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- W2071066568 abstract "Sudden unexpected death syndrome (SUDS) is a leading cause of death in young Southeast Asian men. An epidemiologic survey of young Thai men living along northeastern border of Thailand found that the annual SUDS death rate was 26 to 38 per 100,000 men.1Tungsanga K. Sriboonlue P. Sudden unexplained death syndrome in north-east Thailand.Int J Epidemiol. 1993; 22: 81-87Crossref PubMed Scopus (66) Google Scholar, 2Tatsanavivat P. Chirawatkul A. Klungboonkrong V. Munger R. Chaisiri S. Charerntanyarak L. Saowakontha S. Sudden and unexpected deaths in sleep (Lai Tai) of young men in rural northeastern Thailand.Int J Epidemiol. 1992; 21: 904-910Crossref PubMed Scopus (56) Google Scholar Ventricular fibrillation (VF) is the rhythm leading to cardiac arrest.3Otto C.M. Tauxe R.V. Cobb L.A. Green H.L. Gross B.W. Werner J.A. Burroughs R.W. Samson W.E. Weaver W.D. Trobaugh G.B. Ventricular fibrillation causes sudden death in southeast Asian immigrants.Ann Intern Med. 1984; 100: 45-47Crossref Scopus (110) Google Scholar, 4Baron R.C. Thacker S.B. Gorelkin L. Vernon A.A. Taylor W.R. Choi K. Sudden death among southeast Asian refugees an unexplained nocturnal phenomenon.JAMA. 1983; 250: 2947-2951Crossref PubMed Scopus (108) Google Scholar, 5Gilbert J. Gold R.L. Haffajee G.I. Alpert J.S. Sudden cardiac death in a southeast Asian immigrant clinical, electrophysiologic and biopsy characteristics.PACE. 1986; 9: 912-914Crossref Scopus (15) Google Scholar Episodes mainly occur at night. Typically, the victim wakes up at night with breathing difficulty, in cardiac arrest. Since 1981, there have been reports by the Center of Disease Control that a significant number of young male Southeastern Asian refugees in the United States died suddenly and unexpectedly.6The Centers of Disease ControlSudden unexplained nocturnal deaths among southeast Asian refugees.MMWR. 1981; 30: 518-519Google Scholar, 7US Center for Disease ControlUpdate sudden unexplained death syndrome among southeast Asian refugees: United States.MMWR. 1988; 37: 568-570PubMed Google Scholar The pathophysiology of SUDS is still unknown. Because VF episodes in patients with SUDS usually occur at night, which is different from the timing of sudden death episodes in patients with structural heart disease that usually occur during the morning. Alteration of autonomic modulation may have an important role in the occurrence of VF episodes in these patients. It may also be a guide as to whether certain medications may have beneficial effect or may aggravate VF. We analyzed heart rate variability (HRV) in SUDS survivors compared with controls to determine whether there are changes in autonomic modulation in these patients. We studied 26 patients who survived SUDS-like episodes and were referred for further examination to Siriraj and Bhumibol hospitals. Inclusion criteria were: (1) SUDS survivors were defined as patients who had been apparently healthy before suddenly developing sudden cardiac arrest due to VF and had been successfully resuscitated; and (2) probable SUDS survivors were defined as those who experienced symptoms that reflected the clinical presentation of SUDS, which includes agonal respiration, unresponsiveness after labored respiration usually during sleep, transient symptoms of distress (e.g., moaning, thrashing, grimacing), and syncope without documented VF during symptoms. In this study, patients who were probable SUDS survivors needed to have the Brugada pattern on the electrocardiogram (ECG), defined as right bundle branch block and ST-segment elevation with a J point elevation of ≥1 mV in leads V1 to V3, and inducible polymorphic ventricular tachycardia or VF during electrophysiologic study. We excluded patients who had structural heart disease by echocardiogram, exercise testing, and cardiac catheterization (including coronary angiography), or identifiable causes of cardiac arrest such as prolonged QT syndrome, coronary artery disease, congestive heart failure, or drug-induced arrhythmia. Controls were age-matched healthy men without clinical evidence of heart disease. Controls needed to have normal beats of ≥99% of the total QRS complexes on 24-hour ambulatory