The pandemic caused by the SARS-CoV-2 coronavirus in Wuhan (China) is spreading very strongly. It has already been detected in more than 190 countries around the world. In addition, it causes serious health and economic problems in several countries, including Spain.
Patients infected with SARS-CoV-2 develop covid-19 disease and have different clinical symptoms. The most serious is atypical pneumonia, which also causes a high death rate in elderly patients.
The Coronaviridae comprise a family of RNA viruses with comparable genomic organization and functional mechanisms. They are named after the characteristic crown they exhibit when viewed under high-resolution microscopy.
The life cycle of SARS-CoV2 has not been rigorously established, although it is known to bind to cells via the same receptor as SARS-CoV1, the angiotensin-2 converting enzyme ( ACE2), after which it is internalized.
Due to the pharmacological importance of angiotensin / ACE2 in cardiovascular disease, ACE2 has received a great deal of medical attention and surveillance.
As soon as it enters cells, the viral RNA genome begins to generate its proteins which allow its replication and subsequent release.
It is important to note that the molecular differences underlying the different clinical symptoms between SARS-CoV-2 and SARS-CoV-1, such as prolonged latency, predisposition for people with pre-existing cardiovascular disease, and predilection for myocardial complications, remain to be clarified. .
Clinical presentation and disease progression
In the first multicenter studies of hospital patients in China, the most common symptoms were fever of up to 90%, followed by cough, fatigue, sputum production and shortness of breath.
Less common symptoms include headache, myalgia, sore throat, nausea, vomiting, and diarrhea. In contrast, the average incubation period, or the time between probable exposure and the first symptom, is four days. Additionally, 99% of infected patients develop symptoms within the first 14 days.
Regarding the evidence of cardiac and / or kidney damage on admission, it may be variable, but tends to be absent after the initial hospitalization. Many of the more serious manifestations, such as acute respiratory syndrome, acute kidney injury, and myocardial injury, tend to occur 8-14 days after symptom onset and portend worse outcomes.
Finally, several studies have identified advanced age and the presence of other pathologies, such as diabetes, hypertension, coronary heart disease and / or a history of pulmonary disease, as predictors of a more significant progression of the disease. , with higher hospital admission rates. ICU and death.
Many studies have reported acute heart injury as an important manifestation of COVID-19. This is characterized by elevated markers of myocardial damage isolated or in conjunction with abnormalities of the EKG and / or echocardiography.
The rate of cardiac trauma varies between 7% and 28% of hospitalized patients. Again, patients with signs of this injury tend to be older and have other cardiovascular risk factors. Among them, basal hypertension, diabetes, coronary artery disease and heart failure.
Importantly, the mechanism of heart injury can be multifactorial. It includes, for example, ischemic demand, toxicity due to direct viral injury, stress, inflammation, microvascular dysfunction, or plaque rupture.
In addition to acute heart damage, an increase in the manifestation of arrhythmogenic processes has also been documented. In the first studies carried out, 17% of the 138 patients developed an unspecified arrhythmia during their hospitalization. Likewise, higher rates were observed in covid-19 patients admitted to the ICU (44%).
These results are consistent with the arrhythmias documented in influenza. These are known to cause atrioventricular node dysfunction and ventricular arrhythmias. However, it has not currently been possible to determine what the specific mechanisms of action are.
On the one hand, heart failure and myocardial dysfunction have also been described in patients with COVID-19 in several studies. For example, heart failure was considered a complication in 23% of all patients and 52% of those who died.
Cardiogenic shock has also been documented against the background of high markers of myocardial damage and electrocardiogram (ST segment) abnormalities.
Finally, a reduction in left ventricular systolic function has been observed without any prior obstructive coronary artery disease in patients with COVID-19, while other reports have described myocarditis processes as well.
A way to go
In early estimates in China, myocardial damage or heart failure contributed to 40% of deaths overall, with 7% attributed solely to circulatory failure without respiratory failure.
In summary, covid-19 disease, in addition to presenting with severe lung failure, also occurs in many cases with cardiovascular complications, such as myocardial injury, heart failure, myocarditis and / or arrhythmogenic events. Therefore, it contributes significantly to the increase in fatal events that result in the death of patients with SARS-CoV2. Currently, the molecular and cellular mechanisms of these cardiovascular events are poorly understood.
* Diego Franco Jaime is full professor in the field of cell biology at the University of Jaén
** This article was published on The Conversation and reproduced here under the Creative Commons license. Click here to read the original version
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