But those protections could backfire during hot-weather events, a time when heart attacks are more likely. A new study has found that among people suffering non-fatal heart attacks associated with hot weather, an outsize portion are taking these heart drugs.
“Patients taking these two medications have higher risk,” said Kai Chen, an assistant professor in the Department of Epidemiology (Environmental Health) at the Yale School of Public Health and first author of the study. “During heat waves, they should really take precautions.”
Those precautions include cooling strategies like using air conditioning or visiting a public cooling center.
External environmental factors like air pollution and cold weather can trigger heart attacks. Growing evidence suggests hot weather can do so, too. But epidemiologists are still working to identify which groups of people are most vulnerable to these environmental extremes.
Using a registry, the authors looked at 2,494 cases in which individuals experienced non-fatal heart attacks in Augsburg, Germany during the hot-weather months (May through September) between 2001 and 2014.
In previous research, they had shown that exposure to either heat or cold made heart attacks more likely, and they calculated that heat-related heart attack rates would rise once the planet has warmed by 2 to 3 degrees Celsius.
The current study built on that research by examining patients’ medication use prior to their heart attack.
They analyzed the data in a way that let patients serve as their own controls, by comparing heat exposure on the day of the heart attack versus the same days of the week within the same month. That is, if a person had a heart attack on the third Thursday in June, the authors compared their temperature exposure that day to their temperature exposure on other “control” Thursdays in June.
Two medications tied to risk
It turned out that users of beta blockers or anti-platelet medications were likelier to have heart attacks during the hottest days compared to control days. Anti-platelet medication use was associated with a 63% increase in risk and beta blockers with a 65% increase. People taking both drugs had a 75% higher risk. Non-users of those medications were not more likely to have a heart attack on hot days.
The study doesn’t prove that these medications caused the heart attacks, nor that they make people more vulnerable to heart attack. Although it’s possible that they did increase the risk of heart attacks triggered by hot weather, it’s also possible that patients’ underlying heart disease explains both the prescriptions and the higher susceptibility to heart attack during hot weather.
Still, one clue does suggest the medications could be to blame.
When researchers compared younger patients (25 to 59 years) to older ones (60 to 74 years), they found, as expected, that the younger ones were a healthier group, with lower rates of coronary heart disease. Yet younger patients taking beta blockers and anti-platelet medications were more susceptible to heat-related heart attack than older patients, despite the older ones having more heart disease.
Another clue that these two medication types may render people more vulnerable: For the most part, other heart medications didn’t show a connection to heat-related heart attacks. (An exception was statins. When taken by younger people, statins were associated with an over threefold risk of a heart attack on hot days.)
“We hypothesize that some of the medications may make it hard to regulate body temperature,” Chen said. He plans to try to untangle these relationships in future studies.
This study provides an updated synthesis of the effects of both high temperature and heatwaves on the risk of cardiovascular disease-related mortality and morbidity. Our review of 282 studies strengthened evidence of increased cardiovascular disease health risks related to heat exposures, and provides new evidence that the cardiovascular disease risks vary geographically and are dependent on underlying climate conditions. The meta-analysis of 266 studies showed that for every 1°C increase in temperature above reference temperatures there is an associated 2·1% increase in cardiovascular disease-related mortality and a 0·5% increase in cardiovascular disease-related morbidity. Although positive associations were observed across all cardiovascular disease diagnoses in mortality, stronger risks were shown with stroke (3·8% increased risk) and coronary heart diseases (2·8% increased risk). For morbidity, increased risks were related to arrhythmias and cardiac arrest (1·6%), and out-of-hospital cardiac arrest presented the greatest increased risk (2·1%). Additionally, during heatwaves, the risk of cardiovascular disease-related mortality significantly increased by 11·7%, with the risk increasing as heatwave intensity increased.
