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Background: Capecitabine and other 5-fluorouracil prodrugs are medications widely employed in treating solid tumors, including breast and colorectal cancer. However, they carry a notable risk for cardiotoxicity, including coronary vasospasm, possibly related to their impact on vascular endothelium and smooth muscle. Case Report: We present a case of a 45-year-old male with a pancreatic neuroendocrine tumor who developed exertional chest pain after starting capecitabine. Initial evaluations in the emergency department, including a 12-lead electrocardiogram and cardiac enzymes, were normal, but suspicion for coronary vasospasm persisted due to the temporal relationship with drug initiation and symptom characteristics. A graded exercise test reproduced his symptoms, accompanied by hyperacute peaked T waves and subsequent ST segment elevations in the inferior leads. Coronary angiography revealed patent coronary arteries, rendering provocative testing unnecessary due to a high clinical suspicion of capecitabine-induced vasospasm. Discontinuing the patient's medication was a more efficient approach than continuing additional cardiac workup while the drug was still administered. After multidisciplinary discussion, capecitabine was discontinued, leading to symptom resolution and a negative repeat graded exercise test. Conclusions: This case underscores the potential for capecitabine to induce coronary artery vasospasm, emphasizing the importance of prompt medication cessation. Patients receiving capecitabine therapy and experiencing chest pain should undergo an evaluation with consideration of capecitabine-induced vasospasm in the differential diagnosis. Prompt recognition and medication cessation are critical to prevent serious cardiovascular complications including death. In our patient, discontinuing capecitabine resolved his symptoms, emphasizing the significance of discontinuing the causative drug and seeking alternative chemotherapy regimens. [ABSTRACT FROM AUTHOR]

BACKGROUND: We investigated the usefulness of invasive coronary function testing to diagnose the cause of angina in patients with no obstructive coronary arteries. METHODS: Outpatients referred for coronary computed tomography angiography in 3 hospitals in the United Kingdom were prospectively screened. After coronary computed tomography angiography, patients with unobstructed coronary arteries, and who consented, underwent invasive endotyping. The diagnostic assessments included coronary angiography, fractional flow reserve (patient excluded if ≤0.80), and, for those without obstructive coronary artery disease, coronary flow reserve (abnormal <2.0), index of microvascular resistance (abnormal ≥25), and intracoronary infusion of acetylcholine (0.182, 1.82, and 18.2 μg/mL; 2 mL/min for 2 minutes) to assess for microvascular and coronary spasm. Participants were randomly assigned to disclosure of the results of the coronary function tests to the invasive cardiologist (intervention group) or nondisclosure (control group, blinded). In the control group, a diagnosis of vasomotor angina was based on medical history, noninvasive tests, and coronary angiography. The primary outcome was the between-group difference in the reclassification rate of the initial diagnosis on the basis of coronary computed tomography angiography versus the final diagnosis after invasive endotyping. The Seattle Angina Questionnaire summary score and Treatment Satisfaction Questionnaire for Medication were secondary outcomes. RESULTS: Of 322 eligible patients, 250 (77.6%) underwent invasive endotyping; 19 (7.6%) had obstructive coronary disease, 127 (55.0%) had microvascular angina, 27 (11.7%) had vasospastic angina, 17 (7.4%) had both, and 60 (26.0%) had no abnormality. A total of 231 patients (mean age, 55.7 years; 64.5% women) were randomly assigned and followed up (median duration, 19.9 [12.6-26.9] months). The clinician diagnosed vasomotor angina in 51 (44.3%) patients in the intervention group and in 55 (47.4%) patients in the control group. After randomization, patients in the intervention group were 4-fold (odds ratio, 4.05 [95% CI, 2.32-7.24]; P<0.001) more likely to be diagnosed with a coronary vasomotor disorder; the frequency of this diagnosis increased to 76.5%. The frequency of normal coronary function (ie, no vasomotor disorder) was not different between the groups before randomization (51.3% versus 50.9%) but was reduced in the intervention group after randomization (23.5% versus 50.9%, P<0.001). At 6 and 12 months, the Seattle Angina Questionnaire summary score in the intervention versus control groups was 59.2±24.2 (2.3±16.2 change from baseline) versus 60.4±23.9 (4.6±16.4 change) and 63.7±23.5 (4.7±14.7 change) versus 66.0±19.3 (7.9±17.1 change), respectively, and not different between groups (global P=0.36). Compared with the control group, global treatment satisfaction was higher in the intervention group at 12 months (69.9±22.8 versus 61.7±26.9, P=0.013). CONCLUSIONS: For patients with angina and no obstructive coronary arteries, a diagnosis informed by invasive functional assessment had no effect on long-term angina burden, whereas treatment satisfaction improved. [ABSTRACT FROM AUTHOR]

X-ray coronary angiography is the most common tool for the diagnosis and treatment of coronary artery disease. It involves the injection of contrast agents into coronary vessels using a catheter to highlight the coronary vessel structure. Typically, multiple 2D X-ray projections are recorded from different angles to improve visualization. Recent advances in the development of deep-learning-based tools promise significant improvement in diagnosing and treating coronary artery disease. However, the limited public availability of annotated X-ray coronary angiography image datasets presents a challenge for objective assessment and comparison of existing tools and the development of novel methods. To address this challenge, we introduce a novel ARCADE dataset with 2 objectives: coronary vessel classification and stenosis detection. Each objective contains 1500 expert-labeled X-ray coronary angiography images representing: i) coronary artery segments; and ii) the locations of stenotic plaques. These datasets will serve as a benchmark for developing new methods and assessing existing approaches for the automated diagnosis and risk assessment of coronary artery disease. [ABSTRACT FROM AUTHOR]

Epicardial-derived cells (EPDCs) are involved in the regulation of myocardial growth and coronary vascularization and are critically important for proper development of the atrioventricular (AV) valves. SOX9 is a transcription factor expressed in a variety of epithelial and mesenchymal cells in the developing heart, including EPDCs. To determine the role of SOX9 in epicardial development, an epicardial-specific Sox9 knockout mouse model was generated. Deleting Sox9 from the epicardial cell lineage impairs the ability of EPDCs to invade both the ventricular myocardium and the developing AV valves. After birth, the mitral valves of these mice become myxomatous with associated abnormalities in extracellular matrix organization. This phenotype is reminiscent of that seen in humans with myxomatous mitral valve disease (MVD). An RNA-seq analysis was conducted in an effort to identify genes associated with this myxomatous degeneration. From this experiment, Cd109 was identified as a gene associated with myxomatous valve pathogenesis in this model. Cd109 has never been described in the context of heart development or valve disease. This study highlights the importance of SOX9 in the regulation of epicardial cell invasion—emphasizing the importance of EPDCs in regulating AV valve development and homeostasis—and reports a novel expression profile of Cd109 , a gene with previously unknown relevance in heart development. [Display omitted] • SOX9 controls epicardial-derived cell invasion into the developing heart. • Epicardial-derived cells are needed to maintain atrioventricular valve homeostasis. • Cd109 is identified as novel gene associated with valve development and disease. [ABSTRACT FROM AUTHOR]

