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BACKGROUND: We prospectively assessed the reproducibility of a novel low-dose single-volume dynamic computed tomography (CT) myocardial blood flow measurement technique. METHODS: Thirty-four pairs of measurements were made under rest and stress conditions in 13 swine (54.3 ± 12.3 kg). One or two acquisition pairs were acquired in each animal with a 10-min delay between each pair. Contrast (370 mgI/mL; 0.5 mL/kg) and a diluted contrast/saline chaser (0.5 mL/kg; 30:70 contrast/saline) were injected peripherally at 5 mL/s, followed by bolus tracking and acquisition of a single volume scan (100 kVp; 200 mA) with a 320-slice CT scanner. Bolus tracking and single volume scan data were used to derive perfusion in mL/min/g using a first-pass analysis model; the coronary perfusion territories of the left anterior descending (LAD), left circumflex (LCx), and right coronary artery (RCA) were automatically assigned using a previously validated minimum-cost path technique. The reproducibility of CT myocardial perfusion measurement within the LAD, LCx, RCA, and the whole myocardium was assessed via regression analysis. The average CT dose index (CTDI) of perfusion measurement was recorded. RESULTS: The repeated first (Pmyo1) and second (Pmyo2) single-volume CT perfusion measurements were related by Pmyo2 = 1.01Pmyo1 - 0.03(ρ = 0.96; RMSE = 0.08 mL/min/g; RMSE = 0.07 mL/min/g) for the whole myocardium, and by Preg2 = 0.86Preg1 + 0.13(ρ = 0.87; RMSE = 0.31 mL/min/g; RMSE = 0.29 mL/min/g) for the LAD, LCx, and RCA perfusion territories. The average CTDI of the single-volume CT perfusion measurement was 10.5 mGy. CONCLUSION: The single-volume CT blood flow measurement technique provides reproducible low-dose myocardial perfusion measurement using only bolus tracking data and a single whole-heart volume scan. RELEVANCE STATEMENT: The single-volume CT blood flow measurement technique is a noninvasive tool that reproducibly measures myocardial perfusion and provides coronary CT angiograms, allowing for simultaneous anatomic-physiologic assessment of myocardial ischemia. KEY POINTS: A low-dose single-volume dynamic CT myocardial blood flow measurement technique is reproducible. Motion misregistration artifacts are eliminated using a single-volume CT perfusion technique. This technique enables combined anatomic-physiologic assessment of coronary artery disease.

The article discusses the prevalence of heart failure (HF) as a major disease burden in Europe, exacerbated by comorbidities such as chronic kidney disease, anaemia, obesity, and diabetes. It highlights the systemic nature of HF, requiring an interdisciplinary approach for prevention and treatment. The new COST Action EU-METAHEART aims to address metabolic alterations in HF through research areas focusing on cardiomyocyte metabolism, coronary vascular dysfunction, immunometabolism, and mitochondrial redox alterations. The Action seeks to improve understanding, identify treatment targets, and train the next generation of scientists in this field. [Extracted from the article]

Hypoxia, or the lack of oxygen, has multiple impacts on the vascular system. The major molecular sensors for hypoxia at the cellular level are hypoxia inducible factor and heme oxygenase. Hypoxia also acts on the vasculature directly conveying its damaging effects through disruption of the control of vascular tone, particularly in the coronary circulation, enhancement of inflammatory responses and activation of coagulation pathways. These effects could be particularly detrimental under pathological conditions such as obstructive sleep apnea and other breathing disorders. Introduction: The effect of conjugate 2-(3,4-Dihydroxyphenyl)-6-{[1-(2'-bromo-3',4'-dimethoxyphenyl)-6,7-dimethoxy-3,4-dihydroisoquinolin-2(1H)-yl]methyl}-3,5,7-trihydroxychroman-4-one (DHQ-11) on hypoxia-induced vasorelaxation was investigated in rat aortic rings using standard organ bath techniques. Materials and methods: Hypoxia was stimulated by a superfusion of aortic rings with a glucose-free Krebs solution bubbled with 95% N2/5% CO2. The effect of conjugate DHQ-11 was assessed after a 60-min period of hypoxia on aortic rings precontracted with 50 mM KCl or 1µM phenylephrine (PE). The conjugate DHQ-11 significantly attenuated hypoxia-induced vasorelaxation in the endothelium-intact aortic rings precontracted with KCl or PE in a concentration-dependent manner. Results and discussion: This effect of conjugate DHQ-11 was more potent in aortic rings precontracted with PE than those with KCl where it maximally reduced hypoxia-induced vasorelaxation from 44.7 ± 3.7 to 5.4 ± 3.7 and 33.9 ± 3.4 to 10.8 ± 4.2%, respectively. The removal of the endothelium attenuated the effect of conjugate DHQ-11 on hypoxia-induced vasorelaxation. Similarly, pretreatment of endothelium-intact aortic rings with L-NAME and methylene blue also attenuated the effect of conjugate DHQ-11 on hypoxia-induced vasorelaxation. Furthermore, the blockade of the ATP-sensitive KATP channel with glibenclamide and the calcium-activated large conductance BKCa channel with TEA also significantly attenuated the effect of conjugate DHQ-11 on hypoxia-induced vasorelaxation. Collectively, these results indicated that conjugate DHQ-11 attenuated the hypoxia-induced vasorelaxation suggesting that it alleviated the oxidative damage of vasculature. Conclusions: This effect of conjugate DHQ-11 possible is mediated through several mechanisms including the blockage of the extracellular Ca2+ entry via the voltage-dependent and receptor-operative Ca2+ channels, as well as inhibition of sarcoplasmic reticulum Ca2+ release via the inositol triphosphate pathway. In addition, endothelium and NO/sGC/cGMP/PKG pathway, as well as KATP and BKCa channels most likely participate in protection by conjugate DHQ-11 against hypoxia-induced vasorelaxation. [ABSTRACT FROM AUTHOR]

Background: This study examines the role of extracorporeal life support flow in the development of acute kidney injury in cardiogenic shock. Methods: We performed a retrospective analysis of 465 patients placed on extracorporeal life support at our institution between January 2015 and December 2020 for cardiogenic shock. Flow index was calculated by dividing mean flow by body surface. Stages of acute kidney injury were determined according to Kidney Disease: Improving Global Outcomes (KDIGO) organization guidelines. Results: There were 179 (38.5%) patients who developed acute kidney injury, 63.1% of which were classified as Stage 3--the only subgroup associated with 1-year mortality (hazard ratio = 2.03, p <.001). Risk of k idney injury increased up to a flow index of 1.6 L/min/m2, and kidney injury was more common among patients with flow index greater than 1.6 L/min/m2 (p =.034). Those with kidney injury had higher baseline lactate levels (4.4 vs 3.1, p =.04), and Stage 3 was associated wit higher baseline creatinine (p <.001). Conclusions: In our cohort, kidney injury was common and Stage 3 kidney injury was associated with worse outcomes compared to other stages. Low flow was not associated with increased risk of kidney injury. Elevated baseline lactate and creatinine among patients with acute kidney injury suggest underlying illness severity, rather than flow, may influence kidney injury risk. [ABSTRACT FROM AUTHOR]

Antegrade cardioplegia is routinely given during cardiac surgery. The delivery of antegrade cardioplegia from the cardiopulmonary bypass machine has many variables. Many perfusionists rely exclusively on cardioplegia system pressure to ensure safe antegrade delivery. Our group reviewed antegrade cardioplegia delivery in 50 patients undergoing coronary artery bypass graft. The data collected included the cardioplegia system pressure and the patient's direct aortic root pressure. The analysis of the data found weak correlation between the two pressures with a large mean difference and a wide standard deviation. The results suggest the direct measurement of aortic root pressure as guidance to antegrade cardioplegia instead of relying solely on cardioplegia system pressure. [ABSTRACT FROM AUTHOR]

