A role for Sfrp2 in cardiomyogenesis in vivo.

Cardiomyogenesis, the process by which the body generates cardiomyocytes, is poorly understood. We have recently shown that Sfrp2 promotes cardiomyogenesis in vitro. The objective of this study was to determine if Sfrp2 would similarly promote cardiomyogenesis in vivo. To test this hypothesis, we tracked multipotent cKit(+) cells in response to Sfrp2 treatment. In control adult mice, multipotent cKit(+) cells typically differentiated into endothelial cells but not cardiomyocytes. In contrast, Sfrp2 switched the fate of these cells. Following Sfrp2 injection, multipotent cKit(+) cells differentiated solely into cardiomyocytes. Sfrp2-derived cardiomyocytes integrated into the myocardium and exhibited identical physiological properties to preexisting native cardiomyocytes. The ability of Sfrp2 to promote cardiomyogenesis was further supported by tracking EdU-labeled cells. In addition, Sfrp2 did not promote the formation of new cardiomyocytes when the cKit(+) cell population was selectively ablated in vivo using a diphtheria toxin receptor-diphtheria toxin model. Notably, Sfrp2-induced cardiomyogenesis was associated with significant functional improvements in a cardiac injury model. In summary, our study further demonstrates the importance of Sfrp2 in cardiomyogenesis.

Serum pro-B-type natriuretic peptide levels and cardiac index as adjunctive tools of blunt cardiac injury.

BACKGROUND: Blunt cardiac injury (BCI) has a variety of symptoms that may be a potentially life-threatening injury that can lead to death. Depending on the diagnosis of BCI, treatment direction and length of stay may vary. In addition, the utility of other diagnostic tests for cardiac disease as diagnostic tools for BCI remain unclear. The purpose of this study was to investigate the competence of N-terminal pro-B-type natriuretic peptide (NT pro-BNP) and cardiac index (C.I) as adjunctive diagnostic tools for BCI. METHODS: From January 2018 to March 2020, severe trauma patients with sternum fracture who were admitted to the traumatic intensive care unit (TICU) were included this study. Patients with sternum fracture, 18 years of age or older, and with an injury severity score > 16 who required intensive care were included. Invasive measurement for the analysis of the pulse contour for C.I monitoring and intravenous blood sampling for NT pro-BNP measurement were performed. Sampling and 12-lead electrocardiogram were performed at different time points as follows: immediately after TICU admission and at 24 h and 48 h after trauma. RESULTS: Among 103; 33 patients with factors that could affect NT pro-BNP were excluded; therefore, 63 patients were included in this study. According to the American Association for the Surgery of Trauma Cardiac Injury Scale, 33 patients were diagnosed with non-BCI, and 30 patients constituted with BCI. The median ages of the patients were 58 (52-69), and 60 (45-69) years in the non-BCI and BCI groups, respectively (p = 0.77). The median NT pro-BNP values were higher in the BCI group on admission, hospital day (HD) 2, and HD 3, however, no statistical difference was observed (125 (49-245) vs. 130 (47-428) pg/mL, p = 0.08, 124 (68-224) vs. 187 (55-519) pg/mL, p = 0.09, and 121(59-225) vs. 133 (56-600) pg/mL, p = 0.17, respectively). On the contrary, significantly lower values were observed in the median C.I measurement on admission and HD 3 in the BCI group (3.2 (2.8-3.5) vs. 2.6 (2.3-3.5) L/min/m2, p < 0.01 and 3.2 (3.1-3.9) vs. 2.9 (2.4-3.2) L/min/m2, p < 0.01, respectively); however, no significant difference was observed on HD 2 (3.4 (3.0-3.7) vs. 2.6 (2.4-3.4) L/min/m2, p = 0.17), Furthermore, The median lactate levels in the BCI group upon admission, HD 2, and HD 3 were significantly higher than those in the non-BCI group (1.8 (1.1-2.6) vs. 3.1 (2.1-4.4) mmol/L, p < 0.01; 1.3 (0.8-2.3) vs. 3.0 (2.2-4.7) mmol/L, p < 0.01; and 1.5 (0.9-1.5) vs. 2.2 (1.3-3.7) mmol/L, p < 0.01, respectively). CONCLUSION: Consecutive values of NT pro-BNP and C.I show no correlation with ECG-based BCI diagnosis. However, lactate level measurement may help in the early recognition of BCI as an adjunctive tool. It should be noted that this is a hypothesis-generating study for BCI diagnosis. Further studies should be conducted in larger populations with a prospective approach.

