As the consequences of the COVID‑19 pandemic have been studied, more information has emerged about the non‑respiratory effects of coronavirus infection. Controlled studies have established that the virus causing COVID‑19, SARS‑CoV‑2, most often affects several organ systems, especially the lungs and heart of humans [1].

Signs of myocardial injury, as determined by elevated cardiac biomarkers (particularly high‑sensitivity troponin and/or creatine kinase‑MB), are common in patients with COVID‑19. In a meta‑analysis by cardiologists from Brown University (Providence, USA), which included 26 studies involving 11,685 patients with confirmed COVID‑19, the prevalence of significant myocardial injury based on cardiac enzyme levels ranged from 5% to 38%, depending on the criteria used, and averaged over 20% [2].

Similar data were obtained in a retrospective study conducted by cardiologists at Saint Luke’s Heart Institute and the University of Missouri‑Kansas City (Missouri, USA). In the study by Sammour YM et al. [3], data from 32,636 patients with COVID‑19 enrolled in the American Heart Association (AHA) COVID‑19 Cardiovascular Disease Registry were analyzed. Of the total cohort, 6,234 patients (19.4%) had cardiac troponin measured in venous blood; mean age was 68.7±16.0 years, 56.5% male, 51.5% Caucasian. A more than five‑fold elevation of cardiac troponin was recorded in 1,365 patients (21.6%) of this subgroup. In the multicenter study (55 centers), the average rate of invasive coronary angiography was 0.1% (MOR 1.5). Echocardiography with assessment of left ventricular ejection fraction (LVEF) was performed in 25.5% of cases (MOR 3.0). Intensive care unit admission was noted in 41.7% of patients (MOR 2.2). In‑hospital mortality was 20.9% (MOR 1.7). Analytical reviews of this problem have shown that significant myocardial injury, accompanied by elevated cardiac troponin (cTn), is associated with adverse outcomes in patients with SARS‑CoV‑2 infection [4]. Possible causes of cardiac injury in these conditions may include myocarditis, acute myocardial infarction (MI), stress cardiomyopathy, cardiac arrhythmia, sepsis‑related myocardial injury, pulmonary embolism, endothelial and systemic damage [5]. Among these, acute MI is the primary diagnosis that must be promptly recognized to optimize treatment and outcomes. Acute type 1 MI is a diagnosis for which established care protocols exist, including invasive treatment with coronary angiography and timely revascularization to optimize outcomes, especially in ST‑segment elevation MI (STEMI) and high‑risk non‑ST‑segment elevation MI (NSTEMI) [6]. In patients with COVID‑19, mere suspicion of acute MI poses an additional clinical challenge: the risk of unwarranted diagnostic and therapeutic interventions increases because several COVID‑associated changes may mimic MI in the absence of obstructive coronary artery disease (MINOCA) [7].

Morphological studies during the COVID‑19 period have shown that in patients with acute coronary syndrome (ACS), in addition to plaque rupture and thrombosis, other pathogenetic factors contribute to acute myocardial injury in COVID‑19. According to members of the ESC Working Group on Cellular Biology of the Heart, the main causes of cardiac injury in COVID‑19 are:a) coagulopathy with micro‑ (and, to a lesser extent, macro‑) vascular occlusion;b) direct infection of myocardial cells;c) effects of cytokine storm;d) mechanisms related to coagulopathy derivatives [8].

The likely mechanisms of myocardial injury in COVID‑19 are multifactorial and include:

According to specialists from an Iranian interventional cardiology center, the development of STEMI in patients with COVID‑19 is characterized by specific angiographic findings — massive and multi‑vessel thrombosis, often independent of atherosclerotic coronary artery disease — which is associated with a poor prognosis and creates new therapeutic challenges [9]. Baseline demographic, clinical, and procedural characteristics of patients were obtained from national registries of COVID‑19‑associated MI, in particular the North American COVID‑19 Myocardial Infarction Registry. Univariate logistic regression was performed using candidate predictor criteria, and multivariate logistic regression using backward stepwise selection was conducted for independent predictors of in‑hospital mortality. In‑hospital mortality occurred in 118 of 425 (28%) patients [10]. Eight clinical variables identifiable at the time of STEMI diagnosis (respiratory rate >35/min, cardiogenic shock, oxygen saturation <93%, age >55 years, presence of infiltrates on chest radiography, history of cardiovascular disease, diabetes mellitus, and dyspnea) were included in a model, each assigned a weighted numerical value. In‑hospital mortality increased exponentially with increasing integrated risk score (Cochran‑Armitage test). The prognostic model demonstrated good discriminatory ability (c‑statistic = 0.81) and acceptable calibration (Hosmer‑Lemeshow test). Increasing risk category was directly associated with higher in‑hospital mortality — from 3.6% in the low‑risk group to 60% in the very high‑risk group [10].

Canadian cardiologists from the Department of Cardiology, University of Saskatchewan College of Medicine (Shavadia JS et al.) analyzed data from the North American COVID‑19 Myocardial Infarction Registry, including 853 patients with STEMI and COVID‑19 from the United States, of whom 112 (13%) were enrolled in the registry [11]. The registry included adults (≥18 years) hospitalized from March 1, 2020, to December 31, 2021, meeting the following inclusion criteria: (1) ST‑segment elevation in 2 contiguous leads (or new left bundle branch block), (2) ischemic equivalent, and (3) confirmed or suspected COVID‑19 infection. Covariates included year of enrollment, country, sex, age <66 years, overweight or obesity (by BMI), Caucasian race, current smoking status, hypertension, diabetes mellitus, prior MI, stroke or transient ischemic attack, signs of congestive heart failure, presence of pulmonary infiltrates, and development of shock during PCI. Clinical outcomes of patients enrolled in the USA (n=741) compared to Canada (n=112) were as follows: in‑hospital mortality 28% (n=209) vs. 16% (n=18); stroke rate 1.8% (n=13) vs. 0% (n=0); recurrent MI 2% (n=15) vs. 0% (n=0). The composite endpoint (death, stroke, or recurrent MI) occurred in 30% of US patients (n=225) and 16% of Canadian patients (n=18). Analysis showed that the risk of in‑hospital mortality was significantly higher in unvaccinated compared to vaccinated patients with STEMI–COVID (OR 4.7). Currently, as worldwide, the COVID‑19 pandemic requires the implementation of hospital care systems using an Incident Management System to ensure timely access to reperfusion therapy. Primary PCI was the monitored reperfusion strategy, with no difference in door‑to‑balloon (D2B) time (see Table 1).

