Feasibility, safety, and mid-term efficacy of cardiac resynchronization therapy in patients with severe heart failure and ventricular conduction delay: Chulalongkorn experience.

BACKGROUND: Heart failure is a major and growing public health problem in developed and developing countries. Despite major advances in medical therapy, morbidity and mortality remain high. Cardiac resynchronization therapy (CRT) has been proposed as an adjunctive therapy in patients with drug-refractory heart failure and ventricular conduction delay. Short and long-term studies have demonstrated the clinical benefits of CRT. OBJECTIVE: The present study was designed to assess the feasibility, safety, and mid-term efficacy of CRT in patients with severe heart failure and ventricular conduction delay in the institute. MATERIAL AND METHOD: Ten patients with severe heart failure in New York Heart Association (NYHA) functional class III or IV with left ventricular ejection fraction (LVEF) < 35%, QRS duration >120 ms with left bundle branch block morphology received CRT At baseline, and 6 months after implantation, the following parameters were evaluated: NYHA class, QRS duration, LVEF N-terminal pro-brain natriuretic peptide (NT-pro BNP) level, 6-minute walking distance, SF-36 quality-of-life (QOL) score, and number of heart failure visit. RESULTS: All clinical parameters improved significantly at 6 months. NYHA class decreased from 3.5 +/- 0.5 to 2.4 +/- 0.7 (p < 0.01). QRS duration decreased from 145 +/- 22 ms to 126 + 6 ms (p < 0.01). LVEF increasedfrom 21 +/- 6% to 31 +/- 12% (p < 0.01). NT-pro BNP level decreased from 2503 +/- 1953 pg/ml to 767 +/- 342 pg/ml (p < 0.01). The 6-minute walking distance increased from 153 +/- 122 m to 278 +/- 128 m (p < 0.01). QOL score improved from 66 +/- 14 to 98 +/- 25 (p < 0. 01). The number of heart failure visits was reduced from 3.8 +/- 3.7 per year to 0.5 +/- 0.8 visit per year (p < 0.01). Seventy percent of patients were free of heart failure visit for one year after implantation. One patient had sudden cardiac death eleven months after implantation. There was no procedure-related mortality. One patient had left ventricular lead dislodgement 3 months after implantation. CONCLUSION: In the present study, CRT was safe and effective in improving heart failure symptom, functional status, LV function, and quality of life. CRT also reduced heart failure hospitalization in the presented severe heart failure and ventricular conduction delay patients.

The temporal variations of presumptive sudden death of Thai people in Singapore and Taiwan.

BACKGROUND: Sudden Unexplained Death Syndrome (SUDS) is the major cause ofsudden death in Thai adults, especially Thai migrant workers in Singapore and Taiwan. Temporal variations of sudden death of Thai people abroad are not well known. OBJECTIVE: To study the month, day and time of death of presumptive sudden death (PSD) in Singapore, Taiwan. MATERIAL AND METHOD: The authors reviewed the death certificates of Thai people who died in Singapore and Taiwan and previously SUDS reported cases form Singapore. The time, day and month ofPSD and Non-PSD deaths in Singapore and Taiwan were compared. RESULTS: From January 1994 to January 1995, 46 SUDS died in Singapore (gr A), from May 2000 to August 2002, 39 PSD died in Singapore (gr B), from January 1999 to May 2002, 100 presumptive or probable sudden unexplained death syndrome (PSUDS) died in Taiwan (gr C) and 254 Non-PSD death aboard (gr D) as controls. The annual SUDS/PSD death rates (per 100,000) in Singapore were 91.1 in 1994, 30.7 in 2001 and 33.5 in Taiwan in 2000. All but two SUDS/PSD cases were male. The mean age in gr A + B and C were 34.9 + 7.5 and 33.1 +/- 6.0 years old respectively. In gr. A, B and C, compared with gr D, Tuesday was the weekday of lowest SUDS/PSD death rate and Saturday was the highest. (p < 0.05). Time of death in gr B and C were peak during midnight to 8 a.m. and there was some trend of seasonal variation in occurrence of SUDS/PSD with the peak death rate in April and trough death rate in September; which is significantly different from gr D (1.49% vs 10.89% of all deaths, p < 0.01). CONCLUSION: The presented data demonstrate some temporal variations in SUDS/PSD death aboard. The sudden death of Thai people in Singapore and Taiwan may be more prevalent in the "work-to-rest" than "rest-to-work" periods.

HLa-class II (DRB & DQB1) in Thai sudden unexplained death syndrome (Thai SUDS) families (Lai-Tai families).

Thai Sudden Unexplained Death Syndrome (Thai SUDS), or Lai-Tai, is a major health problem among rural residents of northeastern Thailand. The cause has been identified as a genetic disease. SUDS, a disorder found in Southeast Asia, is characterized by an abnormal electrocardiogram with ST-segment elevation in leads V1-V3, identical to that seen in Brugada Syndrome (Brugada Sign, BS) and sudden death due to ventricular fibrillation and cardiac arrest (represents an arrhythmogenic marker that identifies high-risk for SUDS). SUDS victims have a sleeping disorder (narcolepsy). The HLA-DR locus is tightly associated with narcoleptic Japanese patients and HLA-DR2, DQ haplotypes were also found in Oriental narcoleptic patients. These circumstances prompted us to study the association between the disease and HLA Class II by HLA DNA typing using a PCR-SSO method, with five Thai SUDS families (18 BS-positive subjects as the cases, and 27 BS-negatives as the controls). We found that the HLA-DRB1 *12021 allele was significantly increased in BS-positive subjects (p = 0.02; OR = 4.5), the same as the HLA-DRB1*12021-DQB1 *0301/09 haplotype (p = 0.01; OR = 7.95). Our data suggests that the HLA-DRB1* 12021 allele associated with BS and the HLA-DRB1*12021-DQB1 *0301/09 is a haplotype susceptible to arrhythmogenic markers that can identify a high risk for SUDS.

Linkage analyses and SCN5A mutations screening in five sudden unexplained death syndrome (Lai-tai) families.

Sudden Unexplained Death Syndrome (SUDS) (or in Thai Lai-tai) share the same ECG pattern as Brugada Syndrome: RSR' and ST segment elevation in V1 to V3. Brugada Syndrome is a genetic disorder with the inheritance pattern of autosomal dominant (using the ECG pattern and unexplained sudden death as phenotype) and the cardiac sodium channel gene (SCN5A) mutations caused this syndrome. To determine whether SUDS was associated with the same mutations as Brugada Syndrome, the authors performed a linkage studies on 5 SUDS families with the Brugada Syndrome ECG pattern and found one family could not be excluded from linkage to SCN5A. However, the direct sequencing in 8 reported mutations on exon 5, 12, 17, 18 and 28 in this family failed to demonstrate the mutations. It was concluded that SUDS mutations maybe a novel mutation different from previously reported mutations, further genetic studies in SCN5A and other candidate genes might elucidate the molecular basis of SUDS.