In a select subgroup of patients who have been undergoing evaluation for lung volume reduction surgery and had both Doppler echocardiography and right heart catheterization, Bach and co-workers (Bach et al 1998) did not find a significant correlation between the actual and estimated sPAP but suggested that this difference was due to a single outlying patient. measurement of pulmonary pressures. The combined effects of swelling, GW-1100 endothelial cell dysfunction, and angiogenesis appear GW-1100 to contribute to the development of PH associated with COPD. Systemic vasodilators have not been found to be effective therapy. Selective pulmonary vasodilators including inhaled nitric oxide and phosphodiesterase inhibitors are encouraging treatments for individuals with COPD connected PH but further evaluation of these medications is needed prior to their routine use. Keywords: COPD, pulmonary hypertension Intro Chronic obstructive pulmonary disease (COPD) is definitely a significant health care burden worldwide and is the only major cause of death in the United States for which both mortality and morbidity are increasing (Murray and Lopez 1997; Hurd 2000). This disease process is definitely manifest by progressive airflow limitation, hyperinflation and air trapping, hypoxemia, hypercapnea, and elevations in pulmonary vascular pressures. Clinically, individuals with COPD develop breathlessness, cough, sputum production and disease exacerbations that impair quality of life. Factors that portend a poor prognosis include severity of airflow limitation, ventilatory capacity, hypercapnea, and pulmonary hypertension (Burrows and Earle 1969; Weitzenblum et al 1981; Anthonisen et al 1986). Survival correlates negatively with pulmonary arterial pressure and pulmonary vascular resistance and individuals with COPD and PH have improved morbidity and risk for hospitalizations for acute COPD exacerbations (Burrows et al 1972; Weitzenblum et al 1984; Kessler et al 1999; Barbera et al 2003). PH associated with COPD is definitely progressively recognized as a contributing element to the medical manifestations, morbidity, and mortality of the COPD disease process. This recognition offers stimulated further study into the cellular and molecular processes contributing to the pathogenesis of PH associated with COPD and the development and screening of new restorative interventions. This review will examine the epidemiology GW-1100 of PH associated with COPD, its medical manifestations, methods of analysis, pathophysiology, and treatment strategies. Prevalence The prevalence of pulmonary hypertension (PH) in COPD has not been accurately measured in large epidemiologic studies because of the risks and expense of invasive pressure measurement by right heart catheterization. Most studies have utilized noninvasive measures to estimate pulmonary arterial pressures. Estimations of the prevalence of PH in COPD will also be confounded by individual selection. Studied individuals have varying severity of obstructive lung disease as well as different levels of oxygenation. Finally, over the last several decades, different organizations have used numerous minimal pressures to define PH Rabbit polyclonal to AdiponectinR1 and severe PH (Table 1). Therefore, estimations of the prevalence of PH in individuals with COPD vary widely based upon the definition of PH, the methods used to determine pulmonary pressures, and the physiologic characteristics of the analyzed population. Table 1 Varying thresholds defining pulmonary hypertension and severe pulmonary hypertension
Weitzenblum et al 1981mPAP >20Oswald-Mammosser et al 1991mPAP 20Van Dijk, 1996 (149)mPAP >20 and/or PA systolic 30Pilates et al 2000mPAP >25Kessler et al 2001mPAP >20Arcasoy et al 2003PA systolic 45Doi et al 2003mPAP >20Scharf et al 2002mPAP >20 or PA systolic >30mPAP >30 or PA systolic >45Thabet et al 2005mPAP >25mPAP >45Stevens et al 2000mPAP 40Chaouat et al 2005mPAP 40 Open in a separate windowpane Abbreviations: mPAP, imply pulmonary artery pressure; PA, systolic pulmonary artery systolic pressure. Earlier autopsy studies shown anatomic evidence of right ventricular hypertrophy in individuals with COPD. TwoCthirds of individuals with chronic bronchitis had evidence of right ventricular hypertrophy shown by increased excess weight of the right ventricle (Millard and Reid 1974). Similarly, 71% of 20 individuals dying of COPD experienced right ventricular hypertrophy (Scott 1976). In contrast, oneCthird of 104 individuals with emphysema experienced autopsy evidence of right ventricular hypertrophy (Leopold and Gough 1957). Subsequent studies have suggested a correlation between right ventricular hypertrophy and hypoxemia in individuals with COPD (Calverley et al 1992). Recent studies utilizing magnetic resonance imaging (MRI) to measure right ventricular wall thickness and volume nonCinvasively demonstrated a significant increase in right ventricular wall mass that was classified as concentric hypertrophy in individuals with severe COPD and either normoxemia or slight hypoxemia (Vonk-Noordegraaf et al 2005). Several studies have identified pulmonary pressures by right heart catheterization in groups of COPD individuals with varying levels of physiologic impairment. In a series of 175 individuals with moderate to severe COPD (FEV1% = 40.2 11.1%) and mild hypoxemia (40.6% with PaO2 <60 mmHg), 62 (35%).