations (33.5% versus 18.0%), smaller decreases in ferritin level (+3.0 versus--13.7 ng/ml), and a lower incidence of depleted iron stores (0/8 versus 5/9) than the control group (all data: P < 0.05). Anemic children after cardiopulmonary bypass for surgical repair of congenital heart disease thus benefit from iron supplementation within the first postoperative weeks.
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PMID:Iron supplementation in children after cardiopulmonary bypass for surgical repair of congenital heart disease. 799 33

Using an enzyme-linked immunosorbent assay, we measured anti-adenine nucleotide translocater (ANT) antibody in control subjects and in patients with dilated cardiomyopathy (DCM), myocarditis, and other heart disease. Analysis with sodium dodecyl sulfate-polyacrylamide gel electrophoresis, Western blotting, and immunoabsorption tests confirmed accurate purification of the ANT protein and correct measurement of anti-ANT auto-antibody. Anti-ANT antibody was detected in 6 of 37 cases (16%) of DCM and in 5 of 12 cases (42%) of myocarditis. This antibody was not positive in other heart diseases or in apparently healthy controls. There were no differences between anti-ANT autoantibody-positive and -negative DCM or myocarditis patients in any of the cardiac parameters examined (left ventricular ejection fraction, LVEF; left ventricular end-diastolic dimension, LVDd; and cardiothoracic ratio, CTR). Moreover, in patients who were positive for anti-ANT auto-antibody, no positive correlations were found between the parameters and anti-ANT antibody titers in either DCM or myocarditis. Although these results indicate that the detection of anti-ANT antibody was achieved at a high specificity and could have certain diagnostic value in DCM and myocarditis, there was no statistically significant relationship between the cardiac parameters (LVEF, LVDd, and CTR) and anti-ANT antibody titers in either DCM or myocarditis. Some compensatory mechanism of ventricular function may mask the effects of the anti-ANT auto-antibody or alternatively, this auto-antibody may have mimic effects on the pathogenesis and/or progression of DCM and myocarditis.
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PMID:Auto-antibody against adenine nucleotide translocator in dilated cardiomyopathy and myocarditis--incidence and relation to cardiac function and morphology. 828 7

Thromboembolism is a prominent but poorly understood feature of eosinophilic, or Loeffler's endocarditis. Eosinophil (EO) specific granule proteins, in particular major basic protein (MBP), accumulate on endocardial surfaces in the course of this disease. We hypothesized that these unusually cationic proteins promote thrombosis by binding to the anionic endothelial protein thrombomodulin (TM) and impairing its anticoagulant activities. We find that MBP potently (IC50 of 1-2 microM) inhibits the capacity of endothelial cell surface TM to generate the natural anticoagulant activated protein C (APC). MBP also inhibits APC generation by purified soluble rabbit TM with an IC50 of 100 nM without altering its apparent Kd for thrombin or Km for protein C. This inhibition is reversed by polyanions such as chondroitin sulfate E and heparin. A TM polypeptide fragment comprising the extracellular domain that includes its naturally occurring anionic glycosaminoglycan (GAG) moiety (TMD-105) is strongly inhibited by MBP, whereas its counterpart lacking the GAG moiety (TMD-75) is not. MBP also curtails the capacity of TMD-105 but not TMD-75 to prolong the thrombin clotting time. Thus, EO cationic proteins potently inhibit anticoagulant activities of the glycosylated form of TM, thereby suggesting a potential mechanism for thromboembolism in hypereosinophilic heart disease.
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PMID:Eosinophil cationic granule proteins impair thrombomodulin function. A potential mechanism for thromboembolism in hypereosinophilic heart disease. 838 94

Abnormal myocardial long-chain fatty acid uptake is suspected of being involved in certain types of heart disease, but the mechanism by which the heart takes up long-chain fatty acids remains unclear. The sulfo-N-succinimidyl derivatives of long-chain fatty acids have been reported to undergo covalent binding to a membrane protein and to irreversibly inhibit the transport of long-chain fatty acids by rat adipocytes (Harmon et al., 1991). It has been suggested that the membrane protein bound by these derivatives is a candidate transporter for long-chain fatty acids in adipocytes. However, myocardial membrane long-chain fatty acid-binding proteins have not yet been fully investigated. Rat hearts were isolated and perfused with a sulfo-N-succinimidyl derivative of tritium-labeled palmitate ([3H]SSP). Then the [3H]SSP-binding protein was characterized by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) autoradiography and histological autoradiography. Myocardial palmitic acid uptake was examined after pretreatment of isolated perfused rat hearts with SSP. The SSP-binding protein was isolated from bovine hearts by successive chromatography, and the amino acid sequences of lysylendopeptidase-digested peptide fragments were determined. SDS-PAGE autoradiography revealed that [3H]SSP bound to an 85-90 kDa protein derived from the myocardial microsomal fraction, and histological autoradiography demonstrated that [3H]SSP radioactivity was localized to the myocardial cell membrane. Pre-incubation with SSP inhibited palmitic acid uptake by isolated perfused rat hearts. A [3H]SSP-binding protein was also found in canine and bovine hearts, and was isolated from the bovine cardiac membrane fraction. Amino acid sequencing revealed that four peptide fragments showed strong sequence homology with rat adipocyte membrane protein, which is implicated in the binding or transport of long-chain fatty acids (Abumrad et al., 1993). We conclude that the SSP-binding protein is localized to the myocardial cell membrane and might be involved in the uptake or transport of long-chain fatty acids.
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PMID:Isolation of myocardial membrane long-chain fatty acid-binding protein: homology with a rat membrane protein implicated in the binding or transport of long-chain fatty acids. 852 24


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