The left atrial appendage: from embryology to prevention of thromboembolism.

The left atrial appendage (LAA) is the main source of thromboembolism in patients with non-valvular atrial fibrillation (AF). As such, the LAA can be the target of specific occluding device therapies. Optimal management of patients with AF includes a comprehensive knowledge of the many aspects related to LAA structure and thrombosis. Here we provide baseline notions on the anatomy and function of the LAA, and then focus on current imaging tools for the identification of anatomical varieties. We also describe pathogenetic mechanisms of LAA thrombosis in AF patients, and examine the available evidence on treatment strategies for LAA thrombosis, including the use of non-vitamin K antagonist oral anticoagulants and interventional approaches.

Heart failure due to right ventricular apical pacing: the importance of flow patterns.

In patients receiving permanent cardiac electrical stimulation, a high burden of apical right ventricular pacing is associated with an increased incidence of heart failure. Despite the large body of electrocardiographic, echocardiographic, and pathological data, mechanisms underlying this serious complication are not fully understood. Moreover, the empirical use of alternative right ventricular pacing sites, both in the experimental and in the clinical setting, has not provided better results in terms of clinical outcome. Recent data derived by echocardiographic particle image velocimetry of intracardiac flows have shown abnormal flow patterns in patients with dyssynchrony of left ventricular wall contraction, and the reversion to normal flow dynamics after successful electrical cardiac resynchronization therapy. This suggests that a normal intraventricular flow pattern is strongly dependent on the highly coordinated contraction of the ventricular wall segments and that an abnormal sequence of wall contraction may trigger the development of overt heart failure. This review summarizes the state of the art on this topic, highlighting postulated underlying basic mechanisms linking abnormal flow with the development of pacing-induced heart failure. This research line suggests the importance of studying intraventricular fluid dynamics as a new powerful tool for a more complete understanding of mechanisms involved, and ultimately to prevent pacing-related heart failure.

Therapeutic strategies aiming at the reduction of the antiplatelet intensity should not overlook the ischemic risk in patients with coronary syndromes.

De-escalation of dual antiplatelet therapy (DAPT) is gaining traction as a strategy to reduce bleeding risks while ensuring ischemic outcomes. Undiscriminating de-escalation, notably in patients with high ischemic risk, might expose them to major adverse cardiac events. Platelet function and genetic tests are emerging tools to guide de-escalation, but both present specific drawbacks. Recent meta-analyses have aimed to consolidate the findings of individual trials to provide clearer insights. Yet, limitations remain for patients with concomitant high bleeding and ischemic risks. These high-risk patients are frequently underrepresented in clinical trials, and, therefore, currently available guidelines lack evidence-based recommendations for this subset. While DAPT de-escalation strategies hold promise, the choice of approach, whether clinically or assay-guided, remains complex and should be individualized.

Intraventricular flow patterns during right ventricular apical pacing.

Objectives: To assess differences in blood flow momentum (BFM) and kinetic energy (KE) dissipation in a model of cardiac dyssynchrony induced by electrical right ventricular apical (RVA) stimulation compared with spontaneous sinus rhythm. Methods: We cross-sectionally enrolled 12 consecutive patients (mean age 74±8 years, 60% male, mean left ventricular ejection fraction 58%±6 %), within 48 hours from pacemaker (PMK) implantation. Inclusion criteria were: age>18 years, no PMK-dependency, sinus rhythm with a spontaneous narrow QRS at the ECG, preserved ejection fraction (>50%) and a low percentage of PMK-stimulation (<20%). All the participants underwent a complete echocardiographic evaluation, including left ventricular strain analysis and particle image velocimetry. Results: Compared with sinus rhythm, BFM shifted from 27±3.3 to 34±7.6° (p=0.016), while RVA-pacing was characterised by a 35% of increment in KE dissipation, during diastole (p=0.043) and 32% during systole (p=0.016). In the same conditions, left ventricle global longitudinal strain (LV GLS) significantly decreased from 17±3.3 to 11%±2.8% (p=0.004) during RVA-stimulation. At the multivariable analysis, BFM and diastolic KE dissipation were significantly associated with LV GLS deterioration (Beta Coeff.=0.54, 95% CI 0.07 to 1.00, p=0.034 and Beta Coeff.=0.29, 95% CI 0.02 to 0.57, p=0.049, respectively). Conclusions: In RVA-stimulation, BFM impairment and KE dissipation were found to be significantly associated with LV GLS deterioration, when controlling for potential confounders. Such changes may favour the onset of cardiac remodelling and sustain heart failure.

