Doppler ultrasound surveillance of TIPS-patency in the era of covered stents - retrospective analysis of a large single-center cohort.

PURPOSE: The purpose of this study was to determine accuracy and necessity of long-term Doppler ultrasound (DU) surveillance of transjugular intrahepatic portosystemic shunt (TIPS) patency after implantation of an ePTFE-covered stent-graft (Viatorr). METHODS: This single-center retrospective study includes 228 consecutive cirrhotic patients with TIPS implantation due to portal hypertensive complications. Standardized DU surveillance was scheduled 3 - 5 days, 3 months, and 6 months after TIPS implantation and every 6 months thereafter. Portal venography was performed in case of DU findings suspicious of TIPS dysfunction, clinical signs of recurrent portal hypertension, or refractory hepatic encephalopathy. RESULTS: During a mean follow-up of 16.6 ±â€Š23.4 months, 866 DU examinations were performed. Twenty-two cases of TIPS dysfunction were observed in 16 patients with no first dysfunction more than 4 years after implantation. Routine DU in asymptomatic patients had little therapeutic impact (0.75 %). DU and venography were concordant in 39/46 (84.8 %) paired examinations, and 1-, 2-, and 5-year primary TIPS patency was 87.4 %, 83.7 %, and 79.97 %, respectively. Patients with TIPS dysfunction and subsequent successful revision during the first 2 years of follow-up had a significantly higher risk (p = 0.001) of new dysfunction compared to those without TIPS dysfunction. Cumulative 1-, 2-, and 5-year survival was 68.7 %, 61.3 %, and 42.7 %, respectively. CONCLUSIONS: Despite acceptable accuracy, scheduled DU surveillance proved to have minor therapeutic impact. Thus, detailed DU surveillance is not useful in asymptomatic patients after 2 years of unremarkable follow-up. In contrast, long-term DU surveilleance should be performed in patients after successful revision of TIPS dysfunction and patients with prothrombotic states (e. g., portal vein thrombosis, Budd-Chiari syndrome).

Extreme Metabolic Alkalosis and Acute Kidney Injury in a 38-Year-Old Male Patient.

Repeated vomiting may lead to profound loss of fluid and electrolytes. We describe a case with life-threatening acid-base disturbances due to vomiting. A 38-year-old man presented to an emergency department with weakness and decreased urine output after having vomited up to 20 times per day over a period of 7 days. Arterial blood gas analysis revealed a metabolic alkalosis with partial respiratory compensation. Initial management consisted of oxygen therapy and intravenous fluid therapy with normal saline and potassium chloride. To prevent further gastric losses of HCl, proton-pump inhibitors and metoclopramide were administered. The vomiting was caused most likely by a temporary duodenal stenosis due to portal hypertension of unknown etiology. In our opinion, this case demonstrates the successful management of a life-threatening condition by simple measures. Despite extensive diagnostic procedures, the effective treatment of the underlying condition consisted of watchful waiting.

Reversal of Mitochondrial Transhydrogenase Causes Oxidative Stress in Heart Failure.

Mitochondrial reactive oxygen species (ROS) play a central role in most aging-related diseases. ROS are produced at the respiratory chain that demands NADH for electron transport and are eliminated by enzymes that require NADPH. The nicotinamide nucleotide transhydrogenase (Nnt) is considered a key antioxidative enzyme based on its ability to regenerate NADPH from NADH. Here, we show that pathological metabolic demand reverses the direction of the Nnt, consuming NADPH to support NADH and ATP production, but at the cost of NADPH-linked antioxidative capacity. In heart, reverse-mode Nnt is the dominant source for ROS during pressure overload. Due to a mutation of the Nnt gene, the inbred mouse strain C57BL/6J is protected from oxidative stress, heart failure, and death, making its use in cardiovascular research problematic. Targeting Nnt-mediated ROS with the tetrapeptide SS-31 rescued mortality in pressure overload-induced heart failure and could therefore have therapeutic potential in patients with this syndrome.

Myocardial energetics in heart failure.

It has become common sense that the failing heart is an "engine out of fuel". However, undisputable evidence that, indeed, the failing heart is limited by insufficient ATP supply is currently lacking. Over the last couple of years, an increasingly complex picture of mechanisms evolved that suggests that potentially metabolic intermediates and redox state could play the more dominant roles for signaling that eventually results in left ventricular remodeling and contractile dysfunction. In the pathophysiology of heart failure, mitochondria emerge in the crossfire of defective excitation-contraction coupling and increased energetic demand, which may provoke oxidative stress as an important upstream mediator of cardiac remodeling and cell death. Thus, future therapies may be guided towards restoring defective ion homeostasis and mitochondrial redox shifts rather than aiming solely at improving the generation of ATP.

Wavefront-optimized ablation profiles: theoretical background.

PURPOSE: To describe a method for calculating wavefront-optimized ablation profiles to precompensate for the spherical aberration and higher-order astigmatism induced by myopic, hyperopic, and astigmatic corneal laser corrections. SETTING: IROC-Institut für Refraktive und Ophthalmo-Chirurgie, and Institute for Biomedical Engineering, Swiss Federal Institute of Technology, Zürich, Switzerland. METHODS: The basic ablation profile for myopic, hyperopic, and astigmatic correction is derived from the 2nd-order Zernike representation of wavefront aberrations. Including 4th-order spherical aberration and higher-order astigmatism in the theoretical calculation of the ablation profile allows precompensation for the expected amount of higher-order aberrations (HOAs). The shapes of wavefront-optimized ablation profiles are compared with the shapes of "classic" ablation profiles for myopic and astigmatic corrections. RESULTS: The introduction of precompensating spherical aberration and higher-order astigmatism leads to a more aspheric ablation profile with a significant increase in ablation depth (up to 35%) in the midperiphery of the optical zone. The central ablation depth remains unchanged in the myopic correction but increases by 3% in cylinder correction. CONCLUSIONS: Wavefront-optimized ablation profiles provide a simple method to precompensate for the expected 4th-order spherical aberration and higher-order astigmatism in the average eye. Further clinical studies must be performed to prove the theoretical results; demonstrate the reduction in HOAs; and predict safety, predictability, and stability of wavefront-optimized ablation profiles.