Penetrating cardiac injury after percutaneous breast core-needle biopsy, unusual life-threatening complication: a case report.

BACKGROUND: Complications after percutaneous breast biopsy are infrequent but may include hematoma, pseudoaneurysm formation, persistent pain, infection, delayed wound healing, vasovagal reaction, hemothorax, pneumothorax, and neoplastic seeding. The risk factors include tumor factors (size, location, vascularity), procedure-related factors (needle diameter, number of biopsies), and interventionist experience. There has been no previous report of a fatal complication resulting from percutaneous breast biopsy. CASE PRESENTATION: We report a 54-year-old Asian woman with a 3 cm BI-RADS® 4B left breast mass in the lower-inner quadrant who was biopsied by a 16 G needle under ultrasound guidance at a province hospital. She experienced dizziness and near-syncope afterward. The initial evaluation showed evidence of cardiac tamponade with hemodynamic instability. She underwent urgent subxiphoid pericardial window and was transferred to our facility. We brought her directly to the operating room to perform an explorative median sternotomy and found a 0.2 cm hole in the right ventricle. The injured site was successfully repaired without cardiopulmonary bypass. Postoperative echocardiography demonstrated mild right ventricular dysfunction without evidence of septal or valvular injury. She survived with no significant complications. DISCUSSION: This case might be the first report of a life-threatening complication related to percutaneous breast core-needle biopsy. The rapid pericardial release is key to the survival of cardiac tamponade. The patient subsequently required cardiac repair and monitoring to avoid long-term complications. In this report, we suggested a safe biopsy method, complications recognition, and appropriate management of penetrating cardiac injury. CONCLUSION: Penetrating cardiac injury resulting from percutaneous breast biopsy is extremely rare but can occur. A biopsy must be done cautiously, and worst-case management should promptly be considered.

Capsinoids Increase Antioxidative Enzyme Activity and Prevent Obesity-Induced Cardiac Injury without Positively Modulating Body Fat Accumulation and Cardiac Oxidative Biomarkers.

BACKGROUND/OBJECTIVES: Capsinoids are potential antioxidant agents capable of reducing oxidative damage and the resulting complications triggered by obesity. Thus, this study aimed to investigate the effects of capsinoids on adiposity and biomarkers of cardiac oxidative stress in obese rats induced by a high-fat diet. METHODS: Male Wistar rats were exposed to a high-fat diet for 27 consecutive weeks. After the characterization of obesity (week 19), some of the obese animals began to receive capsinoids (10 mg/kg/day) by orogastric gavage. Adiposity and comorbidities were assessed. In the heart, remodeling, injury, and biomarkers of oxidative stress were determined. RESULTS: The treatment did not reduce obesity-induced adiposity but was efficient in reducing cholesterol levels. Capsinoid treatment did not cause a difference in heart and LV mass, despite having reduced troponin I concentrations. Furthermore, capsinoids did not reduce the increase in the advanced oxidation of protein products and carbonylated proteins caused by obesity in cardiac tissue. In addition, obese rats treated with capsinoids presented high levels of malondialdehyde and greater antioxidant enzyme activity compared to untreated obese rats. CONCLUSIONS: In conclusion, treatment with capsinoids increases antioxidative enzyme activity and prevents obesity-induced cardiac injury without positively modulating body fat accumulation and cardiac oxidative biomarkers.

Involvement of neutrophils and macrophages in exhaustive exercise-induced liver, kidney, heart, and lung injuries.

Moderate exercise is effective for maintaining or improving overall health. However, excessive exercise that exhausts the adaptive reserve of the body or its ability to positively respond to training stimuli can induce tissue damage and dysfunction of multiple organs and systems. Tissue injury, inflammation, and oxidative stress are reportedly induced in the skeletal muscles, liver, and kidneys after exercise. However, the precise mechanisms underlying acute tissue injury after intense exercise have not yet been fully elucidated. Studies using various experimental models of acute tissue injury, other than intense exercise, have demonstrated infiltration of inflammatory cells, including neutrophils and macrophages. These cells infiltrate injured tissues and induce inflammatory and oxidative stress responses by producing inflammatory cytokines and reactive oxygen species, thereby exacerbating tissue injury. In addition to the activation of blood neutrophils and increase in their levels during and/or after prolonged or intense exercise, chemokines that contribute to leukocyte migration are released, facilitating the migration of neutrophils and monocytes into tissues. Therefore, neutrophils and macrophages, activated by exhaustive exercise, may infiltrate tissues and contribute to exhaustive exercise-induced tissue injury. Recently, the contributions of neutrophils and macrophages to various tissue injuries caused by exhaustive exercise have been reported. In this review, we summarize the involvement of neutrophils and monocytes/macrophages in exhaustive exercise-induced non-skeletal muscle tissue injury. In addition, we present novel data demonstrating the contribution of neutrophils and macrophages to exhaustive exercise-induced cardiac and pulmonary injuries. Our study findings and the evidence presented in this review suggest that neutrophils and macrophages may play pivotal roles in exhaustive exercise-induced tissue injuries.

