Search

Background: Cardiac arrest (CA) is the most severe complication of acute myocardial infarction (AMI). Besides the location and severity of coronary occlusion, different factors may have significant role in the pathogenesis of AMI-related cardiac arrest (CA), but their contribution is still under investigation. The aim of the study was to investigate the cardiac magnetic resonance (CMR) features of myocardial injury associated with a higher risk of CA accompanying an AMI. Methods: In total, 918 myocardial segments from 54 post-AMI patients undergoing CMR imaging with delayed gadolinium enhancement were enrolled in the study, of which 18.54% presented CA during the acute phase of AMI. In all patients, infarct mass, the proportion of high transmurality extent, and scar mass at different myocardial segments were calculated using QMap software (Medis BV). Results: Compared to patients without CA, those with CA had a significantly higher infarct size (p = 0.03) and a higher degree of transmurality (29.28% vs. 14.1%, p = 0.01). The risk of CA during the acute phase was significantly higher in patients in whom the location of myocardial injury was at the level of latero-apical, antero-lateral, and basal anterior segments. Group 1 presented a larger infarct size at the level of the latero-apical (33.9 ± 30.6 g vs. 13.6 ± 17.3 g, p = 0.02), anterolateral (26.5 ± 29.0 g vs. 8.9 ± 12.8 g, p = 0.02), and anterobasal segment (20.1 ± 21.5 g vs. 7.8 ± 14.7 g, p = 0.02). Conclusions: CMR imaging identified infarct mass, high transmurality degree, and large myocardial injury as features associated with an increased risk of CA in the acute phase of AMI, especially at the level of anterolateral segments.

Inflammation is a key factor in the development of atherosclerosis, a disease characterized by the buildup of plaque in the arteries. COVID-19 infection is known to cause systemic inflammation, but its impact on local plaque vulnerability is unclear. Our study aimed to investigate the impact of COVID-19 infection on coronary artery disease (CAD) in patients who underwent computed tomography angiography (CCTA) for chest pain in the early stages after infection, using an AI-powered solution called CaRi-Heart®. The study included 158 patients (mean age was 61.63 ± 10.14 years) with angina and low to intermediate clinical likelihood of CAD, with 75 having a previous COVID-19 infection and 83 without infection. The results showed that patients who had a previous COVID-19 infection had higher levels of pericoronary inflammation than those who did not have a COVID-19 infection, suggesting that COVID-19 may increase the risk of coronary plaque destabilization. This study highlights the potential long-term impact of COVID-19 on cardiovascular health, and the importance of monitoring and managing cardiovascular risk factors in patients recovering from COVID-19 infection. The AI-powered CaRi-Heart® technology may offer a non-invasive way to detect coronary artery inflammation and plaque instability in patients with COVID-19.

The present study aimed to investigate the association between apolipoprotein B (Apo B) and classical features associated with clinical or subclinical atherosclerosis. A total of 811 adult patients from the general Romanian population, included in the national SEPHAR registry on hypertension, were divided into two groups based on Apo B value (low versus high Apo B with a cut-off established at 130 mg/dL) and subsequently into four subgroups according to the cut-offs recommended by the 2021 ESC Guidelines on Cardiovascular Disease Prevention. In all patients, lipid profile, uric acid, full blood count and presence of significant carotid plaques were assessed. Apo B levels were positively correlated with proatherogenic lipids (total cholesterol, triglycerides and LDL-cholesterol, p < 0.0001) and negatively correlated with HDL cholesterol (all p < 0.05). In comparison with patients with low Apo B levels, those with elevated Apo B levels more frequently presented significant carotid plaques (17% vs. 19% vs. 28% vs. 46%, p < 0.0001). Univariate regression analysis identified a strong association between the level of uric acid and increased value of Apo B in the four subgroups (uric acid 4.8 +/− 1.3 vs. 5 +/− 1.6 vs. 5.1 +/− 1.5 vs. 5.8 +/− 1.6, r = 0.2, p < 0.0001). The results of this nationwide registry on hypertension in Romania indicate that high Apo B may be considered as a risk factor for CVD, promoting atherosclerosis and associated with increased expression of classical markers of clinical or subclinical CVD.

Background: The integrated ST segment elevation score (ISSTE) score objectively quantifies the ECG changes before and after primary percutaneous coronary intervention (pPCI) for ST segment elevation myocardial infarction (STEMI). The inflammatory response is a major component in scar formation and remodeling process of the myocardial tissue following myocardial infarction (MI). Cardiac magnetic resonance imaging (CMR) precisely quantifies the cardiac function and assesses the pattern of the myocardial scar tissue. The aim of the study was to evaluate the relations between the ISSTE score and: (1) acute inflammatory biomarkers and (2) extent of the myocardial scar determined by CMR in STEMI treated with pPCI. Material and methods: One hundred thirty STEMI patients were included in the study, who underwent pPCI in the first 12 hours from symptom debut. ISSTE-1 was calculated at presentation and 2 hours following pPCI (ISSTE-2). Inflammatory biomarkers were determined at admission and day 5, followed by LGE-CMR at 4 weeks, with quantification of cardiac function and extent of infarct size (IS) and transmurality. Patients were divided in low and high ISSTE groups based on the median values. Results: No significant differences were noted in terms of CMR parameters or inflammatory biomarkers and between the groups with low or high ISSTE-1. Significantly higher levels of day-5 hs-CRP (p = 0.03) and day-1 IL-6 (p = 0.02), MMP-9 (p = 0.05) were recorded in high ISSTE-2 groups. LV IS mass (23.11 ± 5.31 vs. 57.94 ± 8.33, p = 0.001), percentage (13.55 ± 6.22 vs. 27.15 ± 7.12, p = 0.001) and transmurality (p = 0.001) was significantly higher in ISSTE-2 group. ISSTE-2 significantly correlated with LV IS mass (r = 0.391, p Conclusions: A high ISSTE-2 score is associated with increased inflammatory response exhibited by elevated serum IL-6 and MMP-9 levels determined on the day of admission, and with persistently increased serum hs-CRP levels on day 5 of the acute event. A higher ISSTE-2 score is associated with larger myocardial scar extent expressed by IS, higher transmurality and reduced LV EF at 1-month LGE CMR follow-up.

