Statins After a Stroke Significantly Reduce Recurrence Risk

June 8, 2009

For the last several years, a statin agent has been the "top" prescribed drug in the US, as well as the rest of the world (based on cost), and statins were the largest selling US drug class (also by cost) for a number of years, falling to second in 2008 only because of generic availability.

HMG CoA Reductase inhibitors ("statins") seem to be considered "wonder drugs." They are very widely used, and a major drug expense: For the last several years, a statin agent has been the "top" prescribed drug in the US, as well as the rest of the world (based on cost), and statins were the largest selling US drug class (also by cost) for a number of years, falling to second in 2008 only because of generic availability. Statin therapy has been evaluated for myriad situations other than dyslipidemia. For example, there is an increasing body of evidence that statins reduce both initial and recurrent stroke risk. The original large scale statin studies were done only with patients with dyslipidemia, and largely related to cardiac disease. However, of late more data have become available about stroke risk reduction regardless of lipid status. Stroke risk reduction can be substantial. Unfortunately, long term data on this have been somewhat scant, and the largest studies have focused on high dose treatment with a specific statin agent.

Milionis et al. recently published an article intending to address these matters. They did a retrospective review of stroke admissions (n=794) to several institutions in Greece, and evaluated subsequent followup data for up to 10 years. The primary outcome variables were stroke recurrence and death. The demographics of the statin and no statin treatment groups were equivalent: The only baseline demographic variable related to post-discharge statin use was use of same prior to admission.

Detailed risk factor evaluations and a variety of studies were done during the index hospital admission. European Stroke Initiative guidelines drove dyslipidemia pharmacotherapy, as well as other secondary stroke prevention pharmacotherapy, including antiplatelet and anticoagulant regimens, and treatment of diabetes and hypertension. No particular statin was specifically required, and patients in the study were treated with several different agents. Thereafter, patients were followed prospectively by study investigators. A large body of hospital, clinic and stroke-related investigation study data were reviewed to determine recurrence. Median follow up was about 42 months.

The results are interesting: Statins reduced stroke recurrence a good deal. During the follow up interval, 112 patients (14.1%) had a recurrent event (Statin group: 15/183 (7.6%); No statin group: 97/499 (16.3%); p=0.002). The only analyzed factor which predicted recurrent stroke in the regression analyses was statin treatment (HR 0.61; 0.35—0.92; p<0.01). Mortality was reduced to an even greater degree (adjusted hazard ratio = 0.43; 0.29–0.61; p<0.01).

This study is of particular value as it included a variety of statins (some of which are available as generic formulations in the US) and long term observations. Dyslipidemia was not a specific requirement to receive statin therapy. Also, stroke patients, rather than persons with cardiac disease, were the index population, so these results are more directly applicable to neurologic practice. While this study does elucidate the value of statins in a secondary stroke prophylaxis regimen, an important remaining question is the value of statin therapy as part of primary prophylaxis (ie, prior to first stroke) and the factors guiding patient selection if so used.

Thus, statins reduced stroke recurrence risk, and markedly reduced mortality, in this population. These results should be easily generalized. Perhaps, as some wags have suggested, we should indeed be putting these agents in the water supply.