Jan 22, 2021 This Week in Cardiology Podcast

John M. Mandrola, MD


January 22, 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 January 22, 2021, John Mandrola, MD comments on the following news and features stories.

One thing I hope gets noticed in historical accounts of the COVID pandemic is how the absence of a truly national or even state-level health system is problematic in public health emergencies. The patchwork of private hospitals competing against each other in communities is good for transferring wealth to the healthcare industry, but not so good at delivering health to the community.

COVID Myocarditis

Long before the pandemic, viruses were well known causes of pericarditis and myocarditis. Despite that prior, in mid-2020, two small studies suggested that COVID-19 had special proclivity to cause cardiac inflammation. These studies and their outsized media coverage induced widespread fear. But two studies published recently suggest SARS-CoV-2 may be more like other respiratory viruses: namely, it can cause myocardial inflammation but infrequently.

About a month ago, Circulation published a research letter from Vanderbilt researchers in which they did cardiac magnetic resonance (CMR) imaging in 59 athletes who had had COVID-19, 60 healthy athlete controls, and 27 healthy non-athlete controls. The median time from a positive PCR test for SARS-CoV-2 was 21 days; 78% of the COVID-19+ athletes had mild symptoms and 22% had no symptoms. Only two of the 59 positive athletes met criteria for myocarditis. One athlete had pericarditis.

The athletes with positive scans had normal electrocardiograms (ECG), echocardiograms (echo), and troponin levels. One of the positive athletes developed an ejection fraction (EF) of 45% by echo done for dyspnea on exertion. Most standard CMR parameters were similar between COVID-19+ athletes and athletic controls.

The authors concluded that the incidence of myocarditis after COVID-19 is modest, at 3%; I agree with that. They also concluded that COVID-19 myocarditis may be missed without CMR; I don’t agree with this. The only significant finding, the one athlete with mild decrease in EF, was discovered because of symptoms. I don’t think they can claim that standard clinical screening would have missed anything important.

Finally, their findings confirm that focal inferoseptal right ventricular insertion late gadolinium enhancement (LGE) is common in athletes, may represent remodeling from athletic training, and should not be conflated with myocarditis. This paper highlights the need for proper controls when studying viral myocarditis in athletes with CMR.

JAMA Cardiology published the second post-COVID CMR study in athletes. University of Wisconsin authors reported on 145 student athletes who had COVID-19 and underwent CMR at their center. In all, 49% had mild symptoms; 28% had moderate symptoms; 17% had no symptoms; and none needed to be in the hospital.

Two patients (1.4%) had MRI findings consistent with myocarditis. One patient had marked nonischemic LGE and T2-weighted signal abnormalities over multiple segments, along with an abnormal serum troponin-I level; this patient had non-specific ST and T changes by ECG but a normal left ventricular EF by echo. At 1-month MRI re-evaluation, the LGE findings were unchanged, but T2-weighted signal abnormalities had improved, and the troponin-I level was normal.

The second patient had 1-cm nonischemic mild LGE and mild T2-weighted signal abnormalities, with normal laboratory values. At 1-month MRI follow-up, the T2-weighted signal abnormalities and LGE had resolved. The patient had symptoms from COVID-19 but none at the time of the MRI. The authors concluded that the utility of cardiac MRI as a screening tool for myocarditis in this patient population is questionable.

We need more studies on this virus, but the seriously limited nature of the two earlier CMR studies, coupled with these more recent and larger series suggests that we should not be doing routine CMR in young people after COVID; and it is highly likely that SARS-CoV-2 has no more or no less proclivity to inflame heart cells than the slew of other viruses that can cause cardiac inflammation.


Heart disease remains a major threat to human life. Risk factors such as hypertension and elevated cholesterol increase the risk of major adverse cardiac events (MACE). Of course, these risk factors are modifiable with drugs. But drugs only work if people take them. The notion of the polypill is to put numerous chemicals into one capsule, thereby improving adherence.

