Intravenous tissue plasminogen activator in acute branch atheromatous disease: Does it prevent early neurological deterioration?

- Early neurological deterioration (END) is not uncommon in patients with branch atheromatous disease.
- We evaluated whether tissue plasminogen activator (tPA) can prevent END and improve patient outcome.
- Intravenous tPA may not prevent END and guarantee good functional outcome in branch atheromatous disease.
- More effective strategies should be evaluated for management of branch atheromatous disease.

Early neurological deterioration (END) and poor outcome frequently occur in lenticulostriate artery (LSA) infarction due to branch atheromatous disease (BAD). We evaluate whether the tissue plasminogen activator (tPA) can prevent END and improve the outcome by comparing with anti-platelet treatment in LSA infarction due to BAD. We enrolled the patients with LSA infarction due to BAD who arrived at the hospital within 24 h from onset, and divided those into two groups by whether tPA was given or not. END and good outcome (modified Rankin score: 0-1) at 3 months were examined between two groups. Consecutive 35 patients of LSA infarction due to BAD enrolled in this study. Nine patients were given tPA (tPA group) and 26 patients antiplatelets only (non-tPA group). Patients in tPA group showed no symptomatic hemorrhage. END occurred in 68.6% (24/35) of all patients, 66.7% (6/9) of tPA group and 69.2% (18/26) of non-tPA group (p = 0.886). The proportion of good outcome at 3 months were 25.7% in all patients, 22.2% (2/9) in tPA group and 26.9% (7/26) in non-tPA (p = 0.781). tPA did not adequately prevent END, and did not show better outcome in LSA infarction due to BAD compared with antiplatelet therapy only. More effective treatment strategies are needed for prevention of END and favourable outcome in BAD.