Epidemiology of coronary microvascular obstruction

Primary percutaneous coronary intervention (PPCI) is nowadays the preferred reperfusion strategy for treating ST-elevation myocardial infarction (STEMI) patients, aiming at restoring epicardial infarct-related artery patency and achieving microvascular reperfusion as early as possible, thus limiting the extent of irreversibly injured myocardium. Yet, in a sizeable proportion of patients, PPCI achieves epicardial coronary artery reperfusion but not myocardial reperfusion due to the occurrence of coronary microvascular obstruction (CMVO), a condition clinically known as no-reflow. Prevalence of CMVO is variable, ranging from 5% up to 50%, according to the methods used to assess the phenomenon and to the population under study. Indeed, CMVO can be assessed using different techniques and at different time points after STEMI. In this chapter, we review the available data regarding the incidence of CMVO in STEMI patients according to different reperfusion strategies (PPCI, effective thrombolysis, and rescue PCI) and according to the different modalities of its detection. Finally, we analyzed data in the literature reporting the incidence of CMVO in different clinical subsets (diabetes, chronic kidney disease, women, and latecomers) and different subset of lesions (saphenous vein graft)

The management of non-culprit coronary lesions in patients with acute coronary syndrome

About 50% of patients diagnosed with ST-segment elevation myocardial infarction have multivessel disease on coronary angiography. Recent evidence has shown that a staged percutaneous coronary intervention (PCI) strategy of non-culprit lesions, achieving complete revascularization, significantly reduces the rate of recurrent cardiovascular events compared with a PCI strategy limited to culprit lesion. Although functional evaluation of intermediate coronary stenoses by functional flow reserve (FFR) or instantaneous wave-free ratio (iFR) is widely used to detect residual myocardial ischaemia, the reliability of the study of non-culprit lesions in the acute phase of heart attack is controversial. On the other hand, the excess of new events in patients with acute coronary syndrome in whom PCI was deferred on the basis of FFR/iFR compared to patients with stable CAD could be due to both an inadequate functional evaluation and an intrinsic higher risk, related to the presence of untreated vulnerable plaques. In this context, intra-coronary imaging has shown that the presence of vulnerability features in non-culprit plaques is associated with an increased rate of ischaemic recurrence

Hydrogen storage in MgH2 matrices: A study of Mg-MgH2 interface using CPMD code on ENEA-GRID

The remarkable ability of magnesium to store significant quantities of hydrogen, in the form (MgH2), has fostered intense research efforts in the last years in view of its future applications where light and safe hydrogen-storage media are needed. However, further research is needed since Mg has a high operation temperature and slow absorption kinetics that prevent for the moment the use in practical applications. To improve and optimize the performances of this material a detailed knowledge of the hydrogen diffusion mechanism at the atomic level is needed. Experiments can only provide indirect evidences of the atomic rearrangement during the desorption process. For these reasons a detailed computational study of MgH2 is invoked to characterize the dynamics of hydrogen during desorption. Further insights are gained by characterizing the Mg-MgH2 interface which is supposed to play a major role in the hydrogen diffusion during absorption and desorption cycles. By means of accurate ab initio molecular dynamics simulations based on the density-functional theory with norm-conserving pseudopotentials and plane-wave expansion (CPMD code) an interface is designed and studied. Extensive electronic structure calculations are used to characterize the equilibrium properties and the behavior of the surfaces in terms of total energy considerations and atomic diffusion

Myocardial and microvascular injury due to Coronavirus disease 2019

Over the past few months, health systems worldwide have been put to the test with the coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Even though the leading clinical manifestations of the SARS-CoV-2 infection involve the respiratory tract, there is a non-negligible risk of systemic involvement leading to the onset of multi-organ failure with fatal consequences. Since the onset of COVID-19, patients with underlying cardiovascular disease have been at increased risk of poor clinical outcomes with higher death rates. Moreover, the occurrence of new-onset cardiac complications is not uncommon among patients hospitalised for COVID-19. Of importance, a significant portion of COVID-19 patients present with myocardial injury. Herein, the authors discuss the mechanisms leading to myocardial and microvascular injury in SARS-CoV-2 infection and their clinical implications

