Mechanism Of Syncope In Patients Research Articles

Repeated Syncope During Exercise as a Result of Anomalous Origin of Left Coronary Artery With Intramural Aortic Course in a Teenage Boy

Anomalous origin of the left coronary artery from the opposite sinus of Valsalva with an intramural aortic course (L-ACAOS-IM) can cause syncope, sometimes as a prodrome of lethal events, including sudden cardiac death, in young athletes. The detailed mechanism of syncope in patients with L-ACAOS-IM is still unclear. This case report describes a 17-year-old boy who presented to the hospital because of syncope following chest pain with increasing frequency during exercise, such as playing soccer and running. In a treadmill exercise test, a decrease in blood pressure was seen (from 99/56 mm Hg to 68/38 mm Hg); chest pain and faintness accompanied by ST-segment elevation in lead aVR and ST-segment depression at other leads on electrocardiography were noted. These findings and symptoms disappeared spontaneously within a few minutes while clinicians prepared for emergency medications. Coronary computed tomography angiography (CCTA) showed that the origin of the left coronary artery (LCA) was the opposite sinus of Valsalva, and the course of the LCA was through the aortic wall toward the left coronary sinus. He was diagnosed with L-ACAOS-IM. After surgical treatment by unroofing the intramural part of the LCA and reconstructing a neo-ostium, he no longer experienced syncope during exercise. This case suggests that low cardiac output caused by myocardial ischemia, not life-threatening arrythmia, is a main mechanism of syncope in patients with L-ACAOS-IM. Consideration should be given to performing CCTA before an exercise stress test for young patients with syncope and chest pain to avoid the risk of severe myocardial ischemia.

An unusual case of giant cardiac fibroelastoma mimicking left atrial myxoma in a patient presenting with syncope

Cardiac papillary fibroelastomas are the most common primary valvular tumors. Generally benign, they account only for about 10% of all primary cardiac neoplasms, can occur in normal or diseased hearts, and are associated strongly with open heart surgery and radiotherapy. They are, in most cases, incidental findings, but can be discovered after syncope. We report the case of an elderly female, who was referred for syncope and was found to have a large fibroelastoma at the mitral valve annulus, intermittently obstructing the left ventricular inflow tract, and mimicking the presentation of left atrial myxoma. This case illustrates another potential mechanism of syncope in patients with fibroelastomas.

196 Role of endogenous adenosine during ATP-test in patients with syncope of unexplained origin

For some authors, positive head-up tilt-test (HUT) and/or ATP-test could identify patients with vaso-vagal syncope. It has been shown that endogenous adenosine plays a role in the mechanism of syncope in patients with positive HUT. Indeed, patients with positive HUT have higher adenosine plasma levels (APL) than patients with negative HUT. Moreover, APL increase during HUT, only in patients with positive HUT. Adenosine triphosphate injection can induce in some patients with unexplained syncope a cardio-inhibitory but the role of endogenous adenosine in those patients is unknown. In this prospective study we studied APL before and during ATP-test. Twenty consecutive patients with syncope of unexplained origin were included (56.0 □ 23.1 y., 13 females). They underwent baseline APL measurement followed by ATP-test. Then APL was measured 1, 5 and 15 minutes after ATP injection. APL were determined by High Performance Liquid Chromatography method on venous blood samples obtained in resting patients. ATP-test consisted of the intravenous bolus injection of 20 mg ATP during continuous recording of the surface ECG. The test was considered positive when a ventricular pause of ≥ 6 sec. occurred, due either to complete atrioventricular block or sinoatrial block. Nine patients had positive ATP-test. There was no statistical difference between patients with positive and negative ATP-test at baseline, 1, 5 and 15 minutes after ATP injection: 0.32 □ 0.16 μmol/L vs 0.49 □ 0.61 μmol/L, 0.32 □ 0.16 μmol/L vs 0.37 □ 0.21 μmol/L, 0.29 □ 0.23 μmol/L vs 0.41 □ 0.26 μmol/L, 0.34 □ 0.20 μmol/L vs 0.28 □ 0.13 μmol/L, respectively. There was no variation of APL during ATP-test in patients with positive and negative ATP-test. Endogenous adenosine is not involved in the mechanism of ATP-test. These results suggest that ATP-test and HUT have different mechanism and could identify different groups of patients with syncope of unexplained origin.

