Tag Archives: COVID-19

An Update On ACE2, RAAS and Covid-19: Still No Reason To Stop Or Change Your Blood Pressure Medication

Previously, I wrote a detailed post on concerns that have been raised about certain blood pressure medications potentially  increasing the risk of contracting SARS-CoV-2 or increasing the likelihood of death and serious disease related to the virus.

Millions of patients worldwide with heart failure and hypertension are taking drugs that inhibit pathways in the renal angiotensin aldosterone system termed angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs.)

Lisinopril and ramipril are common ACE inhibitors whereas valsartan, losartan, and irbesartan are common ARBs.

Speculation that these drugs might be contributing to mortality associated with COVID-19 was initiated by a “Rapid Response” published online March 3 by the British Medical Journal in response to an editorial on “preventing a COVID-19 pandemic.” and “Correspondence” to the Lancet published March 7.

Since then I’ve been following this topic closely but nothing has emerged from any new data or new expert analysis to suggest that patients should stop taking ACE inhibitors or ARBs.

Yesterday, an excellent summary of the topic from some of the world’s leading authorities was published in the New England Journal of Medicine entitled “Renin–Angiotensin–Aldosterone System Inhibitors in Patients with Covid-19″

It begins with this wonderful sentence: “The renin–angiotensin–aldosterone system (RAAS) is an elegant cascade of vasoactive peptides that orchestrate key processes in human physiology.”

The authors outline in detail the possible interactions between ACE2 receptors and SARS CoV-2.

For those not interested in the scientific details in the paper, the Cliff’s Notes version of this article is below. Basically, we have insufficient data to know if patients taking RAAS inhibitors are at higher or lower risk for serious SARS-CoV-2 infection.


KEY POINTS RELATED TO THE INTERPLAY BETWEEN COVID-19 AND THE RENIN–ANGIOTENSIN–ALDOSTERONE SYSTEM

  • • ACE2, an enzyme that physiologically counters RAAS activation, is the functional receptor to SARS-CoV-2, the virus responsible for the Covid-19 pandemic
  • • Select preclinical studies have suggested that RAAS inhibitors may increase ACE2 expression, raising concerns regarding their safety in patients with Covid-19
  • • Insufficient data are available to determine whether these observations readily translate to humans, and no studies have evaluated the effects of RAAS inhibitors in Covid-19
  • • Clinical trials are under way to test the safety and efficacy of RAAS modulators, including recombinant human ACE2 and the ARB losartan in Covid-19
  • • Abrupt withdrawal of RAAS inhibitors in high-risk patients, including those who have heart failure or have had myocardial infarction, may result in clinical instability and adverse health outcomes
  • • Until further data are available, we think that RAAS inhibitors should be continued in patients in otherwise stable condition who are at risk for, being evaluated for, or with Covid-19

So my recommendations (and more importantly the recommendations of every major society or organization which has weighted in on this topic) to patients remain the same: don’t stop your ACE inhibitor or ARB due to concerns about coronavirus.

Skeptically Yours,

-ACP

Another Coronavirus Quiz

Al Lewis, at Quizzify continues to provide the public brief quizzes with well-researched answers that help even the well-informed better understand SARS-CoV-2 and COVID-19. Today a fourth quiz was released available here (along with the first three 10 -question quizzes.)

Take a few minutes and see if you can beat my score of 875/1000.

Al’s teaser:

Examples of questions from the quiz:
  • Does UV light destroy the virus?
  • How long does food need to be refrigerated at 36 degrees to be safe?
  • What’s the right way to shield yourself when passing near someone else?
  • How much tonic (quinine) water do you need to drink to equal a dose of chloroquine? [SPOILER ALERT: Don’t even think about it.

Skeptically Yours,

-ACP

How Coronavirus Turns Walking Into Awking

Today a guest post from the  wife of the Skeptical Cardiologist who has invented a new word for these difficult times.


