March 12, 2021 This Week in Cardiology Podcast

John M. Mandrola, MD


March 12, 2021

Please note that the text below is not a full transcript and has not been copyedited. For more insight and commentary on these stories, subscribe to the This Week in Cardiology podcast.

In This Week’s Podcast

For the week ending March 12, 2021, John Mandrola, MD comments on the following news and features stories.


This week marked the one-year anniversary of the pandemic. I was talking this week with my grand-daughter, a second-grader. She was very excited about going back to school next week. I thought to myself how my memories of first and second grade seem a blur. But surely she will remember this past year forever. We all will.

The slope of the falling hospitalization curve here in the United States is shocking in its degree. Locally, we have only 20 patients with COVID in our hospital; this is the lower than even the low summer numbers. A larger hospital system in our city sent an email to employees proclaiming the number of patients with COVID on ventilators: zero.

But the pandemic isn’t quite so over everywhere. As it always has been, COVID remains a regional issue. While Kentucky, Indiana, and West Virginia are doing well, some places are still struggling. For example, I wonder why the cases have plateaued in New York? My friends in Brazil talk of serious stress from rising COVID cases. My thoughts are with them. A study showing real-world data from the Israeli experience of rapid vaccination confirms super high efficacy. Again, good news. The challenge now is to get vaccines out as quickly as possible.

Heart Failure

This week a multi-society, international group of 38 authors has proposed a new universal definition of heart failure (HF) and made major revisions to the staging and classification of this condition. The Journal of Cardiac Failure and the European Journal of Heart Failure published the comprehensive document. The lead author is Prof. Biykem Bozkurt from Baylor. Drs. Antman and Braunwauld wrote an accompanying editorial.

Before I go into the details of the massive document, it is useful to reflect on the term “heart failure.” Here I have to cite the now retired British GP, Dr. Richard Lehman, who is one of the wisest of clinicians I have ever learned from. An aside is that in the early years of this podcast, I would cheat by reading Lehman’s weekly journal reviews in the British Medical Journal, which came out every Monday. This podcast is an attempt to be a fraction as good as those gems.

In 2005, Lehman penned an editorial in the BMJ calling for a new name for HF. He proposed “cardiac impairment.” Lehman noted that the term “heart failure” confuses clinicians and scares patients. Indeed. I often actively refrain from using the term with patients. Recall that the word heart denotes not merely an organ but also an innermost part of something, a courage, an enthusiasm. “This patient has a ton of heart.” When you combine the word failure with these meanings of heart, you do a lot of harm.

But it’s even worse than that, explains Lehman in his lead paragraph. Here he cites Geoffrey Rose: There is no disease that you either have or don't have—except perhaps sudden death or rabies. All other diseases you either have a little or a lot of.... Everyone can have a bit of heart failure if they try hard enough, by physical exertion or even emotional shock.”

In that amazing first paragraph, Lehman also summed up the background info for this new effort to re-define HF. He wrote that, because of widely varying definitions, the epidemiology of heart failure can become almost uninterpretable, with estimates of its prevalence in the United Kingdom varying from 500,000 to 3 million.

Any clinician knows this well. You can get labeled as having congestive HF for hundreds of things—a patient with obesity who is dyspneic, an echo during rapidly conducting atrial fibrillation (AF), having hypertension and eating too much salt and needing a dose of diuretic. The effort to sort all this out with better definitions is laudable.

This paper includes nice summaries on things like cardiomyopathy (CM) and HF. CM is heart muscle disease and HF is a clinical syndrome. There is mention of competing diagnoses, and a nice distinction that patients with renal failure, liver failure, morbid obesity with edema, and chronic respiratory failure hypoventilation syndrome may present with symptoms and signs that mimic HF. For example, a patient has what looks like HF, but it resolves with hemodialysis. That is not HF.

The authors proposed revision of the stages of HF. Previously these had various names—New York Heart Association (NYHA) functional class 1 to 4, or by ejection fraction (EF; HF with preserved EF [HFpEF], HF with reduced EF [HFrEF]), or by etiology (ischemic cardiomyopathy [ICM], non-ICM [NICM]) or the American College of Cardiology/American Heart Association (ACC/AHA) format by disease progression (Stages A to D). All of these are fraught. In the end the authors settled on the ACC/AHA stage A to D format with modifications.

