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Dive into the research topics where Stephan Heller is active.

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Featured researches published by Stephan Heller.


European Radiology | 2006

Superficial femoral artery: current treatment options

Gunnar Tepe; Jörg Schmehl; Stephan Heller; Benjamin Wiesinger; Claus D. Claussen; Stephan H. Duda

Treatment of the superficial femoral artery (SFA) has been among the least effective of all endovascular procedures in terms of long-term patency. The relatively small vessel lumen, in conjunction with a high plaque burden, slow flow, and a high frequency of primary occlusions, contributes to a considerable rate of acute technical failures. Because of these technical limitations a much effort has been made during the past years. This manuscript should summarize the hopes and limitations of different approaches such as brachytherapy, cutting balloons, stents and stent grafts, drug-eluting stents, and drug-coated balloons.


CardioVascular and Interventional Radiology | 2012

Epithelioid Angiosarcoma With Metastatic Disease After Endovascular Therapy of Abdominal Aortic Aneurysm

Jörg Schmehl; Marcus Scharpf; Klaus Brechtel; Günay Kalender; Stephan Heller; Claus D. Claussen; Mario Lescan

Malignancies of the aortic wall represent a rare condition, and only a few reports have covered cases of sarcomas arising at the site of a prosthesis made of Dacron. A coincidence with endovascular repair has only been reported in one case to date. We report a patient with epithelioid angiosarcoma and metastatic disease, which was found in an aneurysmal sac after endovascular aortic repair for abdominal aortic aneurysm.


European Journal of Gastroenterology & Hepatology | 2012

Hepatocellular carcinoma: initial tumour response after short-term and long-interval chemoembolization with drug-eluting beads using modified RECIST.

Roland Syha; Dominik Ketelsen; Stephan Heller; J Schmehl; Stefanie Mangold; Martin Heuschmid; Fabian Springer; Claus D. Claussen; Klaus Brechtel

Objective The aim of this study was to evaluate the initial tumour response after one, respectively, two transarterial chemoembolizations (TACE) with drug-eluting (DC) beads in patients with hepatocellular carcinoma (HCC). Methods A total of 26 patients with clinically approved HCC underwent one or two TACE with DC Beads within 6 weeks and were evaluated after 12 weeks by MRI or computed tomography on the basis of the modified Response Evaluation Criteria in the Solid Tumours guidelines for HCC. For improved comparability of both groups, 16 patients were matched in terms of Child–Pugh classification, Barcelona classification of liver cancer, age and sex. Results The overall tumour response showed progressive disease in 11% and an objective response in 89% for the double TACE group compared with progressive disease in 29.5%, objective response in 34.5% and stable disease in 35% for the single TACE group. In the matched population, absolute tumour shrinkage was 61.1±28.3% for the double TACE group and 14.1±38.5% for the single TACE group (P<0.05). Conclusion This retrospective study shows significantly higher tumour shrinkage in patients who underwent two TACE within 6 weeks compared with patients who underwent a single intervention in terms of the initial response rate after 12 weeks. It emphasizes the use of matched populations for the evaluation of tumour response in HCC after TACE.


Journal of Vascular and Interventional Radiology | 2011

Stent-assisted embolization as "bailout" option in aortic aneurysm.

Klaus Brechtel; Dorothee H.L. Bail; Christian Schwentner; Stephan Heller; Joerg Schmehl; Nora Goebel; Albertus M. Scheule; Claus D. Claussen; Guenay Kalender

The authors report two cases of stent-assisted embolization (SAE) in the aorta. In one case, SAE was performed for treatment of a pseudoaneurysm; the procedure consisted of stent placement and embolization with an AMPLATZER Vascular Plug and detachable coils through the stent struts. In the second case, SAE was performed to stop acute bleeding from an aortoureteral fistula. Before SAE in this case, the aortic bifurcation was reconstructed with self-expandable and balloon-expandable stents. SAE was technically successful in both cases. SAE for aortic pathologic processes may be useful in selected cases as an alternative to surgery or endovascular stent-graft therapy.


Journal of Gastroenterology and Hepatology | 2010

Education and Imaging. Gastrointestinal: Hepatic portal venous gas after cardiogenic shock and intraaortic ballon pulsation therapy.

