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Different types of ACS in COVID-19. Legend: SARS-CoV-2—severe acute respiratory syndrome coronavirus 2; ACS—acute coronary syndrome; UA—unstable angina; AMI—acute myocardial infarction; ACS-NNOCA—acute coronary syndrome with normal or near-normal coronary arteries; INOCA—ischemia with non-obstructive coronary artery disease; MINCA—myocardial infarction with normal coronary arteries; MINOCA—myocardial infarction with non-obstructive coronary artery disease; NSTEMI—non-ST elevation myocardial infarction; STEMI—ST elevation myocardial infarction.
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The COVID-19 pandemic has led to numerous negative implications for all aspects of society. Although COVID-19 is a predominant lung disease, in 10-30% of cases, it is associated with cardiovascular disease (CVD). The presence of myocardial injury in COVID-19 patients occurs with a frequency between 7-36%. There is growing evidence of the incidence...
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Citations
... However, patients with COVID-19 are more likely to develop serious complications that endure for an extended period. This is reflected in studies that showed that the incidence of myocardial infarction increased 5 times within the first 14 days post-COVID-19 acute infection, 25,35 and that COVID-19 patients are 7fold more likely to have a stroke than patients with influenza. In addition, the risk for both acute myocardial infarction and stroke remains high for up to 1 year after infection. ...
This controlled study investigated metabolic changes in non-vaccinated individuals with Long-COVID-19, along with their connection to the severity of the disease. The study involved 88 patients who experienced varying levels of initial disease severity (mild, moderate, and severe), and a control group of 29 healthy individuals. Metabolic risk markers from fasting blood samples were analyzed, and data regarding disease severity indicators were collected. Findings indicated significant metabolic shifts in severe Long-COVID-19 cases, mainly a marked drop in HDL-C levels and a doubled increase in ferritin levels and insulin resistance compared to the mild cases and controls. HDL-C and ferritin were identified as the leading factors predicted by disease severity. In conclusion, the decline in HDL-C levels and rise in ferritin levels seen in Long-COVID-19 individuals, largely influenced by the severity of the initial infection, could potentially play a role in the persistence and progression of Long-COVID-19. Hence, these markers could be considered as possible therapeutic targets, and help shape preventive strategies to reduce the long-term impacts of the disease.
... When the SARS-CoV-2 virus binds with ACE2 receptors, it leads to the downregulation of these receptors, and this increases the activity of angiotensin II. This mechanism results in systemic vasoconstriction, apoptosis, inflammation, and endothelial proliferation, leading to cardiomyocyte damage or the worsening of previous ischemic condition [27]. Another identified mechanism of acute myocardial infarction in COVID-19 patients is coronary embolism, found in 3% of AMI patients [28]. ...
Coronavirus disease 2019 (COVID-19) was a global pandemic with high mortality and morbidity that led to an increased health burden all over the world. Although the virus mostly affects the pulmonary tract, cardiovascular implications are often observed among COVID-19 patients and are predictive of poor outcomes. Increased values of myocardial biomarkers such as troponin I or NT-proBNP were proven to be risk factors for respiratory failure. Although the risk of acute coronary syndromes (ACSs) was greater in the acute phase of COVID-19, there were lower rates of hospitalization for ACSs, due to patients’ hesitation in presenting at the hospital. Hospitalized ACSs patients with COVID-19 infection had a prolonged symptom-to-first-medical-contact time, and longer door-to-balloon time. The mechanisms of myocardial injury in COVID-19 patients are still not entirely clear; however, the most frequently implicated factors include the downregulation of ACE2 receptors, endothelial dysfunction, pro-coagulant status, and increased levels of pro-inflammatory cytokines. The aim of this paper is to evaluate the long-term outcomes and prognosis of COVID-19 survivors that presented an acute myocardial infarction, by reviewing existing data. The importance of the association between this infectious disease and myocardial infarction arises from the increased mortality of patients with SARS-CoV-2 infection and AMI (10–76%, compared with 4.6% for NSTEMI patients and 7% for STEMI patients without COVID-19). The literature review showed an increased risk of cardiovascular events in COVID-19 survivors compared with the general population, even after the acute phase of the disease, with poorer long-term outcomes.
