Search Results (72)

Background: Coronary artery calcium (CAC) scores are a widely used surrogate marker for atherosclerotic burden, but they do not fully reflect plaque vulnerability or coronary inflammation. This study aimed to evaluate the relationship between CACs, coronary plaque characteristics, and perivascular inflammatory activity using advanced CCTA and CaRi-Heart^® analysis. Methods: A total of 250 patients with no prior cardiovascular disease were retrospectively evaluated and stratified by CACs into three groups: 0 (n = 28), 1–100 (n = 121), and >100 (n = 101). Coronary plaque morphology, high-risk plaque (HRP) features, CAD-RADS scores, and AI-derived fat attenuation index (FAI) centiles were assessed. Results: Significant differences across CAC categories were observed for several key parameters. The number of diseased coronary segments increased markedly (from 1.39 ± 1.10 vs. 2.97 ± 1.57 vs. 3.94 ± 2.10; p < 0.0001, one-way ANOVA). A similar upward trend was seen for segment involvement scores, HRP prevalence, and the proportions of mixed and calcified plaque components. Regression analysis demonstrated that CACs correlated significantly with segment burden (r² = 0.2520), CAD-RADS (r² = 0.1352), and the FAI score centile (r² = 0.0568). Conclusions: This study highlights the limitations of CACs as a standalone risk stratification tool. Vulnerable and inflamed plaques may already be present in patients with low or zero CACs. Integrating CCTA with perivascular FAI mapping enables earlier detection of biologically active atherosclerosis and supports more precise clinical decision-making. Full article

Elevated levels of atherogenic lipoproteins are known to be associated with an increased risk of incident and recurrent cardiovascular events. Knowing that the immediate post-acute coronary syndrome (ACS) period is associated with the maximum risk of recurrent events, the gradual escalation of therapy allows the patient to remain above the targets during the most vulnerable period. In addition, the percentage of lipid-lowering levels for each class of drugs is predictable and has a ceiling. Hence, it is prudent to immediately start with a combination of lipid-lowering drugs following ACS according to the baseline lipid levels. Multiple studies with injectable lipid-lowering agents (PCSK9 inhibitors) such as EVOPACS, PACMAN MI, and HUYGENS MI have shown the feasibility of achieving LDL-C goals by day 28 and beneficial plaque modification in non-infarct-related coronary arteries. Recently, a study from India demonstrated that an upfront triple combination of oral lipid-lowering agents was able to achieve LDL-C goals in a majority of patients in the early post-ACS period. This notion is also supported by a few recent lipid-lowering guidelines advocating for an upfront dual combination of a high-intensity statin and ezetimibe following ACS. Henceforth, the goal should not only be the achievement of lipid targets but also their early achievement. However, the impact of this strategy on long-term cardiovascular outcomes is yet to be ascertained. Full article

Optical Coherence Tomography (OCT) is a further light-based intravascular imaging modality and provides a high-resolution, cross-sectional view of coronary arteries. It has a useful anatomic and increasingly physiological evaluation in light of coronary artery disease (CAD). This review provides a critical examination of the increased application of the OCT in assessing coronary artery physiology, beyond its initial mainstay application in anatomical imaging. OCT provides precise information on plaque morphology, which can help identify vulnerable plaques, and is most important in informing percutaneous coronary interventions (PCIs), including implanting a stent and optimizing it. The combination of OCT and functional measurements, such as optical flow ratio and OCT-based fractional flow reserve (OCT-FFR), permits a more complete assessment of coronary stenoses, which may provide increased diagnostic accuracy and better revascularization decision-making. The recent developments in OCT technology have also enhanced the accuracy in the measurement of coronary functions. The innovations may support the optimal treatment of patients as they provide more personalized and individualized treatment options; however, it is critical to recognize the limitations of OCT and distinguish between the hypothetical advantages and empirical outcomes. This review evaluates the existing uses, technological solutions, and future trends in OCT-based physiological imaging and evaluation, and explains how such an advancement will be beneficial in the treatment of CAD and gives a fair representation concerning other imaging applications. Full article