Table 1. Reperfusion in patients undergoing angiography

ProcedureCanada, n (%)USA, n (%)Primary PCI78 (80)415 (70)Urgent PCI9 (9.2)24 (4.0)Thrombolytics3 (3.1)22 (3.7)Medical therapy only7 (7.1)122 (21)Coronary artery bypass grafting1 (1)10 (1.8)

Data are presented as n (%) and were compared using Pearson’s χ² and Fisher’s exact tests as appropriate. The authors concluded that differences in incidence and reperfusion strategies for STEMI–COVID patients were evident between the USA and Canada, with no recorded in‑hospital deaths in Canada. Vaccination, regardless of region, appeared to be associated with a significant reduction in the risk of in‑hospital mortality [11].

In an analysis performed by the TIMI Study Group (Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA) [12], data from the AHA COVID‑19 Cardiovascular Disease Registry from January 14 to November 30, 2020, collected in 105 medical centers, were used. Patient characteristics, resource utilization, and outcomes were summarized and compared by country. Among 15,621 COVID‑19 cases, 54 (0.35%) patients with acute MI were hospitalized. Among STEMI patients, the majority (n=40.7%) underwent transthoracic echocardiography, but only a minority (n=27.5%) underwent coronary angiography. Half of all patients with COVID‑19 and STEMI (n=27.5%) received no primary reperfusion therapy. The incidence of shock of any etiology was significantly higher in STEMI patients compared to non‑STEMI patients (47% vs. 14%). Similarly, STEMI patients more frequently had cardiac arrest (22% vs. 4.8%), acute heart failure (17% vs. 1.4%), and need for renal replacement therapy (11% vs. 4.3%). Differences were statistically significant for all compared parameters. In‑hospital death occurred in 41% of STEMI patients compared to 16% of non‑STEMI patients (p <0.05). The authors concluded that STEMI in hospitalized COVID‑19 patients is rare but associated with adverse in‑hospital outcomes [12].

Initial findings from the North American COVID‑19 Myocardial Infarction Registry were presented by Garcia S et al. [13], from the Minneapolis Heart Institute Foundation (Minneapolis, MN). The registry included patients with STEMI and confirmed COVID‑19 (Group 1) or suspected COVID‑19 (Group 2). A control group (Group 3) comprised age‑ and sex‑matched STEMI patients without COVID‑19 treated in the pre‑pandemic period (2015–2019). Patients were matched 2:1 to the STEMI+COVID group and used to compare treatment strategies and clinical outcomes. The primary outcome was in‑hospital death, stroke, recurrent MI, or unplanned repeat revascularization. As of December 6, 2020, the NACMI registry included 1,185 patients (230 with confirmed COVID‑19, 495 with suspected COVID‑19) and 460 control patients. Patients with COVID‑19 were more often from ethnic minorities (Hispanic 23%, Black 24%) and had a higher prevalence of diabetes mellitus (46%). COVID‑19 patients more frequently had cardiogenic shock (18%) but less often underwent invasive angiography (78%) (all p <0.001 vs. controls). Among COVID‑19 patients who underwent angiography, 71% received primary PCI, and 20% received medical therapy alone (both significantly different from controls). The primary outcome occurred in 36% of COVID‑19 patients, 13% of PUI patients, and 5% of control patients (p <0.001 vs. controls). The authors concluded that patients with COVID‑19 and STEMI represent a high‑risk group with persistently poor clinical outcomes. Primary PCI is technically feasible and remains the dominant reperfusion strategy in these patients, consistent with current clinical guidelines.

Data from the Swiss Cardiovascular SARS‑CoV‑2 Consortium were analyzed in a study by staff of the Department of Cardiology, Bern University Hospital Inselspital, Bern, Switzerland, Koskinas KC et al. [14]. From March 2020 to February 2022, 538 patients were enrolled, including 122 with acute cardiac conditions and 416 controls. Mean age was 68.0±14.7 years, and 75% were predominantly male. Compared to controls, SARS‑CoV‑2‑positive patients more often had acute heart failure (35% vs. 17%) or sustained arrhythmia (31% vs. 9%), but less often had ACS (26% vs. 53%) or severe aortic stenosis (4% vs. 18%). Mortality was significantly higher in cases vs. controls in‑hospital (16% vs. 1%), at 30 days (19.0% vs. 2.2%), and at 1 year (28.7% vs. 7.6%). This was driven primarily (up to 30 days) and exclusively (at 1 year) by higher non‑cardiovascular mortality and was accompanied by greater deterioration of renal function. The researchers concluded that patients hospitalized for acute cardiac conditions with SARS‑CoV‑2 infection had higher all‑cause mortality throughout one year of follow‑up. The results highlight the need for early and comprehensive multidisciplinary management with simultaneous correction of both cardiac and non‑cardiac disorders, as well as the need for long‑term follow‑up of patients with manifest cardiovascular disease complicated by SARS‑CoV‑2 infection.

Mortality of STEMI patients hospitalized during the COVID‑19 outbreak in Italy was analyzed using a nationwide administrative database. The study included STEMI patients hospitalized during the lockdown period (March 11 – May 3, 2020), with comparison to the same time intervals in the previous five years. The study was conducted by staff of the Department of Cardio‑Thoracic and Vascular Medicine and Surgery, San Camillo‑Forlanini Hospital (Rome, Italy) [15]. The observed 30‑day and 6‑month all‑cause mortality rates among STEMI patients with and without COVID‑19 during the lockdown were compared to expected mortality based on the 5‑year trend. During the study period, 32,910 hospitalizations for STEMI were recorded in Italy. In 2020, 4,048 STEMI patients were hospitalized, of whom 170 (4.2%) had confirmed COVID‑19 and 3,878 (95.8%) did not. According to the 5‑year trend analysis, expected 30‑day and 6‑month all‑cause mortality in 2020 was 9.2% and 12.6%, respectively, while observed mortality was 10.8% and 14.4%. After excluding STEMI patients with confirmed COVID‑19, mortality rates matched the expected 5‑year values. After multivariate adjustment, the presence of COVID‑19 remained an independent predictor of all‑cause mortality at 30 days (adjusted OR 4.5) and 6 months (OR 3.6).

In a study conducted under the auspices of the Paris Cardiovascular Research Center PARCC (Paris, France) in 2021, data from a nationwide survey in France were used. Information on STEMI patients admitted from 65 centers for emergency revascularization from March 1 to May 31, 2020, was compared with the same period in 2019. The primary endpoint was in‑hospital mortality or the development of fatal or non‑fatal mechanical complications of acute MI. A total of 6,306 patients were included. During the peak of the pandemic, the number of STEMI hospitalizations decreased by 13.9±6.6% per week. In 2020, the delay from symptom onset to PCI was longer than in 2019 (270 min [IQR 150–705] vs. 245 min [140–646]). The increase in total ischemic time was primarily due to prolongation of the interval from symptom onset to first medical contact (121 min [60–360] in 2020 vs. 150 min [62–420] in 2019). In 2020, the rate of mechanical complications of MI was higher (1.7% vs. 0.9%), leading to an increase in the primary endpoint — 129 patients (7.6%) in 2020 vs. 112 patients (5.6%) in 2019. No significant differences were found in the rates of orotracheal intubation, in‑hospital cardiac arrest, ventricular arrhythmias, or cardiogenic shock. The authors concluded that during the first peak of the COVID‑19 pandemic in France, there was a decrease in hospitalizations for MI, associated with increased ischemic time due exclusively to delays in seeking medical attention, and accompanied by a rise in mechanical cardiovascular complications [16].

