Pulmonary hypertension in patients with pulmonary fibrosis awaiting lung transplant.

Pulmonary hypertension (PH) may complicate idiopathic pulmonary fibrosis (IPF) but the prevalence of PH in IPF remains undefined. The present authors sought to describe the prevalence of PH in IPF. The lung transplant registry for the USA (January 1995 to June 2004) was analysed and IPF patients who had undergone right heart catheterisation (RHC) were identified. PH was defined as a mean pulmonary arterial pressure ((Ppa)) > or =25 mmHg and severe PH as a (Ppa) >40 mmHg. Independent factors associated with PH were determined. Of the 3,457 persons listed, 2,525 (73.0%) had undergone RHC. PH affected 46.1% of subjects; approximately 9% had severe PH. Variables independently associated with mild-to-moderate PH were as follows: need for oxygen, pulmonary capillary wedge pressure (P(pcw)) and forced expiratory volume in one second (FEV(1)). Independent factors related to severe PH included the following: carbon dioxide tension, age, FEV(1), P(pcw), need for oxygen and ethnicity. A sensitivity analysis in subjects with P(pcw) <15 mmHg did not appreciably alter the present findings. Pulmonary hypertension is common in idiopathic pulmonary fibrosis patients awaiting lung transplant, but the elevations in mean pulmonary arterial pressure are moderate. Lung volumes alone do not explain the pulmonary hypertension. Given the prevalence of pulmonary hypertension and its relationship with surrogate markers for quality of life (e.g. activities of daily living), future trials of therapies for this may be warranted.     

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.