**2.2 Cardiovascular complications**

Viruses can cause pericarditis due to systemic inflammation generated in severe cases [21] due to cytotoxic mechanisms. In addition, SARS-CoV-2 infection induces an excessive inflammatory response. This inflammation is responsible for pericardial effusions or cardiac tamponade [20, 22].

Elevated Angiotensin-Converting Enzyme 2 (ACE-2) presence in the cardiovascular system allows direct viral invasion. Then, the immune response and cytokines cause inflammation of the heart muscle, interfering with the conduction system and heart pumping capacity, leading to arrhythmias and cardiac arrest [23].

Infectious processes of viral origin are associated with cardiovascular complications, one of the chief causes of mortality. The effect can persist for up to 10 years after the acute infectious process [20].

Months after the acute phase of SARS-CoV-2 infection, regardless of severity, up to 60% of cases present myocarditis and 71% high-sensitivity troponin T elevation. It is due to a significant decrease in left ventricular ejection fraction [20].

Thrombotic events are considered one of the leading causes of death in patients with COVID-19. Various mechanisms generate a procoagulant state due to an unregulated release of proinflammatory cytokines, resulting in endothelial damage and dysfunction, as an increase in promoters of platelet aggregation and fibrin formation [20].

Different factors favor the presentation of these complications in patients after COVID-19, so an increase in the incidence of this group of diseases in the Mexican population can be expected [20].

#### **2.3 Neurological symptoms and complications**

Among the most frequent symptoms are anosmia, headache, myalgias, and mental fog [20].

Neurological alterations are of great relevance since they may significantly affect the quality of life of those who survived COVID-19 [20].

Different viral infections, including coronavirus infections, can manifest with neurosensory alterations, demyelinating diseases, or cerebral vascular events in surviving patients after recovering. After SARS-CoV-2 infection, neuropsychiatric alterations that persisted up to 4 years after recovery were identified [24].

Since the discovery of SARS-CoV-2, various hypotheses have emerged about the mechanism of development of this complication, including its neuroinvasive potential through the olfactory groove or invasion of the nervous system through the bloodstream [24].

Flores-Silva et al. [1] mention that up to 52% of patients may persist with fatigue 10 weeks after the onset of the disease, independent of the severity. This symptom is considered the most frequent in the long term [24].

After the acute phase, about 5–10% of patients persist with anosmia at 4 weeks, with the probability of developing parosmia. In 20–30% of patients, headache is present for 6 weeks, and in 10–20% for up to 9 months. Myalgias are observed during the acute phase, and some patients may present occasional osteoarticular and muscular pain [20].

Other complications from COVID-19 are cerebral vascular events, especially of the ischemic type, which, compared to patients without COVID-19, are usually more severe and have a worse prognosis. The sequelae can hinder the rehabilitation process and even permanently disable the survivors, making it difficult to reintegrate into working and social life. After the acute symptoms of COVID-19, 30% of patients present memory loss, difficulty concentrating, or insomnia. Other reported symptoms are vertigo, headache, and brain fog—discovered as a cognitive alteration, which combines a state of confusion and disorientation [20].

The factors associated with the development of new in-hospital neurological events seem to be related to the severity of the disease, both in respiratory parameters (PaO 2/FiO 2 ratio, Acute Respiratory Distress Syndrome (ARDS) severity, and chest CT findings) and inflammatory markers (C-reactive protein, D-dimer, and neutrophil/lymphocyte ratio) [24].

*Post-COVID-19 Condition and Its Presence in Mexico DOI: http://dx.doi.org/10.5772/intechopen.111697*

Flores-Silva et al. [1], by including non-specific neurological manifestations such as headache, anosmia, dysgeusia, and myalgia—found a frequency of 69.3%, slightly higher than the reported overall frequency of 56.4% [24].

Neurological manifestations, as previously mentioned, have a variable spectrum of presentation, from headache and alterations in taste and smell to ischemic and hemorrhagic cerebrovascular disease [25].

In Mexico, a study carried out at the Specialty Hospital of the Siglo XXI National Medical Center in hospitalized patients with severe COVID-19 identified neurological manifestations in 78 patients (36.4%) out of 214. The most frequent were from the central nervous system: headache, encephalopathy, and cerebrovascular disease (24.8%). The second most were from the peripheral nervous system: anosmia, dysgeusia, and myopathies (8.9%) [25].

