Table 1.
Cardiovascular conditions, mechanism, and cognitive consequence
| Condition | Dominant mechanism | Cognitive consequence | Key evaluation | Intervention | Key controversy |
|---|---|---|---|---|---|
| Chronic hypertension | Chronic direct: pulsatility, endothelial dysfunction, SVD | WMH, lacunes, dysexecutive and slowed-processing decline | Midlife and current BP, orthostatic vitals, MRI SVD markers | BP control, individualized targets | Late-life BP lowering, J-curve, timing of benefit |
| Atrial fibrillation | Acute direct embolic plus chronic substrate | Overt and covert infarcts, cognitive decline independent of recognized stroke | Rhythm monitoring, MRI for covert infarction, LA structure/function | Anticoagulation when indicated, rate/rhythm control | BRAIN-AF negative; tension with MR mediation through stroke/low CO |
| Atrial cardiopathy | Mixed direct and indirect | Cognitive decline or embolic risk without documented AF | ECG, rhythm monitoring, LA size/function, emerging biomarkers | Risk-factor treatment; anticoagulation uncertain | Whether atrial disease is causal independent of AF |
| Heart failure | Chronic direct hypoperfusion plus indirect neurohormonal/inflammatory | Brain fog, slowed processing, attentional and executive dysfunction | EF, HF phenotype, orthostatics, sleep apnea, renal function | GDMT, perfusion optimization, rehabilitation | Reversibility; HFpEF versus HFrEF mechanisms |
| Coronary disease and MI | Mixed: shared substrate, inflammation, hypoperfusion, procedural injury | Post-MI cognitive change, accelerated long-term decline | Vascular risk profile, delirium screen, cognitive baseline | Secondary prevention, cardiac rehabilitation | Shared burden versus hypoperfusion versus microembolism |
| Aortic stenosis and TAVR | Chronic hypoperfusion plus acute procedural embolic injury | Pre-procedural impairment; possible improvement or decline after intervention | Echo, frailty/cognition baseline, pre/post neuroimaging | Valve replacement, cerebral embolic protection | Whether intervention improves cognition net of embolic risk |
| Carotid stenosis | Chronic hypoperfusion plus microembolic injury | Modest contribution to dysexecutive decline | Carotid imaging, cerebral perfusion, cognitive baseline | Intensive medical therapy; revascularization on stroke-risk grounds | CREST-2: no cognitive benefit in asymptomatic stenosis |
| Cardiac surgery/bypass | Acute direct embolic and hypoperfusion plus delirium | Perioperative neurocognitive disorder, delirium, long-term decline | Baseline cognition, delirium risk, vascular burden | Perfusion/anesthesia management, delirium prevention | Attribution of post-CABG decline versus expected aging |
| Cardiac arrest | Acute direct hypoxic-ischemic injury | HIE, amnestic and executive deficits | Exam, EEG, MRI, biomarkers, serial neuroprognostication | Post-arrest care, TTM, rehabilitation | Prognostic accuracy and selective regional vulnerability |