Ferruh Artunc; Stephan Heller; Martin Heuschmid; Reimer Riessen; Michael Haap

Entrapment of gas in the portal veins has been first described in 1955 by Wolfe and Evens in infants suffering from necrotizing enterocolitis. It generally heralds an abdominal catastrophe requiring urgent surgical intervention. Pathogenetically, portal venous gas results from a breakdown of the mucosal barrier usually following ischemic necrosis of the intestinal wall. We report on a 49-year-old Caucasian patient with primary systemic light-chain (AL) amyloidosis lambda and severe systolic and diastolic heart failure who developed cardiogenic shock requiring intraarotic balloon pump therapy (IABP). Treatment was complicated by upper mesenteric ischemia leading to paralytic ileus (Figure 1) and mucosal injury of the stomach. CT scan showed entrapment of gas in the gastric wall, splenic vein, and the left portal venous system as a consequence of bacterial translocation and gas production (Figure 1). Emergency exploratory laparotomy was not amenable due to poor general status and conservative treatment consisting of antimicrobial therapy (metronidazol, piperacillin/tazobactam and fluconazol) and stimulation of bowel function using enema and neostigmine was commenced. After 2 days, complete recovery of bowel function was achieved and oral diet was well tolerated. Ultrasound revealed the disappearance of the portal venous gas (PVG) and the patient survived without any further need for surgery. The differential diagnosis for portal venous gas includes necrotizing enteritis, arterial and venous mesenteric occlusions, bowel obstruction, perforated gastric ulcer, hemorrhagic pancreatitis, sigmoid diverticulitis, and various iatrogenic causes. Portal venous gas is diagnosed usually by CT scan showing tubular lucencies branching from the porta hepatis to the peripheral liver margin. The appearance arises from the accumulation of gas in the distal portal system, which is carried in a hepatopedal direction by the flow in the portal vein. Portal venous gas must be differentiated from pneumobilia, which tends to accumulate in the large central bile ducts near the liver hilus, due to the hepatofugal biliary flow. This case presents an unusual complication of cardiogenic shock with severe intestinal ischemia possibly related to impairment of splanchnic perfusion caused by IABP therapy and hypotension. Without surgery, mortality rates for PVG have been reported to be as high as 75 %, in particular in those cases of PVG due to intestinal ischemia. In the case of inoperable patients, however, conservative management remains the only option.


Journal of Gastroenterology and Hepatology | 2010

Gastrointestinal: Hepatic portal venous gas after cardiogenic shock and intraaortic ballon pulsation therapy

Ferruh Artunc; Stephan Heller; Martin Heuschmid; Reimer Riessen; Michael Haap

Entrapment of gas in the portal veins has been first described in 1955 by Wolfe and Evens in infants suffering from necrotizing enterocolitis. It generally heralds an abdominal catastrophe requiring urgent surgical intervention. Pathogenetically, portal venous gas results from a breakdown of the mucosal barrier usually following ischemic necrosis of the intestinal wall. We report on a 49-year-old Caucasian patient with primary systemic light-chain (AL) amyloidosis lambda and severe systolic and diastolic heart failure who developed cardiogenic shock requiring intraarotic balloon pump therapy (IABP). Treatment was complicated by upper mesenteric ischemia leading to paralytic ileus (Figure 1) and mucosal injury of the stomach. CT scan showed entrapment of gas in the gastric wall, splenic vein, and the left portal venous system as a consequence of bacterial translocation and gas production (Figure 1). Emergency exploratory laparotomy was not amenable due to poor general status and conservative treatment consisting of antimicrobial therapy (metronidazol, piperacillin/tazobactam and fluconazol) and stimulation of bowel function using enema and neostigmine was commenced. After 2 days, complete recovery of bowel function was achieved and oral diet was well tolerated. Ultrasound revealed the disappearance of the portal venous gas (PVG) and the patient survived without any further need for surgery. The differential diagnosis for portal venous gas includes necrotizing enteritis, arterial and venous mesenteric occlusions, bowel obstruction, perforated gastric ulcer, hemorrhagic pancreatitis, sigmoid diverticulitis, and various iatrogenic causes. Portal venous gas is diagnosed usually by CT scan showing tubular lucencies branching from the porta hepatis to the peripheral liver margin. The appearance arises from the accumulation of gas in the distal portal system, which is carried in a hepatopedal direction by the flow in the portal vein. Portal venous gas must be differentiated from pneumobilia, which tends to accumulate in the large central bile ducts near the liver hilus, due to the hepatofugal biliary flow. This case presents an unusual complication of cardiogenic shock with severe intestinal ischemia possibly related to impairment of splanchnic perfusion caused by IABP therapy and hypotension. Without surgery, mortality rates for PVG have been reported to be as high as 75 %, in particular in those cases of PVG due to intestinal ischemia. In the case of inoperable patients, however, conservative management remains the only option.


