Cardiovascular Journal of Africa: Vol 31 No 6 (November/December 2020)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 6, November/December 2020 AFRICA 337
For patients with COVID-19, there are two possible
pathophysiological mechanisms: (1) type-I MI caused
by anxiety-induced catecholamine discharge, prothrombotic
system activation triggered by severe inflammatory activation,
and plaque rupture, and (2) type-II MI caused by decreased
oxygen delivery due to acute inflammation, respiratory failure
and hypoxia.7,8
Moreover, Huang et al. stated that high concentrations of
interleukin-1β, interferon-γ (IFN- γ), IFN-γ-inducible protein
10 and monocyte chemoattractant protein-1 could be observed
in COVID-19 patients, thereby leading to activated T-helper-1
cell responses.9,10 It was also suggested that invasion by the
virus of angiotensin converting enzyme-II, which is abundantly
present in myocytes and vascular endothelial cells and is also
the binding site of the coronavirus, may be the direct cause of
cardiac involvement.9
In a published study, it was reported that a total of 40%
of patients with positive test results for COVID-19 had
cardiovascular or cerebrovascular disease and 7% had the
possibility to develop acute cardiac injury. In case reports, on
the other hand, the first causes of admission to hospital due
to COVID-19 were heart failure, acute MI, myocarditis and
sudden cardiac arrest.10-12 Shi et al. found that 19.7% of patients
experienced cardiac injury, and the report showed for the first
time that cardiac injury was independently related to an increased
risk of mortality in patients with COVID-19 infection.13
It was also reported that in a significant number of patients
with COVID-19 infection, levels of high-sensitivity cardiac
troponin were increased.14 In a retrospective analysis of 191
patients hospitalised due to COVID-19, it was observed that
levels of troponin were increased in more than 50% of patients
who died.14 In other words, increasing levels of troponin in
patients presenting with COVID-19 infection is an important
indicator of mortality.14
Li et al. reported in a meta-analysis of six studies including
1 527 patients that the prevalence of CVD in patients with
COVID-19 was 16.4%.15 The prevalence of CVD was higher
in patients who required intensive care than those who did not
require it.15 It was also reported that at least 8% of the patients
were troponin positive.15
In their analysis, Guo et al. showed that while in-hospital
mortality rates of intensive care patients who were without CVD
and had normal troponin levels was 7.62%, it was 69.44% in
patients with known CVD and high troponin levels.1 In a study
evaluating 187 patients, troponin elevation, which is an indication
of myocardial injury, was observed in 52 (27.8%) patients, and
while the mortality rate was 59.6% in patients with high troponin
levels, it was 8.9% in those with normal troponin levels.1
For the first time, acute MI was identified at the autopsy
of a 53-year-old woman with chronic renal failure in
Jinyintan Hospital (data not published; obtained via personal
communication with a pathologist from the Chinese Academy
of Science).14
In this study, we present a case of MI with anterior and inferior
ST elevation on ECG, with the sudden onset of chest pain and
increasing dyspnoea while receiving treatment for COVID-19.
These patients may be hypoxic due to pneumonia, and both
catecholaminergic discharge due to stress and plaque rupture
with prothrombotic system activation induced by inflammatory
activation related to COVID-19 may develop and result in
STEMI. Moreover, in these patients, increased thrombophilia
and arterial and venous embolisms are observed.
Our case presented with HT and DM, however, there was
no history of chest pain or dyspnoea. On the fourth day of
hospitalisation, sudden onset of chest pain with ST-segment
elevation in the anteroseptal and inferior leads on ECG were
observed. The Turkish Society of Cardiology (TSC), in its
recently published expert opinion report, recommended
thrombolytic therapy as the first option during STEMI. 4 They
also recommended PPCI in cases of wide anterior wall infarcts.4
We considered PPCI in our patient because of ST elevations
in the V1-6 and inferior leads on ECG, in agreement with
the recommendations of the TSC. PPCI was performed with
coronary angiography for the LAD and right coronary arteries.
In COVID-19 patients, the incidence of CVD together
with multiple cardiovascular risk factors is high. It is difficult
to evaluate chest pain in these patients as they are isolated in
intensive care units and the number of intubated patients is high.
Moreover, ECG and TTE are performed less often due to strict
isolation of these patients. In retrospective analysis, troponin was
determined to be positive in approximately half of the deceased
patients. With co-morbid coronary artery disease and positive
troponin results, these patients were identified as a group with a
significantly higher mortality rate.
Conclusion
Serial ECG monitoring and performing echocardiography as
required in these patients in the intensive care unit could help
to diagnose STEMI or non-STEMI accurately. A true diagnosis
of MI may lead to the administration of appropriate treatment
and lowering of mortality rates. On the other hand, a diagnosis
of MI during an autopsy suggests that the reported rate of MI
diagnosis is lower than the actual rate. High levels of stress and
increased metabolism in these patients may lead to thrombosis
of several coronary arteries with the concurrent occurrence of
two different STEMIs.
References
1. Guo T, Fan Y, Chen M, et al . Cardiovascular implications of fatal
outcomes of patients with coronavirus disease 2019 (COVID-19). J Am
Med Assoc Cardiol Mar 27, 2020. [Epub ahead of print].
2. Ibanez B, James S, Agewall S, et al. ESC Scientific Document Group.
2017 ESC guidelines for the management of acute myocardial infarction
in patients presenting with ST-segment elevation: the task force for the
management of acute myocardial infarction in patients presenting with
ST-segment elevation of the European Society of Cardiology (ESC).
Eur Heart J 2018; 39: 119–177.
3. Clerkin KJ, Fried JA, Raikhelkar R, et al. Coronavirus disease 2019
(COVID-19) and cardiovascular disease. Circulation Mar 21, 2020.
[Epub ahead of print].
4. Aktoz M, Altay H, Aslanger E, et al. Türk Kardiyoloji Derneği
Uzlaşı Raporu: COVID-19 Pandemisi ve Kardiyovasküler Hastalıklar
Konusunda Bilinmesi Gerekenler. Turk Kardiyoloji Dernegi Arsivi 2020;
48(Supp1): 1–48
5. Wu Z, Mc Googan JM. Characteristics of and important lessons from
the corona virus disease 2019 (COVID-19) outbreak in China: summary
of a report of 72 314 cases from the Chinese Center for Disease Control
and Prevention. J Am Med Assoc Feb 24, 2020. [Epub ahead of print].