Systems biology-based analysis exploring shared biomarkers and pathogenesis of myocardial infarction combined with osteoarthritis.

Background: More and more evidence supports the association between myocardial infarction (MI) and osteoarthritis (OA). The purpose of this study is to explore the shared biomarkers and pathogenesis of MI complicated with OA by systems biology. Methods: Gene expression profiles of MI and OA were downloaded from the Gene Expression Omnibus (GEO) database. The Weighted Gene Co-Expression Network Analysis (WGCNA) and differentially expressed genes (DEGs) analysis were used to identify the common DEGs. The shared genes related to diseases were screened by three public databases, and the protein-protein interaction (PPI) network was built. GO and KEGG enrichment analyses were performed on the two parts of the genes respectively. The hub genes were intersected and verified by Least absolute shrinkage and selection operator (LASSO) analysis, receiver operating characteristic (ROC) curves, and single-cell RNA sequencing analysis. Finally, the hub genes differentially expressed in primary cardiomyocytes and chondrocytes were verified by RT-qPCR. The immune cell infiltration analysis, subtypes analysis, and transcription factors (TFs) prediction were carried out. Results: In this study, 23 common DEGs were obtained by WGCNA and DEGs analysis. In addition, 199 common genes were acquired from three public databases by PPI. Inflammation and immunity may be the common pathogenic mechanisms, and the MAPK signaling pathway may play a key role in both disorders. DUSP1, FOS, and THBS1 were identified as shared biomarkers, which is entirely consistent with the results of single-cell RNA sequencing analysis, and furher confirmed by RT-qPCR. Immune infiltration analysis illustrated that many types of immune cells were closely associated with MI and OA. Two potential subtypes were identified in both datasets. Furthermore, FOXC1 may be the crucial TF, and the relationship of TFs-hub genes-immune cells was visualized by the Sankey diagram, which could help discover the pathogenesis between MI and OA. Conclusion: In summary, this study first revealed 3 (DUSP1, FOS, and THBS1) novel shared biomarkers and signaling pathways underlying both MI and OA. Additionally, immune cells and key TFs related to 3 hub genes were examined to further clarify the regulation mechanism. Our study provides new insights into shared molecular mechanisms between MI and OA.

Unmasking the cannabis paradox: in-hospital outcomes of cannabis users admitted with acute myocardial infarction over a 20-year period in the United States.

Introduction: Cannabis is increasingly becoming a socially acceptable substance, with multiple countries having legalised its consumption. Epidemiological studies have demonstrated an association between cannabis use and an increased risk of developing coronary artery disease. However, there is a lack of studies about the influence of cannabis consumption on the outcomes following acute myocardial infarction (AMI). Material and methods: We retrospectively analysed hospitalised patients with a primary diagnosis of AMI from the 2001 to 2020 National Inpatient Sample (NIS). Pearson's χ2 tests were applied to categorical variables, and t-tests for continuous variables. We conducted a 1:1 propensity score matching (PSM). Multivariate regression models were deployed on the PSM sample to estimate the differences in several events and all-cause mortality. Results: A total of 9,930,007 AMI patients were studied, of whom 117,641 (1.2%) reported cannabis use. Cannabis users had lower odds of atrial fibrillation (aOR = 0.902, p < 0.01), ventricular fibrillation (aOR = 0.919, p < 0.01), cardiogenic shock (aOR = 0.730, p < 0.01), acute ischaemic stroke (aOR = 0.825, p < 0.01), cardiac arrest (aOR = 0.936, p = 0.010), undergoing PCI (aOR = 0.826, p < 0.01), using IABP (aOR = 0.835, p < 0.01), and all-cause mortality (aOR = 0.640, p < 0.01), but with higher odds of supraventricular tachycardia (aOR = 1.104, p < 0.01), ventricular tachycardia (aOR = 1.054, p < 0.01), CABG use (aOR = 1.040, p = 0.010), and acute kidney injury (aOR = 1.103, p < 0.01). Conclusions: Among patients aged 18-80 years admitted to hospital with AMI between 2001 and 2020 in the United States, cannabis use was associated with lower risks of cardiogenic shock, acute ischaemic stroke, cardiac arrest, PCI use, and in-hospital mortality.