Because my job can be pretty sedentary sometimes, I try to walk at least two to three miles every day (in addition to my regular cardio). I love Europe – you have to walk everywhere, and so I try to continue that behavior when we are here in the States.

Normally going for walks in my neighborhood, I will encounter occasional dog walkers, or baby walkers, or runners… but not many.

Lately, because of the coronavirus pandemic, it seems that everyone is out walking, even in terrible, dreary, cold weather. I think it’s encouraging that people are so committed to daily exercise now, because it really is so important to stay healthy and positive.

But I’ve noticed a funny phenomenon. Because of the 6 feet distancing in effect, it’s getting more challenging for me to go on walks. I am constantly having to move to the other side of the street or the middle of the road to avoid people.

It’s incredibly awkward because I don’t want to offend anyone and make them feel like I think they are infected. But at the same time, I’m trying to follow the rules and protect myself.

While out walking the other day, I was laughing to myself about this behavior and thinking that someone should invent a term for it. The new word would perfectly describe  “awkwardly & suddenly moving to the other side of the street when you realize you’re sharing a sidewalk with someone coming towards you” (behavior necessitated by a desire for keeping a six foot distance during the COVID-19 pandemic)

I thought of 2 words – awkward and walking, and came up with “Awking“. Then I started to wonder if I could get this on Urban Dictionary (or if somebody had already come up with it.) I looked it up, and there were a couple of definitions for my word, but not the one that I was thinking of. So I looked up how to submit on Urban Dictionary, followed the instructions, and submitted it. Within five minutes they responded and said that my word had been approved!! It’s silly how happy this made me. Me, a humble Gen Xer who is not well-versed in “kids today” language.

My immortal contribution to slang!  🤣  (turns out its not so hard to get a word approved on Urban Dictionary, but hey whatever, ha!)

Now you must excuse me…
I need to cross to the other side of the street to keep 6 feet away from my neighbor.


Speaking of neologisms, a few months ago while scanning the blurb on the wrapper of a keto-friendly snack  I created by accident the portmanteau word, farb. Thus far, I have not submitted it to Urban Dictionary.

Neologically Yours,

-ACP

N.B. The featured image comes from @BDStanley on Twitter. Beatleish lyrics of relevance on that tweet include “We were talking about the space between us all.”

 

In The Time of Coronavirus What Should Be Considered A Normal Temperature And What Is A Fever?

As a medical student, I was taught that the normal temperature of humans is 37.0°C (98.6°F) and that the upper limit of normal temperature is 38.0°C (100.4°F). The criterion for fever during this current SARS-CoV-2 epidemic is still considered to be a temperature over 38.0°C (100.4°F) despite strong evidence supporting a lower temperature cut-point.

Multiple studies in the last 30 years have clearly established that the average human temperature has dropped progressively in the last 150 years and is more accurately considered to be 36.8°C (98.2°F).

Moreover, normal temperature varies between individuals and multiple other variables including according to what time of day it is taken.

For example, when I take my temperature first thing in the morning it is 96.4°F. Later in the day, it rises to 97.4°F. After exercise, it reaches 98.0°F. My overall average is 97.0, significantly lower than the canonical average.

This change in the average normal temperature and the upper limits of normal has significant implications for temperature screening for the determination of fever and consequently who may or may not have a coronavirus infection.

Origins Of 98.6 As Normal

The concept of 98.6 as normal can be traced back 150 years to work from the German scientist Carl Reinhold August Wunderlich who made multiple measurements of axillary temperature in 25000 subjects. Wunderlich reported a range of 36.2°C (97.2°F) to 37.5°C (99.5°F). Although he also noted a significant diurnal variation in temperature, with a nadir in early AM and peak in later afternoon,  he would have considered me hypothermic.

Wunderlich also felt that temperatures >100.4 were “probably febrile.”

Change in Temperature Over Time

Studies since Wunderlich have shown a progressive decline in the average human temperature. Mackowiak, et al, (PDF available here) published  data showing a substantially lower normal human temperature such that  that 98.6 “should be abandoned as a concept relevant to clinical thermometry.”

