COMMENTARY

Stable Angina in Primary Care

Matthew F. Watto, MD; Paul N. Williams, MD

Disclosures

August 27, 2021

This transcript has been edited for clarity.

Matthew F. Watto, MD: Paul, we're back again. What are we talking about tonight?

Paul N. Williams: MD: I'm excited to talk about our topic tonight, which is our podcast on stable angina with the CardioNerds, Dr Dan Ambinder and Dr Rick Ferraro. We talked about the underlying pathophysiology and some of the management principles and evaluation of patients who present with stable angina. You had some thoughts about where to start thinking about stable angina.

Watto: Let's start with basic stable angina. Stable angina is usually not an emergency because it's stable. It's something that builds up slowly over time. The symptoms can be anything: nausea, chest pain, shortness of breath. But they're usually reproducible and are typically caused by exertion. Where it gets confusing is, when does it become unstable angina? Unstable angina has to start somewhere, and we usually think of it as a change.

But our guests pointed out that it's really the pace of symptoms that determines the pace of the workup. If the patient has brand-new symptoms or symptoms occurring at rest, that is someone you are going to work up more rapidly and more urgently than someone who became short of breath with exertion and whose symptoms are reproducible and can be avoided if they don't exert themselves past a certain level.

Because we think of an acute coronary syndrome as either unstable angina or an non–ST segment elevation myocardial infarction (NSTEMI), if we have a positive troponin finding, we usually think that's because the plaque is no longer stable. It has fissured or ruptured, and an acute thrombus is forming and causing the symptoms. But one of our guests said, it's less common now to have unstable angina because the high-sensitivity troponin test is now available. Many events that used to be classified as unstable angina (because the troponin wasn't sensitive enough) are now being called NSTEMIs.

Paul, what was your what was one of your takeaways for primary care doctors relevant to the diagnosis of stable angina?

Stable CAD and Angina

Williams: One thing I liked about our conversation is that they emphasize prevention. It's just a reminder that once a patient has gotten to the stage of stable angina, virtually none of the anti-anginal therapies have any kind of mortality benefit. So the things that we focus on as primary care doctors, such as mitigating risk with statin therapy and lifestyle changes, are the things that really make the substantive difference in patient outcomes. The medications are just good for the symptoms.

They had a 4 + 2 framework for cardiovascular disease (CVD) prevention, which also doubles nicely for management of stable angina. The idea is that there are four steps for risk stratification, and then two fundamental principles for management. 

4 + 2 for CVD Prevention. Image courtesy of the Curbsiders.

In terms of risk stratification, they talked about doing a qualitative risk approximation, which is looking at all the factors that may increase risk for CVD. These are the things that we know and love and deal with every day — diabetes, obesity, tobacco use, et cetera — that we can intervene upon.

In estimating quantitative risk, they are putting a number on how likely that patient is to have an atherosclerotic CVD event within a certain timeframe. The ASCVD risk calculator is the one we're most familiar with. Another way to stratify patients is with risk-enhancing factors. These aren't quite as direct, but they include such things as family history that may enhance other underlying risk factors.

Finally, another method is a little more objective. You can use coronary artery calcium scoring as a way to stratify patients as high or low risk for CVD.

Management of Stable Angina

Williams: In terms of management, this is the part that really spoke to my heart. The first principle is just healthy lifestyle, the things you can counsel everyone on: smoke less, mind your diet, exercise, manage your weight. These are the things that make real substantive long-term differences, as well as the medications (low-dose aspirin, high-intensity statins) and escalation of these medications, which are the cornerstones of both therapy and prevention for CVD. They leaned heavily into the prevention point, which means it's still a primary care problem fundamentally. And we're lucky to have cardiologists to help us out.

It does get a little bit nuanced. It's not all just blocked-up plumbing. It's a little trickier than that.

Watto: I want to swing back to your point about the proven therapies. In terms of medications, we have aspirin and statins. Once we've established that someone has coronary artery disease, those are those are the medicines that patients can be on. But the lifestyle strategies in primary care are other things we can do to move the needle.

Beta-blockers are more for acute coronary syndrome. Patients often think they need to be on beta-blockers. Yes, for heart failure with reduced ejection fraction or in an acute coronary syndrome, but for stable angina, beta-blockers aren't life-prolonging medications. They do have side effects. Middle-aged men don't like to take beta-blockers.

Williams: The experts clarified that point. They may have benefit in angina, but they aren't adding mortality benefit for stable angina as far as we know.

When to Suspect INOCA

Watto: The last point that I wanted to talk about is this concept of INOCA (ischemia with no obstructive coronary artery disease). If there is a myocardial infarction, it's called MINOCA. INOCA is the stable version. If you were to take the patients to the cardiac catheterization lab, they would have what seems like angina. They might even have a positive troponin result or an abnormal EKG or stress test. But when you go to image the large epicardial coronary arteries, you would not see any discrete lesions that are stentable, and not what we classically think of when we think of coronary artery disease. Microvascular disease or dysfunction might be causing this. So if your suspicion is high and the conventional testing is negative, you should consider this diagnosis.

It was more common in women in the ISCHEMIA trial (a trial of stenting for coronary disease). A subset of patients didn't have discrete lesions, so they were studied in a separate trial. Most of those patients who otherwise had stable coronary disease were women, and they were more likely to have INOCA. 

So look out for that, and talk to your local cardiologist. As we found out during the podcast, and afterward on Twitter, cardiac imaging has become very nuanced. There are tons of options. Cardiologists are still kind of fighting this out among themselves. So, if you have selected patients whose conventional testing is negative, but you are still suspicious about them, talk to a cardiologist about advanced CT studies, cardiac MRI, PET scanning, et cetera. These might help get a better idea of the patient's coronary disease and their overall risk. 

This was a great podcast. It was packed with stuff like this. Check it out here: Dominate Stable Angina with the CardioNerds.

Thank you for watching.

The Curbsiders are a national network of students, residents, and clinician educators from across the country representing 15 different institutions. They "curbside" experts to deconstruct various topics in the world of medicine to provide listeners with clinical pearls, practice-changing knowledge, and bad puns. Learn more about their contributors and follow them on Twitter.

Follow Medscape on Facebook, Twitter, Instagram, and YouTube

Comments

3090D553-9492-4563-8681-AD288FA52ACE
Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.
Post as:

processing....