... The COVID pandemic impacting health-care services during the study period is also a possible confounder. [16,17] It has been documented that treatment strategies have been affected due to the pandemic globally. [18] Large-scale vaccination during the pandemic may also be a confounder. ...
OBJECTIVE
Cardiovascular disease is the leading cause of death worldwide. As there is an increase in the global burden of ischemic heart disease, there are multiple scoring systems established in the emergency department (ED) to risk stratify and manage acute coronary syndrome (ACS) in patients with chest pain. The objective of this study was to integrate point-of-care echo into the existing history, electrocardiogram, age, risk factors, and troponin (HEART) score and evaluate a novel scoring system, the echo HEART (E-HEART) score in risk stratification of patients presenting with undifferentiated chest pain to the ED. The E-HEART Score was also compared with existing traditional scoring systems for risk-stratifying acute chest pain.
METHODS
A diagnostic accuracy study involving 250 patients with chest pain at the ED of a single tertiary care teaching hospital in India was conducted. The emergency physicians assessed the E-HEART score after integrating their point-of-care echo/focused echo findings into the conventional HEART score on presentation. The primary endpoint was the occurrence of major adverse cardiovascular events (MACE) within 4 weeks of initial presentation. The accuracy of the E-HEART score was compared with other conventional risk stratification scoring systems such as the thrombolysis in myocardial infarction (TIMI), history, electrocardiogram, age, and risk factors, Troponin Only Manchester ACS (T-MACS), and HEART scores.
RESULTS
A total of 250 patients with a median age of 53 years (42.25–63.00) were part of the study. Low E-HEART scores (values 0–3) were calculated in 121 patients with no occurrence of MACE in this category. Eighty-one patients with moderate E-HEART scores (4–6) were found to have 30.9% MACE. In 48 patients with high E-HEART scores (values 7–11), MACE occurred in 97.9%. The area under receiver operating characteristics (AUROC) of E-HEART score is 0.992 (95% confidence interval: 0.98–0.99), which is significantly higher than AUROC values for HEART (0.978), TIMI (0.889), T-MACS (0.959), and HEAR (0.861), respectively (P < 0.0001). At a cutoff of E-HEART score >6, it accurately predicted ACS with a sensitivity of 92% and a specificity of 99% with a diagnostic accuracy of 97%.
CONCLUSION
The E-HEART score gives the clinician a quick and accurate forecast of outcomes in undifferentiated chest pain presenting to the ED. Low E-HEART scores (0–3) have an extremely low probability for short-term MACE and may aid in faster disposition from the ED. The elevated risk of MACE in patients with high E-HEART scores (7–11) may facilitate more aggressive workup measures and avoid disposition errors. E-HEART is an easily adaptable scoring system with improved accuracy compared to conventional scoring systems.
... Such viruses are human immunodeficiency virus, hepatitis C virus, influenza A and B viruses as well as SARS-CoV 1and 2 viruses [18]. A special mechanism of action was discovered in the SARS-CoV-2 virus, which causes direct damage to cardiomyocytes by acting on Angiotensin II receptors [23,24]. Enteroviruses, which are one of the most common causes of viral myocarditis, bind to specific receptors on cardiomyocytes, multiply, and cell lysis follows. ...
... Preprints (www.preprints.org) | NOT PEER-REVIEWED | Posted: 6 September 2023 doi:10.20944/preprints202309.0327.v124 ...
