Intracerebral haemorrhage is a complication of thrombolytic therapy for acute myocardial infarction, pulmonary embolism, and ischaemic stroke. There is increasing evidence that cerebral amyloid angiopathy (CAA), which itself can cause haemorrhage (CAAH), may be a risk factor for thrombolysis-related intracerebral haemorrhage. CAAH and thrombolysis-related intracerebral haemorrhage share some clinical features, such as predisposition to lobar or superficial regions of the brain, multiple haemorrhages, increasing frequency with age, and an association with dementia. In vitro work showed that accumulation of amyloid-beta peptide causes degeneration of cells in the walls of blood vessels, affects vasoactivity, and improves proteolytic mechanisms, such as fibrinolysis, anticoagulation, and degradation of the extracellular matrix. In a mouse model of CAA there is a low haemorrhagic threshold after thrombolytic therapy compared with that in wild-type mice. To date only a small number of anecdotal clinicopathological relations have been reported; neuroimaging advances and further study of the frequency and role of CAA in patients with thrombolysis-related intracerebral haemorrhage are required.