Coronary artery disease (CAD) is the third leading cause of disability and death globally. Intravascular ultrasound (IVUS) is the most commonly used imaging modality for the characterization of vulnerable plaques. The development of novel intravascular imaging and therapy devices requires dedicated open systems (e.g., for pulse sequences for imaging or thrombolysis), which are not currently available. This paper presents the development of a novel multifunctional FPGA-based pulser/receiver system for intravascular ultrasound imaging and therapy research. The open platform consists of a host PC with a Matlab-based software interface, an FPGA board, and a proprietary analog front-end board with state-of-the-art electronics for highly flexible transmission and reception schemes. The main features of the system include the capability to convert arbitrary waveforms into tristate bipolar pulses by using the PWM technique and by the direct acquisition of raw radiofrequency (RF) echo data. The results of a multicycle excitation pulse applied to a custom 550 kHz therapy transducer for acoustic characterization and a pulse-echo experiment conducted with a high-voltage, short-pulse excitation for a 19.48 MHz transducer are reported. Testing results show that the proposed system can be easily controlled to match the frequency and bandwidth required for different IVUS transducers across a broad class of applications. Full article

Despite significant advances in understanding and management, cardiovascular diseases remain the leading cause of mortality worldwide. Historically, diagnostic and therapeutic strategies have typically targeted obstructive coronary arteries. However, growing evidence supports the pivotal role of non-obstructive mechanisms in myocardial ischemia, prompting a new classification that distinguishes Acute Myocardial Ischemic Syndromes from Non-Acute Myocardial Ischemic Syndromes. In this evolving context, Optical Coherence Tomography (OCT) plays an important diagnostic role in the assessment of both obstructive and non-obstructive ischemic mechanisms. In Acute Myocardial Ischemic Syndromes, OCT enables the identification of major plaque destabilization mechanisms and contributes to the diagnosis of Myocardial Infarction with Non-Obstructive Coronary Arteries, helping to differentiate between atherosclerotic and non-atherosclerotic causes. In Non-Acute Myocardial Ischemic Syndromes, OCT assists in evaluating stenosis severity, plaque morphology, vulnerability, and healing, and may contribute to the diagnosis of Ischemia with Non-Obstructive Coronary Arteries, identifying myocardial bridge and epicardial spasm alongside conventional functional assessment of intermediate stenoses. This narrative review outlines the expanding clinical applications of OCT across the full spectrum of ischemic syndromes, emphasizing its role in bridging obstructive and non-obstructive pathophysiology and supporting a more comprehensive diagnostic approach to ischemic heart disease. Full article

Background/Objectives: Cardiovascular disease remains the leading global cause of death, with atherosclerotic plaque vulnerability, rather than stenosis severity, playing a central role in acute coronary events. Epicardial adipose tissue (EAT) has emerged as a key contributor to coronary atherosclerosis and myocardial ischemia. This study aimed to investigate the relationship between EAT thickness and the development and severity of atherosclerotic plaques in these coronary arteries, and to evaluate the influence of demographic factors on EAT thickness and plaque vulnerability. Methods: A retrospective analysis was conducted on autopsy data from 245 sudden cardiac death (SCD) cases (2021–2023). EAT thickness was measured at the left anterior descending artery (LAD) and left circumflex coronary artery (LCx) levels. From each artery, one segment that showed evidence of an atherosclerotic plaque was collected and sent for histological examination. Additionally, we documented demographic data, including age, sex, and body mass index (BMI) for each case. Results: In the present study, we enrolled 245 subjects with SCD, among whom 175 (71.42%) were male, and 70 (28.58%) were female. The mean age was 62.31 ± 12.69 years, and the mean BMI was 26.12 ± 4.16. We observed a mean EAT thickness value of 0.74 ± 0.26 cm at the LAD artery level and 0.71 ± 0.27 cm at the LCx artery level. We observed a positive correlation between BMI and EAT thickness at the LAD level (r = 0.260, p < 0.001) and similarly at the LCx level (r = 0.260, p < 0.001). Additionally, advancing age is associated with an increase in EAT thickness at both the LAD level (r = 0.188, p = 0.003) and the LCx level (r = 0.242, p < 0.001). Furthermore, we observed a higher EAT thickness at the LAD level (p = 0.0019) and the LCx level (p = 0.0225) among subjects with unstable atherosclerotic plaques. In the logistic regression analysis, the elevated value of EAT thickness was associated with unstable atherosclerotic plaque at LAD (OR: 1.88, p = 0.002) and LCx (OR: 1.51, p = 0.010) for the entire study cohort. Conclusions: Our data revealed that higher baseline values of EAT LCx and EAT LAD are associated with unstable plaque at the level of the left coronary arteries. Furthermore, our findings indicate that male individuals are more susceptible to developing unstable plaques in the coronary arteries. Full article