Coronary Plaque Characterization with T1-weighted MRI and Near-Infrared Spectroscopy to Predict Periprocedural Myocardial Injury.

Purpose To clarify the predominant causative plaque constituent for periprocedural myocardial injury (PMI) following percutaneous coronary intervention: (a) erythrocyte-derived materials, indicated by a high plaque-to-myocardium signal intensity ratio (PMR) at coronary atherosclerosis T1-weighted characterization (CATCH) MRI, or (b) lipids, represented by a high maximum 4-mm lipid core burden index (maxLCBI4 mm) at near-infrared spectroscopy intravascular US (NIRS-IVUS). Materials and Methods This retrospective study included consecutive patients who underwent CATCH MRI before elective NIRS-IVUS-guided percutaneous coronary intervention at two facilities. PMI was defined as post-percutaneous coronary intervention troponin T values greater than five times the upper reference limit. Multivariable analysis was performed to identify predictors of PMI. Finally, the predictive capabilities of MRI, NIRS-IVUS, and their combination were compared. Results A total of 103 lesions from 103 patients (median age, 72 years [IQR, 64-78]; 78 male patients) were included. PMI occurred in 36 lesions. In multivariable analysis, PMR emerged as the strongest predictor (P = .001), whereas maxLCBI4 mm was not a significant predictor (P = .07). When PMR was excluded from the analysis, maxLCBI4 mm emerged as the sole independent predictor (P = .02). The combination of MRI and NIRS-IVUS yielded the largest area under the receiver operating curve (0.86 [95% CI: 0.64, 0.83]), surpassing that of NIRS-IVUS alone (0.75 [95% CI: 0.64, 0.83]; P = .02) or MRI alone (0.80 [95% CI: 0.68, 0.88]; P = .30). Conclusion Erythrocyte-derived materials in plaques, represented by a high PMR at CATCH MRI, were strongly associated with PMI independent of lipids. MRI may play a crucial role in predicting PMI by offering unique pathologic insights into plaques, distinct from those provided by NIRS. Keywords: Coronary Plaque, Periprocedural Myocardial Injury, MRI, Near-Infrared Spectroscopy Intravascular US Supplemental material is available for this article. © RSNA, 2024.

Stroke heart injury: the effect of cerebral reperfusion treatment. A 3-year retrospective study.

BACKGROUND: Cardiac involvement following an acute stroke (Stroke Heart Syndrome-SHS) is an established complication and it is linked to the involvement of sympathetic activation, inflammation, and neuro-endocrine response. Troponin "rise and fall pattern" > 30% is one marker of SHS. The aim of this study was to evaluate the role of reperfusion treatments in the prevention/pathogenesis of SHS with different stroke sizes and locations (OCSP classification). METHODS: We retrospectively analyzed data of 890 patients admitted to the Stroke Unit of Trieste (Italy) between 2018 and 2020. Out of them, 411 met the inclusion criteria (acute ischemic non-lacunar stroke). Clinical data were collected for each patient, imaging characteristics, and markers of cardiac injury [troponin I (TnI), NT-proBNP, "rise and fall pattern" > 30%]. We compared different stroke subtypes according to OCSP, while evaluating any differences in patients with and without SHS. RESULTS: In treated total anterior circulation infarct (TACI) patients, the rate of SHS is lower than in non-treated TACI. Similar SHS rate was found in partial anterior (PACI) and posterior stroke (POCI), and between treated and non-treated patients. Focusing on TACI group, we compared SHS-TACI and non-SHS-TACI, we performed a univariate and multivariate analysis; treatment (OR 0.408 CI95% 0.185-0.900; p = 0.026) and diabetes (OR 2.618 CI95% 1.181-5.803; p = 0.018) were significantly associated to SHS. No clear insular effect was found in SHS development. CONCLUSIONS: In severe anterior stroke (TACI), reperfusion treatment may be effective in preventing SHS. Conversely, diabetes is an independent risk factor for SHS. PACI and POCI have similar troponin elevation rate.

Anti-CTLA-4 m2a Antibody Exacerbates Cardiac Injury in Experimental Autoimmune Myocarditis Mice By Promoting Ccl5-Neutrophil Infiltration.

