Syncope Of Undetermined Etiology Research Articles

Syncope risk stratification in the ED.

Syncope may be the final common presentation of a number of clinical conditions spanning benign (i.e. neurally-mediated syncope) to life-threatening diseases (i.e. cardiac syncope). Hospitalization rate after a syncopal episode is high. An effective risk stratification is crucial to identify patients at risk of poor prognosis in the short term period to avoid unnecessary hospital admissions. The decision to admit or discharge a syncope patient from the ED is often based on the physician's clinical judgment. In recent years, several prognostic tools (i.e. clinical prediction rules and risk scores) have been developed to provide emergency physicians with accurate guidelines for hospital admission. At present, there are no compelling evidence that prognostic tools perform better than physician's clinical judgment in assessing the short-term outcome of syncope. However, the risk factors characterizing clinical prediction rules and risk scores may be profitably used by emergency doctors in their decision making, specifically whenever a syncope patient has to be discharged from ED or admitted to hospital. Patients with syncope of undetermined etiology, who are characterized by an intermediate-high risk profile after the initial evaluation, should be monitored in the ED. Indeed, data suggest that the 48h following syncope are at the highest risk for major adverse events. A new tool for syncope management is represented by the Syncope Unit in the ED or in an outpatient setting. Syncope Unit may reduce hospitalization and length of hospital stay. However, further studies are needed to clarify whether syncope patients' prognosis can be also improved.

Assessment of left ventricular volume by an ambulatory radionuclide monitoring system during head-up tilt in patients with unexplained syncope: Relation to autonomic activity assessed by heart rate variability

Background. Decreased left ventricular volume during head-up tilt plays an important role in triggering syncope in patients with neurally mediated syncope. However, precise changes in left ventricular volume during head-up tilt have not been well investigated. This study was conducted to test the hypothesis that the decline in left ventricular volume during tilt could trigger ventricular mechanoreceptor activation. Methods and Results. To investigate the mechanisms of tilt-induced syncope, we measured the temporal changes in left ventricular volume, ejection fraction, cardiac output, and heart rate variability indices during head-up tilt in 25 patients with syncope of undetermined etiology. Eleven patients had a cardioinhibitory response (CI group), 7 patients showed a vasodepressor response (VD group), and 7 patients demonstrated a negative response (NG group). Before syncope, ejection fraction increased most in the CI group, the left ventricular end-diastolic volume declined most in the VD group (VD group, −11.0% ± 3.3%; CI group, −2.8% ± 4.8%; NG group, −3.4% ± 2.2%; P < .005), and the high-frequency spectra increased most in the CI group (CI group, 25.0% ± 21.0%; VD group, −4.1% ± 11.7%; NG group, −5.3% ± 12.7%; P < .01). The vasodepressor response was dependent on left ventricular volume, whereas the cardioinhibitory response was related to the vagal activity reflected by high-frequency spectra. Conclusions. The precise evaluation of left ventricular volume by an ambulatory radionuclide monitoring system combined with a heart rate variability analysis is considered useful for clarifying the pathophysiology of neurally mediated syncope. (J Nucl Cardiol 2001;8:660-8.)

Autonomic responses to orthostatic stress in head-up tilt testing: relationship to test-induced prolonged asystole.

Prolonged asystole is sometimes an extreme manifestation of neurally mediated syncope. To investigate the mechanism of head-up tilt testing-induced prolonged (life-threatening) cardiac asystole, we measured temporal changes in frequency domain heart rate variability indices in 25 patients with syncope of undetermined etiology. Head-up tilt testing (80 degrees) was performed in 25 patients for up to 40 min or until asystole or syncope occurred. Three patients (Group 1; 37 +/- 13 years, 1 man 2 women) had an episode of prolonged cardiac asystole (> or = 10 s) during testing, necessitating cardiopulmonary resuscitation. Syncope, but no asystole, was induced in 10 patients (Group 2; 48 +/- 31 years, 6 men, 4 women), and 12 patients (Group 3; 55 +/- 20 years, 5 men, 7 women) failed to show asystole or syncope during testing. Power spectra of low (0.04-0.15 Hz) and high (0.15-0.40 Hz) frequency, and total (0.01-1.00 Hz) frequency spectra were measured in consecutive 2 min segments throughout the test. Maximally changed values in heart rate, systolic blood pressure, and heart rate variability indices during testing were compared among the three groups (maximally changed values did not include the values during tilt-induced symptoms). High frequency spectra in Groups 2 and 3, but not in Group 1, decreased during the test. High frequency spectra, low frequency spectra, and total spectra in Group 1 were significantly higher than those in Groups 2 and 3 during testing. In Group 1 patients, findings at test-induced asystole were consistent with exaggerated sympathetic and concurrent persistent parasympathetic activity. Unusual autonomic responses to orthostatic stress can cause prolonged asystole, and this autonomic nerve dysregulation may relate to asystolic episodes associated with cardiovascular collapse.

Tilt test results in young and elderly patients with syncope of unknown origin.

