Respiratory clinicians need to start looking beyond the lung and towards the heart – they may also need to start being nice to cardiologists, an expert says.
Speaking at a session on the impact of comorbidities in COPD Associate Professor Bob Hancox from the University of Otago in New Zealand told delegates that studies had consistently shown that up to half of all patients admitted to hospital with acute exacerbations of COPD had evidence of heart disease that often remained clinically unrecognised.
Despite this, guidelines on lung disease tended to focus on treating respiratory failure and the underlying airways disease, with very little acknowledgement that heart disease was an issue.
“Most of our patients are actually going to die from heart disease so we need to think a little bit more about what we need to do to treat these patients beyond the lung,” he told delegates during a COPD special interest group session on Wednesday morning.
What do cardiac biomarkers tell us?
A study conducted by Professor Hancox and colleagues looked at levels of cardiac biomarkers in 250 patients who were hospitalised with an acute exacerbation of COPD but did not have a clinical diagnosis of heart disease.
Results showed that those with high levels of the cardiac biomarkers NT-proBNP and Troponin T had a fifteen-fold increased risk of dying within 30 days compared to patients who had levels within the normal ranges.
However as neither biomarker was associated with mortality beyond 30 days the findings most likely reflected an acute pathology, Professor Hancox told the audience.
What happens to the heart during an exacerbation?
According to Professor Hancox there are a number of unanswered questions about what actually happens to the heart during an exacerbation.
For instance NT-proBNP was a marker of cardiac stretch but it was unknown whether this was a cause of left or right ventricular disease.
It was also possible that elevated levels of biomarkers could be a consequence of acute pulmonary hypertension associated with the exacerbation itself.
Similarly, raised levels of troponin could indicate silent myocardial infarctions that weren’t being picked up or could be a sign of global ischaemic cardiac damage.
In order to find the answers to some of these questions Professor Hancox and colleagues conducted a small exploratory study where an ECG was performed on patients within 48 hours of an admission for an acute exacerbation.
Those with higher NT-proBNP levels had evidence of impaired left and right ventricular function, although the level of impairment was perhaps not sufficient to be diagnosed by a cardiologist as cardiac failure.
It was also unclear whether elevated troponin levels could be a consequence of underlying heart disease made worse by hypoxia. The presence of hyperinflation that restricted diastolic filling and stress cardiomyopathy could also be potential factors.
“We do have evidence of global cardiac dysfunction among people coming into hospital with COPD exacerbations who have raised cardiac biomarkers…I don’t think it’s just acute RV strain because of the COPD exacerbation, it’s more than just a right ventricular phenomenon” Professor Hancox said.
What should be done about it?
There is very little evidence, particularly from randomised controlled trials, that can help guide clinicians on how manage cardiac disease in patients with COPD, Professor Hancox said.
Although there is some evidence for the use of anti-platelets, statins and ACE inhibitors most of the evidence comes from observational studies that are likely to have bias.
Beta-blockers are one of the most cardio-protective drugs on the market but as COPD patients had been systematically excluded from major studies it was unclear what the risks and benefits were in this patient population.
“That’s one of my big questions…I am happy to start patients on anti-platelets, sort of okay with ACE inhibitors and lipid lowering drugs, if there’s indications for them, but I really don’t know about beta-blockers,” he said.
Professor Hancox and colleagues performed a feasibility study to establish whether a randomised controlled trial was possible in patients with acute exacerbations but were unable to recruit a sufficient number of patients.
He is now looking at conducting a feasibility RCT in patients with stable COPD alongside Dr Christine Jenkins.
Where next?
Summing up Professor Hancox said it was possible that cardiac biomarkers could help to identify a subgroup of patients that might lead to a different treatment approach.
There were a lot of cardiac treatments to try, he said, noting that while a lot of the existing treatments for COPD made a big difference to symptoms they “don’t really save lives”.
“We have to change our thinking about lung disease, maybe the heart does have a role to play after all… we may need to start being nice to cardiologists,” he added.
With his tongue firmly in his cheek he proposed a new definition for cardiology: The branch of respiratory medicine dedicated to the study of disorders of the heart.
Under this definition cardiologists were: Nice people who can (sometimes) be really helpful.