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Genetic susceptibility may influence ischemic heart disease (IHD) predisposition and affect coronary blood flow (CBF) regulation mechanisms. The aim of this study was to investigate the association among single nucleotide polymorphisms (SNPs) of genes encoding for proteins involved in CBF regulation and IHD. A total of 468 consecutive patients were enrolled and divided into three groups according to coronary angiography and intracoronary functional tests results: G1, patients with coronary artery disease (CAD); G2, patients with coronary microvascular dysfunction (CMD); and G3, patients with angiographic and functionally normal coronary arteries. A genetic analysis of the SNPs rs5215 of the potassium inwardly rectifying channel subfamily J member 11 (KCNJ11) gene and rs1799983 of the nitric oxide synthase 3 (NOS3) gene, respectively encoding for the Kir6.2 subunit of ATP sensitive potassium (KATP) channels and nitric oxide synthase (eNOS), was performed on peripheral whole blood samples. A significant association of rs5215_G/G of KCNJ11 and rs1799983_T/T of NOS3 genes was detected in healthy controls compared with CAD and CMD patients. Based on univariable and multivariable analyses, the co-presence of rs5215_G/G of KCNJ11 and rs1799983_T/T of NOS3 may represent an independent protective factor against IHD, regardless of cardiovascular risk factors. This study supports the hypothesis that SNP association may influence the crosstalk between eNOS and the KATP channel that provides a potential protective effect against IHD.

Sodium-glucose cotransporter 2 inhibitors (SGLT2i), initially born as anti-diabetic drugs, have shown many beneficial effects on the cardiovascular system, in particular against heart failure (HF). HF is a complex and multifaceted disease that requires a comprehensive approach. It should not be considered as a simplistic cardiac disease, but a systemic disease that leads to multisystemic organ failure and death. Exploiting their pleiotropic effects, SGLT2i are a very valid tool for HF treatment. Beyond the indication to reduce HF hospitalization and death risk, in patients with diabetes mellitus at high cardiovascular risk or with established cardiovascular event, SGLT2i administration reported beneficial effects regarding the wide spectrum of HF manifestations and stages, independently by diabetes mellitus presence. Recent evidence focuses on HF rehospitalization, cardiac and all-cause death reduction, as well as symptoms and quality of life improvement, in patients with chronic HF or with a recent HF decompensation episode. Given the recent finding about the SGLT2i usefulness in HF patients, further studies are needed to define the best administration timing to maximize the SGLT2i-derived beneficial effects.

Previous research suggests that gender bias is pervasive in health care and has deleterious effects on treatment outcomes for patients. When developing and improving training on gender bias, we need to further our understanding of how such topics arise and are sustained in conversations between healthcare professionals (HCPs). The aim of this study is to analyze the influence of patient gender in HCP decision-making by analyzing how they surface, discuss and manage topics around gender. An ethnomethodological qualitative study using discursive psychology and conversation analysis was implemented to examine 10 simulation debriefs in a specialized mental healthcare simulation centre in London. Video footage was obtained from mental health simulation training courses on bias in clinical decision-making, involving HCPs from mixed healthcare professions. Following transcription of selected segments, the debriefs were analyzed and repeated patterns of interaction were captured in distinct themes. Four main themes were identified from the data, indicating some of the ways in which conversations about gender are managed: collaboration (to encourage discussion), surprise (when unexpected topics arose), laughter (to diffuse tense situations) and silence (demonstrating careful thinking). Patients with mental health conditions were perceived differently in terms of treatment decisions due to existing gender biases. The persistence of gender bias that may result in discrimination in health care with negative consequences attests to the need for greater awareness and training development at various levels to include an intersectional approach.

Background: Heart failure (HF) patients are predisposed to recurrences and disease destabilizations, especially during the COVID-19 outbreak period. In this scenario, telemedicine could be a proper way to ensure continuous care. The purpose of the study was to compare two modalities of HF outpatients’ follow up, the traditional in-person visits and telephone consultations, during the COVID-19 pandemic period in Italy. Methods: We conducted an observational study on consecutive HF outpatients. The follow up period was 12 months, starting from the beginning of the COVID-19 Italy lockdown. According to the follow up modality, and after the propensity matching score, patients were divided into two groups: those in G1 (n = 92) were managed with traditional in-person visits and those in G2 (n = 92) were managed with telephone consultation. Major adverse cardiovascular events (MACE) were the primary endpoints. Secondary endpoints were overall mortality, cardiovascular death, cardiovascular hospitalization, and hospitalization due to HF. Results: No significant differences between G1 and G2 have been observed regarding MACE (p = 0.65), cardiovascular death (p = 0.39), overall mortality (p = 0.85), hospitalization due to acute HF (p = 0.07), and cardiovascular hospitalization (p = 0.4). Survival analysis performed by the Kaplan–Meier method also did not show significant differences between G1 and G2. Conclusions: Telephone consultations represented a valid option to manage HF outpatients during COVID-19 pandemic, comparable to traditional in-person visits.