Background: The aim of this study was to investigate the correlation between serum biomarkers of left ventricular dysfunction and systemic inflammation in the first days after the acute episode, and to investigate their role for early identification of patients at high risk for post-infarction heart failure. Materials and methods: In total, 123 subjects admitted to the Intensive Cardiovascular Care Unit of the Cardiology Clinic of the Târgu Mureș County Clinical Emergency Hospital, Romania, with acute myocardial infarction were retrospectively analyzed in this study. Based on the level of NT-proBNP, the study population was divided into 2 groups: Group 1 (n = 92), with NT-proBNP 3,000 pg/mL. Results: Biomarkers reflecting systemic inflammation presented significantly higher values in patients with elevated NT-proBNP (hs-CRP – 12.3 ± 8.9 mg/L vs. 3.6 ± 6.7 mg/L, p Conclusions: Serum biomarkers of ventricular dysfunction are strongly associated with systemic inflammation and ventricular impairment in the immediate phase after an acute myocardial infarction. Systemic inflammation has a higher impact on the clinical outcomes and progression to heart failure than the local coronary inflammation expressed by cell adhesion molecules.

Contains fulltext : 286832.pdf (Publisher’s version ) (Open Access) BACKGROUND: Direct evaluation of vascular inflammation in patients with COVID-19 would facilitate more efficient trials of new treatments and identify patients at risk of long-term complications who might respond to treatment. We aimed to develop a novel artificial intelligence (AI)-assisted image analysis platform that quantifies cytokine-driven vascular inflammation from routine CT angiograms, and sought to validate its prognostic value in COVID-19. METHODS: For this prospective outcomes validation study, we developed a radiotranscriptomic platform that uses RNA sequencing data from human internal mammary artery biopsies to develop novel radiomic signatures of vascular inflammation from CT angiography images. We then used this platform to train a radiotranscriptomic signature (C19-RS), derived from the perivascular space around the aorta and the internal mammary artery, to best describe cytokine-driven vascular inflammation. The prognostic value of C19-RS was validated externally in 435 patients (331 from study arm 3 and 104 from study arm 4) admitted to hospital with or without COVID-19, undergoing clinically indicated pulmonary CT angiography, in three UK National Health Service (NHS) trusts (Oxford, Leicester, and Bath). We evaluated the diagnostic and prognostic value of C19-RS for death in hospital due to COVID-19, did sensitivity analyses based on dexamethasone treatment, and investigated the correlation of C19-RS with systemic transcriptomic changes. FINDINGS: Patients with COVID-19 had higher C19-RS than those without (adjusted odds ratio [OR] 2·97 [95% CI 1·43-6·27], p=0·0038), and those infected with the B.1.1.7 (alpha) SARS-CoV-2 variant had higher C19-RS values than those infected with the wild-type SARS-CoV-2 variant (adjusted OR 1·89 [95% CI 1·17-3·20] per SD, p=0·012). C19-RS had prognostic value for in-hospital mortality in COVID-19 in two testing cohorts (high [≥6·99] vs low [

Background: The evaluation of site-specific phenotype according to the topographic location of atherosclerotic lesions within the coronary tree has not been studied so far. The present study is based on the premise that the location of coronary plaques can influence their composition and degree of vulnerability. Aim: To evaluate different phenotypes of vulnerable coronary plaques across the three major coronary arteries in terms of composition, morphology, and degree of vulnerability, in patients with chest pain and low-to-intermediate probability of coronary artery disease, using coronary computed tomography angiography (CCTA) and a complex plaque analysis. Material and methods: This was a cross-sectional study on 75 subjects undergoing CCTA for chest pain, who presented at least one vulnerable coronary plaque (VP), defined as the presence of ≥1 CT vulnerability marker (low attenuation plaque, napkin-ring sign, spotty calcifications, positive remodeling). The study included per plaque analysis of 90 vulnerable coronary lesions identified in various locations within the coronary tree as follows: n = 30 VPs in the left anterior descending artery (LAD), n = 30 VPs in the circumflex artery (CXA), and n = 30 VPs in the right coronary artery (RCA). Results: The RCA exhibited significantly longer VPs (p = 0.001), with the largest volume (p = 0.0007) compared to those arising from the LAD and CXA. Vulnerable plaques located in the LAD exhibited a significantly more calcified phenotype (calcified volume: LAD – 44.07 ± 63.90 mm3 vs. CXA – 12.40 ± 19.65 mm3 vs. RCA – 33.69 ± 34.38 mm3, p = 0.002). Plaques from the RCA presented a more non-calcified phenotype, with the largest non-calcified (p = 0.002), lipid rich (p = 0.0005), and fibrotic volumes (p = 0.003). Low-attenuation plaques were most frequent in the RCA (p = 0.0009), while the highest vulnerability degree was present in lesions located in the LAD, which presented the highest number of vulnerability markers per plaque (p = 0.01). Conclusions: Vulnerable plaques arising from the right coronary artery are longer, more vo-luminous and with larger lipid and non-calcified content, whereas those located in the left anterior descending artery present a higher volume of calcium, but also a higher degree of vulnerability. The least vulnerable lesions were present in the circumflex artery.