Although the frequency of myocarditis in the general population is very difficult to accurately determine due to the large number of asymptomatic cases, the incidence of this disease is increasing significantly due to better defined criteria for diagnosis and the development of modern diagnostic method. The multitude of different etiological factors, the diversity of the clinical picture and the variability of the diagnostic findings make this disease often demanding both for the selection of the diagnostic modality and for the proper therapeutic approach. The previously known most common viral etiology of this disease is today overshadowed by new findings based on immune-mediated processes, associated diseases that in their natural course can lead to myocardial involvement, but also the iatrogenic cause of myocarditis due to use of immune checkpoint inhibitors in the treatment of cancer patients. Suspecting that a patient with polymorphic and non-specific clinical signs and symptoms, changes in ECG and echocardiography has myocarditis is the starting point in the diagnostic algorithm. Cardio magnetic resonance imaging is non-invasive diagnostic gold standard for diagnosis and clinical follow-up of thses patients. Endomyocardial biopsy as an invasive method is the diagnostic choice in life-threatening patients with suspicion of fulminant myocarditis where the diagnosis has not yet established or there is no adequate response to the applied therapeutic regimen. The treatment of myocarditis is increasingly demanding and includes conservative methods of treating heart failure, immunomodulatory and immunospressive therapy, methods of mechanical circulatory support and heart transplantation. The goal of developing new diagnostic and therapeutic methods is to reduce mortality from this complex disease, which is still high.
... Patel et al 30-Day Readmissions in COVID- 19 and STEMI are often pulmonary, primary cardiac injury in the form of myocarditis and acute coronary syndrome (ACS) are well described. 2,3 The prevalence of myocardial injury in patients with COVID-19 has been reported with variability, in the range of 15.8% to 51% depending on the cohort of patients being investigated, while the prevalence of COVID-19 in patients with ST-segmentelevation myocardial infarction (STEMI) has been estimated at 1.38%. 4 Despite this variability, the important influence of myocardial injury on patient outcomes in those with COVID-19 is clear. ...
Background
Rates, causes, and predictors of readmission in patients with ST‐segment–elevation myocardial infarction (STEMI) during COVID‐19 pandemic are unknown.
Methods and Results
All hospitalizations for STEMI were selected from the US Nationwide Readmissions Database 2020 and were stratified by the presence of COVID‐19. Primary outcome was 30‐day readmission. Multivariable hierarchical generalized logistic regression analysis was performed to compare 30‐day readmission between patients with STEMI with and without COVID‐19 and to identify the predictors of 30‐day readmissions in patients with STEMI and COVID‐19. The rate of 30‐day all‐cause readmission was 11.4% in patients with STEMI who had COVID‐19 and 10.6% in those without COVID‐19, with the adjusted odds ratio (OR) not being significantly different between the two groups (OR, 0.88 [95% CI, 0.73–1.07], P=0.200). Of all 30‐day readmissions in patients with STEMI and COVID‐19, 41% were for cardiac causes. Among the cardiac causes, 56% were secondary to acute coronary syndrome, while among the noncardiac causes, infections were the most prevalent. Among the causes of 30‐day readmissions, infectious causes were significantly higher for patients with STEMI who had COVID‐19 compared with those without COVID‐19 (29.9% versus 11.3%, P=0.001). In a multivariable model, congestive heart failure, chronic kidney disease, low median household income, and length of stay ≥5 days were found to be associated with an increased risk of 30‐day readmission.
Conclusions
Post‐STEMI, 30‐day readmission rates were similar between patients with and without COVID‐19. Cardiac causes were the most common causes for 30‐day readmissions, and infections were the most prevalent noncardiac causes.
... In contrast, other authors [3,10,13,34,35] have suggested more frequent complications in the acute phase, particularly those that are mechanical in nature. This can be explained by a prolonged period of ischaemia as a result of a longer time before calling for help, particularly in STEMI, as well as the adaptation of therapeutic strategies. ...
Background:
The first wave of the coronavirus disease 2019 pandemic significantly changed behaviour in terms of access to healthcare.
Aim:
To assess the effects of the pandemic and initial lockdown on the incidence of acute coronary syndrome and its long-term prognosis.
Methods:
Patients admitted for acute coronary syndrome from 17 March to 6 July 2020 and from 17 March to 6 July 2019 were included. The number of admissions for acute coronary syndrome, acute complication rates and 2-year rates of survival free from major adverse cardiovascular events or death from any cause were compared according to the period of hospitalization.
Results:
In total, 289 patients were included. We observed a 30±3% drop in acute coronary syndrome admissions during the first lockdown, which did not recover in the 2months after it was lifted. At 2years, there were no significant differences in the combined endpoint of major adverse cardiovascular events or death from any cause between the different periods (P=0.34). Being hospitalized during lockdown was not predictive of adverse events during follow-up (hazard ratio 0.87, 95% confidence interval 0.45-1.66; P=0.67).
