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1
De Sutter, Johan, Piotr Lipiec, and Christine Henri. Heart failure: preserved left ventricular ejection fraction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0028.
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Nearly half of all patients with heart failure present with a preserved left ventricular ejection fraction (HFPEF). HFPEF is a pathophysiologically and clinically heterogeneous disease with an overall similar outcome to heart failure patients with a reduced ejection fraction. It is predominantly seen in elderly patients and comorbidities such as obesity, diabetes, hypertension, a sedentary lifestyle, and myocardial ischaemia play important roles in its development. In this chapter the conventional echocardiographic hallmarks of HFPEF including a preserved ejection fraction, left ventricular hypertrophy, left atrial dilatation, diastolic dysfunction, and pulmonary hypertension are presented. For the evaluation of left ventricular diastolic dysfunction, it is important to keep in mind that no single echocardiographic parameter is sufficiently accurate and reproducible to be used in isolation to make a diagnosis of diastolic dysfunction. The value of newer techniques including three-dimensional echocardiography and longitudinal strain assessment for the diagnosis and follow-up of HFPEF patients are promising but require further evaluation. As exercise-induced dyspnoea may be the first manifestation of HFPEF, the role of exercise echo (or diastolic stress testing) with evaluation of exercise-induced changes in left ventricular filling pressure and pulmonary artery systolic pressure is also presented. This chapter ends with a discussion on the echocardiographic parameters that can be used for risk stratification and follow-up of HFPEF patients.
2
Randerath, Winfried J., and Shahrokh Javaheri. Sleep and the heart. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0040.
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Heart function and sleep are closely associated. While NREM sleep reduces cardiac workload, phasic REM sleep increases sympathetic activity and cardiac vulnerability. Heart failure (HF) patients suffer from disturbed sleep due to frequent awakenings, periodic limb movements, sleep apnea, and depression. Insomnia seems to be associated with incident HF, and, when comorbid, results in a vicious circle. There is much evidence of a relationship between breathing disturbances during sleep and heart diseases. At least 50% of HF patients suffer from obstructive (OSA) or central (CSA) sleep apnea, both associated with impaired prognosis. OSA is a risk factor for arterial hypertension, atrial fibrillation, and HF. Continuous positive airway pressure devices reduce adverse cardiac events and improve outcome in severe OSA in compliant subjects. Adaptive servoventilation (ASV) is superior to other therapeutic options for CSA. However, the use of ASV is contraindicated in severe HF with reduced, but not preserved, ejection fraction.
3
Smiseth, Otto A., Maurizio Galderisi, and Jae K. Oh. Left ventricle: diastolic function. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0021.
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Evaluation of diastolic function by echocardiography is useful to diagnose heart failure with preserved ejection fraction by showing signs of diastolic dysfunction, and regardless of ejection fraction, echocardiography can be used to estimate left ventricular (LV) filling pressure. Diastolic dysfunction occurs in a number of cardiac diseases other than heart failure and mild diastolic dysfunction is part of the normal ageing process. The fundamental disturbances in diastolic dysfunction are slowing of myocardial relaxation, loss of restoring forces, and reduced LV chamber compliance. As a compensatory response there is elevated LV filling pressure. Slowing of relaxation and loss of restoring forces are reflected in reduction in LV early diastolic lengthening velocity (e?) by tissue Doppler. The reduced diastolic compliance is reflected in faster deceleration of early diastolic transmitral velocity by pulsed wave Doppler. Elevated LV filling pressure is reflected in a number of Doppler indices and in enlarged left atrium. This chapter reviews the physiology of diastolic function, the clinical methods and indices which are available, and how these should be applied.
4
Paneni, Francesco, and Massimo Volpe. Co-morbidity (HFrEF and HFpEF): hypertension. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198784906.003.0415_update_001.