  • At-risk for HF (stage A). For patients at risk for HF but without current or prior symptoms or signs of HF and without structural or biomarkers evidence of heart disease.

  • Pre-HF (stage B). For patients without current or prior symptoms or signs of HF, but evidence of structural heart disease or abnormal cardiac function, or elevated natriuretic peptide levels.

  • HF (stage C). For patients with current or prior symptoms and/or signs of HF caused by a structural and/or functional cardiac abnormality.

  • Advanced HF (stage D). For patients with severe symptoms and/or signs of HF at rest, recurrent hospitalizations despite guideline-directed management and therapy (GDMT), refractory or intolerant to GDMT, requiring advanced therapies such as consideration for transplant, mechanical circulatory support, or palliative care.

Change in the dichotomization of HF by preserved or reduced EF:

  1. HF with reduced EF (HFrEF): left ventricular EF (LVEF) of up to 40%.

  2. HF with mildly reduced EF (HFmrEF): LVEF of 41-49%.

  3. HF with preserved EF (HFpEF)HF with an LVEF of at least 50%.

  4. HF with improved EF (HFimpEF): HF with a baseline LVEF of 40% or less, an increase of at least 10 points from baseline LVEF, and a second measurement of LVEF of greater than 40%.

You will notice here two new categories: mildly reduced and improved.

The authors waste no time in their discussion of the mildly reduced category in citing both the subgroup analysis of PARAGON HF, which found benefit in the composite endpoint of hospitalizations for HF and cardiovascular disease in patients with EFs below the median of 57% and the post-hoc combination of PARAGON and PARADIGM showing a continuum of benefit correlating with lower and lower EFs. They also mention the potential overlap in this group; the challenge of using echocardiograms to determine EF; and the fact that people can easily move in and out of the minimally reduced groups.

As for the improved category, the authors make the case that this category may help prevent discontinuation of meds in people with recovered EFs; that is, they still have HF so should stay on meds. Bozkurt stressed that HFimpEF only applies if the EF improves to above 40%. A move from an EF of 10%-20% would still see the patient classified as having HFrEF, but a patient whose EF improved from, say, 30% to 45% would be classified as HFimpEF. To encourage further discussion and acceptance, the editors of the Journal of Cardiac Failure will publish many expandatory perspective pieces starting in May.

Three quick thoughts. First, I worry about categories of ways to define not having HF. As I have said before, not dying young is a good way to be at risk for HF or to have pre-HF. I understand the authors’ point though: for instance, patients with left ventricular hypertrophy due to hypertension would have less chance of getting heart failure with good blood pressure control and counseling on diet and exercise. And patients with diabetes and chronic kidney disease clearly have less HF with SGLT2 inhibitors and having pre-HF categories may help more patients receive these beneficial drugs.

Second, I also understand the HFmrEF problem. These patients are not exactly HFpEF or HFrEF. But I will try to suppress the little voice in my head that says: this category is a way to advance the use of the expensive drug sacubitril/valsartan. As I have discussed, this indication is problematic because it is based on a subgroup analysis of one trial, PARAGON-HF, that had a non-significant primary endpoint and no signal of CV death reduction.

Third, even if you loved these definitions, confusion will remain in American hospitals because clinicians still have to code according to a wholly different and anachronistic schema of acute and chronic systolic or diastolic HF.

DOACs After Heart Surgery

A group of researchers from Cleveland Clinic led by Dr. Ankur Kalra published a research letter on the use of direct acting oral anticoagulants (DOACs) in patients who had surgical valve replacements. They culled data from the Society of Thoracic Surgery registry. Whenever you hear the term registry, remember surgeon Joseph Bavaria’s comment: Science tells us what we can do; trials tell us what we should do; registries show what we are actually doing–that is about it.

