Recent observations indicate that a high proportion of patients affected by the COVID-19 are violations of the heart and blood vessels, and that these disorders contribute to the severity and mortality of the disease.
It is increasingly clear that the coronavirus responsible for the current pandemic of COVID-19 is not a respiratory virus like the others. Of course, the lungs are the main organs affected by the virus, but the medical literature book, a description of the clinical cases extremely strange which had never been described until now for this type of viral infection. Among the physiological systems affected, the heart and the blood vessels are increasingly emerging as a target of predilection of the virus, complicating seriously the treatment of the infection.
Formation of blood clots
One of these phenomena is curious is the high incidence of disorders of the clotting processes in patients affected by the COVID-19. For example, the autopsy of patients who died of disease showed the presence of hundreds of small clots in the lungs, a phenomenon very different from a pneumonia classic where the main feature is to present damage to the alveoli involved in gas exchange.
These thromboses (clots) seem to represent a frequent complication of the COVID-19 : several studies have reported an increase in abnormal phenomena caused by a decrease of blood flow, such as a blue stain in the lower limbs (toes), as well as a high incidence of thrombosis of the veins (phlebitis)1. A recent study reported that 71% of the patients died of the COVID-19 had had multiple blood clots scattered throughout the network of blood vessels, a phenomenon observed in only 0.6% of patients who survived the maladie2. The presence of these blood clots is extremely dangerous, because they can migrate into the bloodstream and block by the result of the vital arteries to cause pulmonary embolism, myocardial infarction or STROKE. Moreover, a recent study has shown that high levels of d-dimer, a marker of thrombosis, was associated with a very high increase (18-fold) in the risk of mortality by the COVID-193.
It was also observed that patients with COVID-19 had often clinical signs of heart problems, including a dramatic rise in blood levels of cardiac troponin I, a highly specific marker of damage to the myocarde4. This phenomenon seems to be widespread and could affect nearly one-quarter of patients hospitalized for the COVID-19.
In some cases, it seems that these cardiac involvements may be the first sign of infection : it has been reported that some patients came to the emergency hospital because of the classic signs of infarction, without symptoms of COVID-19 (cough, fever, breathing difficulties), to finally be diagnosed with the viral disease.
The cells of the heart and blood vessels to possess on their surface large amounts of the protein ACE2, the receptor used by the sars coronavirus to enter the interior of the cells. It is likely, therefore, that infringements of cardiovascular observed in a high proportion of infected patients are caused by a direct attack of the virus on these cells, reinforced by the strong inflammatory response triggered by the infection. These observations may explain also why people who have damage to the blood vessels caused by different pathologies (type 2 diabetes, hypertension, preexisting cardiovascular disease) are at much greater risk of developing severe forms of COVID-19.
1. Llitjos JF et al. High incidence of venous thromboembolic events in anticoagulated severe COVID-19 patients. J. Thromb. Haemost., published April 22, 2020.
2. Tang N et al. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J. Thromb. Haemost. 2020; 18: 844-847.
3. Zhou F et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet 2020; 395: 1054-1062.
4. Wang D et al. Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus–infected pneumonia in Wuhan, China. JAMA 2020; 323:1061-1069.