Exercise-Induced Cardiac Troponin Elevations: From Underlying Mechanisms to Clinical Relevance.

Serological assessment of cardiac troponins (cTn) is the gold standard to assess myocardial injury in clinical practice. A greater magnitude of acutely or chronically elevated cTn concentrations is associated with lower event-free survival in patients and the general population. Exercise training is known to improve cardiovascular function and promote longevity, but exercise can produce an acute rise in cTn concentrations, which may exceed the upper reference limit in a substantial number of individuals. Whether exercise-induced cTn elevations are attributable to a physiological or pathological response and if they are clinically relevant has been debated for decades. Thus far, exercise-induced cTn elevations have been viewed as the only benign form of cTn elevations. However, recent studies report intriguing findings that shed new light on the underlying mechanisms and clinical relevance of exercise-induced cTn elevations. We will review the biochemical characteristics of cTn assays, key factors determining the magnitude of postexercise cTn concentrations, the release kinetics, underlying mechanisms causing and contributing to exercise-induced cTn release, and the clinical relevance of exercise-induced cTn elevations. We will also explain the association with cardiac function, correlates with (subclinical) cardiovascular diseases and exercise-induced cTn elevations predictive value for future cardiovascular events. Last, we will provide recommendations for interpretation of these findings and provide direction for future research in this field.

Effect of Colchicine on Myocardial Injury in Acute Myocardial Infarction.

BACKGROUND: Inflammation is a key factor of myocardial damage in reperfused ST-segment-elevation myocardial infarction. We hypothesized that colchicine, a potent anti-inflammatory agent, may reduce infarct size (IS) and left ventricular (LV) remodeling at the acute phase of ST-segment-elevation myocardial infarction. METHODS: In this double-blind multicenter trial, we randomly assigned patients admitted for a first episode of ST-segment-elevation myocardial infarction referred for primary percutaneous coronary intervention to receive oral colchicine (2-mg loading dose followed by 0.5 mg twice a day) or matching placebo from admission to day 5. The primary efficacy outcome was IS determined by cardiac magnetic resonance imaging at 5 days. The relative LV end-diastolic volume change at 3 months and IS at 3 months assessed by cardiac magnetic resonance imaging were among the secondary outcomes. RESULTS: We enrolled 192 patients, 101 in the colchicine group and 91 in the control group. At 5 days, the gadolinium enhancement-defined IS did not differ between the colchicine and placebo groups with a mean of 26 interquartile range (IQR) [16-44] versus 28.4 IQR [14-40] g of LV mass, respectively (P=0.87). At 3 months follow-up, there was no significant difference in LV remodeling between the colchicine and placebo groups with a +2.4% (IQR, -8.3% to 11.1%) versus -1.1% (IQR, -8.0% to 9.9%) change in LV end-diastolic volume (P=0.49). Infarct size at 3 months was also not significantly different between the colchicine and placebo groups (17 IQR [10-28] versus 18 IQR [10-27] g of LV mass, respectively; P=0.92). The incidence of gastrointestinal adverse events during the treatment period was greater with colchicine than with placebo (34% versus 11%, respectively; P=0.0002). CONCLUSIONS: In this randomized, placebo-controlled trial, oral administration of high-dose colchicine at the time of reperfusion and for 5 days did not reduce IS assessed by cardiac magnetic resonance imaging. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03156816.

Impact of bioprosthetic valve type on peri-procedural myocardial injury and mortality after transcatheter aortic valve replacement.