Objectives: Residual dissection is a concern in endovascular treatment with a DCB, and there is limited knowledge of hemodynamics at a dissection lesion. Therefore, the objective of this study is to evaluate the mean pressure gradient (MPG) and fractional flow reserve (FFR) at a residual dissection after DCB angioplasty for the superficial femoral artery (SFA). Methods: A total of 59 cases with residual SFA dissection treated with DCB angioplasty at a single center were analyzed retrospectively. The dissection was classified into 6 types (A-F). The primary endpoints were MPG and FFR at a residual dissection lesion after DCB angioplasty, using evaluation with a pressure wire. Results: The median lesion length was 70 (40-130) mm with 24% popliteal involvement, and 11 cases (18%) had chronic total occlusion. A completion angiogram revealed dissection of types A (n = 33, 56%), B (n = 18, 31%), C (n = 7, 12%), and D (n = 1, 2%). The median MPGs in type A, B, and C cases were 0 (0-2), 0 (0-4), and 3 (0-6) mmHg, with a significant lower in type C cases than in type A cases (A vs C, P =.021). The median FFRs in type A, B, and C cases of 1.0 (.98-1.00), 1.0 (.96-1.00), and.98 (.95-1.00) did not differ significantly among dissection types (A vs B, P =.86; A vs C, P =.055; B vs C, P =.15). Conclusions: This is the first report of hemodynamics at a SFA dissection. The results suggest that low-grade dissection (types A or B) does not affect MPG and FFR at a SFA lesion. This indicates that a bailout stent may be unnecessary for patients with dissection of types A or B. A further investigation is needed to determine whether a scaffold is required for a SFA lesion with type C dissection. [ABSTRACT FROM AUTHOR]

The article offers a look at technological advancements in cardiac computed tomography (CT). Topics discussed include access to the cardiac catheterization laboratory, energy-integrating detectors, photon-counting detectors and spectral photon-counting CT, image reconstruction relative advances in artificial intelligence (AI) and deep learning, and CT-guided coronary risk stratification and cardiac preventative care.

Background The utilization of postdilatation in primary percutaneous coronary intervention (PCI) is feared to induce suboptimal coronary blood flow and compromise the outcome of the patients. This meta-analysis sought to verify whether postdilatation during primary PCI is associated with worse angiographic or long-term clinical outcomes. Methods Systematic literature searches were conducted on PubMed, The Cochrane Library, ClinicalTrials.gov , EBSCO, and Europe PMC on 10 March 2024. Eligible studies reporting the outcomes of postdilatation among ST-segment elevation myocardial infarction patients were included. The primary outcome was no-reflow condition during primary PCI based on angiographic finding. The secondary clinical outcome was major adverse cardiovascular events (MACEs) comprising all-cause death, myocardial infarction, target vessel revascularization (TVR), and stent thrombosis. Results Ten studies were finally included in this meta-analysis encompassing 3280 patients, which was predominantly male (76.6%). Postdilatation was performed in 40.7% cases. Postdilatation was associated with increased risk of no-reflow during primary PCI [Odd Ratio (OR) = 1.33, 95% Confidence Interval (CI): 1.12–1.58; P =.001)]. Conversely, postdilatation had a tendency to reduce MACE (OR = 0.70, 95% CI: 0.51–0.97; P =.03) specifically in terms of TVR (OR = 0.41, 95% CI: 0.22–0.74; P =.003). No significant differences between both groups in relation to mortality (OR = 0.58, 95% CI: 0.32–1.05; P =.07) and myocardial infarction (OR = 1.5, 95% CI: 0.78–2.89; P =.22). Conclusions Postdilatation after stent deployment during primary PCI appears to be associated with an increased risk of no-reflow phenomenon after the procedure. Nevertheless, postdilatation strategy has demonstrated a significant reduction in MACE over the course of long-term follow-up. Specifically, postdilatation significantly decreased the occurrence of TVR. Key messages: What is already known on this topic? Optimizing stent deployment by performing postdilatation during percutaneous coronary intervention (PCI) is essential for long-term clinical outcomes. However, its application during primary PCI is controversial due to the fact that it may provoke distal embolization and worsen coronary blood flow. What this study adds? In this systematic review and meta-analysis of 10 studies, we confirm that postdilatation during primary PCI is associated with worse coronary blood flow immediately following the procedure. On the contrary, this intervention proves advantageous in improving long-term clinical outcomes, particularly in reducing target vessel revascularization. How this study might affect research, practice, or policy? Given the mixed impact of postdilatation during primary PCI, this strategy should only be applied selectively. Future research should focus on identifying patients who may benefit from such strategy. [ABSTRACT FROM AUTHOR]

Introduction and aim: External validations of the Good Outcome Following Attempted Resuscitation (GO-FAR) score have been in populations where Do Not Attempt Resuscitation (DNAR) is practised. We aim to externally validate the GO-FAR score in a population without a DNAR order. Methods: We studied patients ≥ 18 years old who had an In-hospital cardiac arrest (IHCA) with known outcomes at Al Ain Hospital from January 2017 to December 2019, excluding those who died in the emergency department. Studied variables included demography, location, response time, code duration, initial rhythm, primary diagnosis, admission vital signs, GO FAR score variables, discharge status, and functional outcomes as determined by the cerebral performance category score ranging from 1 (good cerebral performance) to 5 (brain death). Results: 366 patients were studied; 66.7% were males. The median (IQR) age was 70 (55–81) years. Cardiac and respiratory causes were the primary diagnoses in 89 (24.6%) and 67 (18.5%), respectively. IHCA occurred in critical areas such as the intensive care unit, high dependency unit and coronary care unit in 206 (80.8%) patients. The majority, 308 (91.8%), had a non-shockable rhythm, and a return of spontaneous circulation was achieved in 159 (43.4%) of the patients. Thirty-one (8.5%) patients survived to hospital discharge, and 20 (5.5%) patients had cerebral performance category scores of 1 and 2. The area under the curve of the ROC for survival to discharge with good functional outcome was 0.74 (95% CI 0.59–0.88). The best cut-off point for predicting survival with a good neurological outcome was a GO-FAR score of < 4, having a sensitivity of 0.81, a specificity of 0.7, a positive likelihood ratio of 2.7 and a negative likelihood ratio of 0.27. Conclusions: A GO-FAR score of less than 4 predicts survival with a good neurological outcome in a healthcare system with an all-inclusive patient population with no DNAR practice. [ABSTRACT FROM AUTHOR]

Objective: This study aims to assess the consistency of various CT-FFR software, to determine the reliability of current CT-FFR software, and to measure relevant influence factors. The goal is to build a solid foundation of enhanced workflow and technical principles that will ultimately improve the accuracy of measurements of coronary blood flow reserve fractions. This improvement is critical for assessing the level of ischemia in patients with coronary heart disease. Methods: 103 participants were chosen for a prospective research using coronary computed tomography angiography (CCTA) assessment. Heart rate, heart rate variability, subjective picture quality, objective image quality, vascular shifting length, and other factors were assessed. CT-FFR software including K software and S software are used for CT-FFR calculations. The consistency of the two software is assessed using paired-sample t-tests and Bland-Altman plots. The error classification effect is used to construct the receiver operating characteristic curve. Results: The CT-FFR measurements differed significantly between the K and S software, with a statistical significance of P < 0.05. In the Bland-Altman plot, 6% of the points (14 out of 216) fell outside the 95% consistency level. Single-factor analysis revealed that heart rate variability, vascular dislocation offset distance, subjective image quality, and lumen diameter significantly influenced the discrepancies in CT-FFR measurements between two software programs (P < 0.05). The ROC curve shows the highest AUC for the vessel shifting length, with an optimal cut-off of 0.85 mm. Conclusion: CT-FFR measurements vary among software from different manufacturers, leading to potential misclassification of qualitative diagnostics. Vessel shifting length, subjective image quality score, HRv, and lumen diameter impacted the measurement stability of various software. [ABSTRACT FROM AUTHOR]