The risk for suffering immune checkpoint inhibitors (ICIs)-associated myocarditis increases in patients with pre-existing conditions and the mechanisms remain to be clarified. Spatial transcriptomics, single-cell RNA sequencing, and flow cytometry are used to decipher how anti-cytotoxic T lymphocyte antigen-4 m2a antibody (anti-CTLA-4 m2a antibody) aggravated cardiac injury in experimental autoimmune myocarditis (EAM) mice. It is found that anti-CTLA-4 m2a antibody increases cardiac fibroblast-derived C-X-C motif chemokine ligand 1 (Cxcl1), which promots neutrophil infiltration to the myocarditic zones (MZs) of EAM mice via enhanced Cxcl1-Cxcr2 chemotaxis. It is identified that the C-C motif chemokine ligand 5 (Ccl5)-neutrophil subpopulation is responsible for high activity of cytokine production, adaptive immune response, NF-κB signaling, and cellular response to interferon-gamma and that the Ccl5-neutrophil subpopulation and its-associated proinflammatory cytokines/chemokines promoted macrophage (Mφ) polarization to M1 Mφ. These altered infiltrating landscape and phenotypic switch of immune cells, and proinflammatory factors synergistically aggravated anti-CTLA-4 m2a antibody-induced cardiac injury in EAM mice. Neutralizing neutrophils, Cxcl1, and applying Cxcr2 antagonist dramatically alleviates anti-CTLA-4 m2a antibody-induced leukocyte infiltration, cardiac fibrosis, and dysfunction. It is suggested that Ccl5-neutrophil subpopulation plays a critical role in aggravating anti-CTLA-4 m2a antibody-induced cardiac injury in EAM mice. This data may provide a strategic rational for preventing/curing ICIs-associated myocarditis.

Iatrogenic Atrial Septal Defect After MitraClip Transcatheter Edge-to-Edge Repair: To Close or Not to Close?

The evolution of percutaneous procedures that use transseptal puncture to treat left-sided structural heart disease has led to the emergence of iatrogenic atrial septal defects as a potential complication. These defects can result in hemodynamic decompensation and worsening clinical outcomes. Some iatrogenic atrial septal defects require immediate closure, others do not. This case report presents 2 patients who underwent transcatheter edge-to-edge mitral valve repair with transseptal puncture and required iatrogenic atrial septal defect closure (1 immediate and 1 delayed). The goal of this report is to highlight iatrogenic atrial septal defect assessment and the possible need for closure after transseptal puncture.

PEX3 promotes regenerative repair after myocardial injury in mice through facilitating plasma membrane localization of ITGB3.

The peroxisome is a versatile organelle that performs diverse metabolic functions. PEX3, a critical regulator of the peroxisome, participates in various biological processes associated with the peroxisome. Whether PEX3 is involved in peroxisome-related redox homeostasis and myocardial regenerative repair remains elusive. We investigate that cardiomyocyte-specific PEX3 knockout (Pex3-KO) results in an imbalance of redox homeostasis and disrupts the endogenous proliferation/development at different times and spatial locations. Using Pex3-KO mice and myocardium-targeted intervention approaches, the effects of PEX3 on myocardial regenerative repair during both physiological and pathological stages are explored. Mechanistically, lipid metabolomics reveals that PEX3 promotes myocardial regenerative repair by affecting plasmalogen metabolism. Further, we find that PEX3-regulated plasmalogen activates the AKT/GSK3ß signaling pathway via the plasma membrane localization of ITGB3. Our study indicates that PEX3 may represent a novel therapeutic target for myocardial regenerative repair following injury.

A Shot Through the Heart.

We present the case of a patient who was shot through the heart with an air rifle and presented in a stable condition at our emergency department. At the time of presentation, the bullet was still present within the myocardium. Imaging, management, and outcome are discussed in this report.

Cardiac Perforation Caused By Pectus Excavatum Metal Bar Stabilizer: A Case Report.

This paper reports the case of a female patient who underwent minimally invasive repair of pectus excavatum (MIRPE) in another service that evolved with bar rotation and cardiac perforation caused by the left stabilizer. The unique and frightening aspect of the case is that despite having the stabilizer inside the ventricle, the patient was oligosymptomatic: occasional chest pain and respiratory discomfort. Preoperative imaging showed rotation of the bar with stabilizers within the thoracic cavity. During surgery, intense ossification was observed around the prosthesis and it was noted that the left stabilizer had perforated the patient's left ventricle. Cardiac repair required a Clamshell incision and cardiopulmonary bypass. This case reinforces the validity of late radiological follow-up after MIRPE in an attempt to avoid this type of event, and the need to reevaluate the use of stabilizers perpendicular to the bar since they are not safe to prevent rotation of these implants.