Patients (N = 177,915) who underwent surgical aortic valve replacement or mitral valve replacement with either mechanical heart valves or bioprosthetic heart valves between July 2014 and June 2017 were included. About 1% of patients who had mechanical AV and 1% of those who had MV were on DOACs at discharge. That percentage did not change over time. Approximately 5% to 6% of those who had bioprosthetic aortic or mitral valves were on DOACs at discharge. For bioprosthetic valves, the use of DOACs increased over time. We assume most of the oral AC use in bioprosthetic were for AF or venous thromboembolism.

I highlight this study because the authors seem to think the increasing use of DOACs in surgical valves is a bad thing. And it definitely is for patients who have mechanical valves. RE-ALIGN was an RCT of dabigatran vs warfarin and it was stopped for harm in the dabigatran arm. Cardiovascular trialist, Dr. David Cohen, noted in the news story that this very low amount of 1% could be simply due to coding error.

But the title of this study includes the term ‘off-label’ and the authors conclude: “Our study suggests a prevailing off-label use of DOACs in patients with prosthetic heart valves without satisfactory safety data.”

I don’t agree with the ideas that we have to withhold a more convenient AC—at least when AF is the indication. In 2019, the ACC guidelines clarified valvular vs nonvalvular AF. Nonvalvular AF does not imply the absence of valvular heart disease. And valvular AF was narrowly defined as associated with mechanical valve replacement or severe rheumatic mitral stenosis. Everything else was nonvalvular—including bioprosthetic valves. In 2020, a joint consensus document from the European Heart Rhythm Association (EHRA) reiterated the ACC guidelines that ‘valvular AF’ is outdated and proposed a functional EHRA (Evaluated Heartvalves, Rheumatic or Artificial) categorization in relation to the type of OAC use in patients with AF, as follows:

(EHRA) Type 1, which refers to AF patients with ‘VHD (valvular heart disease) needing therapy with a vitamin K antagonist (VKA)

  • Mitral stenosis (moderate-severe, of rheumatic origin)

  • Mechanical prosthetic valve replacement

EHRA Type 2 included everything else, and warfarin or DOAC were acceptable.

A meta-analysis for DOAC use in about 1400 patients with AF and bioprosthetic valves in the pivotal DOAC v Warfarin trials found similar efficacy and mostly similar safety.

In sum, yes, there is not a formal indication for DOAC use post-tissue valve, and, yes, it would be nice to have an RCT, but with the data that we have, and a more than decade long experience with this drug class, it is reasonable to choose DOACs when AC is felt suitable after a bioprosthetic valve. The harder question is the broader one: when should AC be used in post-op patients?

Physician Spending During the Pandemic

The AMA recently put out an economic analysis that found spending on physician services fell 40% between January and April of 2020. The absolute number of how much less is eye-catching: Medicare paid docs $9.4 billion less in the first 6 months of 2020 than historical norms. Among physician specialties, the cumulative reduction in spending from January through June ranged from 6% for nephrology, 14% for internal medicine, and 16% for family medicine to 19% for cardiology, 20% for general surgery, and 29% for ophthalmology.

I highlight this data because I find it remarkable that Medicare paid cardiologists roughly 20% less during that 6-month period. Cardiologists care for patients with heart disease and heart disease is a leading killer. Given the necessity of heart function, 20% less cardiology services seems like it would be a calamity.

Did this lead to worse outcomes? How much extra low-value care do we deliver?

Of course, those of you who think cardiologists exert God-like control over many-things-health-related, will cite the observational studies from the pandemic that found higher rates of in-hospital mortality from acute MI. Maybe, but these sorts of ecological studies are hard to use to make causal conclusions. And it is just one diagnosis. For weeks and months during the spring and early summer of the pandemic, our nuclear cameras and echo machines gathered dust. Our cath lab did only acute PCI for ACS. We in electrophysiology inserted pacers for heart block and ablated only incessant tachycardias. In other words, we did only the necessary work.

I have no doubt that chronic disease management is important, but the question is, how much exactly did the heart health of our patients suffer when we were paid $9.4 billion less? If the delta between how much you produced in 2020 is way less than it was 2019, there are two possibilities: you did too little in 2020, or you did too much in 2019.


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