The effects of aging on the results of prolonged drug-free tilt testing were studied in 175 consecutive patients with unexplained syncope divided into 3 groups: 59 patients < 40 years old; 57 patients between 40 and 60 years; and 59 patients > 60 years old. Tilt-induced vaso-vagal syncope occurred respectively in 17 (29%), 20 (35%), and 18 patients (31%) in the 3 age groups. Vasodepressor, mixed, and cardioinhibitory vaso-vagal syncope occurred similarly in the 3 groups; organic heart disease and systemic hypertension were more frequent in elderly patients without affecting the incidence of tilt-induced syncope. Blood pressure and heart rate variations during syncope were similar in the 3 age groups; in the first 20 minutes of tilt testing, before the appearance of the vaso-vagal reflex, elderly patients showed greater reduction in blood pressure and smaller increase in heart rate than younger patients. Our data indicate that increasing age determines a different blood pressure and heart rate behavior during tilt testing, but apparently does not influence the incidence of vaso-vagal syncope in patients with syncope of undetermined etiology. As the proportion of patients with a positive isoproterenol tilt test was reported to decline with age, our results suggest that the reduced incidence of syncope during isoproterenol tilt testing could be the expression of impaired autonomic response among elderly syncope patients.

Heart rate variability and head-up tilt testing in patients with syncope of undetermined etiology.

Indices of heart rate variability are non-invasive indicators of neural control of the heart. To investigate the significance of changes in heart rate variability in neurally mediated syncope, we performed head-up tilt testing in 45 patients with syncope of undetermined etiology. Seventeen patients showed a negative response and 28 showed a positive response; 18 had a vasodepressor response (systolic blood pressure dropped > or = 50% without a decrease in heart rate) and 10 had a vasovagal response (systolic blood pressure dropped > or = 50% with a decrease in heart rate of > or = 30%). The mean RR-interval, the standard deviation of normal sinus RR-intervals (standard deviation of RR-interval) and power spectra were measured in consecutive 2 min periods throughout the study. Power spectra consisted of low frequency (0.04-0.15 Hz), high frequency (0.15-0.40 Hz) and total spectra (0.01-1.0 Hz). Both high frequency spectra and the low/high frequency spectra ratio significantly changed with head-up tilt testing regardless of the response. However, high frequency, low frequency and total spectra increased in relation to symptoms. These changes were most profound in the high frequency spectra of subjects with a vasovagal response. Since high frequency spectra reflect parasympathetic tone, a profound change in the high frequency spectra implies that parasympathetic activities play a significant role in patients with a vasovagal response. The assessment of heart rate variability during head-up tilt testing can provide new insight into the pathogenesis of syncope of undetermined etiology.

1025-98 Exaggerated Sympathetic and Failed Withdrawal of Parasympathetic Activity During Head-up Tilt Precipitates a Life-threatening Cardiac Asystole

A life-threatening cardiac asystole can be a malignant manifestation of vasovagal syncope induced by head-up tilt (HUT) testing. To investigate the mechanism of HUT-induced life-threatening cardiac asystole (T-LTAS), we measured a temporal change of frequency domain heart rate variability indices (HRV) in 25 patients (pts) with syncope of undetermined etiology. Three pts (37 ± 13 years, 2 male) had T-LTAS episode; asystole ≥ 10 seconds and cardiopulmonary resuscitation was necessary (Group 1, G1). Ten pts (48 ± 31 years, 6 male) had positive test (syncope was induced by HUT) but no asystole (Group 2, G2). and 12 pts (55 ± 20 years, 5 male) in negative test (Group 3, G3). After 10 min in supine (Su), HUT (80°) was performed up to 40 min. Power spectra of low (L, 0.04 Hzl, high (H, 0.15–0.40 Hz) and total (T, 0.01–1.00 Hz) frequency were measured in consecutive 2 min segments throughout the study. Maximally changed values (Mx) in HR, systolic blood pressure (BPs) and HRV during HUT were compared among 3 groups. Mx were obtained at 2 min or 4 min before the moment of T-LTAS or syncope in G1 and G2, respectively. HR (bpm) BP5 (mmHg) H(ms) L (ms) T (ms) G1 (Su/Mx) 60 ± 8/64 ± 13 105 ± 3/87 ± 13 15 ± 11/21 ± 6 # 20 ± 11/58 ± 41 # 30 ± 1/73 ± 29 # G2 (Su/Mx) 9/88 ± 21 * 126 ± 23/79 ± 13 * 11 ± 11/6 ± 4 * 14 ± 11/13 ± 9 28 ± 17/28 ± 1 G3 (Su/Mx) 71 ± 13/90 ± 20 * 138 ± 15/115 ± 15 * 15 ± 12/6 ± 4 * 16 ± 10/14 ± 13 36 ± 18/26 ± 16 mean ± SD * p &lt; 0.05. vs Su # P &lt; 0.05 vs G2, G3 H in G2 and G3 was decreased by HUT, whereas HUT did not decrease H in G1. H, L and T in G1 during HUT were significantly higher than those in G2 and G3, respectively. Findings were consistent with exaggerated sympathetic and failed withdrawal of parasympathetic activity during HUT in patients with T-LTAS. Unusual autonomic responses to orthostatic stress can cause prolonged asystole, and this autonomic nerve dysfunction may lead to sudden cardiac death associated with cardiovascular collapse.