Mackowiak, et al found in 148 individuals the average temperate was 98.2 (36.8). These individuals were monitored over a 48 hour period and the average and range varied considerably

Screen Shot 2020-03-28 at 9.29.19 AM

The average temperature varied according to time of day.

Screen Shot 2020-03-28 at 9.29.35 AM

In the graph above if we look at 6 AM temperature measurement, we see the average is actually 97.5°F. My 6 AM recordings of 96.4°F puts me in the bottom fifth percentile. More importantly, 99% of subjects had a temperature of <98.9°F.

If one is recording a temperature on a patient at 6 AM and it is >98.9 that should probable be considered abnormal. On the other hand, if the temperature is being measured between noon and 6 PM, >99.8 should be considered abnormal.

A publication from earlier this year in eLife confirmed that the average temperature in humans is progressively dropping.

The researchers used measurements from the Union Army Veterans of the Civil War (N = 23,710; measurement years 1860–1940), the National Health and Nutrition Examination Survey I (N = 15,301; 1971–1975), and the Stanford Translational Research Integrated Database Environment (N = 150,280; 2007–2017)

They found:

mean body temperature in men and women, after adjusting for age, height, weight and, in some models date and time of day, has decreased monotonically by 0.03°C per birth decade..

Screen Shot 2020-03-28 at 8.12.20 AM

As you can see from the graph above, the average temperature has dropped from the 1970s to the 2000s. The most recent temperatures from 2007 to 2017 in orange lie consistently below the green temperatures from 1971 to 1975. This is irrespective of gender (men in top two graphs, women in bottom two) and race (white in left boxes, black in right boxes.)

Additionally, in all categories (except perhaps civil war men) average temperature declines significantly with age.

Choosing A Cut-point Temperature To Decide Fever

All of this temperature variation data would be simply of academic interest but given the COVID-19 pandemic, the definition of fever has become incredibly important.

If we choose a cut-point that is too high we risk missing cases. If we choose one too low we risk overwhelming the limited testing resources and unnecessarily alarming patients.

What I have decided to do is to establish a norm for myself based on time of day. If I record a temperature >1.8 °F over my norm I will consider myself as having a fever.

Clearly, this doesn’t work for widespread screening of the public which is occurring now at multiple sites as most individuals have not established what is their normal average temperature, let alone their average temperature by time of day.

At a minimum, though, it seems to me that public health authorities should recognize the lower normal average temperature and the corresponding lower cut-point fever that has been known since 1997.

Adjusting the cut-point to >99.8°F for abnormal would align more closely with what is currently known about the range of normal human temperatures.

Thermoregulatorily Yours,

-ACP

Atrial Fibrillation In The Time of Coronavirus: A Call For More Personal Remote ECG Monitoring

What is the best strategy for doctors and patients dealing with atrial fibrillation during the COVID-19 pandemic?

Clearly, at this time everyone needs to minimize visits to the doctor’s office, emergency room, urgent care center or hospital. But patients with paroxysmal atrial fibrillation by definition will have periodic spells during which their heart goes out of rhythm and many of these will occur during this period when we want to minimize contact with individuals outside the home.

In my practice, we are able to manage the majority of these episodes remotely by using a combination of personal ECG monitoring, online cloud ECG review capability, and home adjustment of medications.

Given the presence of coronavirus in the community and the potential for overload of acute care medical resources, outpatient/home management of atrial fibrillation is more important than ever.

I have described in detail in previous posts how we utilize Alivecor’s Kardia device in conjunction with the cloud-based KardiaPro subscription service to manage our afib patients remotely.  (See here and here.) The Apple Watch ECG can also be utilized for this purpose but is more expensive than Kardia and has no online review service.

With this approach we are able to minimize ER visits and hospitalizations. In addition, use of long-term monitors (which also requires a visit to an outpatient center for hook-up) has been greatly reduced.

Given heightened anxiety during the pandemic we are also seeing many patients experiencing palpitations, which are not due to their atrial fibrillation. These can be due to benign premature ventricular contractions or premature atrial contractions.

