The Effect of Everolimus Initiation and Calcineurin Inhibitor Elimination on Cardiac Allograft Vasculopathy in De Novo Recipients: One-Year Results of a Scandinavian Randomized Trial.

Early initiation of everolimus with calcineurin inhibitor therapy has been shown to reduce the progression of cardiac allograft vasculopathy (CAV) in de novo heart transplant recipients. The effect of de novo everolimus therapy and early total elimination of calcineurin inhibitor therapy has, however, not been investigated and is relevant given the morbidity and lack of efficacy of current protocols in preventing CAV. This 12-month multicenter Scandinavian trial randomized 115 de novo heart transplant recipients to everolimus with complete calcineurin inhibitor elimination 7-11 weeks after HTx or standard cyclosporine immunosuppression. Ninety-five (83%) patients had matched intravascular ultrasound examinations at baseline and 12 months. Mean (± SD) recipient age was 49.9 ± 13.1 years. The everolimus group (n = 47) demonstrated significantly reduced CAV progression as compared to the calcineurin inhibitor group (n = 48) (ΔMaximal Intimal Thickness 0.03 ± 0.06 and 0.08 ± 0.12 mm, ΔPercent Atheroma Volume 1.3 ± 2.3 and 4.2 ± 5.0%, ΔTotal Atheroma Volume 1.1 ± 19.2 mm(3) and 13.8 ± 28.0 mm(3) [all p-values ≤ 0.01]). Everolimus patients also had a significantly greater decline in levels of soluble tumor necrosis factor receptor-1 as compared to the calcineurin inhibitor group (p = 0.02). These preliminary results suggest that an everolimus-based CNI-free can potentially be considered in suitable de novo HTx recipients.

17-year trends in incidence and prognosis of cardiogenic shock in patients with acute myocardial infarction in western Sweden.

BACKGROUND: Cardiogenic shock remains the leading cause of in hospital death in acute myocardial infarction (AMI) and is associated with a mortality rate of approximately 50%. Here we investigated the 17-year trends in incidence and prognosis of AMI-induced cardiogenic shock in Västra Götaland in western Sweden, an area with approximately 1.6 million inhabitants. The study period includes the transition from thrombolysis to primary percutaneous coronary intervention (PCI) as the region-wide therapy of choice for patients with ST-elevation myocardial infarction (STEMI). METHODS: Data on patients hospitalized in cardiac care units in Västra Götaland, Sweden between 1995 and 2013 were obtained from the Swedish Websystem for Enhancement of Evidence-based Care in Heart Disease Evaluated According to Recommended Therapies (SWEDEHEART). We determined the incidence of cardiogenic shock among patients diagnosed with AMI and the risk of death associated with developing cardiogenic shock. We fitted logistic regression models to study which factors predicted post-AMI cardiogenic shock. Analyses were performed on complete case data as well as after multiple imputation of missing data. RESULTS: Incidence of cardiogenic shock as a complication of AMI declined in western Sweden in the past decade, from 14% in 1995 to 4% in 2012. The risk of dying once cardiogenic shock had developed increased during the study period (p<0.01). Patients presenting with STEMI were more likely to develop cardiogenic shock than patients presenting with non STEMI (p<0.001). CONCLUSIONS: The incidence of cardiogenic shock has declined but cardiogenic shock carries a worse prognosis today than in 1995.

Transcranial Doppler microembolic signals and serum marker evidence of brain injury during transcatheter aortic valve implantation.

BACKGROUND: Recent studies have shown that transcatheter aortic valve implantation (TAVI) is associated with new foci of restricted diffusion on cerebral magnetic resonance imaging suggestive of cerebral microembolism. The aim of the present investigation was to quantify the cerebral embolic load and to evaluate during which phase of the TAVI procedure microembolism occurs. We also evaluated the association between the cerebral embolic load and post-procedural release of S100B, a serological marker of cerebral injury. METHODS: In 21 patients, we described the extent and intra-procedural distribution of microemboli during the TAVI procedure using the transcranial Doppler technique. S100B, a marker of astroglial injury, was measured for 24 h after the procedure, and the area under the curve (AUC(24h) ) relating S100B to time was calculated. RESULTS: During the TAVI procedure, a mean of 282 ± 169 emboli was detected, 37% occurred during manipulation of the aortic arch/root/valve by guide wires and catheters, 22% occurred immediately after balloon dilatation of the native valve and 41% occurred during frame expansion of the valve prosthesis. S100B increased in all patients with a peak at 1 h after the procedure and returned to baseline after 4 h. There was a positive correlation between the total amount of cerebral microemboli and the AUC(24h) for S100B (r = 0.68, P < 0.001). None of the patients developed neurological impairment. CONCLUSION: TAVI is associated with a substantial amount of cerebral microemboli. The microembolic load correlates to the degree of post-procedural release of a marker of cerebral injury.