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(1) Background: Given its high cardiac specificity and its capacity to directly assess the cardiac function, cardiac myosin-binding protein (MyBP-C) is a promising biomarker in patients with acute heart failure (AHF). The aim of our study was to investigate the clinical utility of this novel marker for diagnosis and short-term prognosis in subjects with AHF. (2) Methods: We measured plasma levels of MyBP-C at admission in 49 subjects (27 patients admitted with AHF and 22 controls). (3) Results: The plasma concentration of MyBP-C was significantly higher in patients with AHF compared to controls (54.88 vs. 0.01 ng/L, p < 0.001). For 30-day prognosis, MyBP-C showed significantly greater AUC (0.972, p < 0.001) than NT-proBNP (0.849, p = 0.001) and hs-TnI (0.714, p = 0.047). In a multivariate logistic regression analysis, an elevated level of MyBP-C was the best independent predictor of 30-day mortality (OR = 1.08, p = 0.039) or combined death/recurrent 30-days rehospitalization (OR = 1.12, p = 0.014). (4) Conclusions: Our data show that circulating MyBP-C is a sensitive and cardiac-specific biomarker with potential utility for the accurate diagnosis and prognosis of AHF.
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Background and Objective: In the landscape of heart failure, non-cardiac comorbidities represent a formidable challenge, imparting adverse prognostic implications. Holter ECG monitoring assumes a supplementary role in delineating myocardial susceptibility and autonomic nervous system dynamics. This study aims to explore the potential correlation between Holter ECG parameters and comorbidities in individuals with ischemic cardiomyopathy experiencing heart failure (HF), with a particular focus on the primary utility of these parameters as prognostic indicators. Materials and Methods: In this prospective inquiry, a cohort of 60 individuals diagnosed with heart failure underwent stratification into subgroups based on the presence of comorbidities, including diabetes, chronic kidney disease, obesity, or hyperuricemia. Upon admission, a thorough evaluation of all participants encompassed echocardiography, laboratory panel analysis, and 24 h Holter monitoring. Results: Significant associations were uncovered between diabetes and unconventional physiological indicators, specifically the Triangular index (p = 0.035) and deceleration capacity (p = 0.002). Pertaining to creatinine clearance, notable correlations surfaced with RMSSD (p = 0.026), PNN50 (p = 0.013), and high-frequency power (p = 0.026). An examination of uric acid levels and distinctive Holter ECG patterns unveiled statistical significance, particularly regarding the deceleration capacity (p = 0.045). Nevertheless, in the evaluation of the Body Mass Index, no statistically significant findings emerged concerning Holter ECG parameters. Conclusions: The identified statistical correlations between non-cardiac comorbidities and patterns elucidated in Holter ECG recordings underscore the heightened diagnostic utility of this investigative modality in the comprehensive evaluation of individuals grappling with HF. Furthermore, we underscore the critical importance of the thorough analysis of Holter ECG recordings, particularly with regard to subtle and emerging parameters that may be overlooked or insufficiently acknowledged.
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Cardiomiopatías , Diabetes Mellitus , Insuficiencia Cardíaca , Isquemia Miocárdica , Humanos , Electrocardiografía Ambulatoria , Proyectos Piloto , Estudios Prospectivos , Isquemia Miocárdica/complicaciones , Isquemia Miocárdica/diagnóstico , Insuficiencia Cardíaca/complicaciones , Cardiomiopatías/complicaciones , Cardiomiopatías/diagnóstico , Frecuencia CardíacaRESUMEN
The overweight status or obesity can be confirmed through classical methods such as the body mass index (BMI) and the waist-to-hip ratio (WHR). Apart from metabolic issues such as atherosclerosis, liver steatosis, or diabetes mellitus, long-term obesity or overweight status can pose a risk for cardiovascular and neurovascular complications. While some acute adverse events like coronary syndromes of strokes are well-documented to be linked to an increased body mass, there are also chronic processes that, due to their silent onset and evolution, are underdiagnosed and not as thoroughly studied. Through this review, we aimed to collect all relevant data with regard to the long-term impact of obesity on cognitive function in all ages and its correlation with an earlier onset of dementia such as Alzheimer's disease (AD). The exact mechanisms through which a decline in cognitive functions occurs in overweight or obese persons are still being discussed. A combination of factors has been acknowledged as potential triggers, such as a sedentary lifestyle and stress, as well as a genetic predisposition, for example, the apolipoprotein E (ApoE) alleles in AD. Most research highlights the impact of vascular dysfunction and systemic inflammation on the nervous system in patients with obesity and the subsequent neurological changes. Obesity during the early to mid-ages leads to an earlier onset of cognitive dysfunction in various forms. Also, lifestyle intervention can reverse cognitive dysfunction, especially dieting, to encourage weight loss.