Peri-procedural myocardial injury (PPMI) is a common complication after transcatheter valve replacement (TAVR), often remaining clinically silent. The role of valve type on PPMI and the association between PPMI and mortality are still unclear. We sought to evaluate predictors and outcome of PPMI after TAVR, and the impact of self-expandable valve (SEV) vs. balloon-expandable valve (BEV) deployment on PPMI. Consecutive patients who underwent successful TAVR in a single-center from January 2014 to December 2019 were included. PPMI was defined according to a modified Valve Academic Research Consortium (VARC)-2 definition as a post-procedure elevation of troponin (with a peak value ≥ 15-times the upper-reference limit) < 72 h after TAVR. We included 596 patients, of whom 258 (43.3%) were men. Mean age was 83.4 ± 5.5 years. We deployed 368 (61.7%) BEV and 228 (38.3%) SEV. PPMI was observed in 471 (79.0%) patients. At multivariable analysis, SEV (OR 2.70, 95% CI 1.64-4.55, p < 0.001), creatinine clearance (OR 0.98, 95% CI 0.97-1.00, p = 0.011), and baseline ejection fraction (OR 1.05, 95% CI 1.02-1.07, p < 0.001) were independent predictors of PPMI; these findings were also confirmed using a propensity-weighted analysis. Thirty-day and 1-year all-cause mortality rates were 2.5% and 8.1%, respectively. No associations between PPMI and 30-day (p = 0.488) or 1-year (p = 0.139) all-cause mortality were found. Independent predictors of 30-day mortality were increasing EUROSCORE II (HR 1.16 per score point, 95% CI 1.08-1.19, p < 0.001) and life-threatening/major bleeding complications (HR 5.87, 95% CI 1.28-26.58, p = 0.019), whereas EUROSCORE II (HR 1.08, 95% CI 1.04-1.13, p = 0.031) and acute kidney injury (HR 2.59, 95% CI 1.20-5.35, p = 0.020) were related to 1-year mortality. PPMI is frequent after TAVR, but it does not affect 30-day or 1-year all-cause mortality. SEV implantation is associated with an increased frequency of PPMI.

Assessment and Treatment of Patients With Type 2 Myocardial Infarction and Acute Nonischemic Myocardial Injury.

Although coronary thrombus overlying a disrupted atherosclerotic plaque has long been considered the hallmark and the primary therapeutic target for acute myocardial infarction (MI), multiple other mechanisms are now known to cause or contribute to MI. It is further recognized that an MI is just one of many types of acute myocardial injury. The Fourth Universal Definition of Myocardial Infarction provides a taxonomy for acute myocardial injury, including 5 subtypes of MI and nonischemic myocardial injury. The diagnosis of MI is reserved for patients with myocardial ischemia as the cause of myocardial injury, whether attributable to acute atherothrombosis (type 1 MI) or supply/demand mismatch without acute atherothrombosis (type 2 MI). Myocardial injury in the absence of ischemia is categorized as acute or chronic nonischemic myocardial injury. However, optimal evaluation and treatment strategies for these etiologically distinct diagnoses have yet to be defined. Herein, we review the epidemiology, risk factor associations, and diagnostic tools that may assist in differentiating between nonischemic myocardial injury, type 1 MI, and type 2 MI. We identify limitations, review new research, and propose a framework for the diagnostic and therapeutic approach for patients who have suspected MI or other causes of myocardial injury.

[Analysis of myocardial injury in patients with COVID-19 and association between concomitant cardiovascular diseases and severity of COVID-19].

Objective: To evaluate the cardiovascular damage of patients with COVID-19, and determine the correlation of serum N-terminal pro B-type natriuretic peptide (NT-proBNP） and cardiac troponin-I (cTnI） with the severity of COVID-19, and the impact of concomitant cardiovascular disease on severity of COVID-19 was also evaluated. Methods: A cross-sectional study was designed on 150 consecutive patients with COVID-19 in the fever clinic of Tongji Hospital in Wuhan from January 19 to February 13 in 2020, including 126 mild cases and 24 cases in critical care. Both univariate and multivariate logistic regression were used to analyze the correlation of past medical history including hypertension, diabetes and coronary heart disease (CHD）, as well as the levels of serum NT-proBNP and cTnI to the disease severity of COVID-19 patients. Results: Age, hypersensitive C-reactive protein(hs-CRP) and serum creatinine levels of the patients were higher in critical care cases than in mild cases(all P<0.05). Prevalence of male, elevated NT-proBNP and cTnI, hypertension and coronary heart disease were significantly higher in critical cases care patients than in the mild cases(all P<0.05). Univariate logistic regression analysis showed that age, male, elevated NT-proBNP, elevated cTnI, elevated hs-CRP, elevated serum creatinine, hypertension, and CHD were significantly correlated with critical disease status(all P<0.05). Multivariate logistic regression analysis showed that elevated cTnI(OR=26.909，95%CI 4.086-177.226，P=0.001) and CHD (OR=16.609，95%CI 2.288-120.577，P=0.005) were the independent risk factors of critical disease status. Conclusions: COVID-19 can significantly affect the heart function and lead to myocardial injury. The past medical history of CHD and increased level of cTnI are 2 independent determinants of clinical disease status in patients with COVID-19.