Uncommon Cause of Syncope in Patient with Bundle Branch Block and Negative Electrophysiological Study

We report a case study of a patient with bifascicular block, episodes of syncope, and negative electrophysiological study (EPS) who diagnosed to have sinus arrest with the help of an implantable loop recorder. This case emphasizes that atrioventricular (AV) block is not the only mechanism of syncope in patients with bundle branch block (BBB) and negative EPS.

Incidence, diagnostic yield and safety of the implantable loop-recorder to detect the mechanism of syncope in patients with and without structural heart disease.

To evaluate the incidence, diagnostic yield and safety of implantable loop recorders (ILRs) in patients with or without structural heart disease (SHD). Two-hospitals, observational, prospective study in consecutive patients with unexplained syncope who underwent an ILR implantation. Between November 1997 and December 2002, a total of 2052 patients with syncope were evaluated (referral population of 590000 inhabitants). The diagnosis remained unexplained in 371 (18%). Of these, 103 patients (5% of total, 28% of unexplained syncope) received an ILR. SHD was present in 38 (37%), and absent in 65 (63%). During a median follow-up of 13 months, syncope was recorded in 52 patients. While patients with and without SHD had similar incidence of syncope recurrence, its mechanism was different. Patients with SHD more frequently had paroxysmal AV block and tachyarrhythmias and patients without SHD more frequently had sinus bradycardia/sinus arrest or no arrhythmia. More patients with SHD finally received an ILR-guided therapy. Sudden death occurred in one patient with SHD. Five syncope-related injuries were noted in 3 patients. The mechanism of syncope is different in patients with and without SHD; diagnostic yield and safety are similar in both groups. About 28% of patients with unexplained syncope have an indication to ILR implantation. The need for ILR implantation in the general population is 34 implants/million inhabitants/year.

Mechanism of syncope in patients with positive adenosine triphosphate tests

Mechanism of syncope in patients with positive adenosine triphosphate tests

Mechanism of syncope in patients with positive adenosine triphosphate tests

ObjectivesWe prospectively evaluated the mechanism of syncope in patients with positive adenosine triphosphate (ATP) tests (defined as the induction of atrioventricular [AV] block with a ventricular pause ≥6 s after an intravenous bolus of 20 mg ATP). BackgroundPatients with unexplained syncope tend to have more positive ATP tests results than those without syncope. MethodsAn implantable loop recorder (ILR) was inserted in 36 ATP-positive patients (69 ± 10 years; 22 women; median of 6 syncopal episodes); 15 of them also had a positive response to tilt testing. ResultsDuring the follow-up of 18 ± 9 months, 18 patients (50%) had syncopal recurrence and 16 (44%) had an electrocardiographically documented episode: AV block (n = 3: paroxysmal in 2 and permanent in 1), AV block followed by sinus arrest (n = 1), sinus arrest (n = 5), sinus bradycardia <40 beats/min (n = 2), normal sinus rhythm (n = 2), sinus tachycardia (n = 1), rapid atrial fibrillation (n = 1), and ectopic atrial tachycardia (n = 1). Bradycardia was documented in a total of 11 cases (69%), and a long ventricular pause (4 to 29 s) was present in eight cases (50%). All three patients with ILR-documented AV block had previously had a negative tilt test, whereas seven of eight with ILR-documented sinus bradycardia or sinus arrest had previously had a positive tilt test. ConclusionsIn patients with adenosine-sensitive syncope, the mechanism of syncope is heterogeneous, although bradycardia is the most frequent finding. Adenosine triphosphate–induced AV block predicts AV block as the mechanism of spontaneous syncope in only a few tilt-negative patients.

A standardized conventional evaluation of the mechanism of syncope in patients with bundle branch block.