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Advances in the treatment of hemophilia have increased the life expectancy of this population and we are currently facing diseases associated with aging, including cardiovascular ones. Coronary atherosclerosis, with acute myocardial infarction as the most severe form of manifestation, has been recognized as part of the comorbidities of hemophiliacs. However, little is known about peripheral artery disease. Available data show that hemophiliacs have cardiovascular risk factors and atherosclerosis similar to the general population. Impaired thrombus formation and phenotype of atheroma plaque rather than the burden of atherosclerosis explains their lower cardiovascular mortality. Since the effect of traditional cardiovascular risk factors overpowers that of decreased coagulability and promotes the onset and progression of atherosclerotic lesions, screening for traditional cardiovascular risk factors and peripheral artery disease should be integrated into standard hemophilia care. There is evidence that invasive treatments and long-term antithrombotic therapy are generally safe, provided that coagulation factor levels are taken into account and replacement therapy is given when necessary.
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Background and Objectives: Cortisol is a valuable marker for assessing the body's response to any form of stress. We conducted this study in order to evaluate the variations of salivary and serum cortisol levels in professional football players in relation to cardiopulmonary exercise testing (CPET) and their significance in potentially evaluating overtraining in athletes. Also, the question of whether salivary cortisol determination could fully substitute serum sampling was addressed. Materials and Methods: A total of 19 male professional football players were evaluated by measuring serum cortisol levels at rest (T0) and immediately after a CPET (T1) and salivary cortisol levels at rest (T0), 10 min after a CPET (T2), and 30 min after a CPET (T3). Results: T0 serum cortisol showed a statistically significant correlation with the oxygen uptake at the anaerobic threshold divided by the body weight (VO2-AT/weight), as did the T2 salivary cortisol with the maximum oxygen uptake at the anaerobic threshold (VO2-AT) and VO2-AT/weight. T0 salivary cortisol was significantly correlated with the subjects' height and the predicted O2 pulse. Conclusions: While some correlations were discovered, they are insufficient to recommend cortisol as a routine biomarker in athletes' evaluation. However, significant correlations were established between salivary and serum determinations, meaning that the non-invasive procedure could substitute venous blood sampling.
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Prueba de Esfuerzo , Hidrocortisona , Humanos , Masculino , Prueba de Esfuerzo/métodos , Consumo de Oxígeno , Oxígeno , AtletasRESUMEN
Atherosclerosis is a significant health concern with a growing incidence worldwide. It is directly linked to an increased cardiovascular risk and to major adverse cardiovascular events, such as acute coronary syndromes. In this review, we try to assess the potential diagnostic role of biomarkers in the early identification of patients susceptible to the development of atherosclerosis and other adverse cardiovascular events. We have collected publications concerning already established parameters, such as low-density lipoprotein cholesterol (LDL-C), as well as newer markers, e.g., apolipoprotein B (apoB) and the ratio between apoB and apoA. Additionally, given the inflammatory nature of the development of atherosclerosis, high-sensitivity c-reactive protein (hs-CRP) or interleukin-6 (IL-6) are also discussed. Additionally, newer publications on other emerging components linked to atherosclerosis were considered in the context of patient evaluation. Apart from the already in-use markers (e.g., LDL-C), emerging research highlights the potential of newer molecules in optimizing the diagnosis of atherosclerotic disease in earlier stages. After further studies, they might be fully implemented in the screening protocols.
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Myocardial ischemia is a pathophysiological state characterized by inadequate perfusion of the myocardium, resulting in an imbalance between myocardial oxygen demand and supply. It is most commonly caused by coronary artery disease, in which atherosclerotic plaques lead to luminal narrowing and reduced blood flow to the heart. Myocardial ischemia can manifest as angina pectoris or silent myocardial ischemia and can progress to myocardial infarction or heart failure if left untreated. Diagnosis of myocardial ischemia typically involves a combination of clinical evaluation, electrocardiography and imaging studies. Electrocardiographic parameters, as assessed by 24 h Holter ECG monitoring, can predict the occurrence of major adverse cardiovascular events in patients with myocardial ischemia, independent of other risk factors. The T-waves in patients with myocardial ischemia have prognostic value for predicting major adverse cardiovascular events, and their electrophysiological heterogeneity can be visualized using various techniques. Combining the electrocardiographic findings with the assessment of myocardial substrate may offer a better picture of the factors that can contribute to cardiovascular death.