Background: Atherosclerotic diseases, including coronary heart disease and cerebrovascular disease, are leading causes of morbidity and mortality worldwide. Atherosclerosis is a chronic vascular condition marked by the accumulation of lipid plaque within arterial walls. These plaques can become unstable and rupture, leading to thrombosis and subsequent cardiovascular events. Therefore, early identification of vulnerable plaque is critical for preventing such events. Objectives: This study aims to develop a novel imaging platform for atherosclerotic plaque by designing a molecular imaging probe based on fluorescent molecules that target lipid necrotic cores. The goal is to specifically detect high-risk plaque, enabling early diagnosis and intervention. Methods: Bioinformatic analysis and immunofluorescence were used to detect CD36 expression in human carotid plaque. CD36pep-ICG was synthesized using the Fmoc solid-phase peptide method. A series of experiments was conducted to characterize the probe’s properties. To assess imaging performance, probe concentration gradients were tested using FLI equipment. Ex vivo imaging was performed on atherosclerotic mice and treatment models to evaluate the probe’s targeting ability and effectiveness in monitoring disease progression. Results: The CD36 expression was significantly elevated in the core of plaque compared to distal regions. The CD36pep-ICG probe, specifically designed to target lipids, was successfully synthesized and exhibited excellent fluorescence properties. In animal models, FLI imaging demonstrated that the CD36pep-ICG probe selectively accumulated in atherosclerotic plaque, enabling precise plaque detection. Moreover, the probe was used to monitor the therapeutic efficacy of anti-atherosclerotic drugs. Conclusions: The CD36pep-ICG probe developed in this study is an effective molecular imaging tool for the specific identification of vulnerable atherosclerotic plaque, offering a novel approach for early diagnosis and treatment. Additionally, the probe shows promise in tracking the therapeutic effects of the drug, potentially advancing the precision treatment of cardiovascular diseases. Full article

Due to the routine use of endovascular revascularization and improved medical therapy, the majority of acute coronary syndrome (ACS) cases now have an uncomplicated course. However, in spite of the currently accepted secondary prevention standards, the residual risk of remote major adverse cardiovascular events (MACEs) after ACS remains high. Ultrasound carotid/subclavian atherosclerotic plaque assessment may represent an alternative approach to estimate the MACE risk after ACS and to control the quality of secondary prevention. Aim: To find the most important clinical predictors of MACEs in contemporary patients with predominantly uncomplicated ACS treated according to the Guidelines, and to study the potential of the longitudinal assessment of quantitative and qualitative ultrasound carotid/subclavian atherosclerotic plaque characteristics for MACE prediction after ACS. Methods: Patients with ACS, obstructive coronary artery disease (CAD) confirmed by coronary angiography, and carotid/subclavian atherosclerotic plaque (AP) who underwent interventional treatment were prospectively enrolled. The exclusion criteria were as follows: death or significant bleeding at the time of index hospitalization; left ventricular ejection fraction (EF) <30%; and statin intolerance. The clinical variables potentially affecting cardiovascular prognosis after ACS as well as the quantitative and qualitative AP characteristics at baseline and 6 months after the index hospitalization were studied as potential MACE predictors. Results: A total of 411 primary patients with predominantly uncomplicated ACS were included; AP was detected in 343 of them (83%). The follow-up period duration was 450 [269; 634] days. MACEs occurred in 38 patients (11.8%): seven—cardiac death, twenty-five—unstable angina/acute myocardial infarction, and six—acute ischemic stroke. In multivariate regression analyses, the most important baseline predictors of MACEs were diabetes (HR 2.22, 95% CI 1.08–4.57); the decrease in EF by every 5% from 60% (HR 1.22, 95% CI 1.03–1.46); the Charlson comorbidity index (HR 1.24, 95% CI 1.05–1.48); the non-prescription of beta-blockers at discharge (HR 3.24, 95% CI 1.32–7.97); and a baseline standardized AP gray scale median (GSM) < 81 (HR 2.06, 95% CI 1.02–4.19). Among the predictors assessed at 6 months, after adjustment for other variables, only ≥ 3 uncorrected risk factors and standardized AP GSM < 81 (cut-off value) at 6 months were significant (HR 3.11, 95% CI 1.17–8.25 and HR 3.77, 95% CI 1.43–9.92, respectively) (for all HRs above, all p-values < 0.05; HR and 95% CI values varied minimally across regression models). The baseline quantitative carotid/subclavian AP characteristics and their 6-month longitudinal changes were not associated with MACEs. All predictors retained significance after the internal validation of the models, and models based on the baseline predictors also demonstrated good calibration; the latter were used to create MACE risk calculators. Conclusions: In typical contemporary patients with uncomplicated interventionally treated ACS, diabetes, decreased EF, Charlson comorbidity index, non-prescription of beta-blockers at discharge, and three or more uncontrolled risk factors after 6 months were the most important clinical predictors of MACEs. We also demonstrated that a lower value of AP GSM reflecting the plaque vulnerability, measured at baseline and after 6 months, was associated with an increased MACE risk; this effect was independent of clinical predictors and risk factor control. According to our knowledge, this is the first demonstration of the independent role of longitudinal carotid/subclavian AP GSM assessment in MACE prediction after ACS. Full article

