My Life After COVID | Crooked Media
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My Life After COVID

FILE - This undated electron microscope image made available by the U.S. National Institutes of Health in February 2020 shows the virus that causes COVID-19. Doctors at Kyoto University Hospital said Thursday, April 8, 2021, they have successfully performed the world’s first lung transplant from living donors to a patient with severe lung damage from the COVID-19.(NIAID-RML via AP, File)

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FILE - This undated electron microscope image made available by the U.S. National Institutes of Health in February 2020 shows the virus that causes COVID-19. Doctors at Kyoto University Hospital said Thursday, April 8, 2021, they have successfully performed the world’s first lung transplant from living donors to a patient with severe lung damage from the COVID-19.(NIAID-RML via AP, File)

It’s been almost four months since Joe Biden’s inauguration, and most of the people in my life say their minds are calmer, they sleep more soundly, their mental health has improved. They entered the new year exhausted but optimistic that it would end better than it began.

I envy them. My mind rattles, my sleep is pathologically poor, and my mental health can no longer be described as such. The political climate in the country may have something to do with it, though under different circumstances, I think I too would’ve enjoyed a psychological dividend from the end of the Trump presidency. But however I thought the year might end for everyone else, until a few weeks ago, I worried I might not survive it.

This is mostly a story about my experience with a form of post-COVID syndrome, what we now call “long COVID,” and what I learned when I finally sought an explanation for my symptoms. 

Or, at least, I think that’s what the story’s about.


By disposition or training, I dislike writing about myself, and rarely do. My opinions are about as much as I wish to share about my inner life, and I can usually accomplish that with a bare minimum number of “I think”-s or “I’d argue”-s. An old editor of mine and I used to swap links to stories written in what I call “first-person indulgent” and tally up the mes and mys for fun. I’ve been trying to write this piece for a month or so, and that aversion has been a major impediment. Who needs another story by another journalist recounting their personal experience of a disease that has infected hundreds of millions of people? But as when I’ve broken my own rule in the past, I think the public purpose makes oversharing worthwhile in this instance. 

When I first got sick on March 5 of 2020, we were in the phase of the pandemic where the former president was encouraging people who may have been infected to go to work. The next day he proposed leaving a cruise ship full of infected Americans anchored offshore, because he “like[d] the numbers being where they are.” As if we were at the end of a non-crisis rather than the beginning of a calamitous one. 

Thanks to Bob Woodward’s reporting, we now know Donald Trump fully understood by then that COVID-19 was highly contagious, airborne, and much more lethal than seasonal flu. Yet at the time, community spread in Washington, DC, remained undetected because the Trump administration had failed to prepare for its arrival. There were no cases because there were no tests—just as Trump wanted; better not to spook the stock market.  

Trump’s deceit warped the country’s sense of risk, including (as a committed skeptic) my own. The virus would probably arrive eventually—it had already been detected on the west coast and was running rampant in New York—but we had some time. We were riding the metro, mingling with coworkers, and coming home to our families. That’s how we now think my wife got sick, before developing symptoms on February 29. 

Neither of us got that sick, though, and with tests tightly limited to those who’d traveled in Wuhan, we vacillated day to day, hour to hour, wondering whether we were among DC’s first coronavirus cases, or whether our persistent, head-jouncing dry cough was just a coincidental symptom of a harmless cold. 

To this day, no one can tell us with medical certainty that we were in fact infected; and as you’ll soon see, this creates a confounding level of uncertainty about everything that’s happened since. But it’s the only explanation that doesn’t rely on unlikely coincidences.

The cough persisted for weeks, and as it did we continued to waver. By late spring, the FDA had authorized a number of antibody tests, and I took two: a crummy pinprick test, and a more reputable-seeming ELISA assay study developed by Abbott Labs. Both came back positive. Case closed! Except…the tests weren’t clinically useful, even in their unanimity. There was a decent chance both positives were false, and that the real answer lay in my wife’s tests, which returned negative. 

