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1
Chronic cardiac disease: Optimizing therapeutic efficacy in heart failure. London: Whurr, 2002.
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2
Rahimi, Kazem. Chronic heart failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0092.
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The European Society of Cardiology defines heart failure as a clinical syndrome in which patients have the following features: symptoms typical of heart failure (breathlessness, fatigue, ankle swelling); signs typical of heart failure (tachycardia, tachypnoea, pulmonary crackles, pleural effusion, raised jugular venous pressure, peripheral oedema, hepatomegaly); and objective evidence of a structural or functional abnormality of the heart at rest (cardiomegaly, third heat sound, cardiac murmurs, abnormality on the echocardiogram, raised natriuretic peptide concentration). Heart failure results in activation of the sympathetic nervous system and the renin–aldosterone–angiotensin system, and release of a number of hormones such as natriuretic peptides, and cytokines, including tumour necrosis factor amongst others. While neurohormone activation is initially compensatory and helps in the short term to maintain circulatory needs, ultimately it has detrimental effects on the myocardium and compromises its function further. These mechanisms are therefore therapeutic targets to improve symptoms and lessen the risk of death.
3
Slaughter, Mark S. Cardiac Surgery in Chronic Renal Failure. Wiley & Sons, Incorporated, John, 2008.
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4
Slaughter, Mark S. Cardiac Surgery in Chronic Renal Failure. Wiley & Sons, Incorporated, John, 2008.
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5
Katritsis, Demosthenes G., Bernard J. Gersh, and A. John Camm. Chronic heart failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199685288.003.0754_update_004.
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The diagnosis and management of chronic heart failure are discussed. Medical therapy and indications for cardiac resynchronization therapy (CRT), implantable cardioverter-defibrillators (ICD), left ventricular assist devices (LVAD), and transplantation are presented. Recommendations by the ACC/AHA and ESC on the management of patients with heart failure have been summarized and tabulated.
6
Goldsmith, David J. Cardiovascular disease and chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0098.
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Even after as full a statistical adjustment as can be made for traditional cardiovascular risk factors has been undertaken, impaired kidney function and raised concentrations of albumin in urine each increase the risk of cardiovascular disease (CVD) by two- to fourfold, the degree increasing with severity. If the patient is also suffering from diabetes (as either the cause of CKD or a complication of it), the risks of CVD increase two- to fourfold again. CKD patients should, therefore, be acknowledged as having perhaps the highest cardiovascular risk of any patient cohort. CVD is underdiagnosed and undertreated in these patients. In early CKD the manifestations of CVD are similar to those of other patients. In late CKD and particularly in patients on dialysis the epidemiology is different. Left ventricular hypertrophy is very common and sudden cardiac death is greatly increased in incidence. Heart failure is a common complication. Calcification of valves and vessels becomes increasingly common and bad CVD outcomes are associated with hyperphosphataemia and other manifestations. The mechanisms by which risks are increased are not fully understood. The evidence base for the effectiveness of established therapies for CVD is relatively light in patients with CKD, but there is evidence for benefit of lipid-lowering therapies and most nephrologists believe that blood pressure and volume control are important for good long-term outcomes. Evidence of impact on CVD of interventions to alter mineral bone disease is disappointingly weak.
7
S, Slaughter Mark, ed. Cardiac surgery in chronic renal failure. Malden, Mass: Blackwell Futura, 2007.
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8
S, Slaughter Mark, ed. Cardiac surgery in chronic renal failure. Malden, Mass: Blackwell Futura, 2007.
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9
S, Slaughter Mark, ed. Cardiac surgery in chronic renal failure. Malden, Mass: Blackwell Futura, 2007.
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10
Bakris, George L. The Kidney in Heart Failure. Springer, 2014.
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11
The Kidney in Heart Failure. Springer, 2012.
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12
Bakris, George L. The Kidney in Heart Failure. Springer, 2012.
