暑い季節に心臓発作のリスクを高める一般的な心臓薬

医師による主な違い

新しい研究によると、ベータブロッカーと抗血小板薬(アスピリンなど)を服用している患者は、非常に暑い時期に心臓発作を起こすリスクが高い.

冠状動脈性心疾患の患者にとって、ベータ遮断薬は生存率と生活の質を改善できる重要な薬です。 同様に、アスピリンやその他の抗血小板薬は、心臓発作のリスクを減らすことができます.

ただし、これらの保護は、心臓発作がすでに起こりやすい暑い天候のイベント中に逆効果になる可能性があります. 8月1日にジャーナルに掲載された新しい研究 Nature 心血管研究 猛暑に関連する致命的ではない心臓発作に苦しんでいる人々の中で、非常に多くの人がこれらの心臓薬を服用していることを発見しました.

「これら2つの薬を服用している患者は、リスクが高くなります」と、イェール大学公衆衛生大学院疫学科(環境衛生)の助教授であり、研究の筆頭著者であるカイ・チェンは述べています。 「熱波の間、彼らは本当に予防策を講じる必要があります。」

これらの安全対策には、エアコンの使用や公共の冷却センターへの訪問などの冷却戦略が含まれます。

大気汚染、寒さ、その他の外部環境要因が心臓発作を引き起こす可能性があります。 暑い気候でもそうなる可能性があることを示唆する証拠が増えています. しかし、疫学者は、どのグループの人々がこれらの極端な環境に対して最も脆弱であるかを特定するためにまだ取り組んでいます.

メソッド

レジストリを使用して、研究者は 2001 年から 2014 年までの暑い時期 (5 月から 9 月) にドイツのアウグスブルクで個人が致命的ではない心臓発作を起こした 2,494 のケースを分析しました。

彼らは以前の研究で、暑さや寒さにさらされると心臓発作が起こりやすくなることをすでに示していました. 彼らはまた、地球が 2 ~ 3 度温暖化すると、熱に関連する心臓発作の発生率が上昇すると計算しました。

摂氏
摂氏スケールとも呼ばれる摂氏スケールは、スウェーデンの天文学者アンデルス・セルシウスにちなんで名付けられた温度スケールです。 摂氏スケールでは、0 °C は水の凝固点であり、100 °C は 1 気圧での水の沸点です。

” data-gt-translate-attributes=”[{” attribute=””>Celsius (3.6 to 5.4 degrees Fahrenheit).

Built on that research, the current study examined patients’ medication use prior to their heart attack.

They analyzed the data in a way that let patients serve as their own controls. This was done 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 researchers 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 antiplatelet medications were likelier to have heart attacks during the hottest days compared to control days. Antiplatelet 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.

Although it shows an association, the study doesn’t prove that these medications caused the heart attacks, nor that they make people more vulnerable to heart attacks. It’s possible that they did increase the risk of heart attacks triggered by hot weather, but 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 the scientists 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 antiplatelet 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.

The results suggest that as climate change progresses, heart attacks might become a greater hazard to some people with cardiovascular disease.

Reference: “Triggering of myocardial infarction by heat exposure is modified by medication intake” by Kai Chen, Robert Dubrow, Susanne Breitner, Kathrin Wolf, Jakob Linseisen, Timo Schmitz, Margit Heier, Wolfgang von Scheidt, Bernhard Kuch, Christa Meisinger, Annette Peters, KORA Study Group and Alexandra Schneider, 1 August 2022, Nature Cardiovascular Research.
DOI: 10.1038/s44161-022-00102-z

The study appears online in Nature Cardiovascular Research. It was funded by the German Foundation of Heart Research, the University of Augsburg, and the University Hospital of Augsburg, Germany.

Professor Robert Dubrow was a co-author and Alexandra Schneider of Germany’s Helmholtz Zentrum Munchen was last author. The other co-authors were Susanne Breitner, Kathrin Wolf, Margit Heier, and Annette Peters, all of the Helmholtz Zentrum München–German Research Center; Jakob Linseisen of Ludwig-Maximilians-Universität München and University Hospital Augsburg; Timo Schmitz, Wolfgang von Scheidt, and Christa Meisinger of University Hospital Augsburg; and Bernhard Kuch of Hospital of Nördlingen (Germany). Brietner and Peters are also affiliated with Ludwig-Maximilians-Universität München, Peters with German Research Center for Cardiovascular Research, and Heier with University Hospital Augsburg.

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