Blood Pressure Profile and Hypertensive Organ Damage in COPD Patients and Matched Controls. The RETAPOC Study

Abstract

BackgroundSeveral studies suggest that there is a pathogenic link between chronic obstructive pulmonary disease (COPD) and cardiovascular diseases. On the other hand, increased sympathetic tone has been described in several respiratory diseases. Our objective was to determine whether hypertension mediated by sympathetic overactivity is a mechanism that explains the association between COPD and cardiovascular diseases.MethodsProspective nested case-control observational study; 67 COPD patients were matched 1:1 by sex and age to controls with smoking history. 24 hour-blood pressure monitoring, urinary catecholamines and their metabolites measurement, echocardiography, carotid ultrasound examination, nocturnal oximetry and retinography were performed.Findingsclassic cardiovascular risk factors and comorbidities were similarly distributed between cases and controls. No significant differences for blood pressure variables (difference for mean systolic blood pressure: -0·13 mmHg; 95% CI: -4·48,4·20; p = 0·94; similar results for all blood presssure variables) or catecholamines values were found between both groups. There was a tendency for lower left ventricle ejection fraction in the COPD cases, that approached statistical significance (64·8 ± 7·4 vs 67·1 ± 6·2, p = 0·05). There were no differences in the retinal arteriovenous ratio, the carotid intima-media thickness, or the number of carotid plaques, between cases and controls. Fibrinogen values were higher in the COPD group (378·4 ± 69·6 vs 352·2 ± 45·6 mg/dL, p = 0·01) and mean nocturnal oxygen saturation values were lower for COPD patients (89·0 ± 4·07 vs 92·3 ± 2·2%, p < 0·0001).InterpretationHypertension induced by sympathetic overactivity does not seem to be a mechanism that could explain the association between COPD and cardiovascular disease.

Looking into the eye of patients with chronic obstructive pulmonary disease: an opportunity for better microvascular profiling of these complex patients

“…They observed no significant difference in AVR between patients with COPD and controls (Golpe et al. ).…”

“…Golpe et al. () determined the AVR in patients with COPD and non‐COPD controls using the average of all vessel calibres measured at arterial and venous intersections (Hubbard et al. ).…”

“…Recent population-based studies demonstrated a strong association between decreased AVR and hypertension, coronary artery disease, diabetes and stroke (Wong et al 2001(Wong et al , 2002aWong et al 2002b;Wong et al 2004). Golpe et al (2016) determined the AVR in patients with COPD and non-COPD controls using the average of all vessel calibres measured at arterial and venous intersections (Hubbard et al 1999). They observed no significant difference in AVR between patients with COPD and controls (Golpe et al 2016).…”

“…Golpe et al (2016) determined the AVR in patients with COPD and non-COPD controls using the average of all vessel calibres measured at arterial and venous intersections (Hubbard et al 1999). They observed no significant difference in AVR between patients with COPD and controls (Golpe et al 2016).…”

Comprehensive, robust, and sensitive UPLC-MS/MS analysis of free biogenic monoamines and their metabolites in urine

“…Abnormally high levels of catecholamines have also been linked with neurological disorders such as Parkinson's disease [10], schizophrenia [11], posttraumatic stress disorder [12]; hypertension [13–15], and myocardial infarction [16]. In addition, several studies have shown that the levels of these neurotransmitters are increased in the plasma and urine of individuals who use tobacco products [17–21].…”