Among 287 midlife adults (mean age 51, 43% women) monitored within 8 months of a myocardial infarction, each standard deviation increase in momentary negative affect (MNA) — a composite of daily sadness, anxiety, anger, distress, and loneliness rated via ecological momentary assessment over 7 days — was associated with a 60% higher risk of major adverse cardiovascular events (MACE) over a median 28-month follow-up. Crucially, MNA outperformed a full battery of standard clinical psychological scales and remained significant independent of baseline depression history.
This preprint, not yet peer-reviewed, adds meaningful nuance to the well-established psychosocial–cardiovascular disease nexus. The finding that real-time, ecologically sampled affect captures residual cardiac risk better than questionnaire-based snapshots aligns with evidence that momentary stress physiology — cortisol fluctuations, sympathetic tone, inflammatory surges — may be the true biological driver rather than trait-level psychological scores. The 60% hazard increase is a clinically substantial effect size for a behavioral marker.
Limitations are notable: 287 participants is a modest cohort, the 7-day monitoring window may not reflect longer-term emotional patterns, and observational design precludes causal inference. Reverse causation — sicker patients feeling worse — cannot be ruled out despite clinical adjustment. Whether interventions targeting momentary negative affect (mindfulness, CBT, biofeedback) would reduce MACE remains entirely untested. If replicated in larger trials, brief ambulatory mood monitoring could become a practical post-MI risk stratification tool.