If an afib patient calls with symptoms of palpitations or rapid heart beat and they have a Kardia device or Apple Watch ECG we can review the recorded ECG, and can quickly make a determination of the cause and best treatment. If they don’t have one of these devices we have no idea what the cause is or the best treatment.

General Advice For Afib Patients 

Obviously, it would be great if patients don’t have episodes of afib during the pandemic.

Paying attention to the eight lifestyle factors which influence afib occurrence I’ve recently posted on is even more important during this stressful period. In particular, afib patients should be limiting the inclination to consume more alcohol and utilizing healthier ways to reduce stress.

Regular exercise has demonstrated benefits in reducing afib episodes and also reduces stress. Gyms are closed or closing, but with spring arriving, outside exercise is always possible. Even if you don’t have exercise equipment in your home there are many exercises you can do inside that provide cardio, strength, and flexibility training. Consider bodyweight exercises, jumping rope, hoping on to a small chair, or go find your old Richard Simmons exercise VHS tape. My wife and I have been enjoying the Seven app lately which takes us through a variety of exercises without the need for equipment. There are tens of thousands of exercise videos on YouTube.

Some afibbers find that meditation or relaxation apps or yoga helps with stress control.

Finally, make sure you have plenty of your prescription medications on hand and that you take them as prescribed without fail. Many pharmacies have home-delivery available for prescriptions.

Regarding medications, please note that good blood pressure control also reduces afib recurrence. Do not stop ACE inhibitors or ARBs as I discussed here.

A Call For More Self Monitoring

Given the importance of staying home right now, afib patients who do not have a method for self monitoring their heart rhythms should consider acquiring a Kardia device or Apple Watch.

Antifibrillatorily Yours,

-ACP

N.B. As I’ve mentioned multiple times I have no connections, financial or otherwise to Apple or Alivecor.

KardiaMobile, the original single lead personal ECG is selling for $84 right now. It’s available also on Amazon.

In my opinion, there is no compelling reason to prefer the Kardia6l, which costs $149 over the single lead KardiaMobile.

Both of these devices work with a Google or iPhone app which is free. To store recorded ECGs on Alivecor’s cloud service requires a subscription fee.

When I enroll my patients into KardiaPro I send them an email invitation which allows them to purchase the KardiaMobile plus have one year of cloud storage and connection to my KardiaPro dashboard for $120. Thereafter the one year KardiaPro service is $60/year.

Apple Watch 5 starts at $399. ECGS are stored in the iPhone app. No cloud storage. ECGs can be emailed as PDF.

Patients with Apple 4 Watches or later can send a PDF of their ECG via email or fax to their cardiologist (https://support.apple.com/en-us/HT208955). Check with your cardiologist if they can view a PDF.

NOTE: Apple has closed all of their retail stores outside of Greater China until March 27. Online stores are open at www.apple.com, or you can download the Apple Store app on the App Store so you can still buy an Apple Watch or an iPhone too.

Cheaper personal ECG devices are available. I’ve reviewed several of these and don’t recommend them. (See here and here.)

Thanks to Mark Goldstein  and Dan Field for review/editing of this post.

A Message From Italy On Coronavirus and COVID-19

Last month the skeptical cardiologist asked Nicola Triglione, a native of Southern Italy who completed his cardiology fellowship in Milan to give us his perspective on the US and Italian health care systems.

Since Italy is now at the European epicenter of the COVID-19 epidemic and second only to China in number of

Screen-Shot-2020-03-15-at-12.02.17-PM.png
From the Center for Systems Science and Engineering (CSSE) at Johns Hopkins University (JHU)

cases and deaths, American scientists and public health officials are now closely scrutinizing Italy’s response and outcomes.

