The impact of coronavirus disease 2019 (COVID-19) on the postoperative course of patients after cardiac surgery is unknown. We experienced a major severe acute respiratory syndrome coronavirus 2 ...(SARS-CoV-2) outbreak in our cardiac surgery unit, with several patients who tested positive early after surgery. Here we describe the characteristics, postoperative course, and laboratory findings of these patients, along with the fate of the health care workers. We also discuss how we reorganize and reallocate hospital resources to resume the surgical activity without further positive patients.
After diagnosis of the first symptomatic patient, surgery was suspended. Nasopharyngeal swabs were performed in all patients and health care workers. Patients who were positive for SARS-CoV-2 were isolated and monitored throughout the in-hospital stay and followed up after discharged until death or clinical recovery.
Twenty patients were found to be positive for SARS-CoV-2 sometime after cardiac surgery (mean age 69 ± 10.4 years; median European System for Cardiac Operative Risk Evaluation II score 3 interquartile range, 5.1); the median time from surgery to diagnosis was 15 days (interquartile range, 11). Among the patients, 18 had undergone cardiac surgery and 2 of them transcatheter aortic valve replacement. Overall mortality was 15%. Specific COVID-19–related symptoms were identified in 7 patients (35%). Among the 12 health care workers infected, 1 developed a bilateral mild-grade interstitial pneumonia.
COVID-19 infection after cardiac surgery, regardless the time of the onset, is a serious condition. The systemic inflammatory state that follows extracorporeal circulation may mask the typical COVID-19 laboratory findings, making the diagnosis more difficult. A strict reorganization of the hospital resources is necessary to safely resume the cardiac surgical activity.
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The decision to treat moderate ischemic mitral regurgitation (IMR) at the time of coronary artery bypass surgery (CABG) remains controversial. We previously conducted a prospective randomized trial ...that showed a benefit of adding restricted annuloplasty to bypass surgery (CABG-Ring group) in terms of IMR grade, New York Heart Association classification, and left ventricle reverse remodeling. Here, we present the long-term (>10 years) follow-up data from this randomized trial.
The original trial arms accounted for 54 patients in the CABG-alone and 48 in the CABG-Ring group; patients were re-contacted for follow-up to obtain relevant clinical and echocardiographic information.
The mean follow-up was 160.4 ± 45.5 months. Survival probabilities in the CABG-alone and CABG-Ring groups were 96% vs 93% at 3 years, 85% vs 89% at 6 years, 79% vs 85% at 9 years, 77% vs 83% at 12 years, and 72% vs 80% at 15 years, respectively (P = .18) Freedom from at least moderate IMR or reintervention at last follow-up was also higher in the CABG-Ring group (P < .001). Compared with the CABG-alone group, the CABG-Ring group had a higher degree of left ventricular reverse remodeling (54.7 ± 6.9 mm vs 51.6 ± 6 mm, respectively; P = .03), lower New York Heart Association class (P < .001), and a lower rate of rehospitalization (P = .002).
Long-term follow-up data from our randomized trial further support the utility of performing restricted annuloplasty at the time of CABG to prevent further progression of IMR, mitral reintervention, and left ventricle remodeling. Untreated IMR was associated with significantly higher New York Heart Association class and rehospitalization.
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Background
Mitral valve apparatus is complex and involves the mitral annulus, the leaflets, the chordae tendinae, the papillary muscles as well as the left atrial and ventricular myocardium. ...Secondary mitral regurgitation is a consequence of regional or global left ventricle remodeling due to an acute myocardial infarction (75% of cases) or idiopathic dilated cardiomyopathy (25% of cases). It is associated with an increase in mortality and poor outcome. There is a potential survival benefit deriving from the reduction in the degree of severity of mitral regurgitation. So the correction of the valve defect can change the clinical course and prognosis of the patient. The rationale for mitral valve treatment depends on the mitral regurgitation mechanism. Therefore, it is essential to identify and understand the pathophysiology of mitral valve regurgitation.
Aim of the Study
The aim of this review is to describe the crucial role of transthoracic and trans‐esophageal echocardiography, in particular with three‐dimensional echocardiography, for the assessment of the severity of secondary mitral regurgitation, anatomy, and hemodynamic changes in the left ventricle. Moreover, the concept that the mitral valve has no organic lesions has been abandoned. The echocardiography must allow a complete anatomical and functional evaluation of each component of the mitral valve complex, also useful to the surgeon in choosing the best surgical approach to repair the valve.