In a study led by the head of cardiology at Westchester Medical Center, New York Medical College (Valhalla, NY, USA), a national inpatient database for 2020 was used to identify all adult hospitalizations with a primary diagnosis of STEMI with and without concomitant COVID‑19. The analysis included data on 159,890 STEMI hospitalizations, of which 2,210 (1.38%) had confirmed COVID‑19. After propensity score matching, patients with STEMI and COVID‑19 had significantly higher in‑hospital mortality compared to patients without COVID‑19 (17.8% vs. 9.1%; OR 1.96). COVID‑19 patients less often underwent PCI on the day of admission (63.6% vs. 70.6%), had a trend toward lower overall PCI rates (74.9% vs. 80.2%), and significantly lower rates of CABG before discharge (3.0% vs. 6.8%). There were no significant differences between groups in the rates of cardiogenic shock, need for mechanical circulatory support, ECMO, cardiac arrest, acute kidney injury, need for dialysis, major bleeding, or stroke.

In STEMI patients with confirmed COVID‑19, undergoing PCI on the day of admission was associated with significantly lower in‑hospital mortality (adjusted OR 0.42). At the same time, the overall cohort of STEMI patients with COVID‑19 had approximately twice the in‑hospital mortality and a lower likelihood of undergoing PCI on the day of admission and of receiving revascularization (PCI and/or CABG) during hospitalization compared to STEMI patients without COVID‑19 [17].

The COVID‑19 pandemic has significantly impacted the functioning of healthcare systems worldwide. Several studies have demonstrated the adverse impact of COVID‑19 on the prognosis of STEMI patients, including those admitted to cardiac intensive care units. In Japan, at the Academic Center for International Medical Assistance in Tokyo, a retrospective observational study was conducted to assess the impact of the COVID‑19 pandemic on the management and outcomes of STEMI patients. Data from 398 patients hospitalized from January 1, 2018, to March 10, 2021, were sequentially included. Hospitalization rates, clinical characteristics, management strategies, and outcomes were compared before and after March 11, 2020 — the date the WHO declared the pandemic.

According to the data, during the COVID‑19 pandemic, the number of STEMI hospitalizations decreased by 10.7% compared to the previous year (117 vs. 131 cases). During the pandemic, there was a significant increase in the proportion of late presentations (26.5% vs. 12.1%) and a significant prolongation of the time from symptom onset to first medical contact (241 min [IQR 70–926] vs. 128 min [66–493]) and the door‑to‑balloon time (72 min [61–128] vs. 60 min [43–90]; p <0.001). In‑hospital mortality was higher during the pandemic than in the pre‑pandemic period (9.4% vs. 5.0%), although the difference did not reach statistical significance. The authors concluded that the COVID‑19 pandemic significantly affected STEMI patients in Tokyo, leading to a moderate decrease in hospitalizations, a marked increase in late presentations and delays in reperfusion therapy, and a trend toward increased in‑hospital mortality. In these conditions, the emergency care system for STEMI patients in Japan requires reorganization [18].

In Israel, a retrospective observational study was conducted using the Clalit Health Services database, covering patients hospitalized for acute MI in several hospitals. The study was performed by authors from the Planning and Strategy Department (Tel Aviv) and the Ruth and Bruce Rappaport Faculty of Medicine, Technion – Israel Institute of Technology (Haifa, Israel). Clinical characteristics and 30‑day mortality were analyzed during three five‑week phases of the first wave of the COVID‑19 pandemic in Israel: before lockdown (n=702), during lockdown (n=584), and after lockdown easing (n=669), with comparison to the same periods in 2018 and 2019. Patients were stratified by MI type: STEMI and NSTEMI. During the lockdown, the number of hospitalizations for acute MI was 17% lower than in the pre‑lockdown period (rate ratio 0.83), and 22% and 31% lower than in the corresponding periods of 2018 and 2019, respectively. The decrease in hospitalizations was primarily due to a reduction in NSTEMI patients (by 26% compared to the pre‑lockdown period in 2020). In the post‑lockdown period, the number of hospitalizations for STEMI and NSTEMI remained moderately reduced compared to the same periods in 2018 and 2019. However, 30‑day mortality rates did not differ across any of the time intervals analyzed. The authors concluded that during the first lockdown and after its lifting, a significant reduction in acute MI hospitalizations occurred in Israel, without changes in 30‑day mortality [19].

A retrospective analysis examined acute MI hospitalizations recorded from December 30, 2018, to May 16, 2020, in 49 hospitals of the Providence – St. Joseph Health system operating in six US states (Alaska, Washington, Montana, Oregon, California, and Texas). Patients ≥18 years with a primary discharge diagnosis of acute MI (STEMI or NSTEMI) were included. Segmented regression analysis was used to assess changes in hospitalization rates. Three time periods were identified: pre‑pandemic (12/30/2018–2/22/2020), early COVID‑19 (2/23/2020–3/28/2020), and late COVID‑19 (3/29/2020–5/16/2020). In‑hospital mortality was risk‑adjusted using observed‑to‑expected (O/E) mortality ratios and multivariate models. The cohort included 15,244 acute MI hospitalizations (4,955 STEMI [33%] and 10,289 NSTEMI [67%]) in 14,724 patients (mean age 68±13 years; 66% male). From February 23, 2020, acute MI hospitalizations decreased by 19.0 cases per week over five weeks (early COVID‑19 period), followed by an increase of +10.5 cases per week in the late period. No significant changes in demographics, cardiovascular comorbidities, or treatment strategies were observed between periods. In the early COVID‑19 period, the risk of in‑hospital mortality increased (OR 1.27), disproportionately in STEMI patients (OR 1.96). In the late period, the overall O/E mortality ratio for acute MI remained elevated (1.23), with the largest contribution again from STEMI patients: the O/E ratio increased sequentially from the pre‑pandemic (1.48) to early (1.96) and late (2.40) COVID‑19 periods. After adjustment for demographic and clinical factors, STEMI patients in the late period still had an elevated mortality risk (OR 1.52). In contrast, the O/E mortality ratio for NSTEMI patients remained consistently below 1.0 throughout all periods.