We might have lost interest in the truth of the matter once our outward symptoms subsided, but for the fact that the healing process didn’t restore my exercise capacity. I had been a fairly avid runner and gym-goer until DC closed down, and it was as though, over the course of a month, whatever virus we’d contracted had completely deconditioned me. My last pre-sickness run was four continuous miles, my first run post-sickness was two blocks. I could still exert myself in spurts, but only brief ones, with lengthy rest periods in between. 

Point COVID. 

We were only a few weeks into the U.S. outbreak, but we already had plenty of anecdotal evidence that mild cases of confirmed disease could cause abrupt and prolonged exercise intolerance. We were also advised not to seek care for non-emergencies so hospitals, still filling up with COVID patients, could husband their resources for the truly ill. Thus, I waited, confident I’d slowly regain my wind, with protective antibodies as a fair tradeoff for a few weeks of recuperation. 

Weeks turned to months and if anything my capacity continued to drop. By November, I was Officially Concerned and went in search of answers, but at first, the best I could do was verify that my symptoms weren’t imaginary. A cardiology tech measured my blood oxygen during a stress test, as did a pulmonology tech during a separate exercise test, and, sure enough, they both found that I desaturated under exertion. Normal blood-oxygen saturation is 95-100 percent; mine would dip into the mid eighties. But my echocardiogram was normal. My chest X-ray was normal. I passed my methacholine challenge, which ruled out asthma. My non-contrast chest CT scan also looked normal, save for some residual scarring at the site of old bullet-wound and chest-tube punctures.

Beneath the surface results, though, my pulmonologist noticed a couple of anomalies; my pulmonary artery, which supplies blood to the lungs for re-oxygenation, was a bit enlarged; the blood speed in my right heart was also on the faster side of normal. He thought these could be indicative of something he called pulmonary hypertension. 

This was January and I couldn’t have been happier to learn that we were closing in on a diagnosis. How hard could it be to treat some kind of hypertension, like every well-fed American eventually develops?

I labored (or exulted) under this delusion for weeks, until I asked Dr. Google whether other long-COVID patients had also developed pulmonary hypertension, and came up with nothing other than a fact sheet, which seemed to peg my new life expectancy at a few years.


Pulmonary hypertension is as much symptom as disease. Like the word “tumor,” it conveys bad news, but only in general terms. It describes high blood pressure specifically in the right side of the heart, which as I would later learn isn’t built to sustain that kind of punishment on a chronic basis. People develop the condition for a host of unrelated reasons, including sleep apnea, connective-tissue disease, blood clots in the lungs, and as a side-effect of the 90s-era, weight-loss drug Fen-Phen, but I had no personal or family history with any of these causes, and my misguided relief over the working diagnosis gave way to hope that it would turn out to be terribly wrong. 

What any of this had to do with COVID remained mysterious to me and my doctors, but none of us were big on coincidences, so we continued investigating. The potential overlap became much clearer when they scanned my lungs for air- and blood-flow abnormalities and found the clots. It was now February, 11 months after the illness.


Blood clots cause a form of pulmonary hypertension called chronic thromboembolic pulmonary hypertension, or CTEPH, and it develops in patients whose clots harden into scar tissue and choke off the arteries connecting the heart and lungs. I remember feeling a mixture of fear and relief when my doctors told me I was likely suffering from CTEPH. We were on the cusp of confirming a diagnosis (relief) but one I was desperate to avoid (fear); the class of pulmonary hypertension they thought I had is theoretically curable (relief), but but: The cure is a highly invasive operation in which some of the most specialized surgeons in the world temporarily disconnect the heart from the body so they can reach the hardened clots and remove them from the lungs in the tree-like shape of human bronchi.