Background/Objectives: Truncus arteriosus communis (TAC) is a rare congenital heart defect characterized by a single arterial trunk that supplies systemic, pulmonary, and coronary circulations. This defect, constituting approximately 1–4% of congenital heart diseases, poses significant challenges in prenatal diagnosis, management, and postnatal outcomes. Methods: A retrospective analysis was conducted at the local tertiary referral center on cases of TAC diagnosed prenatally between 2019 and 2024. Additionally, a systematic literature review was performed to evaluate the accuracy of prenatal diagnostics and the presence of associated anomalies in fetuses with TAC and compare already published data with the local results. The review included studies that especially described the use of fetal echocardiography, the course and outcome of affected pregnancies, and subsequent management strategies. Results: The analysis of local prenatal diagnoses revealed 14 cases. Of the 11 neonates who survived to birth, the TAC diagnosis was confirmed in 7 instances. With all seven neonates undergoing surgery, the intention-to-treat survival rate was 86%, and the overall survival rate was 55%. By reviewing published case series, a total of 823 TAC cases were included in the analysis, of which 576 were diagnosed prenatally and 247 postnatally. The presence of associated cardiac and extracardiac manifestations as well as genetic anomalies was common, with a 22q11 microdeletion identified in 27% of tested cases. Conclusions: Advances in prenatal imaging and early diagnosis have enhanced the management of TAC, allowing for the detailed planning of delivery and immediate postnatal care in specialized centers. The frequent association with genetic syndromes underscores the importance of genetic counseling in managing TAC. An early surgical intervention remains crucial for improving long-term outcomes, although the condition is still associated with significant risks. Long-term follow-up studies are essential to monitor potential complications and guide future management strategies. Overall, a coordinated multidisciplinary approach from prenatal diagnosis to postnatal care is essential for improving outcomes for individuals with TAC. [ABSTRACT FROM AUTHOR]

Introduction: AMI is the leading cause of death for both men and women all over the world. Acute myocardial infarction is myocardial necrosis resulting from acute obstruction of coronary artery. Calcium ions are involved in myocardial contraction, and during acute myocardial infarction. The disruption of blood flow to the heart muscle can lead to an imbalance in calcium levels. This disruption can cause calcium overload with myocardial cells, leading to cellular injury and dysfunction. Magnesium has properties of myocardial cryoprotection, the pathophysiological explanations of which in açute myocardial infarction include prevention of arrythmia, antiplatelet effect, prevention of reperfusion injury and coronary vasodilation. Increased serum uric acid (SUA) levels have been associated with various pathologic processes such as increased oxidative stress, inflammation and endothelial dysfunction. Troponin I is highly specific to cardiac muscle so its presence in the blood stream is a reliable indicator of heart muscle damage. The Elevation in troponin I levels is used as a diagnostic marker for AMI. Material and Methods:A comparative and cross-sectional study was conducted in the Department of Biochemistry in Rangaraya Medical College, Kakinada over a period of 4 months. Sampling Type: Casual sampling of newly diagnosed AMI patients attending the OPD. Controls are recruited from healthy individuals attending the OPD for health checkup. Sample Size: 50 newly diagnosed AMI patients constitute group 1, 50 age and sex matched healthy individuals in group 2. Results: The Group 1 has a higher mean age (54.36±6.70 years) compared to Group 2 (51.3±7.98 years), suggesting that on average, participants in Group 1 are older than those in Group 2. The higher mean calcium level in Group 2 (9.276±1.24 mg/dl) compared to Group 1 (8.548±1.73 mg/dl) suggests that, on average, participants in Group 2 have higher calcium levels than those in Group 1. Comparing the two groups:- Group 2 has a higher mean magnesium level (2.062 mg/dl) compared to Group 1 (1.892 mg/dl). The standard deviation for magnesium levels is smaller in Group 2 (0.41) compared to Group 1 (0.71), indicating that magnesium levels in Group 2 are less variable around the mean compared to Group 1. Group 1 has a mean uric acid level of 7.824 mg/dl with a standard deviation of 5.95 mg/dl. Group 2 has a mean uric acid level of 6.188 mg/dl with a standard deviation of 2.10 mg/dl. Group 1 has a mean Troponin I level of 4463 pg/ml with a standard deviation of 5226.92 pg/ml. Group 2 has a mean Troponin I level of 10.048 pg/ml with a standard deviation of 14.03 pg/ml. Conclusion: Acute MI is the 3rd largest cause of death in the population. If untreated it causes necrosis of the myocardium and finally death of the patient. Magnesium has cytoprotective properties, anti-platelet effect, prevents arrhythmias and reperfusion injury and coronary vasodilation. So it should be estimated. Calcium ions are involved in myocardial contraction. It plays a role in coagulation cascade. It forms blood clots that obstruct blood flow so medications targeting calcium channel to reduce myocardial oxygen load and improve coronary circulation. Uric acid may be a marker for increased cardiovascular risk. Troponin I is highly specific and diagnostic of acute MI. [ABSTRACT FROM AUTHOR]

Purpose: To determine the impact of time profile of tirofiban hydrochloride administration on short-term outcomes in patients with acute myocardial infarction (AMI) undergoing emergency percutaneous coronary intervention (PCI). Methods: A total of 112 patients with AMI who received PCI treatment in The First People's Hospital of Tianshui, Tianshui, China were randomly and equally assigned to study and control groups. The study group received intravenous tirofiban hydrochloride bolus (10 µg/kg) 1 - 2 h before PCI, followed by sustained infusion at 0.15 µg/kg/min for 36 h after the procedure. Control group received the same regimen immediately after PCI. Myocardial injury markers, cardiac functional parameters, ST-segment resolution, myocardial perfusion changes, bleeding complications, and adverse cardiovascular events over 6 months were evaluated. Results: When compared with control group, the study group exhibited significantly lower cardiac troponin T (cTnT) levels and lower serum creatine kinase-MB (CK-MB) levels at 7 days post-PCI (p < 0.05). Furthermore, the study group showed significantly reduced left ventricular end-diastolic diameter (LVEDD), and left ventricular end-systolic diameter (LVESD), along with higher left ventricular ejection fraction (LVEF) after 7 days (p < 0.05). The study group also exhibited superior ST-segment resolution and significant improvement in myocardial perfusion 90 min post-treatment and significantly lower incidence of reperfusion arrhythmias (p < 0.05). Both groups had similar rates of minor bleeding events and no incidence of severe complications or fatalities. Conclusions: Administering tirofiban preoperatively enhances coronary blood flow, improves myocardial perfusion, and reduces the risk of distal embolic events without increasing severe bleeding complications. Larger-scale, multicenter studies with longer follow-up periods are required to confirm these findings and evaluate the safety and efficacy of different administration time for tirofiban infusion in patients with AMI undergoing PCI. [ABSTRACT FROM AUTHOR]

The article explores the impact of bifurcation angles on computed tomography (CT)-derived fractional flow reserve (FFRCT) decline in vessels with no apparent coronary artery disease (CAD). Topics include the correlation between bifurcation angles and FFRCT changes, the identification of optimal cut-off values for bifurcation angles in the left anterior descending (LAD) and left circumflex (LCX) arteries and the significance of vessel length as a predictor of distal FFRCT values.

Patients with unstable angina present clinical characteristics of atherosclerotic plaque vulnerability, contrary to chronic coronary syndrome patients. The process of athersclerotic plaque destabilization is also regulated by microRNA particles. In this study, the investigation on expression levels of microRNAs inhibiting the expression of proteins that protect from atherosclerotic plaque progression (miR-92a inhibiting KLF2, miR-10b inhibiting KLF4, miR-126 inhibiting MerTK, miR-98 inhibiting IL-10, miR-29b inhibiting TGFβ1) was undertaken. A number of 62 individuals were enrolled—unstable angina (UA, n = 14), chronic coronary syndrome (CCS, n = 38), and healthy volunteers (HV, n = 10). Plasma samples were taken, and microRNAs expression levels were assessed by qRT-PCR. As a result, the UA patients presented significantly increased miR-10b levels compared to CCS patients (0.097 vs. 0.058, p = 0.033). Moreover, in additional analysis when UA patients were grouped together with stable patients with significant plaque in left main or proximal left anterior descending ("UA and LM/proxLAD" group, n = 29 patients) and compared to CCS patients with atherosclerotic lesions in other regions of coronary circulation ("CCS other" group, n = 25 patients) the expression levels of both miR-10b (0.104 vs. 0.046; p = 0.0032) and miR-92a (92.64 vs. 54.74; p = 0.0129) were significantly elevated. In conclusion, the study revealed significantly increased expression levels of miR-10b and miR-92a, a regulator of endothelial protective KLF factors (KLF4 and KLF2, respectively) in patients with more vulnerable plaque phenotypes. [ABSTRACT FROM AUTHOR]