Thus, in the Providence – St. Joseph Health system, both a significant decline in acute MI hospitalizations and worsening outcomes, primarily among STEMI patients, were observed during the early and late periods of the COVID‑19 pandemic [20].

Therefore, in patients with confirmed COVID‑19 infection, the prevalence of acute myocardial injury, defined by elevated biochemical markers of myocardial damage, ranges from 5% to 38%, depending on clinical characteristics and disease severity. The COVID‑19 pandemic has significantly impacted the delivery of care to STEMI patients worldwide, including the availability and organization of reperfusion therapy. According to national and international registries, significant changes occurred in the cardiac care system for ACS patients in general and STEMI in particular during the pandemic. Most studies reported a decrease in hospitalizations for severe coronary syndrome compared to the pre‑pandemic period, with overall hospitalizations declining by about 20%. Available data suggest that both the frequency of acute MI hospitalizations and clinical outcomes changed during the early and late periods of the COVID‑19 pandemic. Despite these changes, primary PCI remained the leading reperfusion strategy, and door‑to‑balloon times in several studies did not fundamentally differ from pre‑pandemic levels.

The impact of COVID‑19 infection on treatment strategies and clinical outcomes of hospitalized patients with acute MI was evaluated in several controlled observational studies. One of the largest studies was conducted by the University of Leeds (UK) research group, aiming to assess changes in hospitalization rates, treatment strategies, and 30‑day mortality in patients with acute MI during the COVID‑19 pandemic [25].

The analysis covered hospitalizations for acute MI in 99 hospitals within the national myocardial infarction audit. Hospitalizations were classified in real time as STEMI or NSTEMI from January 1, 2019, to May 22, 2020. Seven‑day moving averages with seasonal adjustment were used to analyze temporal trends. After the introduction of the national lockdown in the UK (March 23, 2020), the median daily number of hospitalizations decreased significantly, more pronounced for NSTEMI (from 69 to 35; IRR 0.51) than for STEMI (from 35 to 25; IRR 0.74), with the lowest values around April 19, 2020.

Patients hospitalized during the lockdown were slightly younger and more often had diabetes mellitus and cerebrovascular disease. For STEMI, primary PCI was performed more frequently during the pandemic period (81.8% vs. 78.8%), with extremely low use of thrombolytic therapy. For NSTEMI, there was a significant reduction in time to coronary angiography (26.2 vs. 64.0 hours), a decrease in length of stay (from 4 to 2 days), with high adherence to secondary prevention pharmacotherapy (>94%). However, 30‑day mortality increased for NSTEMI (from 5.4% to 7.5%; OR 1.41) but decreased for STEMI (from 10.2% to 7.7%; OR 0.73). The authors concluded that the pandemic was associated with a marked reduction in acute MI hospitalizations, with patients presenting later and having more severe disease, especially for NSTEMI.

Similar results were obtained in a Spanish multicenter national retrospective registry including data from 75 specialized STEMI care centers across Spain [26]. Patients were divided into pre‑pandemic and pandemic cohorts with 30‑day follow‑up. Over 94% of patients in both groups received primary PCI. During the pandemic, there was a significant prolongation of total myocardial ischemic time (233 [150–375] vs. 200 [140–332] minutes), with no difference in first medical contact‑to‑reperfusion time. The number of patients with suspected STEMI decreased by 27.6%, and the number of confirmed STEMI cases decreased by 22.7%. In‑hospital mortality was higher during the pandemic (7.5% vs. 5.1%), and the association remained after multivariate adjustment (RR 1.88). The authors noted that the combination of STEMI and SARS‑CoV‑2 infection was relatively rare but was associated with a twofold increase in in‑hospital mortality despite unchanged reperfusion strategies.

Data from the United States, obtained by the University of Rochester School of Medicine research group based on an analysis of Medicare hospitalizations from 2016–2020, demonstrated that increasing hospital COVID‑19 burden was not associated with worse outcomes or lower revascularization rates among STEMI patients, including in racial and ethnic subgroups [27]. At the same time, for NSTEMI during periods of high COVID‑19 burden, increased in‑hospital mortality and decreased revascularization rates were observed.

Initial data from the NACMI registry, presented by Garcia S et al. [13], included patients with STEMI and confirmed COVID‑19, those under investigation (PUI), and a matching pre‑pandemic control group. The primary composite endpoint (in‑hospital death, stroke, recurrent MI, or unplanned revascularization) occurred in 36% of COVID‑19 patients, 13% of PUI patients, and 5% of control patients. COVID‑19 patients more often had cardiogenic shock and were more likely to not undergo invasive treatment, but when coronary angiography was performed, PCI remained the dominant reperfusion strategy. The authors concluded that patients with COVID‑19 and STEMI are a high‑risk group with persistently poor clinical outcomes, and primary PCI remains technically feasible and the preferred reperfusion method, consistent with current guidelines [7].

In Turkey, researchers from the Department of Cardiology, University of Health Sciences Turkey, Şişli Hamidiye Etfal Training and Research Hospital (Istanbul, Turkey) conducted a retrospective study to evaluate the impact of COVID‑19 infection on coronary microcirculation in ACS patients undergoing PCI [28]. The analysis included 165 ACS patients hospitalized from March 1 to June 30, 2020, of whom 26 (15.7%) had confirmed SARS‑CoV‑2 infection. PCR testing was performed in the presence of clinical symptoms or typical CT findings.

To assess reperfusion success, angiographic TIMI frame count (corrected TIMI frame count, cTFC) and myocardial blush grade (MBG) were used — validated markers of coronary blood flow and myocardial perfusion. cTFC is a continuous measure of coronary flow velocity with high reproducibility, and MBG reflects the effectiveness of microvascular perfusion and is a prognostic factor for mortality after primary PCI [29].

COVID‑19 patients had higher cTFC values, indicating slower coronary blood flow, and significantly lower MBG grades (0–1), indicating severe microvascular perfusion impairment. Peak troponin I levels were significantly higher in the COVID‑19 group compared to patients without infection (27,335 vs. 15,959 ng/dL). In addition, COVID‑19 patients more often had reduced LVEF. In‑hospital mortality was significantly higher in the COVID‑19 group (38.4% vs. 7.2%).

Logistic regression analysis showed that cTFC and LVEF were independently associated with in‑hospital mortality in patients with COVID‑19 and ACS. Correlation analysis showed that cTFC was positively correlated with C‑reactive protein level (r=0.340) and peak troponin I (r=0.369). The authors concluded that COVID‑19 infection is associated with slower coronary blood flow and severe microvascular perfusion impairment in ACS patients after primary PCI.

