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)

Subclinical hypothyroidism is defined by elevated concentrations of thyrotropin (TSH) and normal levels of serum thyroxine in the absence of overt symptoms. Autoimmune thyroid disease is the most frequent cause. Prevalence is between 2.5% and 10%, depending on the patient population. The disorder may not be as asymptomatic as previously thought; mild but consistent hypothyroid symptoms may exist in 25% to 50% of patients. Subtle cardiac defects may be present and are probably most clinically relevant in patients with existing heart disease. Mild disturbances in cholesterol metabolism are a more common finding. Treatment of subclinical hypothyroidism must be individualized. The lowest dose of levothyroxine sodium (Levothroid, Levoxine, Synthroid) required to normalize TSH levels and improve symptoms yet avoid unnecessary side effects should be used.
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PMID:Subclinical hypothyroidism. Understanding is the key to decision making. 832 88

Although synthesized as a nonselective beta-adrenergic blocking compound, sotalol has emerged as the prototype of the so-called class III antiarrhythmic compounds. It delays cardiac repolarization by inhibiting the delayed rectifier potassium current, having a lesser effect on the inward rectifying potassium current with little or no effect on the inward calcium or sodium currents. This property of prolonging repolarization with an accompanying increase in the effective refractory period is not due to blockade of the beta-adrenergic receptors. The major electrophysiologic profile of sotalol constitutes the summed effects of beta blockade and prolonged repolarization. Sotalol exerts a potent antifibrillatory action modulated by its antiadrenergic effects. It suppresses premature ventricular contractions and nonsustained ventricular tachycardia while preventing inducible ventricular tachycardia and fibrillation in patients with advanced structural heart disease. The compound is therefore likely to exert a broad spectrum of antiarrhythmic actions in ventricular arrhythmias.
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PMID:Electrophysiologic basis for the antiarrhythmic actions of sotalol and comparison with other agents. 834 31

Speculations about development of tolerance to the inotropic effect of digitalis have been engendered since studies in various in vitro systems and tissues not representative of the heart have shown up-regulation of sodium potassium adenosine triphosphatase (Na,K-ATPase) when exposed to digitalis. Moreover the digitalis receptor (i.e., Na,K-ATPase) concentration in the normal, vital human left ventricle has not been previously determined. On this basis, digitalis receptor concentration was quantified in the left ventricle of explanted hearts from subjects without heart disease and from patients with end-stage heart failure who had received digitalis therapy. This was performed using vanadate-facilitated 3H-ouabain binding to intact tissue samples giving values of 728 +/- 58 (n = 5) and 467 +/- 55 pmol/g wet weight (n = 6) (mean +/- SEM) (p < 0.005), respectively. However, some of the digitalis receptors may have retained digoxin before 3H-ouabain binding and thus may have escaped detection. To eliminate this effect of retained digoxin, samples were exposed to prolonged washing in buffer containing excess digoxin antibody, a method recently shown to clear digoxin from receptors and allow subsequent complete digitalis receptor quantification by 3H-ouabain binding. After washing in digoxin specific antibody, specific digitalis receptor concentration was 760 +/- 58 pmol/g (n = 5) and 614 +/- 47 pmol/g (n = 6) wet weight in samples of the normal and failing hearts, respectively (p < 0.08). Thus, digitalization was associated with occupancy of digitalis receptors in the failing human heart of 24% (p < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:No adaptation to digitalization as evaluated by digitalis receptor (Na,K-ATPase) quantification in explanted hearts from donors without heart disease and from digitalized recipients with end-stage heart failure. 838 May 32