Purpose: Inflamed, prone-to-rupture coronary plaques are an important cause of myocardial infarction and their early identification is crucial. Atherosclerotic plaques are characterized by overexpression of the type-2 somatostatin receptor (SST2) in activated macrophages. SST2 ligand imaging (e.g. with [68 Ga]Ga-DOTA-TOC) has shown promise in detecting and quantifying the inflammatory activity within atherosclerotic plaques. However, the sensitivity of standard axial field of view (SAFOV) PET scanners may be suboptimal for imaging coronary arteries. Long-axial field of view (LAFOV) PET/CT scanners may help overcome this limitation. We aim to assess the ability of [68 Ga]Ga-DOTA-TOC LAFOV-PET/CT in detecting calcified, SST2 overexpressing coronary artery plaques. Methods: In this retrospective study, 108 oncological patients underwent [68 Ga]Ga-DOTA-TOC PET/CT on a LAFOV system. [68 Ga]Ga-DOTA-TOC uptake and calcifications in the coronary arteries were evaluated visually and semi-quantitatively. Data on patients' cardiac risk factors and coronary artery calcium score were also collected. Patients were followed up for 21.5 ± 3.4 months. Results: A total of 66 patients (61.1%) presented with calcified coronary artery plaques. Of these, 32 patients had increased [68 Ga]Ga-DOTA-TOC uptake in at least one coronary vessel (TBR: 1.65 ± 0.53). Patients with single-vessel calcifications showed statistically significantly lower uptake (SUVmax 1.10 ± 0.28) compared to patients with two- (SUVmax 1.31 ± 0.29, p < 0.01) or three-vessel calcifications (SUVmax 1.24 ± 0.33, p < 0.01). There was a correlation between coronary artery calcium score (CACS) and [68 Ga]Ga-DOTA-TOC uptake, especially in the LAD (p = 0.02). Stroke and all-cause death occurred more frequently in patients with increased [68 Ga]Ga-DOTA-TOC uptake (15.63% vs. 0%; p:0.001 and 21.88% vs. 6.58%; p: 0.04, respectively) during the follow-up period. Conclusion: [68 Ga]Ga-DOTA-TOC as a marker for the macrophage activity can reveal unknown cases of inflamed calcified coronary artery plaques using a LAFOV PET system. [68 Ga]Ga-DOTA-TOC uptake increased with the degree of calcification and correlated with higher risk of stroke and all-cause death. [68 Ga]Ga-DOTA-TOC LAFOV PET/CT may be useful to assess patients' cardiovascular risk. [ABSTRACT FROM AUTHOR]

This study explores the synergistic impact of Programmed Death Ligand 1 (PD-L1) and Protein Kinase B (Akt) overexpression in adipose-derived mesenchymal stem cells (AdMSCs) for ameliorating cardiac dysfunction after myocardial infarction (MI). Post-MI adult Wistar rats were allocated into four groups: sham, MI, ADMSC treatment, and ADMSCs overexpressed with PD-L1 and Akt (AdMSC-PDL1-Akt) treatment. MI was induced via left anterior descending coronary artery ligation, followed by intramyocardial AdMSC injections. Over four weeks, cardiac functionality and structural integrity were assessed using pressure–volume analysis, infarct size measurement, and immunohistochemistry. AdMSC-PDL1-Akt exhibited enhanced resistance to reactive oxygen species (ROS) in vitro and ameliorated MI-induced contractile dysfunction in vivo by improving the end-systolic pressure–volume relationship and preload-recruitable stroke work, together with attenuating infarct size. Molecular analyses revealed substantial mitigation in caspase3 and nuclear factor-κB upregulation in MI hearts within the AdMSC-PDL1-Akt group. Mechanistically, AdMSC-PDL1-Akt fostered the differentiation of normal T cells into CD25+ regulatory T cells in vitro, aligning with in vivo upregulation of CD25 in AdMSC-PDL1-Akt-treated rats. Collectively, PD-L1 and Akt overexpression in AdMSCs bolsters resistance to ROS-mediated apoptosis in vitro and enhances myocardial protective efficacy against MI-induced dysfunction, potentially via T-cell modulation, underscoring a promising therapeutic strategy for myocardial ischemic injuries. [ABSTRACT FROM AUTHOR]

The article presents the discussion on invasive study of coronary microvascular disease patients. Topics include phenotype was determined by invasive coronary artery studies in patients with angina, normal left ventricular ejection fraction, and unobstructed coronary arteries; and invasive strategy has the added advantage of being able to induce vasospasm and to quantitate coronary microvascular flow characteristics.

While reperfusion, or restoration of coronary blood flow in acute myocardial infarction, is a requisite for myocardial salvage, it can paradoxically induce a specific damage known as ischemia/reperfusion (I/R) injury. Our understanding of the precise pathophysiological molecular alterations leading to I/R remains limited. In this study, we conducted a comprehensive and unbiased time-course analysis of post-translational modifications (PTMs) in the post-reperfused myocardium of two different animal models (pig and mouse) and evaluated the effect of two different cardioprotective therapies (ischemic preconditioning and neutrophil depletion). In pigs, a first wave of irreversible oxidative damage was observed at the earliest reperfusion time (20 min), impacting proteins essential for cardiac contraction. A second wave, characterized by irreversible oxidation on different residues and reversible Cys oxidation, occurred at late stages (6–12 h), affecting mitochondrial, sarcomere, and inflammation-related proteins. Ischemic preconditioning mitigated the I/R damage caused by the late oxidative wave. In the mouse model, the two-phase pattern of oxidative damage was replicated, and neutrophil depletion mitigated the late wave of I/R-related damage by preventing both Cys reversible oxidation and irreversible oxidation. Altogether, these data identify protein PTMs occurring late after reperfusion as an actionable therapeutic target to reduce the impact of I/R injury. [ABSTRACT FROM AUTHOR]

Background: Inflammation in ST-segment elevation myocardial infarction (STEMI) is an important contributor to both acute myocardial ischemia and reperfusion injury after primary percutaneous coronary intervention (PCI). Methylprednisolone is a glucocorticoid with potent anti-inflammatory properties with an acute effect and is used as an effective and safe treatment of a wide range of acute diseases. The trial aims to investigate the cardioprotective effects of pulse-dose methylprednisolone administered in the pre-hospital setting in patients with STEMI transferred for primary PCI. Methods: This trial is a randomized, blinded, placebo-controlled prospective clinical phase II trial. Inclusion will continue until 378 patients with STEMI have been evaluated for the primary endpoint. Patients will be randomized 1:1 to a bolus of 250 mg methylprednisolone intravenous or matching placebo over a period of 5 min in the pre-hospital setting. All patients with STEMI transferred for primary PCI at Rigshospitalet, Copenhagen University Hospital, Denmark, will be screened for eligibility. The main eligibility criteria are age ≥ 18 years, acute onset of chest pain with < 12 h duration, STEMI on electrocardiogram, no known allergy to glucocorticoids or no previous coronary artery bypass grafting, previous acute myocardial infarction in assumed culprit, or a history with previous maniac/psychotic episodes. Primary outcome is final infarct size measured by late gadolinium enhancement on cardiac magnetic resonance (CMR) 3 months after STEMI. Secondary outcomes comprise key CMR efficacy parameters, clinical endpoints at 3 months, the peak of cardiac biomarkers, and safety. Discussion: We hypothesize that pulse-dose methylprednisolone administrated in the pre-hospital setting decreases inflammation and thus reduces final infarct size in patients with STEMI treated with primary PCI. Trial registration: EU-CT number: 2022–500762-10–00; Submitted May 5, 2022. ClinicalTrials.gov Identifier: NCT05462730; Submitted July 7, 2022, first posted July 18, 2022. [ABSTRACT FROM AUTHOR]

