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First COVID-19 Pill Likely on Its Way


This was a great week. First, we learned that William Shatner—Capt. Kirk himself—is heading into outer space, boldly going where no 90-year-old has gone before. Then, we heard the news that an effective treatment for COVID-19—in pill form—may be headed our way.

Molnupiravir, an experimental small-molecule antiviral oral therapy, may soon be part of your COVID-19 early-treatment arsenal, assuming drugmaker Merck can obtain emergency use authorization (EUA) from the FDA. The drugmaker reported impressive phase 3 clinical trial interim analysis results last week, so securing this EUA should be as safe a bet as an awkward post-game hug between Tom Brady and Bill Belichick.

How impressive were the trial’s interim findings?

So good an independent committee advised investigators to halt the trial. The international trial included 775 unvaccinated high-risk patients with newly diagnosed COVID-19. Molnupiravir was shown to reduce the risk of hospitalization or death by 50% at 29 days after randomization: 7.3% of those who received molnupiravir were hospitalized or died (28/385) vs 14.1% who received placebo (53/377); P=.0012. But no deaths occurred in the treatment group, whereas eight occurred in the control group. We should note that the number needed to treat was relatively high (14.7), so vaccination is still the key to controlling this extremely infectious disease. We also want to emphasize that these results have not yet been published or peer reviewed, and safety data have not been released.

When could this drug be available?

Merck plans to produce enough pills to treat 10 million people by year’s end. The US government has already ordered 1.7 million courses of the treatment at $700 per patient—a fraction of the cost of monoclonal antibody treatment.

We try not to toss around the term “game-changer” like Oprah giving away new cars, but if this experimental drug lives up to its hype of being easily accessible and saving lives, it could be just that. We hope this promising news doesn’t deter patients from receiving the vaccine, which is still our best defense against COVID-19.

Did You Know?

As mentioned, we’ll probably be hearing “molnupiravir” often in the coming months, so let’s dive into the Norse mythology behind the name, so you can impress friends at dinner parties. Molnupiravir was inspired by the term “Mjölnir” (pronounced “MIOL-neer”), the name of Thor’s hammer in Norse mythology. For those of us not up on our Norse mythology (hand raised) or who haven’t seen any of the Marvel movies (hand still up), here’s your crash course. Thor is the god of thunder, lightning, strength, and protection, and only he possesses the strength to lift his mighty hammer. This iconic weapon not only delivers devastating blows against Thor’s enemies (“the Giants”) but also bestows divine blessings. And it boomerangs back to Thor after he uses it.

The drugmakers seem to believe that molnupiravir will smite COVID-19 in the same way that Mjölnir pummels Thor’s opposition. An audacious appellation for sure, but initial data are promising. We would love nothing more than for molnupiravir to be a godsend.

Holy Cow—Dairy Fat Lowers CV Risk?


Apologies upfront for any eye rolls we elicit here—this article lends itself to pun-tificating…

Many patients may be limiting their intake of full-fat dairy products to avoid saturated fat and prevent cardiovascular disease (CVD), but a new study questions this strategy.

Are milk, cheese, and yogurt actually gouda (sorry) for your heart?

Researchers measured the level of serum pentadecanoic acid (15:0), a biomarker of dairy fat consumption, in >4,000 Swedish adults (about half women, median 60 years) to determine an association between dairy intake and CVD events and premature death. After about 16.6 years of follow-up, they noted 578 incident CVD events and 676 deaths, but higher dairy fat intake was not linked to a higher risk of death. Interestingly, their cow-culations showed that the highest amount of dairy fat intake was associated with the lowest risk of CVD (HR 0.75/interquintile range; 95% CI 0.61, 0.93, P=.009). The results proved congruous with the researchers’ meta-analysis of 17 other studies, totaling 43,000 participants. We were udderly surprised by these findings (sorry again, that was cheesy).

Like Swiss cheese…

This study had some holes. The biomarker was assessed only at baseline, so we don’t know if participants consumed dairy consistently throughout the study. Changes in cardiovascular (CV) risk factors, such as smoking, may have skewed the results. And the study did not account for diverse genetics, given that it included only Swedes.

The takeaway is that dairy fat doesn’t appear to cause harm. This doesn’t mean that patients should consume it till the cows come home, but that extra dollop of alfredo may be okay.