Among the most common causes of death worldwide, ischemic heart disease (IHD) is recognized to rank first. Even if atherosclerotic disease of the epicardial arteries is known as the leading cause of IHD, the presence of myocardial infarction with non-obstructive coronary artery disease (MINOCA) is increasingly recognized. Notwithstanding the increasing interest, MINOCA remains a puzzling clinical entity that can be classified by distinguishing different underlying mechanisms, which can be divided into atherosclerotic and non-atherosclerotic. In particular, coronary microvascular dysfunction (CMD), classifiable in non-atherosclerotic mechanisms, is a leading factor for the pathophysiology and prognosis of patients with MINOCA. Genetic susceptibility may have a role in primum movens in CMD. However, few results have been obtained for understanding the genetic mechanisms underlying CMD. Future studies are essential in order to find a deeper understanding of the role of multiple genetic variants in the genesis of microcirculation dysfunction. Progress in research would allow early identification of high-risk patients and the development of pharmacological, patient-tailored strategies. The aim of this review is to revise the pathophysiology and underlying mechanisms of MINOCA, focusing on CMD and actual knowledge about genetic predisposition to it.

To evaluate longitudinal systolic function in patients with myocarditis, its correlation with cardiac magnetic resonance (CMR) features, and its predictive value in functional recovery and arrhythmias onset during follow-up (FU) on optimized medical therapy (OMT). Patients with acute myocarditis, confirmed through CMR criteria, and age- and sex-matched healthy controls were enrolled. Two-dimensional (2D) transthoracic echocardiography, including speckle tracking analysis, was performed at admission and after 6months of FU. Patients of myocarditis group also underwent 24h ECG Holter monitoring during FU. 115 patients with myocarditis (mean age 41 ± 17, 70% males) and 70 healthy subjects were enrolled. Global longitudinal strain (GLS) and sub-epicardial strain were markedly lower in the myocarditis group than in controls (mean GLS%: −14.1 ± 5.1 vs −23.1 ± 3.6, p < 0.001). A strong positive correlation between total scar burden (TSB) on CMR and baseline LV GLS was found (r = 0.67, p < 0.0001). GLS improved after 6months of FU in myocarditis on OMT (mean GLS%: −14.1 ± 5.1 vs −16.5 ± 4.8, p < 0.01). By bivariate correlation analysis, baseline LVEF, GLS, and TSB were all associated with LVEF at 6months of FU. Moreover, by multivariable linear regression analysis, these parameters confirmed to be independent predictors of functional recovery at 6months (LVEF β 0.38, p < 0.01; GLS β −0.35, p < 0.01; total scar burden β −0.52, p < 0.0001). Segmental peak systolic strain was significantly different between segments with and without late gadolinium enhancement on CMR (−13.2 ± 3.1% vs −18.1 ± 3.5%, p < 0.001). A segmental strain of − 12% identified scar with a sensitivity of 79% and a specificity of 84% (AUC = 0.91; 95% CI 0.73–0.97; p < 0.001). In addition, baseline LV GLS in myocarditis resulted predictive of non-sustained ventricular tachycardias (cut-off value > −12%; sensitivity84%; specificity74.4%; AUC = 0.75). Parameters of myocardial longitudinal deformation are importantly associated with the presence of a scar on CMR and are predictors of functional outcome and ventricular arrhythmias in patients with acute myocarditis. Their assessment during ultrasound examination should be considered to get more information about the prognosis and risk stratification of this subset of patients.