The finding of bundle branch block in patients with syncope suggests that paroxysmal AV block may be the cause of syncope, even though its prevalence is unknown. We evaluated 55 consecutive patients with syncope and bundle branch block (mean age 75 +/- 8 years; median of two syncopal episodes per patient) referred to three Syncope Units. The hierarchy and appropriateness of diagnostic tests and the definitions of the final diagnoses followed standardized predefined criteria. Cardiac syncope was diagnosed in 25 patients (45%): AV block in 20, sick sinus syndrome in 2, sustained ventricular tachycardia in 1, aortic stenosis in 2. Neurally mediated syncope was diagnosed in 22 (40%): carotid sinus syndrome in 5, tilt-induced syncope in 15, adenosine-sensitive syncope in 2. Syncope remained unexplained in 8 (15%). Less than half of the patients with bundle branch block have a final diagnosis of cardiac syncope; in these patients, paroxysmal AV block is the most frequent but not the only mechanism supposed.

Mechanism of syncope in patients with bundle branch block and negative electrophysiological test

Background In patients with syncope and bundle branch block (BBB), syncope is suspected to be attributable to a paroxysmal atrioventricular (AV) block, but little is known of its mechanism when electrophysiological study is negative. Methods and Results We applied an implantable loop recorder in 52 patients with BBB and negative conventional workup. During a follow-up of 3 to 15 months, syncope recurred in 22 patients (42%), the event being documented in 19 patients after a median of 48 days. The most frequent finding, recorded in 17 patients, was one or more prolonged asystolic pause mainly attributable to AV block; the remaining 2 patients had normal sinus rhythm or sinus tachycardia. The onset of the bradycardic episodes was always sudden but was sometimes preceded by ventricular premature beats. The median duration of the arrhythmic event was 47 seconds. An additional 3 patients developed nonsyncopal persistent III-degree AV block, and 2 patients had presyncope attributable to AV block with asystole. ...

Mechanism of syncope in patients with isolated syncope and in patients with tilt-positive syncope

Background Because of its episodic behavior, the correlation of spontaneous syncope with an abnormal finding can be considered a reference standard. Methods and Results We inserted an implantable loop recorder in 111 patients with syncope, absence of significant structural heart disease, and a normal ECG; tilt-testing was negative in 82 (isolated syncope) and positive in 29 (tilt-positive). The patients had had ≥3 episodes of syncope in the previous 2 years and were followed up for 3 to 15 months. Results were similar in the isolated syncope group and the tilt-positive group: syncope recurred in 28 (34%) and 10 patients (34%), respectively, and electrocardiographic correlation was found in 24 (23%) and 8 (28%) patients, respectively. The most frequent finding, which was recorded in 46% and 62% of patients, respectively, was one or more prolonged asystolic pauses, mainly due to sinus arrest, preceded for a few minutes by progressive bradycardia or progressive tachycardia-bradycardia. Bradycardia without pa...

Mechanism of Syncope in Patients With Isolated Syncope and in Patients With Tilt-Positive Syncope

Because of its episodic behavior, the correlation of spontaneous syncope with an abnormal finding can be considered a reference standard. We inserted an implantable loop recorder in 111 patients with syncope, absence of significant structural heart disease, and a normal ECG; tilt-testing was negative in 82 (isolated syncope) and positive in 29 (tilt-positive). The patients had had >/=3 episodes of syncope in the previous 2 years and were followed up for 3 to 15 months. Results were similar in the isolated syncope group and the tilt-positive group: syncope recurred in 28 (34%) and 10 patients (34%), respectively, and electrocardiographic correlation was found in 24 (23%) and 8 (28%) patients, respectively. The most frequent finding, which was recorded in 46% and 62% of patients, respectively, was one or more prolonged asystolic pauses, mainly due to sinus arrest, preceded for a few minutes by progressive bradycardia or progressive tachycardia-bradycardia. Bradycardia without pauses was observed in 8% and 12% of cases, respectively. The remaining patients had normal sinus rhythm or sinus tachycardia, except for one, who had ectopic atrial tachycardia. In the tilt-positive group, an asystolic syncope was also recorded when the type of response to tilt-testing was vasodepressor or mixed. Presyncopal episodes were never characterized by asystolic pauses; normal sinus rhythm was the most frequent finding. Homogeneous findings were observed during syncope. In most patients, the likely cause was neurally-mediated, and the most frequent mechanism was a bradycardic reflex. In the other cases, a normal sinus rhythm was frequently recorded. Presyncope was not an accurate surrogate for syncope in establishing a diagnosis.

