Therapeutic Hypothermia Can Treat Cardiac Arrest in Hypertrophic Cardiomyopathy



NEW ORLEANS – Therapeutic hypothermia shows promise as a novel, strikingly effective lifesaving and neuroprotective treatment in patients with hypertrophic cardiomyopathy who experience out-of-hospital cardiac arrest.

In a prospective series of seven consecutive relatively young adult patients with cardiac arrest and hypertrophic cardiomyopathy (HCM) who underwent rapid cooling to a core body temperature of 31.8 -33° F for 24-29 hours followed by gradual rewarming, all seven left the hospital with preserved cognitive, neurologic, and cardiac function. All received implantable cardioverter-defibrillators for secondary prevention and remained asymptomatic 10-56 months post arrest, Dr. Bradley A. Maron said at the annual meeting of the American College of Cardiology.

Dr. Bradley Maron

This experience stands in marked contrast to the outcomes typically seen when cardiac arrest occurs in patients with HCM. In the absence of therapeutic hypothermia, HCM patients are known to have dismal outcomes despite swift cardiopulmonary resuscitation and external defibrillation, noted Dr. Maron of Brigham and Women's Hospital, Boston.

Therapeutic hypothermia is gaining traction as a neuroprotective treatment strategy for out-of-hospital cardiac arrest in unconscious patients, especially those with ischemic heart disease, stroke, or near drowning. But there are no prior reports of it being used in patients with HCM.

Dr. Maron said he got the idea for studying therapeutic hypothermia in patients with HCM and other genetic heart diseases after he noticed that when the therapy is applied in patients with ischemic heart disease and impaired left ventricular function, their LV function tends to worsen because of the increased afterload caused by cold-induced peripheral vasoconstriction.

"I thought, ‘In hypertrophic cardiomyopathy LV function is generally preserved, cardiac index is generally maintained, so maybe this is a population worth looking at to see if they tend to do better with therapeutic hypothermia than other patients [do],’ " he recalled in an interview.

The seven patients, six men and one woman, averaged 47 years of age with a marked mean maximum LV thickness of 23 mm. Four of the seven had LV outflow obstruction of 45-70 mm Hg at rest. Six patients received cardiopulmonary resuscitation within 3 minutes of their cardiac arrest and the other within 6 minutes. The mean time to spontaneous circulation was 19 minutes, with an average of 162 minutes from collapse to initiation of hypothermia. One patient didn’t start therapeutic hypothermia until more than 4 hours had gone by. Each patient was unconscious without meaningful responses at the initiation of therapy. The initial Glasgow Coma Scale score was 3 in all cases.

Prior to their cardiac arrest, none of these patients had risk factors warranting placement of an implantable cardioverter-defibrillator. However, follow-up genetic testing showed that two patients had double sarcomere mutations in the MyBPC3 and TNN13 genes, potentially explaining their high risk for sudden death.

The mean LV ejection fraction was 61% prior to the cardiac arrest and 63% at discharge.

Noting that HCM is the most frequent cause of sudden death in the young, Dr. Maron observed that "since a lot of these deaths are on-field in the athletic arena, we may want to consider the possibility of joining on-field access to an automatic external defibrillator to some form of cooling therapy that can be applied immediately when an athlete goes down."

He said he had no relevant financial disclosures.

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