 

 

I emailed Nicola to see what his situation was and he provided this information and advice for my readers:

Hello everyone from Milan, as you already know Italy is in lockdown over the new coronavirus (Covid-19). The northern regions of Lombardy, Veneto and Emilia-Romagna have been most affected by the outbreak and what’s happening here it’s just surreal. I just wanted to reach out to you because we all have the responsibilities to prevent this. The majority of infections are mild but the pandemic is growing at an exponential speed. The infection is much more aggressive for certain groups: elderly, cancer patients and patient with cardiovascular disease are at higher risk of dying. Hospitals are severely overloaded and the real problem is that medical staff gets sick.

My only take on is: stay home for as long as possible, lots of contagions happen before there are symptoms. Virus doesn’t spread if people don’tinteract. If we can postpone cases the healthcare system will be able to handle contagions much better. I hope the US authorities will stop public gatherings and everything really not necessary. Last but not least, we need to test everybody as limited testing only postpones the problem.

Dott. Nicola Triglione
Medico Chirurgo
Specialista in Cardiologia 

For those who want to learn more about the situation in Italy, watch this video interview with Dr. Cecconi of Humanitas University in Milan discussing the region’s approach to the surge, including clinical and supply management, health care worker training and protection, and ventilation strategies, with JAMA Editor Howard Bauchner.

Antiseptically Yours,
-ACP

Coronavirus and ACE Inhibitors: Do Not Stop Taking Your Blood Pressure Medication

Many of my patients with hypertension and/or cardiovascular disease are taking drugs termed angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs.)

Both types of drugs are mainstays in our treatment of hypertension and heart failure.

Lisinopril and ramipril are common ACE inhibitors whereas valsartan, losartan, and irbesartan are common ARBs.

Speculation that these drugs might be contributing to mortality associated with COVID-19 was initiated by a “Rapid Response” published online March 3 by the British Medical Journal in response to an editorial on “preventing a COVID-19 pandemic.” and “Correspondence” to the Lancet published March 7.

I’ve provided the paragraph in which the authors of the Rapid Response raise the question along with their rationale at the end of this post.

Primarily, however, in this post I want to reproduce comments from experts in this area which confirm my observation that the evidence is not sufficient to ask patients to stop these life-saving drugs.

From the European Society of Cardiology yesterday (March 13, 2020):

Based on initial reports from China, and subsequent evidence that arterial hypertension may be associated with increased risk of mortality in hospitalized COVID-19 infected subjects, hypotheses have been put forward to suggest a potential adverse effects of angiotensin converting enzyme inhibitors (ACE-i) or Angiotensin Receptor Blockers (ARBs). It has been suggested, especially on social media sites, that these commonly used drugs may increase both the risk of infection and the severity of SARS-CoV2. The concern arises from the observation that, similar to the coronavirus causing SARS, the COVID-19 virus binds to a specific enzyme called ACE2 to infect cells, and ACE2 levels are increased following treatment with ACE-i and ARBs.

Because of the social media-related amplification, patients taking these drugs for their high blood pressure and their doctors have become increasingly concerned, and, in some cases, have stopped taking their ACE-I or ARB medications.

This speculation about the safety of ACE-i or ARB treatment in relation to COVID-19 does not have a sound scientific basis or evidence to support it. Indeed, there is evidence from studies in animals suggesting that these medications might be rather protective against serious lung complications in patients with COVID-19 infection, but to date there is no data in humans.

The Council on Hypertension of the European Society of Cardiology wish to highlight the lack of any evidencesupporting harmful effect of ACE-I and ARB in the context of the pandemic COVID-19 outbreak.

The Council on Hypertension strongly recommend that physicians and patients should continue treatment with their usual anti-hypertensive therapy because there is no clinical or scientific evidence to suggest that treatment with ACEi or ARBs should be discontinued because of the Covid-19 infection.

 


 

And from the Science Media Centre:

Prof Tim Chico, Professor of Cardiovascular Medicine and Honorary Consultant Cardiologist, University of Sheffield, said:

“This letter does not report the results of a study; it simply raises a possible question about whether a type of blood pressure and heart disease medication called ACE inhibitors might increase the chances of severe COVID19 infections.  It does not give any evidence that confirms this, simply that it suggests such a relationship should be looked for.