[Clinical feature changes of a COVID-19 patient from mild to critical condition and cardiopulmonary pathological results].

Objective: To analyse the clinical history, laboratory tests and pathological data of a patient who suffered from novel coronavirus pneumonia(COVID-19) and provide reference for the clinical treatment of similar cases. Methods: Data of clinical manifestation, laboratory examination, bronchoscopy, echocardiography and cardiopulmonary pathological results were retrospectively reviewed in a case of COVID-19 with rapid exacerbation from mild to critical condition. Results: This patient hospitalized at day 9 post 2019 novel coronavirus(2019-nCoV) infection, experienced progressive deterioration from mild to severe at day 12, severe to critical at day 18 and underwent extracorporeal membrane oxygenation(ECMO) and continuous renal replacement therapy(CRRT) as well as heart lung transplantation during day 28-45 post infection, and died at the second day post heart and lung transplantation. The patient had suffered from hypertension for 8 years. At the early stage of the disease, his symptoms were mild and the inflammatory indices increased and the lymphocyte count decreased continuously. The patient's condition exacerbated rapidly with multi-organ infections, and eventually developed pulmonary hemorrhage and consolidation, pulmonary hypertension, right heart failure, malignant ventricular arrhythmias, liver dysfunction, etc. His clinical manifestations could not be improved despite viral RNAs test results became negative. The patient underwent lung and heart transplantation and finally died of multi organ failure at the second day post lung and heart transplantation. Pathological examination indicated massive mucus, dark red secretions and blood clots in bronchus. The pathological changes were mainly diffused pulmonary hemorrhagic injuries and necrosis, fibrosis, small vessel disease with cardiac edema and lymphocyte infiltration. Conclusions: The clinical course of severe COVID-19 can exacerbate rapidly from mild to critical with lung, liver and heart injuries.

[Predictive value of early detection of hs-cTnI and sST2 for secondary cardiac damage in severe acute organophosphorus pesticide poisoning].

Objective: To investigate the value of high-sensitivity cardiac troponin I (hs-cTnI) and soluble suppression of tumorigenicity 2 (sST2) in predicting cardiac complications of severe acute organophosphorus pesticide poisoning (SAOPP) . Methods: All 274 SAOPP patients from September 2014 to February 2019 were selected. According to the results of hs-cTnI detection, the patients were divided into non-elevated troponin group (78 cases) and troponin elevation group (196 cases) at 1 hour after admission. 3 days after admission, there were 109 cases of complication and 165 cases of non-complication according to the presence or absence of cardiac complications. The changes of hs-cTnI, sST2, N-terminal B-type brain natriuretic peptide (NT proBNP) , acute physiology and chronic health (APACHE-Ⅱ) , cholinesterase activity, left ventricular ejection fraction (LVEF) , short axis shortening rate (FS) were observed and analyzed. The predictive value of hs-cTnI and sST2 were evaluated by receiver operating characteristic curve (ROC) analysis. Results: The sST2 level in patients with troponin elevation group was significantly higher than that in non-elevated troponin group (P<0.05) . Compared with the non-complication and non-elevated troponin group, the patients with non-complication and troponin elevation group had elevated hs-cTnI, sST2 and decreased cholinesterase (P<0.05) . Compared with other groups, the hs-cTnI, sST2, NT-proBNP, and APACHE-Ⅱ scores in the complication and troponin elevation group were significantly increased, and cholinesterase was significantly reduced (P<0.05) . In the non-complication group, LVEF and FS were in the normal range, and there was no significant difference between the groups (P>0.05) . Compared with other groups, the LVEF and FS of patients with elevated troponin in the complications group were significantly decreased (P<0.05) . Correlation analysis showed that hs-cTnI and sST2 were positively correlated in patients with SAOPP complications (r=0.725, P<0.01) . hs-cTnI, sST2 and APACHE-Ⅱ scores were positively correlated in the complications group (r=0.846, 0.885, P<0.01) . ROC results showed that the areas under the curve for predicting SAOPP secondary heart damage of hs-cTnI (1 hour after admission) and sST2 (3 days after admission) were 0.945 and 0.833, respectively. Conclusion: hs-cTnI and sST2 may have important clinical value in the early diagnosis and prognosis evaluation of patients with SAOPP secondary cardiac damage.

