Holiday Heart Syndrome Studied in Mice

Science Editorial, July 22 (EFE). Vacation heart syndrome is a type of arrhythmia associated with excessive alcohol consumption over a short period of time. A study in mice suggests that it may be linked to the release of a stress protein in the heart.

A team from Ohio State University in the US studied the syndrome and tested a heart-protecting molecule in mice to reduce the surge in stress protein and the resulting irregular heart rhythm.

The study results are preliminary as they have not yet been peer reviewed, but they were presented at the American Heart Association’s 2024 Basic Cardiovascular Sciences Scientific Sessions in Chicago, USA.

Holiday heart syndrome is an arrhythmia, the most common of which is atrial fibrillation (AF), associated with excessive alcohol consumption (five drinks in two hours for men and four drinks in two hours for women, according to research), in just one day or during long holiday periods, such as in the summer.

This type of intoxication can lead to people who have never had heart disease being hospitalized because their heart is racing or beating abnormally, explained the study’s first author, Saugat Khanal.

Previous animal studies have shown that arrhythmias associated with excessive alcohol consumption are caused by increased levels of the stress-induced protein JNK2.

This can cause heart cells to use calcium incorrectly, causing the heart to beat too fast or irregularly.

A new study suggests that the molecule Alda-1, an investigational cardioprotective agent, may prevent the activation of JNK2 that leads to atrial fibrillation.

In the study, more than 70% of mice given alcohol to simulate binge drinking developed atrial fibrillation, compared with none of those also given Alda-1.

Both JNK2 enzyme activity and calcium handling remained normal in cardiac cells from Alda-1-treated mice.

The results suggest that developing new drugs, including Alda-1 and other specific JNK2 inhibitors, may be an effective strategy to combat atrial fibrillation for people with holiday heart syndrome, Khanal said.

The next step will be larger animal studies to translate these findings into clinical application, the researcher said.

A second study, also in mice, looked at why alcohol might negatively affect heart function in women taking estrogen replacement therapy.

In rats that lacked estrogen production to mimic human menopause, alcohol exposure caused negative changes in cardiac function in animals receiving estrogen replacement therapy.

The hormone estrogen helps keep blood vessels open and flexible and is thought to help protect women from heart disease.

In an eight-week study, rats had their ovaries removed to simulate menopause, when the ovaries produce little to no estrogen.

The researchers compared menopausal rats that were regularly exposed to alcohol (delivered as 5% ethanol in a liquid diet) with rats that received alcohol and estrogen replacement therapy.

The study found that menopausal rats given estrogen replacement therapy and alcohol experienced both positive (reduced weight gain and fat mass) and negative (increased blood pressure and heart rate) changes.

The team found the significant effect of estrogen on alcohol-induced cardiac dysfunction surprising, despite its known cardioprotective effects. EFE

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