Speckle tracking echocardiography enables the detection of subclinical left ventricular dysfunction at rest in many heart diseases and potentially in severe liver diseases. It could also possibly serve as a predictor for survival. In this study, 117 patients evaluated for liver transplantation in a single center between May 2010 and April 2016 with normal left ventricular ejection fraction were included according to clinical characteristics of their liver disease: (1) compensated (n = 29), (2) clinically significant portal hypertension (n = 49), and (3) decompensated (n = 39). Standard echocardiography and speckle tracking echocardiography were performed at rest and during dobutamine stress. Follow-up amounted to three years to evaluate survival and major cardiac events. Altogether 67% (78/117) of the patients were transplanted and 32% (31/96 patients) died during the three-year follow-up period. Global longitudinal strain (GLS) at rest was significantly increased (became more negative) with the severity of liver disease (p < 0.001), but reached comparable values in all groups during peak stress. Low (less negative) GLS values at rest (male: >−17/female: >−18%) could predict patient survival in a multivariate Cox regression analysis (p = 0.002). GLS proved valuable in identifying transplant candidates with latent systolic dysfunction.

Terminal heart failure (HF) is the most prevalent cause of death in the Western world and the implantation of a left ventricular assist device (LVAD) has become the gold standard therapy today. Most of the actually implanted devices are driven at a constant speed (CS) regardless of the patient’s physiological demand. A new physiological controller [power ratio (PR) controller], which keeps a constant ratio between LVAD power and left ventricular power, a previous concept [preload responsive speed (PRS) controller], which adds a variable LVAD power to reach a defined stroke work, and a CS controller were compared with an unimpaired ventricle in a full heart computer simulation model. The effects of changes in preload, afterload and left ventricular contractility are displayed by global hemodynamics and ventricular pressure-volume loops. Both physiological controllers demonstrated the desired load dependency, whereas the PR controller exceeded the PRS controller in response to an increased load and contractility. Response was inferior when preload or contractility was decreased. Thus, the PR controller might lead to an increased exercise tolerance of the patient. Additional studies are required to evaluate the controllers

A simple but reliable and safe anaesthetic procedure is required for surgical interventions in small rodents. Combined ketamine and xylazine injections are often used in rats for less invasive surgery, possibly with spontaneous breathing and without airway management. However, there are important pitfalls to be avoided by special precautions and monitoring, as shown subsequently. Observational study. Twenty-four anaesthetic procedures for bile duct ligation, sham operation or carotid artery dilatation in 20 male Sprague-Dawley rats, preoperatively weighing between 440 and 550 g. Intolerable high mortality rates occurred in the first 7 postoperative days while establishing a new experimental model in rats using ketamine-xylazine anaesthesia. Rats were spontaneously breathing ambient air during the first 12 surgeries without airway management. An observed high mortality rate in these animals led to a change in the trial protocol: the insufflation of 2 litres of oxygen per minute via nose cone during the following 12 rat surgeries. Retrospective comparison of the outcome (without oxygen vs. with oxygen insufflation) was conducted. The perioperative mortality rate could be significantly reduced from 58% (7/12) to 17% (2/12) (p = 0.036) by oxygen insufflation via nose cone. Significantly different levels of intraoperative oxygen saturation (SpO₂; 89 ± 4% [without oxygen] vs. 97 ± 0.5% [with oxygen], p < 0.0001), but no significant differences in heart rate (HR; 267 ± 7 beats minute^–1 [bpm] [without oxygen] vs. 266 ± 6 bpm [with oxygen], p = 0.955) were observed. In summary, rats under ketamine-xylazine anaesthesia are susceptible to hypoxia. This may lead to increased delayed mortality related to hypoxia induced lung failure. Apparently, this is an underestimated problem. We highly recommend using additional oxygen insufflation in spontaneously breathing rats under ketamine-xylazine anaesthesia with basic monitoring such as measurement of oxygen saturation.

Cirrhotic patients often suffer from cirrhotic cardiomyopathy (CCM). Previous animal models of CCM were inconsistent concerning the time and mechanism of injury; thus, the temporal dynamics and cardiac vulnerability were studied in more detail. Rats underwent bile duct ligation (BDL) and a second surgery 28 days later. Cardiac function was assessed by conductance catheter and echocardiography. Histology, gene expression, and serum parameters were analyzed. A chronotropic incompetence (P_d31 < 0.001) and impaired contractility at rest and a reduced contractile reserve (P_d31 = 0.03, P_dob-d31 < 0.001) were seen 31 days after BDL with increased creatine (P_d35, P_d42, and P_d56 < 0.05) and transaminases (P_d31 < 0.001). A total of 56 days after BDL, myocardial fibrosis was seen (P_d56 < 0.001) accompanied by macrophage infiltration (CD68: P_group < 0.001) and systemic inflammation (TNFα: P_group < 0.001, white blood cell count: P_group < 0.001). Myocardial expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) was increased after 31 (P_d31 < 0.001) and decreased after 42 (P_d42 < 0.001) and 56 days (P_d56 < 0.001). Caspase-3 expression was increased 31 and 56 days after BDL (P_d31 = 0.005; P_d56 = 0.005). Structural changes in the myocardium were seen after 8 weeks. After the second surgery (second hit), transient myocardial insufficiency with secondary organ dysfunction was seen, characterized by reduced contractility and contractile reserve.

The extent of right ventricular compensation compared to the left ventricle is restricted and varies among individuals, which makes it difficult to define. While establishing a model of acute pulmonary hypertension in pigs we observed two different kinds of compensation in our animals. Looking deeper into the hemodynamic data we tried to delineate why some animals could compensate and others could not. Pulmonary hypertension (mean pressure 45 mmHg) was induced gradually by infusion of a stable thromboxane A₂ analogue U46619 in a porcine model (n = 22). Hemodynamic data (pressure-volume loops, strain-analysis of echocardiographic data and coronary flow measurements) were evaluated retrospectively for the short-term right ventricular compensatory mechanisms and limits (Roehl et al. [2012] Acta Anaesthesiol. Scand., 56:449–58) 10 animals showed stable arterial blood pressures, whereas 12 pigs exhibited a significant drop of 16.4 ± 9.9 mmHg. Cardiac output and heart rate were comparable in both groups. In contrast, right ventricular contractility and coronary flow only rose in the stable group. The unchanging values in the decrease group correlated with an increasing ST-segment depression and a loss of ventricular synchronism and resulted in a larger septum bulging to the right ventricle. Simultaneously, a reduced left-ventricular end-diastolic volume and a missing improvement in contractility in the posterior septal and inferior free wall of the left ventricle have been observed. Our findings suggest that right ventricular compensation during acute pulmonary hypertension is strongly dependent on the individual capability to increase coronary flow. The cause for inter-individual variability could be the dimension and reactivity of the coronary system.