RESUMEN
PURPOSE: To provide information on the outcomes of upper and lower limb surgical embolectomies and the factors influencing amputation and mortality. METHODS: A retrospective, single-center analysis of 347 patients (female, N = 207; male, N = 140; median age, 76 years [interquartile range {IQR}, 63.2-82.6 years]) with acute upper or lower limb ischemia due to thromboembolism who underwent surgery between 2005 and 2019 was carried out. Patient demographics, comorbidities, medical history, the severity of acute limb ischemia (ALI), preoperative medication regimen, embolus/thrombus localization, procedural data, in-hospital complications/adverse events and their related interventions, and 30-day mortality were reviewed in electronic medical records. Statistical analysis was performed using the Mann-Whitney U test and Fisher's exact test; in addition, univariate and multivariate logistic regression was conducted. RESULTS: The embolus/thrombus was localized to the upper limb in 134 patients (38.6%) and the lower limb in 213 patients (61.4%). The median length of hospital stay was 3.8 days (IQR, 2.1-6.6 days). The in-hospital major amputation rates for the upper limb, lower limb, and total patient population were 2.2%, 14.1%, and 9.5%, respectively, and the in-hospital plus 30-day mortality rates were 4.5%, 9.4%, and 7.5%, respectively. In patients with lower limb embolectomy, the predictor of in-hospital major amputation was the time between the onset of symptoms and embolectomy (OR, 1.78), while the predictor of in-hospital plus 30-day mortality was previous stroke (OR, 7.16). In the overall patient cohort, there were two predictors of in-hospital major amputation: 1) the time between the onset of symptoms and embolectomy (OR, 1.92) and 2) compartment syndrome (OR, 3.51). CONCLUSION: Amputation and mortality rates after surgical embolectomies in patients with ALI are high. Patients with prolonged admission time, compartment syndrome, and history of stroke are at increased risk of limb loss or death. To avoid amputation and death, patients with ALI should undergo surgical intervention as soon as possible and receive close monitoring in the peri- and postprocedural periods.
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Síndromes Compartimentales , Enfermedades Vasculares Periféricas , Accidente Cerebrovascular , Humanos , Masculino , Femenino , Persona de Mediana Edad , Anciano , Anciano de 80 o más Años , Recuperación del Miembro , Estudios Retrospectivos , Factores de Riesgo , Enfermedad Aguda , Resultado del Tratamiento , Factores de Tiempo , Amputación Quirúrgica , Extremidad Inferior/cirugía , Embolectomía/efectos adversos , Isquemia , Enfermedades Vasculares Periféricas/cirugía , Accidente Cerebrovascular/etiologíaRESUMEN
PURPOSE: To evaluate factors associated with pseudoaneurysm (PSA) development. METHODS: Between January 2016 and May 2020, 30,196 patients had invasive vascular radiological or cardiac endovascular procedures that required arterial puncture. All patients with PSA were identified. A matched (age, gender, and type of the procedure) control group of 134 patients was created to reveal predictors of PSA formation. RESULTS: Single PSAs were found in 134 patients. Fifty-three PSAs developed after radiological procedures (53/6555 [0.8%]), 31 after coronary artery procedures (31/18038 [0.2%]), 25 after non-coronary artery cardiac procedures (25/5603 [0.4%]), and 25 due to procedures in which the arterial puncture was unintended. Thirty-four PSAs (25.4%) were localized to the upper extremity arteries (vascular closure device [VCD], N = 0), while 100 (74.6%) arose from the lower extremity arteries (VCD, N = 37). The PSA prevalence was 0.05% (10/20478) in the radial artery, 0.1% (2/1818) in the ulnar artery, 1.2% (22/1897) in the brachial artery, and 0.4% (99/22202) in the femoral artery. Treatments for upper and lower limb PSAs were as follows: bandage replacement (32.4% and 14%, respectively), ultrasound-guided compression (11.8% and 1%, respectively), ultrasound-guided thrombin injection (38.2% and 78%, respectively), and open surgery (17.6% and 12%, respectively). Reintervention was necessary in 19 patients (14.2%). The prevalence of PSA for the punctured artery with and without VCD use was 37/3555 (1%) and 97/27204 (0.4%), respectively (OR, 2.94; 95% CI, 1.95-4.34; P<0.001). The effect of red blood cell (RBC) count (P<0.001), hematocrit value (P<0.001), hemoglobin value (P<0.001), international normalized ratio (INR; P<0.001), RBC count-INR interaction (P = 0.003), and RBC count-VCD use interaction (P = 0.036) on PSA formation was significant. CONCLUSION: Patients in whom the puncture site is closed with a VCD require increased observation. Preprocedural laboratory findings are useful for the identification of patients at high risk of PSA formation.