Evaluating the Rates of Mortality and Cardiac Catheterization Using High-Sensitivity Troponin and Conventional Troponin Assays.

Non-ST segment elevation myocardial infarction (NSTEMI) is an acute coronary syndrome event where myocardial ischemia is present, with an increase of cardiac troponins without an elevation of the ST segment. One of the fundamental measures used to diagnose or rule out acute coronary syndrome (ACS) is troponin levels in the blood. Troponin is a broad term used for the category of muscle contraction regulatory proteins and is commonly measured during ACS evaluation. Troponin I is only released by cardiac tissue, while some assay measurements will also pick up troponin released by skeletal muscle injury. This retrospective observational study was performed investigating troponin assays and how they relate to patient's outcomes. The troponin assays used in this Miami hospital where the database of patients was collected between 2018 and 2023 were troponin I (cTnI), the conventional troponin assay, and the newer high-sensitivity troponin I assay (hs-cTn). In this observational study patients who received an admitting diagnosis of NSTEMI corroborated by an independent cardiologist had their respective troponin assay levels included. Patients found to have ECG changes significant for non-ischemic pathologies, or echocardiogram findings suggestive of myocardial dysfunction not clinically correlated to an ACS were excluded from the study. A total of 75 patients were included in this study and the mean age was 75.97 ±14.72 years, with a presentation of chest pain, dyspnea and general weakness recorded in 59% (n = 45) of patients. The median time between troponin samples was 6.63 hours across both assays and hs-cTn showed a 4.99% increase in variation between samples while cTnI had a decrease of 2.53%. The study objective is to support whether there is a difference in rates of cardiac catheterization or mortality based on the type of troponin testing. There was no significant association found between, the type of troponin assay used during hospital admission, and the outcomes of catheterization and death (p > 0.009).

Coronary artery disease and heart failure: Late-breaking trials presented at American Heart Association scientific session 2023.

The late-breaking science presented at the 2023 scientific session of the American Heart Association paves the way for future pragmatic trials and provides meaningful information to guide management strategies in coronary artery disease and heart failure (HF). The dapagliflozin in patient with acute myocardial infarction (DAPA-MI) trial showed that dapagliflozin use among patients with acute MI without a history of diabetes mellitus or chronic HF has better cardiometabolic outcomes compared with placebo, with no difference in cardiovascular outcomes. The MINT trial showed that in patients with acute MI and anemia (Hgb < 10 g/dL), a liberal transfusion goal (Hgb ≥ 10 g/dL) was not superior to a restrictive strategy (Hgb 7-8 g/dL) with respect to 30-day all-cause death and recurrent MI. The ORBITA-2 trial showed that among patients with stable angina and coronary stenoses causing ischemia on little or no antianginal therapy, percutaneous coronary intervention results in greater improvements in anginal frequency and exercise times compared with a sham procedure. The ARIES-HM3 trial showed that in patients with advanced HF who received a HeartMate 3 levitated left ventricular assist device and were anticoagulated with a vitamin K antagonist, placebo was noninferior to daily aspirin with respect to the composite endpoint of bleeding and thrombotic events at 1 year. The TEAMMATE trial showed that everolimus with low-dose tacrolimus is safe in children and young adults when given ≥ 6 months after cardiac transplantation. Providing patients being treated for HF with reduced ejection fraction (HFrEF) with specific out-of-pocket (OOP) costs for multiple medication options at the time of the clinical encounter may reduce 'contingency planning' and increase the extent to which patients are taking the medications decided upon. The primary outcome, which was cost-informed decision-making, defined as the clinician or patient mentioning costs of HFrEF medication, occurred in 49% of encounters with the checklist only control group compared with 68% of encounters in the OOP cost group.

Impact of depression on in-hospital outcomes for adults with type 2 myocardial infarction: A United States population-based analysis.