electrocardiographic monitoring. Controls were studied during the time of enrollment of patients with SUDS. All patients underwent a routine history, physical examination, chest x-ray, electrocardiography, exercise treadmill test using a modified Bruce protocol, Doppler echocardiography, 24-hour ambulatory electrocardiographic monitoring, a signal-averaged ECG, cardiac catheterization (including coronary angiography), and electrophysiologic study. Electrophysiologic study was performed under sedation. Ventricular stimulation was first performed at the right ventricular apex at 3 running cycle lengths: 600, 500, and 400 ms and up to triple ventricular extrastimuli at twice the diastolic current threshold. If there was no inducible ventricular tachycardia or VF, the protocol was then repeated at the right ventricular outflow tract position. The late potentials by signal-averaged ECG were analyzed using Arrhythmia Research Technology 1200 EPX signal-averaged electrocardiographic system (Austin, Texas). The analysis was based on the quantitative time-domain measurements of the filtered vector magnitude of the orthogonal Frank X, Y, and Z leads. QRS complexes of ≥200 beats were amplified, digitized, averaged, and filtered with a high-pass filter (40 Hz). Three parameters were assessed via a computer algorithm: (1) the filtered QRS duration (f-QRS); (2) the root-mean-square voltage of the terminal 40 ms in the filtered QRS complex (RMS40); and (3) the duration of low-amplitude signals <40 μV in the terminal filtered QRS complex (LAS40). In the present study, the positive late potential was defined as ≥2 of the following criteria: f-QRS >114 ms, RMS40 <20 μV, and LAS40 >38 ms. All patients underwent 3-channel electrocardiographic monitoring for 24 hours. A Zymed (Zymed Medical Instrumentation, Camarillo, California) digital recorder was used to obtain the electrocardiographic data. Electrodes were attached at 5 different positions using the standard EASI lead system (Zymed Medical Instrumentation).8Drew B.J. Scheinman M.M. Evans G.T. Comparison of a vector cardiographically derived 12-lead electrocardiogram with the conventional electrocardiogram during wide complex tachycardia, and its potential application for continuous bedside monitoring.Am J Cardiol. 1992; 69: 612-618Abstract Full Text PDF PubMed Scopus (49) Google Scholar All patients were free of medication during ambulatory electrocardiographic monitoring. Patients were instructed to press the event button if they had symptoms such as palpitation, chest pain, or fainting, so that the electrocardiographic playback would automatically display the ECG at that time. Tapes were analyzed with the Zymed system. The sampled electrocardiographic data were transformed from the Zymed scanner to a microcomputer for processing HRV. The electrocardiographic data were scanned and all QRS complexes were classified using the computer program. The accuracy of QRS complex detection and the labeling of QRS complexes were reviewed and manually edited by an experienced cardiologist. The QRS complexes were carefully classified into sinus beats, supraventricular or ventricular ectopic beats, artifacts, or unclassified. The frequency histogram of the normal RR interval was displayed and the ECG of the intervals in both tails of the normal RR distribution were reviewed. Time-domain variables and average heart rate were obtained from the 24-hour electrocardiographic data. Time-domain variables included SD of all normal RR intervals (SDNN) and the average of SD of normal RR intervals every 5 minutes (ASDNN). Frequency-domain variables of HRV were obtained using fast-Fourier transformation throughout the electrocardiographic recording. This technique was first described by Albrecht and Cohen9Albrecht P. Cohen R.J. Estimation of heart rate power spectrum bands from real-world data dealing with ectopic beats and noisy data.Comput Cardiol. 1988; 15: 311-314Google Scholar and modified by Rottman et al.10Rottman J.N. Steinman R.C. Albrecht P. Bigger Jr, J.T. Rolnitzky L.M. Fleiss J.L. Efficient estimation of heart period power spectrum suitable for physiologic and pharmacologic studies.Am J Cardiol. 