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Ventricular assist devices (VADs) have been associated with the development of anti-HLA antibodies ('allosensitization'), but data on devices providing biventricular support in adults are limited. We sought to characterize differences in anti-HLA antibody formation in adult patients receiving left- (LVAD) versus biventricular- (BiVAD) assist devices as bridge to transplantation (BTT) by retrospectively reviewing the records of adult patients who have undergone VAD implantation at our institution. We assessed 82 patients supported with a pulsatile-flow paracorporeal BiVAD and compared them with 40 patients receiving LVAD till 2018. Forty-eight (58.5%) of the BiVAD and 23 (57.5%) of the LVAD patients were eventually transplanted (p = 0.91) with an average time to transplantation 559 and 598 days, respectively (p = 0.73). Evidence of sensitization pre-VAD was found in 11.0% of the BiVAD patients and 15.0% of the LVAD ones (p = 0.53); these percentages rose to 43.9% (p 0.001) and 40.0% (p = 0.01), respectively. The post-VAD sensitization status was not significantly different between the BiVAD and the LVAD group (p = 0.68). De novo sensitization was comparable between the two groups (p = 0.55). Post-transplantation outcomes regarding rejections and cardiac allograft vasculopathy were also similar. Conclusively, BiVAD- and LVAD- induced allosensitization do not appear to differ significantly.

We present the case of a 68-year-old woman, currently asymptomatic but with a history of paroxysmal atrial fibrillation and tachycardia-bradycardia syndrome, for which she underwent a DDD pacemaker implantation and was started on oral anticoagulants. A recent chest X-ray (figure 1), for respiratory infection, was performed and the patient was referred to our institution for evaluation. Following diagnostic procedures, the patient was successfully operated on. heartjnl;105/8/656/F1F1F1Figure 1Preoperative chest X-ray (A) and chest CT with contrast (B). QUESTION: What is the most likely diagnosis?Mitral stenosis.Pericardial cyst.Left atrial appendage aneurysm.Left atrial myxoma.Atrial septal defect.

Pulmonary hypertension and right ventricular (RV) dysfunction may complicate the implantation of a left ventricular assist device (LVAD). We examined whether inhaled vasodilators can sufficiently reduce RV afterload, avoiding the need for temporary RV mechanical support.The study includes 7 patients with RV dysfunction after LVAD insertion. Treatment consisted of inotropes, inhaled nitric oxide (10 ppm), and iloprost (10 μg) in repeated doses. Full hemodynamic profile was obtained before inhalation, during administration of inhaled NO alone (before and after iloprost), as well as after the first two doses of inhaled iloprost. Tricuspid annular velocity was estimated at baseline and before and after adding iloprost.There was a statistically significant reduction in pulmonary vascular resistance (PVR), mean pulmonary artery pressure (MPAP), RV systolic pressure, and pulmonary capillary wedge pressure, and a considerable increase in LVAD flow, LV flow rate index, and tricuspid annular velocity at all points of evaluation versus baseline. By the end of the protocol, MPAP/mean systemic arterial pressure, and PVR/systemic vascular resistance ratios were reduced by 0.17±0.03 (95% confidence interval, 0.10 to 0.25, p=0.001) and 0.12±0.025 (95% confidence interval, 0.06 to 0.18; p=0.003), respectively. The tricuspid annular velocity increased by 2.3±0.18 cm/s (95% confidence interval, 1.83 to 2.73 cm/s; p0.001). Pairwise comparisons before and after iloprost showed an important decrease in PVR (p=0.022), MPAP (p=0.001), pulmonary capillary wedge pressure (p=0.002), and RV systolic pressure (p0.001), and a rise in tricuspid annular velocity (p=0.008).Inhaled vasodilators mainly affected the pulmonary vasculature. Combination treatment with inhaled NO and iloprost sufficiently decreased PVR and MPAP on the basis of an additive effect, improved RV function, and avoided the need for RV assist device.