In the TIPS-3 trial, published this week in The New England Journal of Medicine, Professor Salim Yusef and colleagues studied the use of the polypill to reduce MACE. The 5-year trial of about 5700 patients was conducted in 86 centers in 9 countries. The main comparison was the polypill (simvastatin, atenolol, HCTZ, and ramipril) vs placebo. There was also an aspirin vs placebo arm, and polypill + aspirin vs double placebo arm.

In the main analysis, there was a 4-week run-in period in which one in four people were excluded. The primary endpoint (PEP) was a composite of cardiovascular disease, MI, stroke, cardiac arrest, heart failure, or revascularization. Out of about 6000 patients randomized, 126 patients (4.4%) had a PEP in polypill arm; and 157 patients (5.5%) had a PEP in placebo arm. The only component of the PEP that significantly differed was revascularization. MI, stroke, CVD, HF, and out of hospital cardiac arrest were all non-significant. The aspirin alone vs placebo mirrored the three null trials in 2018 (ARRIVE, ASCEND, ASPREE) and did not show a significant reduction in MACE. Three times more patients in the polypill arm stopped the drug for dizziness or hypotension (despite a 4-week run-in period that selected out patients).

The bottom line is that a pill with solid doses of three blood pressure drugs and one statin had very modest effects in individuals with intermediate to high risk.

Low-Value Care

The Annals of Internal Medicine has published a research letter from a number of authors who attempt to estimate the share of low-value spending on older adults that is directly related to the primary care provider (PCP). The notion is that low-value care is a big problem in our system; and some have felt that increasing the role of PCPs will help reduce low-value care.

The authors took a 20% random sample of a Medicare claims database. They then calculated the percentages of all low-value spending resulting from the PCP or some other doctor. The bottom line was that 15% of low-value services were PCP-performed or ordered; 26% of low-value services were PCP-referred; and 60% of low-value services were performed by non-PCPs. Cardiology accounted for 27% of the low-value spending. The authors conclusion is that PCPs generate only a small part of the $75 billion to $100 billion wasted every year on low-value care.

This paper had some serious limitations. The analysis excluded hospital outpatient services because those claims do not identify the referring physician. But consider that PCPs do not play a big role in the in-patient setting. Thus, I’d conclude that both PCPs and specialists participate in tons of low-value care.

Tricuspid Clipping

One of the goals of this podcast is to help you not be bamboozled. One heuristic or short-cut is to listen for words that ought to put you on guard. One word is ‘single-arm’ to discuss a study; another combo of words is “unmet need.” When you hear these, be on the alert.

In June of 2020, Lancet published the 6-months results of the 85-patient, single-arm TRILUMINATE study of edge-to-edge repair using what Abbott calls the TriClip to reduce tricuspid regurgitation (TR). The main findings of that analysis were that 86% of patients had a reduction in TR by echo, and at 6 months, five (6%) patients experienced a major adverse event, which was less than the authors’ prespecified performance goal of 39% (p<0·0001).

I wrote a column in June expressing serious reservations about normalizing this procedure based on what amounts to what my friend Luis Correia calls an unstudy. The study is without a comparator, and since you can see the clip, it’s utterly impossible to blind echo readers.

This month, JACC published the one-year results. TR was reduced in 71% of patients. The authors reported improvements in NY Heart Association, 6-minute walk, and Kansas City Cardiomyopathy Questionnaire scores, as well as sign reverse right ventricular remodeling in size and function. The overall major adverse event rate and all-cause mortality were both 7% at one year. The authors concluded that “Transcatheter tricuspid valve repair using the TriClip device was found to be safe and effective in patients with moderate or greater TR.” It is fine to report the results of a novel procedure, but it is not fine to make such over-reaching conclusions. First, there was data missing in 1 in 4 patients. Second, safety is a relative term. Safe compared with what? To claim anything useful about safety, you need to have a real control arm. Single-arm studies don’t have that. Third, the clinical endpoints are all subjective. This is important because without blinding, there is surely a placebo effect.

Patrice Wendling has nice coverage of the paper, including references to larger trials that are ongoing or soon to start.


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