Gene function can be described using various measures. We integrated association studies of three types of omics data to provide insights into the pathophysiology of subclinical coronary disease and myocardial infarction (MI). Using multivariable regression models, we associated: (1) single nucleotide polymorphism, (2) DNA methylation, and (3) gene expression with coronary artery calcification (CAC) scores and MI. Among 3106 participants of the Framingham Heart Study, 65 (2.1%) had prevalent MI and 60 (1.9%) had incident MI, median CAC value was 67.8 [IQR 10.8, 274.9], and 1403 (45.2%) had CAC scores > 0 (prevalent CAC). Prevalent CAC was associated with AHRR (linked to smoking) and EXOC3 (affecting platelet function and promoting hemostasis). CAC score was associated with VWA1 (extracellular matrix protein associated with cartilage structure in endomysium). For prevalent MI we identified FYTTD1 (down-regulated in familial hypercholesterolemia) and PINK1 (linked to cardiac tissue homeostasis and ischemia–reperfusion injury). Incident MI was associated with IRX3 (enhancing browning of white adipose tissue) and STXBP3 (controlling trafficking of glucose transporter type 4 to plasma). Using an integrative trans-omics approach, we identified both putatively novel and known candidate genes associated with CAC and MI. Replication of findings is warranted. [ABSTRACT FROM AUTHOR]

The co-occurrence of dilated cardiomyopathy (DCM) and aortic dissection has been rarely reported. Here, we present the case of a patient with co-occurrence of DCM and aortic dissection, wherein multivessel coronary artery dissection eventually occurred, thereby leading to advanced heart failure. She suffered from co-occurrence of DCM and aortic dissection 6 years ago. After the heart failure had briefly stabilized, the myocardial infarction due to coronary artery dissection led to worsening mitral regurgitation and decreased right ventricular function, thereby worsening the status of her heart failure. In addition to cardiovascular abnormalities, the patient was also complicated by short stature (145 cm), mild scoliosis, nonfunctioning pituitary adenoma of 1 cm in size, and retinitis pigmentosa. Coronary artery dissection is a possible complication in patients with co-occurrence of DCM and aortopathy, which could dramatically affect the clinical course of advanced heart failure. [ABSTRACT FROM AUTHOR]

A 41-year-old man with resting angina was diagnosed with a coronary vasospasm and subsequently with Fabry disease exhibiting low serum α-galactosidase A activity. High computed tomography (CT)–derived extracellular volume was detected in the apical inferior wall of the left ventricle suggesting myocardial fibrosis, potentially from vasospasm-related ischemia and/or microvascular dysfunction.

Currently, type 2 myocardial infarction is a rather significant problem, both in terms of diagnosis and treatment. Myocardial infarction without obstructive coronary artery damage occurs in 5-10 % of patients with a myocardial infarction. Optimal strategies for the diagnosis and treatment of patients with myocardial damage associated with non-thrombotic mechanisms have not yet been determined. The article describes a clinical observation of type 2 myocardial infarction on the background of vasospasm, as well as diagnostic and therapeutic tactics in this clinical situation. The main provisions: the patient was 22 years old in the cardiology department due to the pain syndrome behind the sternum for the first time in his life and an increase in body temperature to 37.5 C. From anamnesis: active bodybuilding, taking testosterone in injectable form. The electrocardiogram revealed changes in the type of transmural myocardial ischemia without the dynamics characteristic of myocardial infarction. Troponin I (quantitative test) — 2.1 ng/ml at laboratory reference values of 0.010-0.023 ng/ml. A diagnostic search was conducted for myocardial infarction and acute pericarditis. For the purpose of differential diagnosis, coronary angiography was performed, during which dynamic stenosis of the posterior descending artery was revealed. The decision to stent the vessel was not made. Echocardiography revealed areas of local contractility disorders. The data of the examination showed in favor of myocardial infarction without coronary artery obstruction (type 2). Taking into account the absence of occlusive-stenotic lesions of the coronary arteries, the presence of vasospasm, 1 platelet aggregation inhibitor, medium-dose statins, isosorbide dinitrate, calcium channel blocker, angiotensin-converting enzyme inhibitor was prescribed. Conclusion. Invasive tactics made it more likely to diagnose type 2 myocardial infarction and prescribe the most optimal drug therapy.

This article discusses the importance of atherosclerosis, a chronic disease characterized by the accumulation of fatty and fibrous material in arteries, which can lead to compromised blood flow and tissue ischemia. Atherosclerosis affects multiple vascular beds and is primarily caused by low-density lipoprotein cholesterol. It is the leading cause of vascular disease worldwide and is associated with severe clinical manifestations such as ischemic heart disease, ischemic stroke, and peripheral artery disease. The article also explores molecular mechanisms and potential therapeutic targets for atherosclerosis, including endothelial dysfunction, inflammatory responses, and oxidative stress. Additionally, it discusses the role of intravascular imaging in studying and evaluating coronary plaques and the importance of understanding coronary microvascular dysfunction. [Extracted from the article]

Myocardial bridging is a congenital anatomical anomaly characterized by a coronary artery with an epicardial course that dips into the myocardial tissue before resurfacing on the heart's surface. While it is commonly observed in the left anterior descending coronary artery, it typically occurs in a single coronary artery or a segment thereof. Myocardial bridging is generally asymptomatic and benign; however, in some cases, it can present with symptoms such as chest pain, arrhythmias, myocardial infarction, coronary vasospasm, syncope, and even sudden death. In our case, a patient admitted to our hospital with persistent chest pain for 6 months had myocardial bridges involving two different segments of the left anterior descending artery. Therefore, myocardial bridges should be considered in young patients presenting with angina pectoris. [ABSTRACT FROM AUTHOR]

Pseudo‐Wellens Syndrome (PWS) refers to absence of severe obstructive lesion in the proximal segment of the left anterior descending (LAD) despite having clinical and electrocardiography (ECG) features similar to Wellens Syndrome (WS). In previous reports, PWS most commonly caused by illicit drug use, stress cardiomyopathy, or unknown etiologies In this report, we aimed to present our case in which we detected the development of "memory T wave" secondary to Paroxysmal Supraventricular Tachycardia (PSVT) episodes as an interesting cause of PWS that has not been reported before. [ABSTRACT FROM AUTHOR]

Patent foramen ovale (PFO) is the most common congenital cardiac abnormality and is usually considered a benign finding. This case series suggests a potential link between PFO and vasospastic angina. It also demonstrates PFO closure as a potential therapeutic intervention for individuals with PFO who suffer from refractory vasospastic angina. (Level of Difficulty: Intermediate.)