The World Health Organization (WHO) declared the transmission of SARS-CoV-2 a Public Health Emergency of International Concern. The novel coronavirus has diverse manifestations, usually similar to a common cold or influenza. The majority of patients with coronavirus disease have typical imaging features. The typical CT characteristics of patients with COVID-19 pneumonia are ground-glass opacities and consolidative lesions with a peripheral and posterior distribution. Noninvasive imaging methods are precise and rapid means of diagnosing pneumonia and cardiovascular complications caused by COVID-19 infection. Therefore, it is important for clinicians to understand the implications of this pandemic and to be familiar with the different imaging aspects of the novel coronavirus disease. This review focuses on the most commonly reported imaging findings of COVID-19 infection in different patients from different countries, the expert recommendations, and the cardiac manifestations of SARS-CoV-2 infection.

Background: Multimodality imaging improves the accuracy of cardiac assessment in patients with prior myocardial infarction. The aim of this study was to investigate the association between coronary plaque vulnerability (PV) and myocardial viability in the territory irrigated by the infarct-related artery (IRA). Secondary objectives include evaluation of the systemic inflammation but also different cardiac risk scores (SYNTAX score, Duke jeopardy score, or calcium score) using hybrid imaging models of coronary computed tomography angiography (CCTA) and cardiac magnetic resonance (CMR) in patients who have suffered a previous myocardial infarction (MI). Material and methods: The study included 45 subjects with documented MI in the 30 days prior to study enrolment, who underwent CCTA and CMR examinations. Computational postprocessing of CCTA and CMR images was used to generate fused imaging models. Based on the vulnerability degree of the associated non-culprit lesion located proximally in the IRA, the study population was divided into 3 groups: Group 1 – subjects with no sign of vulnerability (n = 7); Group 2 – subjects with 1 or 2 CT vulnerability features (n = 28); and Group 3 – subjects with >2 features of vulnerability (n = 12). Results: CCTA features indicative for the severity of coronary artery disease were not different between groups in terms of calcium scoring (460 ± 501 vs. 579 ± 430 vs. 432 ± 494, p = 0.7) or SYNTAX score (25 ± 9.2 vs. 24.9 ± 8.3 vs. 20.2 ± 11.9, p = 0.4). However, after 1 month, infarct size and the Duke jeopardy score were associated with increased PV (infarct size 8.77 ± 3.4 g in Group 1, compared to 20.87 ± 8.3 g in Group 2 and 27.99 ± 11.8 g in Group 3 (p = 0.007), while the Duke jeopardy score was 4.4 ± 1.6 in Group 1, vs. 7.07 ± 2.1 in Group 2 vs. 7.5 ± 1.73 in Group 3 (p = 0.01). Inflammatory biomarkers were directly associated with coronary plaque vulnerability (p = 0.007 for hs-CRP and p = 0.038 for MMP-9). Conclusion: In patients with prior myocardial infarction, the size of myocardial scar was directly correlated with the vulnerability degree of coronary plaques and with systemic inflammation quantified during the acute phase of the coronary event. Hybrid imaging may help to identify the hemodynamically significant plaques with superior accuracy.

Multivessel coronary artery disease, defined by the presence of a significant stenosis (≥50% diameter) in two or more epicardial coronary vessels, usually occurs in more than 50% of patients with ST-segment elevation myocardial infarction. The latest guidelines indicate revascularization of the non-culprit artery with a recommendation of class IIB. However, the management of non-culprit lesions in patients with acute coronary syndrome is still a matter of debate. This article presents the most recent concepts related to the management of culprit and non-culprit coronary lesions, based on advanced imaging approaches, in order to identify high-risk patients and prevent further acute coronary syndromes.

