Sleep apnea may offer protection from heart attack

Findings of study show some heart attack patients may actually benefit from mild to moderate sleep-disordered breathing.

sleep apnea test 311 (photo credit: courtesy)
sleep apnea test 311
(photo credit: courtesy)
Doctors have for years warned people suffering from sleep apnea – where they awaken momentarily dozens or even hundreds of times per night – to lose weight and wear so-called continuous positive airway devices on their noses to increase their oxygen supply and reduce their resultant risk for cardiovascular disease.
But a counterintuitive study conducted at the Technion- Israel Institute of Technology in Haifa suggests that some heart attack patients may actually benefit from mild to moderate sleep-disordered breathing.
Apnea and other types of sleep-disordered breathing can boost the numbers and functions of rare cells that help repair and build new blood vessels, according to cell biologist Dr. Lena Lavie, her husband, Prof. Peretz Lavie (president of the Technion and a well-known sleep medicine expert), and their Technion colleagues, Dr. Slava Berger and Prof. Doron Aronson.
They say the findings could help predict which patients are at a greater health risk after a heart attack and might even suggest ways to rebuild damaged heart tissue.
Their study was just published in the American Journal of Respiratory and Critical Care Medicine and was accompanied by an editorial written by Dr. Leila Kheirandish-Gozal of the University of Chicago and Prof. Ramon Farré of the University of Barcelona in Spain.
Sleep-disordered breathing is characterized by cycles of apnea-induced hypoxia in which the sleeper experiences a temporary drop in oxygen levels. Between five percent and 10% of the general adult population suffers from it, but it is much more common – 40% to 60% – among cardiac patients.
Many studies have shown that sleep apnea is a risk factor for everything from high blood pressure to chronic heart failure, Lena Lavie noted. Earlier studies by the Haifa scientists suggest apnea increases oxygen-related stress and inflammation in the heart and blood vessels.
The study could help resolve a puzzling medical issue. If sleep disordered breathing is associated with cardiovascular disease, why is it that people who suffer from breathing disorders in sleep seem to do as well as healthy sleepers after a heart attack?
The Technion researchers examined 40 male patients – a mix of healthy sleepers who served as a control group and others with sleep disordered breathing who had had a heart attack just a few days earlier. Blood samples revealed that the sleep-disordered- breathing heart patients had markedly higher levels of endothelial progenitor cells (EPCs), which give rise to new blood vessels and repair the injured heart. They also had higher levels of other growth-promoting proteins and immune cells that stimulate blood vessel production.
The researchers were able to trigger a similar increase in vessel-building activity in vascular cells taken from a second set of 12 healthy men and women by withholding oxygen from the cells for short periods.
“Indeed, our results point to the possibility that inducing mild-moderate intermittent hypoxia may have beneficial effects,” Lena Lavie said.
The Spanish authors of the accompanying editorial in the journal said the Technion study moved toward reconciling the ideas that apnea can stress the heart but also “precondition” it for repair.
Patients with sleep-disordered breathing, they noted, “are essentially better prepared to harness the recruitment of EPCs when [a heart attack] comes knocking at the door.”
According to Aronson, who is also affiliated with Haifa’s Rambam Medical Center, a heart attack is a “potent stimulus for EPC mobilization.”
He also explained that the cells move from bone marrow to the heart to repair damaged tissue after a heart attack.
“The field of cell-based cardiac repair has struggled to find the best approach to enhance recruitment of EPCs to the heart following myocardial infarction,” he said. The Technion findings, he added, suggest that intermittent periods of oxygen deprivation in heart attack patients “provides a simple and powerful means to boost EPC mobilization.”
According to Lena Lavie, it should be “further investigated if inducing intermittent hypoxia immediately after a heart attack, in patients without sleep disordered breathing, will also have such an effect.”
The researchers hope to test this possibility in animal studies, as well as expand their studies of the underlying mechanisms that activate EPCs and other vessel-building factors.