According to a London physician, women with epilepsy taking antiepileptic drugs can take combined oral contraceptives (OCs). It is usual to recommend a combined OC preparation containing at least 50 mcg of estrogen (Ovran) from patients taking enzyme-inducing antiepileptic drugs; this can be increased to 60 mcg by taking 2 30 mcg pills, and if necessary to 80 mcg. To ensure that ovulation is inhibited, the blood progesterone concentration can be measured on day 21 of the 1st cycle. The higher doses of estrogen should be accompanied by higher doses of progestogen. The commonest fetal malformations are cleft lip and palate and congenital heart disease, usually septal defects. These abnormalities may be caused by all the major antiepileptic drugs. Phenytoin has been particularly implicated and may cause minor defects in up to 30% of infants and major defects in about 5%. The incidence of cleft palate and heart defects with phenytoin is 1.8% compared with 0.7% in the general population. With sodium valproate, neural tube defects occur in about 1.5% of pregnancies. Present evidence suggests that carbamazepine is the safest drug. Folic acid supplements reduce the risk of neural tube defects in women at risk, therefore women taking antiepileptic drugs who are contemplating pregnancy should be given a small folic acid supplement or a diet rich in folate. To reduce the risk of bleeding in the perinatal period, pregnant women taking enzyme-inducing antiepileptic drugs should be given oral phytomenadione (vitamin K1) 20 mg daily for at least 1 week before delivery. Vitamin K1 should be given to the newborn immediately after delivery. Only phenobarbitone and primidone might be contraindicated for breast feeding. Mothers with uncontrolled major epilepsy should not be left alone with small children. If there is already 1 sibling with epilepsy the risk of inheriting epileptic liability rises to about 10% and if both parent have epilepsy the risk is 15-20%.
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PMID:Epilepsy and pregnancy. 824 68

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

Hypertensive crisis is a rare condition with increased blood pressure and evidence of new or progressive severe end-organ damage. The patients should be admitted to hospital, and the blood pressure reduced gradually. Blood pressure should not be normalized, but a reduction in mean arterial pressure of 20-25% or to a diastolic blood pressure > 100-110 mmHg should be achieved. Patients at particular risk for further complications are elderly, patients with hypovolaemia, renal insufficiency, ischaemic heart disease and patients with neurological deficits. The ideal antihypertensive drug for any form of hypertensive crisis does not exist. If the patient can cooperate with oral treatment, nifedipine may be used, usually administered as capsules of 10 mg orally, producing a rapid and safe reduction in blood pressure of 25% within 10-15 minutes with a maximal action after 30-60 minutes. The dose may be repeated after 30 minutes in case of insufficient blood pressure response. Hypotension is rare. Nifedipine in combination with nitroglycerine is of special benefit in hypertensive pulmonary oedema. In cases of treatment failure or if the patient cannot cooperate with oral treatment, the choice of drug lies between labetalol and sodium nitroprusside. Nitroprusside is administered as continuous intravenous infusion, the drug is safe to use and is recommended in conditions where reduction of blood pressure must be performed with extreme caution such as in cases of cerebral infarction and intracranial hemorrhage. Infusion of nitroprusside for more than 48-72 hours is inexpedient because the metabolites of nitroprusside need monitoring as well. Parenteral drug therapy with labetalol is more simple than treatment with nitroprusside, but at the same time somewhat more difficult to titrate. Nitroglycerine is very suitable in moderate hypertension and ischaemic heart disease, but in severe hypertension with heart disease nitroprusside is the treatment of choice. Loop diuretics should not be used as first-line drugs, but only in conditions with evidence of volume-overload. Patients with hypertensive crisis most often show volume depletion which is aggravated by loop diuretics, therefore they should not be used routinely. When the blood pressure has been stabilized, an oral antihypertensive drug should be started concomitantly to a gradual reduction of the initial parenteral drug therapy.
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PMID:[Hypertensive crises. 2. Treatment]. 875 95

Between September 1992 and April 1995, 19 patients at the authors' institution received pneumatic, pulsatile left ventricular assist devices (LVADs) for bridging to cardiac transplantation. The mean (+/- SD) age of the patients was 51 +/- 14 years (range, 19-64 years). Nine (47%) patients had end-stage idiopathic cardiomyopathy, five (26%) had ischemic cardiomyopathy, and five (26%) other recipients were in cardiogenic shock caused by acute myocardial infarction (AMI). Fifteen (79%) patients were supported with an intraaortic balloon pump or centrifugal LVAD at the time of LVAD insertion (duration, 5.5 +/- 4.1 days). Aprotinin was given to limit bleeding; heparin, followed by warfarin sodium, was used for anticoagulation. A vigorous exercise and nutrition protocol was followed. Cardiac index averaged 2.94 +/- 0.87 L/min/m2 immediately after the implantation procedure. No patient required placement of a right VAD. Average duration of LVAD support was 45 +/- 39 days (range, 3-153 days). Major complications included bleeding requiring reoperation (three patients); cerebrovascular accident (three patients); and severe dysrhythmias requiring direct current cardioversion (four patients). Fourteen (74%) patients underwent transplantation, with one patient still being mechanically supported. All of the patients receiving transplants were discharged from the hospital. Of the individuals who died while supported with the LVAD, 75% were patients with AMI. Timely application of LVADs as part of the interdisciplinary management of end-stage heart disease has generated excellent results for transplant candidates. Right ventricular dysfunction has not necessitated right VAD placement in the authors' experience. Patients with AMI have a higher risk of death while being supported with the device than do more chronically ill recipients.
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PMID:Long-term left ventricular assist device use before transplantation. 857 61