Coronary artery disease (CAD) represents one of the leading causes of morbidity and mortality across Europe. Most of the patients do not experience any warning sign before the coronary event develops, therefore screening this group of patients is essential to prevent major cardiac events. Coronary computed tomography angiography (CCTA) offers a noninvasive approach of the coronary arteries, providing information not only on the presence and severity of the coronary stenosis, but is also able to characterize the structure of the coronary wall. CCTA allows complex evaluation of the extension of CAD, and by assessing the structure of the atherosclerotic plaque, it can identify its degree of vulnerability. The napkin-ring sign (NRS) represents a ring-like attenuation of the non-calcified portion of the coronary lesion and has a high specificity (96–100%) for the identification of thin cap fibroatheroma (TCFA) or culprit lesion in acute coronary syndromes (ACS). It is also an independent predictor for ACS events and the strongest predictor for future ACS. Modern CCTA can provide submillimeter isotropic spatial resolution. Thus, CT attenuation-based tissue interpretation enables the assessment of total coronary plaque burden and individual plaque components, with a similar accuracy as intravascular ultrasoud-based investigations. This review aims to present the important role of CCTA as a potent screening tool for patients with CAD, and the current evidences in the detection and quantification of vulnerable plaques.

Extracellular matrix (ECM) plays an important role in the development and progression of atherosclerotic lesions. Changes in the ECM are involved in the pathophysiology of many cardiovascular diseases, including atherosclerosis. Matrix metalloproteinases (MMPs) are a family of zinc-dependent proteases, also known as matrixins, with proteolytic activity in the ECM, being responsible for the process of tissue remodeling in various systemic pathologies, including cardiac and vascular diseases. MMPs play an important role in maintaining normal vascular structure, but also in secondary cardiovascular remodeling, in the formation of atherosclerotic plaques and in their vulnerabilization process. In addition to the assigned effect of MMPs in vulnerable plaques, they have a well-defined role in post-infarction ventricular remodeling and in various types of cardiomyopathies, followed by onset of congestive heart failure, with repeated hospitalizations and death. The aim of this manuscript was to provide a summary on the role of serum matrix metalloproteinases in the process of initiation, progression and complication of atherosclerotic lesions, from a molecular level to clinical applicability and risk prediction in patients with vulnerable coronary plaques.

Decades of research and experimental studies have investigated various strategies to prevent acute coronary events. However, significantly efficient preventive methods have not been developed and still remains a challenge to determine if a coronary atherosclerotic plaque will become vulnerable and unstable. This review aims to assess the significance of plaque vulnerability markers, more precisely the role of spotty calcifications in the development of major cardiac events, given that coronary calcification is a hallmark of atherosclerosis. Recent studies have suggested that microcalcifications, spotty calcifications, and the presence of the napkin-ring sign are predictive vulnerable plaque features, and their presence may cause plaque instability.

Various cardiovascular imaging techniques were developed for the detection of vulnerable atherosclerotic plaques, hoping to be able to predict a cardiovascular event. Plaque vulnerability results from compound pathophysiological mechanisms that lead to structural and morphological changes in lesions. The aim of this review is to present the most recent techniques for the assessment of vulnerable coronary plaques such as cardiac computed tomography angiography (CCTA), optical coherence tomography, or virtual histology intravascular ultra-sound, based on literature data from the last 3 years. CCTA permits direct visualization of the intravascular lumen, together with characterization of the arterial wall. Recent studies maintain that low-attenuation plaques, spotty calcifications, positive vessel remodeling, and the napkin-ring sign are considered main markers of plaque vulnerability and instability. Emerging analytical techniques, such as machine learning or radiomics, will probably demonstrate useful as an auxiliary diagnostic tool for vulnerable plaque detection. The data from the two imaging techniques together provide useful information, especially in patients undergoing a PCI procedure for an acute coronary syndrome. Invasive and noninvasive imaging techniques are able to deliver a large amount of scientific data to assess vulnerable coronary atheromatous plaques. Recent studies demonstrated that information defined by the two techniques is complementary, and using both methods is essential for adequate diagnosis, therapeutic strategy, and prognostic assessment.

Introduction: Spontaneous coronary artery dissection (SCAD) represents a very rare and poorly understood condition that is gaining recognition as an important cause of myocardial infarction, especially among young women. The pathogenesis of SCAD is not well established yet, but several theories have been proposed. Case presentation: We report the case of a 25-year-old woman without any history of cardiovascular disease who presented with acute anterior ST-elevation myocardial infarction (STEMI) due to the luminal obstruction generated by an intramural hematoma from a SCAD of the left main coronary artery, which was successfully treated by coronary artery stenting. Additionally, the patient presented anomalies of coronary origins (ACO) with separate emergences of the left anterior descending (LAD) artery from the left coronary cusp and the left circumflex artery (LCX) from the right coronary cusp, with no apparent clinical significance. Conclusion: SCAD should always be included in the differential diagnosis of young patients presenting with STEMI. In case of prompt diagnosis, SCAD-STEMI patients are successfully treated with percutaneous coronary intervention (PCI). Moreover, it is of vital importance to identify variants of ACO, even without clinical relevance at the moment of the acute event, in order to initiate an appropriate management, since ACO increases the risk of routine PCI.

