COPD: The Current Needs and Goals of Therapy

NOVEMBER 22, 2017
MD Magazine Staff

Byron Thomashow, MD: All of us have been in this field for a very long time. I think all of us would agree that we have better medicines now than we did 10 or 20 years ago. They’re better medicines, they last longer, and you don’t have to take them as often. But it is distressing that in the last 20 years, there’s only been one drug, of a new class, that’s been introduced.

James F. Donohue, MD: Absolutely.

Byron Thomashow, MD: That has to change if we want to move forward. If you look at what’s happening in the cardiac world, where they’ve got 15,000 different classes or drugs that they’re using, we need to move that forward. We can make a difference with what we have, but we need to do better.

Peter L. Salgo, MD: What are the actual goals? What do you try to achieve in goals of therapy here?

Fernando J. Martinez, MD: I’ll speak from my own personal experience in dealing with family members. If you speak to patients, they’re clearly interested in an improvement in their symptoms and their quality of life. This is a disorder that does impact, for reasons that Frank said, multiple components of the patient. And, as we talked about, the decreasing exercise tolerance over time, the complexity of that combination is associated with significant symptoms of breathlessness and exercise limitation. Patients want that to be improved. And so, in all of the therapeutic algorithms that we have, with new drugs incorporating various components, that is key. That’s the key thing that they, patients, see every day when they’re limiting their activities.

Then, there’s been an evolving thought—there are acute events, flares of diseases, or exacerbations, whatever you want to call them, because depending on the part of the country, there are different terms to how that’s described. Not only are patients scared of them, and they really have a dramatic effect on quality of life, which may take months to resolve if it ever is completely resolved, but it’s now become very clear that those events are associated with multiple markers of the progressive components that Frank describes. They’re associated with changes in future health status, functional capacity, potentially even worsening of lung function, and structural abnormalities. A lot of things have been linked to those acute events. So, if you think about the paradigms now, the paradigms are: try to prevent. There are multiple components and approaches to that. Treat the symptoms, and exercise tolerance. Try to get the patient active. In trying to prevent these acute events, these are sort of the key combinations now.

Frank C. Sciurba, MD, FCCP: So, if I can just simplify what Fernando said, not only do we treat the symptoms, and your patient says they feel better, but we adopt the philosophy that the cardiologists have taken for years with antihypertensives and statins. The drug, even if doesn’t immediately have an impact on how you feel, can prevent serious events down the line. Flare-ups and even death, potentially.

Peter L. Salgo, MD: You pointed out that some of these long-acting drugs, if they continually dilate your bronchioles, will eventually result in decreased lung volume, increased lung efficiency, and decreased symptoms. So, what you’re actually doing is making patients not just symptomatically better but physiologically better?

Byron Thomashow, MD: Yes, I think that’s true. Jim can probably talk about it better than I can, but we think of COPD as a disease of obstruction, a problem of getting air out. But increasingly, as the disease progresses, it’s actually a problem with getting air in as well. As a matter of fact, one of the things that we sometimes do is ask people to take a big deep breath in and then take another breath. And that’s really uncomfortable for patients in the COPD world.

Peter L. Salgo, MD: But if you tonically dilate the bronchioles with some of these long-acting agents, they help the lung empty?

James F. Donohue, MD: Yes.

Byron Thomashow, MD: Yes.

James F. Donohue, MD: One of the most important pathophysiologic processes that leads to dyspnea, shortness of breath, is air trapping. Lung volume reduction surgery, bronchoscopic lung volume reduction, all of those things are used to reduce that volume of air in the chest so that maybe some good lung could inflate to be better for you.

Peter L. Salgo, MD: But the tonic volume goes down as long as you can keep the resistance and the caliper better.

James F. Donohue, MD: Exactly, keep the caliper better than the volume of air in the chest. Now, a lot of that is dead space and ineffective, poorly ventilated lung.

Peter L. Salgo, MD: I understand. I don’t want to leave this discussion without talking about escalation/de-escalation strategies. You’ve got to be riding this tide, right?

Fernando J. Martinez, MD: Yes. One of the interesting things is, we have a lot of drugs. We have more drugs with different durations of action, mechanisms that can be combined, that have different devices. Steroids have a role, but not as broad of a role as they had before. One of the concepts that I think all of us have wrestled with in this field is how we provide guidance to a primary care clinician who, as you said, have got 15 diseases they’ve got to deal with and they’ve got 8 minutes at best to do this in, with the concepts of how you can consider adding and withdrawing therapies for individual patients.

What you’re going to notice, and it’s already happened within the last 2 years, is that over the course of the next 4 or 5 years, there are going to be increasing approaches to provide primary care clinicians, because they’re the ones that are dealing with the bulk of this, with relatively simple approaches on when you add, what you add, and when you subtract particular components. In part, they’re used to doing this already. They do this for multiple disorders, whether it’s hypertension, coronary disease, or diabetes. We’re actually learning from them.

Byron Thomashow, MD: And that’s been the asthma approach for a long time. This whole escalation/de-escalation issue, that’s where asthmatic therapy has been for a long time.

Frank C. Sciurba, MD, FCCP: But there’s an important difference between COPD and asthma. In asthma, ICS (inhaled corticosteroids) are the predominant component. Beta-agonists follow if you don’t resolve symptoms. In COPD, bronchodilators are key. These folks are never completely reversible, and inhaled corticosteroids are adjustable based on the individual’s attributes. It’s the opposite. That’s critical. You can’t just use an obstructive airways model across asthma and COPD. They’re different.

Transcript edited for clarity.
 

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