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Introduction: Adequate volume resuscitation is very important for a favorable outcome of critically ill patients. Both over and under filling of intravascular volume could be deleterious. Static indices including central venous pressure, pulmonary capillary wedge pressure, left ventricular end-diastolic area, mean arterial pressure (MAP) and tachycardia are commonly used and are known to be of little value in discriminating responders from non-responders. On the other hand dynamic indices such as pulse pressure variation (PPV), inferior vena cava diameter, superior vena cava diameter, aortic blood flow, which are based on variation on the left ventricular stoke volume, have been shown to be more accurate predictors of fluid responsiveness in mechanically ventilated patients. In this study we are evaluating the ability of stroke volume variation (SVV) obtained by Vigileo–FloTrac device to predict fluid responsiveness in patients with acute circulatory failure under complete passive, volume controlled mechanical ventilation and correlating it to manually calculated PPV. Materials and methods: Twenty five patients aged above 18 years, with acute circulatory failure and at least one sign of tissue hypoperfusion requiring fluid resuscitation and mechanical ventilation were included. Excluded are patients with cardiogenic shock, acute pulmonary edema, LVEF 65 mmHg by norepinephrine, 500 ml of Hes-steril were administered over 10 min. Static and dynamic hemodynamic parameters were taken in supine position before and after fluid challenge. Patients who had an increase of cardiac index measured by trans-thoracic echocardiography ⩾15% of baseline measurement were considered responders. Results: Fourteen patients were fluid responders. Before fluid challenge SVV and PPV were significantly higher in responders than non-responders (p = 0.0001 for each). SVV ⩾ 8.15% predicted responders with a sensitivity of 100% and specificity 81.1% (AUC 0.906). PPV ⩾ 10.2 also predicted responders with a sensitivity of 92.9% and specificity of 90.9% (AUC 0.974). The higher the SVV before fluid challenge the higher the percentage of increase of CI following fluid challenge (r = 0.733, p = 0.00). PPV showed the same correlation pattern with percentage increase of CI (r = 0.798, p = 0.00). Conclusions: Baseline stroke volume variation ⩾8.15% predicted fluid responsiveness in mechanically ventilated patients with acute circulatory failure. The study also confirmed the ability of pulse pressure variation to predict fluid responsiveness.

Objectives: This study sought to assess the impact of baseline left ventricular (LV) outflow, LV ejection fraction (LVEF), and transvalvular gradient on outcomes following transcatheter aortic valve replacement (TAVR) in patients with severe aortic stenosis (AS). Background: Low flow (i.e., reduced stroke volume index [SVi]) can occur with both reduced and preserved LVEF. Low flow is often associated with low gradient despite severe stenosis and with worse outcomes following surgical aortic valve replacement. However, there are few data about the impact of low flow on outcomes following TAVR. Methods: We retrospectively analyzed the clinical, Doppler-echocardiographic, and outcome data prospectively collected in 639 patients who underwent TAVR for symptomatic severe AS in 2 Canadian centers. Results: In this cohort, 334 (52.3%) patients had a low flow (SVi <35 ml/m2) and these patients had increased 30-day mortality (11.4 vs. 5.9%, p = 0.01), 2-year all-cause mortality (35.3 vs. 30.9%, p = 0.005), and 2-year cardiovascular mortality (25.7 vs. 16.8%, p = 0.01) compared with patients with normal flow. Reduced flow was an independent predictor of 30-day mortality (odds ratio: 1.94, p = 0.026), cumulative all-cause mortality (hazard ratio: 1.27 per 10 ml/m² SVi decrease, p = 0.016), and cumulative cardiovascular mortality (hazard ratio: 1.29 per 10 ml/m² decrease, p = 0.04). Despite significant association in univariable analyses, low LVEF and low mean gradient were not found to be independent predictors of outcomes in multivariable analyses. Conclusions: Low flow but not low LVEF or low gradient is an independent predictor of early and late mortality following TAVR in high-risk patients with severe AS. SVi should be integrated in the risk stratification process of these patients. [Copyright &y& Elsevier]

Objectives: The goal of this study was to examine the age-associated differences in ventricular-vascular coupling, defined by the ratio of arterial elastance (EaI) to left ventricular systolic elastance (ELVI), and its components, at rest and during exercise.Background: Ejection fraction (EF) increases during exercise, but the EF reserve decreases with aging. Ejection fraction is inversely related to EaI/ELVI, an index of the interaction between arterial and ventricular properties, which is an important determinant of cardiac performance. Thus, age differences in EaI/ELVI during exercise, due to age differences in EaI, ELVI, or both, may help to explain the age deficit in EF reserve.Methods: We noninvasively characterized EaI/ELVI = end-systolic volume index (ESVI)/stroke volume index (SVI) and its two determinants EaI = end-systolic pressure/SVI, and ELVI = end-systolic pressure/ESVI, at rest and during exercise in 239 healthy men and women (age range, 21 to 87 years). Blood pressures were assessed with cuff sphygomanometry, and cardiac volumes with gated blood pool scintingraphy.Results: Resting EaI/ELVI was not age related in men or women. In both sexes, EaI/ELVI decreased during exercise and declined to a lesser extent in older subjects. There were gender differences in the components of EaI/ELVI during exercise: EaI was greater in older versus young women (p = 0.01) but was unaffected by age in men. Left ventricular systolic elastance increased to a greater extent in young versus older subjects (p = 0.0001 for men, p = 0.07 for women).Conclusions: Age-associated differences in EaI/ELVI occur in both genders during exercise. Sub-optimal ventricular-vascular coupling helps to explain the age-associated blunting of maximal exercise EF, and its underlying mechanisms appear to differ between men and women. [Copyright &y& Elsevier]

The removal of β1-adrenergic receptor (β1AR) autoantibodies by immunoadsorption (IA) has been proposed as a potential mechanism for the improvement of the left ventricular function in dilated cardiomyopathy (DCM). In the present study, the possible association between removal of the autoantibodies against the human β1AR with the hemodynamic improvement induced by IA was investigated.IA was performed in 22 DCM patients (n=22; NYHA III–IV, EF<30%, stable medication). The β1AR autoantibodies from column eluents (CE) were detected by enzyme-linked immunosorbent assay (ELISA) and BIAcore methods. CE of 32% (7/22) of the patients was found to be antibody-positive with ELISA or BIAcore. In addition, a bioassay system was also used for the detection of this autoantibody. Seventy-three percent (16/22) of the patients were found to be antibody-positive by this method. However, independent of the β1AR antibody detection method, both antibody-positive and antibody-negative groups showed similar acute and prolonged hemodynamic improvements during IA therapy. Furthermore, antibody-positive and -negative groups received a comparable improvement of left ventricular ejection fraction.These results suggest that different mechanisms are involved in the hemodynamic improvement induced by IA. The beneficial hemodynamic effects induced by IA are not directly associated with the removal of β1AR autoantibodies. [Copyright &y& Elsevier]