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(1) Background: Acute heart failure (HF) represents a complex clinical syndrome burdened by increased mortality and a high rate of systemic complications. Although natriuretic peptides (e.g., NT-proBNP) currently represent the diagnostic and prognostic gold standard in acute HF, those molecules do not accurately reflect all the pathophysiological mechanisms involved in the progression of this pathology when determined independently. Therefore, the current paradigm tends to focus on a multi-marker approach for the risk stratification of patients with acute HF. Syndecan-1 is a less studied biomarker in cardiovascular diseases; its assessment in patients with acute HF being potentially able to reflect the myocardial pathological changes, such as fibrosis, inflammation, endothelial dysfunction or global wall stress. (2) Methods: We conducted a single center prospective study that enrolled 173 patients (120 patients admitted for acute HF, compared to 53 controls with stable chronic HF). A complete standardized clinical, echocardiography and laboratory evaluation was performed at admission, including serum samples for the determination of syndecan-1 by the enzyme-linked immunosorbent assay (ELISA) method. (3) Results: The serum concentration of syndecan-1 was significantly higher in patients with acute HF, compared to controls [121.4 (69.3-257.9) vs. 72.1 (41.4-135.8) ng/mL, p = 0.015]. Syndecan-1 was a significant predictor for the diagnosis of acute HF, expressed by an area under the curve (AUC) of 0.898, similar to NT-proBNP (AUC: 0.976) or cardiac troponin (AUC: 0.839). Moreover, syndecan-1 was independently associated with impaired kidney and liver function at admission, being also a predictor for early, subclinical organ dysfunction in patients with normal biological parameters at admission. When included in the multi-marker model, syndecan-1 levels influenced mortality more significantly than NT-proBNP or troponin. A multivariable regression including syndecan-1, NT-proBNP and troponin provided additional prognostic value compared to each independent biomarker. (4) Conclusions: Syndecan-1 can be considered a promising novel biomarker in acute HF, exhibiting adequate diagnostic and prognostic value. Additionally, syndecan-1 can be used as a surrogate biomarker for non-cardiac organ dysfunction, as its highs levels can accurately reflect early acute kidney and liver injury.
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Despite the improvements in the treatment of coronary artery disease (CAD) and acute myocardial infarction (MI) over the past 20 years, ischemic heart disease (IHD) continues to be the most common cause of heart failure (HF). In clinical trials, over 70% of patients diagnosed with HF had IHD as the underlying cause. Furthermore, IHD predicts a worse outcome for patients with HF, leading to a substantial increase in late morbidity, mortality, and healthcare costs. In recent years, new pharmacological therapies have emerged for the treatment of HF, such as sodium-glucose cotransporter-2 inhibitors, angiotensin receptor-neprilysin inhibitors, selective cardiac myosin activators, and oral soluble guanylate cyclase stimulators, demonstrating clear or potential benefits in patients with HF with reduced ejection fraction. Interventional strategies such as cardiac resynchronization therapy, cardiac contractility modulation, or baroreflex activation therapy might provide additional therapeutic benefits by improving symptoms and promoting reverse remodeling. Furthermore, cardiac regenerative therapies such as stem cell transplantation could become a new therapeutic resource in the management of HF. By analyzing the existing data from the literature, this review aims to evaluate the impact of new HF therapies in patients with IHD in order to gain further insight into the best form of therapeutic management for this large proportion of HF patients.
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INTRODUCTION: Chronic inflammation plays an essential role in the pathophysiology of both arterial hypertension (HTN) and coronary artery disease (CAD), and is more pronounced in individuals with a non-dipper circadian blood pressure (BP) pattern. A non-dipping BP pattern is in turn is associated with increased cardiovascular morbi-mortality, and a higher risk of atherosclerotic events. Neutrophil to lymphocyte ratio (NLR), monocyte to lymphocyte ratio (MLR) and platelet to lymphocyte ratio (PLR) are readily available predictors of systemic inflammation and cardiovascular risk. The purpose of our study is to evaluate whether NLR, MLR and PLR can be used as cost-effective predictors of a non-dipping blood pressure pattern in hypertensive patients with stable CAD. MATERIALS AND METHODS: We performed a cross-sectional retrospective analysis that included 80 patients with hypertension and stable CAD (mean age 55.51 ± 11.83 years, 71.3% male) referred to a cardiovascular rehabilitation center. All patients underwent clinical examination, 24 h ambulatory blood pressure monitoring (ABPM) and standard blood analysis. RESULTS: Baseline demographic characteristics were similar in both groups. Patients with non-dipper pattern had significantly higher NLR (median = 2, IR (2-3), p < 0.001), MLR (median = 0.31, IR (0.23-0.39), p < 0.001) and PLR (median = 175, IR (144-215), p < 0.001) compared to dippers. CONCLUSION: Our results suggest that MLR and PLR are inexpensive and easily accessible biomarkers that predict a non-dipping pattern in hypertensive patients with stable CAD.