Angina pectoris and myocardial ischemia in the absence of obstructive coronary artery disease: practical considerations for diagnostic tests.

Angina and myocardial ischemia without obstructive coronary artery disease are common clinical findings, often neglected for the assumption of a good prognosis. Most often, such patients are neither further investigated nor offered specific treatment beyond reassurance. However, the absence of significant coronary stenoses on angiography does not necessarily imply a "healthy" coronary tree. In such cases, myocardial ischemia may result from different types of functional disease involving the epicardial coronary arteries, the coronary microcirculation, or both; an accurate assessment of these components should be systematically performed after exclusion of organic epicardial disease because a correct diagnosis has relevant prognostic and therapeutic implications. Here we discuss the basic principles of diagnostic tests in this setting and propose a diagnostic sequence of reasonable practical implementation that may help identify patients at risk of future cardiac events.

The adequacy of myocardial revascularization in patients with multivessel coronary artery disease.

In patients with multi-vessel coronary artery disease (MVCAD) myocardial revascularization may be accomplished either on all diseased lesions--complete myocardial revascularization--or on selectively targeted coronary segments by percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). Complete revascularization has a potential long-term prognostic benefit, but is more complex and may increase in-hospital events when compared with incomplete revascularization. No conclusive agreement has been yet reached on the "optimal" extent of revascularization, and guidelines have only recently mentioned the adequacy of revascularization in the decision whether to submit a patient to CABG or PCI. In the absence of any trial specifically designed to assess the relative benefit of either strategy, the present review explores current concepts about the completeness of revascularization, the growing evidence on the relevance of lesion and myocardial functional evaluation, and analyzes currently available data in relation to different clinical settings, including acute coronary syndromes, diabetes, chronic kidney disease and impaired left ventricular function. Considerations on the adequacy of revascularization should guide the choice among PCI and CABG in patients with MVCAD during the decision-making process, taking into account the clinical presentation, the extent and relevance of ischemia and the presence of other comorbidities.

[Angina with normal coronary arteries: a common but often neglected association]. / Dolore anginoso e coronarie normali: un'associazione frequente, troppo spesso trascurata.

The angiographic evidence of normal coronary arteries or moderate coronary artery disease is a relatively common finding in patients with a history of angina, with a higher prevalence in females. This condition is not a single pathological entity, but comprises several different presentations, such as cardiac syndrome X, vasospastic angina, myocardial bridges, as well as coronary alterations with more doubtful clinical implications, such as serial moderate coronary artery lesions or focal coronary dilations. These pathological conditions are different in pathophysiology, management, and prognosis, and for this reason their correct diagnostic definition, beyond the angiographic evidence of normal coronary arteries, appears mandatory. This review aims at providing an update in the conundrum of entities comprising angina with normal coronary arteries, and at explaining different diagnostic and therapeutic approaches.

Isolated troponin increase after percutaneous coronary interventions: does it have prognostic relevance?

Percutaneous coronary intervention (PCI) is often "associated" with myocardial injury. This event has been considered in the past as an acceptable trade-off for an optimal stent deployment. More recently, in the Universal Definition of myocardial infarction (MI), an increase of either cardiac troponins or creatine kinase-MB >3 times the upper reference limit (URL) has been defined as MI. Although there is no doubt on the accuracy of cardiac troponins in the diagnosis of spontaneous MI, existing data do not support the hypothesis that an isolated elevation of cardiac troponins over such threshold is associated with an adverse prognosis after PCI.