We present here a unique case in which a 63-year-old man developed diffuse coronary vasospasm on postoperative day (POD) 1 following uneventful aortic valve replacement, replacement of ascending aorta, and coronary artery bypass. Subsequent emergent coronary angiogram demonstrated diffuse native coronary artery vasospasm that was only transiently responsive to intracardiac nitroglycerin, resulting in persistent cardiogenic shock and severe biventricular dysfunction. The patient was, thus, placed on femoral-femoral venoarterial (VA) extracorporeal membrane oxygenation (ECMO) with Impella support. This strategy allowed the weaning of vasopressors and enabled the resolution of the vasospasm. The patient was ultimately discharged on POD 17 without further complications. This case demonstrates our management strategy to provide life-saving support for patients facing postcardiac surgery refractory vasospasm. [ABSTRACT FROM AUTHOR]

Acute myocardial infarction (AMI) is a life-threatening disease when sudden blockage of coronary artery occurs. As the most specific biomarker, cardiac troponin I (cTnI) is usually checked separately to diagnose or eliminate AMI, and achieving the accurate detection of cTnI is of great significance to patients' life and health. Compared with other methods, fluorescent detection has the advantages of simple operation, high sensitivity and wide applicability. However, due to the strong fluorescence interference of biological molecules in body fluids, it is often difficult to obtain high sensitivity. In order to solve this problem, in this study, surface acoustic wave separation is designed to purify the target to achieve more sensitive detection performance of fluorescent detection. Specifically, the interference of background noise is almost completely removed on a microfluidic chip by isolating microbeads through acoustic radiation force, on which the biomarkers are captured by the immobilized detection probe. And then, the concentration of cTnI in human serum is detected by the fluorescence intensity change of the isolated functionalized beads. By this way, the detection limit of our biosensor calculated by 3σ/K method is 44 pg/mL and 0.34 ng/mL in PBS buffer and human serum respectively. Finally, the reliability of this method has been validated by comparison with clinical tests from the nephelometric analyzer in hospital. [ABSTRACT FROM AUTHOR]

As a complication of subarachnoid hemorrhage (SAH), vasospasm substantially contributes to its morbidity and mortality. We aimed at analyzing predictors of outcome for these patients including the role of endovascular treatment (ET). Our database was screened for patients with SAH treated in our Neuro-ICU from 2009 to 2019. Clinical parameters including functional outcome (modified Rankin Scale, mRS of 0–2 or 3–6 at discharge and after a median follow-up of 18 months) and details about ET were gathered on 465 patients, 241 (52%) of whom experienced vasospasm. Descriptive analyses were performed to identify explanatory variables for the dichotomized mRS score. A logistic regression model was fitted on 241 patients with vasospasm including age, Hunt and Hess Score, extraventricular drainage (EVD), forced hypertension, ET and delayed cerebral ischemia (DCI). The model found a Hunt and Hess Score of 5 (OR = 0.043, p = 0.008), requirement of EVD (OR = 0.161, p < 0.001), forced hypertension (OR = 0.242, p = 0.001), ET (OR = 0.431, p = 0.043) and DCI (OR = 0.229, p < 0.001) to be negative predictors of outcome while age was not. Use of intraarterial nimodipine alone (OR = 0.778, p = 0.705) or including balloon angioplasty (OR = 0.894, p = 0.902) and number of ETs per patient (OR = 0.757, p = 0.416) were not significant in a separate model with otherwise identical variables. While DCI is clearly associated with poor outcome, the influence of ET on outcome remains inconclusive. Limited by their retrospective nature and an indication bias, these data encourage a randomized assessment of ET. [ABSTRACT FROM AUTHOR]

• Myocardial infarction with non-obstructive coronary arteries (MINOCA) constitutes a significant proportion of patients who are at excess cardiovascular risk and have adverse clinical outcomes. • Coronary microvascular dysfunction (CMD) plays a potential role in the pathogenesis of MINOCA and may affect clinical outcomes, however, the role of functional and structural mechanisms of CMD in MINOCA remains unknown. • CMD can be assessed by various invasive and non-invasive tools depending on availability and clinical settings. • A better understanding of CMD in MINOCA has significant clinical implications for decision-making, identifying novel therapies that target CMD and improve clinical outcomes. In the past decade, scientific and clinical research has provided a translational perspective on myocardial infarction (MI) with non-obstructive coronary arteries (MINOCA). MINOCA is characterized by clinical documentation of an acute MI but angiography shows no significant coronary artery obstruction (stenosis <50%). The prevalence of MINOCA is estimated to range from approximately 6 to 10% among MI patients, and those with this condition have a poor prognosis, experiencing high rates of mortality, rehospitalization, and socioeconomic burden. MINOCA represents a major unmet need in cardiovascular medicine, with uncertain clinical management. It is a complex condition that can be caused by various factors, including atherosclerosis, plaque rupture, coronary vasospasm, and microvascular dysfunction. Effective management of MINOCA depends on identifying the underlying mechanism of the infarction, thus a systematic diagnostic approach is recommended. Contemporary data shows that a significant number of patients exhibit structural and functional abnormalities in coronary microcirculation, which is referred to as coronary microvascular dysfunction (CMD). CMD plays a crucial role in patients with signs and symptoms of myocardial ischemia and non-obstructive coronary artery stenosis, including MINOCA. Furthermore, conducting a thorough evaluation of coronary function can have significant prognostic and therapeutic implications, since personalized patient management strategies based on this assessment have been shown to improve symptoms and prognosis. Therefore, an accurate and timely diagnosis of CMD is essential for effective patient management, which can be achieved through various invasive and non-invasive methods. This review will discuss the pathophysiological understanding, current diagnostic techniques, and management strategies of patients with MINOCA and CMD. [Display omitted] [ABSTRACT FROM AUTHOR]

Objectives: Ferroptosis, a new regulated cell death pathway, plays a crucial part in the development of cardiovascular disease. However, the precise underlying mechanism remains unclear. Therefore, this study aimed to elucidate this. Methods: Herein, an erastin-induced H9C2 cell ferroptosis in vitro model and a myocardial infarction murine model, which was created by ligating the left anterior descending coronary artery, were established. Ferroptosis-related indicators, myocardial injury-related indicators, and Nrf2 signaling-related proteins expression were analyzed to explore the potential mechanism underlying cardiomyocyte ferroptosis-mediated cardiovascular disease development. Results: We demonstrated that Nrf2 downregulation in myocardial tissue, accompanied by ferroptotic events and changes in xCT and GPX4 expressions, induced cardiomyocyte ferroptosis and myocardial injury after myocardial infarction. These events, including ferroptosis and changes in Nrf2, xCT, and GPX4 expressions, were improved by ferrostatin-1 in vivo and in vitro. Besides, Nrf2 deficiency or inhibition aggravated myocardial infarction-induced cardiomyocyte ferroptosis by decreasing xCT and GPX4 expressions in vivo and in vitro. Moreover, ferrostatin-1 directly targeted Nrf2, as evidenced by surface plasmon resonance analysis. Conclusions: These results indicated that myocardial infarction is accompanied by cardiomyocyte ferroptosis and that Nrf2 signaling plays a crucial part in regulating cardiomyocyte ferroptosis after myocardial infarction. Graphical Abstract [ABSTRACT FROM AUTHOR]

