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)

Surgical arrhythmia therapy may be performed for patients failing the catheter ablation approach or incorporated into repair of complex congenital heart disease. Variations in atrial and ventricular anatomy that may limit the catheter approach can be directly addressed surgically assuring lesion depth and continuity of anatomic lines of block. Between July 1992 and August 2002, we performed arrhythmia surgery on 34 patients for refractory atrial (n = 29) or ventricular (n = 5) arrhythmias. Not included in this series are patients who had arrhythmia surgery during Fontan conversion. The majority of patients had various forms of complex congenital heart disease; two had structurally normal hearts. Median age at surgery was 13.0 years (range, 7 days to 45 years). Five patients were infants (mean age, 25 days). Twenty-two patients (65%) had an average of 2.8 previous cardiac procedures; all required resternotomy. Operative mortality was 5.9% (2 of 34 patients) because of low cardiac output in one patient following Mustard takedown and arterial switch operation and in one neonate with Ebstein's anomaly and pulmonary atresia. Ablative surgery for supraventricular tachycardia (atrial re-entry, automatic atrial, atrioventricular nodal re-entry, and atrial fibrillation) had a 93% success rate (25 of 27 patients). Clinical tachycardia recurred in two of 27 surviving patients (7%) with atrial arrhythmia, one after an arrhythmia-free interval of several years. Ventricular tachycardia was inducible postoperatively in two of three patients with ventricular arrhythmias and congenital heart disease. Patient size or anatomic complexity should not be limiting factors in the combined surgical arrhythmia approach. Because older patients undergoing surgical revision of prior surgical repairs of congenital heart disease are at increased risk for the later development of atrial arrhythmias, incorporation of arrhythmia therapy into any planned surgical revision should be routinely considered.
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PMID:Arrhythmia surgery in association with complex congenital heart repairs excluding patients with fontan conversion. 1274 Jul 70

Nkx2.5 is a conserved homeodomain (HD) containing a transcription factor essential for early cardiac development. We generated several mutations modeling some patients with congenital heart disease. Transgenic mice (tg) expressing the wildtype Nkx2.5 under beta-myosin heavy chain (MHC) promoter died during the embryonic stage. However, tg mice expressing this mutation under beta-MHC promoter (beta-MHC-TG(I183P)), the wildtype Nkx2.5 (alpha-MHC-TG(wild)), and a putative transcriptionally active mutant (carboxyl-terminus deletion, alpha-MHC-TG(DeltaC)) under alpha-MHC promoter showed postnatal lethal heart failure. Given the profound atrioventricular conduction abnormalities we recently demonstrated in beta-MHC-TG(I183P) mice, the aim of this study was to determine whether alpha-MHC-TG(wild) and alpha-MHC-TG(DeltaC) mutant mice display similar cardiac electrophysiological phenotypes. Surface ECG recordings and in vivo electrophysiology studies were performed in alpha-MHC-TG(wild) mice and controls at 6 weeks of age, and in alpha-MHC-TG(DeltaC) mice and controls at 10 weeks of age. Ambulatory ECG recordings in alpha-MHC-TG(wild) and controls were obtained using an implantable radiofrequency telemetry system. PR prolongation and atrioventricular nodal dysfunction were detected in alpha-MHC-TG(wild) and alpha-MHC-TG(DeltaC) mice. Bradycardia and prolonged PR interval were seen in ambulatory ECG of alpha-MHC-TG(wild) mice compared to controls. Several alpha-MHC-TG(wild) mice died of bradycardia. Fetal and neonatal mutant Nkx2.5 expression causes severe cardiac conduction failure. Postnatal overexpression of nonmutant (wild) Nkx2.5 also causes conduction abnormalities, although the onset is after the neonatal stage. Bradycardia and AV conduction failure may contribute to the lethal heart failure and early mortality.
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PMID:Cardiac electrophysiological phenotypes in postnatal expression of Nkx2.5 transgenic mice. 1459 38

Atrial fibrillation is the most common arrhythmia in the general population and is frequently associated with organic heart disease. beta-adrenoceptor antagonists (b-blockers) are very effective in preventing atrial fibrillation after coronary artery bypass surgery. It has been shown recently that the beta-blocker metoprolol controlled release/extended release (CR/XL) is also effective in maintaining sinus rhythm after conversion of atrial fibrillation. There is concern that class I antiarrhythmic drugs, such as quinidine, disopyramide, and flecainide in particular, may increase mortality. The risk of proarrhythmia associated with beta-blocker treatment is very low. Therefore b-blockers, such as metoprolol CR/XL, may be the first line of treatment to maintain sinus rhythm, especially after myocardial infarction and in patients with chronic heart failure and in those with arterial hypertension. In patients with persistent atrial fibrillation, AV-nodal conduction-slowing drugs, such as calcium channel antagonists and beta-blockers are used to control the ventricular rate during atrial fibrillation. Several studies clearly show that beta-blockers alone, or in combination with digoxin are very effective in controlling the ventricular rate at rest and during exercise. beta-blockers are effective in maintaining sinus rhythm and controlling the ventricular rate during atrial fibrillation. Given these effects and their favorable effects on mortality, beta-blockers should be considered as first-line agents in the management of patients with atrial fibrillation.
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PMID:Use of beta-blockers in atrial fibrillation. 1472 97