Conclusions
Echocardiography is the first‐line imaging modality for a better selection of patients, according to geometrical modifications of mitral apparatus and left ventricle viability, especially in preoperative phase.
Cardiac resynchronization therapy (CRT) has been shown as a successful strategy in the treatment of patients with heart failure and electrical dyssincrony. However, a significant proportion of ...implanted patients fails to respond sufficiently or in a predictable manner. Consequently, non response to CRT remains a valuable problem in clinical practice. In order to improve CRT response and long-term clinical benefits, the proper evaluation of patient's global frialty, the technology improvement, the multimodality imaging approach and the use of simple and low cost electrographic parameters (to verify effective biventricular capture and QRS narrowing) could play a important role. Therefore, the integration of various medical expertises (clinical cardiology, cardiac advanced imaging, electrophysiology) is a crucial element in order to achive the maximal benefits from this promising tecnique. In the multistep process (from patients evaluation to results verification) the follow-up even from the earliest post implantation phase, should be managed with great attention having the potential for impact the prognosis. This brief review focus the problem of non responder to CRT, giving particular attention to the different variables that may play a role (comorbilities, improvement in the tecnology of device implantation, role of multimodality imaging and electrocardiographic parameters).
Abstract Introduction An inadequate clearance of lung fluid plays a key role in the pathogenesis of transient tachypnea of the newborn (TTN). Objectives To evaluate if left ventricular diastolic ...dysfunction contributes to reduced clearance of lung fluid in TTN. Materials and Methods This was a prospective, observational study. Echocardiography and lung ultrasound were performed at 2, 24 and 48 h of life (HoL) to assess biventricular function and calculate lung ultrasound score (LUS). Left atrial strain reservoir (LASr) provided surrogate measurement of left ventricular diastolic function. Results Twenty‐seven neonates with TTN were compared with 27 controls with no difference in gestation (36.1 ± 2 vs. 36.9 ± 2 weeks) or birthweight (2508 ± 667 vs. 2718 ± 590 g). Biventricular systolic function was normal in both groups. LASr was significantly lower in cases at 2 (21.0 ± 2.7 vs. 38.1 ± 4.4; p < 0.01), 24 (25.2 ± 4.5 vs. 40.6 ± 4.0; p < 0.01) and 48 HoL (36.5 ± 5.8 and 41.6 ± 5.2; p < 0.01), resulting in a significant group by time interaction ( p < 0.001), after adjusting for LUS and gestational diabetes. A logistic regression model including LUS, birth weight and gestational diabetes as covariates, showed that LASr at 2 HoL was a predictor of respiratory support at 24 HoL, with an adjusted odds ratio of 0.60 (CI 0.36–0.99). Conclusions LASr was reduced in neonates with TTN, suggesting diastolic dysfunction, that may contribute to the delay in lung fluid clearance.
The mechanisms underlying the success of propranolol in the treatment of infantile hemangioma (IH) remain elusive and do not fully explain the rapid regression of hemangiomatous lesions following ...drug administration. As autophagy is critically implicated in vascular homeostasis, we determined whether β-blockers trigger the autophagic flux on infantile hemangioma-derived endothelial cells (Hem-ECs) in vitro. MATERIAL AND METHODSFresh tissue specimens, surgically removed for therapeutic purpose to seven children affected by proliferative IH, were subjected to enzymatic digestion. Cells were sorted with anti-human CD31 immunolabeled magnetic microbeads. Following phenotypic characterization, expanded Hem-ECs, at P2 to P6, were exposed to different concentrations (50 μM to 150 μM) of propranolol, atenolol or metoprolol alone and in combination with the autophagy inhibitor Bafilomycin A1. Rapamycin, a potent inducer of autophagy, was also used as control. Autophagy was assessed by Lysotracker Red staining, western blot analysis of LC3BII/LC3BI and p62, and morphologically by transmission electron microscopy. RESULTSHem-ECs treated with either propranolol, atenolol or metoprolol displayed positive LysoTracker Red staining. Increased LC3BII/LC3BI ratio, as well as p62 modulation, were documented in β-blockers treated Hem-ECs. Abundant autophagic vacuoles and multilamellar bodies characterized the cytoplasmic ultrastructural features of autophagy in cultured Hem-ECs exposed in vitro to β-blocking agents. Importantly, similar biochemical and morphologic evidence of autophagy were observed following rapamycin while Bafilomycin A1 significantly prevented the autophagic flux promoted by β-blockers in Hem-ECs. CONCLUSIONOur data suggest that autophagy may be ascribed among the mechanisms of action of β-blockers suggesting new mechanistic insights on the potential therapeutic application of this class of drugs in pathologic conditions involving uncontrolled angiogenesis.