Perioperative Myocardial Injury After Noncardiac Surgery: Incidence, Mortality, and Characterization.

BACKGROUND: Perioperative myocardial injury (PMI) seems to be a contributor to mortality after noncardiac surgery. Because the vast majority of PMIs are asymptomatic, PMI usually is missed in the absence of systematic screening. METHODS: We performed a prospective diagnostic study enrolling consecutive patients undergoing noncardiac surgery who had a planned postoperative stay of ≥24 hours and were considered at increased cardiovascular risk. All patients received a systematic screening using serial measurements of high-sensitivity cardiac troponin T in clinical routine. PMI was defined as an absolute high-sensitivity cardiac troponin T increase of ≥14 ng/L from preoperative to postoperative measurements. Furthermore, mortality was compared among patients with PMI not fulfilling additional criteria (ischemic symptoms, new ECG changes, or imaging evidence of loss of viable myocardium) required for the diagnosis of spontaneous acute myocardial infarction versus those that did. RESULTS: From 2014 to 2015 we included 2018 consecutive patients undergoing 2546 surgeries. Patients had a median age of 74 years and 42% were women. PMI occurred after 397 of 2546 surgeries (16%; 95% confidence interval, 14%-17%) and was accompanied by typical chest pain in 24 of 397 patients (6%) and any ischemic symptoms in 72 of 397 (18%). Crude 30-day mortality was 8.9% (95% confidence interval [CI], 5.7-12.0) in patients with PMI versus 1.5% (95% CI, 0.9-2.0) in patients without PMI (P<0.001). Multivariable regression analysis showed an adjusted hazard ratio of 2.7 (95% CI, 1.5-4.8) for 30-day mortality. The difference was retained at 1 year with mortality rates of 22.5% (95% CI, 17.6-27.4) versus 9.3% (95% CI, 7.9-10.7). Thirty-day mortality was comparable among patients with PMI not fulfilling any other of the additional criteria required for spontaneous acute myocardial infarction (280/397, 71%) versus those with at least 1 additional criterion (10.4%; 95% CI, 6.7-15.7, versus 8.7%; 95% CI, 4.2-16.7; P=0.684). CONCLUSIONS: PMI is a common complication after noncardiac surgery and, despite early detection during routine clinical screening, is associated with substantial short- and long-term mortality. Mortality seems comparable in patients with PMI not fulfilling any other of the additional criteria required for spontaneous acute myocardial infarction versus those patients who do. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifier: NCT02573532.

[Midterm outcomes of surgical treatment of traumatic severe tricuspid insufficiency].

