COMMENTARY

Dec 11, 2020 This Week in Cardiology Podcast

John M. Mandrola, MD

Disclosures

December 11, 2020

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 December 11, 2020, John Mandrola, MD comments on the following news and features stories.

Erratum

Last week I misspoke when I was discussing type I and type 2 MI. I meant to relay this key therapeutic message, which is that type I MI’s should be treated as an acute coronary syndrome, and if an ST elevation MI (STEMI), go emergently to the lab. All other troponin elevations—type 2 MI and acute and chronic injury—should be approached by looking for the cause and treating that condition.

COVID-19 and COVID Vaccination

The United States is struggling with third spike in COVID-19 infections. I don’t know about your situation, but I feel like COVID is everywhere. I probably know a hundred people who have had it, and they know a hundred. This virus’s ability to spread is shocking. Contact tracing is utter folly.

That’s the bad news. The good news is the vaccine. The main results of the phase 3 trial: There were eight cases of COVID-19 among 21,270 participants assigned to the vaccine and 162 cases among the 21,728 assigned to placebo. The FDA committee recommended approval.

Clogged Pipe Theory of CAD

An observational study from Danish authors and published in JACC (Journal of the American College of Cardiology) further refutes our false notions about the clogged-pipe frame of coronary artery disease (CAD). That is, focal stenoses are the culprits. Finding them via stress tests and then angiography and fixing them with revascularization is the engine that drives most cardiology offices. But we know from COURAGE, and BARI 2D and more recently from ISCHEMIA, that finding and fixing these focal manifestations of atherosclerosis does not improve outcomes—no matter the scariness of the blockage.

The Danish study asked whether obstructive CAD (the kind that causes ischemia) provides predictive value beyond its association with calcified plaque burden. The authors used data from a registry to of nearly 24,000 patients who were referred for coronary CT angiography because of suggestive symptoms. The endpoints were MACE (major adverse cardiac events); the follow-up was about 4 years. The results were not surprising:

  1. Event rates go up with increasing number of vessels with obstructive disease.

  2. Event rates also go up with increasing amounts of coronary calcium.

Here’s the key message: when they stratified by calcific burden, the event rate was similar in patients with and without obstructive disease. Plaque burden, not number of stenoses was the main predictor of future events. Thus, patients with a comparable calcified atherosclerosis burden generally carry a similar risk for cardiovascular disease events regardless of whether they have nonobstructive or obstructive CAD. The key clinical implications are that it’s the degree of atherosclerosis that is the issue not the fact that there are focal stenoses; and the authors feel this data should stop the distinction between secondary and primary prevention.

This observational data has oodles of limitations. There could be uncontrolled confounders that account for the findings, and there was a relatively crude and subjective dichotomization of “yes, obstructive” or “no, nonobstructive” disease. But these findings surely comport with clinical trial data that urge and plead and beg us to not see focal stenoses as widow-makers.

I don’t think we need this study to nullify the false distinction between the primary and secondary prevention. All patients with or at risk for atherosclerotic disease ought to be counseled about lifestyle intervention. Daily exercise is a heart pill, for instance. My common advice: eat only on the days you exercise. And as for statins—the drugs reduce cardiac events by 25%. Period. Whether one has had an MI or not.

Paclitaxel and PAD

A recent RCT provided reassuring news on the commonly used drug paclitaxel in peripheral artery disease (PAD). Paclitaxel (or Taxol) is an anti-cancer drug that is also used to coat stents and balloons to prevent normal inflammatory processes from causing restenosis over the long run. This happens because when we “fix” a blockage it may look pretty on an angiogram, but we are actually damaging the vessel wall.

SWEDEPAD is an RCT comparing revascularization of peripheral disease with drug eluting technology vs revascularization without drug-eluting technology. SWEDEPAD launched in November 2014 with a projected enrollment of about 3800, and separate primary end points for the two cohorts: amputation for those with critical limb ischemia and quality of life for patients with claudication. All-cause mortality was a secondary end point in both randomizations.

In 2018, a meta-analysis of studies identified a signal of excess mortality among patients with fem-pop disease who were treated with devices using paclitaxel. This was unexpected. This mortality signal surprised people. But then an evidence review by FDA and other observational studies also found a similar signal. he controversy caused the SWEDEPAD investigators to pause enrollment in their trial, but it resumed in 2019.

The New England Journal of Medicine has published an interim analysis based on the 2289 patients enrolled in the study before the 2018 pause. During a mean follow-up of 2.5 years, 293 patients (25.5%) in the drug-coated–device group died compared with 281 patients (24.6%) in the uncoated-device group, This was not close to a significant difference.

While SWEDEPAD was not a trial designed to look primarily at mortality, this is strong and reassuring data because the total of more than 570 deaths is more than the combined total number of deaths reported in 36 previously published RCTs. This interim analysis may not completely close the question of paclitaxel safety but it surely is enough to reset equipoise and continue ongoing enrollment in clinical trials.

New Performance Measures on AF

An ACC/AHA task force on performance measures (PM) have made two changes to performance measures for adults with atrial fibrillation (AF) or flutter. This was a 2020 update to the 2016 document and adds new ways to measure how a good a clinician is in taking of care of people with AF.

  • PM-1: CHA2DS2-VASc risk score documented prior to discharge

  • PM-2: Anticoagulation prescribed prior to discharge

  • PM-3: INR planned follow-up documented prior to discharge for warfarin treatment

  • PM-4: CHA2DS2-VASc risk score documented during outpatient encounter

  • PM-5: Anticoagulation prescribed during outpatient encounter

Based on these performance measures, a person with a massive left atrium and permanent AF who is age 64.5 years is a CHA2DS2-VASc 0 and should not be on oral anticoagulation, and if you use anticoagulants in this patient, you are not performing well.

Of course, it is good to think about anticoagulation in patients with AF. And whenever we start warfarin there needs to be a plan to check INRs. But these performance measures will simply generate pop-up boxes to click through. Sadly, none of the warning boxes that require clicking through, will have a discussion about the C-statistic of the CHA2DS2-VASc score, which is a measure of a test’s ability to predict future events and is slightly better than a coin toss.

I don’t know the best ways to measure the quality of a clinician. Maybe it’s not possible. For now, the best way through the gauntlet of administrative nonsense is to manage as gracefully as possible.

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