916-88 Simultaneous Measurement of Left Ventricular Volume and Parasympathetic Activity During Head-up Tilt in Vasovagal Syncope

Present study tested the hypothesis that the great decline of left ventricular volume (LVV) during Head-up tilt (HUT) triggers ventricular mechanoreceptor activation and subsequently increases parasympathetic activation associated with hypotension-bradycardia. We measured temporal changes of frequency domain heart rate variability indices (HRV) and LVV using M mode echocardiogarphy during HUT (80° up to 40 min) in 15 patients (pts, 50 ± 23 years) with syncope of undetermined etiology. HRV consisted of low (L, 0.04 Hzl, high (H, 0.15–0.40 Hz) and total (T, 0.01–1.00 Hz) components. For LVV analysis, EDV. ESV and EF were calculated using Teichholtz formula. HRV and LW indices were measured in consecutive 2 min segments throughout the study. Eight pts had positive tests (syncope was induced by HUT; Group 1, G1) and 7 pts in negative tests (Group 2, G2). Data were shown below [SSP, systolic blood pressure; mean in HR and SBP; Suo supine; Δ and Δ%, differenct es between values at 2 min of HUT and maximally changed values (Mx) during HUT; L/H, ratio of Land H components]. HR (bpm) SBP(mmHg) ΔH ΔLJH Δ%EDV Δ%ESV Δ%EF Gl (Su/Mx) 77/64 # 117/79 # 2.8 0.058 -53 + -49 * +23 G2(Su/Mx) 6S/75 # 132/124 -11.6 0.063 -19 -20 +22 * p &lt; 0.05 vs G2 # P &lt; 0.05 vs Su Before syncope, LVVs in G1 gradually and more profoundly declined than those in G2. The values of H significantly increased from supine to 2 min prior to syncope in G1. Also, the values of H at 2 min prior to syncope in G1 was significantly higher than those at Mx in G2 (14 ± 7 vs. 7 ± 4 ms, p &lt; 0.05). Simultaneous measurements of LW and HRV during HUT are useful for evaluating pathophysiology of neurally mediated syncope. Preceding decrease of LVV can trigger exaggerated parasympathetic activity in patients with vasovagal syncope.

Clinical Cardiac Electrophysiology:History, Rationale, and Future

The discipline of clinical cardiac electrophysiology has evolved over the past 40 years. Intense interest has resulted in the clinical application of intracardiac electrophysiologic techniques over the past 20 years. Clinical cardiac electrophysiologic studies have developed since the demonstration that programmed electrical stimulation could be performed in the human heart to evaluate tachyarrhythmias and that cardiac electrical activity that could not be detected on the body surface could be measured with intracardiac electrodes. Clinical electrophysiologic techniques have evolved for the assessment of sinus nodal, AV nodal, and His-Purkinje system function. The evaluation of tachyarrhythmias has progressed rapidly, and pharmacologic, device, and surgical therapy can now be guided by electrophysiologic studies. Invasive electrophysiologic studies have confirmed the utility of noninvasive electrocardiographic analysis and in several circumstances have proved that invasive studies are not necessary. Alternatives to invasive electrophysiologic evaluation continue to be debated. It is clear that when performed by well-trained individuals in appropriately equipped laboratories, electrophysiologic studies are safe and can be shown to be beneficial. Clinical cardiac electrophysiology continues to evolve, and problems of uniformity of methods, definitions of terms, and protocols remain to be resolved. The future of clinical cardiac electrophysiology appears to be one of continued evolution of techniques, refinement of indications, and continued clinical applications.

Electrophysiologic Studies of Patients with Hypertrophic Cardiomyopathy Presenting with Syncope of Undetermined Etiology*

Patients with hypertrophic cardiomyopathy (HC) have a high risk of sudden death. The best clinical predictors of sudden death from HC are young age, strong family history of sudden death, ventricular tachycardia (VT), and progression of symptoms such as syncope. We performed 24-hour Holter monitoring and electrophysiologic studies (EPS) on 26 patients with HC, some with the obstructive form of the disease and some with syncope, in order to predict their vulnerability to syncope and to potentially malignant arrhythmias. Holter monitoring demonstrated supraventricular tachycardia (SVT) in 9/26 patients whereas atrial programmed electrical stimulation induced SVT in 17/26 patients. Of the 17 patients, nine had symptomatic hypotension with SVT while lying supine. Holter monitoring demonstrated nonsustained VT in 7/26 patients whereas ventricular programmed electrical stimulation induced VT or ventricular fibrillation (VF) in 6/26 patients. The patient who had the longest run of nonsustained VT on Holter had VF induced by ventricular programmed electrical stimulation. He was cardioverted to normal sinus rhythm with no untoward effects. We found that atrial programmed electrical stimulation induced SVT with hypotension best predicted a history of syncope in these patients. Although one patient required direct current cardioversion, EPS was conducted safely in all patients. Further long-term studies are needed to demonstrate the value of clinical decisions based upon EPS in patients with HC.