Definition, epidemiology and natural history of COPD.

Chronic obstructive pulmonary disease (COPD) is the fifth cause of morbidity and mortality in the developed world and represents a substantial economic and social burden. Patients experience a progressive deterioration up to end-stage COPD, characterised by very severe airflow limitation, severely limited and declining performance status with chronic respiratory failure, advanced age, multiple comorbidities and severe systemic manifestations/complications. COPD is frequently underdiagnosed and under-treated. Today, COPD develops earlier in life and is less gender specific. Tobacco smoking is the major risk factor for COPD, followed by occupation and air pollution. Severe deficiency for alpha(1)-antitrypsin is rare; several phenotypes are being associated with elevated risk for COPD in the presence of risk factor exposure. Any patient presenting with cough, sputum production or dyspnoea should be assessed by standardised spirometry. Continued exposure to noxious agents promotes a more rapid decline in lung function and increases the risk for repeated exacerbations, eventually leading to end-stage disease. Without major efforts in prevention, there will be an increasing proportion of end-stage patients who can live longer through long-term oxygen therapy and assisted ventilation, but with elevated suffering and huge costs. Smoking prevention and smoking cessation are the most important epidemiological measurements to counteract chronic obstructive pulmonary disease epidemics.     

Congenital dextrocardia complicated by hypertension,coronary artery disease and myocardial infarction

The case record of a seventy-three year old man with congenital dextrocardia and situs inversus viscerum complicated by hypertension, coronary artery disease and myocardial infarction is presented. Electrocardiographic recordings of the limb leads, with and without reversal of the arm lead wires, and of the precordial leads of the V series derived from both right and left chest areas are presented. In this instance the electrocardiographic findings in precordial leads taken over the right chest point to fresh anteroseptal infarction; those leads recorded from the left chest were not informative. This serves to emphasize the fact that precordial leads should be recorded from the right side of the chest rather than the left in order that the exploring precordial electrode may overlie the area of cardiac damage, and thus manifest maximal changes in the electrocardiogram. We agree that the electrocardiogram may best be interpreted by application of the usual criteria to the limb leads taken with the arm lead wires reversed although in this case the limb leads yielded no information of diagnostic significance.