BACKGROUND: Type 2 myocardial infarction (T2MI) is an ischemic myocardial injury in the context of oxygen supply/demand mismatch in the absence of a primary coronary event. However, though there is a rising prevalence of depression and its potential association with type 1 myocardial infarction (T1MI), data remains non-existent to evaluate the association with T2MI. AIM: To identify the prevalence and risk of T2MI in adults with depression and its impact on the in-hospital outcomes. METHODS: We queried the National Inpatient Sample (2019) to identify T2MI hospitalizations using Internal Classification of Diseases-10 codes in hospitalized adults (≥ 18 years). In addition, we compared sociodemographic and comorbidities in the T2MI cohort with vs without comorbid depression. Finally, we used multivariate regression analysis to study the odds of T2MI hospitalizations with vs without depression and in-hospital outcomes (all-cause mortality, cardiogenic shock, cardiac arrest, and stroke), adjusting for confounders. Statistical significance was achieved with a P value of < 0.05. RESULTS: There were 331145 adult T2MI hospitalizations after excluding T1MI (median age: 73 years, 52.8% male, 69.9% white); 41405 (12.5%) had depression, the remainder; 289740 did not have depression. Multivariate analysis revealed lower odds of T2MI in patients with depression vs without [adjusted odds ratio (aOR) = 0.88, 95% confidence interval (CI): 0.86-0.90, P = 0.001]. There was the equal prevalence of prior MI with any revascularization and a similar prevalence of peripheral vascular disease in the cohorts with depression vs without depression. There is a greater prevalence of stroke in patients with depression (10.1%) vs those without (8.6%). There was a slightly higher prevalence of hyperlipidemia in patients with depression vs without depression (56.5% vs 48.9%), as well as obesity (21.3% vs 17.9%). There was generally equal prevalence of hypertension and type 2 diabetes mellitus in both cohorts. There was no significant difference in elective and non-elective admissions frequency between cohorts. Patients with depression vs without depression also showed a lower risk of all-cause mortality (aOR = 0.75, 95%CI: 0.67-0.83, P = 0.001), cardiogenic shock (aOR = 0.65, 95%CI: 0.56-0.76, P = 0.001), cardiac arrest (aOR = 0.77, 95%CI: 0.67-0.89, P = 0.001) as well as stroke (aOR = 0.79, 95%CI: 0.70-0.89, P = 0.001). CONCLUSION: This study revealed a significantly lower risk of T2MI in patients with depression compared to patients without depression by decreasing adverse in-hospital outcomes such as all-cause mortality, cardiogenic shock, cardiac arrest, and stroke in patients with depression.

Spontaneous calcified cerebral emboli: a comprehensive review and proposed diagnostic criteria.

Spontaneous calcified cerebral emboli (SCCE) secondary to aortic valve calcification are a rare and underreported cause of acute ischaemic stroke. Only five cases of SCCE secondary to bicuspid aortic valve calcification have been reported in the literature. This review includes a unique case example of acute ischaemic stroke secondary to SCCE, as the first manifestation of a calcified bicuspid aortic valve. This is the first clinical case of calcified cerebral emboli (CCE) associated with borderzone infarction ('cortical ribbon sign'). Whilst previously assumed that most CCE are secondary to iatrogenic causes, recent literature suggests the majority of CCE are spontaneous and clinically silent. Despite CT imaging widely considered the 'gold standard' for diagnosis, CCE are frequently misdiagnosed and missed entirely. Misdiagnosis of CCE may have catastrophic consequences due to the high risk of recurrence and missed opportunity to prevent neurological disability and death. This review presents a revised CCE diagnostic criteria, using evidence that has emerged over the last decade to create both Compulsory (Major) and Supporting (Minor) criteria. Current CCE management is not evidence based and remains largely speculative. SCCE may be the first manifestation of cardiac or vascular disease and diagnosis should trigger aggressive treatment of emboligenic sources. Future epidemiological studies, analysing symptomatic and asymptomatic SCCE patients, would be beneficial in providing accurate quantification of disease burden. Other future research directions include exploring intracranial stenting for CCE revascularisation and cerebral intravascular lithotripsy.

Enhancing miR-19a/b induced cardiomyocyte proliferation in infarcted hearts by alleviating oxidant stress and controlling miR-19 release.

