Chronic lung disease begins to affect cardiac function at even mild levels of emphysema, data from a large prospective cohort study showed.
A 10-point increase in percent emphysema by lung CT had a linear inverse relationship with left ventricular end-diastolic volume (LVEDV), stroke volume, and cardiac output (P<0.001 for all parameters), researchers reported in the Jan. 21 issue of the New England Journal of Medicine.
Current smoking status increased the magnitude of the association compared with former smokers and nonsmokers, the researchers found.
Left ventricular ejection fraction did not change with increasing percent of emphysema and airflow obstruction.
"Previously, it has been well known that in very severe lung disease, the damage to the lungs affects heart function," lead author R. Graham Barr, MD, of Columbia University in New York, said in an interview.
"What we have shown is that a similar physiology, a similar relationship, would appear to extend up and down the spectrum of lung disease from mild, subclinical COPD and emphysema, all the way to moderately severe lung disease."
Severe COPD can lead to cor pulmonale, characterized by increased vascular resistance and right heart failure, accompanied by reduced left ventricular filling, left ventricular stroke volume, and cardiac output.
However, left ventricular ejection fraction (LVEF) usually is preserved. Whether similar changes occurred with less severe COPD had not been determined, and examining that question was the principal objective of the study by Barr and colleagues.
The study population comprised a subgroup of patients enrolled in the Multi-Ethnic Study of Atherosclerosis (MESA), which is exploring the prevalence, correlates, and progression of subclinical cardiovascular disease. The MESA Lung Study comprised 2,816 MESA participants who underwent cardiac MRI assessment of left ventricular structure and function.
Investigators in the lung study excluded patients who had a restrictive pattern on spirometry, defined as a forced vital capacity (FVC) below the lower limit of normal and an FEV1:FVC ratio >0.7.
Information collected for the lung study included patient demographics, smoking history, medical history, level of physical activity, height, weight, resting blood pressure, serum glucose, C-reactive protein, and fibrinogen levels.
Extent of emphysema was calculated from lung fields of cardiac CT scans, which included 70% of the lung volume from the carina to the base. Investigators defined extent of emphysema as the percentage of voxels below -910 Hounsfield units in the lung windows of cardiac CT scans.
Participants who smoked at least one cigarette in the 30 days before CT or who had urinary cotinine levels >100 ng/mL were classified as current smokers.
The mean age of the lung population was 61, and 51% were women. Current smokers accounted for 13% of the participants, former smokers for 38%, and nonsmokers for 49%. LVEF averaged about 70%.
Mean spirometric measures were normal, as were measures of left ventricular structure and function. Median percent emphysema was 15%. Comparison of percent emphysema with left ventricular measures showed that a 10-point increase in percent emphysema was associated with a:
* 4.1 mL decrement in LVEDV
* 2.7 mL decrement in stroke volume
* 0.19 L/min decrement in cardiac output
The investigators observed no evidence of an association between percent emphysema and LVEF, reflected in a 0.02-point mean increase with each 10-point increase in extent of emphysema.
Smoking status significantly influenced associations of percent emphysema with LVEDV (P<0.001 for interaction) and stroke volume (P=0.008 for interaction).
The magnitude of the association was greater among smokers than former smokers, and greater among former smokers than nonsmokers. However, the associations were evident in smokers and nonsmokers alike.
“The apparent effect of emphysema on left ventricular end-diastolic volume and cardiac output was similar to that of traditional cardiac risk factors previously reported in MESA and, among smokers, was greater than that of traditional cardiac risk factors,” the authors wrote.
The linearity of associations across the study population “suggests that even early-stage COPD influences stroke volume and left ventricular size,” Anton Vonk-Noordegraaf, MD, of Vrije University Medical Center in Amsterdam, wrote in an accompanying editorial.
“Since oxygen delivery is directly related to cardiac output, a lower cardiac output in patients with COPD leads to impaired oxygen delivery,” Vonk-Noordegraaf continued.
“Although the effects on cardiac output were small in this study population, they may be more pronounced in severe cases of emphysema and during exercise, as has been shown previously. The question is whether the striking clinical resemblance between COPD and chronic heart failure can be explained in part by a factor both diseases have in common: decreased cardiac output.”