Albarran-Sánchez et al. [6] report an incidence of alterations in the sense of smell ranging from 4.9 to 85.6%. The incidence of taste disturbances has been highly variable, ranging from 0.3 to 88.8%, referred to as dysgeusia and ageusia. Finally, headache incidence was from 0.6 to 70.3% [25].

The acute cerebrovascular disease has been associated with COVID-19 with a worse prognosis due to increased mortality. It was also the most frequent neurological manifestation in the study conducted by Albarran-Sanchez et al. [25].

#### **2.4 Anosmia**

Anosmia is considered a sequel to COVID-19, caused by damage to the respiratory neuroepithelium. Some studies mention that the damage is driven by the viral invasion of ACE 2 and TMPRSS2 cell receptors—found in the nasal and olfactory epithelium [14].

In the olfactory epithelium, infiltrating leukocytes secrete various proinflammatory cytokines that affect olfactory receptor neurons and the stem cell niche, altering their odorant responses and ability to regenerate [14].

Halabe-Cherem et al. [3] mention that 1 out of 2 patients with COVID-19 will develop anosmia, which affects the quality of life. It influences the ability of people to enjoy smells or detect danger through them [14].

Gutierrez-Bautista et al. [23] observed that 27 of 30 people improved the odor detection threshold 2 months after the onset of the symptoms. Nevertheless, it was not significant in identifying them [23].

#### **2.5 Mental health**

In patients with previous SARS-CoV-2 infection, some mental health symptoms prevail up to 2 years later. Identified risk factors are [20]:


Regarding COVID-19, an increase in these disorders is expected in the Mexican population since 30.2% of the population over 12 years of age report feelings of depression, 35.5% meet the criteria for excessive alcohol consumption, and a

considerable increase in job losses after the pandemic. Within the mental health sequelae secondary to COVID-19, different neuropsychiatric disorders have been identified that can emerge after the acute phase of the disease, as well as an increase in mood-related symptoms, especially in patients with a pre-existing psychiatric illness [20].

A study by Granados-Villalpando et al. [15] which included 203 patients, 96 having prior COVID-19 infection, reported that the most common symptoms of persistent COVID-19 were tiredness, headache, deprivation, and an inconsistent sleep pattern in patients who did not present any previous mental pathology. Meanwhile, in patients who already had some mental pathology before the COVID-19 infection, the symptoms were sleep deprivation, an inconsistent sleep pattern, fatigue, headache, memory problems, brain fog, depression, anxiety, and stress. It shows that the presence of COVID-19 and mental health conditions increases the probability of developing depression, anxiety, or stress [26].

There is a clear relationship between prolonged COVID syndrome and mental disorders [26].

#### **2.6 Obstetric complications**

SARS-CoV-2 infection affects pregnant women and fetuses, causing preterm birth, fetal distress, premature rupture of membranes, and cesarean delivery [27].

ACE-2 in the ovary-which plays several functions-could be a potential target of SARS-CoV-2 [27].

Since the architecture of the tissue changes with each renewal of the menstrual cycle, the consequences of SARS-CoV-2 infection, such as menstrual disorders and fertility problems, could be restarted from one to another [23].

#### **2.7 Male reproductive system**

Patell et al. [15] analyzed the semen of nine hospitalized patients diagnosed with COVID-19 concluding that 39.1% met the criteria for oligospermia [15].

Expression of ACE-2 and TMPRSS2 in spermatogonia, Leydig cells, and Sertoli cells makes it possible for the virus to invade the testes [23].

The problem leads to cell deterioration, interfering with testosterone release and luteinizing hormone surge, altering sperm production [23].

The released proinflammatory cytokines induce a local inflammatory response that can cause orchitis and systemic inflammation, leading to a persistent fever that ultimately affects sperm morphology, motility, and DNA [28, 29].

Batiha et al. [16] reported normal testosterone levels and decreased testosterone/ luteinizing hormone and follicle stimulating hormone/luteinizing hormone ratio without proving causality [28].

## **3. Treatments**

This section presents recommendations for treating post-COVID-19 conditions or complications [30]. In **Table 1**, we summarize the content of this section.


#### **Table 1.**

*Conditions and its treatment.*