Fully restoring the lost population of cardiomyocytes and heart function remains the greatest challenge in cardiac repair post myocardial infarction. In this study, a pioneered highly ROS-eliminating hydrogel was designed to enhance miR-19a/b induced cardiomyocyte proliferation by lowering the oxidative stress and continuously releasing miR-19a/b in infarcted myocardium in situ. In vivo lineage tracing revealed that ∼20.47 % of adult cardiomyocytes at the injected sites underwent cell division in MI mice. In MI pig the infarcted size was significantly reduced from 40 % to 18 %, and thereby marked improvement of cardiac function and increased muscle mass. Most importantly, our treatment solved the challenge of animal death--all the treated pigs managed to live until their hearts were harvested at day 50. Therefore, our strategy provides clinical conversion advantages and safety for healing damaged hearts and restoring heart function post MI, which will be a powerful tool to battle cardiovascular diseases in patients.

Recombinant human placental growth factor-2 in post-infarction left ventricular dysfunction: a randomized, placebo-controlled, preclinical study.

Placental growth factor (PlGF)-2 induces angio- and arteriogenesis in rodents but its therapeutic potential in a clinically representative post-infarction left ventricular (LV) dysfunction model remains unclear. We, therefore, investigated the safety and efficacy of recombinant human (rh)PlGF-2 in the infarcted porcine heart in a randomized, placebo-controlled blinded study. We induced myocardial infarction (MI) in pigs using 75 min mid-LAD balloon occlusion followed by reperfusion. After 4 w, we randomized pigs with marked LV dysfunction (LVEF < 40%) to receive continuous intravenous infusion of 5, 15, 45 µg/kg/day rhPlGF-2 or PBS (CON) for 2 w using osmotic pumps. We evaluated the treatment effect at 8 w using comprehensive MRI and immunohistochemistry and measured myocardial PlGF-2 receptor transcript levels. At 4 w after MI, infarct size was 16-18 ± 4% of LV mass, resulting in significantly impaired systolic function (LVEF 34 ± 4%). In the pilot study (3 pigs/dose), PIGF administration showed sustained dose-dependent increases in plasma concentrations for 14 days without systemic toxicity and was associated with favorable post-infarct remodeling. In the second phase (n = 42), we detected no significant differences at 8 w between CON and PlGF-treated pigs in infarct size, capillary or arteriolar density, global LV function and regional myocardial blood flow at rest or during stress. Molecular analysis showed significant downregulation of the main PlGF-2 receptor, pVEGFR-1, in dysfunctional myocardium. Chronic rhPIGF-2 infusion was safe but failed to induce therapeutic neovascularization and improve global cardiac function after myocardial infarction in pigs. Our data emphasize the critical need for properly designed trials in representative large animal models before translating presumed promising therapies to patients.

Evaluation of a nomogram model for predicting in-hospital mortality risk in patients with acute ST-elevation myocardial infarction and acute heart failure post-PCI.

OBJECTIVES: This study aims to identify the risk factors contributing to in-hospital mortality in patients with acute ST-elevation myocardial infarction (STEMI) who develop acute heart failure (AHF) post-percutaneous coronary intervention (PCI). Based on these factors, we constructed a nomogram to effectively identify high-risk patients. METHODS: In the study, a collective of 280 individuals experiencing an acute STEMI who then developed AHF following PCI were evaluated. These subjects were split into groups for training and validation purposes. Utilizing lasso regression in conjunction with logistic regression analysis, researchers sought to pinpoint factors predictive of mortality and to create a corresponding nomogram for forecasting purposes. To evaluate the model's accuracy and usefulness in clinical settings, metrics such as the concordance index (C-index), calibration curves, and decision curve analysis (DCA) were employed. RESULTS: Key risk factors identified included blood lactate, D-dimer levels, gender, left ventricular ejection fraction (LVEF), and Killip class IV. The nomogram demonstrated high accuracy (C-index: training set 0.838, validation set 0.853) and good fit (Hosmer-Lemeshow test: χ2 = 0.545, p = 0.762), confirming its clinical utility. CONCLUSION: The developed clinical prediction model is effective in accurately forecasting mortality among patients with acute STEMI who develop AHF after PCI.

Cerebral Complications Following Facial Autologous Fat Graft Injection: A Systematic Review and Meta-analysis.