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13
S, Parfrey Patrick, and Harnett John D, eds. Cardiac dysfunction in chronic uremia. Boston: Kluwer Academic Publishers, 1992.
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14
Parfrey, Patrick S. Cardiac Dysfunction in Chronic Uremia. Springer, 2012.
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15
Jardine, Alan G., and Rajan K. Patel. Lipid disorders of patients with chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0102.
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The risk of developing cardiovascular (CV) disease is increased in patients with chronic kidney disease (CKD) and although dyslipidaemia is a major contributory factor to the development of premature CV disease, the relationship is complex. Changes in lipid fractions are related to glomerular filtration rate and the presence and severity of proteinuria, diabetes, and other confounding factors. The spectrum of CV disease changes from lipid-dependent, atheromatous coronary disease in early CKD to lipid-independent, non-coronary disease, manifesting as heart failure, and sudden cardiac death in advanced and end-stage renal disease. Statin-based lipid-lowering therapy is proven to reduce coronary events across the spectrum of CKD. The relative reduction in overall CV events, however, diminishes as CKD progresses and the proportion of lipid-dependent coronary events declines. There is nevertheless a strong argument for the use of statin-based therapy across the spectrum of CKD. The argument is particularly strong for those patients with progressive renal disease who will eventually require transplantation, in whom preventive therapy should start as early as possible. The SHARP study established the benefits and endorses the use of lipid-lowering therapy in CKD 3-4 but uncertainty about the value of initiation of statin therapy in CKD 5 remains. There is, however, no rationale for stopping agents started earlier in the course of the illness for compelling indications, particularly in those who will ultimately be transplanted. The place of high-density lipoprotein-cholesterol raising and triglyceride lowering therapy needs to be assessed in trials. Modifying dyslipidaemia in CKD has demonstrated that lipid-dependent atheromatous cardiovascular disease is only one component of the burden of CV disease in CKD patients, that this is proportionately less in advanced CKD, and that modification of lipid profiles is only one part of CV risk management.
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(Contributor), Khalid Ashai, William Cohn (Contributor), Matthew Forrester (Contributor), Kelly Guglielmi (Contributor), Charles Herzog (Contributor), Rosemary Kelly (Contributor), Rakhi Khanna (Contributor), et al., eds. Cardiac Surgery in Chronic Renal Failure: Clinical Management and Outcomes. Blackwell Publishing Limited, 2007.
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17
Zipes, Douglas, and Silvia Priori. Sudden Cardiac Death: A Handbook for Clinical Practice. Wiley & Sons, Incorporated, John, 2009.
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18
Zipes, Douglas, and Silvia Priori. Sudden Cardiac Death: A Handbook for Clinical Practice. Wiley & Sons, Incorporated, John, 2008.
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19
Cardiac Dysfunction in Chronic Uremia (Topics in Renal Medicine). Springer, 1991.
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20
Visouli, Aikaterini N., and Antonis A. Pitsis. Acute heart failure: heart failure surgery and transplantation. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0054_update_001.
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Cardiac surgery should be considered in all cases of acute heart failure (AHF) or acutely decompensated chronic heart failure (ADCHF) caused, precipitated, or aggravated by surgically correctable causes. Mechanical circulatory support (MCS) and heart transplantation (HTx) may be considered when all conventional measures have failed.
21
Visouli, Aikaterini N., and Antonis A. Pitsis. Acute heart failure: heart failure surgery and transplantation. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0054_update_002.
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Cardiac surgery should be considered in all cases of acute heart failure (AHF) or acutely decompensated chronic heart failure (ADCHF) caused, precipitated, or aggravated by surgically correctable causes. Mechanical circulatory support (MCS) and heart transplantation (HTx) may be considered when all conventional measures have failed.
22
Rahimi, Kazem. Acute heart failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0091.