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Abdominal fat and fat-free masses report a close association with cardiometabolic risks, therefore this specific body compartment presents more interest than whole-body masses. This research aimed to develop accurate algorithms that predict body masses and specifically trunk fat and fat-free masses from easy to measure parameters in any setting. The study included 104 apparently healthy subjects, but with a higher-than-normal percent of adiposity or waist circumference. Multiple linear regression (MLR) and artificial neural network (ANN) models were built for predicting abdominal fat and fat-free masses in patients with relatively low cardiometabolic risks. The data were divided into training, validation and test sets, and this process was repeated 20 times per each model to reduce the bias of data division on model accuracy. The best performance models used a maximum number of five anthropometric inputs, with higher R2 values for ANN models than for MLR models (R2 = 0.96-0.98 vs. R2 = 0.80-0.94, p = 0.006). The root mean square error (RMSE) for all predicted parameters was significantly lower for ANN models than for MLR models, suggesting a higher accuracy for ANN models. From all body masses predicted, trunk fat mass and fat-free mass registered the best performance with ANN, allowing a possible error of 1.84 kg for predicting the correct trunk fat mass and 1.48 kg for predicting the correct trunk fat-free mass. The developed algorithms represent cost-effective prediction tools for the most relevant adipose and lean tissues involved in the physiopathology of cardiometabolic risks.
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This research focused on establishing a hierarchy concerning the influence of various biological markers and body composition parameters on preventing, diagnosing and managing Metabolic Syndrome (MetS). Our cross-sectional cohort study included 104 subjects without any atherosclerotic antecedent pathology, organized in two groups (with and without MetS). All participants underwent clinical and anthropometric measurements, DEXA investigation and blood tests for all MetS criteria, together with adiponectin, leptin, insulin, uric acid and CRP. Based on mathematical logic, we calculated a normalized sensitivity score to compare the predictive power of biomarkers and parameters associated with MetS, upon the prevalence of MetS. Patients with MetS report higher levels of uric acid (p = 0.02), CRP (p = 0.012) and lower levels of adiponectin (p = 0.025) than patients without MetS. The top three biological markers with the highest predictive power of the prevalence of the disease are HDL, insulin, and adiponectin:leptin ratio, and the top three body composition parameters are trunk fat-free percentage, waist-height ratio and trunk fat percentage. Their high sensitivity scores differentiate them from all the other markers analysed in the study. Our findings report relevant scores for estimating the importance of cardiometabolic risks in the prevalence of MetS. The high rank of protective markers, HDL and trunk fat-free percentage, suggest that positive effects have a stronger association with the prevalence of MetS, than negative ones do. Therefore, this risk stratification study provides important support for prevention and management programs regarding MetS.
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Background: Biomarkers, electrocardiogram (ECG) and Holter ECG are basic, accessible and feasible cardiac investigations. The combination of their results may lead to a more complex predictive model that may improve the clinical approach in acute heart failure (AHF). The main objective was to investigate which ECG parameters are correlated with the usual cardiac biomarkers (prohormone N-terminal proBNP, high-sensitive cardiac troponin I) in patients with acute heart failure, in a population from Romania. The relationship between certain ECG parameters and cardiac biomarkers may support future research on their combined prognostic value. Methods: In this prospective case-control study were included 49 patients with acute heart failure and 31 participants in the control group. For all patients we measured levels of prohormone N-terminal proBNP (NT-proBNP), high-sensitive cardiac troponin I (hs-cTnI) and MB isoenzyme of creatine phosphokinase (CK-MB) and evaluated the 12-lead ECG and 24 h Holter monitoring. Complete clinical and paraclinical evaluation was performed. Results: NT-proBNP level was significantly higher in patients with AHF (p < 0.001). In patients with AHF, NT-proBNP correlated with cQTi (p = 0.027), pathological Q wave (p = 0.029), complex premature ventricular contractions (PVCs) (p = 0.034) and ventricular tachycardia (p = 0.048). Hs-cTnI and CK-MB were correlated with ST-segment modification (p = 0.038; p = 0.018) and hs-cTnI alone with complex PVCs (p = 0.031). Conclusions: The statistical relationships found between cardiac biomarkers and ECG patterns support the added value of ECG in the diagnosis of AHF. We emphasize the importance of proper ECG analysis of more subtle parameters that can easily be missed. As a non-invasive technique, ECG can be used in the outpatient setting as a warning signal, announcing the acute decompensation of HF. In addition, the information provided by the ECG complements the biomarker results, supporting the diagnosis of AHF in cases of dyspnea of uncertain etiology. Further studies are needed to confirm long-term prognosis in a multi-marker approach.
