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)

In 184 patients given an event recorder for the evaluation of palpitations, syncope or presyncope, we found that event recorders are useful and relatively inexpensive in the initial evaluation of patients with palpitations regardless of the presence of heart disease, and of syncopal or presyncopal patients without heart disease. In patients with presyncope or syncope who have heart disease and a negative electrophysiology evaluation, event recorders have less utility and are more costly.
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PMID:Utility and cost of event recorders in the diagnosis of palpitations, presyncope, and syncope. 919 28

Although pacemaker recalls are common, the optimal mechanism for risk assessment and triage of patients at risk for sudden loss of device system function is unknown. A retrospective chart review of 120 patients with factory proven failed devices was performed. Logistic regression analysis was used to determine clinical correlates of emergency room versus outpatient clinic presentation at time of device failure. Twenty-two patients (18%) presented to emergency and 98 (82%) to clinic. Sixty-three devices had no device output at the time of presentation. Multivariate logistic regression analysis revealed that antiarrhythmic drug use (odds ratio: 7.4, 95% CI: 2.0-28.0), atrioventricular nodal disease as an indication for pacing (odds ratio: 2.8, 95% CI: 1.2-3.0), and female gender (odds ratio: 2.2, 95% CI: 1.0-4.5) were the only significant correlates of emergency room presentations. Pacemaker dependency (escape heart rate < 40 beats/min) did not correlate with location of presentation even though no device output at the time of presentation was associated with emergency room presentation (odds ratio: 2.5, 95% CI: 1.1-5.8). Neither the presence of structural heart disease nor symptoms at the time of device implantation (syncope or presyncope) were correlated with location of presentation upon unexpected device failure. Although there were no deaths in the 120 failed devices studied, there were 26 deaths in the total group of 227 patients with recalled devices that could not be studied. Antiarrhythmic drug use, electrocardiographic pacing indication, and female gender may be more sensitive predictors of emergency room presentation and significant symptoms in the event of unanticipated pacemaker failure. The inability of any retrospective analysis to accurately assess mortality in the setting of pacemaker system failure underscores the need for prospective databases in recall situations.
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PMID:When pacemakers fail: an analysis of clinical presentation and risk in 120 patients with failed devices. 947 52

The clinical efficacy of electrical algorithms for termination of slow ventricular tachycardia (VT) and ventricular fibrillation (VF) in implantable cardioverter-defibrillators (ICDs) is well established. Such algorithms have not been equally well defined for fast VT reversion. We report the testing of a prospectively designed algorithm for ICDs to treat fast VT that is inherently less responsive to antitachycardia pacing than slow VT. Fourth-generation ICD devices were programmed to three prospectively defined tachycardia detection zones as follows: cycle lengths < or = 260 ms for VF, 270-330 ms for fast VT, and > 330 ms for slow VT. The initial selected therapy for the VF zone was a high-energy biphasic shock (> 15 J), while a 3- or 5-J biphasic shock was usually administered for fast VT, and antitachycardia pacing was initially attempted for slow VT. Initial therapy was followed by backup therapy with high-energy shocks. Twenty-eight patients, 24 of whom were males, all with organic heart disease, with a mean age of 65 +/- 9 years, received either a Medtronic 7219D (23 patients), 7219C (2 patients), 7218SP1 (2 patients), or 7218C (1 patient) ICD with a nonthoracotomy lead system. The defibrillation threshold was 10 +/- 5 J. At predischarge electrophysiologic testing, a single 3- or 5-J shock terminated all episodes of fast VT tested. During a follow-up of 18 +/- 9 months, there were four nonarrhythmic deaths. Fourteen patients (50%) had a total of 21 VF, 44 fast VT, and 202 slow VT episodes. Twenty-three of 24 (96%) VF, 33 of 39 (84%) fast VT, and 193 of 202 (95.5%) slow VT episodes were terminated with the first delivered therapy in each therapy algorithm (p = NS). The overall efficacy of the entire electrical therapy algorithm was 100% for VF, 100% for fast VT, and 98% for slow VT episodes (p = NS). No patient experienced syncope or presyncope during fast VT or VF in this study. We conclude that a third detection and therapy zone can be successfully programmed in ICDs to define a range of fast VT episodes that can be effectively terminated with lower energy cardioversion shocks with comparable success and freedom from arrhythmic symptoms to electrical therapies used for slow VT and VF.
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PMID:Evaluation of a programming algorithm for the third tachycardia zone in a fourth-generation implantable cardioverter-defibrillator. 986 51