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Hypertensive heart disease is a major cause of heart failure (HF) and mortality. Hypertension precedes HF occurrence in 75% of cases, and carries a sixfold increase in HF risk as compared to non-hypertensive individuals. Most importantly, a minority of patients survive 5 years after the onset of hypertensive HF. In hypertensive patients, the heart may present different patterns of adaptive remodelling: concentric remodelling, concentric hypertrophy, and eccentric hypertrophy. Although most hypertensive patients are at high risk of developing concentric hypertrophy, a growing proportion of subjects display a concentric-to-eccentric progression eventually leading to left ventricular dilation and systolic dysfunction. Several factors including myocardial ischaemia, ethnicity, genetic background, history of diabetes, and blood pressure pattern may significantly influence the pathway from hypertension to left ventricular dilation. Patients with a concentric hypertrophy usually develop HF with preserved ejection fraction (HFpEF), whereas those with an eccentric (dilated) phenotype develop HF with reduced ejection fraction (HFrEF). Lowering blood pressure has a striking effect in reducing the risk of HF. Although available antihypertensive drugs are all successful in lowering blood pressure, angiotensin-converting enzyme inhibitors, angiotensin receptor blocker (ARBs), and diuretics are more effective than other drug classes in preventing HF. The combination of the neprilysin inhibitor sacubitril with the ARB valsartan (LCZ696) has recently been shown to be highly effective in reducing HF-related outcomes in hypertensive subjects. An individualized treatment scheme taking into account blood pressure levels, type of HF (HFpEF or HFrEF), and relevant co-morbidities (i.e. renal disease, diabetes) is currently the best approach to improve morbidity and mortality in hypertensive patients with HF.
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Katritsis, Demosthenes G., Bernard J. Gersh, and A. John Camm. Heart failure with preserved left ventricular ejection fraction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199685288.003.0805_update_003.
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6
Lam, Carolyn S. P. Heart Failure with Preserved Ejection Fraction, an Issue of Heart Failure Clinics. Elsevier - Health Sciences Division, 2014.
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7
Heart Failure with Preserved Ejection Fraction, An Issue of Heart Failure Clinics. Elsevier, 2021.
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8
Garcia, Mario J., and Allan L. Klein. Diastology: Clinical Approach to Heart Failure with Preserved Ejection Fraction. Elsevier, 2021.
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9
Reffelmann, Thorsten, and Robert Kloner. Adjunctive Reperfusion Therapy Post-AMI. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0009.
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• Reperfusion of the occluded coronary artery in an ST-segment-elevation myocardial infarction is the most effective approach for reducing infarct size, preserving left ventricular ejection fraction, lowering the incidence and severity of congestive heart failure and improving prognosis• Hence, several pharmacologic agents intended to improve target vessel patency as an adjunct to thrombolysis or primary percutaneous coronary intervention have been shown to be beneficial in patients with reperfusion therapy for acute myocardial infarction, namely antiplatelet and anticoagulation agents• Animal investigations have suggested that coronary reperfusion may also result in undesirable cardiac alterations, termed ‘reperfusion injury’, such as reversible contractile dysfunction (‘stunning’), microvascular obstruction (‘no-reflow’), and in several studies the progression of myocardial necrosis (‘lethal reperfusion injury’)• Clinical investigations of various pharmacologic interventions as an adjunctive therapy to reperfusion to reduce final infarct size, the amount of contractile dysfunction and to improve prognosis have been mostly inconsistent; only a few interventions, e.g. adenosine and atrial natriuretic peptide seem to show promise at least in certain subgroups.
10
Hummel, Scott L., and Matthew C. Konerman. Heart Failure with Preserved Ejection Fraction, an Issue of Cardiology Clinics. Elsevier - Health Sciences Division, 2022.
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11
Zoccali, Carmine, Davide Bolignano, and Francesca Mallamaci. Left ventricular hypertrophy in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0107_update_001.