Atrial fibrillation (AF) is the most commonly encountered sustained arrhythmia. Heart rate control, reduction of symptoms, and prevention of embolism are major goals of treatment. Whether the strategy of cardioversion with subsequent maintenance of sinus rhythm has an advantage over heart rate control is under active investigation. Digoxin, non-dihydropyridine calcium channel antagonists, beta-adrenoceptor antagonists (beta-blockers), and amiodarone are the pharmacologic agents most commonly used to achieve rate control. In patients with drug-resistant AF, atrioventricular nodal ablation (or modification) with implantation of a permanent pacemaker is an alternative therapy. Conversion to sinus rhythm can best be achieved by electrical cardioversion. In selected patients, pharmacologic cardioversion can also be attempted. The use of antiarrhythmic drugs for the maintenance of sinus rhythm depends on several factors: (i) the nature of the arrhythmia (first attack, paroxysmal AF with frequent attacks, paroxysmal AF with infrequent attacks, or persistent AF); (ii) the associated symptoms; (iii) and the risk of severe adverse effects associated with the chosen drug. If the administration of an antiarrhythmic drug is appropriate, the choice of the drug must be tailored to the specific characteristics of the given patient. In lone AF, class Ic antiarrhythmic drugs are the best tolerated. These agents should be combined with a calcium channel antagonist or a beta-blocker to prevent rapid ventricular response in the case of conversion of AF to atrial flutter. In this situation, catheter ablation of atrial flutter at the isthmus (hybrid therapy) should be performed. All class I antiarrhythmic agents should be avoided in patients with structural heart disease. Alternative approaches that may be used if sinus rhythm cannot be maintained with drug therapy include: (i) the ablation of arrhythmogenic pulmonary veins; (ii) the implantation of an atrial defibrillator; (iii) the use of specific pacing sites; (iv) or pacing modes. Whether these approaches will reach clinical relevance merits further investigation. Intraoperative catheter ablation or surgical ablation (maze procedure) seems a promising approach for curing AF in patients undergoing cardiac surgery. Among all of the available treatment options, the most consistent proof of efficacy in reducing mortality and morbidity from AF exists for antithrombotic treatment.
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PMID:Current management of symptomatic atrial fibrillation. 1472 42

Cardiac arrhythmias are the reason of the most sudden deaths in athletes. The annual risk of sudden death at athletes is between 5 to 10 per one million. Benign arrhythmia including bradyarrhythmias, atrial and ventricular premature contractions are common in the athletes. Supraventricular arrhythmias such as atrial fibrillation, nodal reciprocal entrant tachycardia and Wolff-Parkinson-White syndrome are less common. Perhaps the rarest and the most dangerous arrhythmias are ventricular arrhythmias, among them arrhythmias secondary to hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, long QT syndrome, and anomalous origin of coronary arteries. Asymptomatic bradyarrhythmias (if the heart rate in bradyarrhythmia appropriate increases with exercise), supraventricularis tachycardias, and atrial premature contractions without structural heart disease are not the contraindication to sports Athletes with premature ventricular contraction, nonsustained ventricular tachycardia and non structural heart disease are without athletic restrictions as long as the arrhythmias do not worsen and they not cause dyspnea or presyncope during exertion. Frequent or multiform premature ventricular contraction or sustained ventricular tachycardia indicate a higher risk, and all participation in athletic should be restricted.
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PMID:[Cardiovascular diseases as a cause of sudden death in athletes]. 1507 12

Calcium channel blockers are among the most commonly used therapeutic drugs. Nevertheless, the utility of calcium channel blockers for heart disease is limited because of the potent vasodilatory effect that causes hypotension, and other side effects attributable to blockade of noncardiac channels. Therefore, focal calcium channel blockade by gene transfer is highly desirable. With a view to creating a focally applicable genetic calcium channel blocker, we overexpressed the ras-related small G-protein Gem in the heart by somatic gene transfer. Adenovirus-mediated delivery of Gem markedly decreased L-type calcium current density in ventricular myocytes, resulting in the abbreviation of action potential duration. Furthermore, transduction of Gem resulted in a significant shortening of the electrocardiographic QTc interval and reduction of left ventricular systolic function. Focal delivery of Gem to the atrioventricular (AV) node significantly slowed AV nodal conduction (prolongation of PR and AH intervals), which was effective in the reduction of heart rate during atrial fibrillation. Thus, these results indicate that gene transfer of Gem functions as a genetic calcium channel blocker, the local application of which can effectively modulate cardiac electrical and contractile function.
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PMID:Creation of a genetic calcium channel blocker by targeted gem gene transfer in the heart. 1532 42

