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

The arrhythmias in competitive athletes may be classified as "benign," "paraphysiological" due to prolonged athletic training, or "pathological" due to hemodynamic effects on the athletic performance-risk-arrhythmogenic substratum. Pathological arrhythmias include life-threatening forms that are severe enough to produce symptoms (presyncope, syncope, cardiac arrest) during athletic activity. These forms are in particular rapid VT, VF, torsades de pointes, preexcited atrial fibrillation, sinus atrial and AV block. Our study population includes 766 competitive athletes, mean age 21.1 years (74 top international level), investigated with a cardioarrhythmological work-up for symptoms and for arrhythmias from 1974 to June 30, 1991. Three leading categories, represented by 16 aborted sudden death, 8 sudden death, and 7 induced VF (by EES or TAP) athletes, are described. All athletes with life-threatening arrhythmias, previously as asymptomatic or with minor symptoms had an arrhythmogenic substratum due to underlying silent cardiopathy or primary arrhythmic disorders. Athletic activity can be regarded as a trigger of electrical destabilization.
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PMID:Life-threatening tachyarrhythmias in athletes. 138 4

The clinical and pathologic findings of a 10-month-old girl with congenital heart disease who died after rupture of a congenital distal basilar artery aneurysm are reported. The patient developed transient minimal oculomotor nerve paresis 7 days prior to suffering a massive subarachnoid hemorrhage. The finding of transient third nerve dysfunction, particularly in the context of recurrent syncope, should prompt investigation for an intracranial arterial aneurysm.
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PMID:Transient oculomotor nerve paresis in congenital distal basilar artery aneurysm. 138 22

The electrophysiological evaluation of syncope of unknown origin yields a diagnosis in approximately 40% of patients. In the presence of structural heart disease ventricular tachycardia is the most common etiology accounting for 20% of cases. Over the past several years head-up tilt table testing with isoproterenol provocation has highlighted the syndrome of neurocardiogenic syncope. This syndrome accounts for an additional 30-40% of patients with syncope. There is compelling evidence that this syndrome involves the Bezold-Jarisch reflex with excessive stimulation of ventricular mechanoreceptors (C-fibers) located predominantly in the inferoposterior portion of the heart. Tilt table testing is now an established tool both for diagnosis of this syndrome and for guiding therapy with beta blockers, disopyramide, theophylline, or alpha-agonists. Tilt table testing combined with invasive electrophysiological testing significantly increases the diagnostic yield in the evaluation of syncope.
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PMID:Advances in syncope: a combined approach utilizing head-up tilt testing and electrophysiologic evaluation. 145 78

A 62-year-old woman was admitted our hospital because of concussion of the brain. The level of consciousness improved within several days. Cardiac examination was performed because the patient had experienced feelings of fainting since one year previously, and heart murmur also was heard. The electrocardiogram showed WPW configuration. At the same time that she complained of feelings of fainting, the electrocardiogram showed supraventricular tachycardia. The echocardiogram showed displacement of the septal tricuspid leaflet and mild tricuspid valve, regurgitation. Cardiac catheterization was performed and, using the intracardiac electrocardiogram, we confirmed atrialized right ventricle. We diagnosed this patient as having Ebstein's anomaly with WPW syndrome. The clinical manifestations of this anomaly are quite variable, depending upon the spectrum of pathology and the presence of associated malformations. It is well documented that a considerable proportion of these patients are able to survive into adult life. However, the patient who survives into the sixth decade without a sign of heart failure is extremely rare. We speculate that this patient had not developed right ventricular failure until her 60's because she had a milder form of Ebstein's anomaly and did not have any other congenital heart disease.
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PMID:[A 62-year-old survivor with Ebstein's anomaly without right ventricular failure]. 148 Aug 34

Seven out of 829 pediatric cardiac patients (0.84%) were found to have sinus node dysfunction (SND) over the past seven years. Of the seven patients, three had structurally normal hearts. One of these three patients had long QT syndrome. In four patients, structural heart disease was noted. In three of these four patients the sinus node dysfunction was attributed to cardiac surgery. The age of onset of SND ranged from four months to eight years. Presenting symptoms and signs included syncope, near-syncope, seizure and congestive heart failure. Two patients were asymptomatic. Five patients had episodic sinus pause. Sinus or junctional bradycardia was noted in four patients. Three had tachy-bradycardia. High grade atrioventricular block was noted in one patient. Treadmill exercise test revealed a nonsustained ventricular tachycardia in two patients. All seven patients were found to have prolonged maximal corrected sinus node recovery time. Prolonged intra-atrial conduction time was found in three, prolonged AV nodal conduction time in one, and prolonged His-Purkinje conduction time in one patient during the electrophysiologic study. All seven patients showed abnormal results in intrinsic heart rate study. Anti-arrhythmic drugs were prescribed. During the follow-up study, no patient died, but two patients received a pacemaker implantation. Because of the extent of their conduction system diseases, it is recommended that patients with SND should be thoroughly investigated.
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PMID:Sinus node dysfunction in children. 151 8