1990; 66: 1522-1524Abstract Full Text PDF PubMed Scopus (136) Google Scholar The sampling interval was 329 ms for each electrocardiographic recording. A low-pass filter with a window twice the sampling interval was then applied. Gaps in the time series resulting from noise or ectopic beats were filled in with linear splines. A fast-Fourier transformation was computed and the resulting power spectrum was corrected for the attenuating effects of both the filtering and sampling. We computed the 24-hour power spectral density (based on 5-minute interval data) and calculated the power within 2 frequency bands: (1) low-frequency power, 0.04 to 0.15 Hz, which reflects modulation of sympathetic and parasympathetic tone by baroreflex activity, and (2) high-frequency power, 0.15 to 0.40 Hz, which reflects modulation of vagal tone and the calculated total power spectrum. Continuous data were described by mean and SD and categorical variables were described by frequencies and percentages. Comparisons of the 3 groups (SUDS, probable SUDS, and controls) were made by analysis of variance test with least significant difference post hoc analysis. Comparisons between the combined patient group and controls were made by the unpaired t test. Categorical variables were compared by chi-square test. Frequency-domain variables were logarithmic transformed for analysis because the distribution of the data were not normal. Data for the whole 24 hours, during daytime (8:00 a.m. to 8:00 p.m.), and nighttime (12:00 to 6:00 a.m.) were separately compared. A p value ≤0.05 was considered statistically significant. We studied 15 patients with SUDS, 11 patients with probable SUDS, and 42 controls. There was 1 woman in the SUDS group and the rest of the subjects were men. The mean age was 39 ± 9 years in the patients with SUDS, 40 ± 6 years in patients with probable SUDS, and 36 ± 9 years in controls. Twenty patients (76.9%) had SUDS-like symptom between 6 p.m. and 6 a.m. All subjects in the probable SUDS group had right bundle branch block with ST-segment elevation in leads V1 to V3, whereas 6 of 15 patients (40%) in the SUDS group had this pattern on the ECG. No patients in the control group had right bundle branch block with ST-segment elevation. The signal-averaged ECG was considered positive for late potentials (positive 2 of 3 criteria) in 9 patients (34.6%). Late potentials were demonstrated in 8 of 17 patients (47.1%) with right bundle branch block and ST-segment elevation, but only in 1 (11.1%) of those without these factors (p = 0.067). Electrophysiologic study revealed inducible ventricular tachycardia or VF in 19 patients (73.1%). Inducible ventricular tachycardia or VF was found more in patients with right bundle branch block and ST-segment elevation compared with those without (78.9% and 28.6%, p = 0.017). Late potentials were demonstrated in 8 of 19 patients (42.1%) with inducible ventricular tachycardia or VF but only in 1 (14.3%) of those without (p = 0.186). Holter monitoring showed no significant cardiac arrhythmias. Average premature ventricular complex and premature atrial complex count in patients with SUDS were 1.2 ± 4.5 and 0.6 ± 2.3 per 24 hours (range 0 to 14, and 0 to 20 per 24 hours), respectively. No patients had SUDS symptoms during monitoring. Table 1shows the results of ambulatory electrocardiographic monitoring and HRV analysis. Average heart rate tended to be lower during the day and higher during the night in patients with SUDS compared with controls. The difference in heart rate during daytime and nighttime was significantly greater in the control group compared with the SUDS group (21.3 ± 7.4 beats/min for controls vs 7.0 ± 5.6 beats/min for SUDS patients and 9.1 ± 5.9 beats/min for probable SUDS patients, p <0.001). SDNN, ASDNN, and power in all spectrums were lower in patients with SUDS compared with controls. The decrease in HRV variables in patients with SUDS was more obvious at night. FIGURE 1, FIGURE 2 demonstrate a typical variation of heart rate and SDNN during the day and at night in a patient with SUDS and in a control. TABLE 1Ambulatory Electrocardiographic Findings in Controls, Group With SUDS, Group With Probable SUDS, and Combined GroupVariablesControl (n = 42)SUDS (n = 15)Probable SUDS (n = 11)p Value*p value for analysis of variance test of the 3 