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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.

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.

Heart failure is a multifaceted syndrome addressing for a high rate of death among the general population. The common approach to this disease has been always based on the evaluation of the left ventricular ejection fraction by two-dimensional echocardiography with Simpson’s method. Mounting evidences have demonstrated the pitfalls of this method and have suggested that the management of heart failure requires a deep knowledge of the pathophysiological insights of the disease and cannot rely only on the evaluation of the left ventricular ejection fraction. Several advanced imaging technologies overwhelm the evaluation of ejection fraction and could provide a better understanding of the myocardial abnormalities underlying heart failure. Considering the limitation of left ventricular ejection fraction and the systemic involvement of heart failure, classifications of heart failure based on ejection fraction should be substituted with a comprehensive “staging” of multiorgan damage, not only considering the heart but also the lungs, kidneys, and liver, such as the HLM staging system. Such a holistic approach based on the HLM staging system and multimodality imaging can provide a global assessment of patient features allowing for targeted therapies and better heart failure management.

BackgroundDirect oral anticoagulants (DOACs) are recommended as first-line anticoagulants in patients with atrial fibrillation (AF). However, in patients with cancer and AF the efficacy and safety of DOACs are not well established.ObjectiveWe performed a meta-analysis comparing available data regarding the efficacy and safety of DOACs vs vitamin K antagonists (VKAs) in cancer patients with non-valvular AF.MethodsAn online search of Pubmed and EMBASE libraries (from inception to May, 1 2020) was performed, in addition to manual screening. Nine studies were considered eligible for the meta-analysis involving 46,424 DOACs users and 182,797 VKA users.ResultsThe use of DOACs was associated with reduced risks of systemic embolism or any stroke (RR 0.65; 95% CI 0.52–0.81; p 0.001), ischemic stroke (RR 0.84; 95% CI 0.74–0.95; p 0.007) and hemorrhagic stroke (RR 0.61; 95% CI 0.52–0.71; p 0.00001) as compared to VKA group. DOAC use was associated with significantly reduced risks of major bleeding (RR 0.68; 95% CI 0.50–0.92; p 0.01) and intracranial or gastrointestinal bleeding (RR 0.64; 95% CI 0.47–0.88; p 0.006). Compared to VKA, DOACs provided a non-statistically significant risk reduction of the outcomes major bleeding or non-major clinically relevant bleeding (RR 0.94; 95% CI 0.78–1.13; p 0.50) and any bleeding (RR 0.91; 95% CI 0.78–1.06; p 0.24).ConclusionsIn comparison to VKA, DOACs were associated with a significant reduction of the rates of thromboembolic events and major bleeding complications in patients with AF and cancer. Further studies are needed to confirm our results.

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.

A metanalysis of available randomized controlled trials and observational studies comparing self-expanding (SE) and balloon-expandable (BE) bioprostheses in patients with small aortic annulus and aortic stenosis for short- and midterm hemodynamic and clinical outcomes was performed. A total of 21 studies with a total 8,647 patients (SE: n = 4,336 patients vs BE: n = 4,311 patients) were included. SE bioprostheses had a lower postoperative mean gradient at 30 days (Mean Difference [MD] −5.16, 95% confidence interval [CI] 4.7 to 5.5, p <0.001) and at 1 year (MD −6.6, 95%CI 6.1 to 7.03, p <0.001), with a larger indexed effective orifice area (0.17, 95% CI 0.13 to 0.22, p <0.001 and 0.17, 95% CI 0.08 to 0.27, p <0.001) at both time intervals. BE bioprostheses had a higher risk of 30-day and 1-year severe prosthesis-patient mismatch (risk ratio [RR] 1.07, 95% CI 1.04 to 1.09, p <0.001; RR 1.07, 95% CI 1.04 to 1.11, p <0.001). The 30-day and 1 year paravalvular leaks (RR 0.99, 95% CI 0.98 to 0.99, p <0.001; RR 0.89, 95% CI 0.82 to 0.95, p <0.001) and permanent pacemaker implantation (RR 0.97, 95% CI 0.94 to 0.99, p 0.01, I2 = 40%,) were lower in the BE group. BE bioprostheses were associated with a lower risk of in-hospital stroke (RR 0.99, 95% CI 0.98 to 1, p = 0.01). In conclusion, in patients with small aortic annulus and aortic stenosis, SE bioprostheses have superior hemodynamic performance but higher rates of paravalvular leak, permanent pacemaker implantation, and in-hospital stroke. BE bioprostheses were associated with a higher risk of severe prosthesis-patient mismatch. [Display omitted] Self-expandable bioprostheses have superior hemodynamic performance but higher rates of paravalvular leak, permanent pacemaker implantation, and in-hospital stroke. Balloon-expandable bioprostheses were associated with a higher risk of severe prosthesis-patient mismatch.