Acute myocardial infarction (MI) occurs when blood flow to the myocardium is restricted, leading to cardiac damage and massive loss of viable cardiomyocytes. Timely restoration of coronary flow is considered the gold standard treatment for MI patients and limits infarct size; however, this intervention, known as reperfusion, initiates a complex pathological process that somewhat paradoxically also contributes to cardiac injury. Despite being a sterile environment, ischemia/reperfusion (I/R) injury triggers inflammation, which contributes to infarct expansion and subsequent cardiac remodeling and wound healing. The immune response is comprised of subsets of both myeloid and lymphoid-derived cells that act in concert to modulate the pathogenesis and resolution of I/R injury. Multiple mechanisms, including altered metabolic status, regulate immune cell activation and function in the setting of acute MI, yet our understanding remains incomplete. While numerous studies demonstrated cardiac benefit following strategies that target inflammation in preclinical models, therapeutic attempts to mitigate I/R injury in patients were less successful. Therefore, further investigation leveraging emerging technologies is needed to better characterize this intricate inflammatory response and elucidate its influence on cardiac injury and the progression to heart failure. [ABSTRACT FROM AUTHOR]

Background Direct lightning strikes are rare, and multiple organ systems can be involved. Prognosis is dependent on the severity of the injury. Severe myocardial injury associated with transient electrocardiogram changes, which have been previously described, is a hazardous complication. Case summary A 35-year-old man with no known past medical history presented unresponsive following a direct lightning strike while sitting in a portable toilet. High-quality cardiopulmonary resuscitation was started in the field, with return of spontaneous circulation (ROSC) after 1 h. Following ROSC, he received volume resuscitation and was maintained on multiple vasopressors. Electrocardiogram showed significant ST-elevations in inferior leads with elevated troponin I, consistent with inferior ST-elevation myocardial infarction. Labs revealed lactic acidosis, hyperkalaemia, acute kidney, and liver injury. Due to concern for plaque rupture, coronary angiography was performed and revealed no obstructive coronary artery disease. Vasopressor support and volume resuscitation were continued for extensive burns covering greater than 30% body surface area. The patient became progressively hypotensive, eventually precipitating pulseless electrical activity arrest. Emergent labs were notable for severe acidaemia. Despite aggressive interventions, he expired due to severe multi-organ failure. Discussion Direct lightning injuries are rare with serious potential complications. Myocardial damage, either from direct electrical insult or from induced coronary vasospasm, can lead to multi-organ system failure. [ABSTRACT FROM AUTHOR]

Background Coronary air embolism (CAE) is a rare and life-threatening complication of endovascular procedures, mostly due to procedure-related causes. Case summary A 70-year-old man with severe respiratory disorder presented with patent foramen ovale (PFO)-related platypnea-orthodeoxia syndrome (POS). Transcatheter PFO closure was performed under local anaesthesia and intracardiac echocardiographic guidance. After a 5-Fr catheter was passed through the PFO via a 7-Fr femoral vein sheath, the patient suddenly coughed and breathed deeply. Thereafter, intracardiac echocardiography showed massive microbubbles in all cardiac chambers and the ascending aorta, and an electrocardiogram showed ST-segment elevations in the anterior and inferior leads. Emergency coronary angiography confirmed occlusion of the mid-left anterior descending artery, suggesting CAE. As the intracoronary infusion of saline, nitroglycerine, and nicorandil was ineffective, we performed air aspiration using a thrombectomy device, achieving coronary blood flow improvement and ST-segment resolution. Thereafter, positive pressure support using manual bag-valve-mask ventilation under intravenous sedation supported successful transcatheter PFO closure without further air embolization. Discussion In this case with severe respiratory dysfunction, spontaneous deep breathing (spontaneous Valsalva manoeuvre) caused negative intrathoracic pressure and large drops in intravascular pressure. This phenomenon might have induced air contamination during device advancement, either by entrapping or leaving residual air in the gaps between the catheter and the sheath. Additionally, PFO with right-to-left shunts is more likely to cause paradoxical air embolization. Thus, the spontaneous Valsalva manoeuvre should be avoided with appropriate respiratory management to prevent paradoxical air embolization, including CAE, during transcatheter PFO closure under local anaesthesia in severe respiratory dysfunction patients. [ABSTRACT FROM AUTHOR]

Background: Although coronary artery disease and coronary artery spasm (CAS) can lead to acute myocardial infarction, there are clear differences in treatment between coronary heart disease and CAS, and the therapeutic schedule should not be confused. Furthermore, electrocardiogram (ECG) "6+2" phenomenon is recommend as a specific ECG indicator for lesions in the left main coronary artery or multiple vessels. Currently, no reports of this phenomenon in CAS exist. Case Report: A 72-year-old man had history of recurrent chest pain for over 6 years, with episodes lasting about 10 min and resolving with rest. He experienced symptom recurrence and exacerbation due to substance abuse. He was admitted to our Emergency Department for chest pain at rest. His emergency ECG revealed a 6+2 phenomenon, accompanied by troponin levels exceeding 18 times the reference value. Promptly, we conducted coronary angiography, with unexpected normal findings. Following thorough assessment, we postulated the patient could have CAS. Subsequent to medical team intervention, the patient's ECG normalized, leading to his discharge upon condition stabilization. Conclusions: We report a case of CAS in a patient with ECG 6+2 phenomenon, without significant coronary artery stenosis. This differs from transient ST-segment elevation on ECG, a well-recognized hallmark of CAS; however, such a presentation has not been documented before. Additionally, treatment strategies for myocardial ischemic conditions stemming from coronary atherosclerosis diverge from those employed for CAS. Therefore, clinicians should advocate for coronary angiography whenever feasible. This approach serves to elucidate the underlying disease etiology and facilitates the administration of precision-targeted interventions for patients. [ABSTRACT FROM AUTHOR]

Background: During Stent for Life Initiative in Portugal lifetime, positive changes in ST elevation myocardial infarction treatment were observed, by the increase of Primary Angioplasty numbers and improvements in patients' behaviour towards myocardial infarction, with an increase in those who called 112 and the lower proportion attending non primary percutaneous coronary intervention centres. Despite public awareness campaigns and system educational programmes, patient and system delay did not change significantly over this period. The aim of this study was to address the public awareness campaign effectiveness on peoples' behaviour facing STEMI, and how Covid-19 has affected STEMI treatment. Methods: Data from 1381 STEMI patients were collected during a one-month period each year, from 2011 to 2016, and during one and a half month, matching first lockdown in Portugal 2020. Four groups were constituted: Group A (2011); Group B (2012&2013); Group C (2015&2016) and group D (2020). Results: The proportion of patients who called 112, increased significantly (35.2% Group A; 38.7% Group B; 44.0% Group C and 49.6% Group D, p = 0.005); significant reduction was observed in the proportion of patients who attended healthcare centres without PPCI (54.5% group A; 47.6% Group B; 43.2% Group C and 40.9% Group D, p = 0.016), but there were no differences on groups comparison. Total ischemic time, measured from symptoms onset to reperfusion increased progressively from group A [250.0 (178.0–430.0)] to D [296.0 (201.0–457.5.8)] p = 0.012, with statistically significant difference between group C and D (p = 0.034). Conclusions: During the term of SFL initiative in Portugal, patients resorted less to primary health centres and called more to 112. These results can be attributed the public awareness campaign. Nevertheless, patient and system delays did not significantly change over this period, mainly in late years of SFL, probably for low efficacy of campaigns and in 2020 due to Covid-19 pandemic. [ABSTRACT FROM AUTHOR]