Despite these unfavorable pathophysiological changes, professional societies, including the Society for Cardiovascular Angiography and Interventions (SCAI) and the European Association of Percutaneous Cardiovascular Interventions (EAPCI), recommended considering primary PCI as the standard reperfusion strategy for STEMI patients during the COVID‑19 pandemic [30, 31].

In‑hospital outcomes of STEMI patients undergoing PCI during the pandemic were further analyzed in the French national PCI registry (Rangé G et al.) [32]. The study included 2,064 STEMI patients: 1,942 in the pre‑lockdown period and 122 during lockdown restrictions. During the lockdown, the average monthly number of STEMI hospitalizations decreased by 12% (139 vs. 122 cases per month). A significant increase in symptom‑to‑first medical contact time was observed in patients who self‑presented to the emergency department (238 vs. 450 minutes).

During the lockdown, there were higher rates of in‑hospital major adverse cardiovascular events (MACE: death, stent thrombosis, recurrent MI, unplanned revascularization, stroke, major bleeding) and in‑hospital mortality (12.3% vs. 7.7%, and 8.2% vs. 4.9%, respectively), but the differences did not reach statistical significance. The authors concluded that the COVID‑19 outbreak in France was associated with a decrease in STEMI hospitalizations, increased delays in seeking medical care, and a trend toward worse in‑hospital outcomes, despite the continued use of primary PCI.

STEMI patients treated during the COVID‑19 pandemic sometimes require longer time to achieve reperfusion. Delayed reperfusion therapy may increase the risk of out‑of‑hospital cardiac arrest (OHCA) in this patient population. Limited access to medical care, delayed presentation, and healthcare system overload during the pandemic are considered possible factors contributing to increased OHCA risk in STEMI.

Polish cardiologists from the Center for Invasive Cardiology, Electrotherapy and Angiology (Nowy Sącz, Poland) conducted a retrospective study to evaluate the impact of the COVID‑19 pandemic on the timeliness of care and periprocedural outcomes in patients with STEMI complicated by OHCA [33]. The analysis included 5,501 STEMI patients with OHCA who underwent primary PCI with stent implantation. To minimize the effect of non‑randomized design, propensity score matching was used, resulting in 740 pairs of patients treated before and during the COVID‑19 pandemic.

The authors found no significant differences in in‑hospital mortality or periprocedural complication rates between the groups. However, patients treated during the pandemic had a statistically significant increase in time from first medical contact to coronary angiography (101.4±109.8 min vs. 88.8±61.5 min) and a trend toward longer pain‑to‑angiography intervals (227.9±231.4 min vs. 207.3±192.8 min). The authors concluded that despite comparable periprocedural outcomes, treatment of STEMI patients with OHCA during the pandemic was associated with longer delays to reperfusion.

In a Chinese‑American study conducted by specialists from the Department of Global Health, Peking University School of Public Health, and the Department of Health Policy and Management, University of Maryland, the impact of the COVID‑19 pandemic on hospitalizations and quality of specialized care for MI patients was assessed [34]. The primary endpoint was the number of MI readmissions; secondary endpoints were quality of care indicators. Daily hospitalizations during and after the peak of the pandemic were 53% and 38% of the rates in the same period of 2019, respectively. A gap persisted between expected and actual hospitalizations, and some deaths were associated with patients avoiding seeking medical care. In addition, in 2020, door‑to‑balloon time increased (from 17.5 to 34.0 min) and the rate of PCI decreased (from 71.3% to 60.1%).

Data from the AHA COVID‑19 Cardiovascular Disease Registry, analyzed by the TIMI research group, included hospitalizations for COVID‑19 from January 14 to November 30, 2020, across 105 medical centers [12]. Of 15,621 COVID‑19 hospitalizations, STEMI was diagnosed in 54 patients (0.35%). The majority of STEMI patients underwent transthoracic echocardiography, but coronary angiography was performed in less than one‑third, and 27.5% of patients received no reperfusion therapy.

Patients with STEMI and COVID‑19 had significantly more severe complications than non‑STEMI patients, including shock of any etiology (47% vs. 14%), cardiac arrest (22% vs. 4.8%), acute heart failure (17% vs. 1.4%), and need for renal replacement therapy (11% vs. 4.3%). In‑hospital mortality in STEMI patients reached 41% compared to 16% in non‑STEMI patients. The authors concluded that STEMI in hospitalized COVID‑19 patients is relatively rare but associated with an extremely poor prognosis. The low rate of coronary angiography and primary reperfusion in this group underscores the need to adapt healthcare systems to ensure timely and modern treatment of STEMI patients during a pandemic.

In a multicenter Polish study conducted by staff of the hospital in Końskie (Poland), 29,915 STEMI patients were analyzed, of whom 3,139 (10.5%) underwent aspiration thrombectomy [35]. COVID‑19 infection was confirmed in 311 patients (10.8%). The study compared clinical characteristics, angiographic features, and outcomes in STEMI patients with and without COVID‑19. Multivariate logistic regression was used to identify factors associated with thrombectomy.

COVID‑19(+) patients more often had severe clinical status on admission, including Killip class IV heart failure (12.3% vs. 5.8%), and a higher rate of pre‑hospital cardiac arrest (8.0% vs. 4.8%). TIMI‑3 flow after primary PCI was achieved less often in COVID‑19(+) compared to COVID‑19(−) patients (80.5% vs. 87.1%). Periprocedural mortality did not differ significantly between groups. Multivariate analysis showed that the presence of COVID‑19 was an independent predictor of the need for aspiration thrombectomy (OR = 1.23). The authors concluded that STEMI patients with COVID‑19 have more severe clinical status and higher thrombotic burden, and PCI efficacy in this group is lower despite more intensive antithrombotic therapy.

Of particular interest are data from a multicenter retrospective study covering clinics in Italy, Lithuania, Spain, and Iraq, conducted by researchers at the Baylor University Medical Center (Dallas, USA) [36]. The analysis included 78 patients with symptomatic COVID‑19 and STEMI hospitalized from February 1 to April 15, 2020. Median age was 65 [58–71] years, and most had significant comorbidities. During hospitalization, 10% of patients developed acute respiratory distress syndrome, and 18% required invasive mechanical ventilation. Primary PCI was performed in 19 patients (24%), while 59 (76%) received fibrinolytic therapy. In patients who underwent primary PCI, stent thrombosis was diagnosed in 21% of cases, and in‑hospital mortality reached 26%. In the fibrinolysis group, successful reperfusion was achieved in 85% of patients, but the rate of hemorrhagic stroke was high (9%). The authors highlighted the unusually high rate of early stent thrombosis in patients with COVID‑19 and STEMI, indicating the need to revise antithrombotic strategies in this patient population.

