Vasovagal reflex is the most common cause of syncope. Pacemaker with rate drop response (RDR) or closed‐loop stimulation (CLS) anti‐syncope algorithms have been studied in recurrent vasovagal syncope (VVS), with conflicting results. We aim to investigate the role of pacemaker therapy and anti‐syncope pacing mode in cardioinhibitory recurrent VVS. MEDLINE, Cochrane Library and registered clinical trials were searched for single or double‐blind randomized controlled trials on pacing as a treatment for recurrent VVS. Five studies were eligible, overall enrolling 228 patients. After pooling data from all trials, pacemaker therapy showed a 63% reduction in syncope recurrence compared to control [Risk Ratio (RR): 0.37; 95% CI: 0.14‐0.98; I2 = 67%)]. Subgroup analyses suggested that the effect was greater in single‐blind studies (RR: 0.07; 95% CI: 0.01‐0.52, I2 = 0%). When comparing pacing algorithms, the results from RDR versus no pacing trials (n = 2) did not show a significant reduction in syncope recurrence (RR: 0.73; 95% CI: 0.25‐2.16, I2 60 = 75%). In contrast, the data from the CLS versus standard pacing trials (n = 3) evidenced a statistically meaningful reduction in syncopal burden (RR: 0.18; 95% CI: 0.07‐0.47, I2 = 0%). It is unclear whether pacemaker therapy reduces syncopal burden in cardioinhibitory recurrent VVS. However, our results suggest effectiveness of CLS pacing mode.

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In recent years new data on the pathophysiology of cardiorenal syndromes (CRS) has been collected but the impact in acute management is still to be established. Hypothesis: We tried to find different patterns using simple clinical and analytical data that could point to the main decompensated mechanism by accessing the impact of Non-invasive ventilation (NIV), the previous renin angiotensin inhibition and the diuretic strategy, bolus vs perfusion, on these different patterns. Methods: We selected 110 patients with decompensation of heart or renal function but excluded 52 for not having CRS or for presenting acute type 5 (sepsis). Results: Mean age was 76,2 yo. 55,2% males. Mortality was 20,7%. 72,41% had preserved left the ventricular function. There were 2 peaks of time/worst renal function, at first 24hrs and between day 3 and 4. Patients with isolated pulmonary congestion were worst at 2,1 days and peripheral only at 4,3 days p=0,0862. Those with peripheral congestion had the same worsening of renal function with furosemide in bolus versus perfusion despite higher doses. Isolated pulmonary congestion combined with a higher dose of furosemide administered by perfusion had a more severe AKI. Patients doing Non Invasive Ventilation with Jugular Venous Distention or Congestive Liver (N=4 of 37) had worst AKI than those without (p<0,05). Previous RAS-inhibitors at maximum dose were protective vs no RAS-inhibition (p=0,03). Conclusion: In conclusion, there are more subtypes than the traditional classification of the cardiorenal lesion in 5 syndromes and the 3 types of heart failure at least based on the location of congestion.