Lewy bodies (LB) are characteristic pathological findings for idiopathic Parkinson disease, and extracranial organs have also been known to exhibit these structures. Clinically, the possible involvement of LB in cardiac dysfunction has attracted attention based on the findings of studies using [123I] metaiodobenzyl guanidine (MIBG) scintigraphy. The purpose of the present study was to investigate the possible involvement of LB in heart disease. A total of 40 autopsy cases consisting of Lewy body disease and Parkinson syndrome were examined. The former were cases with intracranial LB regardless of clinical symptoms, and the latter were cases with parkinsonism but without intracranial LB. The presence of heart disease or an atrial arrhythmia and the results of an MIBG scintigraphy study were clinically examined. The sinoatrial node was examined microscopically and immunohistochemically. The results showed that heart disease and atrial arrhythmia complications were more frequent in cases with Lewy body disease than in cases with Parkinson syndrome and that LB were frequently found in extracranial organs, especially in the sinoatrial nodal ganglion, in cases with Lewy body disease. In the current report, we hypothesized that neuronal changes involving LB in the sinoatrial nodal ganglion may cause arrhythmia and ischemic heart disease as a result of vasoconstriction.
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PMID:Lewy bodies in the sinoatrial nodal ganglion: clinicopathological studies. 1536 36

African-American (AA) women with breast cancer have higher mortality rates than Caucasian woman, and some studies have suggested that this disparity may be partly explained by unequal access to medical care. The purpose of this study was to analyze racial differences in patterns and costs of care and survival among women treated for invasive breast cancer at a large academic medical center. Subjects included 331 AA and 257 Caucasian women diagnosed with stage I-III breast cancer between 1994 and 1997. Clinical, socio-demographic, and cost data were obtained from the medical record, cancer registry, and hospital financial database. Data were collected on the use of cancer directed treatments (surgery, radiation, chemo and hormonal therapy) up to 1-year post-diagnosis. Survival analyses compared disease-free and overall survival by race adjusting for age, stage, nodal involvement, ER/PR status and a diagnosis of hypertension, diabetes, heart disease and cerebral vascular accident. There were no significant racial differences in treatment utilization and costs. The mean total 1-year treatment costs were US 16,348 dollars for AAs and US 15,120 dollars for Caucasians. While AAs had a significantly higher unadjusted relative risk (RR) of recurrence 2.09 (95% CI: 1.41-3.10) and death 1.56 (95% CI: 1.09-2.25), the multivariate adjusted analyses resulted in no significant differences in recurrence 1.38 (95% CI: 0.85-2.26) or death 1.06 (95% CI: 0.64-1.75). There was no obvious racial disparity in treatment and costs noted. Our findings support the theory that equal treatments produce equal outcomes. Improvement in screening may have an important impact on survival among minority women with breast cancer.
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PMID:Racial disparities in treatment and survival of women with stage I-III breast cancer at a large academic medical center in metropolitan Detroit. 1595 57

A healthy 15-year-old male patient presented with a 6-month history of recurrent attacks of palpitations. On multiple emergency room visits, a sustained wide QRS complex tachycardia with a right bundle branch block and northwest axis deviation was documented. The tachycardia was not terminated by intravenous adenosine, but was suppressed with intravenous verapamil. There was no evidence of structural heart disease, myocarditis, long QT syndrome, or electrolyte imbalance after a series of standard examinations. Idiopathic left ventricular tachycardia (ILVT) was suspected. Electrophysiologic studies revealed 2 inducible tachycardias, which were shown to represent atrioventricular nodal reentrant tachycardia (AVNRT) and ILVT. Transformation from AVNRT to ILVT occurred spontaneously following atrial pacing. Successful ablation of ILVT and the slow atrioventricular nodal pathway resulted in cure of the double tachycardia.
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PMID:Radiofrequency catheter ablation of coexistent idiopathic left ventricular tachycardia and atrioventricular nodal reentrant tachycardia. 1626 63

Swallow syncope is a relatively rare syndrome that is treatable when diagnosed. A 66-year-old woman was referred to the department of cardiology because she had been suffering from recurrent syncopal attacks associated with swallowing. An ambulatory electrocardiogram revealed atrial and ventricular asystoles immediately after swallowing soup or tea that were reproducible (max. RR 3.5 s). An electrophysiological study did not detect sinus nodal or atrioventricular nodal dysfunction. The patient had no underlying esophageal disease or cardiac disorder. The patient's symptoms resolved after permanent pacemaker implantation. This report reviews the diagnosis, mechanism and management of swallow syncope.
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PMID:Swallow syncope, a case report and review of the literature. 1628 32


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