The European Society of Cardiology
Foreword
a Glasgow, UK
b Osaka, Japan
* James Shepherd, MB, Chb, PhD, FRCPath Department of Pathological Biochemistry, University of Glasgow, Glasgow Royal Infirmary, Glasgow, UK.
Coronary heart disease (CHD) no longer remains a concern limited to Western, developed nations; rather, the condition now traverses both ethnic and cultural boundaries. Cardiovascular disease, the world’s leading cause of death, comprises almost one-third of the overall mortality rate, with proportions found regionally in Europe and the Americas, at 52% and 33%, respectively.1 Although CHD still accounts for fewer deaths in Southeast Asian and Western Pacific nations, the disease is rapidly gaining prevalence similar to that of its Western counterparts. We are challenged, then, to compare the nature and course of CHD in these differing cultures and to determine which, if any, of the treatment strategies currently employed in Western populations can be transferred to those in non-Western regions. Since significant advances have been made in recent years regarding the discovery and control of the mechanisms underlying CHD, there already exists a great deal of information to share. With heightened awareness of CHD as a global problem, we stand a much better chance of restricting the scope of the condition and of managing the international population affected by this disease.
The articles presented in this supplement, based on two symposia held during the International Symposium on Atherosclerosis in Kyoto, Japan, in September 2003, confront CHD from a variety of distinct, multi-national viewpoints. This cross-cultural discourse is essential to coordinate an appropriate response to an otherwise overwhelming issue. The authors, while discussing both specific and general aspects of the CHD condition, coincide in addressing one prevailing question: does CHD affect populations in a substantially similar, and easily definable, way?
Ole Faergeman finds three ways in which to distinguish the universal truths of CHD management: first, that clinical benefits are directly related to the magnitude of the reduction of low-density lipoprotein cholesterol (LDL-C); second, that benefits of lipid-lowering therapy are greater in patients with increased CHD risk; and, finally, that benefits from therapy can be achieved independent of baseline concentrations of LDL-C. These axioms have been discovered through years of investigation with statins, among the most promising therapies for CHD, and suggest that successful prevention and treatment of CHD can be attained by the accurate employment of statins in patients at risk for the disease.
Toru Kita, introducing the comparative epidemiology of CHD in Western and non-Western populations, indicates that CHD risk in Japanese patients relates directly to hypercholesterolaemia. Kita also asserts that lifestyle changes may account for the sudden increased prevalence of CHD in a non-Western population such as Japan, diminishing the protection which previously may have been conferred by ethnicity. Studies within Japan are providing important new data on the culture-specific elements of the CHD condition, from which more precise treatment strategies and goals can be formulated.
Because current treatment for CHD focuses primarily on two lipid parameters, levels of LDL-C and high-density lipoprotein cholesterol (HDL-C), Len Kritharides and Philip Barter describe the utility of these measurements in a satisfactory CHD treatment regimen. Kritharides contends that the failure of many patients to achieve LDL-C goals as recommended by clinical practice guidelines results from the inadequacy of their current therapy. Using the more efficacious, yet comparably well-tolerated, statins, more patients achieve their treatment goals. At the same time, Barter illustrates that statins can increase levels of HDL-C, a predictor of CHD risk independent of levels of LDL-C.
Next, W. Virgil Brown and Frank Sacks discuss the course of CHD in patient populations with additional complications, those who consequentially have a high risk for CHD. Brown highlights patients with the metabolic syndrome, heterozygous familial hypercholesterolaemia and hypertension, distinguishing the ways in which each of these groups requires therapy to reduce their CHD risk. Sacks discusses patients hospitalised with an acute coronary syndrome (ACS) and comments on the potential of early intervention with statins to prevent a recurrent ischaemic event. Since the origin of statins’ protective benefit in the ACS patient is unclear, further studies are needed to investigate both the lipid-modifying and anti-inflammatory properties of statins and to determine their exact use in ACS treatment.
Andrew Tonkin discusses in greater depth the problem of the metabolic syndrome, a collection of related risk factors that is poorly defined yet strongly correlated with CHD. Concurring with Brown, Tonkin finds that effective drug therapy can mediate the major effects of the metabolic syndrome, achieving necessary lipid modifications; lifestyle interventions, meanwhile, may address the syndrome’s other central component, abdominal obesity. Once patients in this increased risk state can be properly identified, appropriate treatment may confer important protection against the development of CHD.
In a review of ongoing statin trials, Chris Packard focuses on some remaining unanswered questions about statins. Through explaining the design and aims of these trials, Packard points out key issues at the forefront of the statin research community: namely, the optimal reduction of LDL-C, the use of inflammatory markers as indicators of risk and the ability of statins to prevent recurrent events and to improve survival in patients with chronic heart failure. Although the final results of many of these trials are years in the future, early indications reveal greater benefits from statin therapy than previously envisioned.
M. John Chapman and Muriel Caslake conclude the supplement with another emerging research interest: the use of non-HDL-C as an additional risk factor for CHD. Because non-HDL-C is a measurement including atherogenic lipoproteins, it incorporates more components than LDL-C alone, so its inclusion in the lipid profile may provide increased predictive potential. Statins, which achieve significant reductions in levels of atherogenic lipoproteins, could prove especially effective in this new line of investigation.
From this comprehensive overview of cutting-edge CHD research, the authors present perspectives on the condition that may be applied more generally across disparate cultures. The treatment goals of specific patient populations will vary with corresponding differences in lifestyle, but the principle of strategies, which has been developed from the already long history of CHD in Western nations, will be common. Adopting these tactics, and tailoring them to the needs of individual populations, will construct the strongest barrier against the globally sweeping prevalence of CHD.
References
- World Health Report 2002. Reducing risks, promoting healthy life. Annex Table 2. Geneva, Switzerland: World Health Organization; 2002. Available from: http://www.who.int/whr/2002/en/whr2002_annex2.pdf. Accessed December 8, 2003
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