Coronary microvascular dysfunction (CMD) involves functional or structural abnormalities of the coronary microvasculature resulting in dysregulation of coronary blood flow (CBF) in response to myocardial oxygen demand. This perfusion mismatch causes myocardial ischemia, which manifests in patients as microvascular angina (MVA). CMD can be diagnosed non-invasively via multiple imaging techniques or invasively using coronary function testing (CFT), which assists in determining the specific mechanisms involving endothelium-independent and dependent epicardial and microcirculation domains. Unlike traditional coronary artery disease (CAD), CMD can often occur in patients without obstructive atherosclerotic epicardial disease, which can make the diagnosis of CMD difficult. Moreover, MVA due to CMD is more prevalent in women and carries increased risk of future cardiovascular events. Successful treatment of symptomatic CMD is often patient-specific risk factor and endotype targeted. This article aims to review newly identified mechanisms and novel treatment strategies for managing CMD, and outline sex-specific differences in the presentation and pathophysiology of the disease. [ABSTRACT FROM AUTHOR]

Background: The Uric acid/Albumin ratio (UAR) has recently been identified as a prominent marker in cardiovascular diseases. In this study, we aimed to reveal the effect of UAR on coronary collateral circulation (CCC) in patients with stable coronary artery disease (CAD) patients by comparing it with conventional inflammation-based markers. Methods: In this study, 415 consecutive patients who underwent coronary angiography for stable angina pectoris and were found to have chronic total occlusion in at least one coronary artery were retrospectively included. The study population was divided into two groups as good CCC (Rentrop 2–3) and poor CCC (Rentrop 0–1) according to the Rentrop classification, and the groups were compared in terms of UAR and other traditional inflammation-based markers. Results: In the poor CCC group, C-reactive protein/albumin ratio (CAR), monocyte/high-density lipoprotein cholesterol ratio (MHR), neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), systemic immune-inflammation index (SII) and UAR were found to be significantly high (p <.05, for all). UAR negatively correlated with rentrop classification (r = −0.383, p <.001). In multivariate regression analysis, MHR, NLR, SII and UAR were determined as independent predictors for poor CCC (p <.05, for all). The ability of UAR to predict poor CCC was superior to uric acid and albumin alone (p <.0001, for both). In addition, UAR was found to be superior to other inflammation-based markers in predicting poor CCC (p <.005, for all). Conclusion: UAR was identified as a strong and independent predictor of CCC. In this context, UAR may be a useful biomarker in the risk prediction of patients with stable CAD. [ABSTRACT FROM AUTHOR]

This article provides information on various emergencies that can occur during the postpartum period. It discusses common causes of maternal death, such as infection, hemorrhage, cardiomyopathy, and mental health-related conditions. The article also addresses the increased risk of cardiovascular diseases during this time and provides information on the diagnosis and management of conditions like peripartum cardiomyopathy and pregnancy-associated myocardial infarction. Additionally, it covers specific medical conditions related to pregnancy and the postpartum period, including venous thromboembolism, stroke, and hypertensive disorders. The document emphasizes the importance of prompt recognition and management of these emergencies to prevent adverse outcomes and provides resources for further information and support. [Extracted from the article]

Successful reperfusion of myocardial tissue is the goal of primary percutaneous coronary intervention (pPCI) in patients with ST-segment elevation myocardial infarction (STEMI). We aimed to investigate the association between the De Ritis ratio (AST/ALT) and myocardial reperfusion in patients with STEMI who underwent pPCI. We retrospectively investigated 1236 consecutive patients who were hospitalized for STEMI and underwent pPCI. ST-segment resolution (STR) was defined as the return of the deviated ST-segment to baseline; poor myocardial reperfusion was defined as <70% STR. Patients were divided into 2 groups according to the median De Ritis ratio (.921); 618 patients (50%) were assigned to the De Ritis low group while 618 patients (50%) were assigned to the De Ritis high group. Stent size, neutrophil-to lymphocyte ratio (NLR), and the De Ritis ratio found to be associated with poor myocardial reperfusion (Odds ratio (OR) 1.45, 95% CI 1.07–1.98, P =.01, OR 1.22, 95% CI 1.01–1.48, P =.03 and OR 10.9, 95% CI 7.9–15, P <.001, respectively). A high De Ritis ratio was associated with poor myocardial reperfusion in STEMI patients who underwent pPCI. As an easily obtainable test in clinical practice, the De Ritis ratio may help identify patients at major risk for impaired myocardial perfusion. [ABSTRACT FROM AUTHOR]

Coronary artery ectasia (CAE) is a rare vascular phenotype characterized by abnormal dilation of blood vessels and disruption of coronary artery blood flow, which may promote thrombosis and an inflammatory response. We performed a cross-sectional study to investigate the association of white blood cells to mean platelet volume ratio (WMR) with CAE. Consecutive eligible patients (n = 492) were divided into two groups: including 238 patients with CAE and 254 patients in the normal coronary artery (NCA) group. WMR, the systemic immune-inflammation index (SII), and neutrophil-to-lymphocyte ratio (NLR) were found to be significantly associated with CAE in both univariate and multivariate logistic regression analyses. In multivariate analysis, the presence of WMR was associated with CAE (the odds ratios (OR) = 1.002, 95% CI: 1.001–1.003, P <.001). In the ROC analysis, the statistics (Z-values) of WMR vs SII and WMR vs NLR were 2.427 and 2.670 and were statistically significant (P =.015 and P =.008), indicating that WMR was superior to SII and NLR in distinguishing WMR. The optimal cut-off value was calculated from the point of maximal sensitivity and specificity by using Youden's index, which was determined to be 635.50. WMR has the potential to be a cost-effective tool to monitor CAE. [ABSTRACT FROM AUTHOR]

Dyslipidemia is an important risk factor for cardiovascular morbidity and mortality. Although low-density lipoprotein (LDL) is primarily responsible, the importance of triglyceride (TG) and high-density lipoprotein (HDL) has also been recognized. The present study investigated the effect of the atherogenic index of plasma (AIP), in which atherogenic and protective lipoproteins were evaluated together, on the initial flow in patients with ST elevation myocardial infarction. AIP was calculated as log(TG/HDL-cholesterol). Patients included in the study (n = 1535) were divided into Thrombolysis in Myocardial Infarction (TIMI) flow grade 0 and >0. AIP was found to be significantly different between 2 groups (.55 ±.23 vs.67 ±.21; P <.001). AIP was an independent predictor for pre-intervention TIMI flow (Odds Ratio: 2.778). A moderate correlation was found between TIMI frame count measurements, calculated in patients with TIMI 2–3, and AIP (Pearson correlation coefficient:.63, P <.001). In the receiver operating characteristic analysis, AIP showed the highest area under curve (AUC) compared with other lipid parameters for predicting vascular patency. The AUC of AIP was.634, the cut-off value was.59, and the sensitivity and specificity were 67.6% and 68.4%, respectively (P <.001). In conclusion, AIP was found to be an important marker affecting pre-percutaneous coronary intervention TIMI flow. [ABSTRACT FROM AUTHOR]

Background: This study evaluated the correlation between corrected Thrombolysis in Myocardial Infarction (TIMI) frame count (CTFC) and major adverse cardiovascular events (MACE) within the first month following primary percutaneous coronary intervention (PPCI). Methods: Eighty patients who underwent PPCI at Ayatollah Rouhani teaching Hospital in Babol Eighty patients who underwent PPCI at Ayatollah Rouhani teaching Hospital in Babol were included. CTFC, a measure of coronary blood flow, was assessed. Demographic and clinical data, were collected. ST segment resolution, a criterion for successful PPCI, was evaluated. MACE, including cardiac deaths, need for repeat revascularization of culprit vessels, and recurrent non-fatal myocardial infarction, and CVA (cerebrovascular accident) were recorded. Statistical analyses were performed to assess the association between CTFC and demographic/clinical variables, as well as ST resolution and MACE. Results: The majority of patients were (78.8%) men and (81.2%) nonsmokers. No significant association was found between CTFC and demographic/clinical variables. The left anterior descending (LAD) artery was the most commonly involved vessel (48.8%). ST segment resolution of more than 50% was observed in 51.2% of patients. During the one-month follow-up, 13.7% of patients experienced MACE, including 7 cardiac deaths. However, there was no significant association between CTFC and MACE. (P=0.30) Conclusion: This study concludes that CTFC is not a reliable predictor of MACE within the first month after PPCI. Furthermore, ST segment resolution of more than 50% was associated with a lower prevalence of cardiovascular events. [ABSTRACT FROM AUTHOR]