Conclusions:
We did not observe an increased risk of major cardiovascular events or death at 2years from initial hospitalization for patients hospitalized during the first lockdown, adopted in March 2020 in response to the coronavirus disease 2019 pandemic, potentially as a result of the lack of power of the study.
... Several studies showed that patients infected with SARS-CoV-2 had a higher incidence of acute cardiac injury. Nearly one-third of patients developed a certain phenotype of myocardial injury [1,2,3]. ...
Background:
Coronavirus disease 2019(COVID-19) caused a large number of infections worldwide. Although some patients recovered from the disease, some of the other problems that accompanied it, such as cardiac injury, could affect the patient's subsequent quality of life and prognosis.
Objectives:
To clarify the molecular mechanism of cardiac injury in SARS-CoV-2 Infection.
Methods:
The RNA-Seq dataset (GSE184715) comparing expression profiling of Mock human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and SARS-CoV-2-infected hiPSC-CMs was downloaded from Gene Expression Omnibus (GEO). Differentially expressed genes(DEGs) were performed by the R software. Degs were analyzed by enrichment analysis to clarify the affected pathways. Hub genes were screened out by a PPI network constructed from Degs. Finally, Connectivity Map was used to screen for the treatment of COVID-19 induced cardiac injury.
Results:
2705 differentially expressed genes were identified. Enrichment analysis confirmed that mitochondrial dysfunction was caused by SARS-CoV-2, meanwhile, cardiac muscle contraction was suppressed and NF-κB was activated. Based on the PPI network, 15 hub genes were identified. These 15 down-regulated hub genes were mainly involved in the reduced activity of complexes in the mitochondrial respiratory chain associated with mitochondrial dysfunction. Moreover, 5 candidate drugs were identified to treat cardiac injury.
Conclusion:
In conclusion, SARS-CoV-2 infection of cardiomyocytes causes mitochondrial dysfunction, including reduced mitochondrial respiratory chain complex activity and decreased ATP synthesis, leading to cardiomyocyte apoptosis, while the activated NF-κB also induced cytokine storms, ultimately resulting in cardiac injury.
... With additional data, it could be possible to identify factors that could lead to the increased incidence of AMI, with the ultimate goal of a timely diagnostic and early recognition, as well as the education of the population, especially the elderly, about the signs and symptoms of AMI. [14][15][16] This study showed the influence and significance of circadian rhythms and seasonal variations on the incidence of AMI. A higher incidence was observed in the winter months, especially in January, in the early morning hours. ...
Background/Aim: Acute myocardial infarction (AMI) is a consequence of complete coronary artery occlusion. There is a considerable seasonal variation in the incidence of AMI. The aim of the study was to establish a circadian and seasonal pattern of AMI. Methods: A retrospective observational study was conducted, using the database of the Institute of Emergency Medical Service of the City of Novi Sad. The study included 982 patients, both male and female, diagnosed with AMI (I.21 - ICD-10 code) in the period between 15 March 2018 and 14 March 2022. Data were classified according to the time of the day, days of the week, quarters and months. Data were analysed by using descriptive statistical methods, Mann-Whitney U test, Chi-squared test and Fisher's exact test. Results: AMI most frequently occurred between 6 am and 2 pm (389; 39.6 %). A statistically significant incidence of AMI was calculated for the periods between 6 am and 2 pm (ch2 = 39.69; p < 0.001) and between 2 pm and 10 pm (ch2 = 28.06; p < 0.001). Most cases of AMI were noted on Monday (153; 15.6 %) and in January (93; 9.5 %). The highest incidence of AMI was in the period between 15 March 2021 and 14 March 2022 (304; 31.0 %), while the lowest incidence was noted between 15 March 2019 and 14 March 2020 (190; 19.3 %). Conclusion: Circadian, seasonal and annual rhythm may have a significant impact on the incidence of AMI. This fact can have an important role in the prevention, timely recognition and adequate treatment of acute coronary disease.