Objective: To investigate the indication and midterm outcomes of surgical treatment of traumatic tricuspid insufficiency. Methods: Totally 19 patients with traumatic tricuspid insufficiency who underwent surgical treatment at Department of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University from January 2002 to January 2018 were included in this retrospective study. There were 12 male and 7 female patients, aged (43.1±12.9) years (range: 17-68 years). The main causes of traumatic tricuspid insufficiency included blunt chest trauma following high-speed vehicle accidents (17 patients) and high-fall trauma (2 patients). The preoperative New York Heart Association functional class was class Ⅱ in 5 patients, class Ⅲ in 12 patients, and class Ⅳ in 2 patients. The mechanism of tricuspid insufficiency included anterior chordal rupture in 9 patients, anterior papillary muscle rupture in 3 patients, anterior and posterior chordal or papillary muscle rupture in 4 patients, laceration of leaflet combined with chordal rupture in 2 patients and infection combined with anterior papillary muscle rupture in 1 patient. Anular dilation and enlargement of the right ventricle were observed in all the patients. Paired t test was used to evaluate the echocardiogratic results at preoperation, postoperation and follow-up. Independent sample rank sum test was used to evaluate the intervals between trauma and surgery in tricuspid valve repair group and tricuspid valve replacement group. Results: Tricuspid valve repair was successful in 8 patients, and 11 patients underwent valve replacement. Among the patients who underwent valve replacement, 6 patients received mechanical valve and 5 received bioprosthetic valve. The interval from trauma to surgery of the valve repair group and valve replacement group were 8.5(10.0) months (range: 0.1-13.0 months) and 72.0 (108.0) months (range: 2.0-228.0 months), respectively. Concomitant procedures included debridement in scalp trauma (1 patient), internal fixation of femoral fracture (1 patient). One patient died from liver failure 10 days after operation and the remaining patients survived. Eighteen patients were followed up for (94±50) months, 15 patients were in New York Heart Association functional class Ⅰ and 3 patients in class Ⅱ. One patient received redo-tricuspid valve replacement because of mechanical valve failure at the 11 years of follow-up. Conclusions: The midterm outcomes of surgical treatment of severe traumatic tricuspid insufficiency were satisfactory. Early diagnosis and surgical invention were recommended to achieve successful valve repair.

Expression of Cx43 and Cx45 in Cardiomyocytes of an Overworked Rat Model.

ABSTRACT: Objective To study the effect of overwork stress response on the expression of connexin 43（Cx43） and connexin 45（Cx45） in cardiomyocytes and on cardiac function. Methods The experimental animals were divided into control group, overworked 1-month group and overworked 2-month group. A overworked rat model was established by forcing swimming of overworked group. The expressions of Cx43 and Cx45 in myocardial tissues of experimental animals were detected by Western blotting, while the corresponding myocardial tissues were stained with hematoxylin-eosin （HE） staining and Masson's staining, then histologically observed. Results Western blotting results showed that, compared with the control group, Cx43 expression in myocardial tissues of overworked rats decreased while Cx45 expression increased. HE staining and Masson's staining results showed that hypertrophy, rupture and interstitial fiber tissue hyperplasia were observed in myocardial fibers of overworked rats. Conclusion Overwork stress response may affect cardiac function as an independent factor and may even cause heart failure or arrhythmias and lead to death.

Insights from molecular signature of in vivo cardiac c-Kit(+) cells following cardiac injury and ß-catenin inhibition.

There is much interest over resident c-Kit(+) cells in tissue regeneration. Their role in cardiac regeneration has been controversial. In this study we aim to understand the in vivo behavior of cardiac c-Kit(+) cells at baseline and after myocardial infarction and in response to Sfrp2. This approach can accurately study the in vivo transcript expressions of these cells in temporal response to injury and overcomes the limitations of the in vitro approach. RNA-seq was performed with c-Kit(+) cells and cardiomyocytes from healthy non-injured mice as well as c-Kit(+) cells from 1 day post-MI and 12 days post-MI mice. When compared to in vivo c-Kit(+) cells isolated from a healthy non-injured mouse heart, cardiomyocytes were enriched in transcripts that express anion channels, cation channels, developmental/differentiation pathway components, as well as proteins that inhibit canonical Wnt/ß-catenin signaling. Myocardial infarction (MI) induced in vivo c-Kit(+) cells to transiently adopt the cardiomyocyte-specific signature: expression of a number of cardiomyocyte-specific transcripts was maximal 1 day post-MI and declined by 12 days post-MI. We next studied the effect of ß-catenin inhibition on in vivo c-Kit(+) cells by administering the Wnt inhibitor Sfrp2 into the infarct border zone. Sfrp2 both enhanced and sustained cardiomyocyte-specific gene expression in the in vivo c-Kit(+) cells: expression of cardiomyocyte-specific transcripts was higher and there was no decline in expression by 12 days post-MI. Further analysis of the biology of c-Kit(+) cells identified that culture induced a significant and irreversible change in their molecular signature raising questions about reliability of in vitro studies. Our findings provide evidence that MI induces in vivo c-Kit(+) cells to adopt transiently a cardiomyocyte-specific pattern of gene expression, and Sfrp2 further enhances and induces sustained gene expression. Our approach is important for understanding c-Kit(+) cells in cardiac regeneration and also has broad implications in the investigation of in vivo resident stem cells in other areas of tissue regeneration.