Traumatic pericardial rupture with secondary cardiac herniation in a dog.

OBJECTIVE: To describe the unique finding and treatment of a dog with cardiac herniation due to traumatic pericardial rupture. CASE SUMMARY: A 6.5-year-old entire male Yorkshire Terrier was presented for further management after being hit by a car. Despite suspected significant intrathoracic trauma at that time, the patient regained hemodynamic stability and had orthopedic surgery to correct a right iliac fracture. The patient was readmitted to the hospital 12 days following the initial visit due to considerable respiratory difficulty after accidentally being dropped several feet. Thoracic radiographs revealed an unusual severe mediastinal shift to the left with an atypical position of the cardiac silhouette against the left lateral thoracic wall. Due to the severe respiratory compromise of the patient and newly developed pneumothorax, an exploratory thoracotomy was recommended, where a complete rupture of the pericardium was identified, with secondary left-sided prolapse of the heart. Other more common intrathoracic injuries (ie, lung perforation, rib fractures) were also identified and partially repaired. The patient recovered successfully and was discharged 4 days postoperatively. NEW OR UNIQUE INFORMATION PROVIDED: This is the first case report in the veterinary literature of traumatic pericardial rupture and cardiac herniation. According to human case descriptions, this is a rare and often fatal occurrence, which can be significantly challenging to diagnose preoperatively or antemortem. Emergency veterinary clinicians should be aware of this rare but important complication of blunt thoracic trauma. Surgical intervention may be necessary in cases with suspected or confirmed entrapment of great vessels or cardiac chambers, although these abnormalities were not present in this case.

Impact of neuromuscular block on myocardial injury after non-cardiac surgery (MINS) incidence in the early postoperative stage of older patients undergoing laparoscopic colorectal cancer resection: a randomized controlled study.

BACKGROUND: Myocardial injury after non-cardiac surgery (MINS) is a common and serious complication in older patients. This study investigates the impact of neuromuscular block on the MINS incidence and other cardiovascular complications in the early postoperative stage of older patients undergoing laparoscopic colorectal cancer resection. METHODS: 70 older patients who underwent laparoscopic colorectal cancer resection were separated into the deep neuromuscular block group and moderate neuromuscular block group for 35 cases in each group (n = 1:1). The deep neuromuscular block group maintained train of four (TOF) = 0, post-tetanic count (PTC) 1-2, and the moderate neuromuscular block group maintained TOF = 1-2 during the operation. Sugammadex sodium was used at 2 mg/kg or 4 mg/kg for muscle relaxation antagonism at the end of surgery. The MINS incidence was the primary outcome and compared with Fisher's exact test. About the secondary outcomes, the postoperative pain was analyzed with Man-Whitney U test, the postoperative nausea and vomiting (PONV) and the incidence of cardiovascular complications were analyzed with Chi-square test, intraoperative mean artery pressure (MAP) and cardiac output (CO) ratio to baseline, length of stay and dosage of anesthetics were compared by two independent samples t-test. RESULTS: MINS was not observed in both groups. The highest incidence of postoperative cardiovascular complications was lower limbs deep vein thrombosis (14.3% in deep neuromuscular block group and 8.6% in moderate neuromuscular group). The numeric rating scale (NRS) score in the deep neuromuscular block group was lower than the moderate neuromuscular block group 72 h after surgery (0(1,2) vs 0(1,2), P = 0.018). The operation time in the deep neuromuscular block group was longer (356.7(107.6) vs 294.8 (80.0), min, P = 0.008), the dosage of propofol and remifentanil was less (3.4 (0.7) vs 3.8 (1.0), mg·kg-1·h-1, P = 0.043; 0.2 (0.06) vs 0.3 (0.07), µg·kg-1·min-1, P < 0.001), and the length of hospital stay was shorter than the moderate neuromuscular block group (18.4 (4.9) vs 22.0 (8.3), day, P = 0.028). The differences of other outcomes were not statistically significant. CONCLUSIONS: Maintaining different degrees of the neuromuscular block under TOF guidance did not change the MINS incidence within 7 days after surgery in older patients who underwent laparoscopic colorectal cancer resection. TRIAL REGISTRATION: The present study was registered in the Chinese Clinical Trial Registry (10/02/2021, ChiCTR2100043323).

Podophyllotoxin via SIRT1/PPAR /NF-κB axis induced cardiac injury in rats based on the toxicological evidence chain (TEC) concept.