Journal of Gastroenterology and Hepatology | 2010

Gastrointestinal: Hepatic portal venous gas after cardiogenic shock and intraaortic ballon pulsation therapy: Education and Imaging

Ferruh Artunc; Stephan Heller; Martin Heuschmid; Reimer Riessen; Michael Haap

Entrapment of gas in the portal veins has been first described in 1955 by Wolfe and Evens in infants suffering from necrotizing enterocolitis. It generally heralds an abdominal catastrophe requiring urgent surgical intervention. Pathogenetically, portal venous gas results from a breakdown of the mucosal barrier usually following ischemic necrosis of the intestinal wall. We report on a 49-year-old Caucasian patient with primary systemic light-chain (AL) amyloidosis lambda and severe systolic and diastolic heart failure who developed cardiogenic shock requiring intraarotic balloon pump therapy (IABP). Treatment was complicated by upper mesenteric ischemia leading to paralytic ileus (Figure 1) and mucosal injury of the stomach. CT scan showed entrapment of gas in the gastric wall, splenic vein, and the left portal venous system as a consequence of bacterial translocation and gas production (Figure 1). Emergency exploratory laparotomy was not amenable due to poor general status and conservative treatment consisting of antimicrobial therapy (metronidazol, piperacillin/tazobactam and fluconazol) and stimulation of bowel function using enema and neostigmine was commenced. After 2 days, complete recovery of bowel function was achieved and oral diet was well tolerated. Ultrasound revealed the disappearance of the portal venous gas (PVG) and the patient survived without any further need for surgery. The differential diagnosis for portal venous gas includes necrotizing enteritis, arterial and venous mesenteric occlusions, bowel obstruction, perforated gastric ulcer, hemorrhagic pancreatitis, sigmoid diverticulitis, and various iatrogenic causes. Portal venous gas is diagnosed usually by CT scan showing tubular lucencies branching from the porta hepatis to the peripheral liver margin. The appearance arises from the accumulation of gas in the distal portal system, which is carried in a hepatopedal direction by the flow in the portal vein. Portal venous gas must be differentiated from pneumobilia, which tends to accumulate in the large central bile ducts near the liver hilus, due to the hepatofugal biliary flow. This case presents an unusual complication of cardiogenic shock with severe intestinal ischemia possibly related to impairment of splanchnic perfusion caused by IABP therapy and hypotension. Without surgery, mortality rates for PVG have been reported to be as high as 75 %, in particular in those cases of PVG due to intestinal ischemia. In the case of inoperable patients, however, conservative management remains the only option.


Journal of Vascular and Interventional Radiology | 2009

Endovascular Treatment of Venous Graft Stenosis in the Inferior Vena Cava and the Left Hepatic Vein after Complex Liver Tumor Resection

Klaus Brechtel; Gunnar Tepe; Stephan Heller; Joerg Schmehl; Markus Kueper; Claus D. Claussen; Jakub Wiskirchen

Endovascular treatment has been reported for a variety of conditions that result in venous obstruction in the iliocaval territory. The present report describes a patient who underwent a complex resection of a tumor that infiltrated the retrohepatic segment of the inferior vena cava (IVC), necessitating replacement of the IVC with a polytetrafluoroethylene (PTFE) graft. Postoperatively, symptomatic venous obstruction occurred in the graft and the left hepatic vein. Treatment required stent placement bridging native veins and the graft. The patient underwent placement of a self-expanding stent within the IVC and the PTFE graft with treatment of the hepatic vein stenosis via jugular vein access.


The New England Journal of Medicine | 2008

Local Delivery of Paclitaxel to Inhibit Restenosis during Angioplasty of the Leg

Gunnar Tepe; Thomas Zeller; Thomas Albrecht; Stephan Heller; Uwe Schwarzwälder; Jean-Paul Beregi; M.D. Claus D. Claussen; Anja Oldenburg; Bruno Scheller; Ulrich Speck


Biomaterials | 2006

Reduced thrombogenicity of nitinol stents--in vitro evaluation of different surface modifications and coatings.

Gunnar Tepe; Joerg Schmehl; Hans P. Wendel; Sivio Schaffner; Stephan Heller; Marc Gianotti; Claus D. Claussen; Stephan H. Duda

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Gunnar Tepe

University of Tübingen

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Michael Haap

University of Tübingen

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