Coronary artery disease is a highly prevalent disease that constitutes the leading cause of mortality worldwide. Acute coronary syndromes are the most devastating form of presentation of coronary disease, involving the acute formation of a thrombus within the coronary vessel lumen, further leading to flow limitation and diminished myocardial perfusion. Vulnerable plaques, which are characterized by thin-cap fibroatheroma, a large lipid pool, and macrophage infiltration and spotty calcification of the cap, pose a higher risk of coronary events despite not being flow-limiting. Iterations in intravascular imaging and coronary computed tomography have largely increased the ability to detect and define vulnerable plaques, and its clinical impact in early- and mid-term outcomes has been confirmed in several studies. In this review, we aimed to revise the current concept of vulnerable coronary plaque and its repercussion, to summarize the main pharmacological approaches for its management, and to provide an updated overview of the available evidence on preventive percutaneous interventional strategies in this clinical setting. Full article

Vulnerable coronary atherosclerotic plaque involves a dynamic pathophysiologic process within and surrounding an atheromatous plaque in coronary artery intima. The process drastically increases the risk of plaque rupture and is clinically responsible for most cases of acute coronary syndromes, myocardial infarctions, and sudden cardiac deaths. Early detection of vulnerable plaque is crucial for clinicians to implement appropriate risk-mitigation treatment strategies, offer timely interventions, and prevent potentially life-threatening events. There is an imperative clinical need to develop practical diagnostic pathways that utilize non-invasive means to risk-stratify symptomatic patients. Since the early 1990s, the identification of vulnerable plaque in clinical practice has primarily relied on invasive imaging techniques. In the last two decades, CT coronary angiogram (CTCA) has rapidly evolved into the prevalent non-invasive diagnostic modality for assessing coronary anatomy. There are now validated plaque appearances on CTCA correlating with plaque vulnerability. It is worth noting that in clinical practice, most CTCA reports omit mention of vulnerable plaque details because spatial resolution (0.3–0.5 mm) is often insufficient to reliably detect some crucial features of vulnerable plaques, such as thin fibrous caps. Additionally, accurately identifying vulnerable plaque features requires substantial expertise and time, which many cardiologists or radiologists may lack in routine reporting. Cardiac magnetic resonance imaging (cMRI) is also non-invasive and allows simultaneous anatomic and functional assessment of coronary plaques. Despite several decades of research and development, routine clinical application of cMRI in coronary plaque imaging remains hampered by complex imaging protocols, inconsistent image quality, and cost. Molecular imaging with radiotracers, specifically positron emission tomography (PET) with sodium fluoride (Na¹⁸F PET), have demonstrated significant potential as a sensitive and specific imaging procedure for diagnosing vulnerable coronary artery plaque. The study protocol is robust and brief, requiring minimal patient preparation. Compared to CTCA and cMRI, the diagnostic accuracy of this test is less dependent on the experience and expertise of the readers. Furthermore, validated automated quantitative algorithms complement the visual interpretation of the study, enhancing confidence in the diagnosis. This combination of factors makes Na¹⁸F PET a promising tool in cardiology for identifying high-risk coronary plaques. Full article