BACKGROUND The coronavirus disease 2019 (COVID-19) pandemic has adversely affected diagnosis and treatment of noncommunicable diseases. Its effects on delivery of diagnostic care for cardiovascular disease, which remains the leading cause of death worldwide, have not been quantified. OBJECTIVES The study sought to assess COVID-19`s impact on global cardiovascular diagnostic procedural volumes and safety practices. METHODS The International Atomic Energy Agency conducted a worldwide survey assessing alterations in cardiovascular procedure volumes and safety practices resulting from COVID-19. Noninvasive and invasive cardiac testing volumes were obtained from participating sites for March and April 2020 and compared with those from March 2019. Availability of personal protective equipment and pandemic-related testing practice changes were ascertained. RESULTS Surveys were submitted from 909 inpatient and outpatient centers performing cardiac diagnostic procedures, in 108 countries. Procedure volumes decreased 42% from March 2019 to March 2020, and 64% from March 2019 to April 2020. Transthoradc echocardiography decreased by 59%, transesophageat echocardiography 76%, and stress tests 78%, which varied between stress modalities. Coronary angiography (invasive or computed tomography) decreased 55% (p < 0.001 for each procedure). hi multivariable regression, significantly greater reduction in procedures occurred for centers in countries with lower gross domestic product. Location in a low-income and lower-middle-income country was associated with an additional 22% reduction in cardiac procedures and less availability of personal protective equipment and teteheatth. CONCLUSIONS COVID-19 was associated with a significant and abrupt reduction in cardiovascular diagnostic testing across the globe, especially affecting the world's economically challenged. Further study of cardiovascular outcomes and COVID-19-related changes in care delivery is warranted. (C) 2021 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation.

The new coronavirus (COVID-19) outbreak was declared a pandemic by the World Health Organization on March 11, 2020. Since then, important changes have been observed in the medical world, both in terms of patient management and patient presentations to the hospital. A dramatic decrease in the number of cardiovascular emergencies presenting to the emergency rooms has been reported in every country affected by the COVID-19 pandemic. This resulted mainly from the fear of patients to present at the hospital due to the risk of infection with the new coronavirus. Moreover, a significant increase in the time spent for investigations and specialized treatment has been reported for patients suffering from acute cardiovascular diseases. This adds to the longer times reported from symptom onset to presentation, and also to the longer period spent for triage in the emergency room. The aim of this paper is to highlight the dramatic reduction in the number of cardiovascular emergencies during the COVID-19 period and its possible explanations.

The novel coronavirus disease first appeared in Wuhan (China) is an infectious disease spreading throughout the world, causing life-threatening conditions in vulnerable or even healthy individuals. The great impact of this virus on healthcare urges physicians to investigate all aspects of the disease in order to overcome its complications. A particularly investigated aspect of the SARS-CoV-2 infection is represented by the coagulation disorders among infected and critically ill patients. Several studies observed modified blood coagulation parameters such as D-dimers, fibrinogen, and coagulation times. Moreover, the severe thrombotic complications, mainly pulmonary embolism, could be responsible for the high mortality and poorer outcomes of COVID-19 infected patients. The aim of this article is to present the current knowledge related to thrombosis predisposition in patients infected with the new coronavirus.

The aim of this review is to provide a short update on whether treatment with angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) has beneficial or harmful effects in patients infected with SARS-CoV-2. Epidemiological studies have shown that SARS-CoV-2 infects all age groups, presenting a higher incidence in elderly patients with various comorbidities such as hypertension, diabetes mellitus, and cardiovascular diseases. A large proportion of these patients are treated with ACEIs and ARBs. Since it has been demonstrated that SARS-CoV-2 uses angiotensin converting enzyme type 2 (ACE2) as an entry point into host cells, it is important to know whether ACEIs and ARBs could modify the expression of this enzyme, and thus promote the viral infection. Animal studies and a few studies in humans have shown that renin angiotensin system (RAS) inhibitors increase tissue expression of ACE2, but with potentially beneficial effects. In this context, it is imperative to provide appropriate guidance for clinicians and patients. The major cardiology associations across the world have released statements in which they recommend healthcare providers and patients to continue their treatments for hyper-tension and heart failure as prescribed.

Myocardial infarction with non-obstructive coronary arteries (MINOCA) has been defined as clinical presentation of an acute coronary syndrome with laboratory evidence of myocardial necrosis, but with coronary stenosis of less than 50% on coronary angiography. On the other side, myocarditis is an inflammatory response triggered by viral, bacterial, fungal, lymphocytic, eosinophilic, or autoimmune myocardial injury, which may be associated with elevated myocardial necrosis serum biomarkers. We present the case of a young male patient with acute chest pain, ST-segment elevation, and high-sensitivity troponin levels of 22,162 ng/L.

Myocarditis is one of the relatively common complications of respiratory infection with SARSCoV-2. As several patients confirmed with the new SARS-CoV-2 are known with cardiovascular disease (CVD) and data from the literature show negative prognosis and a higher risk of complications, this subgroup of subjects represents a particular situation. Therefore, an adequate understanding of the mechanisms involved in myocardial injury and interaction between COVID-19 and CVD is essential for optimal further management. Studies have proved that in COVID-19 patient myocarditis is determined via three pathological mechanisms of cardiomyocyte injury: direct viral cell entry and binding to ACE2, vasculitis-mediated injury, and systemic inflammatory response leading to pro-inflammatory cytokine discharge. Studies show that the incidence of myocarditis in patients with SARS-CoV-2 is relatively low, 4.8%, but myocardial damage occurs in more than 25% of critical cases in the form of acute fulminant myocarditis with severe hemodynamic degradation, or develops when the severity of SARS-CoV-2 infection intensifies. The mortality rate in myocarditis from COVID-19 infection ranges between 50–70%, with poorer prognosis and a higher risk of complications in CVD patients. As in all of these cases increased troponin and natriuretic peptide levels proved to be a negative prognostic factor, for risk stratification and prompt treatment, cardiac biomarkers should be evaluated in all patients with COVID-19.