Background: Calcific aortic valve stenosis (CAVS) is seen in a large proportion of individuals over 60 years. It is an active process, influenced by lipid accumulation, mechanical stress, inflammation, and abnormal extracellular matrix turnover. Various biomarkers (BMs) are studied, as regards mechanisms, diagnosis and prognosis. Methods: In the calcified valves calcium deposition, elastin fragmentation and disorganization of cellular matrix were assessed, together with expression of OPN, OPG, osteocalcin (OCN) and RL2. We prospectively studied the following serum BMs in 60 patients with CAVS and compared them to 20 healthy controls, free from any cardiac disease: Matrix metalloproteinases (MMP) 2 and 9 and tissue inhibitor of metalloproteinase 1 (TIMP1), which regulate collagen turnover, inflammatory factors, i.e. tumor necrosis factor a (TNFa), interleukin 2 (IL2), transforming growth factor β1 (TGF-β1) which regulates fibrosis, fetuin-A (fet-A), osteopontin (OPN), osteoprotegerin (OPG), sclerostin (SOST), and relaxin-2 (RL2) which positively or negatively regulate calcification. Monocyte chemoattractant protein 1 (MCP-1) which regulates migration and infiltration of monocytes/macrophages was also studied as well as malondialdehyde (MDA) an oxidative marker. Results: Extent of tissue valve calcification (Alizarin Red stain) was negatively correlated with tissue elastin, and RL2, and positively correlated with tissue OCN and serum TIMP1 and MCP-1 and negatively with MMP9. Tissue OCN was positively correlated with OPN and negatively with the elastin. Tissue OPN was negatively correlated with elastin and OPG. Tissue OPN OPG and RL2 were not correlated with serum levels In the serum we found in patients statistically lower TIMP1, fet-A and RL2 levels, while all other BMs were higher compared to the healthy group. Positive correlations between SOST and IL2, OPG and MDA but negative with TNFa and OPN were found; also MMP9 was negatively correlated with TNFa and MCP-1 was negatively correlated with TIMP1. Conclusion: We found that many BMs expressing calcification, collagen breakdown, or formation, and inflammation are increased in the valve tissue and in the serum of patients with CAVS as compared with healthy group. Our findings may give new insights towards diagnosis but also therapy. Thus antisclerostin, and antiflammatory agents could be tried for preventing aortic calcification progression.

Acute hyperglycemia has been associated with delayed gastric emptying in healthy controls. Erythromycin has recently been found to be a gastrointestinal prokinetic agent in both solids and hypertonic liquids. Our aim was to examine whether the acute steady-state hyperglycemia reduces the erythromycin-induced acceleration of gastric emptying of hypertonic liquids after a fasted state of the stomach in healthy subjects. In 12 healthy subjects scintigraphic measurement of gastric emptying of a hypertonic radiolabeled liquid meal, during normoglycemia (5–8.9 mmol/l glucose) or induced hyperglycemia (16–19 mmol/liter glucose) by intravenous glucose infusion after giving either placebo or 200 mg intravenous erythromycin, was performed on four separate days in random order. In the hyperglycemic state compared with normoglycemia, either after placebo administration or erythromycin, the gastric emptying of the hypertonic liquid was reduced. The lag-phase duration was significantly increased (17.5 ± 5.5 min, and 7.2 ± 4.5 min vs 10.5 ± 3.4 min, and 3.5 ± 2.5 min, respectively, P < 0.0001) as were the overall T1/2 (gastric emptying time of the half meal) (52.5 ± 13 min and 24.5 ± 5.5 min vs 42 ± 10.5 min, and 16 ± 6 min, respectively, P < 0.0001) and the percentage of liquid meal retained in the stomach at 60 and 100 min postprandially (P < 0.001). In conclusion, hyperglycaemia attenuates the acceleration effect of erythromycin and decreases the overall gastric emptying rate of hypertonic liquids in healthy subjects.