Objective: To study the effect of Shexiang Tongxin Dropping Pill (STDP) on angiogenesis in diabetic cardiomyopathy mice with coronary microcirculation dysfunction (CMD). Methods: According to a random number table, 6 of 36 SPF male C57BL/6 mice were randomly selected as the control group, and the remaining 30 mice were injected with streptozotocin intraperitoneally to replicate the type 1 diabetes model. Mice successfully copied the diabetes model were randomly divided into the model group, STDP low-dose group [15 mg/(kg·d)], medium-dose group [30 mg/(kg·d)], high-dose group [60 mg/(kg·d)], and nicorandil group [15 mg/(kg·d)], 6 in each group. The drug was given by continuous gavage for 12 weeks. The cardiac function of mice in each group was detected at the end of the experiment, and coronary flow reserve (CFR) was detected by chest Doppler technique. Pathological changes of myocardium were observed by hematoxylin-eosin staining, collagen fiber deposition was detected by masson staining, the number of myocardial capillaries was detected by platelet endothelial cell adhesion molecule-1 staining, and the degree of myocardial hypertrophy was detected by wheat germ agglutinin staining. The expression of the vascular endothlial growth factor (VEGF)/endothelial nitric oxide synthase (eNOS) signaling pathway-related proteins in myocardial tissue was detected by Western blot. Results: Compared with the model group, medium- and high-dose STDP significantly increased the left ventricular ejection fraction and left ventricular fraction shortening (P<0.01), obviously repaired the disordered cardiac muscle structure, reduced myocardial fibrosis, reduced myocardial cell area, increased capillary density, and increased CFR level (all P<0.01). Western blot showed that high-dose STDP could significantly increase the expression of VEGF and promote the phosphorylation of vascular endothelial growth factor receptor 2, phosphoinositide 3-kinase, protein kinase B, and eNOS (P<0.05 or P<0.01). Conclusion: STDP has a definite therapeutic effect on diabetic CMD, and its mechanism may be related to promoting angiogenesis through the VEGF/eNOS signaling pathway. [ABSTRACT FROM AUTHOR]

Aims Epicardial fat is a metabolically active adipose tissue depot situated between the myocardium and visceral pericardium that covers ∼80% of the heart surface. While epicardial fat has been associated with the development of atherosclerotic coronary artery disease, less is known about the relationship between epicardial fat and coronary vascular function. Moreover, the relations between excess epicardial fat and cardiac morphology and function remain incompletely understood. Methods and results To address these knowledge gaps, we retrospectively analysed data from 294 individuals from our database of women with suspected ischaemia with no obstructive coronary disease (INOCA) who underwent both invasive coronary function testing and cardiac magnetic resonance imaging. Epicardial fat area, biventricular morphology, and function, as well as left atrial function, were assessed from cine images, per established protocols. The major novel findings were two-fold: first, epicardial fat area was not associated with coronary vascular dysfunction. Secondly, epicardial fat was associated with increased left ventricular concentricity (β = 0.15, P = 0.01), increased septal thickness (β = 0.17, P = 0.002), and reduced left atrial conduit fraction (β = −0.15, P = 0.02), even after accounting for age, BMI, and history of hypertension. Conclusion Taken together, these data do not support a measurable relationship between epicardial fat and coronary vascular dysfunction but do suggest that epicardial fat may be related to concentric remodelling and diastolic dysfunction in women with suspected INOCA. Prospective studies are needed to elucidate the long-term impact of epicardial fat in this patient population. [ABSTRACT FROM AUTHOR]

Aims This study aimed to assess the impact of adenosine on quantitative myocardial blood flow (MBF) in a rapid stress–rest protocol compared with a rest–stress protocol using 13N-ammonia positron emission tomography (PET) myocardial perfusion imaging (MPI) and to gain insights into the time dependency of such effects. Methods and results Quantitative MBF at rest (rMBF) and during adenosine-induced stress (sMBF) and myocardial flow reserve (MFR) were obtained from 331 retrospectively identified patients who underwent 13N-ammonia PET MPI for suspected chronic coronary syndrome and who all exhibited no perfusion defects. Of these, 146 (44.1%) underwent a rapid stress–rest protocol with a time interval (Δ t stress–rest) of 20 ± 4 min between adenosine infusion offset and rest imaging, as per clinical routine. The remaining 185 (55.9%) patients underwent a rest–stress protocol and served as the reference. Groups did not differ regarding demographics, risk factors, medication, left ventricular function, and calcium scores. rMBF was significantly higher in the stress–rest vs. the rest–stress group [0.80 (interquartile range 0.66–1.00) vs. 0.70 (0.58–0.83) mL·min−1·g−1, P < 0.001], and, as sMBF was identical between groups [2.52 (2.20–2.96) vs. 2.50 (1.96–3.11), P = 0.347], MFR was significantly lower in the stress–rest group [3.07 (2.43–3.88) vs. 3.50 (2.63–4.10), P = 0.007]. There was a weak correlation between Δ t stress–rest and rMBF (r = −0.259, P = 0.002) and between Δ t stress–rest and MFR (r = 0.163, P = 0.049), and the proportion of patients with abnormally high rMBF was significantly decreasing with increasing Δ t stress–rest. Conclusion Intravenously applied adenosine induces a long-lasting hyperaemic effect on the myocardium. Consequently, rapid stress–rest protocols could lead to an overestimation of rMBF and an underestimation of MFR. [ABSTRACT FROM AUTHOR]

Tribulus terrestris is an annual plant belonging to family Zygophyllaceae, which is extensively dispersed globally. T. terrestris has been used to treat a variety of illnesses, including as heart and circulation problems, sexual dysfunction, and to try to improve body building and athletic performance. This Pharmacological study aims to Preliminary phytochemical study and various pharmacological studies like antioxidant, antimicrobial and anti-inflammatory study of Tribulus terrestris. Crude Ext. of the plant undergoes preliminary phytochemical study by various chemical methods; antioxidant assay was done by DPPH radical scavenging method, superoxide anion radical scavenging activity and Nitric oxide radical scavenging technique, antimicrobial study was done by zone inhibition method and anti-inflammatory study was done by protein denaturation and protein inhibitory study. From the above scientific study, various Phytochemicals like Glycoside, tannins, carbohydrate revealed from Tribulus terrestris, the potential antimicrobial, free radical scavenging activity and anti-inflammatory activity of Tribulus terrestris revealed. [ABSTRACT FROM AUTHOR]

The document titled "2024 ESC Guidelines for the management of peripheral arterial and aortic diseases" is a comprehensive guide that provides recommendations for the evaluation, screening, and treatment of peripheral arterial and aortic diseases. It covers topics such as epidemiology, risk factors, and diagnostic methods for these conditions. The guidelines outline optimal medical treatments, including lifestyle changes and pharmacological therapies, and discuss specific conditions such as peripheral arterial disease and carotid artery disease. The document also addresses aortic diseases, including atheromatous disease and aortic aneurysms, and offers guidance on treatment options such as surgery and endovascular repair. It provides information on genetic and congenital diseases of the aorta, as well as polyvascular peripheral arterial disease. The document concludes with key messages, gaps in evidence, and recommendations for practice, emphasizing the importance of individualized care, multidisciplinary management, and early diagnosis. [Extracted from the article]

Understanding the evolving nature of coronary hemodynamics is crucial for early disease detection and monitoring progression. We require digital twins that mimic a patient's circulatory system by integrating continuous physiological data and computing hemodynamic patterns over months. Current models match clinical flow measurements but are limited to single heartbeats. To this end, we introduced the longitudinal hemodynamic mapping framework (LHMF), designed to tackle critical challenges: (1) computational intractability of explicit methods; (2) boundary conditions reflecting varying activity states; and (3) accessible computing resources for clinical translation. We show negligible error (0.0002–0.004%) between LHMF and explicit data of 750 heartbeats. We deployed LHMF across traditional and cloud-based platforms, demonstrating high-throughput simulations on heterogeneous systems. Additionally, we established LHMFC, where hemodynamically similar heartbeats are clustered to avoid redundant simulations, accurately reconstructing longitudinal hemodynamic maps (LHMs). This study captured 3D hemodynamics over 4.5 million heartbeats, paving the way for cardiovascular digital twins. [ABSTRACT FROM AUTHOR]

