Concealed SARS-CoV-2 interstitial pneumonia unmasked by infarct-like acute myocarditis

A 38-year-old otherwise healthy man presented to the emergency department for sudden-onset oppressive chest pain. On admission, vital parameters were within normal limits and physical examination was unremarkable. Since the ECG showed mild ST-segment eleva- tion in the inferior leads (Panel A), he underwent urgent coronary angiography which ruled out obstructive coronary artery disease (Panel B). Transthoracic echocardiogram showed preserved left ven- tricular (LV) ejection fraction with inferolateral wall hypokinesis. The peak of high-sensitive troponin I was 4038 ng/L (normal value <20). Acute myocarditis was suspected, and a cardiac magnetic resonance (CMR) was performed. High signal intensity (SI) of the mid-basal LV lateral wall on T2 short tau inversion recovery (STIR) sequences con- sistent with myocardial oedema (Panel C) and subepicardial late gado- linium enhancement in the same location (Panel D) were detected. Unexpectedly, areas of high SI on T2-STIR images were also noted on both lungs (Panel C), suggesting a pulmonary inflammatory pro- cess. Despite an initially negative chest X-ray, computed tomography revealed bilateral ground-glass opacity with multifocal consolidation and thickening of interlobular septa consistent with interstitial pneumonia (Panel E). Considering the ongoing coronavirus outbreak, a nasopharyngeal swab was obtained resulting positive for severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection. The patient remained free from either cardiovascular or respiratory symptoms and presented only mild fever (37.5C). Laboratory tests detected an increase of transaminases and C-reactive protein (6.73 mg/dL; normal value <0.5) with stable lymphocytopenia. After 20 days of hospitalization, he was discharged with the diagnosis of infarct-like myocarditis associated with subclinical SARS-CoV-2 respiratory infection. Acute myocarditis in the setting of SARS-CoV-2 infection has been anecdotally reported and its mechanism remains to be elucidated. So far, the SARS-CoV-2 genome has never been detected within the myocardium, suggesting an immune-mediated inflammatory myocardial injury. For the first time we reported a case of subclinical SARS-CoV-2 interstitial pneumonia occasionally unmasked by CMR performed for acute myocarditis

Lamin A/C Missense Mutation R216C Pinpoints Overlapping Features Between Brugada Syndrome and Laminopathies

A 31-year-old man experienced at-rest cardiac arrest. After successful resuscitation, the baseline ECG demonstrated sinus rhythm with concave ST segment elevation in right precordial leads (V1–V3) followed by a negative and symmetrical T-wave. Neither coronary artery disease nor electrolytes’ imbalances were detected. In the following days, ECG showed a spontaneous type 1 Brugada ECG pattern (Figure [A1]), more evident with right precordial leads in II and III intercostal spaces. Transthoracic echocardiography (Figure [A2]) failed to show any cardiomyopathy. Cardiac MRI showed normal chambers dimension, wall thickness, volume, and function (left ventricular end diastolic volume, 67.7 mL/m2; IVS, 1 cm; left ventricular end fraction, 59.7%). Late gadolinium enhancement sequences were negative; adipose and fibrous tissue infiltration were excluded. The patient was implanted with a transvenous single chamber cardioverter defibrillator (Medtronic). Several appropriate ICD interventions on VT and ventricular fibrillation were recorded in the following years. Family history (Figure [B]) was positive for sudden cardiac death: the maternal grandfather died at age 45 years, aII degree maternal cousin died during sleep at age 40 years. The proband’s mother showed a first degree atrioventricular block (PR interval=280 ms) and right bundle branch block (Figure [A3]). A neurological examination in the index case and his mother was negative and creatine phosphokinase levels were normal in both. Informed written consent was obtained from all family members. Study was approved by the Local Ethics Committee (152/2013/O/Oss, June 1, 2013). Molecular genetic analysis was performed by next generation sequencing using PED MASTR Plus assay comprising 52 cardiac electrical disorders related genes, SCN5A included (www.agilent.com)

Reducing the environmental impact of surgery on a global scale: systematic review and co-prioritization with healthcare workers in 132 countries

