Exposure to heat has significant effects on the heart

A direct consequence of climate change is a greater frequency of extreme heat events, which are associated with higher mortality. Striking examples include the European summers of 2003 and 2022, which caused over 70,000 and 60,000 heat-related deaths, respectively. Deaths during extreme heat events are mainly due to cardiovascular events (see here, here, and here). Extreme temperatures significantly increase the risk of ischemic events, such as myocardial infarction (see here, here, and here) and hospitalization or death from coronary artery disease (CAD) (see here and here). These risks are particularly high in adults living with heart disease (see here and here). Despite epidemiological studies demonstrating an association between extreme temperatures and increased cardiac risk, the physiological mechanisms underlying this association remain unknown (see here and here).

Heat-induced myocardial ischemia may be one of the physiological mechanisms underlying the increased cardiac risk associated with extreme temperatures. When exposed to heat, body hyperthermia causes skin vasodilation and sweat production, promoting heat loss. However, these responses result in a redistribution of blood flow and volume toward the skin, decreasing peripheral vascular resistance and central blood volume. These adjustments result in an increase in cardiac output for blood pressure regulation (see here and here). The increase in cardiac output is primarily mediated by an increase in heart rate and cardiac contractility, two determinants of myocardial oxygen consumption (see here and here). These responses require an increase in myocardial blood flow (MBF), which is primarily achieved by coronary vasodilation (see here and here). This may put people living with CAD at risk of ischemia (oxygen deficiency). Moreover, our group has previously observed signs of myocardial ischemia in adults living with coronary artery disease during a 15-minute exposure to a Finnish sauna (80 °C). However, the MBF requirements for heat exposure remained unknown. Identifying these requirements would allow for the establishment of the MBF required to support the cardiovascular demands of heat exposure and would potentially help identify individuals at risk for heat-induced ischemia.

Effects of heat exposure on myocardial blood flow

The main objective of this study conducted by our research team at the Montreal Heart Institute’s EPIC Centre was to determine whether heat exposure increases the MBF. We tested the hypothesis that the MBF would be higher after a 1.5°C increase in core temperature than before exposure. A secondary objective was to determine whether the increase in MBF during heat exposure is modulated by age and the presence of coronary artery disease. Previous studies have shown that healthy older adults have a moderate increase in heart rate during heat exposure. Therefore, we hypothesized that the increase in MBF during heat exposure would be reduced in healthy older adults compared to healthy younger adults. Although little is known about cardiovascular responses to heat exposure in adults with coronary artery disease, we hypothesized that the combination of coronary artery disease and the long-term effect of cardiovascular medications would further attenuate the increase in MBF during heat exposure.

The study included 61 participants: 20 healthy young adults (20–38 years old); 21 adults (60–80 years old); and 20 adults living with CAD (61–79 years old). Participants underwent a PET-CT scan to measure their MBF before and during passive heat exposure. Participants donned a thermostatically controlled suit that covered the entire body except for the head, hands, and feet. After a 30-minute acclimation period at 34°C, the suit temperature was increased to 50°C and maintained at this temperature until the core body temperature increased by 1.5°C. MBF was measured before (baseline) and when core body temperature increased by 0.5°C, 1.0°C, and 1.5°C.

A 1.5°C increase in core body temperature increased MBF by 0.8 mL/min/g, 0.7 mL/min/g, and 0.6 mL/min/g in young and healthy participants, older adults, and older adults with CAD, respectively. Compared with baseline levels, these MBF increases were 2.1-fold, 1.8-fold, and 1.6-fold, respectively. Furthermore, MBF increased proportionally with increases in core body temperature of 0.5°C, 1.0°C, and 1.5°C in all three groups of participants.

We did not observe heat-induced ischemia (lack of oxygen) in older healthy participants. In contrast, PET-CT imaging revealed that 7 (35%) older adults with CAD were ischemic during heat exposure, despite having no symptoms of angina. Ischemia occurred at an increase in core temperature of 0.5°C for 3 participants, 1.0°C for 2 participants, and 1.5°C for 2 participants.

Other effects of heat exposure

Heat exposure increased heart rate by an average of 39 beats per minute (bpm) and systolic blood pressure by an average of 5 mmHg. Heat-induced increases in heart rate were greater in younger participants (45 bpm) than in older healthy participants (34 bpm) or participants with CAD (34 bpm). Systolic blood pressure increases were similar across all three groups. Sweating rates were lower in both older groups than in the younger group. Heat-induced dehydration was moderate in all groups (<2% body weight loss) but lower in older than younger participants.

The results of this study support the hypothesis that higher MBF requirements with a predisposition to myocardial ischemia may be a physiological mechanism underlying the higher cardiac risk associated with extreme temperatures in adults with heart disease. It should be noted that these results are specific to a laboratory study, in which participants were asked not to take antianginal medications (beta-blockers, calcium channel blockers, and nitroglycerin-based medications) for 24 hours before heat exposure and were not allowed to drink during the study. These factors may have contributed to the results, and our results cannot necessarily be generalized to apply to people living normally and taking their prescribed medications.

Higher MBF requirements with ischemia predisposition in adults with heart disease may be sufficient to increase the risk of myocardial infarction. Even with mild to moderate body hyperthermia, older adults living with CAD may benefit from reducing stress on the heart during periods of extreme heat by using a fan, moistening the skin, or adequately hydrating in the absence of air conditioning.