Introduction: In ST-elevation myocardial infarction (STEMI), inflammation is pivotal, with early senescent CD4+CD28null cells implicated in its pathogenesis. However, the functional phenotype of these cells within the coronary circulation remains unclear. Methods: We examined CD4+ cell subpopulations in blood samples from the coronary sinus and vena cava of 24 STEMI patients and the cephalic vein of seven healthy controls. Results: Our findings revealed reduced CD4+ cell counts in STEMI patients compared to controls (1,998, 1,275–3,268 vs. 4,278, 3,595–4,449), alongside an increased proportion of CD4+ cells lacking CD28 expression (20.1 vs. 6.1%). These CD4+CD28null cells in STEMI predominantly exhibited a Th1 phenotype (47.8% vs. 6.6%). Intriguingly, no significant differences were detected in CD4+CD28null cells between coronary sinus and vena cava, and cytokine levels in these compartments remained similar. Conclusion: CD4+CD28null cells are increased in STEMI, mainly polarized toward a Th1 phenotype, and distributed equally between the different vascular beds. [ABSTRACT FROM AUTHOR]

Objective: To report our experience of fetal aortic valvuloplasty (FAV) for critical aortic stenosis (AS), with a focus on the postnatal evolution of the patients. Methods: This was a retrospective study including all fetuses with critical AS which underwent FAV in a single center between January 2011 and June 2022. FAV was performed under ultrasound guidance. Technical success was based upon balloon inflation across the aortic valve and improvement of the antegrade aortic flow across the aortic valve. At birth, a biventricular circulation (BVC) strategy was decided assuming the left ventricular (LV) systolic and diastolic function would ensure the systemic circulation. Results: Sixty‐three FAV procedures were performed in 58 fetuses, at a median (range) gestational age of 26.2 (20.3–32.2) weeks. The procedure was technically successful in 50/58 (86.2%) fetuses. There were 11/58 (19.0%) cases of in‐utero demise and 9/58 (15.5%) terminations of pregnancy. No patient was liveborn after an unsuccessful procedure. Thirty‐eight (65.5%) infants were liveborn, at a median (range) gestational age of 38.1 (29.0–40.6) weeks, of whom 21 (55.3%) required prostaglandin treatment. Twenty‐eight of the 38 (73.7%) liveborn children (48.3% of the study population) entered the BVC pathway at birth. Among them, 20 (71.4%) required an aortic valvuloplasty procedure at birth (11 (55.0%) percutaneous balloon, nine (45.0%) surgical) and eight (28.6%) did not require any treatment at birth, but, of these, five (62.5%) underwent surgical valvuloplasty between day 26 and day 1200 of age. Eleven (39.3%) of the infants with BVC at birth required a second intervention and four (14.3%) of them required a third intervention. Two (7.1%) infants who entered the BVC pathway at birth underwent conversion to univentricular circulation (UVC). None of the surviving children with BVC developed pulmonary hypertension. The overall survival rate in those with BVC at birth was 22/28 (78.6%) at a median (range) follow‐up of 23.3 (2.0–112.6) months. Ten of the 58 (17.2%) patients had UVC at birth. Among these, six (60.0%) received compassionate care from birth and four (40.0%) underwent surgery. Three of the 10 patients who had UVC at birth were still alive at the latest follow‐up assessment, at a median (range) gestational age of 24.3 (8.3–48.7) months. Conclusions: FAV for critical AS led to increase of antegrade aortic flow in 86.2% of fetuses, with BVC being achieved in 48.3% (73.7% of the liveborn cases). Among patients with BVC at birth, the rate of reintervention was high, but 78.6% of these children were alive at the latest evaluation. © 2024 The Authors. Ultrasound in Obstetrics & Gynecology published by John Wiley & Sons Ltd on behalf of International Society of Ultrasound in Obstetrics and Gynecology. [ABSTRACT FROM AUTHOR]

Understanding of the mechanisms contributing to the increased maternal susceptibility for major adverse cardiovascular events in the postpartum period remains poor. Accordingly, this study tested the hypothesis that the balance between coronary blood flow and myocardial metabolism is compromised during the puerperium period (35–45 days post-delivery) in swine. Systemic and coronary hemodynamic responses were assessed in anesthetized, open-chest control (nonpregnant) and puerperium/postpartum swine at baseline and in response to intravenous infusion of dobutamine (1–30 μg/kg/min). Blood pressure and heart rate were lower in postpartum swine at baseline and in response to dobutamine (P < 0.05). Coronary blood flow and myocardial oxygen delivery were significantly diminished at baseline in postpartum swine (P < 0.001), which corresponded with ∼35% reduction in myocardial oxygen consumption (MVO 2) (P < 0.001). Postpartum swine displayed enhanced retrograde coronary flow, larger cardiomyocyte area (P < 0.01) and marked capillary rarefaction (P < 0.01). The relationship between coronary blood flow and heart rate (P < 0.05) or MVO 2 (P < 0.001) was significantly diminished in postpartum swine as dobutamine increased MVO 2 up to ∼135% in both groups. This reduction in myocardial perfusion was associated with decreases in myocardial lactate uptake (P < 0.001), increases in coronary venous PCO 2 (P < 0.01) and decreased coronary venous pH (P < 0.01). These findings suggest an impaired balance between coronary blood flow and myocardial metabolism could contribute to the increased incidence of maternal myocardial ischemia and premature death in the postpartum period. [Display omitted] • Alterations in the structure and function of the coronary circulation characterize postpartum changes to the maternal heart. • Resting coronary flow is diminished in the maternal heart in the postpartum condition. • Indices of under-perfusion are present in maternal swine hearts in the postpartum condition. • Mechanisms contributing to dysregulated coronary control in the postpartum maternal heart require further investigation. [ABSTRACT FROM AUTHOR]

• Ischemia with non-obstructive coronary arteries (INOCA) encompasses a breadth of structural and functional abnormalities of the coronary circulation causing ischemia (and angina) despite the lack of obstructive epicardial atheroma. • Several diagnostic techniques are available, including invasive and non-invasive ones. At present, invasive functional assessment, using both pressure wire and vasoreactivity tests and also termed #FullPhysiology, is the only one allowing comprehensive evaluation of the pathophysiological mechanisms of INOCA. • Leveraging #FullPhysiology, a stratified medical therapy can be implemented, which can mitigate symptoms and positively affect quality of life in patients with INOCA. Ischemia with non-obstructive coronary arteries (INOCA) is an increasingly recognized entity. It encompasses different pathophysiological subtypes (i.e., endotypes), including coronary microvascular dysfunction (CMD), vasospastic angina (VSA) and mixed entities resulting from the variable combination of both. Diagnosing INOCA and precisely characterizing the endotype allows for accurate medical treatment and has proven prognostic implications. A breadth of diagnostic technique is available, ranging from non-invasive approaches to invasive coronary angiography adjuvated by functional assessment and provocative tests. This review summarizes the strength and limitations of these methodologies and provides the rationale for the routine referral for invasive angiography and functional assessment in this subset of patients. [ABSTRACT FROM AUTHOR]

The article discusses the background and clinical implications of coronary computed (CT) tomography angiography (CCTA) and CT-based fractional flow reserve (CT-FFR). Topics covered include the practice of CCTA and CT-FFR, samples of CCTA and CT-FFR protocols and case studies involving CCTA and CT-FFR. It also cited the clinical relevance of CCTA and CT-FFR and the clinical effect of the PLATFORM trial on CT-FFR.