Aims IHD is determined by inadequate coronary blood supply to myocardium and endothelial dysfunction may represent one of the main pathophysiological mechanisms involved. Genetic predisposition to endothelial dysfunction has been associated with IHD and its clinical manifestation. However, studies are often confounding and inconclusive for several reasons, such as interethnic differences. Results validation on larger cohorts and new population is needed. The aim of the study is to evaluate the association among the allelic variants of eNOS rs1799983 single-nucleotide polymorphism, IHD susceptibility, and its clinical presentation. Methods A total of 362 consecutive patients with suspected myocardial ischemia were enrolled. Patients were divided into three groups: G1, coronary artery disease (CAD); G2, coronary microvascular dysfunction (CMD); G3, control group with anatomically and functionally normal coronary arteries. Analysis of three allelic variants, GT, GG, and TT of rs1799983 for NOS3 gene, encoding for eNOS has been performed. Results rs1799983_GT is significantly more expressed by ischaemic groups (G1 and G2) compared with G3. The TT variant is significantly more expressed by G1 group, compared with G2 group. Among ischaemic patients, GT is significantly more expressed in patients with acute coronary syndrome (ACS) presentation, compared to other clinical presentation. At multivariate analysis, the allelic variant GT may represent an independent predictor of IHD and ACS presentation. Conclusions The SNP rs1799983_GT, encoding for eNOS, is an independent risk factor for IHD and, remarkably, for ACS presentation, independently from cardiovascular risk factors. These results may be useful for the prediction of IHD development, in particular with acute clinical manifestation. It may allow the early identification of patients at high risk to develop IHD with an ACS, promoting a genetic-based prevention strategy against IHD.

Proper therapeutic management of patients with heart failure (HF) is a major challenge for cardiologists. Current guidelines indicate to start therapy with angiotensin converting enzyme inhibitors/angiotensin receptor neprilysin inhibitors (ACEi/ARNI), beta blockers (BB), mineralocorticoid receptor antagonists (MRAs) and sodium glucose cotransporter 2 inhibitors (SGLT2i) to reduce the risk of death and hospitalization due to HF. However, certain aspects still need to be defined. Current guidelines propose therapeutic algorithms based on left ventricular ejection fraction values and clinical presentations. However, these last do not always reflect the precise hemodynamic status of patients and pathophysiological mechanisms involved, particularly in the acute setting. Even in the field of chronic management there are still some critical points to discuss. The guidelines do not specify which of the four pillar drugs to start first, nor at what dosage. Some authors suggest starting with SGLT2i and BB, others with ACEi or ARNI, while one of the most recent approach proposes to start with all four drugs together at low doses. The aim of this review is to revise current gaps and perspectives regarding pharmacological therapy management in HF patients, in both the acute and chronic phase.

Heart failure with preserved ejection fraction (HFpEF) is a complex clinical syndrome responsible for high mortality and morbidity rates. It has an ever growing social and economic impact and a deeper knowledge of molecular and pathophysiological basis is essential for the ideal management of HFpEF patients. The association between HFpEF and traditional cardiovascular risk factors is known. However, myocardial alterations, as well as pathophysiological mechanisms involved are not completely defined. Under the definition of HFpEF there is a wide spectrum of different myocardial structural alterations. Myocardial hypertrophy and fibrosis, coronary microvascular dysfunction, oxidative stress and inflammation are only some of the main pathological detectable processes. Furthermore, there is a lack of effective pharmacological targets to improve HFpEF patients’ outcomes and risk factors control is the primary and unique approach to treat those patients. Myocardial tissue characterization, through invasive and non-invasive techniques, such as endomyocardial biopsy and cardiac magnetic resonance respectively, may represent the starting point to understand the genetic, molecular and pathophysiological mechanisms underlying this complex syndrome. The correlation between histopathological findings and imaging aspects may be the future challenge for the earlier and large-scale HFpEF diagnosis, in order to plan a specific and effective treatment able to modify the disease’s natural course.