BACKGROUND: With the increasing use of autologous fat (AF) grafting in plastic surgery, the occurrence of complications has garnered the attention from plastic surgeons. This study aims to estimate the cerebral complications following facial AF graft injection objectively and systematically with newly published literature. METHODS: A comprehensive literature search was conducted systematically on PubMed, Embase, Web of Science, Cochrane, and ClinicalTrials.gov for articles published between 2000 and 2023. A systematic review and meta-analysis were performed in accordance with PRISMA guidelines. RESULTS: A total of 11 articles comprising of 37 participants were included, all of which are case reports. For AF facial filling, the incidence rate of cerebral embolism among cases of cerebral and ocular embolism was found to be 60% (95% CI 0.41-0.79). The incidence of cerebral embolism presenting with initial symptoms of unconsciousness was 69% (95% CI 0.48-0.9), with limb movement disorders was 55% (95% CI 0.26-0.84), and with vision loss was 30% (95% CI 0.12-0.49). The incidence of cerebral embolism with ophthalmic artery occlusion was 36% (95% CI 0.20-0.53), compared to was 71% (95% CI 0.48-0.95) without ophthalmic artery occlusion. CONCLUSIONS: AF grafting is generally safe and minimally invasive. However, with its widespread use as facial injection filling for cosmetic enhancement, the incidence of cerebral complications, such as cerebral infarction, has also increased. It is imperative to properly manage high-risk factors for cerebral embolism during the perioperative period to prevent its occurrence. LEVEL OF EVIDENCE III: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

The cardiovascular risk in bullous pemphigoid: Insights from a population-based study.

BACKGROUND: The risk of life-threatening major cardiovascular outcomes among patients with bullous pemphigoid (BP) is inconsistent in the current literature. OBJECTIVE: To evaluate the risk and prognostic outcomes of myocardial infarction (MI), cerebrovascular accident (CVA), peripheral vascular disease (PVD) and pulmonary embolism (PE) in patients with BP. We additionally aimed to explore the influence of different therapeutic approaches on the risk of these outcomes. METHODS: A population-based retrospective cohort study was conducted to compare BP patients (n = 3924) with age-, gender- and ethnicity-matched control subjects (n = 19,280) with regard to incident cases of MI, CVA, PVD and PE. Adjusted hazard ratio (HR) and 95% confidence intervals (CI) were estimated by multivariate Cox regression analysis. Data were retrieved from Clalit Health Services' computerized database. RESULTS: Relative to their matched controls, patients with BP were at an elevated risk of MI (fully-adjusted HR: 1.44; 95% CI: 1.14-1.81; p = 0.002), CVA (fully-adjusted HR: 1.24; 95% CI: 1.06-1.45; p = 0.007), PVD (fully-adjusted HR: 1.60; 95% CI: 1.27-2.03; p = 0.003) and PE (fully-adjusted HR: 1.72; 95% CI: 1.28-2.32; p < 0.008). Patients with BP experienced heightened risk of all-cause mortality in the presence of comorbid MI (fully-adjusted HR: 1.61; 95% CI: 1.44-1.81; p < 0.001), CVA (fully-adjusted HR: 1.70; 95% CI: 1.52-1.89; p < 0.001), PVD (fully-adjusted HR: 1.38; 95% CI: 1.20-1.58; p < 0.001) and PE (fully-adjusted HR: 1.44; 95% CI: 1.10-1.88; p = 0.007). The therapeutic approach utilized to manage BP did not significantly influence the risk of cardiovascular outcomes. CONCLUSIONS: BP is associated with an elevated risk of MI, CVA, PVD, PE and cardiovascular mortality. Primary, secondary and tertiary cardiovascular prevention measures should be implemented among patients with BP.

Pre-hospital heparin is not associated with infarct vessel patency and mortality in ST-segment elevation myocardial infarction patients with out-of-hospital cardiac arrest.

