Heart failure (HF) is an extremely major health problem with gradually increasing incidence in developed and developing countries. HF may lead to cardiac remodeling; thus, advanced imaging techniques are required to comprehensively evaluate cardiac mechanics. Recently, three-dimensional speckle-tracking echocardiography (3D-STE) has been developed as a novel imaging technology that is based on the three-dimensional speckle-tracking on the full volume three-dimensional datasets. Three-dimensional speckle-tracking echocardiography allows a more accurate evaluation of global and regional myocardial performance, assessment of cardiac mechanics, detection of subclinical cardiac dysfunction, and prediction of adverse clinical events in a variety of cardiovascular diseases. Therefore, this review summarizes the clinical usefulness of 3D-STE in patients with HF.

The acute and chronic myocardial ischemia results in oxidative stress that impairs myocardial contractility and eventually leads to heart failure. However, the underlying regulatory molecular mechanisms are not fully understood. The heat shock protein 22 (Hsp22), a small-molecular-weight protein preferentially expressed in the heart, was found to be dramatically increased in the cardiac oxidative stress conditions in both human and animal models after the acute and chronic ischemia. Overexpression of Hsp22 largely protects the heart against ischemic damage. Mechanistically, overexpression of Hsp22 attenuates hypoxia-induced oxidative phosphorylation in mitochondrial and the high rate of superoxide production. Short term gene delivery of Hsp22 reduces the infarct size caused by the ischemia/reperfusion, providing a clinical therapeutic potential. This review discusses the new progress of the studies on Hsp22 by focusing on its protective effect against the excessive cardiac oxidative stress, including its adaptive induction in myocardium upon the oxidative stress, its protective role in myocardial ischemia/reperfusion, its regulation in mitochondrial oxidative phosphorylation and the underlying molecular signaling pathways promoting cell survival. This information will increase our understanding of the molecular regulation of cardiac adaption under the oxidative stress and the potential therapeutic relevance.

Patients with heart failure (HF) have high morbidity and mortality. Accurate assessment of right ventricular (RV) function has important prognostic significance in patients with HF. However, conventional echocardiographic parameters of RV function have limitations in RV assessments due to the complex geometry of right ventricle. In recent years, speckle tracking echocardiography (STE) has been developed as promising imaging technique to accurately evaluate RV function. RV longitudinal strain (RVLS) using STE, as a sensitive index for RV function evaluation, displays the powerfully prognostic value in patients with HF. Therefore, the aim of the present review was to summarize the utility of RVLS in patients with HF.

Primary cardiac tumors (PCTs) are rare, with benign PCTs being relatively common in approximately 75% of all PCTs. Benign PCTs are usually asymptomatic, and they are found incidentally by imaging. Even if patients present with symptoms, they are usually nonspecific. Before the application of imaging modalities to the heart, our understanding of these tumors is limited to case reports and autopsy studies. The advent and improvement of various imaging technologies have enabled the non-invasive evaluation of benign PCTs. Although echocardiography is the most commonly used imaging examination, it is not the best method to describe the histological characteristics of tumors. At present, cardiac magnetic resonance (CMR) and cardiac computed tomography (CCT) are often used to assess benign PCTs providing detailed information on anatomical and tissue features. In fact, each imaging modality has its own advantages and disadvantages, multimodality imaging uses two or more imaging types to provide valuable complementary information. With the widespread use of multimodality imaging, these techniques play an indispensable role in the management of patients with benign PCTs by providing useful diagnostic and prognostic information to guide treatment. This article reviews the multimodality imaging characterizations of common benign PCTs.

Heat shock protein 22 (Hsp22) is a small heat shock protein predominantly expressed in skeletal and cardiac muscle. Previous studies indicate that Hsp22 plays a vital role in protecting the heart against cardiac stress. However, the essential role of Hsp22 in the heart under physiological conditions remains largely unknown. In this study, we used an Hsp22 knockout (KO) mouse model to determine whether loss of Hsp22 impairs cardiac growth and function with increasing age under physiological conditions. Cardiac structural and functional alterations at baseline were measured using echocardiography and invasive catheterization in Hsp22 KO mice during aging transition compared to their age-matched wild-type (WT) littermates. Our results showed that Hsp22 deletion induced progressive cardiac dilation along with declined function during the aging transition. Mechanistically, the loss of Hsp22 impaired BCL-2–associated athanogene 3 (BAG3) expression and its associated cardiac autophagy, undermined cardiac energy metabolism homeostasis and increased oxidative damage. This study showed that Hsp22 played an essential role in the non-stressed heart during the early stage of aging, which may bring new insight into understanding the pathogenesis of age-related dilated cardiomyopathy.

Valosin-containing protein (VCP) was found to play a vital protective role against cardiac stresses. Genetic mutations of VCP are associated with human dilated cardiomyopathy. However, the essential role of VCP in the heart during the physiological condition remains unknown since the VCP knockout in mice is embryonically lethal. We generated a cardiac-specific dominant-negative VCP transgenic (DN-VCP TG) mouse to determine the effects of impaired VCP activity on the heart. Using echocardiography, we showed that cardiac-specific overexpression of DN-VCP induced a remarkable cardiac dilation and progressively declined cardiac function during the aging transition. Mechanistically, DN-VCP did not affect the endogenous VCP (EN-VCP) expression but significantly reduced cardiac ATPase activity in the DN-VCP TG mouse hearts, indicating a functional inhibition. DN-VCP significantly impaired the aging-related cytoplasmic/nuclear shuffling of EN-VCP and its co-factors in the heart tissues and interrupted the balance of the VCP-cofactors interaction between the activating co-factors, ubiquitin fusion degradation protein 1 (UFD-1)/nuclear protein localization protein 4 (NPL-4) complex, and its inhibiting co-factor P47, leading to the binding preference with the inhibitory co-factor, resulting in functional repression of VCP. This DN-VCP TG mouse provides a unique functional-inactivation model for investigating VCP in the heart in physiological and pathological conditions.