The efficacy of the dialysis in the heart failure non responsive to the traditional methods is well known. In our study we have evaluated the effects of three different dialytic methods (UFI: ultrafiltration isolate; HF: hemofiltration; CAVH: continuous arteriovenous hemofiltration). These methods are used to cause a good depletion in the patients with intractable heart failure following from ischaemic valvular or primitive cardiomiopathy. We have treated 18 patients (6 for each method) and the patients with organic or functional renal disease were treated with the methods (HF and CAVH) that have depletive and depurative effects. Each of these methods is capable, without important differences, of achieving the following aim: the hydro-sodium depletion, the correction of the haemodynamic alteration and the re-establishment of the response to the traditional medical treatment. Using the hemofiltration and continuous arteriovenous hemofiltration, both soft methods, we have obtained values of dehydratation, absolute and for each session, higher than isolated ultrafiltration. The follow-up has not pointed out differences, of both prognosis and survival among patients treated with the three methods studied, whose effects are always only temporary; only the heart transplantation or the valvular correction, by operating in a very important way on the basal cardiopathy, is the resolutive event.
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PMID:[Treatment of refractory heart failure with different dialysis technics]. 872 82

In transiently transfected mammalian cells we have identified pharmacological consequences of a naturally occurring deletion mutation, delta KPQ, of the human heart Na+ channel alpha subunit that previously has been linked to one form of the long QT syndrome, an inherited heart disease. Our results show that the Class IB antiarrhythmic agent lidocaine blocks maintained inward current through and slows recovery from inactivation of delta KPQ-encoded Na+ channels. Block is greater for maintained than for peak current. Because incomplete inactivation of mutant Na+ channels is now thought to underlie the prolonged ventricular action potential, which is the phenotype of this disease, and we find that the delta KPQ mutation speeds the recovery from inactivation of drug-free mutant channels, our results provide evidence, for the first time, that clinically relevant dysfunctional properties of an ion channel can be selectively targeted on the basis of the molecular properties conferred on the channel by an inherited genetic disorder.
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PMID:Lidocaine block of LQT-3 mutant human Na+ channels. 892 57

This study examined possible selective impairment of endothelial dysfunction in the peripheral vascular bed in patients with chronic heart failure in the absence of confounding factors influencing endothelial function (i.e. hypertension, hypercholesterolaemia and diabetes mellitus). Several recent studies have suggested that endothelium-dependent peripheral vasodilation is impaired but endothelium-independent vasodilation is preserved in patients with chronic heart failure. However, a classical paper has demonstrated that sodium nitrite-mediated calf blood flow is clearly depressed in patients with valvular heart disease and cardiomyopathy. We examined forearm blood flow changes mediated by acetylcholine and nitroprusside in patients with valvular heart disease (n = 55) or congenital heart disease (n = 13), and a comparison was made with healthy volunteers (n = 21). The blood flow changes mediated by acetylcholine and nitroprusside were significantly impaired in both patient groups (P < 0.01). When blood flow responses were collected from all patients, two types of vasodilatory capacity were found to have decreased significantly with increasing clinical severity of heart failure (New York Heart Association functional class; P < 0.01). This suggests that the peripheral vasodilatory responses mediated by endothelium-dependent and endothelium-independent vasodilators are significantly impaired in patients with symptomatic chronic heart failure due to non-ischaemic heart disease.
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PMID:Endothelium-dependent vasodilatation is not selectively impaired in patients with chronic heart failure secondary to valvular heart disease and congenital heart disease. 896 Apr 11


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