Abstract Background Healthcare cannot achieve net-zero carbon without addressing operating theatres. The aim of this study was to prioritize feasible interventions to reduce the environmental impact of operating theatres. Methods This study adopted a four-phase Delphi consensus co-prioritization methodology. In phase 1, a systematic review of published interventions and global consultation of perioperative healthcare professionals were used to longlist interventions. In phase 2, iterative thematic analysis consolidated comparable interventions into a shortlist. In phase 3, the shortlist was co-prioritized based on patient and clinician views on acceptability, feasibility, and safety. In phase 4, ranked lists of interventions were presented by their relevance to high-income countries and low–middle-income countries. Results In phase 1, 43 interventions were identified, which had low uptake in practice according to 3042 professionals globally. In phase 2, a shortlist of 15 intervention domains was generated. In phase 3, interventions were deemed acceptable for more than 90 per cent of patients except for reducing general anaesthesia (84 per cent) and re-sterilization of ‘single-use’ consumables (86 per cent). In phase 4, the top three shortlisted interventions for high-income countries were: introducing recycling; reducing use of anaesthetic gases; and appropriate clinical waste processing. In phase 4, the top three shortlisted interventions for low–middle-income countries were: introducing reusable surgical devices; reducing use of consumables; and reducing the use of general anaesthesia. Conclusion This is a step toward environmentally sustainable operating environments with actionable interventions applicable to both high– and low–middle–income countries

[Arrhythmogenic left ventricular cardiomyopathy: beyond magnetic resonance imaging]

Arrhythmogenic left ventricular cardiomyopathy: beyond magnetic resonance imagin

Long-term clinical outcome based on aspirin and clopidogrel responsiveness status after elective percutaneous coronary intervention: a 3T/2R (tailoring treatment with tirofiban in patients showing resistance to aspirin and/or resistance to clopidogrel) trial substudy

Objectives The purpose of this study was to investigate the long-term outcome after elective percutaneous coronary intervention in low-risk patients screened for aspirin and/or clopidogrel responsiveness in the 3T/2R (Tailoring Treatment With Tirofiban in Patients Showing Resistance to Aspirin and/or Resistance to Clopidogrel) trial. Background The impact of aspirin and/or clopidogrel poor response on long-term outcome is debated. Methods Aspirin and clopidogrel response was measured with the VerifyNow system aspirin and P2Y12 assays. After percutaneous coronary intervention (PCI), death, stroke, and myocardial infarction were assessed up to 1 year. Results Overall, 1,277 patients were screened, and 826 (65%) were treated with PCI. In all, 124 patients were found to be aspirin poor responders, and there were 179 clopidogrel poor responders (totally, 278 poor responders). The 1-year end point was significantly higher in poor responders as compared to full responders (15.8% vs. 8.6%, p = 0.002), which is principally due to more myocardial infarction occurrence. At multivariable analysis, clopidogrel poor response emerged as an independent predictor (hazard ratio: 1.15, 95% confidence interval: 1.03 to 1.28). Receiver-operator characteristic analysis identifies ≤23 of percentage of platelet inhibition and <208 of P2Y12 reactivity units as optimal cut offs to predict 1-year end point. Excluding periprocedural events, also peri-PCI myocardial infarction, which is strongly related to aspirin/clopidogrel poor response, was an independent predictor (hazard ratio: 1.25, 95% confidence interval: 1.14 to 1.37). Glycoprotein IIb/IIIa inhibitor administration reduces this risk in poor responders (21.2% vs. 34.7%, p = 0.02), but not in full responders (6.3% vs. 6.5%, p = 0.8). Conclusions Poor response to clopidogrel is an independent predictor of periprocedural myocardial infarction and worse 1-year outcome in low-risk patients undergoing PCI, whereas poor response to aspirin failed to predict a worse outcome. Contrary to what was observed in poor responders, glycoprotein IIb/IIa inhibitor therapy failed to provide a benefit in aspirin and/or clopidogrel full responders

