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

Palpitations are a nonspecific symptom and do not necessarily imply serious heart disease. The vast majority of palpitations are benign. Goals in evaluation include detecting and identifying an arrhythmia, clarifying symptom severity, and defining the extent of underlying heart disease. If palpitations are infrequent and not accompanied by angina, congestive heart failure, or syncope, outpatient transtelephonic monitoring yields useful clinical information in most patients and is more cost-effective than Holter monitoring. Patients with major symptoms require hospitalization for aggressive cardiac evaluation and, possibly, electrophysiologic testing to guide treatment.
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PMID:Palpitations and arrhythmias. Separating the benign from the dangerous. 172 76

A 9-year-old patient who had had a syncope was found to have atrial flutter in a resting electrocardiogram (ECG). Brief phases of sinus arrest had previously occurred after drug conversion to sinus rhythm. Structural heart disease was excluded by cardiac catheterization and angiography. Electrophysiologic study revealed a sick sinus syndrome, associated with diffuse impairment of the conduction system (supra-, infra-, and intrahisian block). Epimyocardial and an endocardial pacemaker implantation failed because of high stimulation threshold, after 3 years and 2 weeks, respectively. At the third implantation a steroid-eluting endocardial pacing lead was used and satisfactory pacing was still present 2 years later.
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PMID:Sick sinus syndrome and diffuse impairment of the conduction system in a child: successful pacing with a steroid eluting endocardial pacing lead. 173 68

Our aim was to assess the incidence and clinical characteristics of carotid sinus hypersensitivity in a group of subjects suffering from syncope. The total number of patients was 118. Twenty-four of them (20%) were diagnosed as epileptics (first attack) and 38 (32%) as vasodepressors. 56 patients with unexplained syncope underwent carotid sinus massage during electrocardiographic registration and pressure monitoring. 41 patients were found to have carotid sinus hypersensitivity. 34 of these 41 patients received implantation of a pacemaker. Abnormal sinus node function was noted in 30, abnormal atrioventricular node function in 3 and combined abnormal sinus node and AV node function in 1. Furthermore three other patients who were negative to massage were implanted with a pacemaker because they had an organic heart disease and recurrent syncope. Different tests as 24-hour monitoring ecg and electrophysiologic study showed no better results in the diagnosis of syncope. Our data demonstrates the diagnostic importance of carotid sinus massage in the diagnosis of syncope. The validity of this method is confirmed by the 24 month follow-up.
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PMID:[Hypersensitivity of the carotid sinus in syncope and its diagnostic role: therapeutic implications and follow-up]. 174 29

The long-QT syndrome (LQT; Ward-Romano syndrome) is a cardiac disorder that is inherited as an autosomal dominant trait. Affected family members suffer from recurrent syncope and sudden death due to ventricular arrhythmias. Recently, we identified a DNA marker on the short arm of chromosome 11 (the Harvey ras-1 locus [H-ras-1]) that was completely linked to the LQT locus in one large family. In the study presented here, we performed linkage investigations on six new and unrelated families with LQT. The LQT locus was again completely linked to the H-ras-1 locus in all families examined, with a combined lod score of 5.25 at a recombination fraction of 0. This work confirms our previous assignment of the LQT locus to chromosome 11p and supports the hypothesis that LQT is genetically homogeneous. As no obligate recombinants were identified in either this or our previous study, the H-ras-1 protooncogene remains a candidate for the LQT disease gene. Identification of LQT families with locus homogeneity is an important step in the development of a refined genetic map of this locus and will help determine whether the H-ras-1 marker would be of general use for presymptomatic diagnosis of this potentially fatal, but treatable, disorder.
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PMID:Consistent linkage of the long-QT syndrome to the Harvey ras-1 locus on chromosome 11. 174 60

Torsades de pointes (TdP) is a life-threatening ventricular tachycardia that occurs in the setting of a prolonged QT interval and is most frequently related to administration of antiarrhythmic drugs. Patients with organic heart disease, with low serum electrolyte levels, with a previous episode of TdP and with bradycardia or baseline QT prolongation may be at increased risk of developing TdP. After initiation of a QT prolonging therapy, the dosage should be modified if the QT interval reaches 560-600 ms. Cessation of medication and immediate hospitalization are indicated in the presence of lightheadedness, syncope, or increased frequency and complexity of ventricular premature beats. The conventional therapy of TdP with isoproterenol or cardiac pacing, although usually effective, has certain disadvantages. Isoproterenol is contraindicated in patients with hypertension or ischemic heart disease, whereas institution of cardiac pacing requires skilled personnel and fluoroscopy. Recently, infusion of magnesium sulfate has been shown to abolish TdP both in the clinical and experimental setting. Compared with conventional therapy, magnesium sulfate has the advantage of safety and simplicity of its administration. In doubtful cases, if does not aggravate a ventricular tachycardia that is not TdP, as may occur with isoproterenol. This advantage and the prompt effectiveness of the drug in four clinical series, including 31 patients, support the use of magnesium sulfate as the first line of therapy for TdP.
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PMID:Torsades de pointes: prevention and therapy. 185 60

