Coronary Subclavian Steal Syndrome (CSSS) is a rare condition of blood flow reversal, in patients who have undergone Coronary Arterial Bypass Graft (CABG) with a Left Internal Mammary Artery (LIMA) to Left anterior descending (LAD) graft, who have concomitant left subclavian artery stenosis. The left subclavian artery stenosis results in retrograde blood flow from the coronary circulation through the LIMA- LAD graft to the left subclavian artery, causing cardiac ischemia. We report a case of a 77-year-old Female with previous CABG (LIMA to LAD graft) who presented to the Emergency department (ED) with chest pain. Her Electrocardiogram (ECG) showed ST elevations in aVR and widespread ST depressions in the anterior, lateral and inferior leads with a raised high sensitivity Troponin. A diagnosis of Non-ST Elevation Myocardial Infarction (NSTEMI) was made, and she underwent Coronary Angiogram which revealed relatively patent grafts that could not explain her presentation. She was found to have left subclavian artery stenosis and subclavian artery angioplasty was performed successfully. Coronary Subclavian Steal Syndrome is a rare but significant pathology. It is important for Emergency physicians to consider it as a differential in patients with history of CABG and suggestive clinical features. A Computed Tomography (CT) Angiogram or Aortogram should be performed, and Vascular Surgery should be activated early for timely intervention.
Coronary subclavian steal syndrome (CSSS) is a rare phenomenon that occurs due to severe stenosis of the subclavian artery, resulting in retrograde vertebral and left internal mammary artery (LIMA) flow. We present a 60-year-old man with severe peripheral artery disease (PAD) and coronary artery bypass graft (CABG) involving the LIMA-left anterior descending artery (LAD) who presented with left arm claudication, vertigo, angina, and heart failure. This case highlights a patient with a complex set of symptoms across multiple organs with one unifying culprit in the left subclavian artery. Prompt identification and treatment of a total subclavian occlusion resulted in restoration of vertebral and LIMA-LAD flow with resolution of angina, vertigo, and left ventricular systolic dysfunction. Coronary subclavian steal syndrome is an underrecognized diagnosis that should be on the differential for patients with inter-arm pressure differences and a history of CABG involving the LIMA-LAD. Routine surveillance should be pursued in high-risk patients. Early detection and treatment may improve symptoms and potentially contribute to recovery of left ventricular systolic dysfunction in select patients.
Distal revascularization with interval ligation (DRIL) is widely regarded as the gold standard for dialysis access-associated steal syndrome (DASS), yet high-level comparative evidence remains scarce. We performed a systematic review and meta-analysis to evaluate whether DRIL truly outperforms alternative reconstructive strategies, particularly proximalization of the arterial inflow (PAI). A PRISMA-compliant systematic search identified observational studies reporting outcomes after DRIL, PAI, or RUDI for DASS. The review protocol was prospectively registered in the International Prospective Register of Systematic Reviews (PROSPERO; CRD420261329250) prior to data extraction and study selection. The primary endpoint was symptom resolution. Secondary outcomes included primary patency and postoperative complications. Subgroup analyses and meta-regression were performed to explore technique-related differences and heterogeneity. Eight studies were included. Overall symptom resolution reached 92% (95% CI 87-96%), with moderate heterogeneity (I2 = 58%). DRIL achieved a pooled resolution rate of 91%, while PAI demonstrated 93%, with no significant between-technique difference (P = 0.62). No statistically significant difference in complication rates was detected between DRIL and PAI (P = 0.56). No statistically significant difference in primary patency was detected between techniques (P = 0.34). Meta-regression did not identify publication year or study size as significant moderators. Influence diagnostics confirmed robustness of pooled estimates. The available observational evidence - derived exclusively from small retrospective cohorts predominantly at serious risk of bias - did not demonstrate a statistically significant difference between DRIL and PAI with respect to symptom resolution, complications, or primary patency. These results should not be interpreted as equivalence or as justification for abandoning DRIL as a cornerstone technique. Rather, they reflect the limitations of the current evidence base. In the absence of randomized data, an individualized, anatomy-driven approach is recommended, and prospective comparative studies are urgently needed.