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Alterations in left ventricular (LV) mass and geometry and LV dysfunction increase in prevalence from stage 2 to stage 5 in CKD. Nuclear magnetic resonance is the most accurate and precise technique for measuring LV mass and function in patients with heart disease. Quantitative echocardiography is still the most frequently used means of evaluating abnormalities in LV mass and function in CKD. Anatomically, myocardial hypertrophy can be classified as concentric or eccentric. In concentric hypertrophy, the muscular component of the LV (LV wall) predominates over the cavity component (LV volume). Due to the higher thickness and myocardial fibrosis in patients with concentric LVH, ventricular compliance is reduced and the end-diastolic volume is small and insufficient to maintain cardiac output under varying physiological demands (diastolic dysfunction). In those with eccentric hypertrophy, tensile stress elongates myocardiocytes and increases LV end-diastolic volume. The LV walls are relatively thinner and with reduced ability to contract (systolic dysfunction). LVH prevalence increases stepwisely as renal function deteriorates and 70–80% of patients with kidney failure present with established LVH which is of the concentric type in the majority. Volume overload and severe anaemia are, on the other hand, the major drivers of eccentric LVH. Even though LVH may regress after renal transplantation, the prevalence of LVH after transplantation remains close to that found in dialysis patients and a functioning renal graft should not be seen as a guarantee of LVH regression. The vast majority of studies on cardiomyopathy in CKD are observational in nature and the number of controlled clinical trials in these patients is very small. Beta-blockers (carvedilol) and angiotensin receptors blockers improve LV performance and reduce mortality in kidney failure patients with LV dysfunction. Although current guidelines recommend implantable cardioverter-defibrillators in patients with ejection fraction less than 30%, mild to moderate symptoms of heart failure, and a life expectancy of more than 1 year, these devices are rarely offered to eligible CKD patients. Conversion to nocturnal dialysis and to frequent dialysis schedules produces a marked improvement in LVH in patients on dialysis. More frequent and/or longer dialysis are recommended in dialysis patients with asymptomatic or symptomatic LV disorders if the organizational and financial resources are available.
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Farmakis, Dimitrios, John Parissis, George Papingiotis, and Gerasimos Filippatos. Acute heart failure. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0051_update_001.
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Acute heart failure is defined as the rapid development or change of symptoms and signs of heart failure that requires urgent medical attention and usually hospitalization. Acute heart failure is the first reason for hospital admission in individuals aged 65 or more and accounts for nearly 70% of the total health care expenditure for heart failure. It is characterized by an adverse prognosis, with an in-hospital mortality rate of 4–7%, a 2–3-month post-discharge mortality of 7–11%, and a 2–3-month readmission rate of 25–30%. The majority of patients have a previous history of heart failure and present with normal or increased blood pressure, while about half of them have preserved left ventricular ejection fraction. A high prevalence of cardiovascular or non-cardiovascular comordid conditions is further observed, including coronary artery disease, arterial hypertension, atrial fibrillation, diabetes mellitus, renal dysfunction, chronic lung disease, and anaemia.
13
Moonen, Marie, Nico Van de Veire, and Erwan Donal. Heart failure: risk stratification and follow-up. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0027.
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An increasing number of two- and three-dimensional echocardiographic, Doppler, and speckle imaging-derived parameters and values can be related to prognosis in heart failure with left ventricular (LV) systolic dysfunction. This chapter discusses both conventional and new indices, including their advantages and potential limitations. There is increasing evidence for the use of new indices, including three-dimensional LV ejection fraction and global longitudinal strain. The follow-up and monitoring of heart failure patients using two-dimensional transthoracic echocardiography is also discussed in this chapter, including how to estimate the LV filling pressures and quantify LV reverse remodelling.
14
Farmakis, Dimitrios, John Parissis, and Gerasimos Filippatos. Acute heart failure: epidemiology, classification, and pathophysiology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0051.