The efficacy and safety of primary PCI in patients with STEMI and concomitant COVID‑19 infection were also analyzed in a single‑center observational study by interventional cardiologists at Barts Heart Centre, London [37]. COVID‑19(+) patients had significantly higher thrombotic burden, including multi‑vessel coronary thrombosis, more frequent use of aspiration thrombectomy and glycoprotein IIb/IIIa inhibitors. Biochemically, these patients had higher troponin T, D‑dimer, and C‑reactive protein levels with lymphopenia. LVEF and myocardial perfusion grade were significantly lower than in patients without COVID‑19. Moreover, higher doses of heparin were required to achieve target activated partial thromboplastin time (aPTT). STEMI patients with COVID‑19 more often required intensive care and had more severe disease. The authors concluded that COVID‑19 infection is accompanied by a marked shift in hemostatic balance toward hypercoagulation, leading to high thrombotic burden and worse outcomes.

The main findings of British interventional studies were developed in an editorial in the Journal of the American College of Cardiology (September 2020), in which Dauerman H.L. noted that primary PCI in patients with COVID‑19 and STEMI is technically more challenging and requires increased caution [38]. Massive coronary thrombotic burden (modified thrombus grade 4–5) was found in 75% of COVID‑19(+) STEMI patients compared to 31.4% of patients without COVID‑19. Multi‑vessel thrombosis and early stent thrombosis were also significantly more common.

Despite the higher thrombotic burden, in‑hospital mortality in British cohorts of COVID‑19(+) STEMI patients was moderately higher than in COVID‑19(−) patients (17.9% vs. 6.5%), which differs from some US and Italian studies where mortality reached 40–75% [40, 41]. However, about one‑quarter of COVID‑19(+) patients had cardiac arrest, underscoring the extreme severity of myocardial involvement.

The high thrombotic burden in patients with STEMI and COVID‑19 is likely due to the marked systemic inflammatory response characteristic of SARS‑CoV‑2 infection. It is accompanied by activation of endothelium, platelets, leukocytes, and vascular smooth muscle cells, as evidenced by elevated C‑reactive protein and D‑dimer levels [43–45]. The association between viral infections (particularly influenza) and increased MI risk has been described previously [46, 47], but COVID‑19 has a more aggressive inflammatory and thrombogenic potential, leading to thrombosis in multiple vascular beds.

The development of hypercoagulability in severe COVID‑19 patients is confirmed by elastography and clinical observations, demonstrating an increased incidence of venous thrombosis, pulmonary embolism, ischemic stroke, and disseminated intravascular coagulation [44, 48, 49]. These data indicate the need to revise and individualize antithrombotic therapy in patients with COVID‑19, especially those who are critically ill or have concomitant ACS [50].

In comments by French authors from the European Hospital Georges Pompidou (Department of Cardiology, Paris, France) [51], based on data from Choudry FA et al. (2020), it is emphasized that the optimal anticoagulation regimen for STEMI patients with concomitant COVID‑19 undergoing PCI remains uncertain. The authors note that in clinical practice, intravenous low‑molecular‑weight heparin (LMWH), particularly enoxaparin, may have several advantages over unfractionated heparin (UFH), including a more predictable dose‑response relationship, stable anticoagulant activity, and no need for constant laboratory monitoring and dose adjustment. This makes LMWH a potentially attractive alternative to UFH in combination with dual antiplatelet therapy, especially in view of alignment with current STEMI guidelines [7, 52, 78] and proven efficacy of LMWH in venous thromboembolic complications in COVID‑19 patients [44].

The problem of choosing the optimal strategy and method of revascularization for STEMI occurring during COVID‑19 was discussed in detail in a review by American authors Yerasi C et al. (2020) [53], from the Department of Interventional Cardiology, MedStar Washington Hospital Center (USA). The authors noted that at the beginning of the pandemic, there were no randomized trials directly comparing different treatment strategies for STEMI in the setting of COVID‑19. As a guide, recommendations from Chinese specialists in Sichuan Province [54] proposed fibrinolytic therapy for STEMI patients with symptom duration <12 hours and performing PCI only after obtaining a negative SARS‑CoV‑2 test. This approach was based on assessing the risk of infection spread during invasive procedures and assumed conservative management until respiratory status stabilized.

However, this strategy proved difficult to implement in clinical practice for several reasons. A significant proportion of patients had contraindications to fibrinolysis (prior ischemic or hemorrhagic stroke, active bleeding, advanced age, multiorgan failure, cytokine storm in COVID‑19) [43]. Moreover, in patients with ECG signs of STEMI, alternative causes of ST‑segment elevation were often found, including Takotsubo syndrome, myopericarditis, and spontaneous coronary artery dissection, complicating clinical interpretation and treatment decisions [55, 56]. Fibrinolytic use was also associated with increased healthcare resource utilization due to longer hospital stays and the need for intensive monitoring.

Pre‑pandemic data from 29,190 STEMI patients in 229 hospitals participating in the Get With The Guidelines — Coronary Artery Disease (GWTG-CAD) program showed that in‑hospital mortality with fibrinolysis was higher than with primary PCI (4.6% vs. 3.3%), length of stay was longer (4 vs. 3 days), and the proportion of patients staying >4 days reached 39% vs. 28% in the primary PCI group [57]. Additional concern came from pandemic‑period data showing that approximately 31% of COVID‑19 patients develop acute respiratory distress syndrome, which may be exacerbated by the increased risk of alveolar hemorrhage with thrombolytic therapy [43, 58].

A review by American researchers from the Georgia Heart Institute [59] emphasizes that primary PCI remains the first‑line reperfusion strategy for STEMI in most countries, although the proportion of fibrinolysis‑oriented strategies in current practice varies from 2% to 13% [60]. During the COVID‑19 pandemic, there were significant reperfusion delays compared to the pre‑pandemic period, caused by late patient presentation, heightened infection control measures, potential risk to healthcare personnel, and increased emergency department waiting times, leading to prolonged door‑to‑balloon times. In these circumstances, broader use of fibrinolytic therapy in certain STEMI patient subgroups was discussed [6].

Similar conclusions were presented in a review by interventional cardiologists from the Manchester Heart Centre (UK) [61], emphasizing that despite the proven superiority of PCI over fibrinolysis and its status as the gold standard for STEMI treatment in Western countries, pharmacoinvasive strategies continue to be used in some regions. These approaches were studied in detail in the randomized STREAM trial [62], in which a pharmacoinvasive strategy (fibrinolysis followed by PCI 6–24 hours later) was non‑inferior to primary PCI when an unavoidable delay to invasive treatment was present, although it was associated with a higher risk of intracranial hemorrhage.