BACKGROUND: Nocturnal hemodialysis (nHD) restores the attenuated brachial artery vasodilator responsiveness of patients receiving conventional intermittent hemodialysis (iHD). Its impact on coronary vasodilatation is unknown. METHODS: We evaluated 25 patients on hemodialysis who fulfilled transplant criteria: 15 on iHD (4-hour sessions, 3 d/wk) and 10 on nHD (≈40 h/wk over 8-10-hour sessions) plus 6 control participants. Following diagnostic angiography, left anterior descending (LAD) coronary flow reserve and mean luminal diameter were quantified at baseline and during sequential intracoronary administration of adenosine (infusion and bolus), nitroglycerin (bolus), acetylcholine (infusion), acetylcholine coinfused with vitamin C, and, finally, sublingual nitroglycerin. RESULTS: Coronary flow reserve in those receiving nHD was augmented relative to iHD (3.28±0.26 versus 2.17±0.12 [mean±SEM]; P<0.03) but attenuated, relative to controls (4.80±0.63; P=0.011). Luminal dilatations induced by intracoronary adenosine and nitroglycerin were similar in nHD and controls but blunted in the iHD cohort (P<0.05 versus both). ACh elicited vasodilatation in controls but constriction in both dialysis groups (both P<0.05, versus control); vitamin C coinfusion had no effect. Sublingual nitroglycerin increased mid-left anterior descending diameter and reduced mean arterial pressure in controls (+15.2±2.68%; -16.00±1.60%) and in nHD recipients (+14.78±5.46%; -15.82±1.32%); iHD responses were markedly attenuated (+1.9±0.86%; -5.89±1.41%; P<0.05, all comparisons). CONCLUSIONS: Coronary and systemic vasodilator responsiveness to both adenosine and nitroglycerin is augmented in patients receiving nHD relative to those receiving iHD, whereas vasoconstrictor responsiveness to acetylcholine does not differ. By improving coronary conduit and microvascular function, nHD may reduce the cardiovascular risk of patients on dialysis. [ABSTRACT FROM AUTHOR]

This article discusses the issue of flow-related thrombosis in prosthetic heart valves (PHVs) and presents the "StreamlineValve Project," which aims to address this problem. Valvular heart disease affects millions of people worldwide, and while PHVs have improved survival rates, they still encounter flow-related thrombosis. The project plans to use passive flow control strategies inspired by nature to modulate the flow field and reduce factors contributing to coagulation on PHVs. The goal is to create a flow-controlled PHV that acts as a self-cleaning valve, improving durability and patient safety. [Extracted from the article]

Cardiovascular disease remains the leading cause of death worldwide, with acute myocardial infarction and anticancer drug-induced cardiotoxicity being the significant factors. The most effective treatment for acute myocardial infarction is rapid restoration of coronary blood flow by thrombolytic therapy or percutaneous coronary intervention. However, myocardial ischemia–reperfusion injury (MI/RI) after reperfusion therapy is common in acute myocardial infarction, thus affecting the prognosis of patients with acute myocardial infarction. There is no effective treatment for MI/RI. Anthracyclines such as Doxorubicin (DOX) have limited clinical use due to their cardiotoxicity, and the mechanism of DOX-induced cardiac injury is complex and not yet fully understood. N6-methyladenosine (m6A) plays a crucial role in many biological processes. Emerging evidence suggests that m6A methylation plays a critical regulatory role in MI/RI and DOX-induced cardiotoxicity (DIC), suggesting that m6A may serve as a novel biomarker and therapeutic target for MI/RI and DIC. M6A methylation may mediate the pathophysiological processes of MI/RI and DIC by regulating cellular autophagy, apoptosis, oxidative stress, and inflammatory response. In this paper, we first focus on the relationship between m6A methylation and MI/RI, then further elucidate that m6A methylation may mediate the pathophysiological process of MI/RI through the regulation of cellular autophagy, apoptosis, oxidative stress, and inflammatory response. Finally, briefly outline the roles played by m6A in DIC, which will provide a new methodology and direction for the research and treatment of MI/RI and DIC. [ABSTRACT FROM AUTHOR]

Tissue perfusion can be affected by physiology or disease. With the advent of total-body PET, quantitative measurement of perfusion across the entire body is possible. [11C]-butanol is a perfusion tracer with a superior extraction fraction compared with [15O]-water and [13N]-ammonia. To develop the methodology for total-body perfusion imaging, a pilot study using [11C]-butanol on the uEXPLORER total-body PET/CT scanner was conducted. Methods: Eight participants (6 healthy volunteers and 2 patients with peripheral vascular disease [PVD]) were injected with a bolus of [11C]-butanol and underwent 30-min dynamic acquisitions. Three healthy volunteers underwent repeat studies at rest (baseline) to assess test-retest reproducibility; 1 volunteer underwent paired rest and cold pressor test (CPT) studies. Changes in perfusion were measured in the paired rest-CPT study. For PVD patients, local changes in perfusion were investigated and correlated with patient medical history. Regional and parametric kinetic analysis methods were developed using a 1-tissue compartment model and leading-edge delay correction. Results: Estimated baseline perfusion values ranged from 0.02 to 1.95 mL·min-1·cm-3 across organs. Test-retest analysis showed that repeat baseline perfusion measurements were highly correlated (slope, 0.99; Pearson r = 0.96, P < 0.001). For the CPT subject, the largest regional increases were in skeletal muscle (psoas, 142%) and the myocardium (64%). One of the PVD patients showed increased collateral vessel growth in the calf because of a peripheral stenosis. Comorbidities including myocardial infarction, hypothyroidism, and renal failure were correlated with variations in organ-specific perfusion. Conclusion: This pilot study demonstrates the ability to obtain reproducible measurements of total-body perfusion using [11C]-butanol. The methods are sensitive to local perturbations in flow because of physiologic stressors and disease.

To investigate the relationships between inflammatory parameters, including neutrophil‐to‐lymphocyte ratio (NLR), platelet‐to‐lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR) and systemic immune-inflammation index (SII), and quantitative flow ratio (QFR) in stable coronary artery disease (CAD) patients (n = 450) enrolled in this cross-sectional study. Logistic regression was performed to evaluate the associations of NLR, PLR, MLR, and SII evaluated as continuous and binary variables with QFR ≤0.80. When treated as continuous variables, lnNLR was associated with QFR ≤0.80 with borderline significance in univariable (odds ratio (OR) = 1.60, p =.05) and multivariable analysis (OR = 1.72, p =.05), while lnMLR was associated with QFR ≤0.80 significantly in univariable analysis (OR = 1.87, p =.03) and with borderline significance in multivariable analysis (OR = 1.91, p =.05). When treated as binary variables, high levels of MLR and SII were significantly associated with QFR ≤0.80 in univariable (MLR: OR = 1.91, p =.02; SII: OR = 2.42, p =.006) and multivariable analysis (MLR: OR = 1.83, p =.04; SII: OR = 2.19, p =.02). NLR, MLR, and SII, but not PLR, were significantly associated with the severity of coronary physiology in stable CAD patients. [ABSTRACT FROM AUTHOR]

Accurate modeling of blood dynamics in the coronary microcirculation is a crucial step toward the clinical application of in silico methods for the diagnosis of coronary artery disease. In this work, we present a new mathematical model of microcirculatory hemodynamics accounting for microvasculature compliance and cardiac contraction; we also present its application to a full simulation of hyperemic coronary blood flow and 3D myocardial perfusion in real clinical cases. Microvasculature hemodynamics is modeled with a compliant multi-compartment Darcy formulation, with the new compliance terms depending on the local intramyocardial pressure generated by cardiac contraction. Nonlinear analytical relationships for vessels distensibility are included based on experimental data, and all the parameters of the model are reformulated based on histologically relevant quantities, allowing a deeper model personalization. Phasic flow patterns of high arterial inflow in diastole and venous outflow in systole are obtained, with flow waveforms morphology and pressure distribution along the microcirculation reproduced in accordance with experimental and in vivo measures. Phasic diameter change for arterioles and capillaries is also obtained with relevant differences depending on the depth location. Coronary blood dynamics exhibits a disturbed flow at the systolic onset, while the obtained 3D perfusion maps reproduce the systolic impediment effect and show relevant regional and transmural heterogeneities in myocardial blood flow (MBF). The proposed model successfully reproduces microvasculature hemodynamics over the whole heartbeat and along the entire intramural vessels. Quantification of phasic flow patterns, diameter changes, regional and transmural heterogeneities in MBF represent key steps ahead in the direction of the predictive simulation of cardiac perfusion. [ABSTRACT FROM AUTHOR]