Finding the BP Target Bullseye in Older Adults


Speaking of CV risk, what’s the appropriate systolic blood pressure (SBP) target for reducing CV events in older adults? According to a multicenter, randomized, controlled trial (the STEP trial) of Chinese patients aged 60 to 80 years, it’s 110 to <130 mm Hg.

More than 8,500 older adults with a history of hypertension (but not stroke) were assigned to either intensive treatment to lower their SBP to 100 to <130 mm Hg or standard treatment to meet a goal of 130 to <150 mm Hg. At one year, the groups averaged 127.5 mm Hg (intensive treatment) and 135.3 mm Hg (standard treatment). Researchers looked at a composite of stroke, acute coronary syndrome, acute decompensated heart failure, atrial fibrillation, coronary revascularization, or all CV deaths. After a 3.34-year follow-up, more favorable results for both composite and individual component outcomes occurred in the intensive-treatment group:

  • Primary-outcome events: HR 0.74, 95% Cl 0.60-0.92: p=.007
  • Stroke: HR 0.67, 95% Cl 0.47-0.97
  • Acute coronary syndrome: HR 0.67, 95% CI 0.47-0.94
  • Coronary revascularization: HR 0.69, 95% CI 0.40-1.18
  • Atrial fibrillation: HR 0.96, 95% CI 0.55-1.68
  • Death from CV causes: HR 0.72, 95% CI 0.39-1.32

“Great, but what about the risk of hypotension with intensive treatment?” asks Debbie Downer, insisting that she is simply a realist.

Well, Debbie, you have a valid point. The relative risk of hypotension was 31% higher in the intensive-treatment group, so it is something to keep an eye on. Risk of hypotension was the only significant safety difference between the two groups; the incidence of dizziness and worsening of renal function did not differ significantly between the two groups.

So, what’s the takeaway here? Cardiologist Ty Gluckman put it best: “Modest reductions in BP make a big difference. 8 mm Hg is a big enough change to see meaningful clinical improvements. This study reaffirms the findings from the SPRINT trial that lower is better!”

When Patients With Depression Start Feeling Better


It’s easy to know when to stop a full course of antibiotics after symptom resolution, but as many of you can attest, it’s not always easy to know when to taper or discontinue the use of antidepressants in patients whose depressive symptoms or number of episodes has improved. Researchers from across the pond set out to provide more data in this area.

This randomized, double-blind trial examined 478 patients (average 54 years, 73% women) across 150 primary care practices in the UK. All had experienced at least two prior episodes of depression or had been on the antidepressants citalopram, fluoxetine, sertraline, or mirtazapine for at least two years but were now (at the start of the trial) feeling well enough to consider stopping antidepressant therapy. Participants were split into the treatment maintenance group or the taper and discontinuation (with a matching placebo) group for 52 weeks.

To maintain or not to maintain?

In the maintenance group, 39% of patients relapsed; but in the discontinuation group, 56% relapsed, leaving a sizable gap between the lines of the hazard ratio graph (HR 2.06, 95% CI 1.56-2.70, P<.001). Also of note, adherence was 70% in the maintenance group and only 52% in the discontinuation group. A final mark in the maintenance group’s favor was its fewer number of symptoms of depression, anxiety, and withdrawal.

Patients may inquire about stopping their antidepressants as soon as they feel better, but similar to discontinuing a course of antibiotics, this can have serious consequences if done too soon. It’s tempting to wean patients off antidepressants once they start feeling better, but this study is a reminder to use caution and to consider the patient’s risk of relapse.

Rapid-Fire COVID-19 Updates


  • WHO issues new guidance on the use of monoclonal antibodies in COVID-19

  • J&J says COVID-19 vaccine booster two months after first shot increases protection

  • CDC strengthens its vaccination recommendation for pregnant people

  • Pfizer officially requests authorization from the FDA to use its COVID-19 vaccine for kids ages 5 to 11 years

Interested in more healthcare news? Here are some other articles we don’t want you to miss:

Morning Report is written by:

  • Alissa Scott, Lead Author
  • Aylin Madore, MD, MEd, Author and Editor
  • Shira Page, RN, NP, Author and Editor

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Please note that the summaries in Morning Report are intended to provide clinicians with a brief overview of an article, and while we do our best to select the most salient points, we ask that you please read the full article linked in each summary for clarification before making any practice-changing decisions.

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