Background/objectives: Acute coronary syndrome (ACS) is a major global health issue primarily caused by the rupture or erosion of vulnerable coronary plaques. Non-invasive identification of these plaques through coronary computed tomography angiography (CCTA) can be improved with radiomics, which extracts and analyses quantitative features from medical images. This systematic review aims to comprehensively evaluate the literature surrounding the role of radiomics in assessing coronary plaques via CCTA. Methods: A systematic search of Medline, EMBASE, and Web of Science was conducted up to July 2024. Nine studies met the inclusion criteria, and their methodological quality was assessed using the radiomic quality score (RQS) and the QUADAS-2 tool. Results: All studies that evaluated radiomic models for plaque vulnerability reported area under the curve (AUC) values exceeding 0.7, indicating at least modest diagnostic performance. In the four studies that made direct comparisons, radiomic models consistently outperformed conventional CCTA markers. However, RQS scores ranged from 2.7% to 41.7%, reflecting variability in study quality and underscoring the need for more robust validation. Conclusions: Radiomics has the potential to enhance CCTA-based identification of vulnerable coronary plaques, offering a promising non-invasive approach to predicting major adverse cardiovascular events. However, the current body of research is limited by the lack of external validation, reliance on small, single-centre retrospective studies, and methodological inconsistencies, which impact the generalisability and reproducibility of findings. Future research should prioritise prospective, multi-centre studies with standardised protocols and rigorous validation frameworks to effectively incorporate radiomics into clinical practice. Full article

Atherosclerotic plaque development constitutes the primary substrate of coronary artery disease (CAD) and is the outcome of an intricate process involving endothelial damage, inflammation, and lipid retention. The clinical efficacy of many lipid-lowering therapies in patients with CAD has been well established. Over the past few decades, a substantial and significant advance regarding the use of invasive and non-invasive imaging modalities has been observed. Numerous studies have been conducted using these imaging techniques and have investigated the changes in morphology (e.g., atheroma volume) and composition (e.g., lipid burden, fibrous cap thickness, macrophage accumulation) at the plaque level that explain the improved clinical outcomes by various pharmacological interventions. Lipid-lowering agents, such as statins and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, demonstrate direct effects on plaque volume and composition that enhance plaque stabilization and/or regression beyond the reduction of low-density lipoproteins. An increasing amount of clinical research is also focused on the role of inflammation in plaque vulnerability and future adverse cardiac events. Consequently, there is a pressing need to explore therapeutic strategies that are capable of disrupting the inflammatory response as well as reducing atheroma burden and modifying high-risk plaque characteristics. This review provides a comprehensive analysis of the current evidence regarding the effects of traditional and novel therapeutic strategies targeting modification of the lipid profile and inflammatory processes on reversing plaque growth and attenuating vulnerable features, thereby promoting plaque stabilization and passivation. Full article

Background and Objectives: Atherosclerotic disease is a major contributor to heart failure, stroke, and myocardial infarction, significantly lowering the quality of life and life expectancy and placing a significant burden on healthcare. Not all lesions deemed non-significant are benign, and conversely, not all significant lesions are causative of ischemia. Fractional flow reserve (FFR) provides a functional assessment of coronary lesions, while optical coherence tomography (OCT) offers detailed imaging of plaque morphology, aiding in therapeutic decision-making. The objective of this study was to evaluate the utility of OCT and FFR as adjunctive tools in the catheterization laboratory for guiding therapeutic decisions in patients with multivessel disease for non-culprit vessels. Specifically, we aimed to assess how OCT and FFR influence therapeutic decision-making in patients with multivessel coronary artery disease. Materials and Methods: A total of 36 patients with acute coronary syndrome (ACS) and multivessel disease were randomized 1:1 into two groups: one guided by FFR alone and the other by a combination of FFR and OCT. For the FFR group, revascularization decisions for non-culprit lesions were based solely on FFR measurements. If the FFR was >0.8, the procedure was concluded, and the patient received maximal medical treatment. If the FFR was ≤0.8, a stent was placed. For the FFR + OCT group, if the FFR was >0.8, the revascularization decision was based on OCT findings. If there were no vulnerable plaques (VP), the procedure was concluded, and the patient received maximal medical treatment. If OCT imaging indicated VP, then the patient underwent revascularization. If the FFR was ≤0.8, the patient underwent revascularization regardless of OCT findings. Results: OCT imaging altered the therapeutic decision in 11 cases where FFR measurements were above 0.8, but the lesions were characterized as VP. Analyzing the total change in the decision to stent, 4 cases in the FFR group and 15 cases in the FFR and OCT groups (4 based on FFR and 11 on OCT) revealed a statistically significant difference (p = 0.0006; Relative Risk = 0.2556; 95% CI: 0.1013 to 0.5603). When analyzing the change in the total decision both to stent and not to stent, we observed a statistically significant difference, with Group 1 having 7 cases and Group 2 having 15 cases (p = 0.0153; Relative Risk = 0.4050; 95% CI: 0.2004 to 0.7698. Conclusions: Based on the findings of this study, OCT significantly increases the percentage of stenting procedures by identifying vulnerable lesions. The use of intracoronary imaging facilitates the timely identification and treatment of these vulnerable lesions. This underscores the crucial role of OCT in enhancing the precision of coronary interventions by ensuring timely intervention for vulnerable lesions, thereby potentially improving patient outcomes. Full article

