In addition, another study explored the
clinical characteristics and prognosis of new patients with COVID-19
combined with cardiovascular disease (CVD). A retrospective analysis was
performed on 112 COVID-19 patients with CVD admitted to the western
district of Union Hospital in Wuhan, from January 20, 2020, to February
15, 2020. They were divided into a critical group (n = 16) and general
group (n=96) according to the severity of the disease and the patients
were followed up until the clinical outcome. Observation indicators
included blood count, C-reactive protein (CRP), arterial blood gas
analysis, myocardial injury markers, coagulation function, liver and
kidney function, electrolyte, procalcitonin (PCT), type B natriuretic
peptide (BNP), blood lipids, pulmonary CT and pathogen detection.
Compared with the general group, the lymphocyte count was extremely
lower in the critical group, CRP (106.98 (81.57, 135.76) mg / L vs.
34.34 (9.55.76.54) mg / L, p <0.001) and PCT (0.20 (0.15.0.48)
µg / L vs. 0.11 (0.06.0.20) µg / L, p <0.001) were
significantly higher in critical group. The BMI of the critical group
was significantly higher than that of the general group (25.5 (23.0,
27.5) kg/m2 vs. 22.0 (20.0, 24.0)
kg/m2, p = 0.003). Patients were divided into a
non-surviving group (17, 15.18%) and a surviving group (95, 84.82%).
Among non-survivors, there were 88.24% (15/17) patients with
BMI> 25 kg/m2, which was significantly
higher than that of survivors (18.95% (18/95), p<0.001).
Compared with surviving patients, the oxygenation index (130 (102, 415)
vs. 434 (410, 444), p<0.001) was significantly lower and
lactic acid (1.70 (1.30, 3.00) mmol/L vs. 1.20 (1.10, 1.60) mmol/L,
p<0.001) was significantly higher in non-survivors. Therefore,
COVID-19 patients combined with CVD are associated with an increased
risk of mortality. Critical patients are characterized by fewer
lymphocytes. Higher BMI is more often seen in critically ill,
non-survivors. The use of angiotensin converting enzyme inhibitor and
angiotensin receptor blockers (ACEI and ARB) does not affect the
morbidity and mortality of COVID-19 combined with CVD. Aggravating
causes of death include fulminant inflammation, accumulation of lactic
acid and thrombotic events
[2].
Another study included patients with acute myocardial infarction with
ST-segment elevation (STEMI) admitted by the Accident and Emergency
Department and in whom the percutaneous coronary interventions (PCI) was
performed in Wuhan-China. The focus spanned the period since January 25,
2020, when city hospitals began instituting emergency infection
protocols to contain COVID-19. This required hospitals to suspend all
non-essential visits and adjust internal and external clinical services.
PCI nominations were in accordance with international guidelines. The
criteria included hospitalized STEMI (n=1), STEMI with unknown onset of
symptoms (n=3) and patients with cardiac arrest (n=2). The time between
the onset of the symptom and the first medical contact is defined as the
time from the beginning of the chest discomfort reported by the patient
until the moment of the first medical contact. The door-to-device time
is defined as the time of arrival from the Accident and Emergency
Department until the cable runs successfully during PCI. The time of
arrival at the catheterization device is defined as the time between the
patient’s arrival at the catheterization laboratory and the time that
the wire passes successfully. From January 25, 2020, to February 10,
2020, we observed changes in the temporal components of treatment with
STEMI among the aggregate group of 7 consecutive patients undergoing
PCI. They were compared with data from 108 patients with STEMI treated
with PCI in the previous year, from February 1, 2018, to January 31,
2019 (n = 108). These 7 patients did not suffer from COVID-19 infection
and 6 out of 7 went to our hospital during regular work hours [3].
