19 September 2019
Chronic obstructive pulmonary disease (COPD) and left ventricular diastolic dysfunction (LVDD) are major causes of morbidity and mortality and have overlapping symptomatology including cough and dyspnea. Whether COPD is a risk factor for LVDD remains largely unclear.
The objective of this meta-analysis was to determine if the prevalence of the LVDD as determined by echocardiographic parameters is increased in COPD patients.
We used a time-and-language-restricted search strategy resulting in identification of 4,912 studies of which 15 studies met our apriori inclusion criteria; 4,897 were excluded, such duplicates, foreign language articles were excluded. We performed a meta-analysis of standard echo parameters on the fifteen case control studies related to diastolic dysfunction. The meta-analysis was performed using Review Manager, version 5.3 (Cochrane Collaboration).
A total of 15 studies with 1,403 subjects were included. There were no differences in left ventricular ejection fraction between COPD and non-COPD population. Patients with COPD had prolonged isovolumetric relaxation time (IVRT) (mean difference 20.84 [95% CI 12.21, 29.47]; P< 0.00001), lower E/A ratio (mean difference - 0.24 [95% CI −0.34, 00.14]; P < 0.00001), higher transmitral A wave peak velocity (Apv) (mean difference 11.71 [95% CI 4.80, 18.62]; P< 0.00001), higher E/e’ ratio (mean difference 1.88 [95% CI 1.23, 2.53]; P< 0.00001), lower mitral E wave peak velocity (Epv) (mean difference −8.74 [95% CI −13.63, −3.85]; P< 0.0005), prolonged deceleration time (DT) (mean difference 50.24 [95% CI 15.60, 84,89]; P< 0.004), a higher right ventricular end diastolic diameter (RVEDD) (mean difference 8.02 [95% CI 3.45, 12.60]; P< 0.0006) compared to controls. COPD patients had a higher pulmonary arterial pressure (mean difference 10.52 [95% CI 3.98, 17.05]; P< 0.002). Differences in septal e’ velocity (mean difference −2.69 [95% CI −6.07, 0.69]; P< 0.12) and in lateral e’ velocity (mean difference −2.84 [95% CI 5.91, 0.24]; P< 0.07) trended towards significance but did not meet our cutoff for statistical significance (p < 0.05).
Patients with COPD are more likely to have LVDD as established by echocardiographic parameters. Our findings are likely explainable, in part, by factors such as lung hyperinflation, chronic hypoxia, hypercapnia, systemic inflammation, increased arterial stiffness, subendocardial ischemia, as well as ventricular interdependence; all of which might contribute to the pathogenesis of diastolic dysfunction. Further research is needed to elucidate the pathophysiologic mechanisms of increased LVDD in the COPD population with the potential impact on developing effective therapeutic interventions for these serious disorders.