“It is very important that this letter is not interpreted or reported as saying that ACE inhibitors are proven to worsen COVID19 disease.  With more information we will begin to be able to understand whether the relationships between disease severity and existing disease and treatment.

“I strongly advise anyone on heart medications not to stop or change these without discussion with their doctor.  If a patient stops their medication and worsens to the point of requiring admission to hospital at the same time as we are dealing with an increase in COVID19 cases, that would pose the patient a considerable risk and put further strain on the healthcare services.”

 

Prof Peter Sever, Professor of Clinical Pharmacology & Therapeutics, Imperial College London, said:

“There are some questions about whether certain drugs such as angiotensin converting enzyme inhibitors and angiotensin receptor blockers, commonly taken by patients with hypertension, heart failure and diabetes might increase susceptibility to corona virus infection.  On the other hand these drugs could reduce the risk of serious lung disease following infection.

“At the present time we have no evidence as to whether either of these two possibilities are true.

“Patients could be put at risk by stopping these drugs, which are effective treatments for their current condition, without medical supervision, and until further evidence is available should be encouraged to continue their current treatment.”

 

Prof Hugh Montgomery, UCL Professor of Intensive Care Medicine, UCL, said:

“There is no proof yet that the use of ACE inhibitors worsen Coronovirus infection.  There are theoretical reasons, in fact, why they might offer benefit in serious disease.  I would not advocate people ceasing such medication until the evidence has been weighed and clear guidance issued.”

 

Dr Dipender Gill, Specialist Registrar in Clinical Pharmacology and Therapeutics at Imperial College Healthcare NHS Trust, and a Postdoctoral Researcher at Imperial College London, said:

“Evidence is currently lacking and it is too early to make robust conclusions on any link between use of angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type-I receptor blockers with risk or severity of novel coronavirus disease 2019 (COVID-19) infection.  Furthermore, the acute implications of stopping such medications in relation to effects on risk or severity of COVID-19 infection are not known.  Patients should be advised to follow public health guidance rather than alter their medications without proper and informed consultation with their medical doctor.”

 



Let me repeat my main message: Do Not Stop Your Blood Pressure Medication Based On This Speculation.

I will keep monitoring this area and update you as information arises.

 

Skeptically Yours,

-ACP

This article has been updated with additional information as of 3/30/20 with a newer post here.

N.B. It is not unreasonable to raise questions but before making substantial changes in treatment we need more data. Below, the BMJ Rapid Response

The question is, does there exist a connection between the use of these drugs and severe sequela of Covid-19? While the epidemiological association has not been investigated yet, several indicators underline the hypothesis of the link between ACE inhibitors and Covid-19:

On the one hand, it has been shown that the Covid-19 agent (also known as SARS-CoV-2), uses the SARS-COV receptor angiotensin converting enzyme (ACE) 2 for entry into target cells [4]. The interface between ACE2 and the viral spike protein SARS-S has been elucidated and the efficiency of ACE2 usage was found to be a key determinant of SARS-CoV transmissibility [4].

On the other hand, it could be shown in animal experiments that both the ACE-inhibitor lisinopril and the angiotensin-receptor blocker losartan can significantly increase mRNA expression of cardiac ACE2 (5-fold and 3-fold, respectively) [5]. Further, losartan also significantly increases cardiac ACE2 activity [5].

Is a link between these observations possible? Is the expression of ACE2 receptor in the virus targeted cells increased by the use of ACE-inhibitor/angiotensin-receptor blocker and is the patient therefore more at risk for a severe course? We need rapid epidemiological and preclinical studies to clarify this relationship. If this were the case, we might be able to reduce the risk of fatal Covid-19 courses in many patients by temporarily replacing these drugs.

Most Important Coronavirus Question: Will I Get Sick And Die?

Alex Berenow at the American Council on Science and Health has written a helpful analysis of the COVID-19 case fatality rate.

With his permission, I’ve reproduced the article in its entirety below.