The use of radiofrequency energy for the treatment of supraventricular tachycardia in pediatric patients has gained widespread acceptance, especially for tachyarrhythmias associated with palpitations, dizziness, presyncope or syncope, cardiomyopathy, and cardiac arrest. Ablation of the substrate supporting atrioventricular reentry, atrioventricular node reentry, and automatic atrial tachycardia yields a 90%-98% success rate with low incidence (< 1%) of complications and adverse side-effects. Ablation of intra-atrial reentry, including atrial flutter and fibrillation, appears to be promising and would be a significant advance in the management of patients following extensive atrial surgery for congenital heart disease. Radiofrequency energy is also used to treat various forms of idiopathic ventricular tachycardia. Finally, radiofrequency energy has been extended to control the ventricular rate associated with malignant atrial tachycardia by either modification or ablation of the atrioventricular node, and subsequent pacemaker implant. Long-term outcome of radiofrequency ablation is unknown, but the short-to-intermediate (1-5 yrs) outcome is excellent, with low recurrence rate of the tachycardia, no proarrhythmic effect, and excellent clinical state.
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PMID:The use of radiofrequency energy in pediatric cardiology. 1015 20

Syncope in the patient with structural heart disease and a nondiagnostic noninvasive workup is a generally accepted indication for an invasive electrophysiologic study. However, if the electrophysiologic evaluation is not highly sensitive, arrhythmic causes of syncope may not be discovered. In these patients, recurrent syncope and even sudden death may be observed at follow-up. Thus, we evaluated long-term follow-up in 68 consecutive patients who presented with syncope, coronary artery disease, and who had a negative invasive electrophysiologic evaluation. At a mean follow-up of 30 +/- 18 months (range 1 to 65), there have been 2 sudden deaths and 1 episode each of ventricular fibrillation and ventricular tachycardia in patients treated with an implantable cardioverter-defibrillator. All 4 arrhythmias occurred in patients with left ventricular fractions < or = 25%. Seventeen patients had recurrent presyncope or syncope. Bradycardia causing syncope was found in 8 of these patients. A bundle branch block at the initial evaluation predicted for the occurrence of bradycardia at follow-up. We conclude that in patients with coronary artery disease and syncope, noninducibility at electrophysiologic study predicts a lower risk of sudden death and ventricular arrhythmias. However, in patients with a reduced ejection fraction, the risk of sudden death and ventricular arrhythmias remains up to 10%/year and these patients may warrant treatment with implantable cardioverter-defibrillators. Recurrent syncope is common, and frequently a bradyarrhythmia is found to be the cause. Treatment of selected patients (especially those with bundle branch blocks) with permanent pacemakers may be justified.
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PMID:Long-term outcome of patients with syncope associated with coronary artery disease and a nondiagnostic electrophysiologic evaluation. 1023 91

Vasovagal syncope is the most common cause of syncope, but its risk for driving remains uncertain. We analyzed the clinical characteristics of patients who had syncope during driving and subsequently underwent the head-up tilt test (HUTT). Of the 245 consecutive patients undergoing HUTT, 23 (9%) had > or =1 episode of syncope during driving. HUTT was positive in 19 (group A) and negative in 4 (group B) patients. No patient had structural heart disease. In group A, the driving incident occurred on the first syncope in 3 patients, and the other 16 patients had 1 to 4 episodes of prior syncope not associated with driving. In group B, the driving incident occurred on the first syncope in 1 patient, and the other 3 patients had prior syncope (3 episodes in each) not associated with driving. Seven group A and 1 group B patients had 2 syncope-related driving incidents, and the remaining patients had only 1 syncope-related driving incident. The syncope-related driving incidents caused personal injury in 7 group A and 2 group B patients. One incident in 1 group A patient caused the death of another driver. After HUTT, all but 1 patient in group A received medical treatment and only 1 patient in group B received empirical beta-blocker therapy. During the follow-up of 51+/-26 months, 1 patient died and another was lost to follow-up. Of the remaining patients, 4 patients had recurrence of syncope and 2 patients had presyncope in group A. One of these patients had another syncope-related driving incident. No group B patient had syncope recurrence. A second etiology of syncope was never found in any patient. We conclude that vasovagal syncope during driving is not uncommon in patients referred for syncope evaluation. Early medical attention to patients with vasovagal syncope may help reduce syncope-related driving incidents.
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PMID:Potential risk of vasovagal syncope for motor vehicle driving. 1095 74

Left ventricular outflow tract (LVOT) tachycardia is an uncommon form of idiopathic ventricular tachycardia (IVT). The underlying mechanism of this arrhythmia appears to be cyclic AMP-medicated triggered activity. The tachycardia occurs in the absence of structural heart disease and is generally benign, presenting commonly as palpitations and presyncope. It can manifest either a right or left bundle branch block morphology with an inferior axis. Subtle variations in the QRS morphology in leads I, V1, and V2 can help in localizing the anatomic site of origin (SOO). The arrhythmia is typically responsive to a variety of pharmacologic agents (beta-blockers, calcium channel blockers, Class I and II agents). Radiofrequency catheter ablation of LVOT tachycardia SOO as determined by pace mapping is quite efficacious (success rates of 90%). Magnetic electroanatomic mapping augments this by permitting three-dimensional catheter mapping and reproducible localization of the SOO. Catheter ablation should be considered relatively early in patients who experience severe symptoms with their arrhythmia and have failed, or are reluctant to take medications for the disorder.
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PMID:Clinical characteristics and catheter ablation of left ventricular outflow tract tachycardia. 1140 89