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Sustained physical activity induces morphological and functional changes in the cardiovascular system. While mostly physiological, they can also become a trigger for major adverse cardiovascular events, the most severe of which are sudden cardiac arrest and sudden cardiac death. Therefore, any novel method which can help more accurately estimate the cardiovascular risk should be considered for further studying and future implementation in the standard protocols. The study of biomarkers is gaining more and more ground as they have already established their utility in diagnosing ischemic cardiac disease or in evaluating cardiac dysfunction in patients with heart failure. Nowadays, they are being implemented in the screening of apparently healthy individuals for the assessment of the cardiovascular risk. The aim of this paper is to gather published data regarding the measurements of cardiac biomarkers in athletes, i.e., troponins, myoglobin, CK-MB, NT-proBNP, and D-Dimers, and their potential use in the field of sports cardiology.
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(1) Background: Pulmonary embolism (PE) represents the third most important cardiovascular cause of death after myocardial infarction and stroke. The proper management of this condition is dependent on adequate risk stratification, due to the life-threatening complications of more aggressive therapies such as thrombolysis. Copeptin is a surrogate marker of vasopressin which is found increased in several cardiovascular conditions. The Mastora score is an imagistic evaluation of the degree of pulmonary arteries thrombotic burden based on computed tomography angiography. In this study, we aimed to evaluate the diagnostic and prognostic role of copeptin in patients with acute PE. Furthermore, we analyzed the relationship between copeptin and Mastora score and their role in PE risk profiling. (2) Methods: We conducted a single center prospective study that included 112 patients with PE and 53 healthy volunteers. Clinical and paraclinical parameters, together with plasma levels of copeptin and the Mastora score, were evaluated in all patients after admission. (3) Results: Copeptin levels were significantly increased in PE patients compared with the general population (26.05 vs. 9.5 pmol/L, p < 0.001), while receiver operating characteristic (ROC) analysis revealed an AUC of 0.800 (95% CI 0.728−0.873, p < 0.001). Copeptin directly correlated with the Mastora score (r = 0.535, p = 0.011) and both parameters were strong predictors for adverse clinical events and death. Receiver operating characteristic (ROC) analysis for death within 30 days revealed a copeptin cut-off of 38.36 pmol/L, which presented a specificity of 79.6% and a sensitivity of 88.9%, and a Mastora score cut-off of 82 points, which presented a specificity of 74.8% and a sensitivity of 77.8%. (4) Conclusions: Our results showed that copeptin and the Mastora score are both correlated with adverse cardiovascular events and mortality in PE patients, and this may pave the way for their use in clinical practice, helping physicians to select the best therapeutical management.
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(1) Background: Acute heart failure (HF) represents one of the most common yet extremely severe presentations in emergency services worldwide, requiring prompt diagnosis, followed by an adequate therapeutic approach, and a thorough risk stratification. Natriuretic peptides (NPs) are currently the most widely implemented biomarkers in acute HF, but due to their lack of specificity, they are mainly used as ruling-out criteria. Growth differentiation factor-15 (GDF-15) is a novel molecule expressing different pathophysiological pathways in HF, such as fibrosis, remodeling, and oxidative stress. It is also considered a very promising predictor of mortality and poor outcome. In this study, we aimed to investigate the GDF-15's expression and particularities in patients with acute HF, focusing mainly on its role as a prognosis biomarker, either per se or as part of a multimarker panel. (2) Methods: This unicentric prospective study included a total of 173 subjects, divided into 2 subgroups: 120 patients presented in emergency with acute HF, while 53 were ambulatory-evaluated controls with chronic HF. At admission, all patients were evaluated according to standard clinical echocardiography and laboratory panel, including the assessment of GDF-15. (3) Results: The levels of GDF-15 were significantly higher in patients with acute HF, compared to controls [596 (305−904) vs. 216 (139−305) ng/L, p < 0.01]. GDF-15 also exhibited an adequate diagnostic performance in acute HF, expressed as an area under the curve (AUC) of 0.883 [confidence interval (CI) 95%: 0.828−0.938], similar to that of NT-proBNP (AUC: 0.976, CI 95%: 0.952−1.000), or troponin (AUC: 0.839, CI 95%: 0.733−0.944). High concentrations of GDF-15 were significantly correlated with mortality risk. In a multivariate regression model, GDF-15 was the most important predictor of a poor outcome, superior to NT-proBNP or troponin. (4) Conclusions: GDF-15 proved to be a reliable tool in the multimarker assessment of patients with acute HF. Compared to the gold standard NT-proBNP, GDF-15 presented a similar diagnostic performance, doubled by a significantly superior prognostic value, making it worth being included in a standardized multimarker panel.