Postliver transplant ascites occurs in 5%-7% of recipients. This report describes splenic artery steal syndrome, causing refractory post-transplant ascites and ischemic biliopathy requiring splenectomy. A 65-year-old man with alcohol-related cirrhosis underwent orthotopic liver transplantation (Model for End-Stage Liver Disease 12) with pretransplant splenomegaly and splenic-artery dilatation. Postoperatively, computed tomography demonstrated persistent ascites, splenic-to-hepatic artery ratio of 2.5, and reduced hepatic arterial perfusion. Endoscopic retrograde cholangiopancreatography identified an anastomotic stricture with intrahepatic biliopathy. Two splenic artery embolization procedures were unsuccessful. Salvage splenectomy achieved resolution of ascites, cholestasis, and biliopathy. Splenic artery steal syndrome is an under-recognized cause of refractory post-transplant ascites which may benefit from splenectomy after embolization failure.
Coronary-subclavian steal syndrome (CSSS) is an uncommon but potentially serious complication following coronary artery bypass grafting (CABG). In the presence of significant proximal left subclavian artery stenosis, blood flow within the left internal mammary artery (LIMA) may reverse, leading to myocardial ischemia in the left anterior descending artery (LAD) territory. CSSS typically manifests months to years after CABG, whereas intraoperative onset during the procedure is exceedingly rare and very few cases previously documented. We report a patient who developed acute CSSS during off-pump CABG. Prompt intraoperative diagnosis was achieved using transit-time flow measurement (TTFM), and the condition was successfully managed by immediate LIMA graft reconstruction. This case highlights the critical role of intraoperative flow assessment and timely surgical decision-making in the management of rare but life-threatening complications during CABG.
One observation that has not received much attention and has not been described in detail to date is temporary hypoenhancement in the arterial phase of contrast-enhanced ultrasound (CEUS) in the surrounding liver parenchyma of well-vascularized lesions. This phenomenon is described and distinguished from other CEUS phenomena and artifacts. Even though this phenomenon has no specific differential diagnostic significance, knowledge of it can contribute to an overall understanding of CEUS.
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Congenital coronary artery anomalies are uncommon but clinically significant conditions associated with myocardial ischemia, malignant ventricular arrhythmias, and sudden cardiac death, particularly in young individuals. Among these anomalies, anomalous origin of the right coronary artery from the pulmonary artery (ARCAPA) is exceptionally rare, with a reported prevalence of approximately 0.002%. Although ARCAPA may remain clinically silent for many years due to collateral circulation from the left coronary system, it carries a persistent risk of myocardial ischemia caused by a coronary steal phenomenon and may result in sudden cardiac death. We report the case of a 19-year-old Somali male with no prior medical history who presented with a several-month history of recurrent syncope occurring both at rest and during exertion, without preceding chest pain, palpitations, dyspnea, seizure-like activity, or prodromal symptoms. He presented following a prolonged syncopal episode and was found to be hemodynamically unstable, with a blood pressure of 86/54 mmHg and sinus tachycardia. Initial laboratory investigations, including complete blood count, renal function, serum electrolytes, coagulation profile, and cardiac biomarkers, were within normal limits. Electrocardiography demonstrated diffuse ST-segment depression in the inferolateral leads with reciprocal ST-segment elevation in lead aVR, raising concern for global subendocardial ischemia. Transthoracic echocardiography revealed preserved left ventricular systolic function, with an ejection fraction of 65%, a mildly dilated main pulmonary artery, and mild pulmonary regurgitation. Due to the unavailability of coronary computed tomography angiography, urgent invasive coronary angiography was performed approximately 4 hours after presentation. Angiography revealed anomalous origin of the right coronary artery from the pulmonary artery with retrograde flow into the pulmonary trunk, consistent with a significant coronary steal phenomenon. No obstructive coronary artery disease was identified. Approximately 30 minutes after angiography, the patient developed sudden hemodynamic collapse and progressed to cardiac arrest. Despite prolonged advanced cardiopulmonary resuscitation, return of spontaneous circulation was not achieved. The presumed cause of death was malignant ventricular arrhythmia secondary to myocardial ischemia related to ARCAPA; however, the exact mechanism could not be definitively established. This case highlights the potential for rapid fatal deterioration in ARCAPA despite preserved ventricular systolic function. Recurrent syncope and ischemic electrocardiographic abnormalities should be recognized as high-risk features. The electrocardiographic pattern observed may reflect diffuse myocardial ischemia due to coronary steal rather than atherosclerotic coronary artery disease. ARCAPA should be considered in young patients presenting with unexplained recurrent syncope and high-risk electrocardiographic findings. Early recognition, appropriate use of multimodality imaging, close monitoring, and prompt surgical referral are essential to prevent catastrophic outcomes.