Environmental factors may have an important role in the development of coronary heart disease. However, it is not clearly understood yet how the genetic factors interplay with the environmental ones in the onset of acute myocardial infarction. The early onset of coronary artery disease in cases with a positive family history suggests a certain role of genetic predisposition, but the open question remains: could environmental differences contribute to this predisposition? This case report describes similar coronary angiographic findings of two brothers who developed acute myocardial infarction in their early 40s, after being exposed to different environmental risk factors.

The recent technological developments in the field of cardiac imaging have established coronary computed tomography angiography (CCTA) as a first-line diagnostic tool in patients with suspected coronary artery disease (CAD). CCTA offers robust information on the overall coronary circulation and luminal stenosis, also providing the ability to assess the composition, morphology, and vulnerability of atherosclerotic plaques. In addition, the perivascular adipose tissue (PVAT) has recently emerged as a marker of increased cardiovascular risk. The addition of PVAT quantification to standard CCTA imaging may provide the ability to extract information on local inflammation, for an individualized approach in coronary risk stratification. The development of image post-processing tools over the past several years allowed CCTA to provide a significant amount of data that can be incorporated into machine learning (ML) applications. ML algorithms that use radiomic features extracted from CCTA are still at an early stage. However, the recent development of artificial intelligence will probably bring major changes in the way we integrate clinical, biological, and imaging information, for a complex risk stratification and individualized therapeutic decision making in patients with CAD. This review aims to present the current evidence on the complex role of CCTA in the detection and quantification of vulnerable plaques and the associated coronary inflammation, also describing the most recent developments in the radiomics-based machine learning approach for complex assessment of plaque-associated risk.

Background: Atrial fibrillation (AF), a common arrhythmia in clinical practice, is associated with a high rate of complications and an increased risk for thromboembolic events. Pulmonary vein ablation is a new therapeutic option to cure AF; however, it remains associated with a high rate of recurrence. In this study we aimed to identify the clinical characteristics and imaging-based features that may predict the risk of recurrence after pulmonary veins ablation in atrial fibrillation. Materials and method: Twenty-four patients with paroxysmal and persistent AF, who underwent radiofrequency catheter ablation and a 12-month follow-up were included in the study. Group 1 included 8 patients with AF recurrence, and group 2 included 16 patients with no AF recurrence. In all cases, cardiovascular risk factors, ejection fraction, left atrial diameter, atrial volumes, and epicardial fat volume were analyzed. Results: CT analysis revealed that patients with AF recurrence presented a significantly larger mean index of left atrial volume (59.57 ± 8.52 mL/m2 vs. 49.99 ± 10.88 mL/m2, p = 0.04), right atrial volume (58.94 ± 8.37 mL/m2 vs. 43.21 ± 6.4 mL/m2, p Conclusion: Left atrial diameter, indexed atrial volumes, and epicardial fat volume may be used as factors to identify patients at risk for developing recurrence after pulmonary vein ablation.

Coronary artery anomalies represent a heterogeneous group of congenital diseases with various clinical presentations. Over time, the subject of coronary anomalies has been constantly changing in terms of definition, morphology, clinical manifestations, prognosis, and treatment. We present the case of a male patient, aged 53, with coronary artery disease and a medical history of high blood pressure and diabetes mellitus, who had undergone a coronary computed tomography angiography during the one-year follow-up after a percutaneous coronary intervention with drug-eluting stent implantation for a critical stenosis in the middle segment of the left anterior descending artery. Axial images revealed a separate origin of the left anterior descending and circumflex arteries from the left aortic coronary sinus, with the absence of the left main coronary artery.

(1) Background: The inflammatory response following MI plays an important role in the healing, scar formation, and left ventricle (LV) remodeling. Cardiac magnetic resonance (CMR) imaging can accurately quantify the extent of myocardial scarring. The study aimed to investigate: (a) the relationship between acute inflammatory response and the CMR parameters of the scarring extent, and (b) the predictive power of inflammatory biomarkers and myocardial scarring for 2-year mortality. (2) Methods: The study included 202 STEMI patients, who underwent pPCI. Serum hs-CRP, IL-6, P-selectin, E-selectin, I-CAM, and V-CAM levels were determined at admission, and hs-CRP on the fifth day. Patients underwent LGE-CMR after 1 month, for LV volumes, ejection fraction (EF), infarct size (IS), and transmurality. Subjects were divided into tertiles according to the IS, and 2-year all-cause mortality was determined. (3) Results: IL-6 was associated with IS (r = 0.324, p = 0.01), increased transmurality index (r = 0.3, p = 0.01), and lower LVEF (r = −0.3, p = 0.02). Admission hs-CRP levels were not associated with IS, transmurality, or mortality, while hs-CRP at day 5 was a significant predictor for IS (AUC = 0.635, p = 0.05) as well as IL-6 levels (AUC = 0.685, p < 0.001). Mortality was significantly higher in the upper IS tertiles (6% vs. 8.7% vs. 24.52%, p = 0.005). IS was a significant predictor of 2-year mortality (AUC = 0.673, p = 0.002), with a cut-off value of 28.81 g, as well as high transmurality (AUC = 0.641, p = 0.013), with a cut off value of 18.38 g. (4) Conclusions: The serum levels of IL-6 and day-5 hs-CRP predict IS and transmurality, and day-5 hs-CRP levels are independent predictors of 2-year mortality in STEMI patients treated with pPCI. The CMR pattern of myocardial scarring after 1 month, as expressed by the magnitude of IS and transmurality, is a significant predictor for 2-year mortality after revascularized STEMI.