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Atherosclerosis is the basis of the cardiovascular continuum in peripheral artery disease (PAD) patients. Limiting functional decline and increasing quality of life are the main objectives for these patients. We conducted a prospective cohort study on 101 patients with PAD admitted to a single center in Northeast Romania. We used an index score to evaluate the 10-year mortality risk assessment and based on the scores we divided the patients into two groups: a low and low-intermediate risk mortality group (49 cases, 48.5%) and a high-intermediate and high-risk mortality group (52 cases, 51.5%). We analyzed demographics, comorbidities, clinical and paraclinical parameters and we aimed to identify the parameters associated with an unfavorable prognosis. Patients in the high-intermediate and high-risk mortality group were associated more with cardiovascular risk factors. Hypertension (p = 0.046), dyslipidemia (p < 0.001), diabetes mellitus (p < 0.001), and tobacco use (p = 0.018) were statistically significant factors. Lipid profile (low-density lipoprotein cholesterol, p = 0.005) and fasting blood glucose (p = 0.013) had higher mean serum values in the high-intermediate and high-risk mortality group, with a positive correlation between them and the ankle-brachial index value (p = 0.003). A multidisciplinary assessment and, especially, correction of associated cardiovascular risk factors prevent complications, and thus, improve the prognosis in the medium and long term.
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Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a global public health concern and is characterized by an exaggerated inflammatory response that can lead to a large variety of clinical manifestations such as respiratory distress, sepsis, coagulopathy, and death. While it was initially considered primarily a respiratory illness, different data suggests that COVID-19 can lead to a pro-inflammatory milieu and a hypercoagulable state. Several mechanisms attempt to explain the pro-coagulant state seen in COVID-19 patients, including increased fibrinogen concentration, different receptor binding, exhausted fibrinolysis, cytokine storm, and endothelial dysfunction. Some hematological parameters, such as elevated D-dimers and other fibrinolytic products, indicate that the essence of coagulopathy is massive fibrin formation. Moreover, elevated D-dimer levels have emerged as an independent risk factor for a worse outcome, including death, indicating a potential risk for deep vein thrombosis and pulmonary thromboembolism. Prophylactic anticoagulation is recommended in all in-patients with COVID-19 to reduce the incidence of thrombosis. Those with elevated D-dimer values or with a higher risk of developing thromboembolic events should be treated with higher doses of anticoagulant. Anticoagulation may not be enough in some circumstances, highlighting the need for alternative therapies. An understanding of the complex cross-talk between inflammation and coagulopathy is necessary for developing direct appropriate interventional strategies.
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Given the possible pathophysiological links between myocardial ischemia and SARS-CoV-2 infection, several studies have focused attention on acute coronary syndromes in order to improve patients' morbidity and mortality. Understanding the pathophysiological aspects of myocardial ischemia in patients infected with SARS-CoV-2 can open a broad perspective on the proper management for each patient. The electrocardiogram (ECG) remains the easiest assessment of cardiac involvement in COVID-19 patients, due to its non-invasive profile, accessibility, low cost, and lack of radiation. The ECG changes provide insight into the patient's prognosis, indicating either the worsening of an underlying cardiac illnesses or the acute direct injury by the virus. This indicates that the ECG is an important prognostic tool that can affect the outcome of COVID-19 patients, which important to correlate its aspects with the clinical characteristics and patient's medical history. The ECG changes in myocardial ischemia include a broad spectrum in patients with COVID-19 with different cases reported of ST-segment elevation, ST-segment depression, and T wave inversion, which are associated with severe COVID-19 disease.