Abstract
Goal: The effect of pulse pressure and interactions with type of antihypertensive therapy on mortality after acute ischemic stroke has not been previously evaluated. Materials and Methods: A retrospective cohort study was conducted to evaluate the independent and interactive effects of pulse pressure and antihypertensive class (specifically angiotensin converting enzyme inhibitor/angiotensin type 1 receptor blocker, or beta blocker) on mortality following acute ischemic stroke. Findings/Conclusions: 343 patients were identified with 49 months of follow-up. Baseline pulse pressure was 64 mmHg and age was 66.5 years. Patients were divided at a pulse pressure of 70. Patients with pulse pressure ≥ 70 were older (p < 0.001) and had higher comorbid vascular burden (p = 0.031) than those with pulse pressure < 70. Pulse pressure did not remain a significant predictor of follow-up mortality after adjustment for baseline comorbidities. Angiotensin converting enzyme inhibitor/angiotensin type 1 receptor blocker based therapy was associated with lower follow-up mortality when beta blocker was not used in pulse pressure < 70 group (odds ratio 0.07, 95% confidence interval 0.01 - 0.48). Prospective analysis will be needed to confirm the protective effect of angiotensin converting enzyme inhibitor/angiotensin type 1 receptor blocker based on pulse pressure in acute ischemic stroke.
Highlights
The relationship between blood pressure (BP) control and short and long term outcomes in patients with acute ischemic stroke (AIS) is highly complex and not well understood with conflicting data
Prospective analysis will be needed to confirm the protective effect of angiotensin converting enzyme inhibitor/angiotensin type 1 receptor blocker based on pulse pressure in acute ischemic stroke
We examined whether treatment of hypertension modulates adverse effects of widened pulse pressure (WPP) in ischemic stroke
Summary
The relationship between blood pressure (BP) control and short and long term outcomes in patients with acute ischemic stroke (AIS) is highly complex and not well understood with conflicting data. The IST evaluation demonstrated a U-shaped relationship between SBP at both 14-day and 6 month outcomes. Significantly elevated BP in AIS is deleterious, rapid reduction of SBP has been associated with a higher mortality [3] with cerebral hypoperfusion and increased cardiac events [4]. The 2013 ACC/AHA Guidelines for the “Early Management of Patients with Acute Ischemic Stroke” did not specify BP targets and suggest using “best clinical judgment” and “to initially lower the SBP by 15% and monitor for neurological deterioration related to the (blood) pressure lowering” [2]
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