BACKGROUND: Pre-hospital heparin administration has been reported to improve prognosis in patients with out-of-hospital cardiac arrest (OHCA). This beneficial effect may be limited to the subgroup of ST-segment elevation myocardial infarction (STEMI) patients. METHODS: To assess the impact of pre-hospital heparin loading on TIMI (Thrombolysis in Myocardial Infarction) flow grade and mortality in STEMI patients with OHCA, we analyzed data from 2,566 consecutive patients from two hospitals participating in the prospective Feedback Intervention and Treatment Times in ST-segment Elevation Myocardial Infarction (FITT-STEMI) trial. RESULTS: In 394 participants with OHCA, 272 (69%) received heparin from the emergency medical service (EMS). Collapse witnessed by EMS (odds ratio (OR) = 3.53, 95%-confidence interval (CI) = 1.54-8.09; p = 0.003) and pre-hospital ECG recording (OR = 3.32, 95% CI = 1.06-10.35; p = 0.039) were identified as parameters significantly associated with pre-hospital heparin use. In univariate analysis, in-hospital mortality was lower in the group receiving heparin in the pre-hospital setting (26.8% vs. 42.6%, p = 0.002). However, in a regression model, pre-hospital heparin use was no longer a significant predictor of mortality (OR = 0.992; p = 0.981). Patency of the infarct artery prior to coronary revascularization, as measured by TIMI flow grade, was not associated with pre-hospital administration of heparin in OHCA patients (OR = 0.840; p = 0.724). CONCLUSIONS: In STEMI patients with OHCA, pre-hospital use of heparin is neither associated with improved early patency of the infarct artery nor with a better prognosis. Our results do not support the assumption of a positive effect of heparin administration in the pre-hospital treatment phase in STEMI patients with OHCA. TRIAL REGISTRATION: ClinicalTrials.gov: NCT00794001.

SGLT1 contributes to glucose-mediated exacerbation of ischemia-reperfusion injury in ex vivo rat heart.

Hyperglycaemia is common during acute coronary syndromes (ACS) irrespective of diabetic status and portends excess infarct size and mortality, but the mechanisms underlying this effect are poorly understood. We hypothesized that sodium/glucose linked transporter-1 (SGLT1) might contribute to the effect of high-glucose during ACS and examined this using an ex-vivo rodent heart model of ischaemia-reperfusion injury. Langendorff-perfused rat hearts were subjected to 35 min ischemia and 2 h reperfusion, with variable glucose and reciprocal mannitol given during reperfusion in the presence of pharmacological inhibitors of SGLT1. Myocardial SGLT1 expression was determined in rat by rtPCR, RNAscope and immunohistochemistry, as well as in human by single-cell transcriptomic analysis. High glucose in non-diabetic rat heart exacerbated reperfusion injury, significantly increasing infarct size from 45 ± 3 to 65 ± 4% at 11-22 mmol/L glucose, respectively (p < 0.01), an association absent in diabetic heart (32 ± 1-37 ± 5%, p = NS). Rat heart expressed SGLT1 RNA and protein in vascular endothelium and cardiomyocytes, with similar expression found in human myocardium by single-nucleus RNA-sequencing. Rat SGLT1 expression was significantly reduced in diabetic versus non-diabetic heart (0.608 ± 0.08 compared with 1.116 ± 0.13 probe/nuclei, p < 0.01). Pharmacological inhibitors phlorizin, canagliflozin or mizagliflozoin in non-diabetic heart revealed that blockade of SGLT1 but not SGLT2, abrogated glucose-mediated excess reperfusion injury. Elevated glucose is injurious to the rat heart during reperfusion, exacerbating myocardial infarction in non-diabetic heart, whereas the diabetic heart is resistant to raised glucose, a finding which may be explained by lower myocardial SGLT1 expression. SGLT1 is expressed in vascular endothelium and cardiomyocytes and inhibiting SGLT1 abrogates excess glucose-mediated infarction. These data highlight SGLT1 as a potential clinical translational target to improve morbidity/mortality outcomes in hyperglycemic ACS patients.

Impact of cardiac patch alignment on restoring post-infarct ventricular function.