Atrial fibrillation (AF) is the most widely recognized arrhythmia. Systemic arterial hypertension, diabetes, obesity, heart failure, and valvular heart diseases are major risk factors for the onset and progression of AF. Various studies have emphasized the augmented anxiety rate among AF patients due to the poor quality of life; however, little information is known about the possibility of triggering atrial fibrillation by anxiety. The present review sought to underline the possible pathophysiological association between AF and anxiety disorders and suggests that anxiety can be an independent risk factor for AF, acting as a trigger, creating an arrhythmogenic substrate, and modulating the autonomic nervous system. The awareness of the role of anxiety disorders as a risk factor for AF may lead to the development of new clinical strategies for the management of AF.

Background Early detection of myocardial involvement can be relevant in coronavirus disease 2019 (COVID-19) patients to timely target symptomatic treatment and decrease the occurrence of the cardiac sequelae of the infection. The aim of the present study was to assess the clinical value of cardiovascular magnetic resonance (CMR) in characterizing myocardial damage in active COVID-19 patients, through the correlation between qualitative and quantitative imaging biomarkers with clinical and laboratory evidence of myocardial injury. Methods In this retrospective observational cohort study, we enrolled 27 patients with diagnosis of active COVID-19 and suspected cardiac involvement, referred to our institution for CMR between March 2020 and January 2021. Clinical and laboratory characteristics, including high sensitivity troponin T (hs-cTnT), and CMR imaging data were obtained. Relationships between CMR parameters, clinical and laboratory findings were explored. Comparisons were made with age-, sex- and risk factor–matched control group of 27 individuals, including healthy controls and patients without other signs or history of myocardial disease, who underwent CMR examination between January 2020 and January 2021. Results The median (IQR) time interval between COVID-19 diagnosis and CMR examination was 20 (13.5–31.5) days. Hs-cTnT values were collected within 24 h prior to CMR and resulted abnormally increased in 18 patients (66.6%). A total of 20 cases (74%) presented tissue signal abnormalities, including increased myocardial native T1 (n = 11), myocardial T2 (n = 14) and extracellular volume fraction (ECV) (n = 10), late gadolinium enhancement (LGE) (n = 12) or pericardial enhancement (n = 2). A CMR diagnosis of myocarditis was established in 9 (33.3%), pericarditis in 2 (7.4%) and myocardial infarction with non-obstructive coronary arteries in 3 (11.11%) patients. T2 mapping values showed a moderate positive linear correlation with Hs-cTnT (r = 0.58; p = 0.002). A high degree positive linear correlation between ECV and Hs-cTnT was also found (r 0.77; p < 0.001). Conclusions CMR allows in vivo recognition and characterization of myocardial damage in a cohort of selected COVID-19 individuals by means of a multiparametric scanning protocol including conventional imaging and T1–T2 mapping sequences. Abnormal T2 mapping was the most commonly abnormality observed in our cohort and positively correlated with hs-cTnT values, reflecting the predominant edematous changes characterizing the active phase of disease.

Background/Objectives: The increasing use of endovascular procedures with common femoral artery (CFA) access has led to a rise in iatrogenic arterial injuries at this site. The most frequent injuries are pseudoaneurysms (PSA), retrograde dissections (RD), arteriovenous fistulas (AVF), and arterial perforations. Surgical repair is the standard treatment; however, the use of covered stents (CS) may represent a valid alternative, despite current instructions for use (IFU) not recommending CFA implantation. Methods: We conducted a single-center retrospective study on a prospectively maintained database. Patients undergoing transcatheter aortic valve repair (TAVR), endovascular aortic repair EVAR, diagnostic or therapeutic coronary angiography, or peripheral percutaneous transluminal angioplasty, who were subsequently treated for CFA injury with CS implantation between February 2015 and May 2024, were included. Endpoints were technical success (complete arterial repair), 30-day mortality, overall mortality, reintervention rates, and long-term stent patency. Results: A total of 41 patients were included: 10 (24.4%) PSA, 3 (7.3%) AVF, 27 (65.8%) perforations, and 2 (4.9%) RD. Of which 28 (68.3%) were treated with self-expandable CS and 13 (31.7%) with balloon-expandable CS. Additionally, 33 (80.5%) underwent urgent treatment. Technical success was achieved in 97.5%. Thirty-day mortality was 7.3%, with no procedure-related deaths. At a mean follow-up of 50.8 months (range 1–109), survival was 63.4%, with 100% stent patency and no procedure-related reinterventions. Conclusions: CS implantation for CFA iatrogenic injuries achieved high technical success and excellent long-term patency, representing a viable alternative to open repair. Further studies are needed to integrate CS use for CFA injuries into treatment algorithms and to update device IFUs accordingly.

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.