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1.
Urology ; 142: 226-230, 2020 08.
Artículo en Inglés | MEDLINE | ID: mdl-32348806

RESUMEN

OBJECTIVE: To report the initial case of robotic-assisted level IV inferior vena cava (IVC) tumor thrombectomy, with the supra- and infradiaphragmatic caval segments managed purely by a robotic-assisted technique. METHODS: A 67-year-old female presented with a 5.3 × 2.4 cm right renal tumor and a level IV IVC tumor thrombus, 16.5 cm in length, extending 1.5 cm into the right atrium. Through a robotic trans-abdominal approach, the infrarenal and retrohepatic IVC, left renal vein and right kidney were secured. Using a robotic transthoracic approach, the thrombus was milked out of the right atrium. The intrapericardial caval segment was secured and the right atrium was excluded. No cardiopulmonary bypass was used. A cavotomy was made at the right renal vein os and the tumor thrombus was extracted en bloc in a retrograde manner under transesophageal echocardiographic visualization. RESULTS: Total operative time was 211 minutes, including robotic docking, with 90 minutes spent on taking down intraabdominal adhesions. Caval clamp time was 13 minutes. Estimated blood loss was 100 mL. Postoperatively, the patient developed atrial fibrillation with rapid ventricular rate (RVR) requiring diltiazem infusion (Clavien Grade II). Hospital stay was 5 days. There were no further complications. Pathology revealed an Angiomyolipoma and negative surgical margins. CONCLUSION: This is the initial report of a purely robotic-assisted level IV IVC tumor thrombectomy. We used this technique for an angiomyolipoma with tumor thrombus extending 1.5cm into the right atrium, managing both the supra- and infradiaphragmatic caval segments robotically. This report further extends the field of robotic surgery.


Asunto(s)
Procedimientos Quirúrgicos Robotizados , Trombectomía/métodos , Vena Cava Inferior , Trombosis de la Vena/cirugía , Anciano , Femenino , Humanos , Trombosis de la Vena/patología
3.
Ann Thorac Surg ; 101(4): e107-9, 2016 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-27000611

RESUMEN

Here we present the case of a patient that suffered a cardiac arrest due to pulmonary embolus. The patient was resuscitated using extracorporeal membrane oxygenation and treated with ultrasound-accelerated catheter-directed thrombolysis during support on extracorporeal membrane oxygenation, with an excellent outcome. This case demonstrates that the use of extracorporeal membrane oxygenation and ultrasound-accelerated catheter-directed thrombolysis can be highly effective for managing select patients with pulmonary embolus and cardiac arrest.


Asunto(s)
Cateterismo Periférico/métodos , Oxigenación por Membrana Extracorpórea/métodos , Paro Cardíaco/terapia , Heparina/administración & dosificación , Embolia Pulmonar/complicaciones , Terapia Trombolítica/métodos , Angiografía , Anticoagulantes/administración & dosificación , Arteria Femoral , Vena Femoral , Estudios de Seguimiento , Paro Cardíaco/diagnóstico por imagen , Paro Cardíaco/etiología , Humanos , Infusiones Intraarteriales , Masculino , Persona de Mediana Edad , Embolia Pulmonar/diagnóstico , Embolia Pulmonar/fisiopatología , Tomografía Computarizada por Rayos X , Ultrasonografía , Función Ventricular Derecha/fisiología
4.
ASAIO J ; 60(6): e1-2, 2014.
Artículo en Inglés | MEDLINE | ID: mdl-25232772

RESUMEN

Left ventricular assist devices (LVADs) have become more important in the management of patients with advanced heart failure. New generation rotary blood pumps demonstrated survival benefits and improved functional status and quality of life in these patients. Although a variety of relevant advances have been achieved in the field of device technology, the risk of severe complications remains. In this report, we describe the application of intracardiac echocardiography in the management of postoperative LVAD complications.


Asunto(s)
Ecocardiografía/métodos , Corazón Auxiliar/efectos adversos , Complicaciones Posoperatorias/diagnóstico por imagen , Insuficiencia Cardíaca/cirugía , Humanos , Masculino , Persona de Mediana Edad , Complicaciones Posoperatorias/diagnóstico , Complicaciones Posoperatorias/terapia , Falla de Prótesis , Taquicardia Ventricular/diagnóstico por imagen , Taquicardia Ventricular/etiología , Taquicardia Ventricular/terapia
6.
Arch Intern Med ; 170(20): 1827-31, 2010 Nov 08.
Artículo en Inglés | MEDLINE | ID: mdl-20696949