Three cases of symptomatic bradycardia due to topical ocular timolol administration are reported. Two patients had syncope related to atrioventricular block, and the other one complained of dizziness due to sinus bradycardia. Heart disease was not present in any case, although a right bundle branch block was observed in one patients. A normal sinus rhythm resumed in all patients after discontinuation of timolol.
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PMID:[Bradyarrhythmias secondary to the use of ophthalmic timolol. A report of 3 cases]. 154 65

Guidelines for the use of electrophysiologic studies in syncope have not yet been formulated. To confirm the sensitivity and specificity of a previously derived model to predict the results of electrophysiologic testing in syncope, the importance of 6 clinical predictors was assessed in a new data set of 141 consecutive patients with unexplained syncope who were referred for electrophysiologic studies. The 6 predictors were: organic heart disease; premature ventricular beats, sinus bradycardia, first-degree heart block and bundle branch block by electrocardiogram; and nonsustained ventricular tachycardia by Holter monitor. Organic heart disease and nonsustained ventricular tachycardia by Holter monitoring were highly sensitive for serious ventricular tachyarrhythmias at electrophysiologic study (sensitivity 100%), whereas sinus bradycardia, first-degree heart block or bundle branch block by electrocardiogram were sensitive for bradyarrhythmic outcomes (sensitivity 79%). Because these variables are so sensitive for serious outcomes of electrophysiologic testing in syncope, invasive studies in patients without these clinical predictors are likely to be of very low diagnostic yield.
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PMID:Usefulness of clinical characteristics in predicting the outcome of electrophysiologic studies in unexplained syncope. 156 76

Syncope is a clinical entity of diverse cause. The historical features surrounding the syncopal event and the presence or absence of heart disease are the most important features in establishing the cause for syncope. Passive head-up tilt study provides a means of identifying many patients with vasodepressor syncope. Electrophysiologic study is important in the elucidation of syncope in patients who have syncope undefined after noninvasive evaluation. With proper use of the modalities available, few patients will have an undefined cause for syncope.
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PMID:Syncope. 156 73

This study examined the role of electrophysiologic study in the evaluation of patients with unexplained syncope. The incidence of abnormalities (conduction disease, supraventricular tachycardia, ventricular tachycardia) was compared in patient groups with and without heart disease, and the effect of treatment of these abnormalities on recurrence of syncope was examined. Electrophysiologic study was performed in 111 consecutive patients with syncope, with antiarrhythmic medications being discontinued 1 week prior to study. There was no mortality associated with the procedure and only 9 patients (8%) had complications (groin haematoma, atrial fibrillation or brady-arrhythmias persisting after the procedure). Abnormalities were detected in 31 of 73 patients with heart disease (42%) but in only 6 of 38 patients with no heart disease (16%, P less than 0.01). During follow-up, syncope recurred in 2 of 37 patients (5%) treated because of abnormal findings, compared with a recurrence rate of 24% (18 of 74 patients) in the untreated group (P less than 0.05). Probability of remaining free from syncope at 2 years was 0.94 in the treated group and 0.72 in the untreated group (P less than 0.05). Mortality during follow-up was confined to the heart disease group with 5 of 30 treated patients in this group dying (17%) compared with 3 of 43 untreated patients (7%, P = not significant). Syncope patients with heart disease were thus more likely to have a diagnostically useful study than patients with normal hearts. Treatment directed at correction of abnormalities detected at electrophysiologic study reduced recurrence of syncope but did not significantly affect mortality. Syncope did not appear to be a prelude for sudden death in patients with normal hearts. Electrophysiologic study had no mortality and low morbidity.
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PMID:Electrophysiologic studies in patients with unexplained syncope. 157 41

A number of practical office and bedside clues to cardiac disease in infants and children have been passed on through the years. They relate to the history, to the inspection and palpation components of the physical examination, and to knowledge of the specific cardiac defects that are likely to be associated with certain clinical syndromes. With the possible exception of coarctation of the aorta, the clues are not diagnostically specific. In many instances, however, they serve to narrow a broad array of diagnostic possibilities to 2 or 3 and, with the aid of other clues and auscultation, they can often be distinguished from one another. When a primary care physician is confronted with a child who has an incidental murmur that is "probably" innocent but could be organic, useful clues favoring an organic murmur are a history of congenital heart disease in a first-degree relative; a history of maternal rubella syndrome, alcohol use, or teratogenic drug use during pregnancy; a history of inappropriate sweating; a history of syncope, chest pain, or squatting; maternal diabetes mellitus; premature birth; birth at a high altitude; cyanosis; abnormal pulsations; recurrent bronchiolitis or pneumonia; chronic unexplained hoarseness; asymmetric facies with crying; and a physical appearance suggestive of a clinical syndrome.
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PMID:Clues in diagnosing congenital heart disease. 157 99


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