Randomised trials and meta-analyses of double vs triple antithrombotic therapy for atrial fibrillation-ACS/PCI: A critical appraisal

•The optimal antithrombotic regimen to be used in patients with AF and PCI or ACS is still debated.•Each of the six randomised controlled trials comparing double to triple therapy has limitations.•None was powered to assess differences between treatment arms in ischaemic event rates.•The contrasting results regarding ischaemic events within published meta-analyses can be explained by heterogeneity, incompleteness and varying definitions of stent thrombosis.•The overall reduced bleeding rates, but increased early definite and probable stent thrombosis rates with double versus triple antithrombotic therapy encourage consideration of triple therapy during the first weeks from PCI followed by double therapy

Peptidomic approach for the identification of peptides with potential antioxidant and anti-hyperthensive effects derived from Asparagus by-products

Asparagus waste represents products of great interest since many compounds with high biological value are located in the lower portion of the spears. The extraction of bioactive compounds from asparagus by-products is therefore crucial for the purpose of adding value to these by-products. In this paper, bioactive peptides from asparagus waste were extracted, digested, purified and identified. In particular, Alcalase® was chosen as the enzyme to use to obtain protein hydrolysate due to its low cost and, consequently, the possibility of implementing the method on a large scale. In order to simplify the peptide extract to reach better identification, the hydrolysate was fractionated by reversed-phase chromatography in 10 fractions. Two tests were carried out for antioxidant activity (ABTS-DPPH) and one for antihypertensive activity (ACE). Fractions with a higher bioactivity score were identified by peptidomics technologies and screened for bioactivity with the use of bioinformatics. For ACE-inhibitor activity, two peptides were synthetized, PDWFLLL and ASQSIWLPGWL, which provided an EC50 value of 1.76 µmol L-1 and 4.02 µmol L-1, respectively. For the antioxidant activity, by DPPH assay, MLLFPM exhibited the lowest EC50 value at 4.14 µmol L-1, followed by FIARNFLLGW and FAPVPFDF with EC50 values of 6.76 µmol L-1 and 10.01 µmol L-1, respectively. A validation of the five identified peptides was also carried out. The obtained results showed that peptides obtained from asparagus by-products are of interest for their biological activity and are suitable for being used as functional ingredients

Microvascular Dysfunction in Heart Failure With Preserved Ejection Fraction

Heart failure with preserved ejection fraction (HFpEF) is an increasingly studied entity accounting for 50% of all diagnosed heart failure and that has claimed its own dignity being markedly different from heart failure with reduced EF in terms of etiology and natural history (Graziani et al., 2018). Recently, a growing body of evidence points the finger toward microvascular dysfunction as the major determinant of the pathological cascade that justifies clinical manifestations (Crea et al., 2017). The high burden of comorbidities such as metabolic syndrome, hypertension, atrial fibrillation, chronic kidney disease, obstructive sleep apnea, and similar, could lead to a systemic inflammatory state that impacts the physiology of the endothelium and the perivascular environment, engaging complex molecular pathways that ultimately converge to myocardial fibrosis, stiffening, and dysfunction (Paulus and Tschope, 2013). These changes could even self-perpetrate with a positive feedback where hypoxia and locally released inflammatory cytokines trigger interstitial fibrosis and hypertrophy (Ohanyan et al., 2018). Identifying microvascular dysfunction both as the cause and the maintenance mechanism of this condition has opened the field to explore specific pharmacological targets like nitric oxide (NO) pathway, sarcomeric titin, transforming growth factor beta (TGF-β) pathway, immunomodulators or adenosine receptors, trying to tackle the endothelial impairment that lies in the background of this syndrome (Graziani et al., 2018;Lam et al., 2018). Yet, many questions remain, and the new data collected still lack a translation to improved treatment strategies. To further elaborate on this tangled and exponentially growing topic, we will review the evidence favoring a microvasculature-driven etiology of this condition, its clinical correlations, the proposed diagnostic workup, and the available/hypothesized therapeutic options to address microvascular dysfunction in the failing heart