Peripheral arterial disease (PAD) is highly prevalent among patients requiring hemodialysis access and reflects advanced systemic atherosclerosis. We evaluated whether PAD severity is associated with increased postoperative complications and loss of primary patency following dialysis access creation and performed stratified analyses by access type: arteriovenous fistula (AVF) and arteriovenous graft (AVG). We used the Vascular Quality Initiative database from 2011 to 2024, including patients undergoing upper-extremity hemodialysis access creation. PAD status was categorized as no PAD, asymptomatic PAD, claudication, or chronic limb-threatening ischemia (CLTI). Postoperative outcomes included 30-day mortality, prolonged length of stay, bleeding, thrombosis, and steal syndrome. Six-month primary patency was defined as time to first intervention, thrombosis, failure, or abandonment. Multivariable logistic and Cox regression analyses were performed in the overall cohort, followed by subgroup analyses stratified by AVF and AVG. A total of 78,607 patients were included (25,718 [32.7%] no PAD; 47,771 [60.8%] asymptomatic PAD; 2079 [2.6%] claudication; and 3039 [3.9%] CLTI). In the overall cohort, increasing PAD severity was independently associated with worse postoperative outcomes. Compared with patients without PAD, asymptomatic PAD (adjusted odds ratio [aOR] 1.55; 95% confidence interval [CI], 1.27-1.90; P < .001), claudication (aOR 2.20; 95% CI, 1.52-3.18; P < .001), and CLTI (aOR 3.01; 95% CI, 2.24-4.06; P < .001) were associated with progressively higher odds of 30-day mortality. Asymptomatic PAD (aOR 1.41; 95% CI, 1.16-1.71; P < .001) and CLTI (aOR 2.27; 95% CI, 1.82-2.83; P < .001) were associated with prolonged length of stay. Asymptomatic PAD was also associated with increased odds of postoperative bleeding (aOR 1.30; 95% CI, 1.01-1.69; P = .043). Claudication (aOR 3.57; 95% CI, 1.33-9.59; P = .012) and CLTI (aOR 2.87; 95% CI, 1.21-6.82; P = .017) were associated with increased odds of steal syndrome, whereas PAD severity was not associated with postoperative thrombosis. At 6 months, all PAD stages were strongly associated with loss of primary patency: asymptomatic PAD (adjusted hazard ratio [aHR] 5.09; 95% CI, 3.15-8.22; P < .001), claudication (aHR 4.79; 95% CI, 2.86-8.02; P < .001), and CLTI (aHR 5.05; 95% CI, 3.14-8.10; P < .001). Findings were consistent in analyses stratified by AVF and AVG. To our knowledge, this is the first study to comprehensively evaluate the impact of PAD and PAD progression on outcomes and patency of dialysis access. PAD severity is independently associated with increased postoperative complications, 30-day mortality, and loss of primary patency following dialysis access creation. Notably, even asymptomatic PAD confers significantly increased risk of mortality and loss of primary patency at 6 months. These findings highlight the importance of incorporating PAD status into preoperative risk stratification and dialysis access planning.