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Aneurisma Falso/epidemiología , Arteria Braquial/cirugía , Procedimientos Endovasculares/efectos adversos , Arteria Femoral/cirugía , Anciano , Aneurisma Falso/etiología , Aneurisma Falso/patología , Arteria Braquial/fisiopatología , Femenino , Arteria Femoral/fisiopatología , Humanos , Extremidad Inferior/fisiopatología , Extremidad Inferior/cirugía , Masculino , Persona de Mediana Edad , Punciones/efectos adversos , Resultado del Tratamiento , Ultrasonografía Intervencional/efectos adversos , Dispositivos de Cierre Vascular/efectos adversosRESUMEN
OBJECTIVE: Stenting is the preferred, minimally invasive treatment for innominate artery (IA) stenosis or occlusion. Stent fractures in the IA have not been assessed in larger cohorts. In this retrospective study, we examined the frequency and risk factors of IA stent fractures. METHODS: The final analysis included 32 patients (15 women; mean age, 59.4 ± 12.0 years) with 32 balloon-expandable stents (2000 to 2009). In 2010, the patients were asked to come back for a fluoroscopic examination of the implanted stents. Stent fractures and their relationship to atherosclerotic risk factors, lesion characteristics, postprocedural symptoms, and in-stent restenosis were analyzed. Fisher exact test and univariate Cox regression analysis were used in the statistical evaluation. RESULTS: Lesions were >20 mm in 14 patients (44%) or heavily calcified in 13 (41%). The mean follow-up time was 33.4 ± 21.0 months. Postprocedural symptoms were noted in nine patients (28%). Significant restenosis was detected in 22% of the implanted stents, and 11 stent fractures (34%) were found. The prevalence of heavily calcified lesions, postprocedural symptoms, and in-stent restenosis did not differ significantly between groups with and without fracture. Long lesions were associated with an increased incidence of stent fracture (hazard ratio, 5.09; 95% confidence interval, 1.33-19.48; P = .017). No correlation was observed between stent fractures and old age (≥70 years), female gender, smoking, hypertension, hyperlipidemia, or diabetes mellitus. CONCLUSIONS: IA stent fractures are common but seem to have no effect on symptoms and in-stent restenosis rates.
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Angioplastia de Balón/instrumentación , Arteriopatías Oclusivas/terapia , Tronco Braquiocefálico , Falla de Prótesis , Stents , Adulto , Anciano , Anciano de 80 o más Años , Angioplastia de Balón/efectos adversos , Arteriopatías Oclusivas/diagnóstico , Tronco Braquiocefálico/diagnóstico por imagen , Constricción Patológica , Femenino , Humanos , Masculino , Persona de Mediana Edad , Modelos de Riesgos Proporcionales , Radiografía , Recurrencia , Estudios Retrospectivos , Índice de Severidad de la Enfermedad , Factores de Tiempo , Resultado del Tratamiento , Calcificación Vascular/terapiaRESUMEN
Recent studies have highlighted a significant association between the severity of atherosclerosis and bone mineral density (BMD) among healthy subjects, although its connection to angiographically determined peripheral artery disease (PAD) has never been investigated. We evaluated the connection between the angiographic severity and site specificity of peripheral atherosclerosis and osteoporosis among patients with chronic lower limb ischemia. In our cross-sectional study we investigated 172 patients with PAD. The anatomic sites of the lesions were analyzed. The severity of atherosclerosis was diagnosed using the Bollinger angiographic score (BS). BMD was measured at the lumbar spine (l-BMD) and at femoral (f-BMD) and radial (r-BMD) sites by dual-energy X-ray absorptiometry. Dyslipidemia, the level of vitamin D(3), and different bone turnover markers were also noted. Among PAD patients, regardless of the lesion site, we did not find any association between BMD and BS. Among patients with iliac disease, BS was associated with l-BMD (p = 0.038, r = -0.467) and with f-BMD (p = 0.002, r = -0.642). The level of r-BMD among patients with iliac disease was not associated with BS (p = 0.233, r = -0.306). We did not find any difference between the group of patients with and that without dyslipidemia and low or normal levels of vitamin D(3). Our results show a connection between the severity of atherosclerosis and osteoporosis among patients with PAD, specific to the site of the lesion. The findings regarding dyslipidemia, bone markers, and site specificity support the hypothesis that reduced blood flow is the key factor responsible for the inverse association of BMD with atherosclerosis.