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Heart failure is a clinical syndrome characterized by an inadequate cardiac output for the needs of the body in the absence of low filling pressures, and reflects abnormal cardiac structure or function. Although various definitions for acute heart failure (AHF) exist, here AHF is defined as new-onset heart failure or an acute exacerbation of chronic heart failure, requiring urgent therapy. Patients with AHF typically have clinical features of organ hypoperfusion, with or without pulmonary and peripheral oedema.
23
Visouli, Aikaterini N., and Antonis A. Pitsis. Acute heart failure: heart failure surgery and transplantation. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0054.
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Cardiac surgery should be considered in all cases of acute heart failure that is attributed to surgically correctable causes. Surgical revascularization, repair of mechanical complications of myocardial infarction, valve repair or replacement, mechanical circulatory support, and heart transplantation represent the main surgical interventions that may be offered in the setting of acute (de novo or decompensated chronic) heart failure. Percutaneous aortic valve replacement should also be considered for patients who are deemed inoperable.
24
Mebazaa, Alexandre, and Mervyn Singer. Therapeutic strategy in cardiac failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0152.
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The fundamental therapeutic principles of heart failure management are for acute heart failure with mainly signs of pulmonary congestion, normal or high blood pressure, and no signs of low cardiac output to reduce pulmonary congestion without affecting blood pressure. Management principles of cardiogenic shock management comprise improvement of forward flow with restoration/maintenance of adequate organ perfusion. Appropriate management requires sound appreciation of the underlying pathophysiology, awareness of the actions and potential side-effects of each therapeutic intervention, and a level of monitoring and investigation sophisticated enough to assess disease severity, and the effectiveness (or otherwise) of any treatment being given. Where possible, consideration of previous comorbidity factors and chronic symptomatology should guide how aggressive intervention should be. However, these must be based on documented fact, rather than hearsay or supposition. The patient should always be given the benefit of the doubt.
25
Choudhary, Rajiv, Kevin Shah, and Alan Maisel. Biomarkers in acute heart failure. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0037.
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Acute heart failure continues to be a worldwide medical problem, associated with frequent readmissions, high mortality, and a profound economic impact on national health care systems. In the past decade, biomarkers have shifted the way in which acute heart failure is managed by the cardiologist. The search for the ideal biomarker to aid in the diagnosis, prognosis, and treatment of acute heart failure is ongoing. The natriuretic peptides have proved extremely useful in determining whether acute dyspnoea has a cardiac aetiology. In addition, recent trials have demonstrated the use of natriuretic peptides in inpatient and outpatient prognosis, as well as in titrating medications in outpatients with chronic heart failure to prevent acute heart failure hospitalizations. Other emerging acute heart failure biomarkers include mid-regional pro-adrenomedullin, mid-regional proatrial natriuretic peptide, troponin, ST2, and neutrophil gelatinase-associated lipocalin.
26
Choudhary, Rajiv, Kevin Shah, and Alan Maisel. Biomarkers in acute heart failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0037_update_001.
Full textAbstract:
Acute heart failure continues to be a worldwide medical problem, associated with frequent readmissions, high mortality, and a profound economic impact on national health care systems. In the past decade, biomarkers have shifted the way in which acute heart failure is managed by the cardiologist. The search for the ideal biomarker to aid in the diagnosis, prognosis, and treatment of acute heart failure is ongoing. The natriuretic peptides have proved extremely useful in determining whether acute dyspnoea has a cardiac aetiology. In addition, recent trials have demonstrated the use of natriuretic peptides in inpatient and outpatient prognosis, as well as in titrating medications in outpatients with chronic heart failure to prevent acute heart failure hospitalizations. Other emerging acute heart failure biomarkers include mid-regional pro-adrenomedullin, mid-regional proatrial natriuretic peptide, troponin, ST2, and neutrophil gelatinase-associated lipocalin.
27
Choudhary, Rajiv, Kevin Shah, and Alan Maisel. Biomarkers in acute heart failure. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0037_update_002.