Micronutrients are ions and vitamins humbly required by the human body. They play a main role in several physiological mechanisms and their imbalance is strongly associated with potentially-fatal complications. Micronutrient imbalance is associated with many cardiovascular diseases, such as arrythmias, heart failure, and ischemic heart disease. It has been also observed in coronavirus disease 2019 (COVID-19), particularly in most severe patients. The relationship between cardiovascular diseases and COVID-19 is mutual: the latter triggers cardiovascular disease onset and worsening while patients with previous cardiovascular disease may develop a more severe form of COVID-19. In addition to the well-known pathophysiological mechanisms binding COVID-19 and cardiovascular diseases together, increasing importance is being given to the impact of micronutrient alterations, often present during COVID-19 and able to affect the balance responsible for a good functioning of the cardiovascular system. In particular, hypokalemia, hypomagnesemia, hyponatremia, and hypocalcemia are strongly associated with worse outcome, while vitamin A and D deficiency are associated with thromboembolic events in COVID-19. Thus, considering how frequent the cardiovascular involvement is in patients with COVID-19, and how it majorly affects their prognosis, this manuscript provides a comprehensive review on the role of micronutrient imbalance in the interconnection between COVID-19 and cardiovascular diseases.

IHD is determined by an inadequate coronary blood supply to the myocardium, and endothelial dysfunction may represent one of the main pathophysiological mechanisms involved. Genetic predisposition to endothelial dysfunction has been associated with IHD and its clinical manifestation. However, studies are often confounding and inconclusive for several reasons, such as interethnic differences. Validation of results in larger cohorts and new populations is needed. The aim of this study is to evaluate the associations between the allelic variants of the eNOS rs1799983 single-nucleotide polymorphism, IHD susceptibility and its clinical presentation. Methods: A total of 362 consecutive patients with suspected myocardial ischemia were enrolled. Patients were divided into three groups: G1, coronary artery disease (CAD), G2, coronary microvascular dysfunction (CMD), and G3, a control group with anatomically and functionally normal coronary arteries. Analysis of three allelic variants, GT, GG and TT, of rs1799983 for the NOS3 gene, encoding for eNOS, was performed. Results: rs1799983_GT was significantly more expressed by the ischemic groups (G1 and G2) compared to G3. The TT variant was significantly more expressed by the G1 group, compared to the G2 group. Among ischemic patients, GT was significantly more expressed in patients with acute coronary syndrome (ACS) presentation, compared to other clinical presentations. In the multivariate analysis, the allelic variant GT was found to potentially represent an independent predictor of IHD and ACS presentation. Conclusion: The presence of the SNP rs1799983_GT, encoding for eNOS, is an independent risk factor for IHD and, remarkably, for ACS presentation, independently of cardiovascular risk factors. These results may be useful for the prediction of IHD development, particularly with an acute clinical manifestation. They may allow the early identification of patients at high risk of developing IHD with an ACS, promoting a genetic-based prevention strategy against IHD.

Background Heart failure (HF) is the pandemic of the third millennium with the highest mortality among general population, while lung cancer is the second most common cause of death. As cancer, HF can affect close organs, as lungs, or can reach peripheral organs (kidney, liver, brain), leading to multi-organ dysfunction, like cancer metastasis. Purpose We proposed a new staging system named HLM, analogous to TNM classification used in oncology, which refers to heart damage (H), lung involvement (L), and malfunction (M) of peripheral organs. The aim of this study is a comparison between HLM and NYHA, ACC/AHA and MAGGIC scores to assess the most accurate prognosis of HF patients in terms of rehospitalization for acute HF (AHF) or major adverse cardiac and cerebrovascular events (MACCE), and cardiac death. Methods We performed a single-center observational study of HF patients. All parameters for heart, lungs and peripheral organs function were examined. Each patient was classified according to HLM, NYHA, ACC/AHA and MAGGIC score at the entrance and at the discharge. Rehospitalization for MACCE or AHF and cardiac death were checked at 12 months follow up. Results We enrolled 2054 patients: 68.5% males, 31.3% females, mean age 70.18±7.48 years. Among them, overall survival curves regarding rehospitalization for MACCE, AHF and cardiac death at 12 months, show that HLM classification is as valid as the others (p Conclusion(s) According to our results, HLM classification has greater prognostic power compared to other nosologies in terms of rehospitalization for MACCE, AHF and cardiac death for HF patients, thanks to a more accurate evaluation of the systemic impact of heart failure. Such a multivariable, holistic approach should be used in HF patients, rather than a “cardiocentric” approach, in order to address the pathophysiological mechanisms underlining heart abnormalities, improving clinical management and costs. Funding Acknowledgement Type of funding source: None

Ischemic heart disease still represents a large burden on individuals and health care resources worldwide. By conventions, it is equated with atherosclerotic plaque due to flow-limiting obstruction in large–medium sized coronary arteries. However, clinical, angiographic and autoptic findings suggest a multifaceted pathophysiology for ischemic heart disease and just some cases are caused by severe or complicated atherosclerotic plaques. Currently there is no well-defined assessment of ischemic heart disease pathophysiology that satisfies all the observations and sometimes the underlying mechanism to everyday ischemic heart disease ward cases is misleading. In order to better examine this complicated disease and to provide future perspectives, it is important to know and analyze the pathophysiological mechanisms that underline it, because ischemic heart disease is not always determined by atherosclerotic plaque complication. Therefore, in order to have a more complete comprehension of ischemic heart disease we propose an overview of the available pathophysiological paradigms, from plaque activation to microvascular dysfunction.

