SARS-CoV-2 acts like no pathogen humanity has ever seen
In Brescia, Italy, a 53-year-old woman walked into the emergency room of her local hospital with all the classic symptoms of a heart attack, including telltale signs in her electrocardiogram and high levels of a blood marker suggesting damaged cardiac muscles. Further tests showed cardiac swelling and scarring, and a left ventricle—normally the powerhouse chamber of the heart—so weak that it could only pump one-third its normal amount of blood. But when doctors injected dye in the coronary arteries, looking for the blockage that signifies a heart attack, they found none. Another test revealed why: The woman had COVID-19.
How the virus attacks the heart and blood vessels is a mystery, but dozens of preprints and papers attest that such damage is common. A 25 March paper in JAMA Cardiology documented heart damage in nearly 20% of patients out of 416 hospitalized for COVID-19 in Wuhan, China. In another Wuhan study, 44% of 36 patients admitted to the ICU had arrhythmias.
The disruption seems to extend to the blood itself. Among 184 COVID-19 patients in a Dutch ICU, 38% had blood that clotted abnormally, and almost one-third already had clots, according to a 10 April paper in Thrombosis Research. Blood clots can break apart and land in the lungs, blocking vital arteries—a condition known as pulmonary embolism, which has reportedly killed COVID-19 patients. Clots from arteries can also lodge in the brain, causing stroke. Many patients have “dramatically” high levels of D-dimer, a byproduct of blood clots, says Behnood Bikdeli, a cardiovascular medicine fellow at Columbia University Medical Center.
“The more we look, the more likely it becomes that blood clots are a major player in the disease severity and mortality from COVID-19,” Bikdeli says.
Infection may also lead to blood vessel constriction. Reports are emerging of ischemia in the fingers and toes—a reduction in blood flow that can lead to swollen, painful digits and tissue death.
In the lungs, blood vessel constriction might help explain anecdotal reports of a perplexing phenomenon seen in pneumonia caused by COVID-19: Some patients have extremely low blood-oxygen levels and yet are not gasping for breath. It’s possible that at some stages of disease, the virus alters the delicate balance of hormones that help regulate blood pressure and constricts blood vessels going to the lungs. So oxygen uptake is impeded by constricted blood vessels, rather than by clogged alveoli. “One theory is that the virus affects the vascular biology and that’s why we see these really low oxygen levels,” Levitt says.
If COVID-19 targets blood vessels, that could also help explain why patients with pre-existing damage to those vessels, for example from diabetes and high blood pressure, face higher risk of serious disease. Recent Centers for Disease Control and Prevention (CDC) data on hospitalized patients in 14 U.S. states found that about one-third had chronic lung disease—but nearly as many had diabetes, and fully half had pre-existing high blood pressure.
Mangalmurti says she has been “shocked by the fact that we don’t have a huge number of asthmatics” or patients with other respiratory diseases in HUP’s ICU. “It’s very striking to us that risk factors seem to be vascular: diabetes, obesity, age, hypertension.” [Continue reading…]