For epidemiologists, the most important unanswered question about the Wuhan coronavirus, or COVID-19, is the case-fatality rate. But for the general public, the question is much more personal: “Might I – or anyone I love – get sick and die?” from it.

This article was originally published at Geopolitical Futures.


The first person to die from coronavirus on American soil passed away on Feb. 29 at a Seattle area hospital – incidentally, the same hospital where my daughter was born just ten and a half months ago.

For epidemiologists, the most important unanswered question about the Wuhan coronavirus, or COVID-19, is the case-fatality rate. But for the general public, the question is much more personal: “Might I – or anyone I love – get sick and die?” When faced with uncertainty, people make decisions cautiously, and they base them on emotion and personal experience instead of statistics. If enough people answer “Yes,” there could be major repercussions as panic sets in around the world. Small behavioral modifications, such as telecommuting or reducing factory activity to avoid spreading the disease, made by millions of people can have a large impact. The United Nations already estimated $50 billion worth of exports worldwide will be affected, excluding non-trade economic activities such as travel tourism, as manufacturing slows and governments impose measures like port restrictions. This is why it is necessary to develop a “risk of death” profile for COVID-19.

The first substantial effort to do just that was published by the Chinese Center for Disease Control and Prevention. Though these numbers should be thought of as preliminary (and perhaps specific to only China), they allow us to begin to comprehend the risk that our global society is facing. After analyzing 44,672 confirmed cases, Chinese health officials estimated the case-fatality rates by age group:

Of the 416 children aged 0 to 9 who contracted COVID-19, precisely zero died. This is unusual for most infectious diseases, but not for coronaviruses; the SARS coronavirus outbreak also had minimal impact on children. For patients aged 10 to 39, the case-fatality rate is 0.2 percent. The case-fatality rate doubles for people in their 40s, then triples again for people in their 50s, and nearly triples yet again for people in their 60s. A person who contracts COVID-19 in their 70s has an 8 percent chance of dying, and a person in their 80s a nearly 15 percent chance of dying.

The virus can be lethal in a variety of ways. Viral infections in the lungs can trigger an immune response so strong that it fatally damages the lungs. In others, a systemic immune response, called a “cytokine storm,” can cause multiple organ failure. This could explain why some young, healthy people are killed by the virus, such as Dr. Li Wenliang, the 34-year-old doctor who died shortly after alerting the world to this new strain of coronavirus. An older person’s immune system may not be able to fight a respiratory virus. Underlying conditions such as high blood pressure or diabetes can worsen outcomes.

The above statistics are no doubt frightening numbers. But there are at least three major mitigating factors. First, the number of mild or asymptomatic cases is unknown and probably substantial. Second, China is still a poor country with low-quality health care and, at the epicenter of the outbreak in Hubei province, was overwhelmed by the virus. (The case-fatality rate in Chinese provinces outside Hubei, where hospitals aren’t overloaded, is much lower.) Third, smoking is much more prevalent in China than America, especially among men (52 percent in China versus 16 percent in the U.S.), and smoking is a risk factor for poor responses to respiratory infections. Together, this means the case-fatality rate is likely inflated, and it would be a mistake to apply these figures to the United States or other advanced nations.

The real question, then, is how inflated the case-fatality rates are. At this point, it’s impossible to determine because scientists are still collecting data on how widespread the virus is. But to get a sense of how exaggerated these numbers might be, it is useful to examine the case-fatality rate for seasonal influenza. For the 2018-19 influenza season, the U.S. Center for Disease Control and Prevention provides estimates for the number of cases (defined here as “symptomatic illnesses”) and deaths. From these, we can derive case-fatality rate estimates by age group.