Thus, during the COVID‑19 pandemic, delayed patient presentation for STEMI, organizational constraints, increased infection risk, and prolonged door‑to‑balloon times contributed to the reappraisal of reperfusion strategies. Despite a temporary expansion of indications for pharmacoinvasive approaches in some regions, primary PCI retained its status as the preferred revascularization method. At the same time, patients with STEMI and COVID‑19 had high thrombotic burden and a lower rate of achieving TIMI‑3 flow after PCI, despite more intensive antiplatelet and anticoagulant therapy. These features underscore the need for further research to optimize antithrombotic and revascularization strategies in patients with acute MI during COVID‑19.

COVID‑19 is associated with an increased propensity for thrombotic complications in both venous and arterial circulation. This is due to the combined effects of systemic inflammation, platelet activation, endothelial dysfunction, and venous stasis. The combination of these mechanisms creates a hypercoagulable state that significantly increases the risk of thromboembolic complications in COVID‑19 patients [63].

An additional clinical challenge is that a significant proportion of patients already receiving antithrombotic therapy for thrombotic diseases may develop COVID‑19, requiring a reassessment of drug choice, dosing, and laboratory monitoring. Antithrombotic therapy and prevention of thromboembolic complications are mandatory components of the management of hospitalized COVID‑19 patients, as established in Russian and US national clinical guidelines [7, 64]. This approach is based on the key role of thrombo‑inflammatory mechanisms in the pathogenesis of organ injury in SARS‑CoV‑2 infection.

Patients with severe forms of COVID‑19 often show hemostatic abnormalities resembling other systemic coagulopathies associated with severe infections, including disseminated intravascular coagulation (DIC) and thrombotic microangiopathy [65]. However, coagulopathy in COVID‑19 has several distinct features. The combination of mild thrombocytopenia, prolongation of prothrombin time, and markedly elevated D‑dimer levels may indicate a DIC‑like state, but its laboratory profile differs from classic sepsis‑associated DIC [66]. In sepsis, more pronounced thrombocytopenia and less marked D‑dimer elevation are typically seen than in COVID‑19. Importantly, most COVID‑19 patients do not meet the diagnostic criteria for DIC of the International Society on Thrombosis and Haemostasis (ISTH) [67].

In some patients with severe COVID‑19, clinically significant but often unrecognized venous and arterial thromboembolic complications develop [66, 67]. According to early cohort studies, the frequency of thromboembolic events in hospitalized COVID‑19 patients reaches 35–45%, and the presence of coagulopathy is associated with a substantially increased risk of death [6, 9].

Many controlled studies have shown that characteristic laboratory signs of coagulopathy in COVID‑19 are a marked increase in D‑dimer concentration, a moderate decrease in platelet count, and prolongation of prothrombin time [69, 70]. In intensive care unit patients, the median D‑dimer level was significantly higher (2.4 mg/L; IQR 0.6–14.4) than in non‑ICU patients (0.5 mg/L; IQR 0.3–0.8) [70]. A D‑dimer level >1.0 mg/L was associated with an >18‑fold increase in the risk of death in COVID‑19 patients [43].

Coronavirus infection is also accompanied by activation of the fibrinolytic system. Endothelial cell damage leads to massive release of tissue plasminogen activators, which may explain the extremely high levels of D‑dimer and fibrin degradation products in patients with severe COVID‑19 [63].

Mild thrombocytopenia (platelet count <150 × 10⁹/L) is found in 70–95% of patients with severe COVID‑19. Thrombocytopenia is generally not an independent predictor of disease progression or adverse outcome [65, 70]. According to dynamic observations, only about 5% of patients have platelet counts below 100 × 10⁹/L [69, 70].

Fibrinogen concentration in most COVID‑19 patients is at the upper limit of normal or elevated, likely reflecting an acute phase inflammatory response. However, in some patients shortly before death, a sharp drop in plasma fibrinogen below 1.0 g/L has been described, possibly indicating depletion of coagulation potential [68].

Thrombotic microangiopathy develops as a result of pathological platelet‑vessel wall interaction mediated by ultra‑large von Willebrand factor multimers released from damaged endothelial cells. Under normal conditions, the activity of these multimers is regulated by the metalloprotease ADAMTS13. In systemic inflammatory conditions, including severe infections, a relative deficiency of ADAMTS13 may occur. However, data on the status of the ADAMTS13 system in patients with ACS, MI, and severe COVID‑19 are currently limited [63].

In clinical practice, prophylactic and therapeutic use of heparins in COVID‑19 patients, including those with concomitant ACS and MI, is considered. In a retrospective study from China including 449 COVID‑19 patients, it was shown that in patients with coagulopathy receiving prophylactic heparin, mortality was lower compared to patients not receiving anticoagulants (40% vs. 64%) in the subgroup with sepsis‑associated coagulopathy [68]. The effect was particularly pronounced in patients with D‑dimer levels exceeding the upper limit of normal by more than six‑fold.

Evidence supports the efficacy of prophylactic LMWH for preventing venous thromboembolism in critically ill COVID‑19 patients [71]. Given the hypercoagulable profile of the disease, most hospitalized COVID‑19 patients without contraindications should receive thromboprophylaxis. If LMWH is unavailable, unfractionated heparin may be used, but it requires more frequent administration and laboratory monitoring. Fondaparinux is an alternative, but its potential anti‑inflammatory effects, characteristic of heparins, remain underexplored [63].

Patients with severe forms of COVID‑19 may require higher doses of anticoagulants compared to standard prophylaxis due to the pronounced hypercoagulable state [72]. This hypothesis is currently being evaluated in several multicenter randomized clinical trials (NCT04372589, NCT04345848, NCT04366960).

The nature of coagulation abnormalities and their role in coronary thrombosis in patients with confirmed STEMI during COVID‑19 were studied in detail in a study performed in the Department of Cardiology, Barts Heart Centre, St Bartholomew’s Hospital (London, UK) [37]. STEMI patients with concomitant COVID‑19 had higher troponin T levels, marked lymphopenia, and significantly elevated D‑dimer and C‑reactive protein concentrations. Angiographically, these patients had a significantly higher thrombotic burden, frequent multi‑vessel coronary thrombosis, and stent thrombosis. During primary PCI, aspiration thrombectomy and glycoprotein IIb/IIIa inhibitors were used more often, and higher heparin doses were required to achieve therapeutic aPTT. The authors concluded that STEMI patients with COVID‑19 exhibit a pronounced shift in hemostatic balance toward hypercoagulation, associated with greater thrombotic burden and less favorable clinical outcomes. This underscores the need for routine COVID‑19 testing in all STEMI patients and further research to refine criteria for coronary thrombosis and indications for more aggressive antithrombotic therapy in specific clinical situations.