Background: The prognostic nutritional index (PNI) and different glucose metabolisms have been separately reported to be correlated with long-term prognosis in patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI). However, PNI application in patients with an impaired glucose metabolism has not been well validated, especially in pre-diabetic patients. This study evaluated whether PNI influences a long-term risk of mortality along different glucose metabolism statuses. Methods: A total of 17,697 patients with AMI and a history of PCI were enrolled in this retrospective observational cohort study from January 2007 to December 2020. Three subgroups with different glucose metabolism statuses, including normal glucose regulation (NGR), pre-diabetes mellitus (pre-DM), and diabetes mellitus (DM), were divided into three groups according to the tertiles of PNI, respectively. Results: All-cause mortality occurred in 2613 (14.8%) patients within a median of 4.1 years of follow-up. Upon analyzing the Kaplan–Meier plots for the NGR, pre-DM, and DM groups, the incidence of all-cause or cardiovascular mortality in the low PNI (PNI-L, ≤ 42.7) subgroup was significantly higher than that in the median PNI (PNI-M, > 42.7 and ≤ 48.2) and high PNI (PNI-H, > 48.2) subgroups (all, P < 0.001). After adjusting for confounding factors, the hazard ratio (HR) for all-cause mortality in the PNI-L group significantly increased compared to that in the PNI-H subgroups of the NGR group (HR, 1.35; 95% CI 1.14–1.66; P < 0.001), pre-DM group (HR, 1.29; 95% CI 1.02–1.62; P < 0.001), and DM group (HR, 1.36; 95% CI 1.13–1.63; P < 0.001). Given that there was evidence of interactions between PNI and different glucose statuses (P for interaction < 0.001), patients were divided into nine subgroups, and we found that DM patients with PNI-L statuses had the highest risk of all-cause mortality compared to NGR patients with PNI-H statuses (HR, 1.69; 95% CI 1.42–2.01; P < 0.001). Conclusion: Lower PNI is a significant and independent risk factor for all-cause mortality in AMI patients undergoing PCI with different glucose metabolism statuses, and this risk further increases with DM compared to NGR or pre-DM statuses. [ABSTRACT FROM AUTHOR]

Background: Adenosine stress cardiac magnetic resonance (CMR) imaging is increasingly utilized for evaluating patients with known or suspected coronary artery disease (CAD). This study aims to assess the safety and clinical impact of adenosine stress CMR in a tertiary care setting in Thailand. Methods: A total of 3,768 consecutive patients aged 18 years and above who underwent adenosine stress CMR between 2017 and 2020 were included in the study. Patient records were reviewed to collect data on clinical characteristics, hemodynamic measurements, complications during or immediately after CMR, and the rates of clinical changes resulting from CMR. Results: Among the included patients, the primary indications for adenosine stress CMR were risk stratification in suspected CAD (70.8%) and the assessment of myocardial ischemia/viability in patients with known CAD (26.5%). There were no reported deaths or acute myocardial infarctions during the procedure. Major complications, specifically acute pulmonary edema requiring hospital observation or admission for further management, occurred in four patients (0.11%), all of whom were elderly (ranging from 75 to 91 years) with a history of heart failure. Non-major complications were observed in 13.7% of patients, with dyspnea (9.8%) and mild chest pain (5.6%) being the most common. CMR provided a completely new diagnosis in 26.2% of patients. Overall, stress CMR resulted in a change in diagnosis or management for 48% of patients. Conclusion: Adenosine stress CMR was found to be safe and to have a significant impact on clinical management in Asian patients with known or suspected CAD. These findings support the use of adenosine stress CMR as a valuable tool for evaluating and guiding treatment decisions in this patient population. [ABSTRACT FROM AUTHOR]

Introduction: World Health Organization clinically defines a stroke as ‘the rapid development of clinical signs and symptoms of a focal neurological disturbance lasting more than 24 hours or leading to death with no apparent cause other than vascular origin’. Hypomagnesaemia leads to neuromuscular hyperirritability, tremors, increased vascular resistance, coronary vasospasm and hypertension. Hypomagnesaemia triggers vasoconstriction enhancing vascular endothelial injury and hence leads to atherosclerosis. Subjects and Methods: It was a case control study, undertaken in the Department of Medicine in S Nijalingappa medical college and HSK Hospital during the period of July 2021–December 2022. 30 patients with acute ischemic cerebral stroke fulfilling the inclusion criteria were selected. 2 ml venous sample for serum magnesium level was taken within 24 hours. Magnesium levels in patients after acute cerebral ischemic stroke were documented in patients, receiving standard management protocol of ischemic stroke. The correlation co-efficient of Hypomagnesaemia with modified Rankin Scale Score was calculated. Results: The mean age of patients was 45-80 years, 36 (60 %) patients were male and 24 (40 %) were females and there was male preponderance. The mean serum magnesium levels were measured. The present study observed a statistically significant correlation between modified Rankin Scale score measured at three months and serum magnesium level. Conclusion: It was concluded through the results of this study that Hypomagnesaemia in the body can cause more severe ischemic stroke. [ABSTRACT FROM AUTHOR]

Background: Photon‐counting‐detector CT (PCD‐CT) enables the production of virtual monoenergetic images (VMIs) at a high spatial resolution (HR) via simultaneous acquisition of multi‐energy data. However, noise levels in these HR VMIs are markedly increased. Purpose: To develop a deep learning technique that utilizes a lower noise VMI as prior information to reduce image noise in HR, PCD‐CT coronary CT angiography (CTA). Methods: Coronary CTA exams of 10 patients were acquired using PCD‐CT (NAEOTOM Alpha, Siemens Healthineers). A prior‐information‐enabled neural network (Pie‐Net) was developed, treating one lower‐noise VMI (e.g., 70 keV) as a prior input and one noisy VMI (e.g., 50 keV or 100 keV) as another. For data preprocessing, noisy VMIs were reconstructed by filtered back‐projection (FBP) and iterative reconstruction (IR), which were then subtracted to generate "noise‐only" images. Spatial decoupling was applied to the noise‐only images to mitigate overfitting and improve randomization. Thicker slice averaging was used for the IR and prior images. The final training inputs for the convolutional neural network (CNN) inside the Pie‐Net consisted of thicker‐slice signal images with the reinsertion of spatially decoupled noise‐only images and the thicker‐slice prior images. The CNN training labels consisted of the corresponding thicker‐slice label images without noise insertion. Pie‐Net's performance was evaluated in terms of image noise, spatial detail preservation, and quantitative accuracy, and compared to a U‐net‐based method that did not include prior information. Results: Pie‐Net provided strong noise reduction, by 95 ± 1% relative to FBP and by 60 ± 8% relative to IR. For HR VMIs at different keV (e.g., 50 keV or 100 keV), Pie‐Net maintained spatial and spectral fidelity. The inclusion of prior information from the PCD‐CT data in the spectral domain was able to improve a robust deep learning‐based denoising performance compared to the U‐net‐based method, which caused some loss of spatial detail and introduced some artifacts. Conclusion: The proposed Pie‐Net achieved substantial noise reduction while preserving HR VMI's spatial and spectral properties. [ABSTRACT FROM AUTHOR]

