Speaking at Hospital Healthcare Europe’s Clinical Excellence in Cardiovascular Care event, our panel of interventional cardiology specialists shared ideas and insights into the progress of techniques, procedures and devices for chronic coronary disease, including coronary sinus reducers. Drs Alex Zaphiriou and Sundeep Kalra and Pierluigi Costanzo discussed their evolving approaches to patients previously labelled as having no hope, the crucial need for multidisciplinary working and training, and the exciting trials set to transform clinical practice.
The past two decades – and even the past two years – have been particularly impressive within the realm of interventional cardiology, with significant advances changing clinical practice and offering patients additional solutions for difficult-to-treat conditions.
This formed the basis of a fascinating discussion between three Clinical Excellence event panellists who shared their take on this changing landscape.
Taking charge of the questions, the session chair was Dr Brian Halliday, consultant cardiologist and clinical lecturer in cardiomyopathy, at the Royal Brompton and Harefield Hospitals and the National Heart and Lung Institute in London.
He was joined by Dr Alex Zaphiriou, consultant in interventional cardiology at Queen Elizabeth Hospital, Birmingham; Dr Sundeep Kalra, consultant interventional cardiologist at London’s Royal Free Hospital; and Dr Pierluigi Costanzo, consultant interventional and structural cardiologist and clinical lead for coronary intervention at Royal Papworth Hospital NHS Foundation Trust in Cambridge.
What is the most notable recent advancement in treating patients with angina and coronary disease?
Dr Zaphiriou: The last 12 to 18 months have been exciting for a range of patients, particularly those previously labelled as having no hope, such as those with intractable angina. Data is accumulating, which means we have more effective pharmacological and other treatments available to us. There is a group of patients who have no revascularisation options and are on the maximum tolerated medical therapy but still suffer with severe angina that is very intrusive and affects their quality of life.
Now, we have more evidence to support the use of a coronary sinus reducer. It’s not so new now, but its use is expanding, and we have more evidence to suggest that it is an effective anti-anginal therapy over and above medical therapy and revascularisation. There are a few centres now that offer this technology.
It has to be said that it’s not for every patient, but, with careful selection, the results can be very encouraging, and this has been proven with two large, double-blind, placebo-controlled trials.
Dr Halliday: Indeed, my colleague Rasha Al-Lamee at Imperial did the ORBITA-COSMIC trial, which had encouraging results showing symptom benefit in a placebo-controlled trial. Should we wait for placebo or sham controlled trials before using these types of devices?
Dr Zaphiriou: Rasha has done exceptional work, and the way she and her team ensured that the placebo effect was neutralised is exemplary. I think she has set a new standard in terms of placebo-controlled trials and, if the condition allows it, I think we should follow that route.
We’ve proven that a coronary sinus reducer reduces symptoms, and there are lots of hypotheses about how it works, but do we need to know exactly how it does that?
Dr Zaphiriou: I think it does matter. There are several hypotheses regarding how it works and the one that is substantiated with data from research is that perhaps there is a redistribution of the blood flow from the epicardium to the subendocardium aspect of the heart muscle. We know that what gets ischemic first in coronary artery disease is exactly that part of the heart muscle – the one near the endocardium.
So, Rasha’s very detailed MRI study has demonstrated that perhaps that’s the mechanism because there is redistribution. The total flow to the heart muscle, interestingly, in this study, was unchanged, but there was redistribution from the less ischemic segments to the more ischemic segments, and that’s the most likely mechanism of action.
Do you think that coronary sinus reducer should be a mainstay of therapy for patients with intractable angina, and do we need to train more people to do the procedure?
Dr Kalra: It definitely gives us a new facet of treating this group of patients. It’s not going to be a bread-and-butter treatment strategy, because most patients we can treat with revascularisation or with medical therapy. So, it’s a small group of patients, but a group of patients that we’ve historically treated very poorly.
I think with any interventional procedure, you need to be doing sufficient volume to be able to deliver it correctly, and to optimise patient selection. We still quite haven’t worked out the responders and non-responders, and as we get more clinical experience with the device outside of research trials, we’ll understand which are the groups of patients that may benefit more from this.
But, in saying that, I don’t think this should be rolled out to every single cath lab in the country at this moment in time. You have to commit to having an infrastructure to support this technology. This means having a refractory angina multidisciplinary team so you can discuss these patients and group learn on which patients will respond and having follow-on for these patients. You need patient advocates in your hospital, your nurse specialists, your doctors and the specialists in the technology to actually be able to deliver this more effectively.
I don’t think it should be widespread that everyone suddenly does this type of procedure. In the first instance, I think we should localise it to the Centres of Excellence where they have advanced chronic total occlusion programmes. We need to really make sure there are no percutaneous or surgical revascularisation strategies before we say we’re going to implant a coronary sinus reducer in someone.