Full textAbstract:
Acute heart failure continues to be a worldwide medical problem, associated with frequent readmissions, high mortality, and a profound economic impact on national health care systems. In the past decade, biomarkers have shifted the way in which acute heart failure is managed by the cardiologist. The search for the ideal biomarker to aid in the diagnosis, prognosis, and treatment of acute heart failure is ongoing. The natriureticfc peptides have proved extremely useful in determining whether acute dyspnoea has a cardiac aetiology. In addition, recent trials have demonstrated the use of natriuretic peptides in inpatient and outpatient prognosis, as well as in titrating medications in outpatients with chronic heart failure to prevent acute heart failure hospitalizations. Other emerging acute heart failure biomarkers include mid-regional pro-adrenomedullin, mid-regional proatrial natriuretic peptide, troponin, ST2, and neutrophil gelatinase-associated lipocalin.
28
Choudhary, Rajiv, Kevin Shah, and Alan Maisel. Biomarkers in acute heart failure. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0037_update_003.
Full textAbstract:
Acute heart failure continues to be a worldwide medical problem, associated with frequent readmissions, high mortality, and a profound economic impact on national health care systems. In the past decade, biomarkers have shifted the way in which acute heart failure is managed by the cardiologist. The search for the ideal biomarker to aid in the diagnosis, prognosis, and treatment of acute heart failure is ongoing. The natriureticfc peptides have proved extremely useful in determining whether acute dyspnoea has a cardiac aetiology. In addition, recent trials have demonstrated the use of natriuretic peptides in inpatient and outpatient prognosis, as well as in titrating medications in outpatients with chronic heart failure to prevent acute heart failure hospitalizations. Other emerging acute heart failure biomarkers include mid-regional pro-adrenomedullin, mid-regional proatrial natriuretic peptide, troponin, ST2, and neutrophil gelatinase-associated lipocalin.
29
Cruz, Dinna N., Anna Giuliani, and Claudio Ronco. Acute kidney injury in heart failure. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0248.
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Acute kidney injury (AKI) occurring during heart failure (HF) has been labelled cardiorenal syndrome (CRS) type 1. CRS is defined as a group of ‘disorders of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other’. This consensus definition was proposed by the Acute Dialysis Quality Initiative, with the aim to standardize those disorders where cardiac and renal diseases coexist. Five subtypes have been proposed, according to which organ is affected first (cardiac vs renal) and whether the dysfunction is acute or chronic. Another subtype which includes systemic conditions leading to both heart and kidney dysfunction is also described.The term ‘worsening renal function’ has been regularly used to describe the acute and/or subacute changes that occur in the kidneys following HF. However, the AKI classification according to the current consensus definition better represents the entire spectrum of AKI in the setting of HF.The pathophysiology of heart–kidney interaction is complex and still poorly understood. Factors beyond the classic haemodynamic mechanisms appear to be involved: neurohormonal activation, venous congestion, and inflammation have all been implicated.Diuretics are still a cornerstone in the management of HF. Intravenous administration by bolus or continuous infusion appears to be equally efficacious. Biomarkers and bioelectrical impedance analysis can be helpful in estimating the real volume overload and may be useful to predict and avoid AKI. The role of ultrafiltration remains controversial, and it is currently recommended only for diuretic-resistant patients as it has not been associated with better outcomes. The occurrence of AKI during HF is associated with substantially greater short- and long-term mortality.
30
Dalzell, Jonathan R., Colette E. Jackson, Roy Gardner, and John JV McMurray. Acute heart failure: early pharmacological therapy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0052.