... The risk variable results of this study are comparable with many studies that found the traditional CAD risk factors aggravate COVID-19. [19][20][21] In this study, dyslipidemia doesn't aggravate COVID-19, but it is one of the risk factors that trigger ACS because atherogenicity has been linked to lifting the low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL) cholesterol, yet it lowers HDL cholesterol levels. These changes increase the risk of cardiovascular disease, and when accumulated with the atherosclerotic plaque and rupture, ulceration, or erosion, cause intraluminal thrombus development and restrict myocardial blood flow; resulting in myocardial necrosis. ...
Background : During the COVID-19 outbreak, the number of patients who have developed acute coronary syndromes (ACS) has soared rapidly, cardiovascular disease and mortality are influenced by the elevated inflammatory biomarkers. The aim of this study is to compare inflammatory markers between patients with ACS who hadn’t previously had COVID-19 and those who’d be infected within the preceding three months; as well as, evaluating the effect of statins on inflammatory biomarkers.
Methods : This is a comparative cross-sectional study of 42 patients who presented with ACS and had previously had COVID-19 and 48 patient who had never had COVID-19, who were admitted to the coronary care unit at the Iraqi Center for Heart Disease and Baghdad Teaching Hospital, Iraq. Inflammatory biomarkers (TNF-α, IL-6, and HS-CRP) levels were determined in serum samples of all patients at admission to these centers then one month later, after administration of statins daily using the Sandwich-ELISA Principle, and Immunofluorescence technique for these markers.
Result: The baseline for patients who had ACS and COVID-19 three months previously, were IL6 (85.87 ±45.80), HS-CRP (23.19 ± 14.49), and TNF-α (161.94± 240.96) were higher than patients that had ACS but not COVID-19; IL6 (50.77±22.48), HS-CRP (13.64± 12.09), and TNF-α (117.73 ±71.23),(p<0.0001), (p=0.003) and (p=0.201) for IL6, HS-CRP, and TNF-α respectively. Rosuvastatin showed a significant reduction in HS-CRP and IL6 (P<0.001), while Atorvastatin a significant reduction in HS-CRP (P<0.001) after one month of therapy. Yet there was no significant difference in the level of TNF α in these two groups at the end of this study. Conclusions: The patients with previous COVID-19 still had higher inflammatory markers than those who didn’t. Rosuvastatin 40mg had a more reduction in IL6 than Atorvastatin 40mg after one month and both of them could reduce HS-CRP, but neither could reduce TNF-α in this short period.
Giant cell myocarditis is a rare but extremely severe disease with a frequent need for heart transplantation and a high mortality rate. To this day, the most common reason for the occurrence of this disease has not been precisely determined, but its frequent association with autoimmune diseases speaks in favor of autoimmune etiology. Clinically, it is presented to the greatest extent by symptoms and signs of acute heart failure and ventricular rhythm disturbances, which are registered in as many as half of the patients. Arrhythmias can be accompanied by the occurrence of palpitations, repeated syncope, and even sudden cardiac death. A severe degree of acute heart failure in hemodynamically unstable patents who respond inadequately to the administered therapy for heart failure and refractory heart rhythm disorders and/or conduction disorders that are common in these patients should always raise suspicion of giant cell myocarditis. Given that changes in electrocardiogram, echocardiography and positive biomarker values are not strictly specific for this disease, the diagnosis of giant cell myocarditis is most often established by endomyocardial biopsy, especially in patients with the fulminant form of the disease. Timely endomyocardial biopsy enables not only quick and accurate diagnosis, but also early administration of immunosuppressive therapy, which greatly improves the outcome in these patients. Pathohistological verification of this disease is important so as to rule out cardiac sarcoidosis and other granulomatous infectious and non-infectious diseases. Given that in a large number of patients the disease has a fulminant course, early and rapid diagnosis, application of inotropic stimulation and mechanical circulatory support in hemodynamically unstable patients and adequate modern therapeutic regimen can largely reduce mortality in these patients, which is still high despite modern diagnostics and therapeutic progress of medicine.