The arterial anatomy of the lips is highly variable, influencing both reconstructive and aesthetic procedures. Despite extensive anatomical studies, potential perfusion relationships within the perioral region remain underexplored. This review introduces a new anatomical hypothesis, the "steal phenomenon", which describes a possible redistribution of perfusion (or filler material) from the upper lip toward the nasal and ophthalmic territories through pre-existing anastomoses. Electronic databases, including Medline (PubMed), Embase, Scopus, and Web of Science, were systematically searched to gather studies examining the blood supply to the lips. Twenty-three studies were included. The superior labial artery (SLA) was absent in 3.55% of cases; when present, it most commonly originated above the oral commissure (OC) (80.71%) at a mean distance of 11.95 mm. The inferior labial artery (ILA) was absent in 13.45% of cases and most frequently located below the OC (72.44%) at an average distance of 21.99 mm. Both arteries most commonly coursed through the submucosal plane, with the SLA and ILA, reported in this layer in up to 84.8 and 81.25% of cases, respectively. Mean arterial depths were approximately 5.2 mm for both vessels. This review highlights the considerable variability of the labial vasculature and its implications for procedural safety. No lip plane can be regarded as entirely free of vascular structures, emphasizing the need for individualized, anatomically guided injection technique. The proposed steal phenomenon offers a theoretical explanation for the upper lip's greater susceptibility and underscores the importance of cautious, patient-specific practice supported by ultrasound when available. 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 .
Coronary artery fistulas (CAFs) are uncommon coronary anomalies that are often asymptomatic but may present later in life due to the coronary steal phenomenon, leading to myocardial ischemia and related complications. We report the case of a 76-year-old male presenting with anginal chest pain. Coronary computed tomography angiography performed after inconclusive prior cardiac testing revealed a direct fistulous communication between the right coronary artery (RCA) and the left anterior descending artery (LAD), an exceptionally rare configuration. Imaging also demonstrated a double RCA, an uncommon congenital variant characterized by two parallel right coronary arteries arising from a single or separate ostia, which may coexist with other coronary anomalies and complicate interpretation. The study showed a tortuous fistulous tract with features consistent with chronic high-flow physiology and coronary steal, correlating with the patient's clinical presentation. This case highlights the importance of considering rare coronary anomalies in elderly patients with new-onset angina and underscores the value of coronary computed tomography angiography in providing detailed three-dimensional visualization of coronary anatomy, enabling definitive diagnosis and guiding clinical management in complex coronary vascular anomalies.
Moyamoya disease is a progressive steno-occlusive cerebrovascular disorder in which cerebral perfusion may become highly dependent on systemic arterial pressure, arterial carbon dioxide tension, and collateral flow. Encephaloduroarteriosynangiosis (EDAS) is an indirect revascularization procedure that promotes neovascularization over weeks to months but does not immediately augment cerebral blood flow intraoperatively. Anesthetic management therefore requires preservation of cerebral oxygen delivery during a period of persistent physiologic vulnerability. This narrative review presents a practical perioperative framework for EDAS anesthesia, emphasizing maintenance of mean arterial pressure near baseline or modestly above baseline, avoidance of hypotension and hypovolemia, normoxia, normothermia, and careful regulation of carbon dioxide. Hyperventilation should be avoided because hypocapnia can reduce cerebral blood flow through vasoconstriction, while excessive hypercapnia may contribute to regional maldistribution or steal physiology. Raw electroencephalography may provide cortical ischemia surveillance where available, whereas somatosensory evoked potentials, motor evoked potentials, near-infrared spectroscopy, and transcranial Doppler should be considered adjunctive and institution-dependent. A structured algorithm that integrates hemodynamics, ventilation, oxygen delivery, anesthetic depth, neuromonitoring, and surgical communication may support the timely recognition and correction of intraoperative hypoperfusion.
