Abhiram Prasad, Professor of Interventional Cardiology & Honorary Consultant Cardiologist at St George’s Hospital, University of London, UK, speaks to Cardio Debate about stress cardiomyopathy and Takotsubo syndrome.
Stress cardiomyopathy: What is it? How do you diagnose this and how frequent is it?
Stress cardiomyopathy is often considered a relatively new syndrome. It has probably always been around but we’ve just got better at diagnosing it. It probably accounts for about two per cent of all heart attack or myocardial infarction patients, and if you just take women alone it’s probably as high as six per cent of women presenting with myocardial infarction.
The diagnosis is a diagnosis of exclusion – so in other words we don’t have a single test that can diagnose this, so different institutions and investigators have put out diagnostic criteria as a result – the Mayo Clinic Criteria is perhaps one of the most commonly used, which has four different criteria in it. And diagnosis is made when all those criteria are met.
Essentially you need to exclude conditions that mimic it, for example obviously acute myocardial infarction, but myocarditis, spontaneous coronary artery dissection and so on. These have to be excluded, and then you make the diagnosis of stress cardiomyopathy as a result.
Is it benign?
When we first recognised the condition we were mostly recognising people presenting with the emotional triggers, and certainly that group of patients seemed to do very well, and long-term outcomes seemed to be quite good.
Over time we started recognising patients with all sorts of other triggers, particularly physical triggers in the hospital, sick patients and intensive care units and so on. So some of the more recent data suggest that perhaps the outcomes are not as benign as we thought in the past, and probably very similar to patients with acute myocardial infarction.
That said, if you look at patients who survive their initial hospitalisation in many studies the long-term outcomes seem to be very similar to controls and the majority of the deaths seem to be non-cardiac.
It’s still a way off ongoing research and we’ll learn a lot more in the years to come.
What are the treatments?
Again, it’s a condition in which we don’t understand the pathophysiology in detail yet, and until we do so targeted treatments do not exist.
So we treat the condition very much like other conditions that present with a reduction in systolic function. So initially it’s very much supportive treatment – treatment of acute heart failure, arrhythmias, and so on, very much like a heart attack – but once the patient has got through that acute period we usually treat them for systolic dysfunction – beta blockers and ACE inhibitors. We don’t know if that helps recovery but we don’t want to miss a patient who has been misdiagnosed, for example, didn’t really have stress cardiomyopathy but say, has a myocardial infarction. I think it’s important not to miss that early window of remodeling so we must treat them with beta-blockers and ACE inhibitors.
And then after about 6 to 8 weeks, once repeat imaging has confirmed that the heart function has recovered and indeed the diagnosis was stress cardiomyopathy then the treatment can be tailored a little bit. And at that point we enter the area of the unknown. We don’t really know whether we should continue long-term beta-blockers, or ACE inhibitors for that matter.
My personal practice is to stop the ACE inhibitors at that time, at some point after a few months, and then continue long-term beta-blocker therapy with a view of preventing recurrences given that we think the underlying causes is a catecholamine-mediated mechanism.