The Underestimated Role of Platelets in Severe Infection a Narrative Review

Beyond their role in hemostasis, platelets have emerged as key contributors in the immune response; accordingly, the occurrence of thrombocytopenia during sepsis/septic shock is a well-known risk factor of mortality and a marker of disease severity. Recently, some studies elucidated that the response of platelets to infections goes beyond a simple fall in platelets count; indeed, sepsis-induced thrombocytopenia can be associated with—or even anticipated by—several changes, including an altered morphological pattern, receptor expression and aggregation. Of note, alterations in platelet function and morphology can occur even with a normal platelet count and can modify, depending on the nature of the pathogen, the pattern of host response and the severity of the infection. The purpose of this review is to give an overview on the pathophysiological interaction between platelets and pathogens, as well as the clinical consequences of platelet dysregulation. Furthermore, we try to clarify how understanding the nature of platelet dysregulation may help to optimize the therapeutic approach

Endothelial dysfunction and increased platelet reactivity in patients with acute coronary syndrome and undiagnosed COPD: insights into the SCAP trial

In conclusion, to our best knowledge, this is the first study to show that patients with ACS and concomitant UCOPD have increased endothelial dysfunction and on-treatment platelet reactivity. Moreover, we showed that ticagrelor may contribute to improve both parameters. Accordingly, any further effort for early identification and treatment of patients with UCOPD should be encouraged

Cardiac troponin elevation predicts all-cause mortality in patients with acute exacerbation of chronic obstructive pulmonary disease: Systematic review and meta-analysis

Cardiovascular disease, especially ischemic heart disease, is a major comorbidity in chronic obstructive pulmonary disease (COPD) patients. Several studies suggested that after acute exacerbation of COPD (AECOPD), there is a significant increase of mortality (cardiac and all-cause) and of myocardial infarction. Whether cardiac troponin (Tn) elevation during AECOPD could be considered a prognostic marker of all-cause mortality is still debated

C subunit of F1/FO-ATP synthase as target for preventing the detrimental effect of myocardial ischemia/reperfusion injury

Objective: The pathophysiological effects of coronary heart diseases are imputable to the hurtful consequences of ischemia-reperfusion injury (IRI). The opening of a large pore in the mitochondrial membrane, namely, the mitochondrial permeability transition pore (mPTP), is widely recognized as the final step of IRI and is responsible for mitochondrial and cardiomyocyte death. We provided evidences that c subunit of the F1/FO-ATP synthase (FFAS) owns a pivotal role in mPTP formation and activity and thus we sought to test a new mPTP opening inhibitor directed against the c subunit, namely IB13, for the treatment of IRI in ex-vivo model of myocardial infarction

Antiplatelet Treatment Reduces All-Cause Mortality in COPD Patients: A Systematic Review and Meta-Analysis

Previous studies clearly showed that patients with chronic obstructive pulmonary disease (COPD) are at high risk for cardiovascular events. Platelet activation is significantly heightened in these patients, probably because of a chronic inflammatory status. Nevertheless, it is unclear whether antiplatelet treatment may contribute to reduce all-cause mortality in COPD patients. To clarify this issue, we performed a systematic review and meta-analysis including patients with COPD (outpatients or admitted to hospital for acute exacerbation). The primary endpoint was all-cause mortality. We considered studies stratifying the study population according the administration or not of antiplatelet therapy and reporting its relationship with the primary endpoint. Overall, 5 studies including 11117 COPD patients were considered (of those 3069 patients were with acute exacerbation of COPD). IHD was present in 33% of COPD patients [95%CI 31%–35%). Antiplatelet therapy administration was common (47%, 95%CI 46%–48%), ranging from 26% to 61%. Of note, IHD was considered as confounding factor at multivariable analysis in all studies. All-cause mortality was significantly lower in COPD patients receiving antiplatelet treatment (OR 0.81; 95%CI 0.75–0.88). The data was consistent both in outpatients and in those with acute exacerbation of COPD. The pooled studies analysis showed a very low heterogeneity (I2 : 8%). Additional analyses (meta-regression) showed that antiplatelet therapy administration was effective independently (to potential confounding factors as IHD, cardiovascular drugs and cardiovascular risk factors. In conclusion, our meta-analysis suggested that antiplatelet therapy might significantly contribute to reduce all-cause mortality in COPD patients