groups.Combined (n = 26)p Value†p value for unpaired t test between the combined group and controls.Average HR75 ± 875 ± 1467 ± 80.06672 ± 120.202Average HR (d)81 ± 978 ± 1271 ± 100.01075 ± 120.011Average HR (n)60 ± 871 ± 1562 ± 60.00267 ± 120.007ASDNN66 ± 2143 ± 1965 ± 140.00153 ± 200.014ASDNN (d)56 ± 1839 ± 1561 ± 150.00248 ± 180.078ASDNN (n)80 ± 2747 ± 2275 ± 17<0.00159 ± 240.001SDNN164 ± 4994 ± 30123 ± 21<0.001106 ± 30<0.001SDNN (d)109 ± 3775 ± 24108 ± 170.00389 ± 260.019SDNN (n)118 ± 3679 ± 27112 ± 210.00193 ± 290.005Total power3.6 ± 0.33.2 ± 0.33.6 ± 0.2<0.0013.4 ± 0.30.006Total power (d)3.4 ± 0.33.2 ± 0.33.5 ± 0.20.0143.3 ± 0.30.176Total power (n)3.8 ± 0.33.3 ± 0.43.7 ± 0.2<0.0013.5 ± 0.30.001LF2.9 ± 0.32.5 ± 0.32.9 ± 0.2<0.0012.7 ± 0.30.002LF (d)2.8 ± 0.32.5 ± 0.42.8 ± 0.30.0062.6 ± 0.40.023LF (n)3.0 ± 0.32.6 ± 0.42.9 ± 0.3<0.0012.7 ± 0.40.001HF2.5 ± 0.52.2 ± 0.42.6 ± 0.30.0392.4 ± 0.40.196HF (d)2.3 ± 0.52.1 ± 0.42.5 ± 0.30.1132.3 ± 0.40.972HF (n)2.8 ± 0.52.4 ± 0.52.8 ± 0.30.0112.5 ± 0.50.032Average HR = average heart rate (beats per minute); d = day, HF = spectrum in high-frequency range (ms2), LF = spectrum in low-frequency range (ms2), n = night, Total = total power spectrum (ms2).* p value for analysis of variance test of the 3 groups.† p value for unpaired t test between the combined group and controls. Open table in a new tab FIGURE 2Twenty-four-hour heart rate (upper panel) and SDNN (lower panel) in a control subjects. Normal diurnal changes in heart rate and HRV are demonstrated.View Large Image Figure ViewerDownload (PPT) Average HR = average heart rate (beats per minute); d = day, HF = spectrum in high-frequency range (ms2), LF = spectrum in low-frequency range (ms2), n = night, Total = total power spectrum (ms2). SUDS in southeast Asian has been named differently. In Thailand, it is called “Lai Tai.”1Tungsanga K. Sriboonlue P. Sudden unexplained death syndrome in north-east Thailand.Int J Epidemiol. 1993; 22: 81-87Crossref PubMed Scopus (66) Google Scholar, 2Tatsanavivat P. Chirawatkul A. Klungboonkrong V. Munger R. Chaisiri S. Charerntanyarak L. Saowakontha S. Sudden and unexpected deaths in sleep (Lai Tai) of young men in rural northeastern Thailand.Int J Epidemiol. 1992; 21: 904-910Crossref PubMed Scopus (56) Google Scholar It is called “Pokkuri” in Japan11Gotoh K. A histopathological study on the conduction system of the so-called ‘pokkuri disease’ (sudden unexpected cardiac death of unknown origin in Japan).Jpn Circ J. 1976; 40: 753-768Crossref PubMed Scopus (53) Google Scholar and “Bangungut” in Philippines.12Aponte G.E. The enigma of bangungut.Ann Intern Med. 1960; 52: 1258-1263Crossref PubMed Scopus (46) Google Scholar Most patients who experience SUDS are young (approximately 28 to 34 years), the male:female ratio is 20:1, 68% of SUDS death occur between 9 p.m. and 4 a.m., and death is usually preceded by agonal respiration described as choking or gasping.4Baron R.C. Thacker S.B. Gorelkin L. Vernon A.A. Taylor W.R. Choi K. Sudden death among southeast Asian refugees an unexplained nocturnal phenomenon.JAMA. 1983; 250: 2947-2951Crossref PubMed Scopus (108) Google Scholar, 13Goh KT, Chao TC, Chew CH. Sudden nocturnal death among Thai construction workers in Singapore. Lancet 1990;335:1154Google Scholar Patients with SUDS are unresponsive, difficult to arouse, and have no obvious prodomal symptoms or precipitating factors. Death usually occurs within minutes. SUDS has a considerable economic impact because of the high incidence and fatality rate, and also because it usually strikes the working heads of families who are in the very productive years of their lives. Although data show that SUDS is hereditary, it is not known how the syndrome is passed from one generation to the next. Approximately 27% to 40% of the cases had relatives who succumbed to a similar pattern of death. Familial clustering of patients with SUDS has also been reported.14Tatsanavivat P. Chirawatkul A. Klungboonkrong V. Saowakontha S. Familial clustering of presumptive sudden unexplained death syndrome (PSUDS).Southeast Asian J Trop Med Public Health. 