It’s Now Time to Worry About Long-Term Cardiac Consequences of COVID-19

A study published yesterday in JAMA has the skeptical cardiologist very concerned about the long-term cardiac effects of COVID-19 infection.

The investigators performed cardiac MRI (CMR) on 100 patients with documented COVID-19. Cardiac MRI is now considered the gold-standard for noninvasively measuring pathologic changes in cardiac muscle.

In this study of a cohort of German patients recently recovered from COVID-19 infection, CMR revealed cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%), independent of preexisting conditions, severity and overall course of the acute illness, and time from the original diagnosis. These findings indicate the need for ongoing investigation of the long-term cardiovascular consequences of COVID-19.

These patients were evaluated a mean of 71 days after confirmed COVID-19 diagnosis,

Note that left ventricular ejection fraction (LVEF), the most common measure of the systolic or pumping function of the heart although lower in the COVID-19 patients was not depressed below normal values. This means these cardiac abnormalities would not be detected on more commonly available cardiac diagnostic methods like echocardiography.

Also note that risk-factor matched controls have a fair number of CMR abnormalities and that we don’t know what cardiac MRI would show in a comparison group of patients recovering from the flu.

Despite these limitations, given reports of ongoing cardiac symptoms in many post-COVID-19 patients, I have to agree with these words from an accompanying JAMA editorial.

We wish not to generate additional anxiety but rather to incite other investigators to carefully examine existing and prospectively collect new data in other populations to confirm or refute these findings. We hope these findings represent that of a select cohort of patients. Yet, if this high rate of risk is confirmed, the pathologic basis for progressive left ventricular dysfunction is validated, and especially if longitudinal assessment reveals new-onset heart failure in the recovery phase of COVID-19, then the crisis of COVID-19 will not abate but will instead shift to a new de novo incidence of heart failure and other chronic cardiovascular complication

Gadoliniumly Yours,


Source: Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered From Coronavirus Disease 2019 (COVID-19) | Cardiology | JAMA Cardiology | JAMA Network


14 thoughts on “It’s Now Time to Worry About Long-Term Cardiac Consequences of COVID-19”

    • I’ve been following the development of this revision based on criticism from Professor Darrel Francis on Twitter of discrepancies in the data. My overall opinion is that the German investigators make a few mistakes in data presentation that don’t change the overall conclusions. Overall I think the science is good and there are limitations to the conclusions that can be drawn but it remains an important study that has me worried about long term cardiac complications of COVID-19
      You can read a full discussion from the investigators standpoint here …

      • Thanks for your thoughts. One question regarding the revision, did LV mass index change from significant to non significant in comparison to COVID vs healthy controls? My understanding (which is woefully poor) is that LV hypertrophy can cause a whole lot of issues, and I thought this was the main concern elucidated from the study. Or does the study worry cardiologists because of the subclinical myocarditis (I assume its subclinical b/c its not detected by echo and there are no apparent symptoms, again I might be totally wrong on this and please correct me if I am)and the long term repercussions of chronic inflammation. Sorry for the probably silly questions but I am trying to fully appreciate the concern.

        • LVMI significance did change. I did not find the LVMI difference on my initial look at the data to be of concern. The minor differences in this parameter could easily have been noise.
          It is the cardiac MRI changes in T1 and T2 and LGE suggesting myocardial inflammation that worries me.

          • Thanks for the further explanation. I see now what you mean, although at this point after spending about 2 hours reading about inversion times and inversion recoveries I have come to realize yet again that I’m not nearly as smart as I thought I was. I guess I will have to rely on the chart you posted to spell it out for me “significantly abnormal” accompanied by a bigger number than cohort and control, I can understand that!. On a positive note though after all of my reading I figured out what your closing meant “gandoliniumly yours”. I guess that’s good, right?

  1. Could you please comment about the opinion piece by Dr. Harvey Risch in the link below. In the practice I work in, we have a large pool of high risk cardiac patients. Based on the comments of Dr. Fauci and the statements released by the FDA, I have not considered prescribing azithromycin and hydroxycholoquine for our high risk patients. However, Dr. Risch makes a compelling case for using the drug combination.

  2. Follow up question, in the 2nd paragraph you said Cardiac MRI is now considered the gold-standard for non-invasively measuring pathologic changes in cardiac muscle”. I believe this answers the question about measuring ischemia. Is there a more accurate test (invasive) than CMR that more accurately measures ischemia?

    • Currently, I would consider PET MPI scanning with FFR as the gold-standard. CCTA also allows the calculation of FFR as a measure of ischemia but I haven’t seen enough studies to be confident in the techique

  3. This is interesting. I do wonder, as you pointed out, if the change in LVEF is similar in non COVID flu patients or other illnesses that involve an elevated immune response. I also wonder if the convalescent stage of COVID is longer as well? My other question about this study is, what were the treatment protocols for the patients and at what point were they administered?

    From a cardiologist’s perspective, I was also curious, are changes in EF ever transient to that degree? Is ishemic damage quantified based on EF and troponin levels or are there other tests that can better determine that?

  4. I have a few patients with HF symptoms but normal echo and pro-BNP following COVID. Struggling with how to manage them. Referred to Cards but our local services are so impacted that it’s hard to get them in. Suggestions? Medical management assuming HF even without diagnostic support?

    • In my opinion if the patient has a normal echo and normal pro BNP heart failure is not the cause of their symptoms.
      This comes with a big caveat. The echo must include well-done parameters of diastolic function (LAVI, E/E’, TR velocities).
      I’m guessing the symptoms are shortness of breath and fatigue? These would be common post a serious respiratory infection of any kind.


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