Our data demonstrate that more than one-third of patients clinically diagnosed as having pulmonary embolism presented with elevated serum troponin I concentrations. Troponin I tests helped to identify patients with RV dilatation who had significantly more segmental defects in lung scans. Thus, troponin I assays are useful to detect minor myocardial damage in pulmonary embolism.

Background-Assessment of risk and appropriate management of patients with acute pulmonary embolism (PE) remains a challenge. Cardiac troponins I (cTnI) and T (cTnT) are reliable indicators of myocardial injury and may be associated with right ventricular dysfunction in PE. Methods and Results-The present prospective study included 106 consecutive patients with confirmed acute PE. cTnI was elevated (Ն0.07 ng/mL) in 43 patients (41%), and cTnT (Ն0.04 ng/mL) was elevated in 39 (37%). Elevation of cTnI or cTnT was significantly associated with echocardiographically detected right ventricular dysfunction (Pϭ0.001 and PϽ0.05, respectively). Moreover, a significant correlation was found between elevation of cTnI or cTnT and the two major end points overall mortality and complicated in-hospital course. The negative predictive value of cardiac troponins for major clinical events was 92% to 93%. Importantly, there was obvious escalation of in-hospital mortality, the rate of complications, and the incidence of recurrent PE, when patients with high troponin concentrations (cTnI Ͼ1.5; cTnT Ͼ0.1 ng/mL) were compared with those with only moderately elevated levels (cTnI, 0.07 to 1.5; cTnT, 0.04 to 0.1 ng/mL). Logistic regression analysis confirmed that the mortality risk (OR) was significantly elevated only in patients with high cTnI (Pϭ0.019) or cTnT (Pϭ0.038) levels. Furthermore, the risk of a complicated in-hospital course was almost 5 times higher (15.47 versus 3.16) in the high-cTnI group compared with patients with moderate cTnI elevation. Conclusions-Our results indicate that cTnI and cTnT may be a novel, particularly useful tool for optimizing the management strategy in patients with acute PE.

In chronic obstructive pulmonary disease (COPD), the sympathetic nervous system, as well as the renin-angiotensin system, is activated with possible negative systemic effects on skeletal muscles. Angiotensin II type-1 receptor blockers inhibit the sympathetic and reninangiotensin systems and might improve skeletal and respiratory muscle strength in patients in whom these systems are activated.The effects of the angiotensin receptor blocker irbesartan given over 4 months was evaluated in 60 patients with COPD and a forced expiratory volume in one second of ,50% of the predicted value and without obvious cardiovascular disease that would necessitate the administration of an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker.Irbesartan was well tolerated, but did not exert a significant effect on the primary end-point maximum inspiratory pressure. Spirometric results were not affected, but total lung capacity was reduced. Irbesartan led to a significant decrease in haematocrit (46.4¡3.6 to 43.9¡4.3% versus 47.5¡2.4 to 48.7¡3.0% with placebo).In conclusion, respiratory muscle strength in chronic obstructive pulmonary disease patients was not influenced by angiotensin II receptor blockade. However, the changes in haematocrit and total lung capacity following irbesartan raise the possibility that well-known cardiovascular drugs can produce unanticipated beneficial effects in chronic obstructive pulmonary disease patients.