RESUMEN

BACKGROUND: Vena cava filters represent an alternative treatment option for patients with contraindications to anticoagulation, or they might serve as adjunctive treatment for continued emboli despite anticoagulation. The fracture of a filter strut with subsequent end-organ embolization is a rarely reported but potentially life-threatening occurrence. METHODS: We sought to determine the prevalence of fracture and embolization of the Bard Recovery (first generation) and the Bard G2 (second generation) vena cava filters. A retrospective, single-center, cross-sectional study was conducted by evaluating all patients who received either a Bard Recovery or Bard G2 filter from April 2004 until January 2009. A total of 189 patients had undergone implantation: 1 pregnant woman and 35 patients who died were excluded from our study. In addition, 10 patients who had the filter removed were also excluded. Ultimately, 80 patients participated in the trial. Subjects underwent fluoroscopy to assess the filter's integrity. Embolized struts were localized by fluoroscopy. Echocardiography and cardiac computed tomography were performed in patients with fragment embolization to the heart. RESULTS: Thirteen of 80 patients had at least 1 strut fracture (16%). At least 1 strut in 7 of the 28 Bard Recovery filters fractured and embolized (25%). In 5 of these 7 cases, patients had at least 1 fragment embolize to the heart (71%). Three patients experienced life-threatening symptoms of ventricular tachycardia and/or tamponade, including 1 patient who experienced sudden death at home. Six of 52 Bard G2 filters fractured (12%). In 2 of these 6 cases, the patients had asymptomatic end-organ fragment embolization. CONCLUSION: The Bard Recovery and Bard G2 filters had high prevalences of fracture and embolization, with potentially life-threatening sequelae.


Asunto(s)
Taponamiento Cardíaco/etiología , Migración de Cuerpo Extraño/complicaciones , Lesiones Cardíacas/etiología , Embolia Pulmonar/prevención & control , Filtros de Vena Cava , Vena Cava Inferior/cirugía , Adulto , Anciano , Taponamiento Cardíaco/epidemiología , Taponamiento Cardíaco/cirugía , Remoción de Dispositivos , Femenino , Fluoroscopía , Estudios de Seguimiento , Migración de Cuerpo Extraño/epidemiología , Migración de Cuerpo Extraño/cirugía , Lesiones Cardíacas/epidemiología , Lesiones Cardíacas/cirugía , Humanos , Masculino , Persona de Mediana Edad , Prevalencia , Pronóstico , Diseño de Prótesis , Falla de Prótesis , Estudios Retrospectivos , Tomografía Computarizada por Rayos X , Vena Cava Inferior/diagnóstico por imagen , Adulto Joven
7.
Proc Natl Acad Sci U S A ; 101(33): 12277-81, 2004 Aug 17.
Artículo en Inglés | MEDLINE | ID: mdl-15304656

RESUMEN

Stem cell therapy holds great promise for the replacement of damaged or dysfunctional myocardium. Nitric oxide (NO) has been shown to promote embryonic stem (ES) cell differentiation in other systems. We hypothesized that NO, through NO synthase gene transfer or exogenous NO exposure, would promote the differentiation of mouse ES cells into cardiomyocytes (CM). In our study, NO treatment increased both the number and the size of beating foci in embryoid body (EB) outgrowths. Within 2 weeks, 69% of the inducible NO synthase-transduced EB displayed spontaneously beating foci, as did 45% of the NO donor-treated EB, compared with only approximately 15% in controls. Cardiac-specific genes and protein expression were significantly increased in NO-treated ES. Electron microscopy and immunocytochemistry revealed that these NO-induced contracting cells exhibited characteristics consistent with CM. At day 7 in culture, troponin T was expressed in 45.6 +/- 20.6% of the NO-treated ES cells but in only 9.25 +/- 1.77% of control cells. Interestingly, 50.4 +/- 18.4% of NO-treated ES cells were troponin T-negative and annexin V-positive. This apoptotic phenotype was seen in <1% of the control ES cells. These data strongly support our hypothesis that mouse ES cells can be accelerated to differentiate into CM by NO treatment. NO may influence cardiac differentiation by both inducing a switch toward a cardiac phenotype and inducing apoptosis in cells not committed to cardiac differentiation.


Asunto(s)
Miocitos Cardíacos/citología , Miocitos Cardíacos/efectos de los fármacos , Óxido Nítrico/farmacología , Células Madre Pluripotentes/citología , Células Madre Pluripotentes/efectos de los fármacos , Animales , Apoptosis/efectos de los fármacos , Diferenciación Celular/efectos de los fármacos , Línea Celular , Regulación del Desarrollo de la Expresión Génica/efectos de los fármacos , Ratones , Microscopía Electrónica , Miocitos Cardíacos/metabolismo , Fenotipo , Células Madre Pluripotentes/metabolismo , ARN Mensajero/genética , ARN Mensajero/metabolismo
8.
Ann Thorac Surg ; 51(5): 705-710, 1991 May.
Artículo en Inglés | MEDLINE | ID: mdl-28327311

RESUMEN

Hypercalcemic reperfusion of the postischemic heart has been associated with ventricular dysfunction and with ultrastructural changes in the mitochondria. The isolated working rat heart model was used to correlate ventricular function, mitochondrial damage, and high-energy phosphate content with degree and timing of hypercalcemia during reperfusion. When administered early during reperfusion, calcium chloride caused a dose-dependent deterioration in ventricular function, whereas calcium augmented function when it was administered after a 15-minute period of normocalcemic reperfusion. Hearts treated with calcium early during reperfusion demonstrated more mitochondrial damage and decreased stores of adenosine triphosphate than those in which calcium administration was delayed. The data indicate that a period of normocalcemic reperfusion should precede calcium administration in the postischemic heart. Mitochondrial damage resulting in decreased synthesis of adenosine triphosphate is likely the cause of ventricular dysfunction associated with calcium administration in the postischemic heart.

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