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Acute heart failure syndromes consist of a spectrum of clinical presentations due to an impairment of some aspect of the cardiac function. They represent a final common pathway for a vast array of pathologies and may be either a de novo presentation or, more commonly, a decompensation of pre-existing chronic heart failure. Despite being one of the most common medical presentations, there are no definitively proven prognosis-modifying treatments. The mainstay of current therapy is oxygen and intravenous diuretics. However, within this spectrum of presentations, there is a crucial dichotomy which governs the ultimate treatment approach, i.e. the presence, or absence, of cardiogenic shock. Patients without cardiogenic shock may receive vasodilators, whilst shocked patients should be considered for treatment with inotropic therapy or mechanical circulatory support, when appropriate and where available.
31
Dalzell, Jonathan R., Colette E. Jackson, Roy Gardner, and John JV McMurray. Acute heart failure: early pharmacological therapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0052_update_001.
Full textAbstract:
Acute heart failure syndromes consist of a spectrum of clinical presentations due to an impairment of some aspect of the cardiac function. They represent a final common pathway for a vast array of pathologies and may be either a de novo presentation or, more commonly, a decompensation of pre-existing chronic heart failure. Despite being one of the most common medical presentations, there are no definitively proven prognosis-modifying treatments. The mainstay of current therapy is oxygen and intravenous diuretics. However, within this spectrum of presentations, there is a crucial dichotomy which governs the ultimate treatment approach, i.e. the presence, or absence, of cardiogenic shock. Patients without cardiogenic shock may receive vasodilators, whilst shocked patients should be considered for treatment with inotropic therapy or mechanical circulatory support, when appropriate and where available.
32
Fye, W. Bruce. Treating Heart Failure and Preventing Cardiovascular Disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199982356.003.0019.
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Heart failure may result from coronary disease, valve disease, or hypertensive heart disease. The first effective pills to treat hypertension and fluid retention were introduced in the 1950s. Cardiac transplantation was first performed in a human in 1967. This radical approach to treat patients with so-called end-stage heart failure presented a series of problems, such as organ rejection and ethical issues surrounding the definition of death. The large gap between the number of patients who might benefit from transplantation and the number of available donor organs contributed to a costly and controversial program to develop an artificial heart. During the final third of the twentieth century, preventive cardiology gained momentum. The goal was to identify cardiac risk factors and to attempt to treat them. Controlled clinical trials became increasingly important in the evaluation of competing treatments. Organizations used trial results as raw materials to produce clinical practice guidelines.
33
Arntz, Hans-Richard. Sudden cardiac death: epidemiology and prevention. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0005.
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Even if sudden cardiac death is considered to be the most frequent cause of death in adults in industrialized countries, its incidence varies widely, depending on the definition and the source and quality of underlying data. It is estimated that about 70-80% of cases are due to coronary heart disease. The remaining 20% are attributable to a wide variety of inborn, genetically determined or acquired diseases, including a small group with hitherto undefined background. Prevention primarily encompasses the treatment of cardiovascular risk factors to avoid manifestations of coronary heart disease. Furthermore, preventive strategies are targeted to define groups of patients with an increased risk for sudden cardiac death or individuals at risk in specific populations, e.g. competitive athletes. A major target group are patients with impaired left ventricular function, preferentially due to myocardial infarction. These patients, and some less clearly defined patient groups with non-ischaemic cardiomyopathy and heart failure, may benefit from the insertion of an implantable cardioverter-defibrillator. With regard to pharmacological prevention, treatment of the underlying condition is the mainstay, since no antiarrhythmic substance-with the exemption of beta-blockers in some situations-has shown to be of efficacy.
34
O’Mahony, Constantinos. Hypertrophic cardiomyopathy: prevention of sudden cardiac death. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0354.