Myocardial infarction with nonobstructive coronary arteries (MINOCA) is a distinct subtype of myocardial infarction (MI), occurring in about 8–10% of spontaneous MI cases referred for coronary angiography. Unlike MI with obstructive coronary artery disease, MINOCA's pathogenesis is more intricate and heterogeneous, involving mechanisms such as coronary thromboembolism, coronary vasospasm, microvascular dysfunction, dissection, or plaque rupture. Diagnosing MINOCA presents challenges and includes invasive and non-invasive strategies aiming to differentiate it from alternative diagnoses and confirm the criteria of elevated cardiac biomarkers, non-obstructive coronary arteries, and the absence of alternate explanations for the acute presentation. Tailored management strategies for MINOCA hinge on identifying the underlying cause of the infarction, necessitating systematic diagnostic approaches. Furthermore, determining the optimal post-MINOCA medication regimen remains uncertain. This review aims to comprehensively address the current state of knowledge, encompassing diagnostic and therapeutic approaches, in the context of MINOCA while also highlighting the evolving landscape and future directions for advancing our understanding and management of this intricate myocardial infarction subtype. [ABSTRACT FROM AUTHOR]

Due to the high degree of curvature of the coronary arteries, normal blood flow patterns are disrupted, making them susceptible sites for stenosis and atherosclerosis, leading to decrease in flow. Myocardial ischemia and infarction are the results of this reduced myocardial flow perfusion. Therefore, we conducted an extensive hemodynamic analysis on a patient suspected to have chest pain because of coronary artery disease in order to recognize the processes behind behaviors instigated by intricate geometry of the coronary artery. First, using coronary computed tomography angiography data, which were obtained from an ethically approved data provider, a patient-specific model was reconstructed. Open-circuit resemblance lumped parameter network coupled with zero-three dimensional (0D-3D) model was built to mimic coronary pressure and flow. Hemodynamic parameters such as the flow streamlines, time-average wall shear stress, oscillatory shear index, flow rate, and relative resilience time were investigated using computational fluid dynamics. It is critical for cardiac specialists to adequately care for their patients and provide corrective therapies at early onset of coronary problems caused by myocardial infarctions and demand coronary bypass surgery and stenting. The open loop modeling approach with lumped parameter-based physiologically and geometrically realistic outflow pressures will assist cardiologists in analyzing blood dynamics using the medically imaged coronary arteries of their patients and computing the magnitude of the hemodynamic parameters to provide them with a reliable assessment of the risk of coronary arterial disease for their patients. [ABSTRACT FROM AUTHOR]

Noreflow is a condition associated with a poor prognosis in ST segment elevation myocardial infarction patients. It has been shown that many inflammatory markers and index such as procalcitonin, C-reactive protein, neutrophil to lymphocyte ratio, systemic immune inflammatory index (SII), are associated with noreflow. We used a brand-new index pan-immune-inflammation value (PIV) to retrospectively evaluate the relationship between PIV and noreflow. A total of 1212 patients were included for analysis. Noreflow was observed in 145 patients. In multivariate analysis, PIV (odds ratio (OR): 1.025; [1.002–1.115], p < 0.001), baseline ejection fraction (OR: 0.963; [0.934–0.993], p = 0.015), stent length (OR: 1.032; [1.010–1.054], p = 0.004), age (OR: 1.034; [1.014-1.053], p = 0.001) and pain to PCI time (OR: 1.003 [1.002–1.005], p < 0.001) were observed to be the independent predictors of noreflow. ROC curve analysis showed that the best cut off value of PIV for predicting noreflow was ≥889 with 77.2% sensitivity and 77.5% specificity (AUC, 0.828; 95% CI [0.806-0.849]). A ROC curve comparison analysis was performed to compare PIV and SII. The predictive power of PIV was higher than SII (differences between areas: 0.154; p < 0.001). According to our findings, an increase in PIV is an independent predictor of noreflow in patients with STEMI. [ABSTRACT FROM AUTHOR]

Background: Mesenchymal stromal cell (MSC) transplantation can improve the left ventricular ejection fraction (LVEF) after an acute myocardial infarction (AMI). Transplanted MSCs exert a paracrine effect, which might be augmented if repeated doses are administered. This study aimed to compare the effects of single versus double transplantation of Wharton's jelly MSCs (WJ-MSCs) on LVEF post-AMI. Methods: We conducted a single-blind, randomized, multicenter trial. After 3–7 days of an AMI treated successfully by primary PCI, 70 patients younger than 65 with LVEF < 40% on baseline echocardiography were randomized to receive conventional care, a single intracoronary infusion of WJ-MSCs, or a repeated infusion 10 days later. The primary endpoint was the 6-month LVEF improvement as per cardiac magnetic resonance (CMR) imaging. Results: The mean baseline EF measured by CMR was similar (~ 40%) in all three groups. By the end of the trial, while all patients experienced a rise in EF, the most significant change was seen in the repeated intervention group. Compared to the control group (n = 25), single MSC transplantation (n = 20) improved the EF by 4.54 ± 2%, and repeated intervention (n = 20) did so by 7.45 ± 2% when measured by CMR imaging (P < 0.001); when evaluated by echocardiography, these values were 6.71 ± 2.4 and 10.71 ± 2.5%, respectively (P < 0.001). Conclusions: Intracoronary transplantation of WJ-MSCs 3–7 days after AMI in selected patients significantly improves LVEF, with the infusion of a booster dose 10 days later augmenting this effect. Trial registration: Trial registration: Iranian Registry of Clinical Trials, IRCT20201116049408N1. Retrospectively Registered 20 Nov. 2020, https://en.irct.ir/trial/52357 [ABSTRACT FROM AUTHOR]