Background: Management of patients with co-existent coronary and carotid disease is a controversial and challenging issue. The risk for stroke after coronary artery bypass grafting (CABG) in patients with hemodynamically significant carotid stenosis is up to 30%. In these patients a common practice is to proceed first with the restoration of cerebral perfusion and then perform the coronary revascularization. The rationale is that this strategy will reduce perioperative neurological morbidity and mortality. However, what happens when the carotid procedure is acutely complicated by cardiac instability which necessitates the interruption of the carotid procedure? Case report: We describe a case of a patient with unstable angina and high grade asymptomatic bilateral carotid stenosis who underwent emergency combined CABG and carotid endarterectomy (CEA). Due to hemodynamic instability, ST-T changes, hypotension and bradycardia, upon completion of endarterectomy we placed a carotid shunt and the patient was put on cardiopulmonary bypass through median sternotomy. After triple CABG (duration of 90 minutes) we concluded the interrupted CEA procedure with primary closure of the carotid arteriotomy with the shunt in place. The postoperative course was uneventful and the patient was discharged after a week. In extreme cases with bilateral severe carotid stenosis and coronary artery disease where the carotid procedure should be interrupted, we suggest the use of carotid shunt which can provide adequate cerebral perfusion giving time to cardiac surgeon to perform the life saving cardiac procedure first. Background Management of patients with co-existent coronary and carotid disease is a controversial and challenging issue [1]. The risk for stroke after coronary artery bypass grafting (CABG), in patients with hemodynamically significant carotid stenosis is up to 30% [2]. Therefore, in these patients a common practice is to proceed first with the restoration of cerebral perfusion and then perform the coronary revascularization. The rationale is that this strategy will reduce perioperative neurological morbidity and mortality. However, according to our knowledge, there is no published data concerning combined carotid endarterectomy (CEA) and CABG where intraoperatively the carotid procedure was acutely complicated by cardiac instability necessitating the interruption of the carotid procedure. We describe our experience using a temporary carotid shunt in order to maintain cerebral perfusion until CABG was completed and then the operation was concluded with the closure of carotid arteriotomy. Case presentation Patient’s history and management A 80 year old male patient with a history of coronary artery disease (CAD) and severe left ventricular dysfunction was urgently admitted in our institution with unstable angina. Ejection fraction was 20%. Coronary angiography revealed severe triple vessel disease. Moreover, duplex

Stentless aortic bioprostheses are designed to offer better hemodynamics, less mechanical stress to the leaflets and as a result less degeneration. Although encouraging results are reported, little evidence has been published regarding reoperations of stentless valves. We are reporting a case of a structural valve dysfunction of an O'Brien-Angell stentless prosthesis, which could not be extracted during reoperation without damaging the aortic root. We are presenting a simple, quick and effective surgical solution, the surgical 'valve within a valve' technique for the avoidance of a redo complex root procedure.

Background: Acute hyperglycemia has been associated with delayed gastric emptying of solid foods in healthy control subjects. Erythromycin has been found to be a gastrointestinal prokinetic agent in humans. We examined whether acute steady-state hyperglycemia reduces the erythromycin-induced acceleration of gastric emptying of a solid meal after a fasted state in healthy subjects. Methods: Twelve healthy subjects ate standard solid meals that had been radiolabeled. Gastric emptying was measured by scintigraphy during normoglycemia (5–8.9 mmol/L glucose) and hyperglycemia induced by intravenous glucose (16–19 mmol/L glucose) after administration of placebo or 200 mg of erythromycin intravenously. Emptying was measured randomly on 4 different days. Results: Administration of erythromycin during normoglycemia or induced hyperglycemia compared with placebo accelerated the gastric emptying of the solid meal but did not completely normalize the delay caused by hyperglycemia versus normoglycemia (p < 0.001). In both conditions, erythromycin versus placebo significantly reduced the lag-phase duration (9.7 ± 2.3 min and 22.0 ± 3.9 min vs. 38.3 ± 5.7 min and 49.5 ± 6.0 min, respectively; p < 0.001), gastric emptying of the half meal (39.2 ± 4.0 min and 52.0 ± 7.1 min vs. 75.7 ± 11.8 min and 94.0 ± 13.4 min, respectively; p < 0.001), and the percentage of meal retained in the stomach 120 min postprandially (p < 0.001). Conclusion: The erythromycin-induced acceleration effect on gastric emptying was related to the plasma glucose level. Hyperglycemia might have chosen a cholinergic antagonist pathway that delayed gastric emptying of solids. Even though induced hyperglycemia inhibited gastric emptying, erythromycin accelerated the gastric emptying rate through two distinct pathways: cholinergic and noncholinergic.