Sleep apnoea syndrome in Ramathibodi Hospital: clinical and polysomnographic baseline data.

OBJECTIVE: The aim of this study was to determine clinical and baseline polysomnographic data on obstructive sleep apnoea (OSA) in Thai patients. This prospective study was performed at the Sleep Laboratory Center, Ramathibodi Hospital, Mahidol University, Thailand. METHODOLOGY: Ninety adult cases clinically suspected of having OSA were studied. The study included clinical, blood chemistry, electrocardiogram, chest radiograph, arterial blood gas, spirometry and full night polysomnography. RESULTS: Fifty-nine cases (65.6%) out of a total of 90 cases had an abnormal apnoea (i.e. apnoea index (AI) of 5 or more). The incidence of upper airway abnormality among cases with AI of 5 or more was 79.7% (47/59 cases). Among 59 patients with abnormal AI, associated medical problems comprised hypertension (n=22), obesity hypoventilation (n=9), hypothyroidism (n=4), chronic airflow obstruction (n=4), diabetes mellitus (n=3) and chronic renal failure (n=1). Obstructive sleep apnoea was present in all 59 cases. Central apnoea and mixed apnoea were rare. CONCLUSION: Symptoms and signs suggestive of OSA can lead to a high detection rate and confirmation of OSA by polysomnography. The OSA characteristics of Thai patients were similar to the patients in the Western world.

Arrhythmogenic marker for the sudden unexplained death syndrome in Thai men.

BACKGROUND: Between 1981 and 1988, the Centers for Disease Control and Prevention reported a very high incidence of sudden death among young male Southeast Asians who died unexpectedly during sleep. The pattern of death has long been prevalent in Southeast Asia. We carried out a study to identify the clinical markers for patients at high risk of developing sudden unexplained death syndrome (SUDS) and long-term outcomes. METHODS AND RESULTS: We studied 27 Thai men (mean age, 39.7+/-11 years) referred because they had cardiac arrest due to ventricular fibrillation, usually occurring at night while asleep (n=17), or were suspected to have had symptoms similar to the clinical presentation of SUDS (n=10). We performed cardiac testing, including EPS and cardiac catheterization. The patients were then followed at approximately 3-month intervals; our primary end points were death, ventricular fibrillation, or cardiac arrest. A distinct ECG abnormality divided our patients who had no structural heart disease (except 3 patients with mild left ventricular hypertrophy) into two groups: group 1 (n=16) patients had right bundle-branch block and ST-segment elevation in V1 through V3, and group 2 (n=11) had a normal ECG. Group 1 patients had well-defined electrophysiological abnormalities: group 1 had an abnormally prolonged His-Purkinje conduction time (HV interval, 63+/-11 versus 49+/-6 ms; P=.007). Group 1 had a higher incidence of inducible ventricular fibrillation (93% for group 1 versus 11% for group 2; P=.0002) and a positive signal-averaged ECG (92% for group 1 versus 11% for group 2; P=.002), which was associated with a higher incidence of ventricular fibrillation or death (P=.047). The life-table analysis showed that the group 1 patients had a much greater risk of dying suddenly (P=.05). CONCLUSIONS: Right bundle-branch block and precordial injury pattern in V1 through V3 is common in SUDS patients and represents an arrhythmogenic marker that identifies patients who face an inordinate risk of ventricular fibrillation or sudden death.

Nocturnal physiological and biochemical changes in sudden unexplained death syndrome: a preliminary report of a case control study.

Sudden nocturnal deaths among "healthy" workers in Southeast Asia have been termed "sudden unexplained nocturnal death syndrome (SUNDS)" or "sudden unexplained death syndrome (SUDS)". The pathogenesis is still unknown. The paucity of publications on nocturnal monitoring and scientific data stimulated us to perform this study, which included biochemical tests and physiological monitoring during the night in 11 males north-eastern Thai workers. Group 1 (G1) consisted of 5 subjects with neither a previous history of near-SUDS (NSUDS) nor a familial history of SUDS (FHSUDS). Group 2 (G2) consisted of 6 subjects with a family history of either SUDS or NSUDS. Two subjects in G2 presented with NSUDS. Two-day nocturnal monitoring included blood sugar, electrolytes, and respiratory parameters. 24-hour Holter ECGs were monitored for 2 days. The subjects underwent exercise stress tests on the 2nd day of this study. Significant nocturnal hypoxia was more common in G2 than G1 and this abnormality was aggravated by exercise. There were no significant findings in sleep apnea (apnea indices) or in nocturnal biochemical changes, eg blood sugar, electrolytes, thiamine. The recordings of the Holter-ECGs were within normal limits in both groups. We conclude that nocturnal hypoxia might be the primary abnormality in SUDS, and this abnormality was aggravated by the day-time exercise. The cause of nocturnal hypoxia requires further studies.