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Abstract
C
hronic obstructive pulmonary disease (COPD) is a preventable and treatable disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases, primarily caused cigarette smoking. Although COPD affects the lung it also produces significant systemic consequences.
COPD is often associated with changes of the structure and function of the heart. Although functional abnormalities of the right ventricle have been well described in COPD patients.
The classic view of the development of the right ventricle ( RV ) hypertrophy in patients with COPD is that a reduction of the pulmonary vascular bed and hypoxia-induced pulmonary vasoconstriction increase pulmonary vascular resistance.
Chronic inflammation is a critical feature of chronic obstructive pulmonary disease ( COPD ). Assessing air way inflammation is important for investigating the underlying mechanism of many lung diseases.
The present study includes 50 patients with COPD based on the Global Initiative for Chronic Obstructive Pulmonary Disease ( GOLD ), 2004 which were classified into three groups :
Group A: consists of 28 patients with severe COPD with FEV1 less than 50%
Group B: consists of 12 patients with moderate COPD with FEV1 50 – 70%
Group C: consists of 10 patients with mild COPD with FEV1 more than 70%
The study also includes 20 healthy non smokers subjects who were served as a control group (Group D).
The primary finding of the present study was that there was a highly significant increase in right ventricular wall thickness in COPD patients during exacerbation as compared to the control group, whereas left ventricular wall thickness did not differ significantly between both groups.
Stroke volume was significantly lower in COPD group since the heart rate in COPD group was higher than the control subjects, cardiac output was similar between patient groups and control subjects.
Another finding of the present study was that both right ventricular end-diastolic volume and end-systolic volume were significantly lower compared to the control subjects. While left ventricular end-diastolic volume was lower among patients groups compared to the control subjects, Left ventricular end-systolic volume was within normal range.
Structural changes in the right ventricle might also alter left ventricle structure and filling due to the phenomenon of ventricular interdependency. This might explain lowered left ventricular end-diastolic volumes found in COPD patients.
Finally, the data obtained in the present study indicate that concentric right ventricular hypertrophy is already present in COPD patients with normoxemia probably due to intermittent increases in pulmonary artery pressure that occur during exercise and/or sleep. Concentric right ventricular hypertrophy does not impair right ventricular and left ventricular systolic functions.