Full textAbstract:
Acute heart failure is defined as the rapid development or change of symptoms and signs of heart failure that requires urgent medical attention and usually hospitalization. Acute heart failure is the first reason for hospital admission in individuals aged 65 or more and accounts for nearly 70% of the total health care expenditure for heart failure. It is characterized by an adverse prognosis, with an in-hospital mortality rate of 4-7%, a 2-3-month post-discharge mortality of 7-11%, and a 2-3-month readmission rate of 25-30%. The majority of patients have a previous history of heart failure and present with normal or increased blood pressure, while about half of them have a preserved left ventricular ejection fraction. A high prevalence of cardiovascular or non-cardiovascular comordid conditions is further observed, including coronary artery disease, arterial hypertension, atrial fibrillation, diabetes mellitus, renal dysfunction, chronic lung disease, and anaemia. Different classification systems have been proposed for acute heart failure, reflecting the clinical heterogeneity of the syndrome; the categorization to acutely decompensated chronic heart failure vs de novo acute heart failure and to hypertensive, normotensive, and hypotensive acute heart failure are among the most widely used and clinically relevant classifications. The pathophysiology of acute heart failure involves several pathogenetic mechanisms, including volume overload, pressure overload, myocardial loss, and restrictive filling, while several cardiovascular and non-cardiovascular causes or precipitating factors lead to acute heart failure through a single of these mechanisms or a combination of them. Regardless of the underlying mechanism, peripheral and/or pulmonary congestion is the hallmark of acute heart failure, resulting from fluid retention and/or fluid redistribution. Myocardial injury and renal dysfunction are also involved in the precipitation and progression of the syndrome.
15
Mebazaa, Alexandre, and Mervyn Singer. Pathophysiology and causes of cardiac failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0151.
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Organ congestion upstream of the dysfunctional left and/or right ventricle, with preserved stroke volume, is the most frequkeywordent feature of myocardial failure.Clinical manifestations do not necessarily correlate with the degree of left ventricular systolic dysfunction (i.e. left ventricular ejection fraction).Systolic and/or diastolic dysfunction may be present, with systolic dysfunction usually predominating.Pulmonary oedema is related to left ventricular diastolic dysfunction. Compensatory mechanisms (within the heart and/or periphery) may prove paradoxically disadvantageous on ventricular stroke work and stroke volume.
16
Lancellotti, Patrizio, and Bernard Cosyns. Assessment of Diastolic Function. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713623.003.0005.
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Diastole is the part of the cardiac cycle starting at aortic valve closure and ending at mitral valve closure. Evaluation of diastolic function by echocardiography is useful to diagnose heart failure with preserved ejection fraction, and regardless of ejection fraction, echocardiography can be used to estimate left ventricular filling pressure. Assessment of diastolic function includes analysis of left ventricular relaxation and compliance, left atrial and left ventricular filling pressures. This chapter describes the phases of diastole and covers the integrated approach of LV diastolic function through M-Mode and 2D/3D echocardiography, pulsed-wave Doppler echocardiography, and pulsed-wave tissue Doppler echocardiography.
17
Gielen, Stephan, Alessandro Mezzani, Paola Pontremoli, Simone Binno, Giovanni Q. Villani, Massimo F. Piepoli, Josef Niebauer, and Daniel Forman. Physical activity and inactivity. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0012.
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In this chapter the current evidence for regular aerobic exercise in primary prevention is discussed and recommendations for exercise interventions in the general population are given. Regular physical exercise is an established therapeutic strategy in a number of cardiovascular diseases and with stable chronic heart failure. In these disease entities moderate-intensity aerobic endurance training is the basis of most training programmes. However, high-intensity interval training is more effective in improving cardiovascular exercise capacity without any measurable additional risks. Resistance training can be used as an optional training component in patients with pronounced loss of lean muscle. In recent years new areas for application of exercise-based intervention have been explored: training interventions proved to be safe and effective in pulmonary hypertension, heart failure with preserved ejection fraction, and compensated subcritical valvular heart disease. However, in contrast to training in coronary artery disease and heart failure, the prognostic benefit is not yet established.
18
Cardinale, Daniela, and Carlo Maria Cipolla. Anthracycline-related cardiotoxicity: epidemiology, surveillance, prophylaxis, management, and prognosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0290.