Both periodontal disease and atherosclerosis are chronic disorders with an inflammatory substrate that leads to alteration of the host’s immune response. In PD, inflammation is responsible for bone tissue destruction, while in atherosclerosis, it leads to atheromatous plaque formation. These modifications result from the action of pro-inflammatory cytokines that are secreted both locally at gingival or coronary sites, and systemically. Recently, it was observed that in patients with PD or with cardiovascular disease, COVID-19 infection is prone to be more severe. While the association between PD, inflammation and cardiovascular disease is well-known, the impact of COVID-19-related inflammation on the systemic complications of these conditions has not been established yet. The purpose of this review is to bring light upon the latest advances in understanding the link between periodontal–cardiovascular diseases and COVID-19 infection.

The COVID-19 pandemic has had a major impact on cardiovascular emergencies. The aim of this study was to investigate the impact of the COVID-19 pandemic on a regional network for management of ST-segment elevation acute myocardial infarction (STEMI). Methods: We report a single center’s experience of patients hospitalized for ACS in a high-volume hub of a STEMI network during the lockdown (in the first pandemic trimester), compared with the same time interval of the previous year and including all consecutive patients referred for an AMI during the second trimester of 2020 (from April to June) or during the same time interval of the previous year, 2019. Results: The absolute number of hospital admissions for AMI decreased by 22.3%, while the non-AMI hospitalizations decreased by 77.14% in Q2-2020 compared to Q2-2019 (210 vs. 48, p &lt, 0.0001). As a consequence, the percentage of AMI cases from the total number of hospital admission increased from 38% to 68% (p &lt, 0.0001), AMI becoming the dominant pathology. In the STEMI group there was a significant reduction of 55% in the absolute number of late STEMI presentations. Functionality of the STEMI network at the hub level did not present a significant alteration with only a minor increase in the door-to-balloon time, from 34 min to 41 min. However, at the level of the network we recorded a lower number of critical cases transferred to the interventional center, with a dramatic reduction of 56.1% in the number of critical STEMI cases arriving in the acute cardiac care unit (17.0% vs. 7.3%, p-0.04 for KILLIP class III, and 21.17% vs. 11.11%, p = 0.08 for resuscitated out of hospital cardiac arrest). Conclusions: The COVID-19 outbreak did not have a major impact on the interventional center’s functionality, but it limited the capacity of the regional STEMI network to bring the critical patient with complicated STEMI to the cathlab in time during the first months of the lockdown. Even a very well-functioning STEMI network like the one in Central Romania had difficulties bringing the most critical STEMI cases to the cathlab in time.

Atherosclerosis is the elemental precondition for any cardiovascular disease and the predominant cause of ischemic heart disease that often leads to myocardial infarction. Systemic risk factors play an important role in the starting and progression of atherosclerosis. The complexity of the disease is caused by its multifactorial origin. Besides the traditional risk factors, genetic predisposition is also a strong risk factor. Many studies have intensively researched cardioprotective drugs, which can relieve myocardial ischemia and reperfusion injury, thereby reducing infarct size. A better understanding of abnormal epigenetic pathways in the myocardial pathology may result in new treatment options. Individualized therapy based on genome sequencing is important for an effective future medical treatment. Studies based on multiomics help to better understand the pathophysiological mechanism of several diseases at a molecular level. Epigenomic, transcriptomic, proteomic, and metabolomic research may be essential in detecting the pathological phenotype of myocardial ischemia and ischemic heart failure.

Heart failure is a clinical syndrome that appears as a consequence of a structural disease, and the most common cause of left ventricular systolic dysfunction results from myocardial ischemia. Cardiac remodeling and neuroendocrine activation are the major compensatory mechanisms in heart failure. The main objective of the study is to identify the association between serum biomarkers illustrating the extent of myocardial necrosis (highly sensitive troponin as-says), left ventricular dysfunction (NT-proBNP), and systemic inflammatory response (illustrated via serum levels of hsCRP and interleukins) during the acute phase of a myocardial infarction, and the left ventricular remodeling process at 6 months following the acute event, quantified via speckle tracking echocardiography. The study will include 400 patients diagnosed with acute myocardial infarction without signs and symptoms of heart failure at the time of enrollment that will undergo a complex clinical examination and speckle tracking echocardiography. Serum samples from the peripheral blood will be collected in order to determine the inflammatory serum biomarkers. After 6 months, patients will be divided into 2 groups according to the development of ventricular remodeling, quantified by speckle tracking echocardiography: group 1 will consist of patients with a remodeling index lower than 15%, and group 2 will consist of patients with a remodeling index higher than 15%. All clinical and imaging data obtained at the baseline will be compared between these two groups in order to determine the features associated with a higher risk of deleterious ventricular remodeling and heart failure.