Selenoprotein N (SEPN1) is a protein of the endoplasmic reticulum (ER) whose inherited defects originate SEPN1-related myopathy (SEPN1-RM). Here, we identify an interaction between SEPN1 and the ...ER-stress-induced oxidoreductase ERO1A. SEPN1 and ERO1A, both enriched in mitochondria-associated membranes (MAMs), are involved in the redox regulation of proteins. ERO1A depletion in SEPN1 knockout cells restores ER redox, re-equilibrates short-range MAMs, and rescues mitochondrial bioenergetics. ERO1A knockout in a mouse background of SEPN1 loss blunts ER stress and improves multiple MAM functions, including Ca2+ levels and bioenergetics, thus reversing diaphragmatic weakness. The treatment of SEPN1 knockout mice with the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) mirrors the results of ERO1A loss. Importantly, muscle biopsies from patients with SEPN1-RM exhibit ERO1A overexpression, and TUDCA-treated SEPN1-RM patient-derived primary myoblasts show improvement in bioenergetics. These findings point to ERO1A as a biomarker and a viable target for intervention and to TUDCA as a pharmacological treatment for SEPN1-RM.
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•SEPN1 interacts with the endoplasmic-reticulum-stress-induced oxidoreductase ERO1A•Upregulation of ERO1A is a hallmark of the SEPN1-RM preclinical models•Targeting ERO1A improves the muscle disease phenotype of SEPN1-RM•TUDCA, a pan ER stress inhibitor, is an effective pharmacological strategy for SEPN1-RM
SEPN1-related myopathy (SEPN1-RM) is a congenital muscle disorder with no approved pharmacological treatment. Germani et al. show an interaction between SEPN1 and ERO1A and that targeting ERO1A improves the muscle phenotype of SEPN1-RM. Furthermore, they find that TUDCA, an FDA-approved drug, is an effective pharmacological strategy for SEPN1-RM.
The objective of this cross-sectional study was to evaluate the degree of glycaemic control and the frequency of diabetic complications in Italian people with diabetes who were treated with ...continuous subcutaneous insulin infusion (CSII).
Questionnaires investigating the organisation of diabetes care centres, individuals' clinical and metabolic features and pump technology and its management were sent to adult and paediatric diabetes centres that use CSII for treatment in Italy. Information on standard clinical variables, demographic data and acute and chronic diabetic complications was derived from local clinical management systems. The sample consisted of 6623 people with diabetes, which was obtained from 93 centres. Of them, 98.8% had type 1 diabetes mellitus, 57.2% were female, 64% used a conventional insulin pump and 36% used a sensor-augmented insulin pump. The median glycated haemoglobin (HbA1c) level was 60 mmol/mol (7.6%). The HbA1c target (i.e. <58 mmol/mol for age <18 years and <53 mmol/mol for age >18 years) was achieved in 43.4% of paediatric and 23% of adult participants. Factors such as advanced pump functions, higher rate of sensor use, pregnancy in the year before the study and longer duration of diabetes were associated with lower HbA1c levels.
The most common chronic complications occurring in diabetes were retinopathy, microalbuminuria and hypertension. In the year before the study, 5% of participants reported ≥1 episode of severe hypoglycaemic (SH) episodes (SH) and 2.6% reported ≥1 episode of ketoacidosis.
Advanced personal skills and use of sensor-based pump are associated with better metabolic control outcomes in Italian people with diabetes who were treated with CSII. The reduction in SH episodes confirms the positive effect of CSII on hypoglycaemia.
NCT 02620917 (ClinicalTrials.gov).
•The study marks the largest Italian study on glucose control in CSII-treated people.•The median HbA1c level among all participants was 60.0 mmol/mol (7.6%).•Patient skills on sensor use are associated with lower HbA1c levels.•The frequency of severe hypoglycaemia and ketoacidosis episodes was very low.
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