BACKGROUND: The study of cardiotoxicity of drugs has become an important part of clinical safety evaluation of drugs. It is commonly known that podophyllotoxin (PPT) and its many derivatives and congeners are broad-spectrum pharmacologically active substances. Clinical cardiotoxicity of PPT and its derivatives has been raised, basic research on the mechanism of cardiotoxicity remains insufficient. PURPOSE: In present study, our group's innovative concept of toxicological evidence chain (TEC) was applied to reveal the cardiac toxicity mechanism of PPT by targeted metabolomics, TMT-based quantitative proteomics and western blot. METHODS: The injury phenotype evidence (IPE) acquired from the toxicity manifestations, such as weight and behavior observation of Sprague-Dawley rat. The damage to rat hearts were assessed through histopathological examination and myocardial enzymes levels, which were defined as Adverse Outcomes Evidence (AOE). The damage to rat hearts was assessed through histopathological examination and myocardial enzyme levels, which were defined as evidence of adverse outcomes.Overall measurements of targeted metabolomics based on energy metabolism and TMT-based quantitative proteomics were obtained after exposure to PPT to acquire the Toxic Event Evidence (TEE). The mechanism of cardiac toxicity was speculated based on the integrated analysis of targeted metabolomics and TMT-based quantitative proteomics, which was verified by western blot. RESULTS: The results indicated that exposure to PPT could result in significant elevation of myocardial enzymes and pathological alterations in rat hearts. In addition, we found that PPT caused disorders in cardiac energy metabolism, characterized by a decrease in energy metabolism fuels. TMT-based quantitative proteomics revealed that the PPAR (Peroxisome proliferators-activated receptor) signaling pathway needs further study. It is worth noting that PPT may suppress the expression of SIRT1, subsequently inhibiting AMPK, decreasing the expression of PGC-1α, PPARα and PPARγ. This results in disorders of glucose oxidation, glycolysis and ketone body metabolism. Additionally, the increase in the expression of p-IKK and p-IκBα, leads to the nuclear translocation of NF-κB p65 from the cytosol, thus triggering inflammation. CONCLUSION: This study comprehensively evaluated cardiac toxicity of PPT and initially revealed the mechanism of cardiotoxicity,suggesting that PPT induced disorders of energy metabolism and inflammation via SIRT1/PPAR/NF-κB axis, potentially contributing to cardiac injury.

Rare case of multiple self-inflicted gunshot wounds to the chest in Poland.

Multiple gunshot suicides are relatively rare and present significant challenges for investigators and forensic pathologists. In such cases, assessing the possibility of more than one shot being fired can be crucial in distinguishing homicide from suicide. We present a rare case of multiple self-inflicted gunshot wounds to the chest with severe injury to the heart and left lung. Both the sudden, unexpected death of the man, the unknown source of the firearm, and the number and nature of the injuries sustained seemed quite unusual. The investigation revealed that the wounds were self-inflicted at close range, and the interval between successive shots (estimated by witnesses at up to 2 min) suggests that even multiple gunshot wounds perforating the heart and lungs may not necessarily cause immediate incapacitation. Forensic investigations in such cases should be multi-faceted and include full autopsy and ballistics expertise, as well as witness testimony and medical history.

Right ventricle pierced by a traditional sharp hair straightener: a case report.

The case presents a traumatic ventricular perforation of a girl, accidentally felt on a sharp instrument. The uniqueness of the case presented is due to the very high infrequency of injuries with this type of sharp object. The 7-year-old girl was transported to the hospital after accidentally falling on a sharp instrument. The child had no signs of heart failure. On opening the chest, it was found that the metal object was lodged in the right ventricle. Quickly proceeded to remove the object and suture the entry hole. After a short hospitalization, the child was discharged completely cured.

Needle Decompression Complicated by Cardiac Injury in a Prehospital Environment.

Needle decompression is a mainstay intervention for tension pneumothorax in trauma medicine. It is used in combat and prehospital medicine when definitive measures are often not available or ideal. It can temporarily relieve increased intrathoracic pressure and treat a collapsed lung or great vessel obstruction. However, when done incorrectly, it can result in underlying visceral organ and vessel trauma. This is a case of an adult male who presented to the emergency department after sustaining multiple stab wounds during an altercation. On arrival, the patient had a 14-gauge angiocatheter inserted at the 4th intercostal space (ICS), left of the parasternal line traversing the right ventricle and interventricular septum and terminating in the left ventricle. The case emphasizes the importance of understanding the landmarks of performing needle decompression in increasing the procedure's efficacy and reducing iatrogenic complications.