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Heart failure in Southeast Asia: facts and numbers
1National Heart Centre Singapore, 5 Hospital Drive, Singapore, 169609, Duke-NUS, 8 College Road, Singapore, 169857.
Abstract:
Southeast Asia is home to a growing population of >600 million people, the majority younger than 65 years, but among whom, rapid epidemiological transition has led to high rates of premature death from non-communicable diseases (chiefly cardiovascular disease) (up to 28% in the Philippines vs. 12% in UK). There is a strikingly high prevalence of stage A heart failure (HF) risk factors in Southeast Asia, particularly hypertension (>24% in Cambodia and Laos vs. 13-15% in UK and USA), tobacco smoking (>36% in Indonesia), physical inactivity (>50% in Malaysia) and raised blood glucose (10-11% in Brunei, Malaysia, Singapore and Thailand) in spite of a low prevalence of overweight/obesity (21-26% in Southeast Asia vs. 67-70% in UK and USA). Accordingly, the prevalence of symptomatic HF appears to be higher in Southeast Asian countries compared with the rest of the world. Epidemiologic trends in Singapore showed a sharp 38% increase in age-adjusted HF hospitalizations (from 85.4 per 10 000 in 1991 to 110.3 per 10 000 in 1998) with notable ethnic differences (hospitalization rates ~35% higher in Malays and Indians vs. Chinese; mortality 3.5 times higher in Malays vs. Indians and Chinese). Furthermore, Southeast Asian patients present with acute HF at a younger age (54 years) compared with USA patients (75 years) but have more severe clinical features, higher rates of mechanical ventilation, longer lengths of stay (6 vs. 4.2 days) and higher in-hospital mortality (4.8 vs. 3.0%). Finally, there is under-usage of guideline-recommended HF medical therapies (prescribed in 31-63% of patients upon discharge) and device therapies in Southeast Asia. Large gaps in knowledge that need to be addressed in Southeast Asia include the prevalence of HF with preserved ejection fraction, clinical outcomes, barriers to recommended therapies and their cost-effectiveness, as well as possible ethnicity-specific pathophysiologic mechanisms.
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