Bacterial Infection Test Helps Diagnose Heart Disease

Patients admitted to the emergency department (ED) can often present a confusing picture of overlapping and vague symptoms. Two common diseases that tend to look similar at first glance are pneumonia and heart failure. They share many of the same symptoms-shortness of breath, rapid heart rate, coughing and wheezing, lack of appetite and fatigue. Both situations can produce infiltrates and hypoxia to varying degrees. Even basic lab tests initially can fail to separate the two. Normal or mildly elevated white blood count and fever would seem to indicate infection, but these findings are common to many patients who enter the ED.

Ironically, a test that helps diagnose severe infection-procalcitonin (PCT)-has come to help us diagnose and speed treatment to patients with heart failure and often other non-infectious pulmonary processes.

PCT is the natural pro-hormone of calcitonin and happens to be a highly expressed biomarker during systemic bacterial infections. Researchers first learned about 15 years ago that elevated PCT was common with severe infection.¹Many cells release PCT during the course of immune response to these infections.²It is now established that PCT can be used to precisely determine a bacterial infection immune response from viral and inflammation not caused by infection at all.³We use it in many ways, initially for a new patient suspected of having a significant bacterial infection in the ED to help confirm and differentiate a bacterial infectious process from an ambiguous or overlapping situation. PCT is also helpful in cases of symptom overlap between pneumonia and congestive heart failure. It provides a strong positive predictive value if high, and is a good negative predictor if the level is normal.

A patient who enters our ED with these symptoms and possible pneumonia would have three PCT tests performed in the first 12 hours akin to cardiac enzymes. We use a rapid test called VIDAS^®B·R·A·H·M·S PCT^®(bioMerieux), which can generate a reading in well under an hour. A rising level would confirm the presence of a bacterial infection given the right clinical circumstances. PCT typically surges within the first 12 hours of systemic infection. Once the patient starts improving, we use it every other day, comparing the levels to the peak level. A declining level would suggest appropriate treatment. If the level does not drop in 24-48 hours or if it rises, it would suggest the therapy needs to be changed. Re-culturing would be appropriate.

If, however, the PCT level is normal and remains flat, this tells clinicians within 12-24 hours that something else is wrong. By this point, the lab and physician most likely will also have some telling troponin or BNP tests. Combined, these heart markers and PCT can help you make a more accurate diagnosis in a much shorter time frame.

Over the last year, two patients in our cardiothoracic ICU spiked high post-operative fevers. The first patient showed a rapid increase in PCT levels (4-5ng/mL) plus febrile illness. Chest X-ray was reported as "infiltrate, possibly atelectasis or pneumonia." Appropriate cultures were sent and antibiotics were started. The levels came back down to close to baseline by Day 5, when antibiotics were stopped.

In the other patient, the PCT level did not rise significantly with fever, despite similar chest X-ray changes. Serial PCT levels did not rise above 0.5-1.0 ng/mL, and antibiotics were de-escalated at 48 hours to treat for probable bronchitis. In both cases, cultures were negative.

We have also been more aggressive in obtaining tissue from patients with fever, pulmonary infiltrates and hypoxia who have normal PCTs and have diagnosed Bronchiolitis Obliterans Organizing Pneumonia as well as acute hypersensitivity pneumonitis. Ordinarily this would have been delayed for several days or longer while waiting for antibiotics to take effect.

Dr. Amin is medical director of Critical Care Services, Morton Plant Hospital, and assistant professor of Medicine, Department of Family Practice, University of South Florida at Morton Plant Hospital, Morton Plant Mease Health Care, Clearwater.

References

1. Assicot M, et al. High serum procalcitonin concentrations in patients with sepsis and infection. Lancet 1993;341:515-8.

2. Muller B, et al. Ubiquitous expression of the calcitonin-I gene in multiple tissues in response to sepsis. J Clin Endocrinol Metab 2001;86:396-404.

3. Eberhard OK, et al. Usefulness of procalcitonin for differentiation between activity of systemic autoimmune disease (systemic lupus erythematosus or systemic anti-neutrophil cytoplasmic antibody-associated vasculitis) and invasive bacterial infection. Arthritis Rheum 1997;40:1250-6.