Cardiac Perforation by Migrated Fractured Strut of Inferior Vena Cava Filter Mimicking Acute Coronary Syndrome.

We present a rare late complication after inferior vena cava filter (IVC) placement. A 52-year-old woman with an IVC presented with sudden onset of chest pain. Cardiac catheterisation and echocardiography revealed an embolised IVC filter strut penetrating the right ventricle. Endovascular retrieval was considered but deemed unsafe due to proximity to the right coronary artery and concern for migration to pulmonary circulation. Urgent removal of the strut was performed via sternotomy. The postoperative course was uneventful. Two weeks later, she was asymptomatic. Minimally invasive approaches have been described for retrieval of intact IVC filters that have migrated to the right heart but not for embolised filter fragments. We recommend traditional sternotomy as the preferred method of retrieval as it limits the likelihood of further migration or trauma.

Penetrating cardiac injury resulting in a bullet embolus: a case report.

Bullet embolism is a potential complication of a gunshot wound, especially with a low-velocity missile. This is because the trajectory of the low-velocity bullet can be significantly slowed as it passes through tissue. An unusual form of travel can occur in which the bullet enters the vasculature but does not have enough kinetic energy to create a through-and-through wound, leading it to remain inside the vasculature. Once inside the vasculature, the bullet could migrate to different parts of the body, potentially causing complications such as ischemia, becoming a source of thromboembolism, or functioning as a nidus for infection. The management of a bullet embolism varies from case to case, as each patient with this issue has a unique body habitus that can result in infinite possibilities of the trajectory and destination of the bullet embolus. Additional damage to surrounding vasculature or tissue can occur, as well as embolization of the bullet to critical areas of the body. Here we present the case of a 72-year-old man who had a self-inflicted gunshot wound to the chest with a low-velocity bullet, which penetrated the right atrium of the heart. It traveled into the venous vasculature through the right atrium, into the inferior vena cava, and eventually settled in the right internal iliac vein. He refused further intervention and management after initial workup and resuscitation.

Right Ventricular Perforation by Fractured Sternal Wires: A Narrative Review.

INTRODUCTION: Migration of a fragmented sternal wire is an unusual and rare phenomenon following cardiovascular surgery. It can present with variable clinical presentations, ranging from incidental findings to hemodynamic instability. Here, we described two cases of fragmented sternal wire migration to the right ventricle. METHODS: Retrospective review of the clinical course of two patients presenting with a fragmented sternal wire embedded in the right ventricle after sternotomy for cardiovascular surgery. We also conducted a literature review to identify similar cases, compared them based on reported clinical variables, and discussed the role of diagnostic imaging and management. RESULTS: We identified 13 patients (11 from the literature), of which 85% were men, and the median age was 64 years; 46% presented with hemorrhagic shock, another 46% had other cardiovascular symptoms, and 8% were asymptomatic. The presentation was bimodal, 54% presented within three weeks of the original sternotomy, while 46% had sternotomy more than a year before. Sternal dehiscence/instability was observed in 61% of cases. Computed tomography scan was the most common diagnostic modality (54%). Two patients did not undergo surgery, and two others died after surgery, while others had a successful surgical repair. CONCLUSION: Migration of a fragmented sternal wire is a phenomenon presented on a dehisced and unstable sternum that can occur days or years after sternotomy. These findings and the associated cardiac injury can be easily missed on computed tomography scan reporting if one is not looking for it. After diagnosis, treatment should be individualized according to the patient's needs.

Long noncoding RNA MCM3AP-AS1 attenuates sepsis-induced cardiomyopathy by improving inflammation, oxidative stress, and mitochondrial function through mediating the miR-501-3p/CADM1/STAT3 axis.