Atherosclerotic disease of the carotid arteries is a crucial risk factor in predicting the likelihood of future stroke events. In addition, emerging studies suggest that carotid stenosis may also be an indicator of plaque load on coronary arteries and thus have a correlation with the risk of acute cardiovascular events. Furthermore, although in symptomatic patients the degree of stenosis is the main morphological parameter studied, recent evidence suggests, especially in asymptomatic patients, that plaque vulnerability should also be evaluated as an emerging and significant imaging parameter. The reference diagnostic methods for the evaluation of carotid stenosis are currently ultrasonography, magnetic resonance imaging (MRI), and computed tomography angiography (CTA). In addition, other more invasive methods such as 123I-metaiodobenzylguanidine (MIBG) scintigraphy and PET-CT, as well as digital subtraction angiography, can be used. Each method has advantages and disadvantages, and there is often some confusion in their use. For example, the usefulness of MRI is often underestimated. In addition, implementations for each method have been developed over the years and are already enabling a significant increase in diagnostic accuracy. The purpose of our study is to make an in-depth analysis of all the methods in use and in particular their role in the diagnostic procedure of carotid stenosis, also discussing new technologies. Full article

Recent studies reported that circulating microRNAs (miRNAs) can target different metalloproteases (MMPs) involved in matrix remodeling and plaque vulnerability. Consequently, they might have a role in the diagnosis and prognosis of coronary artery disease. To quantify circulating miRNAs (miRNA126, miRNA146, and miRNA21) suggested to have possible cardiovascular implications, as well as levels of MMP-1 and MMP-9, and to determine their association with left ventricular (LV) function and with arterial function, in patients with either ST-segment elevation acute myocardial infarction (STEMI) or stable ischemic heart disease (SIHD). A total of 90 patients with coronary artery disease (61% men, 58 ± 12 years), including 60 patients with STEMI and 30 patients with SIHD, were assessed within 24 h of admission, by measuring serum microRNAs, and serum MMP-1 and MMP-9. LV function was assessed by measuring ejection fraction (EF) by 2D and 3D echocardiography, and global longitudinal strain (GLS) by speckle tracking. Arterial function was assessed by echo tracking, CAVI, and peripheral Doppler. Circulating levels of miRNA146, miRNA21, and MMP1 were significantly increased in patients with STEMI vs. SIHD (p = 0.0001, p = 0.0001, p = 0.04, respectively). MiRNA126 negatively correlated with LVEF (r = −0.33, p = 0.01) and LV deformation parameters (r = −0.31, p = 0.03) in patients with STEMI and negatively correlated with ABI parameters (r = −0.39, p = 0.03, r = −0.40, p = 0.03, respectively) in patients with SIHD. MiRNA146 did not have any significant correlations, while higher values of miRNA21 were associated with lower values of GLS in STEMI patients and with higher values of GLS in SIHD patients. Both MMP1 and MMP9 correlated negatively with LVEF (r = −0.27, p = 0.04, r = −0.40, p = 0.001, respectively) and GLS in patients with STEMI, and positively with arterial stiffness in patients with SIHD (r = 0.40 and r = 0.32, respectively; both p < 0.05). MiRNA126, miRNA21, and both MMP1 and MMP9 are associated with LV and arterial function parameters in patients with acute coronary syndrome. Meanwhile, they inversely correlate with arterial function in patients with chronic atherosclerotic disease. However, further studies are needed to establish whether these novel biomarkers have diagnosis and prognosis significance. Full article