Americans are not healthy in the default case. Start the assumption with Hypertension (130 mmHg or higher systolic) and/or Obesity, and suddenly the blood clots make a lot of sense. These people are probably already predisposed to get blood clots... what pushes them over the edge is some kind of stressful situation. Under normal conditions, these people wouldn't die.
But guess what? Strapping someone to a ventilator, while your own lungs malfunction (forcing an external machine to breath for you), is hardly a "normal situation". Add on 2-weeks of sitting still on a hospital bed, with your legs immobile the whole time, and its no surprise that blood clots develop, causing strokes.
Granted you aren't a doctor, but that's a pretty unsatisfying answer IMO.
Two additional links. WAPO had a story today on the issue of blood-clotting: https://www.washingtonpost.com/health/2 ... ood-clots/
I think the whole article is useful for contextualizing the phenomenon, but some particularly relevant quotes:
Helen W. Boucher, an infectious-disease specialist at Tufts Medical Center, said there’s no reason to think anything is different about the virus in the United States. More likely, she said, the problem was more obvious to American doctors because of the unique demographics of U.S. patients, including large percentages with heart disease and obesity that make them more vulnerable to the ravages of blood clots. She also noted small but important differences in the monitoring and treatment of patients in ICUs in this country that would make clots easier to detect.
The body’s cardiovascular system often is described as a network of one-way streets that connect the heart to other organs. Blood is the transport system, responsible for moving nutrients to the cells and waste away from them. A common cold or a cut on the finger can lead to changes that help repair the damage, but when the body undergoes a more significant trauma, the blood can overreact, leading to an imbalance that can cause excessive clots or bleeding — and sometimes both...
Harlan Krumholz, a cardiac specialist at the Yale-New Haven Hospital Center, said no one knows whether blood complications are a result of a direct assault on blood vessels, or a hyperactive inflammatory response to the virus by the patient’s immune system. “One of the theories is that once the body is so engaged in a fight against an invader, the body starts consuming the clotting factors, which can result in either blood clots or bleeding. In Ebola, the balance was more toward bleeding. In covid-19, it’s more blood clots,” he said.
So health demographics of Americans are likely contributing to the higher number of observed moralities that have evidence of blood clotting, but again the biological mechanism of why
, or how COVID-19, causes those clots is still not definitive. The hypothesis that clotting factors are being consumed in severe cases of COVID-19 is a plausible idea to me (as a layman).
The other link (pulled from the WAPO article) is a paper (just published) that really focused in on the issue of clotting. It's completely outside my discipline so a lot of it isn't really digestible to me, but there are two paragraphs that are relatively layman friendly.http://www.onlinejacc.org/content/early ... 020.04.031
There are several ways in which the COVID-19 pandemic may affect the prevention and management of thrombotic and thromboembolic disease (hereafter collectively referred to as thrombotic disease for brevity). First, the direct effects of COVID-19 or the indirect effects of infection, such as through severe illness and hypoxia, may predispose patients to thrombotic events. Preliminary reports suggest that hemostatic abnormalities, including disseminated intravascular coagulation (DIC), occur in patients affected by COVID-19 (7,8). Additionally, the severe inflammatory response, critical illness, and underlying traditional risk factors may all predispose to thrombotic events, similar to prior virulent zoonotic coronavirus outbreaks (Table 1) (9,10). Second, investigational therapies for treating COVID-19 may have adverse drug-drug interactions with antiplatelet agents and anticoagulants. Third, the pandemic, because of resource allocations or social distancing recommendations, may adversely affect the care of patients without COVID-19 but who present with thrombotic events. For example, (mis)perception that antithrombotic agents confer increased risk for contracting COVID-19, may lead to untoward interruption of anticoagulation by some patients.
It's a big picture paragraph, but another mention that traditional risk factors may predispose COVID-19 patients to blood clotting. But also interestingly, some of the treatments/therapies for COVID-19 might also lead to the undesired consequence of blood clotting.
Nevertheless, it is yet unknown whether these hemostatic changes are a specific effect of SARS-CoV-2 or are a consequence of cytokine storm that precipitates the onset of systemic inflammatory response syndrome (SIRS), as observed in other viral disease (30-33). Another consideration which has not yet been investigated is that the hemostatic changes seen with COVID-19 infection are related to liver dysfunction (34). A recent study reported 3 cases with severe COVID-19 and cerebral infarction, one associated with bilateral limb ischemia, in the 11 setting of elevated antiphospholipid antibodies. Whether antiphospholipid antibodies play a major role in pathophysiology of thrombosis associated with COVID-19 requires further investigation (35)
Talking more specifically about mechanisms, they conjecture it could be related to the "cytokine storm" (the more technical term for the WAPO quote I linked), or possibly even related to liver dysfunction in COVID-19 patients.