Angina with nonobstructive coronary arteries (ANOCA) is increasingly recognized and may affect nearly one-half of patients undergoing invasive coronary angiography for suspected ischemic heart disease. This working diagnosis encompasses coronary microvascular dysfunction, microvascular and epicardial spasm, myocardial bridging, and other occult coronary abnormalities. Patients with ANOCA often face a high burden of symptoms and may experience repeated presentations to multiple medical providers before receiving a diagnosis. Given the challenges of establishing a diagnosis, patients with ANOCA frequently experience invalidation and recidivism, possibly leading to anxiety and depression. Advances in scientific knowledge and diagnostic testing now allow for routine evaluation of ANOCA noninvasively and in the cardiac catheterization laboratory with coronary function testing (CFT). CFT includes diagnostic coronary angiography, assessment of coronary flow reserve and microcirculatory resistance, provocative testing for endothelial dysfunction and coronary vasospasm, and intravascular imaging for identification of myocardial bridging, with hemodynamic assessment as needed. [Display omitted] • ANOCA is a common clinical presentation that is variably recognized and managed. • Standardization is needed for the identification, diagnosis, and treatment of patients with ANOCA. • Comprehensive coronary function testing is important for identifying underlying causes of ANOCA in individual patients. [ABSTRACT FROM AUTHOR]

Systemic sclerosis (SSc) is an autoimmune disease associated with increased mortality and poor morbidity, impairing the quality of life in patients. Whilst we know that SSc affects multiple organs via vasculopathy, inflammation, and fibrosis, its exact pathophysiology remains elusive. Microvascular injury and vasculopathy are the initial pathological features of the disease. Clinically, the vasculopathy in SSc is manifested as Raynaud's phenomenon (reversible vasospasm in reaction to the cold or emotional stress) and digital ulcers due to ischemic injury. There are several reports that medications for vasculopathy, such as bosentan and soluble guanylate cyclase (sGC) modulators, improve not only vasculopathy but also dermal fibrosis, suggesting that vasculopathy is important in SSc. Although vasculopathy is an important initial step of the pathogenesis for SSc, it is still unclear how vasculopathy is related to inflammation and fibrosis. In this review, we focused on the clinical evidence for vasculopathy, the major cellular players for the pathogenesis, including pericytes, adipocytes, endothelial cells (ECs), and myofibroblasts, and their signaling pathway to elucidate the relationship among vasculopathy, inflammation, and fibrosis in SSc. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of coenzyme Q10 combined with tegrel on unstable angina pectoris of coronary heart disease and its influence on coronary blood flow parameters. 128 patients with unstable angina pectoris of coronary heart disease admitted to our hospital from October 2020 to October 2022 were selected as the study subjects. All patients were divided into observation group and matched group by random number table method, with 64 patients in each group. The patients in the matched group were treated with conventional western medicine. The observation group added coenzyme Q10 combined with tegrel on the basis of the matched group to compare the clinical treatment effect of the two groups, Visual Analogue Pain Scale (VAS) was used to assess the pain of angina pectoris in the two groups, and the daily attack frequency, duration of each time, and daily amount of nitroglycerin were compared. The cardiac function indexes and coronary blood flow parameters of the two groups were measured before and after treatment. Results: The total effective rate of treatment in the observation group was higher than that in the matched group (P<0.05); The pain score, daily attack frequency, duration of each time and daily nitroglycerin dosage in the observation group were significantly lower than those in the matched group (P; There was no difference in the 6-minute walking distance, LVEF and BNP between the two groups before treatment (P>0.05). After treatment, the 6-minute walking distance and LVEF of the two groups increased, and the level of BNP in the observation group was higher than that in the matched group, while the level of BNP in the observation group was lower than that in the matched group (P<0.05); There was no difference between the two groups before treatment in terms of diastolic time velocity integral, left anterior descending systolic peak velocity, left anterior descending diastolic peak velocity, and coronary flow velocity reserve value (P>0.05). After treatment, the two groups increased in terms of diastolic time velocity integral, left anterior descending systolic peak velocity, left anterior descending diastolic peak velocity, and coronary flow velocity reserve value, and the observation group was higher than the matched group (P<0.05). Conclusion: Coenzyme Q10 combined with tegrel has a significant effect on the treatment of unstable angina pectoris of coronary heart disease. It can reduce the degree of angina pectoris, reduce the frequency, duration and nitroglycerin consumption of patients, improve the level of cardiac function, improve coronary blood flow parameters, and is worthy of clinical application and promotion. [ABSTRACT FROM AUTHOR]

Backgrounds. Serum total bilirubin (STB) is recently more regarded as an antioxidant with vascular protective effects. However, we noticed that elevated STB appeared in unstable angina pectoris (UAP) patients with diffused coronary lesions. We aimed to explore STB's roles in UAP patients, which have not been reported by articles. Methods and Results. 1120 UAP patients were retrospectively screened, and 296 patients were finally enrolled. They were grouped by Canadian Cardiovascular Society (CCS) angina grades. The synergy between PCI with TAXUS stent and cardiac surgery score (SYNTAX score) and corrected thrombolysis in myocardial infarction flow count (CTFC) were adopted to profile coronary features. The results showed that STB, mean platelet volume (MPV), hs-CRP, fasting blood glucose (FBG), red blood cell width (RDW), and CTFC elevated significantly in the CCS high-risk group. STB (B = 0.59 , 95% CI: 0.39-0.74, P < 0.01) and MPV (B = 0.86 , 95% CI: 0.42-1.31, P < 0.01) could indicate SYNTAX score changes for these patients. STB (≥21.7 μmol/L) could even indicate a coronary slow flow condition (AUC: 0.88, 95% CI: 0.84-0.93, P < 0.01). Moreover, UAP patients with elevated STB had a lower event-free survival rate by the Kaplan-Meier curve. STB ≥21.7 μmol/L could reflect a poor coronary flow status and indicate 1-year poor outcomes for these patients (HR: 2.01, 95% CI: 1.06-3.84, P < 0.01). Conclusion. Elevated STB in UAP patients has a close relationship with changes in SYNTAX score. STB (over 21.7 μmol/L) could even indicate a coronary slow flow condition and poor outcomes for the UAP patients. [ABSTRACT FROM AUTHOR]

High-density lipoprotein (HDL) functionality has been reported to be associated with coronary artery disease (CAD). However, little is known about the impact of HDL functionality on coronary atherosclerosis. Thirty-eight type 2 diabetic patients with CAD who underwent percutaneous coronary intervention were examined. Coronary atheroma burden and plaque composition of the culprit lesions were assessed using conventional gray-scale and integrated backscatter intravascular ultrasound. HDL-mediated cholesterol efflux capacity (HDL-CEC) and HDL antioxidant capacity, estimated as HDL inflammatory index (HII), were examined. The associations between HDL functionality and coronary plaques were analyzed using multivariate data analysis, including principal components analysis and orthogonal partial least squares (OPLS) models. Percent atheroma volume was correlated with HDL-CEC (r = 0.34, p = 0.04) but not with HII (p = 0.65). The OPLS model demonstrated that the percentage lipid volume was significantly associated with HDL functionality [coefficient (95% confidence interval); HDL-CEC: −0.26 (−0.49, −0.04); HII: 0.34 (0.08, 2.60), respectively]. HII exhibited the highest variable importance in projection score, indicating the greatest contribution. HDL functionality was associated with coronary plaque composition, a key component of plaque vulnerability. Our findings highlight the potential importance of HDL functionality for coronary plaque stabilization. [ABSTRACT FROM AUTHOR]