Acute myocardial infarction (MI) leads to a loss of cardiac function which, following adverse ventricular remodeling (AVR), can ultimately result in heart failure. Tissue-engineered contractile patches placed over the infarct offer potential for restoring cardiac function and reducing AVR. In this computational study, we investigate how improvement of pump function depends on the orientation of the cardiac patch and the fibers therein relative to the left ventricle (LV). Additionally, we examine how model outcome depends on the choice of material properties for healthy and infarct tissue. In a finite element model of LV mechanics, an infarction was induced by eliminating active stress generation and increasing passive tissue stiffness in a region comprising 15% of the LV wall volume. The cardiac patch was modeled as a rectangular piece of healthy myocardium with a volume of 25% of the infarcted tissue. The orientation of the patch was varied from 0 to 150 ∘ relative to the circumferential plane. The infarct reduced stroke work by 34% compared to the healthy heart. Optimal patch support was achieved when the patch was oriented parallel to the subepicardial fiber direction, restoring 9% of lost functionality. Typically, about one-third of the total recovery was attributed to the patch, while the remainder resulted from restored functionality in native myocardium adjacent to the infarct. The patch contributes to cardiac function through two mechanisms. A contribution of tissue in the patch and an increased contribution of native tissue, due to favorable changes in mechanical boundary conditions.

A Rare Case of Multiple Bone Infarctions and Abnormal Pulmonary Function Tests in a Patient With Compound Heterozygous Hemoglobin S and Type 2 Hereditary Persistence of Fetal Hemoglobin.

Sickle cell disease (SCD) is a group of inherited blood disorders characterized by abnormal hemoglobin production, affecting individuals worldwide with varying prevalence across different populations. Manifestations vary, ranging from severe to mild. SCD is characterized by the presence of hemoglobin S (HbS), which distorts erythrocytes upon deoxygenation, leading to sickling. This results in hemolytic anemia, painful vaso-occlusive crises (VOC), and multiple organ damage, including bones, due to microinfarcts. Sickle cell trait (SCT), or carrier status, is not considered an SCD and often runs a benign course. We report a 44-year-old man of African descent presenting with a one-month history of pain in his ankles and feet. He had a prior diagnosis of sickle cell "trait" without previous VOC. Hematological indices were normal. Hemoglobin electrophoresis showed absent HbA, elevated HbS, elevated HbF, and normal HbA2. X-rays and MRI revealed bilateral bone infarction in diaphyses of right proximal and bilateral distal tibias. Molecular analysis of [Formula: see text]-globin revealed compound heterozygous hemoglobin S and type 2 deletion of persistence of fetal hemoglobin (HPFH). Pulmonary function tests revealed restrictive lung disease. A literature review from 1946 to May 2024 via PubMed, EMBASE, and Medline was performed, revealing two cases of HbS-HPFH with avascular necrosis affecting the femoral neck were briefly reported more than 60 years ago. Although pulmonary function tests in SCD typically show a mild restrictive pattern with decreased diffusion capacity and rarely an obstructive pattern, no cases of HbS-HPFH were identified. In conclusion, multiple bone infarctions are extremely rare in HbS-HPFH. Lung and bone diseases might be unrecognized in this unique disorder.

Anterior Spinal Cord Infarction: A Rare Diagnosis With an Uncommon Presentation.

Spinal cord infarction (SCI) is a rare vascular event accounting for 1% of all strokes. Neurological syndromes may vary according to the arterial territory involved. This condition may differ in onset, severity, and recovery, making it a diagnostic challenge for clinicians. Diagnosis is made on a clinical basis, and neuroimaging (magnetic resonance imaging (MRI)) provides confirmatory evidence. A 72-year-old male, with a medical history of being overweight, hyperuricemia, dyslipidemia, and cigarette smoking presented to our emergency department (ED) with sudden-onset leg weakness. He reported chest pain with radiation to the back, followed by sudden arm and leg weakness, evolving to inferior limb plegia within four hours. He also noticed a loss of sensation below the breast region. On admission, vital signs were stable. Neurological examination demonstrated paraplegia of inferior limbs with absent deep tendon reflexes. Both pinprick, vibrational, and proprioceptive sensitivities were absent below T6. A diagnostic workup revealed lactescent serum suggesting severe hypertriglyceridemia. A clinical diagnosis of spinal cord infarction was made, which was later confirmed with MRI demonstrating an acute ischemic lesion in the anterior spinal artery (ASA) with the "owl's eye" sign, from T5 with extension to the cone. Neurological examination remained unaltered. He started aspirin and insulin perfusion. Since spinal cord injury is an uncommon cause of paraplegia, physicians should be extremely cautious. Despite the results of magnetic resonance imaging, the clinical picture was not consistent, which was finally explained by perilesional edema. To our knowledge, this is a rare case combining SCI with hypertriglyceridemia. Notwithstanding the lack of evidence linking reducing triglyceride levels to neurological recovery, insulin infusion was carried out given the hazards associated with sustaining such high levels of triglycerides. We aim to emphasize some characteristic MRI findings and the wealth of possible etiologies contributing to this clinical entity.