In addition, cardiovascular metabolic comorbidities made patients more
susceptible to COVID-19 and exacerbated the infection. Thus, a study
analyzed the association of cardiovascular metabolic diseases with the
development of COVID-19. A meta-analysis of eligible studies was
performed that summarized the prevalence of cardiovascular metabolic
diseases in COVID-19 and compared the incidences of comorbidities in
Intensive Care Units (ICU)/critically ill and non-ICU/critically ill
patients. A total of six studies with 1527 patients were included in
this analysis. The proportions of hypertension, cardio-cerebrovascular
disease, and diabetes in patients with COVID-19 were 17.1%, 16.4%, and
9.7%, respectively. The incidences of hypertension,
cardio-cerebrovascular diseases and diabetes were two to three times and
twice, respectively, higher in ICU/severe cases than in non-ICU/severe
patients. At least 8.0% of patients with COVID-19 suffered the acute
cardiac injury. The incidence of acute cardiac injury was about 13 times
higher in the ICU/critically ill patients compared to non-ICU/critically
ill patients. Patients with previous cardiovascular metabolic diseases
may face an increased risk of progressing to a serious condition and
comorbidities can also greatly affect the prognosis of COVID-19.
Therefore, COVID-19 can aggravate damage to the heart [4].
Also, a systematic literature review was carried out with meta-analysis,
using three databases to evaluate clinical, laboratory, imaging and
results of cases confirmed with COVID-19. Observational studies and also
case reports were included and analyzed separately. Was performed a
meta-analysis of the random-effects model to calculate the combined
prevalence and 95% confidence interval (95% CI). 660 articles were
recovered for the period (1/1/2020 to 2/23/2020). After screening, 27
articles were selected for evaluation in full text, 19 were finally
included for qualitative and quantitative analyzes. In addition, 39 case
report articles were included and analyzed separately. For 656 patients,
fever (88.7%, 95% CI 84.5-92.9%), cough (57.6%, 40.8-74.4%) and
dyspnea (45.6%, 10.9 -80.4%) were the most prevalent manifestations.
Among the patients, 20.3% (95% CI 10.0-30.6%) required an ICU, 32.8%
had acute respiratory distress syndrome (ARDS) (95% CI 13.7- 51.8),
6.2% (95% CI 3.1 -9.3) with shock. Approximately 13.9% (95% CI
6.2-21.5%) of hospitalized patients had fatal results. COVID-19 places
an enormous burden on health services, especially in patients with
comorbidities. The ICU was necessary for approximately 20% of
polymorphic patients infected with COVID-19 and hospitalization was
associated with a fatal results above 13% [5].
Therefore, patients with COVID-19 combined with cardiovascular disease
are associated with an increased risk of mortality. Critical patients
are characterized by fewer lymphocytes. Higher BMI is more often seen in
critically ill, non-survivors. The use of ACEI/ARB does not affect the
morbidity and mortality of COVID-19 combined with CVD. Aggravating
causes of death include fulminant inflammation, accumulation of lactic
acid and thrombotic events. Therefore, cardiovascular metabolic
comorbidities made patients more susceptible to COVID-19 and exacerbated
the infection [5].
COVID-19 disease is associated with a high inflammatory load that can
induce vascular inflammation, myocarditis, and cardiac arrhythmias.
Thus, cardiovascular risk factors and conditions must be carefully
controlled according to the evidence-based guidelines [6]. Mortality
is strongly associated with cardiovascular disease, diabetes, and
hypertension. These disorders share the underlying pathophysiology
related to the renin-angiotensin system (SARS) which can be clinically
illuminating. In particular, the activity of the angiotensin-converting
enzyme 2 (ACE2) is unregulated in cardiovascular diseases, and this
enzyme is used by the coronavirus to initiate infection [6].
Cardiovascular disease and SARS pharmacological inhibition increase ACE2
levels, which can increase coronavirus virulence in the lung and heart
[7]. On the other hand, there is evidence that coronavirus infection
can decrease ACE2, leading to toxic over-accumulation of angiotensin II,
which induces acute respiratory distress syndrome and fulminant
myocarditis. Inhibition of SARS can reduce this effect [7].
In addition, there is scientific evidence that SARS-CoV-2 can chemically
bond to the heme group of hemoglobin and thus cause the release of iron
ions (Fe2+ and Fe3+) that can damage
tissues, including the lungs and heart [8]. Another important
information is that the heme group is produced by mitochondria and, in
this case, the oral or intramuscular use of Coenzyme Q10 (ubiquinone) is
strongly recommended, as it stimulates the increase in mitochondrial
production [9,10]. Therefore, the use of chelators of iron ions is
notorious, as well as the administration of Coenzyme Q10 as a treatment
for patients infected with SARS-CoV-2.