The heat effects on poor cardiovascular outcomes relate to the multiple physiological pathways that initiate human cardiovascular responses to passive heat stress and exogenous heat gain. These pathways leading to heat-induced impairment of cardiovascular health are overlapping and complex, with potential systemic effects. Briefly, when heat gain exceeds the capacity of the body to lose heat, a series of pathological events can eventually result in cardiovascular impairment.8, 33 Increased sweating and skin blood flow can lead to water loss and dehydration and increase the risk of stroke. The accompanying decrease in plasma volume and increase in the concentration of red blood cells and other blood constituents, together with an increase in blood viscosity and an elevated cholesterol concentration, might cause thromboembolism, leading to increased risk of ischemic stroke and heart disease.34 Thermal stress has been shown to increase the risk of cardiovascular dysfunction such as hypertension, heart rate disturbances, and ischemic heart disease.35 Vasodilation of peripheral blood vessels reduces systolic blood pressure and so decreases coronary blood flow, leading to the risk of arrhythmias and cardiac arrest.36 Additionally, a heat-induced elevated heart rate and cardiac contractility can increase myocardial oxygen consumption, which might also pose a threat of fatal arrhythmias.37
Our results support and update the findings of previous reviews associating high temperatures5, 38, 39, 40 and heatwaves3, 6, 38 with cardiovascular disease-related mortality. We also found associations with cardiovascular disease-related morbidity, and our findings are in line with a 2016 meta-analysis that reported a 1% increased risk associated with elevated temperatures and a 6·1% increased risk for heatwaves.4 However, some meta-analyses and original epidemiological studies reported either weak or no apparent associations between increased temperature and cardiovascular disease-related morbidity.41, 42, 43, 44, 45 This might be explained by a variety of indicators being used in morbidity studies, including hospital admissions, emergency department visits, and ambulance attendances. Moreover, differences in effect estimates exist even for the same heat-associated cardiovascular disease outcome depending on the type of health outcome indicators the study used;6 this might be a plausible explanation for the observed difference in associations for hypertensive mortality and morbidity. Furthermore, studies based on morbidity data might have underestimated the true heat effects if patients had difficulty accessing health-care services during extreme temperatures.46 On the other hand, patients who die during heatwaves might be inpatients in hospitals (particularly hospitals without air conditioning), or those with acute cardiovascular disease conditions might die before being admitted to hospital for medical treatment,47 and this might explain the observed higher overall effect on mortality than on morbidity and the high out-of-hospital morbidity for conditions such as cardiac arrest.
Inter-study heterogeneity was detected, indicating inherent differences between the studies, in aspects such as study areas and population structures, study designs, and statistical models used. Meteorological variables (wind speed, air pressure, and relative humidity) and air pollutants were considered and adjusted for as confounders in most of the included studies. However, different covariates included in analyses might also contribute to the heterogeneity of the results. The series of sensitivity analyses indicated consistency in the direction and magnitude of the associations in the reviewed studies (appendix pp 58–61). Additionally, heterogeneity was not reduced in any of these associations (in either the main analysis or sensitivity analyses), indicating that other unmeasured factors might be contributing to the heterogeneity, warranting future research.
