A study published February 25 in the European Journal of Heart Failure, reveals that lung function and obstructive airway diseases are associated with a higher incidence of heart failure
According to the researchers of the large population-based study, this link was apparent in individuals who never smoked and was still apparent after adjusting for smoking status and number of years smoking. They say that this suggests “that our results are not primarily confounded by smoking.”
Heart failure is the primary cause for acute hospital admission. In Europe, approximately 30 million individuals have heart failure and its incidence is still rising: more individuals are living longer, more people are surviving a heart attack (but with damage to the heart muscle), and more cases are being identified.
The researchers found reduced lung function, as measured by forced expiratory volume (FEV1) by spirometry, increased the long-term risk of developing heart failure. The findings were not altered by cardiovascular risk factors (including smoking), age, or prior heart disease.
Results from the study were acquired from the Atherosclerosis Risk In Communities (ARIC) study, a population-based cohort from the United States. The study involved approximately 16,000 individuals aged 45 to 65 years old who were followed for an average of 15 years. The research was funded by the National Heart, Lung and Blood Institute (NHLBI), part of the National Institutes of Health.
A common co-morbidity in individuals with heart failure is chronic obstructive pulmonary disease (COPD), and vice versa. However, COPD has only just now been established as a long-term risk factor for heart failure. According to an associated report the study now “strengthens the hypothesis that pulmonary obstruction itself is a major risk factor for heart failure.”
The report continues: “thinking of heart failure as a possible cause in any patient with shortness of breath and fatigue, or an increase in such symptoms, irrespective of other disease labels, including COPD, means that physicians need to ‘reset’ their clinical reasoning,” and review their pharmacological management.
The researchers collected baseline data of the ARIC cohort between 1987 and 1989. The data included information on medical history, socioeconomic indicators, cardiovascular risk factors, family history, medication use, lung volumes, ECGs, and serum chemistries.
After the baseline visit, 3 re-examinations were conducted, along with yearly telephone interviews and active surveillance of hospitalizations and death. Incident heart failure was determined from hospital records and death certificates up to 2005 in 13,660 eligible patients.
The researchers calculated hazard ratios for heart failure according to quartiles of FEV1 in both men and women. After adjusting for smoking, height, and age, the team found that the ratios increased steadily over descending quartiles of FEV1.
Further adjustment for CVD risk factors revealed that the hazard ratio for heart failure, comparing the lowest with highest quartile FEV1, was 3.03 for white men, 3.91 for white women, 2.23 for black men and 2.11 for black women. The researchers observed these connections at all levels of smoking.
According to the researchers, this finding indicates that a low FEV1 reading by spirometry “was strongly predictive” of heart failure, independent of other CVD risk factors.
Lead researcher of the study, Dr. Sunil Agarwal from the University of North Caroline, Chapel Hill, USA, explains that the results, when translated in the context of current scientific evidence, backs a temporal association between development of heart failure and low lung capacity.
“This risk, given a low FEV1, is similar in magnitude – and may be stronger – than that seen for common and modifiable risk factors such as diabetes or hypertension. The public health implications are huge, particularly since smoking and air pollution affect lung function adversely. So it will be important to determine whether interventions that sustain or improve FEV1 are associated with lower risk of heart failure.”
One possible explanation for the link is “multiple drivers”, such as environmental or genetic factors, said Dr. Agarwal. Even though smoking is known to be linked to heart failure, results from the study indicated that the associated with low FEV1 was also present in individuals who never smoked.
Agarwal highlights a recent study by Barr and colleagues, published in the New England Journal of Medicine. Results from the study demonstrated a connection between subclinical emphysema with impaired relaxation of the heart, a process which may be involved in the development of heart failure.
“Whether pulmonary shunting of blood due to COPD, pulmonary hypertension or arrhythmias also drive this association remains unclear at this time.
Our study does add to a growing literature indicating that COPD of low FEV1 influence one’s risk of heart failure, even if the observed association cannot be equated with causation. So we have to focus on interventions to prevent or reverse COPD or improve FEV1, and to test whether such interventions reduce the risk of heart failure. Given the complex interaction between the respiratory and cardio-circulatory functions, causation will be hard to disentangle.”
Senior researcher of the study, Dr. Gerardo Heiss, explained:
“COPD is coming in patients with heart failure, but we cannot infer from our results that screening for COPD will reduce the risk of heart failure, or that managing COPD in heart failure patients will improve outcomes. However, our results should add to the growing awareness among practitioners that patients with COPD do have a higher risk of heart failure, and that shortness of breath or impaired vigour should not be ascribed prima facie to COPD without careful consideration of the presence of heart failure.”
Written by Grace Rattue Source: European Society of Cardiology