Atherosclerosis is a slow, progressive disease, its most common manifestation and most severe consequence being coronary artery disease, one of the main causes of mortality and morbidity worldwide. The vast majority of cardiovascular deaths are caused by complications of atherosclerosis, most often being represented by the rupture of an unstable coronary plaque, regularly triggered by inflammation. A vulnerable plaque is characterized by a large, lipid-rich necrotic core, a thin fibrous cap with macrophage infiltration, and the presence of multiple specific biomarkers such as positive remodeling, irregular calcifications, and low attenuation visible with coronary computed tomography angiography (CCTA). Identifying biomarkers that could predict the risk of plaque rupture with high accuracy would be a significant advance in predicting acute cardiac events in asymptomatic patients, furthermore guiding treatment of patients with this disease. The main indication of noninvasive imaging is to identify patients at risk based on the presence or absence of symptoms that can be related to myocardial ischemia. The diagnostic objective is to confirm or to exclude the presence of coronary plaques. Coronary imaging in asymptomatic individuals is used to estimate the risk of future cardiac events through the identification of non-obstructive high-risk plaques. The possibility to monitor the evolution of vulnerable plaques via noninvasive imaging techniques, prior to the occurrence of an acute clinical event, is the main goal in plaque imaging. This manuscript will be focusing on recent advances of noninvasive imaging of vulnerable coronary plaques.

Coronary computed tomography angiography (CCTA) is a reliable screening method of patients with coronary artery disease (CAD). CCTA is capable to assess both coronary stenosis and plaque morphology, but does not provide hemodynamic characterization of the coronary lesions. However, the severity of coronary stenosis does not always reflect the hemodynamic significance of the plaque. Invasive fractional flow reserve (FFR) is considered the gold standard for the functional evaluation of a potential ischemia-causing stenosis. FFR derived from CCTA (FFR-CT) is a new noninvasive diagnostic tool, using a typically acquired CCTA, without the need for any further radiation or medication. Additional functional assessment of the coronary lesions permits a more complex characterization of CAD patients. Based on the FFR-CT examination, patients who need invasive coronary intervention can be selected more precisely, and a more personalized and optimized treatment can be provided.

With coronary artery disease (CAD) projected to remain the leading cause of global mortality, prevention strategies seem to be the only effective approach able to reduce the burden and improve mortality and morbidity. At this moment, diagnostic strategies focus mainly on symptomatic patients, ignoring the occurrence of major cardiovascular events as the only manifestation of CAD. As two thirds of fatal myocardial infarction are resulting from plaque rupture, an approach based on the “vulnerable plaque” concept is mandatory in order to improve patient diagnosis, treatment, and, by default, prognosis. Given that the main studies focus on a plaque-centered approach, this is a prospective observational study that will perform a complex assessment of the features that characterize unstable coronary lesions, in terms of both local assessment via specific coronary computed tomography angiography markers of coronary plaque vulnerability and systemic approach based on serological markers of systemic inflammation in patients proved to be “vulnerable” by developing acute cardiovascular events.

Out-of-hospital cardiac arrest (OHCA) has a poor prognosis and is the most severe complication of any cardiac event. It is known from previous studies that the location of the culprit lesion in ST-segment elevation myocardial infarction (STEMI) patients with cardiac arrest may affect the post resuscitation survival rate. However, due to the low number of cases, the association between the localization of the culprit lesion within the coronary tree and the occurrence of cardiac arrest is not widely discussed, because resuscitated cardiac arrest patients are excluded from the vast majority of clinical trials. This is a prospective observational study that aims to develop a prediction model for OHCA in patients who present with STEMI, based on differences related to culprit lesion location. The primary objective of the study is to evaluate the differences related to the location of the culprit lesion in patients with STEMI who present OHCA versus patients without cardiac arrest.

Background: Myocardial infarction (MI) with no obstructive coronary arteries (MINOCA) is a special form of the acute coronary syndrome. The heterogeneous pathophysiology of MINOCA is not well elucidated and includes cardiac and non-cardiac causes. Slow flow phenomenon on coronary angiography can be associated with several possible causes of MINOCA confirmed by optical coherence tomography (OCT). Therefore, the aim of this study is to assess the underlying mechanism of the delayed washout phenomenon on coronary angiography and the potential role of subintimal coronary artery dissection (SD) in the setting of an acute MI. Methods and design: This clinical prospective, descriptive research will enroll patients diagnosed with acute MI (STEMI or NSTEMI) identified by coronary angiography, followed by OCT imaging of the coronary arteries at the Emergency Clinical County Hospital of Târgu Mureş, Romania. The enrolled patients will be separated into two groups based on OCT examination, patients with SD and patients with no SD. Conclusion: The underlying mechanisms of MINOCA with delayed washout phenomenon on coronary angiography is still poorly understood. Modern invasive imaging techniques are capable to assess the microstructure of the coronary artery wall and are able to offer the much needed information to elucidate the pathophysiological changes which ultimately cause the acute event. The current study offers a new, complex – clinical, invasive and noninvasive imaging, as well as biomarker-based – approach, which may lead to a better understanding and treatment of this pathology.