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Aterosclerosis/fisiopatología , Densidad Ósea , Enfermedad Arterial Periférica/fisiopatología , Absorciometría de Fotón , Anciano , Aterosclerosis/diagnóstico por imagen , Aterosclerosis/etiología , Colecalciferol/sangre , Estudios Transversales , Dislipidemias/complicaciones , Dislipidemias/fisiopatología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Osteoporosis/diagnóstico por imagen , Osteoporosis/etiología , Osteoporosis/fisiopatología , Enfermedad Arterial Periférica/complicaciones , Enfermedad Arterial Periférica/diagnóstico por imagenRESUMEN
It has been previously reported that serum levels of 70-kDa heat shock protein (Hsp70) are elevated in peripheral artery disease. The aim of the present study was to examine whether increased serum Hsp70 levels are related to the extent of arterial calcification and standard laboratory parameters of patients with peripheral artery disease, as well as to markers of inflammation (C-reactive protein), atherosclerosis (homocysteine), and calcification (fetuin-a). One hundred eighty chronic atherosclerotic patients with significant carotid stenosis and/or lower extremity vascular disease were enrolled in this cross-sectional study. Systemic atherosclerosis and calcification was assessed by ultrasound (carotid intima-media thickness (IMT), presence of calcification at the abdominal aorta, carotid and femoral bifurcations, and aortic and mitral cardiac valves). Standard serum markers of inflammation, diabetes, renal function, ankle-brachial indexes, and traditional risk factors for atherosclerosis were noted. Serum Hsp70 levels were measured with enzyme-linked immunosorbent assay. Standard laboratory parameters (clinical chemistry), C-reactive protein (CRP), and homocysteine levels were determined by an autoanalyzer using the manufacturer's kits. Fetuin-a levels were measured by radial immunodiffusion. Patients' median age was 64 (57-71) years, 69% were men, and 34.5% had diabetes. Serum heat shock protein 70 levels were significantly higher in patients with more severe arterial calcification (p < 0.02) and showed significant positive correlations with serum bilirubin (r = 0.23, p = 0.002) and homocysteine levels (r = 0.18, p = 0.02). Serum Hsp70 did not correlate with body mass index, IMT, CRP, or fetuin-a levels in this cohort. Logistic regression analysis confirmed the association between sHsp70 and calcification score (OR, 2.189; CI, 1.156-4.144, p = 0.016) and this correlation remained significant (OR, 2.264; CI, 1.021-5.020, p = 0.044) after the adjustment for age, sex, eGFR, smoking, CRP, and homocysteine levels. Our data show that serum Hsp70 levels correlate with the severity of atherosclerosis in patients with carotid artery disease and chronic lower limb ischemia. These data support a putative role for plasma Hsp70 in the development of arterial calcification. Nevertheless, further studies are required to investigate the usefulness of circulating Hsp70 level as a marker of atherosclerotic calcification.
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Arterias/patología , Calcinosis/sangre , Proteínas HSP70 de Choque Térmico/sangre , Arterias/metabolismo , Bilirrubina/sangre , Estenosis Carotídea/sangre , Femenino , Homocisteína/sangre , Humanos , Masculino , Persona de Mediana Edad , SolubilidadRESUMEN
BACKGROUND: Fetuin-A is a glycoprotein that inhibits extraosseous and vascular calcification. Its serum level is lower in patients with atherosclerosis compared with healthy controls, but its role is unknown in aneurysmal diseases. The aim of our study was to investigate the association of serum fetuin-A levels with aortic aneurysms of different aetiology: Marfan syndrome and atherosclerosis. MATERIAL AND METHODS: In a single centre cross-sectional observational study, 105 patients (30 with atherosclerotic aortic aneurysm, 15 with Marfan syndrome, 30 with peripheral arterial disease and 30 healthy controls) were examined; sera were analysed for fetuin-A, standard markers of possible inflammation, lipid profile, kidney and hepatic disease and diabetes. Systemic atherosclerosis was assessed by carotid intima-media thickness (IMT) measurement and arterial calcification score of cardiac valves, carotids, aorta and femoral arteries determined by ultrasound. RESULTS: Serum fetuin-A levels (median and IQR) were significantly lower in the atherosclerotic aneurysm cohort than in patients with Marfan syndrome: 708 µg mL⻹ (612-780) and 756 µg mL⻹ (708-816), respectively, (P = 0·0428). Fetuin-A levels were 754 µg mL⻹ (713-777) in the control group and 654 µg mL⻹ (600-756) in patients with peripheral arterial disease. Mean and maximum IMT, ACS values and homocysteine levels were significantly higher in patients with atherosclerosis: P < 0·0001, P < 0·0001, P < 0·0001 and P = 0·0034, respectively. There was no significant difference between aneurysm groups analysing the results of lipid profile and acute-phase markers. CONCLUSIONS: The significantly lower serum level of fetuin-A in the atherosclerotic aneurysm group supports the protective role of fetuin-A in the evolution of arterial calcification.