Stroke: After stroke, do not intensify statin treatment, or greatly increase the mortality rate

The secondary stroke prevention guidelines recommend high-concentration statins to prevent ischemic stroke caused by atherosclerosis or recurrent stroke in patients with transient ischemic attack (TIA)
.

The evidence base supporting the recommendations of this guideline mainly comes from a single large randomized controlled clinical trial-SPARCL (Stroke Prevention by Aggressive Reduction in Cholesterol Levels), in which atherosclerotic stroke and low-density lipoprotein (LDL) Patients with a level of 100 to 190 mg/dL were randomly assigned to high-energy statin or no statin

Stroke prevention of the trial showed that in five years, the subsequent ischemic stroke and cardiac vascular events absolute risk reduction of 2.

According to blood cholesterol treatment guidelines, patients with non-atherosclerotic stroke should use statins
.

Patients with non-atherosclerotic stroke and diabetes should receive at least moderate-intensity statins

Cholesterol diabetes

Therefore, most patients with ischemic stroke may be eligible to take moderate-to-high-intensity statins due to stroke mechanisms, comorbidities, or cardiovascular risks
.

In this way, Jennifer L.
Dearborn-Tomazos and others of Harvard University used observational studies to describe the statin medication mode of veterans after recent ischemic stroke or TIA in a large national sample
.

Using observational research, in a large national sample, described the statin medication mode of veterans after recent ischemic stroke or TIA
.

Using observational research, in a large national sample, described the statin medication mode of veterans after recent ischemic stroke or TIA

Core hypothesis: Compared with patients receiving moderate or high-intensity statins, non-use of statins, low-intensity statins, and reduced doses are associated with increased mortality
.

The study population included patients with ischemic stroke or TIA who occurred in 134 veterans' health management institutions during 2011
.

They used the electronic clinic’s pharmacy file to determine the dose of statins on admission and within 7 days after discharge

manage

In addition, they created 6 mutually exclusive (mutually exclusive) groups to reflect the effectiveness of statins from admission to discharge: target (efficacy) to target (efficacy), low to target, target to low or target to Nothing, nothing to nothing, nothing to low, and low to low
.

Finally, logistic regression was used to compare the 30-day and 1-year mortality rates of statins in each group

The study subjects included 9,380 men (96.
3%) who were predominantly white (71.
1%) who were hospitalized due to stroke or TIA
.

34.
1% of patients (n=3194) did not take statins when they were discharged from the hospital
.

14.

Compared with target-to-target, desensitization and nothing to nothing are associated with a higher chance of death
.

Using propensity-weighted scores to adjust for differences in baseline characteristics showed similar results
.

The significance of this study lies in the findings: In about one-third of ischemic stroke or TIA veterans, underuse of statins was observed, including non-treatment or under-dose after stroke, and reaching statin prescriptions The mortality rate is higher than that of patients with the target dose
.

In approximately one-third of ischemic stroke or TIA veterans, underuse of statins was observed, including untreated or under-dose after stroke, and mortality compared with patients who reached the prescribed dose target of statins Higher
.

In approximately one-third of ischemic stroke or TIA veterans, underuse of statins was observed, including untreated or under-dose after stroke, and mortality compared with patients who reached the prescribed dose target of statins Higher

Original source:
Dearborn-Tomazos JL, Hu X, Bravata DM, et al.

Deintensification or No Statin Treatment Is Associated With Higher Mortality in Patients With Ischemic Stroke or Transient Ischemic Attack.
Stroke.
2021;52(8):2521-2529.
doi:10.
1161/STROKEAHA.
120.
030089

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