Acute Myocardial Infarction and Risk of Cognitive Impairment and Dementia: A Review

SIMPLE SUMMARY: Cognitive impairment (CI) and dementia are common in patients with heart attacks, and both share common cardiovascular risk factors. In our ageing population, the management and recognition of both becomes increasingly relevant. In this review, we explore the pathophysiology behind this relationship between CI and heart attacks/heart disease. We also discuss risk factors for CI in patients with heart attacks, including the impact of age, sex, and heart failure after the heart attack. We explore how interventions for heart attacks, including percutaneous coronary angiography and bypass surgery, seem to be associated with higher rates of CI, though it is not clear whether this is related to the procedure itself or to the similar underlying risk factors. Finally, we explore how medical management, including most medications prescribed for heart attack patients, can have a positive impact on reducing the risk of CI in patients post-heart attack, though one medication (beta-blocker) may be associated with functional decline in patients with existing CI. The early identification of those with dementia or CI who present with a heart attack is important, as the subsequent tailoring of management strategies can potentially improve outcomes as well as guide prognosis. ABSTRACT: Cognitive impairment (CI) shares common cardiovascular risk factors with acute myocardial infarction (AMI), and is increasingly prevalent in our ageing population. Whilst AMI is associated with increased rates of CI, CI remains underreported and infrequently identified in patients with AMI. In this review, we discuss the evidence surrounding AMI and its links to dementia and CI, including pathophysiology, risk factors, management and interventions. Vascular dysregulation plays a major role in CI, with atherosclerosis, platelet activation, microinfarcts and perivascular inflammation resulting in neurovascular unit dysfunction, disordered homeostasis and a dysfunctional neurohormonal response. This subsequently affects perfusion pressure, resulting in enlarged periventricular spaces and hippocampal sclerosis. The increased platelet activation seen in coronary artery disease (CAD) can also result in inflammation and amyloid-β protein deposition which is associated with Alzheimer’s Dementia. Post-AMI, reduced blood pressure and reduced left ventricular ejection fraction can cause chronic cerebral hypoperfusion, cerebral infarction and failure of normal circulatory autoregulatory mechanisms. Patients who undergo coronary revascularization (percutaneous coronary intervention or bypass surgery) are at increased risk for post-procedure cognitive impairment, though whether this is related to the intervention itself or underlying cardiovascular risk factors is debated. Mortality rates are higher in dementia patients with AMI, and post-AMI CI is more prevalent in the elderly and in patients with post-AMI heart failure. Medical management (antiplatelet, statin, renin-angiotensin system inhibitors, cardiac rehabilitation) can reduce the risk of post-AMI CI; however, beta-blockers may be associated with functional decline in patients with existing CI. The early identification of those with dementia or CI who present with AMI is important, as subsequent tailoring of management strategies can potentially improve outcomes as well as guide prognosis.