To describe the technical feasibility and early clinical outcomes of basilic vein to fistula outflow vein transposition as an autogenous salvage option for malfunctioning forearm arteriovenous fistulas (AVFs) with venous outflow obstruction at the elbow level and a patent basilic vein. This single-center retrospective technical note reviewed nine patients who underwent basilic vein to fistula outflow vein transposition between December 2023 and March 2026. Clinical indications, reasons for selecting surgical transposition over further endovascular treatment, operative details, time to postoperative dialysis use, complications, reinterventions, and individual access outcomes were summarized descriptively. The mean age was 67.8 ± 7.2 years; seven patients were male. Hypertension was present in all patients and diabetes mellitus in two patients. The main clinical triggers for intervention were venous hypertension during hemodialysis, thrombotic occlusion of the cephalic outflow vein, and inadequate dialysis blood flow. The mean preoperative basilic vein diameter was 2.0 ± 0.28 mm. After reconstruction, all patients had restoration of a normal access thrill and resolution of abnormal fistula pulsatility, while intradialytic venous hypertension improved compared with the preoperative status. All AVFs were successfully used for hemodialysis within 48 h after surgery. Two patients had wound hemorrhage that resolved after bedside management. During follow-up, five patients required reintervention for restenosis, including PTA and open thrombectomy. No early thrombosis, hematoma, nerve injury, wound infection, clinically significant steal syndrome, or access abandonment occurred during the available follow-up. In patients with a functioning forearm AVF, preserved arterial inflow, elbow-level venous outflow obstruction, and a suitable basilic vein, basilic vein-to-fistula outflow vein transposition may represent a practical autogenous salvage option. These findings should be interpreted as preliminary technical experience.
Coronary-bronchial artery fistulas are rare vascular anomalies between the coronary and bronchial circulations. They are most often detected incidentally and may be congenital or acquired, particularly in the setting of chronic pulmonary disease. Origin from the sinoatrial nodal artery is exceptional. If haemodynamically significant, these communications may lead to a coronary steal phenomenon and represent a potential cause of myocardial ischaemia. Recognition is also crucial prior to bronchial artery embolization to avoid inadvertent coronary complications. Multimodality imaging plays a key role in their diagnosis and characterization. A 58-year-old man with psoriasis presented with atypical chest pain. Exercise stress echocardiography was electrically equivocal, prompting invasive coronary angiography. No significant coronary artery disease was identified. However, contrast injection into the proximal right coronary artery demonstrated a prominent atrial branch with opacification of the right pulmonary parenchyma. Coronary computed tomography angiography revealed a retroaortic sinoatrial nodal artery originating from the proximal right coronary artery. Its left branch communicated with a hypertrophied bronchial artery, which followed a tortuous trajectory towards the right middle lobe. Chest computed tomography demonstrated cylindrical and varicose bronchiectasis in the right middle and lower lobes. No haemoptysis occurred. This case illustrates a rare coronary-bronchial artery fistula arising from the sinoatrial nodal artery in association with bronchiectasis. Multimodality imaging enabled accurate anatomical characterization and suggested possible haemodynamic relevance. Such fistulas may represent a potential cause of myocardial ischaemia and should be recognized both in the evaluation of chest pain and prior to interventional procedures.
In wireless communication, the multipath effect and the time-varying channel due to mobility will directly lead to the key update cycle lagging far behind the channel change, which is difficult to effectively resist various malicious attacks and stealing behaviors, and affects the effect of privacy data protection in wireless communication. To this end, a deep learning-based dual chaos encryption method is proposed for wireless communication privacy data. Combining the chaotic characteristics of one-dimensional Logistic mapping and two-dimensional Henon mapping, the dual chaotic key is generated to extend the key space and improve the anti-attack ability; and the bidirectional long and short-term memory network (BiLSTM) is used to analyze the data such as key usage records, accurately predict the timing of the key updating, and generate a new key when anomalies are detected, and then distribute it securely. Taking the updated double chaotic key as input, the AES algorithm is used to realize wireless communication privacy data encryption through key expansion, initial round encryption, multiple rounds of iterative encryption and final round encryption, while the decryption process restores the plaintext by inverse operation. Experiments demonstrate that the method can effectively realize wireless communication privacy data encryption, and the security index can reach more than 0.94 in the face of different types of network attacks. It demonstrates that the proposed method can have the ability to resist all kinds of attacks and protect the security of private data.
We present a case and literature review regarding posterior ischemic optic neuropathy (PION) in the context of orbital hemorrhage following cosmetic blepharoplasty. A 49-year-old male patient, who underwent resection of residual fat from a previous blepharoplasty, developed acute orbital hemorrhage six hours postoperatively, with sudden visual loss, painful proptosis, and a relative afferent pupillary defect. Urgent decompressive surgery was performed. Ultimately, the patient did not experience visual improvement, and optic atrophy was evident one month later, confirming the diagnosis of PION. Potential pathophysiological mechanisms include direct nerve compression, venous stasis, epinephrine-induced vasoconstriction, vascular steal phenomena, orbital fat traction, and alterations in coagulation and blood pressure. The various hemodynamic, orbital, and systemic mechanisms demonstrate the importance of considering PION as a possible cause of acute visual loss after eyelid procedures.