The significant, higher mortality risk of heat impacts on people aged 65 years and over than those younger than 65 years are evident from our findings. Older people usually exhibit low physiological tolerance to heat. In addition to age-related physiological changes in thermoregulation, the cardiovascular capacity of the human body naturally declines with age.48 During heat exposure, older individuals generally respond with attenuated sweat gland outputs, reduced blood flow to the skin, smaller increases in cardiac output, and decreased redistribution of blood from the splanchnic and renal circulations.49 Moreover, people 65 years and older tend to have a higher rate of pre-existing conditions than younger people (eg, hypertension, diabetes mellitus, hyperlipidaemia, and coronary artery disease), and associated medication use, which might also explain the observed increased risk of cardiovascular disease outcomes in response to heat.50
The importance of estimating exposure–response effects in different climate regions has been previously identified.4 In this study, our subgroup analyses showed higher risk estimates of cardiovascular disease outcomes among individuals living in tropical climates than in those living in other climate zones examined, suggesting that the risk is not uniform.51 This finding might be explained by the higher extreme heat frequency and lower interannual variability in tropical regions than other climate regions.52 The variations in heat-related cardiovascular disease risks between regions might also be associated with differences in humidity at high temperatures.9 Future studies investigating these geographical variations by population structure, socioeconomic status, and public health intervention capacity are needed. Additionally, for every 1°C increase in temperature, the pooled effect estimates for cardiovascular disease-related mortality and morbidity were higher in countries with lower national income, although LMICs are often in warmer regions than high-income countries.53
This systematic review of 282 studies included diverse populations and study areas. A key strength of this review is that it addresses the gaps in knowledge about the quantitative effects of high temperatures and heatwaves (stratified by intensity) on cardiovascular disease health outcomes in different climate zones. The studies have been assessed on the basis of best practice guidelines developed specifically for environmental health research, and several sensitivity analyses attest the robustness of our findings.54
Limitations should be acknowledged. Firstly, we only considered peer-reviewed literature published in English. Secondly, the Peer Review of Electronic Search Strategies (PRESS) checklist was not adopted for peer-review of search strategies,20 and tools (such as Medline Transpose) were not used to translate search terms between databases. However, our search strategy was developed using recognised search guides and in consultation with an academic librarian, which might have enabled us to retrieve the most relevant studies. Thirdly, although we included studies from several countries with diverse climates, there were a low number of estimates in some subgroups. For example, only a few were from LMICs and tropical areas that might have increased susceptibility to the effects of a warming climate. Despite our efforts to account for the differences between climate zones, caution should be taken when interpreting these pooled effect estimates owing to the high observed heterogeneity that indicates the possible unaccounted factors within each climate zone. Moreover, many primary studies reviewed did not include data on modifying factors such as pre-existing cardiovascular disease illness, comorbidities, and use of medication.
As the global temperature rises, the population ages, and cardiovascular disease incidence and prevalence increases worldwide, tailored strategies for preventing the negative effects of ambient heat on cardiovascular disease can have a substantial effect on heat-related health burdens. However, data are sparse on interventions specifically aimed at reducing cardiovascular disease-related health risks from heat,55 the effectiveness of the interventions, and whether they can be adequately received by the most vulnerable groups (eg, those with low education levels, people who are homeless, and people older than 65 years).56, 57 Another challenge is in determining a threshold at which hot weather conditions become sufficiently harmful to human health to warrant intervention.56, 58 To support this effort, collaboration should be enhanced between local government bodies, public health professionals, primary health-care providers, and cardiologists, in heat-health planning, research, education, and advocacy campaigns on global climate and health. Moreover, future studies improving understanding of the impact of ambient heat exposure on cardiovascular disease health that consider the differences in underlying climate pattern and age structure, and which involve the monitoring of health status and risks of heart disease before the onset of summer, are warranted.
In summary, this study provides updated evidence regarding the elevated risk of cardiovascular disease-related mortality and morbidity due to heat exposures and indicates avenues for future research. Findings also highlight that underlying regional climate conditions need to be accounted for when assessing the risk of heat-related cardiovascular disease health outcomes, as well as societal lifestyle factors, population characteristics, and disease subgroups. Findings from this review have important implications for the evaluation of current risks of adverse cardiovascular disease effects during hot weather and future health-care prevention strategies and resource allocation for high-risk populations. As rising temperatures already confer an increased risk of quantifiable and avoidable cardiovascular disease events in the general population, implementation of policy measures to achieve a zero-carbon emission economy should be a high priority.
reference link :https://www.thelancet.com/journals/lanplh/article/PIIS2542-5196(22)00117-6/fulltext#seccestitle130
More information: Kai Chen et al, Triggering of myocardial infarction by heat exposure is modified by medication intake, Nature Cardiovascular Research (2022). DOI: 10.1038/s44161-022-00102-z