Aims The recent coronavirus disease 19 (COVID‐19) pandemic outbreak forced the adoption of restraint measures, which modified the hospital admission patterns for several diseases. The aim of the study is to investigate the rate of hospital admissions for heart failure (HF) during the early days of the COVID‐19 outbreak in Italy, compared with a corresponding period during the previous year and an earlier period during the same year. Methods and results We performed a retrospective analysis on HF admissions number at eight hospitals in Italy throughout the study period (21 February to 31 March 2020), compared with an inter‐year period (21 February to 31 March 2019) and an intra‐year period (1 January to 20 February 2020). The primary outcome was the overall rate of hospital admissions for HF. A total of 505 HF patients were included in this survey: 112 during the case period, 201 during intra‐year period, and 192 during inter‐year period. The mean admission rate during the case period was 2.80 admissions per day, significantly lower compared with intra‐year period (3.94 admissions per day; incidence rate ratio, 0.71; 95% confidence interval [CI], 0.56–0.89; P = 0.0037), or with inter‐year (4.92 admissions per day; incidence rate ratio, 0.57; 95% confidence interval, 0.45–0.72; P

Background Whether increasing body mass index (BMI) is independently associated with parallel increased prevalence of hypertensive vascular and cardiac target organ damage (TOD) needs further clarification. Methods We analyzed 8815 hypertensive patients without prevalent cardiovascular disease, participating in the Campania Salute Network, grouped into BMI classes (normal 20–24.9kg/m 2 , overweight 25–29.9kg/m 2 and obese ≥30kg/m 2 ). Vascular and cardiac TOD was defined as ultrasound plaque (intima-media thickness>1.5mm) in >1 of the common or internal carotid arteries and echocardiographic left ventricular (LV) hypertrophy (LVH) (LV mass/height 2.7 >47g/m 2.7 in women and >50g/m 2.7 in men), respectively. Results A majority of patients were either overweight (49%) or obese (27%). In spite of more use of combination therapy, the obese group had higher blood pressure (BP) and prevalence of TOD. In multivariate logistic analyses, obesity was associated with a 6.9 times higher prevalence of LVH (95% confidence interval [CI] 5.84–8.17, p =0.0001), independent of significant associations with female sex, age, diabetes mellitus, office systolic BP, antihypertensive and antiplatelet treatment. In contrast, only a 17% increased prevalence of carotid plaques (OR=1.17; 95% CI 1.02–1.33, p =0.02) was found in obese patients independent of significant effect of male sex, older age and higher clinic systolic BP, an association that disappeared once effect of metabolic risk factors and related therapy was also considered. Conclusions In hypertensive patients participating in the Campania Salute Project, concomitant obesity was associated with a modestly increased prevalence of carotid plaques and a pronounced increase in prevalent LVH.

Aims Ischaemic heart disease is classically associated with coronary artery disease. Recent evidences showed the correlation between coronary microvascular dysfunction and ischaemic heart disease, even independently of coronary artery disease. Ion channels represent the final effectors of blood flow regulation mechanisms and their genetic variants, in particular of Kir6.2 subunit of the ATP-sensitive potassium channel (KATP), are reported to be involved in ischaemic heart disease susceptibility. The aim of the present study is to evaluate the role of KATP channel and its genetic variants in patients with ischaemic heart disease and evaluate whether differences exist between coronary artery disease and coronary microvascular dysfunction. Methods A total of 603 consecutive patients with indication for coronary angiography due to suspected myocardial ischaemia were enrolled. Patients were divided into three groups: coronary artery disease (G1), coronary microvascular dysfunction (G2) and normal coronary arteries (G3). Analysis of four single nucleotide polymorphisms (rs5215, rs5216, rs5218 and rs5219) of the KCNJ11 gene encoding for Kir6.2 subunit of the KATP channel was performed. Results rs5215 A/A and G/A were significantly more represented in G1, while rs5215 G/G was significantly more represented in G3, rs5216 G/G and C/C were both more represented in G3, rs5218 C/C was more represented in G1 and rs5219 G/A was more represented in G1, while rs5219 G/G was significantly more represented in G2. At multivariate analysis, single nucleotide polymorphism rs5215_G/G seems to represent an ischaemic heart disease independent protective factor. Conclusions These results suggest the potential role of KATP genetic variants in ischaemic heart disease susceptibility, as an independent protective factor. They may lead to a future perspective for gene therapy against ischaemic heart disease.