Lesser Omental Infarction: Clinical Insights and Diagnostic Challenges in a Rare Case of Acute Abdominal Pain.

Intraperitoneal focal fat infarction (IFFI) is a rare condition characterized by infarction of fatty tissue within the abdominal cavity. Lesser omental infarction, a relatively rare type of IFFI, occurs when there is an infarction of fat within the lesser omentum. Patients typically present with acute abdominal pain that can mimic more serious conditions. This case report highlights the clinical presentation, diagnostic challenges, and management strategies for patients presenting to the emergency department with lesser omental infarction. A 63-year-old female presented to the emergency department with a chief complaint of epigastric abdominal pain that had been persisting for approximately a week and a half. The pain, which initially seemed like a sore muscle, became increasingly sharp and intermittent, with tenderness upon palpation of the epigastric area. Computed tomography (CT) imaging revealed an omental infarct in the lesser sac with focal inflammation in the fat of the lesser omentum. Through conservative management with analgesics and anti-inflammatory medication, the patient experienced resolution of her symptoms within a few days and had a follow-up with the gastrointestinal team several weeks later. Lesser omental infarction typically results from compromised blood flow due to torsion or thrombosis, leading to ischemia and necrosis of the fatty tissue. CT imaging is crucial for its diagnosis and reveals fat-density lesions with surrounding inflammatory changes. Conservative management is typically effective, though in rare cases, surgical intervention may be necessary when significant vital signs and electrolyte derangements occur.

Predictive value of initial Lp-PLA2, NT-proBNP, and peripheral blood-related ratios for heart failure after early onset infarction in patients with acute myocardial infarction.

OBJECTIVE: To analyze the predictive value of lipoprotein-associated phospholipase A2 (Lp-PLA2), N-terminal prohormone of brain natriuretic peptide (NT-proBNP), and peripheral blood-related ratios at the initial diagnosis for heart failure (HF) after early-onset infarction in patients with acute myocardial infarction (AMI). METHODS: This retrospective analysis included 151 patients first diagnosed with AMI at Xianyang Central Hospital from February 2020 to February 2023. Patients were classified into two groups: those who developed HF during hospitalization (HF group, n=45) and those who did not (non-HF group, NHF, n=106). Differences in Lp-PLA2, NT-proBNP, and peripheral blood ratios at initial diagnosis were compared between the groups. Binary logistic regression was used to identify independent risk factors for HF, and a nomogram model was developed based on these factors. RESULTS: HR (P=0.032), C-reactive protein (CRP) (P<0.001), alanine aminotransferase (ALT) (P=0.015), coronary artery lesion score (CALDS) (P<0.001), D-dimer (D-D) (P=0.021), neutrophil-to-lymphocyte ratio (NLR) (P<0.001), Lp-PLA2 (P<0.001), and NT-proBNP (P<0.001) were significantly higher in the HF group than in the NHF group. Left ventricular end-systolic diameter (LVESD) (P<0.001) and left ventricular end-diastolic diameter (LVEDD) (P<0.001) were significantly lower in the HF group. Multifactorial logistic regression identified HR (P=0.034), CRP (P=0.028), CALDS (P=0.007), NLR (P=0.001), Lp-PLA2 (P=0.001), and NT-proBNP (P=0.002) as independent predictors of HF. The AUCs for NLR, Lp-PLA2, and NT-proBNP were 0.806, 0.849, and 0.780, respectively. The nomogram model achieved an AUC of 0.964, significantly outperforming individual indicators per Delong's test, highlighting its superior predictive efficacy. CONCLUSION: HR, CRP, CALDS, NLR, Lp-PLA2, and NT-proBNP were identified as independent predictors of HR post-AMI myocardial infarction. The constructed nomogram model provides an effective tool for early clinical identification of high-risk patients, potentially improving prognosis and guiding therapeutic strategies.