Mechanisms

The study frames post-stroke cognitive impairment as multifactorial across vascular, demographic, socioeconomic, psychological, behavioural, and nutritional pathways. Stroke can directly contribute to vascular cognitive impairment through brain injury and indirectly through comorbidities and functional decline. Physical activity may protect cognition after stroke through neurotransmitter, mood, cerebral blood volume, and brain volume mechanisms. Low BMI may reflect nutritional and biological factors linked to cognitive decline after stroke. COPD exacerbations may increase cardiovascular risk through systemic inflammation, respiratory stress, and medication effects. Hypoxaemia and acid-base imbalance can destabilise cardiac conduction, which may explain common arrhythmias. Heart failure decompensation was plausibly frequent because exacerbations impose fluid and pressure loads on compromised ventricles. Acute coronary syndrome was rare, possibly because short-term respiratory stress less directly triggers plaque rupture.