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Right Ventricle
Published in Takahiro Shiota, 3D Echocardiography, 2020
The three parts of the RV are not in the same plane as seen in a 3D echocardiogram from a normal subject (Figure 4.1). The RV inflow tract contracts earlier than the infundibulum. The response of these three segments to medications, sympathetic stimulation, and volume and pressure overload may be different. For example, animal and human studies suggested that the inotropic response of the infundibulum may be greater than that of the inflow tract.
Physiological interpretation of pressure waveforms
Published in John Edward Boland, David W. M. Muller, Interventional Cardiology and Cardiac Catheterisation, 2019
Interaction of ventricles RV pressure overload (primary pulmonary hypertension)RV volume overload (large left to right shunt)
Cardiogenic shock
Published in Ian Mann, Christopher Critoph, Caroline Coats, Peter Collins, The Junior Doctor’s Guide to Cardiology, 2017
Ian Mann, Christopher Critoph, Caroline Coats, Peter Collins
Pulmonary embolism. A massive PE may cause signs of right-sided pressure overload on echocardiography, including dilated right atrium and right ventricle, tricuspid regurgitation and raised pulmonary pressure. Occasionally embolus may be directly visualised in the right heart. The proximal pulmonary trunk can usually be seen with echocardiography.
The role of autophagy and mitophagy in cancers
Published in Archives of Physiology and Biochemistry, 2022
Beclin1 (BECN1), which is an ortholog of the Atg6/vacuolar protein sorting (Vps)-30 protein in yeast, plays a major role in the critical step of the autophagic process by interacting with class III-type phosphoinositide 3-kinase (Class III PI3K, also known as Vps34). The activation of the kinase activity of the Beclin1-Vps34 complex promotes the production of phosphatidylinositol 3-phosphate, thereby promoting cargo recruitment, lipid membrane extension and autophagosome maturation (Kihara et al.2001). Beclin1 and Vps34 form two distinct complexes. The Beclin1-Vps34 complex I, in which Atg14L cross-links between Beclin1 and the Vps34-p150 complex, mediates autophagosome formation. Beclin1-Vps34 complex II, in which Beclin1 and the Vps34-p150 complex are bridged by UVRAG, regulates the vacuolar protein-sorting pathway (Itakura et al.2008). Some endogenous factors, including transcriptional factors and microRNAs, modulate autophagy during pressure overload (PO) by regulating Beclin1 levels (Yin et al.2013). Cardiac pressure overload, such as those caused by aortic stenosis and systemic hypertension, commonly results in cardiac hypertrophy, and may lead to the development of heart failure. Hypertrophic stimuli, such as PO and angiotensin II, downregulate miR-30a, which stimulates autophagy through the upregulation of Beclin1 (Yin et al.2013). The overexpression of Beclin1 in breast cancer cells promotes autophagy and inhibits the malignant phenotype (Qu et al.2003).
Emerging therapeutic targets for cardiac hypertrophy
Published in Expert Opinion on Therapeutic Targets, 2022
Alexander J. Winkle, Drew M. Nassal, Rebecca Shaheen, Evelyn Thomas, Shivangi Mohta, Daniel Gratz, Seth H. Weinberg, Thomas J. Hund
Currently, there are several strategies that aim to reduce the extent of hypertrophy by targeting cell-surface receptors with the goal of minimizing activation of the neurohumoral stress response. The renin-angiotensin-aldosterone system (RAAS) is a major regulator of this response and target of these therapies. Angiotensin converting enzyme (ACE) inhibitors, β-adrenergic receptor blockers, and angiotensin receptor blockers fall under this umbrella and have been clinically administered demonstrating favorable outcomes [95,96]. An additional route often explored is reduction of the pressure overload that stimulates this stress response. Often termed antihypertensives, these treatments can include the RAAS treatments above, and similarly aim to reduce activation of stress response. More recently, therapeutic strategies have focused on action within the cell. A promising class of these therapies are histone de-acetylase (HDAC) inhibitors. These compounds have shown promise in reducing the growth of cardiomyocytes and reducing the effects of hypertrophy within the context of increased load [8,97,98]. Schiattarella et al. even posit using these agents in a targeted manner to ‘sculpt’ ventricular mass through the progression of disease [4].
Usefulness of echocardiographic McConnell’s sign in the computerized-medicine-era
Published in Acta Cardiologica, 2019
Carmine Siniscalchi, Alessandro Palumbo, Anna Rocci, Manuela Basaglia, Nicola Gaibazzi
We described the case of 30-year-old man was admitted to the Emergency Room for acute dyspnoea and chest pain. Echocardiogram revealed RV pressure overload and significant systolic dysfunction in four-chamber view, consisting in hypokinesia of the free wall compared with hyperkinesia of the RV apex, the so-called McConnell’s Sign (Figure 1, Supplementary material Movie 1, Supplementary material Movie 2). Enlargement of the right atrium and moderate-severe tricuspid regurgitation were also detected. Chest X-ray suggested signs of RV pressure overload (Figure 2). A Multi-slice Computed Tomography (MSCT) was also performed. In Figure 3: A shows the large saddle pulmonary thrombus and encroaching clots into lobar artery lumen; B: dilatation of the right ventricle and septal flattening/deviation; C: reduction of blood flow into pulmonary vessels causes oligaemia; D picture depicts the dilatation of pulmonary artery trunk using 3D volume-rendering.