Angina pectoris may arise from obstructive coronary artery disease (CAD) or in the absence of significant CAD (ischemia with nonobstructed coronary arteries [INOCA]). Therapeutic strategies for patients with angina and obstructive CAD focus on reducing cardiovascular events and relieving symptoms, whereas in INOCA the focus shifts toward managing functional alterations of the coronary circulation. In obstructive CAD, coronary revascularization might improve angina status, although a significant percentage of patients present angina persistence or recurrence, suggesting the presence of functional mechanisms along with epicardial CAD. In patients with INOCA, performing a precise endotype diagnosis is crucial to allow a tailored therapy targeted toward the specific pathogenic mechanism. In this expert opinion paper, we review the evidence for the management of angina, highlighting the complementary role of coronary revascularization, optimal medical therapy, and lifestyle interventions and underscoring the importance of a personalized approach that targets the underlying pathobiology. • Angina pectoris may arise from obstructive CAD or in the absence of significant CAD. • Functional mechanisms may be involved in determining angina both in obstructive CAD and in ischemia with nonobstructed coronary arteries. • Revascularization and medical therapy play complementary roles in achieving optimal outcomes for patients with angina. • Management of angina is shifting toward a more personalized approach, moving away from the traditional one-size-fits-all strategy. [ABSTRACT FROM AUTHOR]

Caffeine is the most popular and widely consumed behaviourally active substance in the world. This review describes the influence of caffeine on the cardiovascular system, with a special focus on blood platelets. For many years, caffeine was thought to have a negative effect on the cardiovascular system mainly due to increasing blood pressure. However, more recent data suggest that habitual caffeine consumption may reduce the risk of cardiovascular disease and hypertension. This could be a significant finding as cardiovascular disease is the leading cause of death worldwide. Caffeine is known to inhibit A1 adenosine receptors, through which it is believed to modulate inter alia coronary blood flow, total peripheral resistance, diuresis, and heart rate. It has been shown that coffee possesses antiplatelet activity, but depending on the dose and the term of its use, caffeine may stimulate or inhibit platelet reactivity. Also, chronic exposure to caffeine may sensitize or upregulate the adenosine receptors in platelets causing increased cAMP accumulation and anti-aggregatory effects and decrease calcium levels elicited by AR agonists. The search for new, selective, and safe AR agonists is one of the new strategies for improving antiplatelet therapy involving targeting multiple pathways of platelet activation. Therefore, this review examines the AR-dependent impact of caffeine on blood platelets in the presence of adenosine receptor agonists. [ABSTRACT FROM AUTHOR]

Background: Clinical events such as angina pectoris, acute coronary syndrome, and sudden death caused by myocardial bridge (MB) have attracted increasing attention. It is still a challenge to diagnose whether MB can cause the symptoms of patients with MB. For most MB patients, medication remains the primary treatment. Case presentation: This article reports a case of chest pain in a patient with MB in the middle segment of the left anterior descending artery (LADm) with moderate stenosis in the proximal segment (LADp). Through functional assessment, we found that neither MB nor fixed stenosis had sufficient effect on coronary blood flow to cause myocardial ischemia, but their synergistic effect resulted in myocardial ischemia. Finally, a stent was implanted in LADp and good clinical results were achieved. Conclusions: For symptomatic patients with MB combined with fixed stenosis, functional evaluation may be necessary, which has significant guiding significance for treatment strategy selection. For asymptomatic patients, early detection of myocardial ischemia may also improve the prognosis of patients. [ABSTRACT FROM AUTHOR]

Understanding the mechanisms underlying vascular regeneration in the heart is crucial for developing novel therapeutic strategies for myocardial ischemia. This study investigates the contribution of bone marrow-derived cells to endothelial cell populations in the heart, and their role in cardiac function and coronary circulation following repetitive ischemia (RI). Chimeric rats were created by transplanting BM cells from GFP female rats into irradiated male recipients. After engraftment chimeras were subjected to RI for 17 days. Vascular growth was assessed from recovery of cardiac function and increases in myocardial blood flow during LAD occlusion. After sorting GFP+ BM cells from heart and bone of Control and RI rats, single-cell RNA sequencing was implemented to determine the fate of BM cells. Our in vivo RI model demonstrated an improvement in cardiac function and myocardial blood flow after 17 days of RI with increased capillary density in the rats subjected to RI compared to Controls. Single-cell RNA sequencing of bone marrow cells isolated from rats' hearts identified distinct endothelial cell (EC) subpopulations. These ECs exhibited heterogeneous gene expression profiles and were enriched for markers of capillary, artery, lymphatic, venous, and immune ECs. Furthermore, BM-derived ECs in the RI group showed an angiogenic profile, characterized by upregulated genes associated with blood vessel development and angiogenesis. This study elucidates the heterogeneity of bone marrow-derived endothelial cells in the heart and their response to repetitive ischemia, laying the groundwork for targeting specific subpopulations for therapeutic angiogenesis in myocardial ischemia. [ABSTRACT FROM AUTHOR]

This article explores the role of electrocardiograms (ECGs) in diagnosing and localizing occlusions in the coronary arteries during acute myocardial infarction (heart attack). The study involved 112 patients and found that ECG criteria, such as ST segment elevation and depression in specific leads, can accurately predict the location of the occlusion. The results highlight the importance of ECGs in determining the need for early reperfusion therapy and assessing the extent of myocardial injury. The study's findings align with previous research in this area. [Extracted from the article]

Heart transplantation (HT) in patients with failing univentricular circulation is often challenging. This is compounded by the ever-increasing number of patients with prior Norwood-type reconstruction of the aorta, large aortic root, and often dense adhesions from multiple prior operations. We aimed to elucidate differences in outcomes of HT in patients with prior univentricular palliations, with and without prior Norwood-type aortic arch reconstruction (ArchRec). All patients who underwent HT for failed univentricular palliation during the 1990–2022 period were included in the study. Of 45 patients, 18 had undergone ArchRec. Hospital mortality improved in the recent era (17.4% before 2006 vs 0% after 2006; p=0.11), despite a higher proportion of patients with ArchRec (17.4% before 2006 vs 60.8% after 2006, p=0.002). Patients with ArchRec had a higher number of prior cardiac surgeries (4.1±1.5 vs 3.2±1.3, p=0.04), longer cardiopulmonary bypass time (320±23 vs 242±21 min, p=0.02), more concomitant arch reconstruction (33.3% vs 0%, p=0.02), greater need for post-HT extracorporeal membrane oxygenation (33.3% vs 3.7%; p=0.01) and longer hospital stay (37.1±30.5 days vs 23.6±11.8 days, p=0.04). Freedom from death or retransplantation for all patients was 91%, 73%, 67%, and 53% at 1, 5, 10, and 15-years, respectively. Prior ArchRec, Fontan procedure, and earlier eras were not risk factors for death. The outcomes of HT after univentricular palliation have improved in recent times and low operative mortality can be achieved. Despite increased complexity, good similar outcomes can be achieved in patients with and without prior arch reconstruction regardless of the palliation stage. [ABSTRACT FROM AUTHOR]

Coronary artery disease (CAD) is a condition where the coronary arteries, which supply blood to the heart muscle, become narrowed or blocked. The most common cause of CAD is atherosclerosis, which is a condition in which plaque builds up inside the arteries, causing them to harden and narrow. These are critical conditions due to their high prevalence, adverse impact on health and quality of life, and potential for severe complications. Early detection, prevention, and effective management are essential to mitigate their effects, which delves critically on the understanding of blood flow dynamics (hemodynamics) in these arteries. While fluid dynamics simulations incorporating the deformability of blood vessels have proven to be immensely useful in this context, their outcomes remain far from being amenable for clinical decision making in real-life medical practice because of their limitations in capturing the implications of certain key physiological features such as the stiffnesses of the artery walls and the plaque deposits formed therein. In an effort to circumvent these deficits, here we report the development and deployment of a fluid–structure interaction model that unveils the sensitive dependence of the clinically relevant hemodynamic parameters on the arterial wall and plaque stiffness, bringing in explicit quantitative assessment of the pathophysiology of arterial disease progression. Our results enable direct quantification of the time-averaged wall shear stress, offering clinical insights into the biomechanical environment and the endothelial response that are critical in the initiation and progression of atherosclerotic plaques. In addition, our results pinpoint the alterations in the fractional flow reserve due to changes in the deformability of the arterial walls and plaques, providing a functional assessment of the impact of these plaques on coronary blood flow. Our simulation platform thus helps in a comprehensive assessment of cardiovascular risk, enabling better prediction, prevention, and treatment of atherosclerosis-related conditions—a paradigm that has remained to be elusive in clinical practices thus far. [ABSTRACT FROM AUTHOR]