To obtain the normal ranges for 2D echocardiographic (2DE) indices of myocardial work (MW) from a large group of healthy volunteers over a wide range of ages and gender.

Echocardiographic parameters provide additional information compared to other variables routinely used in clinical practice to identify patients at higher risk of hemodynamic deterioration and poor in-hospital outcome, allowing prompt institution of appropriate pharmacological treatment and adequate mechanical support.

Antineoplastic therapies have significantly improved the prognosis of oncology patients. However, these treatments can bring to a higher incidence of side-effects, including the worrying cardiovascular toxicity (CTX). Substantial evidence indicates multiple mechanisms of CTX, with redox mechanisms playing a key role. Recent data singled out mitochondria as key targets for antineoplastic drug-induced CTX; understanding the underlying mechanisms is, therefore, crucial for effective cardioprotection, without compromising the efficacy of anti-cancer treatments. CTX can occur within a few days or many years after treatment. Type I CTX is associated with irreversible cardiac cell injury, and it is typically caused by anthracyclines and traditional chemotherapeutics. Type II CTX is generally caused by novel biologics and more targeted drugs, and it is associated with reversible myocardial dysfunction. Therefore, patients undergoing anti-cancer treatments should be closely monitored, and patients at risk of CTX should be identified before beginning treatment to reduce CTX-related morbidity. Genetic profiling of clinical risk factors and an integrated approach using molecular, imaging, and clinical data may allow the recognition of patients who are at a high risk of developing chemotherapy-related CTX, and it may suggest methodologies to limit damage in a wider range of patients. The involvement of redox mechanisms in cancer biology and anticancer treatments is a very active field of research. Further investigations will be necessary to uncover the hallmarks of cancer from a redox perspective and to develop more efficacious antineoplastic therapies that also spare the cardiovascular system. Antioxid. Redox Signal. 00, 000-000.

In hypertensive patients, STE provides more detailed information than conventional echocardiography and TDI, since it reveals a systolic dysfunction before hypertrophy occurs (Stage A of ACC/AHA classification of HF) and identifies some early LV mechanic changes that might improve the clinical management of these patients.

Antineoplastic drugs can be associated with several side effects, including cardiovascular toxicity (CTX). Biochemical studies have identified multiple mechanisms of CTX. Chemoterapeutic agents can alter redox homeostasis by increasing the production of reactive oxygen species (ROS) and reactive nitrogen species RNS. Cellular sources of ROS/RNS are cardiomyocytes, endothelial cells, stromal and inflammatory cells in the heart. Mitochondria, peroxisomes and other subcellular components are central hubs that control redox homeostasis. Mitochondria are central targets for antineoplastic drug-induced CTX. Understanding the mechanisms of CTX is fundamental for effective cardioprotection, without compromising the efficacy of anticancer treatments. Type 1 CTX is associated with irreversible cardiac cell injury and is typically caused by anthracyclines and conventional chemotherapeutic agents. Type 2 CTX, associated with reversible myocardial dysfunction, is generally caused by biologicals and targeted drugs. Although oxidative/nitrosative reactions play a central role in CTX caused by different antineoplastic drugs, additional mechanisms involving directly and indirectly cardiomyocytes and inflammatory cells play a role in cardiovascular toxicities. Identification of cardiologic risk factors and an integrated approach using molecular, imaging, and clinical data may allow the selection of patients at risk of developing chemotherapy-related CTX. Although the last decade has witnessed intense research related to the molecular and biochemical mechanisms of CTX of antineoplastic drugs, experimental and clinical studies are urgently needed to balance safety and efficacy of novel cancer therapies.

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Accessory mitral valve tissue (AMVT) is a rare congenital cardiac anomaly sometimes responsible for left ventricular outflow tract (LVOT) obstruction. It is diagnosed during both neonate-childhood and adult periods in patients usually symptomatic for dyspnoea, chest pain, palpitations, fatigue, or syncope. Nevertheless, AMVT is often an incidental finding. AMVT is most often associated with other cardiac and vascular congenital malformations, such as septal defects and transposition of the great arteries. Surgery is indicated only in cases of significant LVOT obstruction and in patients undergoing correction of other cardiac malformations or exploration of an intracardiac mass. Two-dimensional echocardiography, both transthoracic and transoesophageal, is considered the main imaging modality for AMVT diagnosis and patient follow-up. The recent introduction of three-dimensional echocardiography allows a more realistic characterization of this entity. We present three clinical cases in which AMVT was incidentally diagnosed during standard echocardiography and an updated review of the literature highlighting the usefulness of echocardiography for AMVT morphological and functional characterization as well as the most relevant clinical implications due to its discovery.

In patients with cryptogenic stroke and migraine, there is a fair concordance (k = 0.89) between TCD and TEE in PFO recognition. Accordingly, TCD should be recommended as a simple, noninvasive, and reliable technique, whereas TEE indication should be restricted to selected patients. TTE is a very specific technique, whose major advantage is the ability to detect a large right-to-left shunt, particularly if associated with an atrial septal aneurysm.