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.
METHODS: 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.
CONCLUSIONS: 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.
CONCLUSIONS: 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.

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.

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.

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.

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.

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.

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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.

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/GSK3β 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.

OBJECTIVE: To describe the unique finding and treatment of a dog with cardiac herniation due to traumatic pericardial rupture.
METHODS: 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.
CONCLUSIONS: 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.