Background: Acute blood pressure (BP) elevation in acute ischemic stroke (AIS) is common, yet the link with collateral circulation remains elusive due to lack of longitudinal data on premorbid hypertension (HTN) and serial BP changes within an individual. Precision medicine for AIS and management of HTN requires an understanding of collateral circulation.
Methods: The Interventional Management of Stroke III angiography core lab prospectively evaluated collateral circulation utilizing the ASITN scale prior to endovascular therapy. We used these data to discern the relationship of clinical and imaging markers of premorbid HTN with acute, serial BP measures and collaterals.
Results: Collaterals at angiography were graded in 276/331 (83%) subjects. Higher initial BP was associated with impaired collateral status, driven by diastolic BP (ASITN 0-1: mean 88.9 ± 23.5 mmHg (n=70); 2: 82.7 ± 18.5 mmHg (n=106); 3-4: 79.4 ± 15.0 mmHg (n=95); p=0.002) but not systolic BP (ASITN 0-1: mean 153.7 ± 31.5 mmHg (n=71); 2: 147.8 ± 29.0 mmHg (n=107); 3-4: 146.8 ± 28.3 mmHg (n=95); p=0.153). Premorbid HTN was linked with worse collaterals (ASITN 0-1: 88.9% (64/72); 2: 78.7% (85/108); 3-4: 64.2% (61/95); p=0.001). Admission anti-hypertensive medications were tied to worse collaterals (ASITN 0-1: 76.4% (55/72); 2: 64.8% (70/108); 3-4: 57.3% (55/96); p=0.036). Prior infarction on baseline imaging was also a marker of worse collaterals (ASITN 0-1: 33.3% (24/72); 2: 24.3% (26/107); 3-4: 19.1% (18/94); p=0.039). Serial BP from pre-randomization to post-tPA, however, was unrelated to collateral status. Multivariate modeling to predict collateral grade revealed that history of HTN (OR 0.29 95%CI (0.13, 0.64); p=0.002) and diastolic BP measured post-stroke but pre-randomization (per 10 mm Hg) (OR 0.80 95%CI (0.69, 0.93); p=0.004) were both distinct markers of impaired collaterals. The poorest collaterals were seen in those with both history of HTN and acutely elevated BP.
Conclusions: Chronic and acute HTN are both potent predictors of impaired collaterals in AIS. Understanding how HTN affects the structure and function of collaterals and response to acute BP changes is critical for future hypertensive management and collateral augmentation.