Moreover, not everyone with CTEPH can be cured. Depending upon the size and location of the clots, some cases are inoperable; more than the surgery per se I feared that my doctors would conclude I wasn’t a candidate for it. To cope, I thought “optimistic” thoughts of undergoing open-heart surgery at age 38, recovering and regaining what I’d lost as quickly as possible, before encroaching middle age could eat away at it permanently in the normal course of things. 

That best-case scenario was months off, though, and the interim course of treatment entailed urgent anticoagulation therapy—blood thinning—in the form of a pill taken twice daily indefinitely, both to dissolve any unhardened emboli, and prevent new ones from forming. We knew I had clotted, but as loudly as Occam screamed COVID-19, we couldn’t say for certain why. 

My hematologist has since ruled out genetic blood-clotting disease. But in 2008 I underwent major trauma surgery, including a splenectomy, which increases risk of developing blood clots. Maybe I developed them after that operation and they hid out quietly until COVID-19 added new inflammation to the mix. Maybe I picked them up on a plane over the holidays. Of course COVID-19 is now known to increase the risk of blood clots and it is the most likely and unifying hypothesis—but it may remain a hypothesis forever. While none of my doctors could say with certainty what caused the blood clots or when exactly they formed, they all seemed pretty confident that they’d been around for at least 11 months, since the start of my exercise intolerance. And, unfortunately, they seemed equally certain that leaving blood clots untreated for the best part of a year was just too long for this all to resolve harmlessly.

They would thus confirm the diagnosis by measuring the blood pressure in my right heart directly. The procedure, called catheterization, entails lying on an exam table, awake under conscious sedation, while a doctor strings a gauge down the jugular into the right side of the heart. 

Awaiting final confirmation of the diagnosis, I did what any reasonable person in my predicament would do, and pondered whom to blame. This was a mostly pointless exercise but it led me to some interesting thought experiments. If the clots first formed after the long-ago trauma surgery when my spleen was removed, but only became life threatening 12 years later, might the mugger who shot me, wherever he is, transform into my murderer? A moral philosopher would say yes but federal prosecutors in DC probably would not

Weaving up and down a crowded hospital hallway with a pulse oximeter strapped to my forehead, I wondered whether I might have escaped this nightmare if Trump had done the right thing and briefed the whole country, instead of just Bob Woodward, last January. What if he’d done everything exactly the same except for botching the tests? I’d spent over a year scandalized by these failures as a journalist, not realizing I was, in a direct if unprovable sense, a victim of them. My blood desaturated five times in six minutes; two nurses looking on, counting my laps, became alarmed and readied an oxygen tank.


Just a few days later, weeks into anticoagulation therapy and 36 hours before they’d insert the catheter, an uncanny sensation washed over me, as if the machinery in my chest clicked into gear and started working a bit better. I couldn’t explain how exactly, and still can’t, other than that things just felt—smoother—all of a sudden. 

I underwent the procedure on February 19. We were deep enough into the vaccine rollout and I found it kind of funny that the cardiologist tasked with invading my heart kept allowing his mask to slip under his nose, but I also wondered why he seemed so puzzled.

“What tests did you have before you were sent here?” I remember him asking as he read my pressures. “These are all completely normal. You don’t have CTEPH. This is good news.” 

His procedure notes suggested something else was going on; perhaps even that the blood thinners I’d started so many months after the clots formed might’ve kept me out of the danger zone after all. “No pulmonary hypertension…. No apparent indication for pulmonary hypertension therapies at present. Consider alternative diagnosis for hypoxia, right heart dilation and decreased function, including possibility of acute or subacute changes of pulmonary embolism that have improved with anticoagulant therapy.”

Three months later, fingers tightly crossed, it seems like a fair guess. Over the course of the year, I’d worked with a trainer to build an exercise program around my post-COVID limitations. On March 20, he took me to a nearby track and layered running drills into our typical session. First, 100 yard dashes; then a full lap; then a full lap at max speed; then two consecutive. Somewhere along the line running had become achievable again. Altogether it added up to just a mile and a half, but little miracles often feel like the biggest blessings.