The mechanism of syncope in patients with bundle branch block

The mechanism of syncope in patients with bundle branch block

The mechanism of syncope in patients with bundle branch block

The mechanism of syncope in patients with bundle branch block

Absence of Increased Systemic Vascular Resistance During Syncopal Episodes in Patients with Tilt‐Positive Neurocardiogenic Syncope

BackgroundThe purpose of this study was to elucidate the mechanism of syncope in patients with neurocardiogenic syncope (NCS) by measuring hemodynamic parameters continuously during a head‐up tilt (HUT) test.MethodsTwenty‐three adults (mean age 22.6 ± 9.8, range 15–62) participated in the study: 16 with a history of syncope suggesting NCS and 7 healthy volunteers who served as controls. The subjects underwent a 45‐minute 60° tilt test. Heart rate and blood pressure were monitored continuously. The stroke volume was measured every minute by noninvasive impedance cardiography, and systemic vascular resistance was calculated from these measurements. The test was terminated when syncope occurred or after 45 minutes in an upward position.ResultsEight of the 16 patients had a positive HUT, while all control subjects had a negative HUT. Decreased stroke volume and cardiac index were observed in all subjects and subgroups in the upward position, compared to the rest position (P &lt; 0.01). Systemic vascular resistance rose in patients with a negative HUT and all controls (P &lt; 0.03), but did not change in the HUT‐positive patients (P = 0.25), during the HUT. Systemic vascular resistance was significantly lower in the upward position in the positive HUT than in the other groups (P &lt; 0.04), but there were no differences in the cardiac index.ConclusionsFailure to achieve an appropriate increase in systemic vascular resistance may be an important mechanism in some cases of NCS and should be taken in account when considering therapeutic options. Impedance cardiography is a noninvasive technique for the detection of this abnormal response and can be used to assess the effect of drug therapy on systemic vascular resistance. A.N.E. 1999; 4(2):121–129

912-43 Sick Sinus Syndrome. A Cardiac or a Neurocardiogenic Disorder?

The commonly proposed mechanism of syncope in patients (pts) with sick sinus syndrome (SSS) is a long sinus pause without an effective escape rhythm. Nevertheless, the probability of a coexistent neurally mediated syncope (NMS) component has not been adequatelly investigated in these pts. We studied 3 groups: Gl: 12 syncopal pts (age: 58 ± 12 years, M/F: 9/3) with SSS (unexplained sinus bradycardia with inadequate chronotropic response to exercise or atropine, long sinus node recovery or sinoatrial conduction times and low intrinsic heart rate), G2; 52 pts (37 ± 17 years, M/F; 18/12) with syncope of unknown etiology and G3: 20 healthy controls (HC) (34 ± 9 years, M/F: 16/4). The same tilt table test (TTT) protocol was used (20 min in 80° upright followed by three 10 min stages in the same position under graded isoproterenol intravenous infusion at 1 – 3μg/min). TTT was considered positive (pos) if induced pre or syncope due to hypotension with or without bradycardia. A pos TTT was observed in 7 Gl pts (58.3%) and 30 G2 pts (57.7%) (p: NS). In contrast, only 4 of the G3 HC (20%) developed syncope (p &lt; 0.005). The mean pos TTT duration was similar in both pts with SSS and pts with NMS (57 ± 18 vs 55 ± 17 min, p: NS). The mean posm duration was longer in the 4 HC with an induced vagotonic reaction when compared to the 30 NMS pts of G2168 ± 10 vs 55 ± 17 min, p &lt; 0.05). We conclude that syncopal SSS pts commonly demonstrate a pos TTT. This might explain the occasional failure to avoid recurrence of syncope in SSS pts treated with cardiac pacing.

Investigation of the mechanism of syncope in patients with hypertrophic cardiomyopathy

Investigation of the mechanism of syncope in patients with hypertrophic cardiomyopathy