While the results of this study are not surprising, they provide us with both the validation to continue practice according to existing recommendations, particularly the avoidance of monotherapy with beta-lactam antibiotics. The study also provides us with the imperative to take the lead in developing evidence-based pneumonia pathways at our own hospitals.
7. Pham MX, Whooley MA, Evans GT Jr, et al. Prognostic value of low-level cardiac troponin-I elevations in patients without definite acute coronary syndromes. Am Heart J. 2004;148: 776-82.
With the availability of rapid and highly sensitive and specific troponin testing, many patients admitted to the hospital with non-cardiac diagnoses have been recognized as having abnormal serum troponin-I or troponin-T levels, often just slightly above the reference cutoff for “normal.” While the clinical assumption is often that the elevated enzyme level does not reflect an acute coronary syndrome per se, its significance regarding the patient’s underlying cardiac health is often unclear.
Pham et al. retrospectively reviewed the 1-year mortality of 366 patients who were admitted to the San Francisco VA without evidence of acute MI or ACS either clinically or by EKG, but who had low-level troponin-I elevations (up to 3.0 ng/mL—a level that the authors state was reached by institutional consensus, and which was measured by a “first-generation” assay). These patients were admitted for a broad spectrum of diagnoses ranging from CHF to COPD to sepsis. Ninety-six percent of the patients were men; their average age was 69.
Follow-up was accomplished after a mean of 288 days and included 97% of patients. The primary endpoint was MI or death due to cardiac disease at one year; secondary endpoints were revascularization or admission for unstable angina. The primary endpoint was reached by 11% of patients with cTn-I between 1.0 and 3.0 ng/mL, and 4% of the patients with cTn-I up to 1.0 ng/mL (adjusted HR 3.4, 95% CI, 1.3 to 9.4), and the higher the cTn-I, the higher the risk. However, the authors did not test for the level of risk by specific diagnosis, so they caution against overgeneralizing their findings.
The findings of this study add to the evidence that any evidence of myocardial injury implies an increased risk of underlying heart disease and accompanying long—term cardiac complications– even if such injury occurs in the absence of ACS or known heart disease. Hospitalists often see such injury in the setting of acute infection and pulmonary disease and may be the first to recognize the possibility of CHD in a given patient. To date, guidelines addressing optimal prospective risk stratification have not been developed. Until they are, hospitalists should be aware of the ramifications of “troponin leak” and be prepared to initiate necessary inpatient monitoring and treatments, and to coordinate appropriate follow-up for these patients.
8. Saposnik G, Young B, Silver B, et al. Lack of improvement in patients with acute stroke after treatment with thrombolytic therapy: predictors and association with outcome. JAMA. 2004; 292: 1839-44.
Recombinant tissue plasminogen activator (tPA) has been shown to be one of the most efficacious therapies for acute stroke treatment. This was a systematic evaluation of predictors for outcomes at 24 hours after tPA therapy and of the prognostic significance of lack of improvement at 24 hours for long-term outcomes at 3 months.
The trial was a prospective cohort study of 216 consecutive patients admitted with acute ischemic stroke to a university hospital. The decision to treat with tPA was based on the NINDS protocol with one difference: patients with involvement of more than one third of the middle cerebral artery on the baseline CT scan were excluded. A control CT scan was performed at 24 hours to determine the presence of new infarction, cortical involvement, and extension of the ischemic lesion.