Oxidative stress and inflammation are highly important for sepsis-mediated myocardial damage. The long noncoding RNA (lncRNA) MCM3AP-AS1 is involved in inflammatory diseases, but its function in acute myocardial injury during sepsis has not been fully elucidated. LPS and cecal ligation and puncture (CLP) were used to construct in vitro and in vivo sepsis-induced myocardial damage models, respectively. qRT-PCR was used to evaluate alterations in MCM3AP-AS1 and miR-501-3p alterations. After the MCM3AP-AS1 and miR-501-3p knockdown or overexpression models were established, the viability, apoptosis, inflammation, oxidative stress, and mitochondrial function of the myocardial cells were examined. Dual luciferase activity assay, RNA immunoprecipitation, and fluorescence in situ hybridization (FISH) confirmed the correlation among MCM3AP-AS1, miR-501-3p, and CADM1. Previous studies revealed that MCM3AP-AS1 was downregulated in sepsis patients, myocardial cells treated with LPS, and in the CLP mouse sepsis model, whereas miR-501-3p expression was increased. MCM3AP-AS1 overexpression hampered myocardial damage mediated by LPS and abated inflammation, oxidative stress, and mitochondrial dysfunction in myocardial cells and THP-1 cells. In contrast, MCM3AP-AS1 knockdown or miR-501-3p overexpression promoted all the effects of LPS. In vivo, MCM3AP-AS1 overexpression increased the survival rate of CLP mice; ameliorated myocardial injury; decreased the levels of TNF-α, IL-1ß, IL-6, iNOS, COX2, ICAM1, VCAM1, PGE2, and MDA; and increased the levels of SOD, GSH-PX, Nrf2, and HO-1. Mechanistic studies demonstrated that MCM3AP-AS1 acted as a competitive endogenous RNA to repress miR-501-3p, enhance CADM1 expression, and dampen STAT3/nuclear factor-kappaB (NF-κB) activation. MCM3AP-AS1 suppresses myocardial injury elicited by sepsis by mediating the miR-501-3p/CADM1/STAT3/NF-κB axis.

Risk factors for myocardial injury during living donor liver transplantation in pediatric patients with biliary atresia.

BACKGROUND: Cold ischemia-reperfusion of the liver is an inevitable occurrence in liver transplantation that may also cause damage to the heart. Perioperative myocardial injury during liver transplantation can increase the incidence of postoperative mortality, but there is little research on the incidence of myocardial injury in children who undergo living donor liver transplantation (LDLT). Therefore, this study mainly explores the independent risk factors for myocardial injury in children who undergo LDLT. AIM: To analyze the data of children who underwent LDLT to determine the risk factors for intraoperative myocardial injury. METHODS: We retrospectively analyzed the inpatient records of pediatric patients who underwent LDLT in Tianjin First Central Hospital from January 1, 2020, to January 31, 2022. Recipient-related data and donor-related data were collected. The patients were divided into a myocardial injury group and a nonmyocardial injury group according to the value of the serum cardiac troponin I at the end of surgery for analysis. Univariate analysis and multivariate logistic regression were used to evaluate the risk factors for myocardial injury during LDLT in pediatric patients. RESULTS: A total of 302 patients met the inclusion criteria. The myocardial injury group had 142 individuals (47%), and the nonmyocardial injury group included 160 patients (53%). Age, height, and weight were significantly lower in the myocardial injury group (P < 0.001). The pediatric end-stage liver disease (PELD) score, total bilirubin, and international standardized ratio were significantly higher in the myocardial injury group (P < 0.001). The mean arterial pressure, lactate, hemoglobin before reperfusion, duration of the anhepatic phase, cold ischemic time, incidence of postreperfusion syndrome (PRS), and fresh frozen plasma transfusion were significantly different between the two groups (P < 0.05). The postoperative intensive care unit stay and peak total bilirubin values in the first 5 d after LDLT were significantly higher in the myocardial injury group (P < 0.05). The pediatric patients with biliary atresia in the nonmyocardial injury group who underwent LDLT had a considerably higher one-year survival rate than those in the myocardial injury group (P = 0.015). Multivariate logistic regression revealed the following independent risk factors for myocardial injury: a high PELD score [odds ratio (OR) = 1.065, 95% confidence interval (CI): 1.013-1.121; P = 0.014], a long duration of the anhepatic phase (OR = 1.021, 95%CI: 1.003-1.040; P = 0.025), and the occurrence of intraoperative PRS (OR = 1.966, 95%CI: 1.111-3.480; P = 0.020). CONCLUSION: A high PELD score, a long anhepatic phase duration, and the occurrence of intraoperative PRS were independent risk factors for myocardial injury during LDLT in pediatric patients with biliary atresia.