If COVID-19 ends up being similar to seasonal influenza, then the case-fatality rates for COVID-19 are inflated by a factor of 20 to 100. Dr. Anthony Fauci, head of the U.S. NIAID, co-authored an editorial for the New England Journal of Medicine in which he wrote:

“If one assumes that the number of asymptomatic or minimally symptomatic cases is several times as high as the number of reported cases, the case fatality rate may be considerably less than 1%. This suggests that the overall clinical consequences of Covid-19 may ultimately be more akin to those of a severe seasonal influenza (which has a case fatality rate of approximately 0.1%) or a pandemic influenza (similar to those in 1957 and 1968) rather than a disease similar to SARS or MERS, which have had case fatality rates of 9 to 10% and 36%, respectively.” [Emphasis added]

We have reason to believe this view is closest to reality. In South Korea, public health officials screened about 100,000 people and detected over 7,300 cases. So far, the death toll is 50, which translates to a case-fatality rate of 0.7 percent. That’s still seven times worse than seasonal flu, but it’s far lower than the initial reports from China.

The Future of COVID-19

Stat News describes two possible scenarios that epidemiologists envision for the future of COVID-19. In the first, COVID-19 becomes just another cold virus, and possibly evolves to become less lethal as well. What we call the “common cold” is actually caused by roughly 200 different viruses. Each year, about 25 percent of common colds are due to four coronaviruses, and some scientists think COVID-19 could eventually join this group as its fifth member. In the second scenario, COVID-19 behaves more like a severe seasonal flu, vanishing in the summer and returning to hit us hard in the winter.

In neither scenario does COVID-19 resemble the Spanish flu of 1918, which disproportionately killed young people. In neither scenario does the virus mutate to become more lethal. Most likely, the opposite will be true. There is an inverse relationship between lethality and contagiousness; that is, the most contagious viruses tend to be less lethal. Evolutionary pressures – namely, the biological imperative to reproduce as far and wide as possible (which means not killing people) – may push COVID-19 down this path.

For now, influenza remains the far bigger global public health threat. Each year, about 1 billion people become infected with seasonal flu, killing some 300,000 to 500,000. This season alone (2019-20), about 20,000 Americans have died from fluincluding 136 children. Yet, very few people fear the flu. Society has accepted it as part of reality, and people carry about their daily lives without excessive concern over influenza. This is the likely future for COVID-19.

Until then, perhaps the last word should be given to virologist Dr. Lisa Gralinski, who told The Scientist, “If you’re over fifty or sixty and you have some other health issues and if you’re unlucky enough to be exposed to this virus, it could be very bad.” While everyone else should remain vigilant and take proper precautions (e.g., washing hands and avoiding crowds) until more data comes in, from a scientific perspective the public alarm is disproportionate to the risk.

© 2020 Geopolitical Futures. Republished with permission. (The original is here.)


Skeptically Yours,

-ACP

Test Your Knowledge of Coronavirus With These Two Quizzes

Since COVID-19 has been sucking all the oxygen out of the information atmosphere I have lost any desire to post on my usual array of semi-cardiovascular topics.

However, Al Lewis  has been hard at work providing us with COVID-19 information relevant to employee wellness through his blog and his company,  Quizzify.

You can test your knowledge of the coronavirus by taking Quiz1 or Quiz2.

Al’s  typically engaging description follows.

When was the last time a sequel was better than the original?  Toy Story 2? Superman 2? A Shot in the Dark

Our first coronavirus quiz did indeed live up to its name by going viral, and will be highlighted in Employee Benefit News next week.

As with the first, doctors at Harvard Medical school have reviewed this new content. As with the first, the sequel also features 10 engaging and reliable coronavirus employee health education questions.  This quiz covers, among other things:

  • boosting your immune system
  • the value of zinc tablets
  • how far a sneeze can spread it, and
  • how to avoid a surprise bill for treating it.

As with the previous quiz, Quizzify customers have much more flexibility, control, visibility and support in their deployment of the quiz than you will. However, owing to the public health emergency, we are making the actual quiz freely available for you to share, eating a loss and forgoing a profit opportunity.*


If your hankering for coronavirus information has not been sated by the quizzes check out his post on 5 easy ways to reduce coronavirus risk you didn’t think of.

Handwashingly Yours,

ACP