Why does any of this matter? Beyond, perhaps, as a backward looking glimpse into the obvious fact that leaving terrible people in charge of historic crises is a mistake.

I can think of at least a couple reasons. 

At some point, we’ll have to decide what to do about the tens of millions of Americans who contracted and survived unconfirmed cases of COVID-19, particularly those of them who will suffer lasting or chronic medical conditions as a result. Many of them will be uninsured or underinsured, and even those who enjoy what passes for good insurance (people like me) will find their paths to care obstructed. My insurance company rejected preauthorization for almost every test and scan my doctors ordered. Its effort to deny me care created numerous delays as my doctors pleaded my case to the physicians who work for Aetna; patients with worse doctors, or less flexibility might have given up. We should eliminate this abusive system for everyone, but in the immediate term, undisrupted care for COVID survivors is a more reachable goal, and it should be extended to those who were unable to confirm their infections because policymakers failed them. I may find at the end of my acute treatment phase that I have lasting lung damage, enough to inhibit me from regaining my full function, but not enough that an insurance company will pay for treatments that might restore it. There is a procedure called pulmonary angioplasty that can essentially reopen obstructed pulmonary arteries; I might be a candidate for this procedure, but probably not if my insurance company has its way—particularly now that they can google me and find out I’m able to jog again.

This policy problem points to the larger, global challenge of seeking out as much of the invisible damage the virus did as possible. Doctors have known that COVID increases the risk of blood clots since early in the pandemic, but that’s because they were treating very sick patients who were clotting in their hospital beds; many of them died, those who didn’t were treated with due haste. At the time we found my clots, they knew much less about how commonly people with mild or moderate cases of COVID develop clots, and in some instances weren’t even investigating. I’ve reached out privately to a small number of people who’ve described experiencing the same mysterious collapse in peak performance, the same symptoms, after recovering from COVID. None of them had been scanned for blood clots. 

My hope of course is that what happened to me turns out to be extremely rare; but on the scale of a runaway pandemic the math of rareness can be punishing. If only one in 100 people who contract COVID develop blood clots, and all but one in 100 of those patients reabsorb their clots without incident, we are indeed dealing with something rare; but if a billion people around the world get COVID before the pandemic is over, then 100,000 people will be in urgent need of blood thinning; those who don’t get it will scar permanently, and some of them will surely die. 

And that’s just one kind of post-COVID syndrome. 

Eventually these two challenges may resolve one another in tandem: Over time, we’ll learn more about the lasting damage COVID-19 can do, doctors will become better at identifying unusual symptoms in their patients and attributing them to past infections, and the treatments could come with a government guarantee. But without intervention, the global population of COVID-19 survivors will include contingents of quiet sufferers and walking dead, and their misery would be a legacy of failure.


These recent months taught me an important lesson, in an unwelcome way, about the nature of human frailty; that the trauma of mortal limbo grows with the length of uncertainty; that an extreme but brief brush with early death like a shooting can leave few obvious mental scars, but the mind can’t so easily shake off two months of contemplating it. Even when it turns out to be illusory. 

Now in May, I run several miles at a time, much slower than before, but continuously. In the lull between medical appointments, I can’t know whether to attribute the lingering drag to a lost year, or to residual clots that will never go away. It may be a combination of the two. Once we repeat the whole battery of tests and scans I underwent this winter, my team of doctors may even give me the all clear to taper off the blood thinners, under tight monitoring. 

As a path to healthier times has become shorter and clearer, the rattle has quieted a bit. The clots made me a vaccination priority and my hospital invited me for my first shot in early March; the rest of my family has been vaccinated, too, as have most of my friends. The ability to travel and reunite and socialize leaves me less time to dwell on the damage branching through my lungs, and when those thoughts return, I can distract myself with work, and, at long last, normal exercise. I told myself when I began this essay that after writing the final word, I’d lace up and run through the horizon until my legs gave out—for hours, if they’ll allow it. So off I go.