The objectives of this study were to: (1) define the incidence of presyncope and/or syncope in patients with paroxysmal junctional tachycardias, (2) determine their causes, and (3) determine the outcome of symptoms. Syncope is a frequent problem and is often caused by paroxysmal tachycardia. The mechanism of hemodynamic instability is unknown. The population study consisted of 281 patients, consecutively recruited because they had paroxysmal tachycardia and a sinus rhythm on a normal electrocardiogram. Fifty-two patients (group I) had presyncope and/or syncope associated with tachycardia. The remaining patients (group II) had no loss of consciousness. Transesophageal programmed atrial stimulation used 1 and 2 atrial extrastimuli, delivered in a control state, and if necessary, after infusion of 20 to 30 microg of isoproterenol. Arterial blood pressure was monitored. Vagal maneuvers and echocardiogram were performed in all patients. Paroxysmal tachycardia was induced in 51 group I patients and 227 group II patients. Comparisons of groups I and II revealed that age (50 +/- 21 vs 49 +/- 17 years), presence of heart disease (10% vs 10%), mechanism of tachycardia with a predominance of atrioventricular nodal reentrant tachycardia (70.5% vs 76%), and rate of tachycardia (196 +/- 42 vs 189 +/- 37 beats/min) did not differ between the groups. However, there were differences in both groups with regard to significantly higher incidences of positive vasovagal maneuvers (35% vs 4%, p <0.01), isoproterenol infusion required to induce tachycardia (55% vs 17%, p <0.001), and vasovagal reaction at the end of tachycardia (41% vs 4%, p <0.05). Thirty-seven group I patients underwent radiofrequency ablation of the reentrant circuit, which suppressed presyncope and/or syncope in 36 of the 37 patients. Thus, presyncope and/or syncope frequently complicated the history of patients with paroxysmal junctional tachycardia (18.5%). Several mechanisms are implicated, but vasovagal reaction was the most frequent cause. Treatment of the tachycardia typically suppressed presyncope and/or syncope.
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PMID:Incidence and mechanism of presyncope and/or syncope associated with paroxysmal junctional tachycardia. 1144 9

When faced with a patient with exercise-induced syncope, it is important to exclude heart disease. Nevertheless, neurally-mediated syncopes should be taken into account in the differential diagnosis and the tilt table test is essential to establish this diagnosis. We report the case of an 11-year-old boy, who presented recurrent exercise-induced fainting. The results of cardiac and neurologic tests were negative. The tilt table test with pharmacological challenge with isoproterenol infusion induced arterial hypotension and presyncope, and a diagnosis of neurally-mediated syncope was made. After initiating beta-blocker treatment, the patient has remained asymptomatic during a follow-up of 10 months.
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PMID:[Exercise-induced syncope]. 1179 47

The flecainide test is widely used in Brugada syndrome. However, its reproducibility and safety remain ill-defined. This study included 22 patients (18 men, mean age 34 years). Mutations in the SCN5A gene were found in eight patients. Two patients had aborted sudden cardiac death, 8 had syncope/presyncope, and 12 were asymptomatic. The ECG was diagnostic in 19 patients and suggestive in 3. At baseline, 21 of 22 patients underwent a flecainide test (2 mg/kg IV bolus over 10 minutes). In 21 of 21 patients the test was diagnostic or amplified the typical ECG pattern. At the end of drug infusion, sustained VT lasting 7-10 minutes developed in two patients. A second flecainide test was performed within 2 months in 20 patients. The test was not repeated in the two patients with prior development of VT. The flecainide test was diagnostic in 20 of 20 patients. Sustained VT occurred in one patient and recurrent VF in another. The reproducibility of the flecainide test was 100%. In 4 (18%) of 22 patients major VAs were documented after the end of flecainide infusion. VA occurred in 3 (43%) of 7 patients with, versus 1 (7%) 15 without SCN5A gene mutation (P < 0.05). No diagnostic ECG changes or arrhythmias developed in 25 control patients without structural heart disease who underwent the same study protocol. This study shows a high flecainide reproducibility, supporting its diagnostic value in Brugada syndrome. However, the occurrence of major VA, significantly higher in patients with documented SCN5A gene mutation, including in asymptomatic patients, mandates the performance under appropriate medical supervision. Whether a slower rate of drug infusion can lower the risk of VA induction, while maintaining the sensitivity of the test should be explored.
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PMID:Flecainide test in Brugada syndrome: a reproducible but risky tool. 1268 41


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