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(Stroke. 2003;34:1615.)
© 2003 American Heart Association, Inc.

Original Contributions

Editorial Comment—Decline in Stroke Mortality: Splitters and Lumpers

Michel T. Torbey, MD, MPH, Guest Editor

Stroke Critical Care Program, Neurointensive Care Unit, Department of Neurology and Neurosurgery, Medical College of Wisconsin, Milwaukee, Wisconsin

Over the last 3 decades, it has been rewarding to observe the steep decline in stroke mortality in many countries. In part, epidemiologists have attributed this decline to improvements in treatment of hypertension.² Unfortunately, during the last several years some of these countries have experienced a slowdown of the declining trend. A plethora of studies have been published since attempting to explain this phenomenon.

It seems unlikely that flattening of the stroke mortality curve is an indication of a floor effect of primary and secondary prevention efforts.³ Rather, it seems more likely to be masking a relapse in hypertension prevention. Although screening for high blood pressure has increased in the 1980s, still only half of hypertensive patients received treatment from their physicians in the 1990s,⁴ and only 69% are even aware that they have elevated blood pressure.⁵ It is also possible that the increase in incidence of other stroke risk factors, such as diabetes,⁶ obesity,⁷ and alcohol drinking,⁸ may be contributing to the slowdown in mortality decline.

In the accompanying article, Peeters and colleagues focused on a more optimistic hypothesis. The investigators tested the hypothesis that the increase in CHD cases, secondary to improvement in survival, could lead to an increase in stroke mortality that will eliminate the previously observed decline. First, they estimated the annual rate of decline in stroke mortality in the United States during 1981–1991 on the basis of ICD-9 codes data from the Compressed Mortality Database.⁹ Probability models were used to identify whether improvements in survival after CHD could plausibly eliminate the stroke mortality rate decline observed. The results of the study showed that changes in survival after CHD are unable to cause the 3% to 4% annual increase in stroke mortality rate required to eliminate the stroke mortality rate decline observed in United States before 1991. The investigators found no reasonable scenario in which the increase in stroke mortality rate was more than even 1% per year.

The study in the accompanying article has several methodological strengths. The multistate life-table analysis was based on age-specific transition rates derived from 46 years of follow-up of the Framingham Heart Study.¹⁰ The study therefore provided an accurate way to link changes in one age group with outcomes in future age groups. The strengths of this approach are in part offset by several limitations. The life-table analysis was based primarily on a white American homogeneous population and was not very reflective of changes in trends on a larger demographic scale. Interestingly, Howard et al¹¹ found that the pattern of decline in stroke mortality in the United States was heterogeneous, with substantial variations among population groups, geographic areas, race, and sex.¹¹

As survival of patients with CHD improves, the pool of people at high risk of stroke is expected to increase. This hypothetically will increase stroke mortality rates. However, in the accompanying article Peeters et al provided enough evidence to reject this hypothesis; the only shortcoming in their argument was that they lumped all stroke subtypes into 1 group. Although cerebral infarct shares similar risk factors with CHD,¹² its risk profile is different from intracerebral hemorrhage (ICH) or subarachnoid hemorrhage. Hypertension is among the few risk factors common to both ischemic stroke and ICH. In some reports, ischemic stroke risk factors were even found to have a protective effect on ICH.¹³ Such risk factors included history of cardiovascular disease, high cholesterol levels, being mildly overweight, smoking, and hormone replacement therapy.^13–15

The difference between stroke subtypes was not only limited to risk factor profiles. Lawlor et al¹⁶ demonstrated different mortality trends associated with different stroke subtypes. In the period 1981–1991, ischemic stroke mortality dropped from 18% to 11%, whereas ICH mortality increased only by 1% from 28%. The stroke subtype that had the largest mortality changes was the "ill defined cerebrovascular disease" subtype in which mortality increased from 53% in 1981 to 60% in 1999. This group included patients with ICD-9 codes 342, 344, and 436 to 438.¹⁶ The authors also demonstrated a 4-fold increase in the ratio of cerebral infarct to cerebral hemorrhage, from 0.5 in the 1930s to 2.0 by the 1990s.¹⁶ This ratio seemed to plateau in the 1990s. Interestingly, the combined decline in mortality rate for all stroke subtypes was 3% during 1981–1991. Similar rates have been reported by Peeters et al in the accompanying article and by others.¹⁷ This decline rate dropped to 0% during 1991–1999.

It appears that differences in risk factors and secular trends between stroke subtypes may be playing an important role in the flattening of stroke mortality curve. Hence, it is important to consider splitting rather than lumping the different subtypes of stroke to better understand epidemiological trends and long-term effectiveness of primary and secondary prevention efforts.

	References

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