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Anthracycline-induced cardiotoxicity is of considerable concern, as it may compromise the clinical effectiveness of treatment, affecting both quality of life and overall survival in cancer patients, independently of the oncological prognosis. It is probable that anthracycline-induced cardiotoxicity is a unique and continuous phenomenon starting with myocardial cell injury, followed by progressive left ventricular ejection fraction (LVEF) decline that, if disregarded and not treated progressively leads to overt heart failure. The main strategy for minimizing anthracycline-induced cardiotoxicity is early detection of high-risk patients and prompt prophylactic treatment. According to the current standard for monitoring cardiac function, cardiotoxicity is usually detected only when a functional impairment has already occurred, precluding any chance of its prevention. At present, anthracycline-induced cardiotoxicity can be detected at a preclinical phase, very much before the occurrence of heart failure symptoms, and before the LVEF drops by measurement of cardiospecific biochemical markers or by Doppler myocardial and deformation imaging. The role of troponins in identifying subclinical cardiotoxicity and treatment with angiotensin-converting enzyme inhibitors, in order to prevent LVEF reduction is an effective strategy that has emerged in the last 15 years. If cardiac dysfunction has already occurred, partial or complete LVEF recovery may still be achieved if cardiac dysfunction is detected early after the end of chemotherapy and heart failure treatment is promptly initiated.
19
Haugaa, Kristina H., Francesco Faletra, and João L. Cavalcante. Cardiac rhythm disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0063.
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Cardiac rhythm disorders require diagnostic, prognostic, and guidance of therapeutic procedures by echocardiography. The most common sustained cardiac arrhythmia is atrial fibrillation (AF) leading to an increased risk for mortality, heart failure, and thromboembolic events. Echocardiography is performed to assess the aetiology of AF which most commonly is associated with diseases leading to enlarged atria. Furthermore, echocardiography is crucial to evaluate thromboembolic risk by assessing the morphology and function of the left atrial appendage among other parameters. Non-invasive imaging modalities including two-dimensional transthoracic (TTE) and transoesophageal echocardiography (TOE) with three-dimensional imaging are often indicated. Finally, TOE can help in the preprocedural planning and providing guidance for interventions such as pulmonary vein ablation and percutaneous left atrial appendage closure. In patients with ventricular arrhythmias, TTE is the first-line diagnostic tool for assessing the aetiology of ventricular arrhythmias. Ischaemic heart disease, either acute or chronic fibrosis, is the most common causes of ventricular tachycardias. Left ventricular ejection fraction remains the most important parameter for indication of an implantable cardioverter defibrillator for primary prevention therapy, although newer strain echocardiographic measures may add incremental prognostic information.
20
Sidhu, Kulraj S., Mfonobong Essiet, and Maxime Cannesson. Cardiac and vascular physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0001.
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This chapter discusses key components of cardiovascular physiology applicable to clinical practice in the field of anaesthesiology. From theory development to ground-breaking innovations, the history of cardiac and vascular anatomy, as well as physiology, is presented. Utilizing knowledge of structure and function, parameters created have allowed adequate patient clinical assessment and guided interventions. A review of concepts reveals the impact of multiple physiological variables on a patient’s haemodynamic state and the need for more accurate and efficient measurements. In particular, it is noted that a more reliable index of ventricular contractility is the end-systolic elastance rather than the ejection fraction. Constant direct preload assessment has not yet been achieved but continues to be determined through surrogate variables, and continuous cardiac output monitoring for oxygen delivery, although advancing, has limitations. Considering the effect of compound factors perioperatively, especially heart failure, modifies the goals and interventions of anaesthetists to achieve improved outcomes. Therefore, medical management prior to surgery and complete assessment through history, physical examination, and diagnostic tests are a priority. This chapter also details the expectations following volume expansion to augment haemodynamics during surgery, the concept of functional haemodynamic monitoring, and limitations to the parameters applied in assessing fluid responsiveness. Challenging the accuracy of conventional indices to predict volume status led to the use of goal-directed therapy, reducing morbidity and minimizing length of hospital stay. The mainstay of this chapter is to reinforce the relevance of advances in haemodynamic monitoring and homeostasis optimization by anaesthetists during surgery, using fundamental concepts of cardiovascular physiology.