COVID‑19 may predispose patients to thrombotic complications in both venous and arterial circulation due to systemic inflammatory response, platelet activation, endothelial dysfunction, and blood stasis. An additional complexity is that patients already receiving antithrombotic therapy for thrombotic diseases may develop COVID‑19, necessitating reconsideration of drug choice, dosing, and laboratory monitoring. During the pandemic, particular attention is also given to optimizing care for non‑COVID‑19 patients with thrombotic diseases, including ACS and acute MI. The use of antithrombotic agents as modulators of endothelial dysfunction improves the function of damaged endothelium. It is important to consider that when antithrombotic drugs are combined with lopinavir/ritonavir, through inhibition of cytochrome P450 CYP3A4 enzymes, antivirals can affect the activity of P2Y₁₂ inhibitors, leading to reduced concentrations of active metabolites of clopidogrel and prasugrel, and increased concentrations of ticagrelor. If a P2Y₁₂ inhibitor is required, prasugrel is the preferred agent [77].

A literature review by researchers at Columbia University (New York, USA) examined current concepts of pathogenesis, epidemiology, and clinical outcomes of thrombotic complications in COVID‑19 patients, including those with venous and arterial thrombosis, patients with pre‑existing thrombotic diseases, and those requiring continuation of antithrombotic therapy in special clinical situations, including pregnancy [44]. According to available data, COVID‑19 patients often show hemostatic abnormalities resembling DIC, but with a distinct laboratory profile [73]. Severe inflammatory reaction, critical illness, and presence of risk factors may contribute to thrombotic complications, which were previously noted in other highly virulent zoonotic coronavirus infections [74, 75]. In addition, the potential for drug interactions between medications used to treat COVID‑19 and antiplatelet or anticoagulant agents is emphasized [44, 78].

The impact of secondary prevention pharmacotherapy on the course of MI in COVID‑19 patients was also analyzed in a study by cardiologists from the Leeds Institute for Data Analytics and the University of Leeds (UK) [25]. The authors evaluated the impact of the COVID‑19 pandemic on inpatient treatment patterns and 30‑day mortality from acute MI in 99 hospitals as part of the national myocardial ischemia audit. The rate of prescribing secondary prevention medications remained stable and exceeded 94% in all subgroups analyzed. However, 30‑day mortality increased for NSTEMI patients (from 5.4% to 7.5%; OR 1.41), while it decreased for STEMI patients (from 10.2% to 7.7%; OR 0.73). The authors concluded that during the COVID‑19 pandemic, it was NSTEMI patients who had worse short‑term prognosis.

It is important to remember that in patients with cardiovascular disease, drug safety is particularly critical, as most have several risk factors for adverse drug effects (elderly age, multiple pathologies, need for ≥2 medications, history of allergies) [78].

Standards for managing hospitalized patients with complicated forms of COVID‑19 include complex antiviral, antibacterial, antithrombotic, anti‑inflammatory, hormonal, and symptomatic therapy. The impact of such pathogenetic and symptomatic therapy on the clinical outcomes of ACS and MI is limited. In a prospective observational study performed at the Regional Center for Public Health in Milan, the role of ACE inhibitors and angiotensin receptor blockers in STEMI patients hospitalized during the first wave of the pandemic was analyzed [76]. It was shown that in 2020, symptom‑to‑hospitalization time was significantly longer than in pre‑pandemic periods, and the proportion of patients with late‑presenting STEMI increased markedly. The use of ACE inhibitors and ARBs, as well as in‑hospital outcomes including mortality and hemodynamic complications, did not differ significantly from previous years.

Summarized data from the literature review are presented in a structured Table 2.

Table 2. Summary table: tactics and features of managing patients with COVID‑19 and ST‑segment elevation myocardial infarction

Aspect / CategoryKey findings and features1. Epidemiology and pandemic impactDecrease in STEMI hospitalizations by ~20% during the pandemic.Increased time to care: delays in presentation, prolonged door‑to‑balloon time.Worse outcomes: increased in‑hospital mortality (28–41%), mechanical complications, cardiogenic shock.2. Clinical features of STEMI in COVID‑19High prevalence of myocardial injury: 5–38% of COVID‑19 patients have myocardial injury.Pronounced thrombotic burden: multi‑vessel thrombosis, stent thrombosis often independent of atherosclerosis.Microcirculation impairment: slow coronary flow (↑cTFC), reduced myocardial perfusion (↓MBG).High risk of complications: more frequent shock, cardiac arrest, acute heart failure, need for renal replacement therapy.3. Reperfusion strategyPrimary PCI remains the method of choice despite increased technical challenges and risk to staff.Reduced access to invasive procedures: coronary angiography and primary PCI less often performed on admission day.Fibrinolysis considered an alternative when PCI is unavailable or delayed, but associated with bleeding risk, especially in COVID‑19.Lower reperfusion efficacy: TIMI‑3 flow achieved less often, aspiration thrombectomy more frequently required.4. Antithrombotic therapyHypercoagulation is a key pathogenetic feature (↑D‑dimer, ↑CRP).Need for intensified/individualized therapy: higher heparin doses, frequent use of glycoprotein IIb/IIIa inhibitors.Interactions with antivirals: lopinavir/ritonavir may reduce clopidogrel activity.Thromboprophylaxis recommended for all hospitalized COVID‑19 patients.5. Prognosis and outcomesIn‑hospital mortality significantly higher (up to 28–41%) compared to STEMI without COVID‑19.Independent predictors of poor prognosis: presence of COVID‑19, older age, tachypnea, low oxygen saturation, cardiogenic shock.Vaccination associated with significant reduction in mortality risk.6. Organizational aspectsMultidisciplinary approach needed, considering systemic inflammation and thrombogenic risk.Protocol adaptation necessary: logistics optimization, infection control measures, ensuring access to invasive procedures.Importance of early diagnosis: routine COVID‑19 testing for all STEMI patients.

Thus, management of STEMI patients with COVID‑19 is a complex clinical challenge requiring an aggressive reperfusion strategy (preferably primary PCI), intensive and individualized antithrombotic therapy, and optimized healthcare organization during a pandemic to improve outcomes.

In summary, coagulation abnormalities mimicking systemic coagulopathies, including DIC, are common in COVID‑19 patients but have specific pathophysiological features. Patients with STEMI and concomitant COVID‑19 have higher levels of myocardial injury and inflammatory markers, pronounced thrombotic burden, more frequent multi‑vessel thrombosis and stent thrombosis, and require more intensive anticoagulant therapy. At the same time, the principles of secondary prevention in MI patients during the COVID‑19 pandemic remain largely unchanged, and the use of ACE inhibitors and ARBs, according to available data, does not significantly affect clinical outcomes.