We describe a case of a 79-year-old man with pacemaker who presented to the Emergency Department due to asthenia and acute confusional state. He had a history of atrial fibrillation, anemia and colostomy and he was on treatment with diuretics. The electrocardiogram (ECG) showed pacemaker-induced ventricular activity, QRS complexes excessively wide with sine-wave appearance, tall and peaked T waves, without electrically evident atrial activity. Potassium concentration on arterial blood gas analysis was 8.8 mmol/L. ECG abnormalities disappeared after therapy with calcium chloride and spontaneous cardiac activity reappeared.

Background Ischemic heart disease (IHD) is classically associated with coronary artery disease (CAD) and conventional cardiovascular risk factors. However, IHD may exhibit in the absence of CAD, because of different pathophysiological mechanisms, such as the presence of specific genetic variants of ion channels, which act mainly in the microcirculation. Recently, we reported the correlation between some single nucleotide polymorphisms (SNPs) of ion channels genes and the presence of IHD, independently from the presence of conventional cardiovascular risk factors. The goal of this study is to confirm the results of the previous study on a bigger population and discover new SNPs of ion channels genes which may be associated with IHD. Methods A prospective, observational, single-center study was conducted on patients candidates for coronary angiography. Patients were divided in three groups: G1, coronary artery disease; G2, microvascular disfunction; G3, normal. Genetic polymorphisms relative to KCNJ11 encoding for the Kir6.1 and Kir6.2 subunits of K-ATP channels and KCNE1 encoding for the MinK subunit of IKs channels were analyzed. Results 603 consecutive patients (G1: 409; G2:76; G3:118) were enrolled. Genetic analysis for the three groups showed a statistically significant difference for the SNP S38G of KCNE1 (p=0.001) and for the variants rs5215, rs5218, rs5219 of KCNJ11 (p Conclusion These results confirm the importance of genetic susceptibility and the role of SNPs of ion channels genes in the determinism of IHD, independently from the conventional cardiovascular risk factors. Moreover, these results may represent a future perspective for a genic therapy for IHD.

Echocardiography is a noninvasive imaging technique useful to provide clinical data regarding physiological adaptations of athlete's heart. Echocardiographic characteristics may be helpful for the clinicians to identify structural cardiac disease, responsible of sudden death during sport activities. The application of echocardiography in preparticipation screening might be essential: it shows high sensitivity and specificity for identification of structural cardiac disease and it is the first-line imagining technique for primary prevention of SCD in athletes. Moreover, new echocardiographic techniques distinguish extreme sport cardiac remodeling from beginning state of cardiomyopathy, as hypertrophic or dilated cardiomyopathy and arrhythmogenic right ventricle dysplasia. The aim of this paper is to review the scientific literature and the clinical knowledge about athlete's heart and main structural heart disease and to describe the rule of echocardiography in primary prevention of SCD in athletes.

Ischemic heart disease (IHD) has several risk factors, among which diabetes mellitus represents one of the most important. In diabetic patients, the pathophysiology of myocardial ischemia remains unclear yet: some have atherosclerotic plaque which obstructs coronary blood flow, others show myocardial ischemia due to coronary microvascular dysfunction in the absence of plaques in epicardial vessels. In the cross-talk between myocardial metabolism and coronary blood flow (CBF), ion channels have a main role, and, in diabetic patients, they are involved in the pathophysiology of IHD. The exposition to the different cardiovascular risk factors and the ischemic condition determine an imbalance of the redox state, defined as oxidative stress, which shows itself with oxidant accumulation and antioxidant deficiency. In particular, several products of myocardial metabolism, belonging to oxidative stress, may influence ion channel function, altering their capacity to modulate CBF, in response to myocardial metabolism, and predisposing to myocardial ischemia. For this reason, considering the role of oxidative and ion channels in the pathophysiology of myocardial ischemia, it is allowed to consider new therapeutic perspectives in the treatment of IHD.

