A new study debunks the theory that acid reflux is partially responsible for triggering severe asthma symptoms — while other research indicates that reflux drugs may raise the risk of major adverse cardiovascular (CV) events.

Studies show that anywhere from 32% to 84% of Americans suffering from asthma also have gastroesophageal reflux (GER). Approximately half of those patients have silent GER (acid reflux associated with mild or no symptoms). Cough, chest discomfort, and other symptoms of asthma can be difficult to distinguish from GER–related problems. The relationship between the two conditions is complex, and the role of GER in the development or persistence of asthma symptoms is unknown.

Asthma guidelines suggest anti–reflux treatment for individuals with poorly controlled asthma and silent GER, but this suggestion is mainly based on findings regarding asthma patients with symptomatic GER (for whom GER treatment is recommended).

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Investigators randomly assigned 412 patients with silent GER and poorly controlled asthma to treatment with a proton pump inhibitor (PPI) or placebo. Over six months, both groups experienced a similar number of episodes of poor asthma control.

“Despite a high prevalence of asymptomatic GER among patients with poorly controlled asthma, treatment with PPIs does not improve asthma control,” researchers conclude (N Engl J Med. 2009;360:1487-1499). “Asymptomatic GER is not a likely cause of poorly controlled asthma.”

The CV study, presented in May at the Society for Cardiovascular Angiography and Interventions 32nd Annual Scientific Sessions, in Las Vegas, analyzed claims from 16,690 patients taking clopidogrel (Plavix) for a full year following coronary stenting. A total of 41% also took a PPI for an average of nine months. PPIs are frequently prescribed with clopidogrel to counteract pre–existing stomach disease or reduce the risk of nausea and heartburn.

The overall combined risk of hospitalization for major adverse CV events was 51% higher among the patients taking PPIs, which can interfere with the liver enzymes needed to activate the anti–clotting effects of clopidogrel.