Mitral Valve Prolapse (MVP) is a common cardiac disorder in our community. It is estimated that 4% to 15% of the general population have the anatomical defect of prolapsed mitral valve leaflets during ventricular systole. Patients with MVP that suffer from chest pain, dyspnea, fatigue, dizziness, syncope, palpitations, cardiac arrhythmias, anxiety, and panic attacks are diagnosed as having Mitral Valve Prolapse Syndrome. There is much controversy in the medical literature as to the causes of MVPS symptomatology. Some scientists believe that autonomic dysfunction, adrenergic, and vagal responsiveness are factors which appropriately explain the symptoms of MVPS. Pharmacological therapy, depending on the severity of the symptoms, is one option for treatment. Education on the etiology of their symptoms, instruction on lifestyle modifications, and reassurance from their physician are appropriate methods for the management of MVPS patients.
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PMID:Mitral valve prolapse. 186 Oct 97

Syncope usually has a cardiovascular source, so neurologic evaluation has a low diagnostic yield in these patients. Cardiac arrhythmias in persons with or without structural heart disease can produce syncope. Neurocardiogenic dysfunction that results in diminished venous return and hypercontractility is another frequent cause. Postural hypotension or left ventricular outflow obstruction may also be to blame. Careful history taking and physical examination, head-up tilt testing, echocardiography or radionuclide isotope imaging, and electrophysiologic study are often diagnostic. However, syncope remains undiagnosed in some patients, and they may require periodic reassessment. Treatment options are available for most cardiovascular disorders, among them use of pharmacologic agents; catheter, surgical, or radio-frequency modification of certain tachycardias; and permanent pacing.
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PMID:Cardiovascular causes of syncope. Identifying and controlling trigger mechanisms. 161 Apr 34

Forty patients (36 men and 4 women) with life-threatening arrhythmia received an implantable cardioverter defibrillator (ICD). Mean age was 63 years (range, 46 to 80 years). All patients had structural heart disease, with coronary artery disease in 32 patients, idiopathic cardiomyopathy in 7 patients, and hypertensive heart disease in 1 patient. Mean left ventricular ejection fraction was 29 +/- 13%. The clinical arrhythmia was out-of-hospital cardiac arrest in 14 patients (35%), symptomatic sustained ventricular tachycardia in 21 patients (53%), and episodes of syncope without documented spontaneous ventricular arrhythmia but ventricular tachycardia that was easily provoked at the time of electrophysiologic testing in 5 patients (13%). Sustained ventricular tachycardia was induced in 37 patients (93%) at basic electrophysiologic testing. The average number of drug failures was 2.9 +/- 1.4 per patient. One patient (2.5%) died perioperatively because of intractable ventricular tachycardia and ventricular fibrillation. During a median follow-up period of 5.5 months (range 2-21 months) 2 sudden deaths occurred. No patient had a serious complication during the follow-up period. Ten patients (25%) received antiarrhythmic drugs to suppress spontaneous ventricular tachycardia. Appropriate shock treatment was received by 18 patients (45%), and inappropriate shock treatment was received by 2 patients (5%). Several issues regarding use of the ICD must be considered, but the device seems to be useful, and it is associated with an acceptable rate of complications and good long-term success at the present time.
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PMID:Clinical experience in patients with implantable cardioverter defibrillators. 188 Aug 99

To assess the potential for ventricular tachycardia (VT), ventricular extrastimulus testing was performed in 33 young patients with complex ventricular ectopic activity defined as multiform ventricular premature complexes (VPCs), couplets or nonsustained VT, or a combination, found during electrocardiographic monitoring. There were 21 male and 12 female patients with a mean age of 11 years (range 1 to 18). Patients were divided into 2 groups based on the presence (14 patients) or absence (19 patients) of syncope. Patients with syncope had ostensibly normal hearts (9 patients) or miscellaneous heart disease (5 patients). Patients without syncope had ostensibly normal hearts (8 patients) or miscellaneous heart disease (11 patients). Ventricular stimulation protocol consisted of burst pacing and 1 to 4 programmed extrastimuli decreasing to refractoriness at 3 drive-train cycle lengths, and at 2 pacing sites (right ventricular apex and outflow tract) during the drug-free baseline state and isoproterenol infusion. No patient had VT induced with 1 or 2 extrastimuli. VT was induced in 13 of 14 patients (93%) with syncope, and in 9 of 19 patients (47%) without syncope (p less than 0.05). Using a 3-extrastimuli protocol, 8 of 14 patients (57%) with and 3 of 19 patients (16%) without syncope had VT induced (p less than 0.05). These findings suggest that VT may be the cause of syncope in young patients with complex ventricular ectopic activity.
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PMID:Complex ventricular ectopic activity in patients less than 20 years of age with or without syncope, and the role of ventricular extrastimulus testing. 189 81

Syncope is a common clinical problem. Patients with cardiac syncope have a poor prognosis and a high incidence of sudden death during follow-up. The most common diagnosis in these patients is ventricular tachycardia in the setting of coronary artery disease. Patients with syncope and structural heart disease should undergo EP testing to exclude ventricular tachycardia. The use of SAE may be helpful in selecting patients who are likely to have ventricular tachycardia at EP testing. Patients with syncope and a normal heart have an excellent survival, but about 30 percent have recurrent spells. Those patients with a normal heart and syncope in the upright position often have neurally mediated syncope, and the diagnosis can be confirmed by tilt testing. Patients defying diagnosis should undergo loop monitoring to document the cardiac rhythm during syncope.
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PMID:New diagnostic modalities for the evaluation of the patient with syncope. 189 74


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