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There has been an exponential increase in the amount of information available on the pathophysiology and management of heart diseases. Meanwhile, understanding of the underlying pathology and physiology has deepened and broadened with new methodologies to monitor cardiac structure and function. These developments have led to an overwhelming amount of information available to students, trainees, and physicians. What is in short supply is a comprehensive yet concise and clear description of the important cardiac conditions and disorders, an approach to their management, and an easily consulted and well-indexed summary to be used at the bedside or in the clinic. This book addresses that need.

Many of them will need multiple valve surgeries over their lifetime, which increases their risk of morbidity and mortality.1 The advances in interventional cardiology and the introduction of the Melody valve, a balloon expandable pulmonary valve2 in 2000 have radically altered the management options for these patients by reducing the need for redo surgical interventions.3 We herein discuss the existing and future catheter-based valve replacement and repair options for adult CHD. Studies evaluating the timing of PVR in patients with severe chronic PR have suggested that normalisation of right ventricular (RV) volume will not occur if severe dilation has already ensued (indexed RV end-diastolic volume >150 mL/m2 or indexed RV end-systolic volume >80 mL/m2).6–8 Furthermore, it is likely that earlier PVR could result in improved exercise tolerance especially in patients with predominant PS.9 10 While there is little evidence that such an approach results in improved clinical outcomes such as decreased mortality, some experts argue that all patients with RV outflow dysfunction (PR, PS or both) should undergo PVR prior to the development of RV dilation or dysfunction.9 The introduction of transcatheter valve therapies is lowering the threshold for PVR, however, this approach must be weighed against the potential for infective endocarditis (IE), procedural risks and decrease in internal diameter of the conduits secondary to multiple transcatheter valve implants.11 Transcatheter PVR (TPVR) can alleviate RV outflow tract (RVOT) conduit dysfunction whether due to stenosis or regurgitation or both. Potential complications of TAVR include perivalvular leak, conduction abnormalities, thromboembolism, valve embolisation, aortic root rupture, coronary occlusion and iliac artery rupture.43 TAVR in AS due to bicuspid aortic valve has been shown to be feasible and effective with favourable valve performance, and similar outcomes as TAVR in trileaflet AS, and while some studies demonstrated a higher rate of PVL compared with TAVR in trileaflet AS, the newer generation valves, such as the Sapien 3 and the Lotus valve show lower rates of perivalvular leak (PVL).44 45 In our experience, TAVR in patients with other forms of CHD is feasible, such as a patient with D -transposition of the great arteries status postarterial switch and valve sparing aortic root repair with recurrent AR (figure 4). Furthermore, the Melody valve has been modified and surgically placed in all four valvular positions as an expandable valve in infants and children allowing for future balloon dilations and by that accommodating somatic outgrowth, hopefully reducing the number of future surgeries.48 49 Importantly, while transcatheter valve implantation in CHD is reducing the need for surgical intervention, with its associated morbidities, as well as getting women through childbearing age without the need for systemic anticoagulation as would be necessary with mechanical valves, the trade-off is the concern for valve durability, and the need for reintervention relative to the surgical valves, especially as these valves are being implanted at a much younger age in patients with CHD.

Memoir by Stuart Jamieson, a member of the second generation of cardiothoracic surgical pioneers, from his early years in Africa to his career as an innovative heart surgeon.

In a randomized trial, patients with tricuspid regurgitation who were treated with transcatheter edge-to-edge repair had more favorable clinical outcomes at 1 year than did patients who received medical therapy.

\"Can a paper heart be like a real heart for a little puppet who longs for love?\"--P. [4] of cover.

Myocardial cell death is initiated by excessive mitochondrial Ca(2+) entry causing Ca(2+) overload, mitochondrial permeability transition pore (mPTP) opening and dissipation of the mitochondrial inner membrane potential (ΔΨm). However, the signalling pathways that control mitochondrial Ca(2+) entry through the inner membrane mitochondrial Ca(2+) uniporter (MCU) are not known. The multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is activated in ischaemia reperfusion, myocardial infarction and neurohumoral injury, common causes of myocardial death and heart failure; these findings suggest that CaMKII could couple disease stress to mitochondrial injury. Here we show that CaMKII promotes mPTP opening and myocardial death by increasing MCU current (I(MCU)). Mitochondrial-targeted CaMKII inhibitory protein or cyclosporin A, an mPTP antagonist with clinical efficacy in ischaemia reperfusion injury, equivalently prevent mPTP opening, ΔΨm deterioration and diminish mitochondrial disruption and programmed cell death in response to ischaemia reperfusion injury. Mice with myocardial and mitochondrial-targeted CaMKII inhibition have reduced I(MCU) and are resistant to ischaemia reperfusion injury, myocardial infarction and neurohumoral injury, suggesting that pathological actions of CaMKII are substantially mediated by increasing I(MCU). Our findings identify CaMKII activity as a central mechanism for mitochondrial Ca(2+) entry in myocardial cell death, and indicate that mitochondrial-targeted CaMKII inhibition could prevent or reduce myocardial death and heart failure in response to common experimental forms of pathophysiological stress.

Accurate assessment of cardiac function is crucial for the diagnosis of cardiovascular disease , screening for cardiotoxicity and decisions regarding the clinical management of patients with a critical illness . However, human assessment of cardiac function focuses on a limited sampling of cardiac cycles and has considerable inter-observer variability despite years of training . Here, to overcome this challenge, we present a video-based deep learning algorithm-EchoNet-Dynamic-that surpasses the performance of human experts in the critical tasks of segmenting the left ventricle, estimating ejection fraction and assessing cardiomyopathy. Trained on echocardiogram videos, our model accurately segments the left ventricle with a Dice similarity coefficient of 0.92, predicts ejection fraction with a mean absolute error of 4.1% and reliably classifies heart failure with reduced ejection fraction (area under the curve of 0.97). In an external dataset from another healthcare system, EchoNet-Dynamic predicts the ejection fraction with a mean absolute error of 6.0% and classifies heart failure with reduced ejection fraction with an area under the curve of 0.96. Prospective evaluation with repeated human measurements confirms that the model has variance that is comparable to or less than that of human experts. By leveraging information across multiple cardiac cycles, our model can rapidly identify subtle changes in ejection fraction, is more reproducible than human evaluation and lays the foundation for precise diagnosis of cardiovascular disease in real time. As a resource to promote further innovation, we also make publicly available a large dataset of 10,030 annotated echocardiogram videos.