Heart failure is a complex syndrome responsible for high rates of death and hospitalization. Ischemic heart disease is one of the most frequent causes of heart failure and it is normally attributed to coronary artery disease, defined by the presence of one or more obstructive plaques, which determine a reduced coronary blood flow, causing myocardial ischemia and consequent heart failure. However, coronary obstruction is only an element of a complex pathophysiological process that leads to myocardial ischemia. In the literature, attention paid to the role of microcirculation, in the pathophysiology of ischemic heart disease and heart failure, is growing. Coronary microvascular dysfunction determines an inability of coronary circulation to satisfy myocardial metabolic demands, due to the imbalance of coronary blood flow regulatory mechanisms, including ion channels, leading to the development of hypoxia, fibrosis and tissue death, which may determine a loss of myocardial function, even beyond the presence of atherosclerotic epicardial plaques. For this reason, ion channels may represent the link among coronary microvascular dysfunction, ischemic heart disease and consequent heart failure.

Modern epistemology is in the peculiar position of retaining its trust in man’s ability to acquire knowledge without being capable of specifying the reasons for our gnosis success. Popper was the first to state that any conclusion concerning the possibility or impossibility of knowing is a transcendental statement and he states, also, that man reaches knowledge while trying to guess. In my opinion, we know things because we assume to have always been aware of them, in the sense that some form of immediate awareness has promptly enabled us to perceive them, identify them, use them. But one needs to ascertain whether the reason is the most suitable faculty to ensure the positive development of knowledge. At last, Kuhn claims the impossibility of comparing different theories. But if we establish a comparison between theories in terms of their complexity, then we must admit that there occurs some progress.

Among cardiovascular disease, ischemic heart disease (IHD) is the most frequent cause of mortality all over the world1. However, as well known, CAD and IHD are not always synonymous. In fact, there are other pathophysiological mechanisms which have a role in IHD development2,3. Possible underlying mechanisms include coronary microvascular dysfunction (CMD), coronary spasm and coronary dissection.&nbsp

Diabetes mellitus is one the strongest risk factors for cardiovascular disease and, in particular, for ischemic heart disease (IHD). The pathophysiology of myocardial ischemia in diabetic patients is complex and not fully understood: some diabetic patients have mainly coronary stenosis obstructing blood flow to the myocardium; others present with coronary microvascular disease with an absence of plaques in the epicardial vessels. Ion channels acting in the cross-talk between the myocardial energy state and coronary blood flow may play a role in the pathophysiology of IHD in diabetic patients. In particular, some genetic variants for ATP-dependent potassium channels seem to be involved in the determinism of IHD.

Protein mussel-inspired adhesive polymers, characterized by the presence of catechol groups, possess superior muco-adhesive properties and have great potentiality in wound healing. Suitable materials for wound dressing should properly combine muco-adhesiveness and antimicrobial activity. In this work, catechol-functionalized chitosan was obtained by reaction with hydrocaffeic acid (HCAF), in order to investigate how catechol introduction at different content could affect the intrinsic antimicrobial activity of the polymer itself. Unexpectedly, an enhancement of chitosan antimicrobial activity was observed after catechol functionalization, with a fourfold reduction in the polymer minimum inhibitory concentration versus Staphylococcus epidermidis. Additionally, a commercial wound dressing coated with one of the synthesized CS-HCAF derivatives showed a significant reduction in the adhesion of S. epidermidis compared to the uncoated dressing (3-log reduction). The CS-HCAF derivatives also showed an interesting antioxidant property (EC50 ranging from 20 to 60 μg/mL), which further confirms the potentiality of these materials as wound dressings. © 2017 Elsevier Ltd

BACKGROUND Lowering systolic blood pressure (SBP) below the conventional threshold (140 mm Hg) reduces left ventricular (LV) hypertrophy and incident cardiovascular (CV) events. We assessed whether different thresholds of SBP as the average value during follow-up (FU) have different impact on changes in target organ damage (TOD). METHODS From the Campania Salute Network registry, we selected 4,148 hypertensive patients with average SBP-FU