Author(s): ASHWORTH, E., Institution: BASEL UNIVERSITÄT, Country: SWITZERLAND, Abstract-ID: 1634

INTRODUCTION:
Heat stress increases cardiovascular mortality, likely through ischemic pathways. Although myocardial blood flow rises during passive heating, the pressure–time determinants of coronary perfusion and their interaction with ventricular loading remain incompletely defined due to measurement limitations. The hypothesis that disease phenotypes operate with a reduced coronary perfusion reserve margin that is further compressed during thermal stress was assessed using computational models of heat stress.

METHODS:
A validated CircAdapt model was calibrated to represent an older adult phenotype and extended to heart failure with preserved ejection fraction (HFpEF) and pulmonary hypertension (PH). Acute heat stress was imposed using literature-aligned perturbations in systemic vascular resistance, chronotropy, and inotropy across progressive increases equivalent to 0.5, 1.0, and 1.5 °C elevations in core temperature observed during passive heating in older adults (1). Primary outcomes included coronary perfusion pressure (CPP), a diastolic pressure–time index (DPTI), and left ventricular end-diastolic pressure (LVEDP).

RESULTS:
At baseline, diseased phenotypes exhibited lower CPP (HFpEF 44.2 mmHg; PH 42.6 mmHg) compared with the older phenotype (53.4 mmHg), alongside higher LVEDP. Baseline DPTI was likewise reduced in HFpEF and PH relative to older. Progressive heat stress produced modest reductions in CPP across all phenotypes (1.5 °C: HFpEF 41.5 mmHg; PH 41.0 mmHg; older 50.6 mmHg), preserving between-group separation at each thermal level. DPTI declined proportionally with increasing thermal load in all groups, remaining consistently lower in disease. LVEDP increased across phenotypes, maintaining higher absolute filling pressures in HFpEF and PH (13.7 and 13.6 mmHg at 1.5 °C) compared with older (10.7 mmHg). Across thermal increments, disease phenotypes operated with a persistently narrower perfusion–demand margin rather than an accelerated deterioration slope.
CONCLUSION:
Although heat imposes similar relative perfusion compression across phenotypes, diseased hearts operate closer to subendocardial supply–demand imbalance throughout. This reduced reserve margin provides a mechanistic framework linking thermal stress to ischemic vulnerability. Further computational studies are warranted to explore the determinants of cardiac perfusion during passive heating and to examine subfactors that may predispose certain individuals to thermal intolerance.

Reference
1. Gagnon D, Romero SA, Ngo H, Poh PY, Cramer MN, Jay O. Healthy aging does not compromise the augmentation of cardiac function during heat stress. Journal of Applied Physiology. 2016;121(4):885–893. doi:10.1152/japplphysiol.00337.2016.