1991; 22: 195-199PubMed Google Scholar Van den Berg and colleagues15Van den Berg M.P. Wilde A.A.M. Viersma J.W. Brouwer J. Haaksma J. Van der Hout A.H. Stolte-Dijkstra I. Bezzina C.R. Van Langen I.M. Beaufort-Krol G.C.M. Cornel J.H. Crijns H.J.G.M. Possible bradycardic mode of death and successful pacemaker treatment in a large family with features of long QT syndrome type 3 and Brugada syndrome.J Cardiovasc Electrophysiol. 2001; 12: 630-636Crossref PubMed Scopus (121) Google Scholar described a possible bradycardic mode of death in patients with long QT and Brugada syndromes. They also state that SUDS can be prevented by the use of pacemakers. The influence of the autonomic nervous system on ST-segment elevation in patients with Brugada syndrome has been studied.16Miyazaki T. Mitamura H. Miyoshi S. Soejima K. Aizawa Y. Ogawa S. Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome.J Am Coll Cardiol. 1996; 27: 1061-1070Abstract Full Text PDF PubMed Scopus (621) Google Scholar Isoproterenol has been demonstrated to normalize ST elevation, and an increase in vagal activity can cause ST-segment elevation. These findings raise the concern of using β blocker in this group of patients. The fact that VF episodes in patients with SUDS occur mainly at night has led to the question of the role of autonomic modulation in these patients. If high vagal tone is dangerous to patients, then β blockers, which are excellent drugs for the prevention of sudden death in patients with coronary artery disease, may have detrimental effects in patients with SUDS and should not be used. Among patients with Brugada syndrome and inducible VF, late potentials were found in 19 of 22 patients (86.4%) by Kanda et al17Kanda M. Shimizu W. Matsuo K. Nagaya N. Taguchi A. Suyama K. Kurita T. Aihara N. Kamakura S. Electrophysiologic characteristics and implications of induced ventricular fibrillation in symptomatic patients with Brugada syndrome.J Am Coll Cardiol. 2002; 39: 1799-1805Abstract Full Text Full Text PDF PubMed Scopus (124) Google Scholar and 8 of 15 patients (53.3%) in our study. In our study, we cannot conclude whether the finding of late potentials merely reflects the slow conduction from right bundle branch block per se or reflects the reentrant circuit because it is closely related to both right bundle branch block with ST-segment elevation and inducible VF. Nademanee et al18Nademanee K. Veerakul K. Nimmannit S. Chaowakul V. Bhuripanyo K. Likittanasombat K. Tangsanga K. Kuasirikul S. Malasit P. Tansupasawadikul S. Tatsanavivat P. Arrhythmogenic marker for the sudden unexplained death syndrome in Thai men.Circulation. 1997; 96: 2595-2600Crossref PubMed Scopus (462) Google Scholar reported that the clinical outcomes were worse in patients with SUDS who had abnormal electrocardiographic patterns compared with those without abnormal patterns. The main findings from our study indicate that HRV is lower in patients with SUDS. Previous reports on HRV mainly studied patients with coronary artery disease and used 24-hour HRV study as the predictor of future events. However, in our study we investigated the changes in HRV, especially during the night, because the timing of events in patients with SUDS is different from episodes that occur in patients with coronary artery disease. Our findings demonstrated that not only is the 24-hour HRV less in patients with SUDS compared with controls, but also that the depressed HRV was more obvious during the night. Markedly decreased vagal tone at night may be a mechanism contributing to VF episodes. This finding is consistent with the nighttime episodes in patients with SUDS. In conclusion, we studied HRV in 26 patients with SUDS and 42 controls to determine whether there were changes in autonomic modulation in the patients with SUDS. Results of this study showed that patients with SUDS had higher heart rates at night, lower day- to-night heart rate differences, and decreases in time- and frequency-domain HRV, especially at night, which may explain the occurrence of VF episodes at night in these patients. The investigators greatly appreciate the technical assistance of Charuwan Kangkagate, MS." @default.
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- W2071066568 title "Heart rate variability in patients with sudden unexpected cardiac arrest in Thailand" @default.
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