Achilles tendon rupture is a rare but potentially career-altering injury in elite basketball athletes. Contemporary data specific to National Basketball Association (NBA) players are limited, particularly regarding return-to-play (RTP) timing, functional outcomes, and long-term incidence trends in the modern high-pace era. To evaluate RTP rates, time to return, postinjury performance changes, and temporal patterns of Achilles tendon rupture in NBA players over a 25-year period. Descriptive epidemiology study. NBA players with a confirmed Achilles tendon rupture between the 2000-2001 and 2024-2025 seasons were identified through multisource verification, including team announcements, league injury reports, Basketball Reference records, NBA.com injury logs, and contemporaneous reporting from major sports media outlets. RTP was defined as participation in at least one official NBA regular season or postseason game after the index rupture. Season-level performance metrics were extracted for the final full preinjury season and the first full postreturn season. Paired pre- versus postinjury comparisons were performed, effect sizes were calculated using Cohen d, and selected metrics were normalized per 48 minutes to account for changes in playing time. The annual rupture incidence was evaluated in relation to league-wide pace using Pearson correlation. A total of 22 NBA players sustained a confirmed Achilles rupture. Among athletes with adequate follow-up (n = 15), 13 players (86.7%) returned to NBA competition. The mean time to RTP was 10.8 ± 4.3 months. Significant declines were observed in minutes per game (-7.6 minutes; P < .001), points per game (-5.4; P < .001), effective field goal percentage (-0.055; P = .005), rebounds (-1.3; P = .008), assists (-1.0; P = .002), defensive rebounds (-1.01; P = .014), steals (-0.28; P = .001), and blocks (-0.19; P = .026). When normalized per 48 minutes, scoring production still decreased significantly (-3.36 points; P = .004), while defensive metrics were preserved. Games started decreased substantially (-44 percentage points; P = .003). Annual rupture incidence remained low overall, with a notable spike in the 2024-2025 season, but no significant correlation with league pace was observed. This study showed that most NBA players with adequate follow-up returned to professional play after Achilles tendon rupture, typically within approximately 11 months. However, reductions in playing time, scoring output, offensive efficiency, and starting role prevalence were common after return. Per-48-minute analyses suggested that scoring decline persisted even after accounting for reduced playing time, whereas several defensive and rebounding metrics were relatively preserved. Annual rupture incidence remained low overall, although a notable cluster was observed during the 2024-2025 season. These data may be helpful for counseling players regarding performance expectations and decision-making after Achilles tendon rupture in elite basketball players.
Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA, or Bland-White-Garland syndrome) is a rare congenital anomaly associated with a high risk of ischaemic cardiomyopathy and sudden cardiac death. Non-cardiac surgery in patients with uncorrected anomaly is exceedingly rare and standardised peri-operative risk models are lacking. This case report highlights the complex physiological considerations and tailored anaesthetic management of a 13-year-old girl with uncorrected ALCAPA undergoing general anaesthesia for dental extractions. Pre-operative echocardiography demonstrated left ventricular dilatation (52.2 mm) with a preserved ejection fraction (68%) and mild mitral regurgitation. Cardiac magnetic resonance imaging revealed extensive subendocardial scarring and inducible stress perfusion defects, indicating ongoing ischaemic and arrhythmogenic risk. Following a multidisciplinary consensus, the procedure was performed under strict haemodynamic control. General anaesthesia was carefully titrated to maintain the balance between myocardial oxygen supply and demand, and to prevent the exacerbation of coronary steal, with advanced ischaemia monitoring and immediate defibrillator availability. The patient remained haemodynamically stable throughout the peri-operative period. This case demonstrates that by integrating detailed anatomic and functional imaging data, anaesthetic strategies can be precisely tailored to manage the severe physiological vulnerabilities of patients with uncorrected ALCAPA.