Is coronary sinus reducer a simple procedure, or one requiring significant time, training and skill?
Dr Costanzo: It is a simple procedure but, like any simple procedure, it does involve some technical skills. Effectively, you’re going through the jugular vein, so the punctures need to be pristine.
In our centre, we buddy up with electrophysiologists who do cardiac resynchronisation therapy (CRT) as they are much more familiar with getting into the coronary sinus. It shouldn’t be difficult, but occasionally, even in the CRT world, we can still dissect or cause problems in the coronary sinus.
The deployment is fairly straightforward as well. Most of the time, the complications are either that you won’t manage to do the procedure because you don’t get into the coronary sinus, or you’d have a bleeding complication from the puncture. But again, it requires a certain level of skill and familiarity with the right side of the heart.
Do you expect the effect of these devices to be persistent in future, say over 10 or 15 years, and is there any evidence for this yet?
Dr Zaphiriou: One very interesting thing is that the benefit doesn’t happen straight away. On average, it takes 70 days, and up to three months, to see the full effect. So far, the longest data we have is five years. It seems that for the people who respond, the benefit is sustained, certainly between two and five years. The hope is that it’s going to be a sustainable effect. But only time will show that.
Have any new developments or techniques emerged in terms of revascularising patients with very advanced, often calcified disease or disease with chronic total occlusions?
Dr Kalra: In the realms of the chronic total occlusions (CTO), we’ve had massive advances in the technology: the wires, the microcatheters, the types of kit that we have available to us to make these procedures a lot more achievable. We are getting much better results as we’ve learned new procedures and techniques.
There’s a lot of collaboration internationally now where we’re sharing knowledge and expertise through lots of joint live cases where we are able to learn from each other. I think what we are able to deliver is advanced and, historically, what may have been patients untreatable with percutaneous revascularisation, we are achieving a lot more nowadays.
How do you select who will most benefit from these procedures and how do you navigate risk?
Dr Kalra: Anatomy is key. The presence of a CTO doesn’t mean you should undertake a procedure on a patient. Non-CTO operators will often see a chronic total occlusion and feel that it’s something that can be referred for treatment. But anatomy is absolutely key. This has to be a bilateral conversation with a CTO operator.
We’re talking about stable angina here, so we’ve got time to treat these patients. We don’t have to rush into doing things. We should effectively counsel them and see them in the non-acute clinic setting to talk about the procedure and the risks involved.
We also have to look at the comorbidity and the overall goal that we’re trying to achieve. The data we’re looking at and what we’re trying to achieve with CTO percutaneous coronary intervention (PCI) is for symptom control. There’s no real convincing data at this moment in time that this is going to improve prognosis.
Dr Costanzo: I totally echo what Sundeep has mentioned there. In terms of CTO techniques, we are in a different world compared to even five years ago. There are different ways to deal with a CTO. Patients with stable angina do not see improved mortality with CTO PCI. It’s just to relieve the angina, make sure that the patient is on the maximum tolerated medical therapy and then you can embark on what is an antegrade approach. This means putting a catheter on the artery that is blocked, essentially doing the procedure from upstream and techniques have been refined in terms of coronary wires.
Techniques are refined and the technology keeps advancing. It is a high-risk procedure, as you might guess with all this manipulation. Within time, the risk of complications will go down, but I doubt that it will ever be as low risk as a normal PCI.
Dr Zaphiriou: I agree. The perforation risk has been reported to be as high as 4%, which is much higher than the usual PCI, and mortality perhaps is 2%, rather than the usual 1%. We have to take all of that into consideration.
The key issue for more general cardiologists or PCI operators is that it’s important that we develop networks. Find who your friendly CTO operator is, join them, do a procedure together, invite conversation and participation and don’t give up.
There are so many new things we now have at our disposal – so many new technologies and equipment – and it’s unbelievable what can be achieved, providing you team up with your experienced CTO operator, and that’s a very important message.
Do you rely on cardiac imaging to select patients and guide your treatment, and what imaging techniques do you use the most?
Dr Kalra: Multimodality imaging is used, and angiograms are just part of the equation. Patients will, almost invariably in my care, get some form of effusion imaging – cardiac magnetic resonance imaging is usually what I prefer – as we want to get an accurate burden of ischemia assessment.
But another key thing is CT coronary angiography. You want to understand what you’re dealing with, where the calcium is, where stumps are on vein graphs, where the inlet of the lesion is. Then you can assess everything with all the information before we put that patient on the table for a procedure that’s higher risk than usual PCI.
This article is part of our Clinical Excellence series, which offers valuable first-hand insights into how experts from renowned Centres of Excellence are pursuing innovative approaches to optimise patient care across the UK and Europe.