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Sudden cardiac death (SCD) secondary to ventricular arrhythmias is the most common mode of death in hypertrophic cardiomyopathy (HCM) and can be effectively prevented with an implantable cardioverter defibrillator (ICD). The risk of SCD in HCM relates to the severity of the phenotype and regular risk stratification is an integral part of routine clinical care. For the primary prevention of SCD, risk stratification involves the assessment of seven readily available clinical parameters (age, maximal left ventricular wall thickness, left atrial diameter, left ventricular outflow tract gradient, non-sustained ventricular tachycardia, unexplained syncope, and family history of SCD) which are used to estimate the risk of SCD within 5 years of clinical evaluation using a statistical risk prediction model (HCM Risk-SCD). The 2014 European Society of Cardiology Guidelines provide a framework to aid clinical decisions and consider patients with a 5-year risk of SCD of less than 4% as low risk and recommend regular assessment while those with a risk of 6% or higher should be considered for an ICD. In patients with an intermediate risk (4% to <6%) ICD implantation may also be considered after taking into account age, co-morbid conditions, socioeconomic factors, and the psychological impact of therapy. Survivors of ventricular fibrillation arrest should receive an ICD for secondary prevention unless their life expectancy is less than 1 year. Following device implantation, patients should be followed up for device- and disease-related complications, particularly heart failure and cerebrovascular disease.
35
Balik, Martin. Perioperative cardiac care of the high-risk non-cardiac patient. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0076.
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Non-cardiac surgery conveys a cardiac risk related to the status of the patient’s cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additional tests. The indications for further cardiac testing and treatments are the same as in the non-operative setting, but their timing is dependent on the urgency of surgery, and patient-specific and surgical risk factors. A delay in surgery, due to the use of both non-invasive and invasive preoperative testing, should be limited to those circumstances in which the results of such tests will clearly affect patient management. In high-risk patients, the result of the cardiac assessment helps to choose adequate perioperative monitoring and to indicate for an intensive care unit stay perioperatively. Chronic medications can be adjusted, according to the current knowledge on perioperative management. Drugs with the potential to reduce the incidence of post-operative cardiac events and mortality include beta-blockers, statins, and aspirin. Chronic platelet anti-aggregation and anticoagulation therapies have to be adapted by weighing the risk of bleeding against the risk of thrombotic complications.
36
Balik, Martin. Perioperative cardiac care of the high-risk non-cardiac patient. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0076_update_001.
Full textAbstract:
Non-cardiac surgery conveys a cardiac risk related to the status of the patient’s cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additional tests. The indications for further cardiac testing and treatments are the same as in the non-operative setting, but their timing is dependent on the urgency of surgery, and patient-specific and surgical risk factors. A delay in surgery, due to the use of both non-invasive and invasive preoperative testing, should be limited to those circumstances in which the results of such tests will clearly affect patient management. In high-risk patients, the result of the cardiac assessment helps to choose adequate perioperative monitoring and to indicate for an intensive care unit stay perioperatively. Chronic medications can be adjusted, according to the current knowledge on perioperative management. Drugs with the potential to reduce the incidence of post-operative cardiac events and mortality include beta-blockers, statins, and aspirin. Chronic platelet anti-aggregation and anticoagulation therapies have to be adapted by weighing the risk of bleeding against the risk of thrombotic complications.
37
Balik, Martin. Perioperative cardiac care of the high-risk non-cardiac patient. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0076_update_002.
Full textAbstract:
Non-cardiac surgery conveys a cardiac risk related to the status of the patient’s cardiovascular system. Cardiac-related risk of surgery can be assessed by integrating the risk and urgency of the procedure with cardiovascular risk factors, which include age, ischaemic heart disease, heart failure, stroke, diabetes mellitus, chronic obstructive pulmonary disease, and renal dysfunction. An individual assessment can include simple multivariate scoring systems, developed with the aim of evaluating cardiac risk prior to non-cardiac surgery. Patient assessment can be extended for indicated additional tests. The indications for further cardiac testing and treatments are the same as in the non-operative setting, but their timing is dependent on the urgency of surgery, and patient-specific and surgical risk factors. A delay in surgery, due to the use of both non-invasive and invasive preoperative testing, should be limited to those circumstances in which the results of such tests will clearly affect patient management. In high-risk patients, the result of the cardiac assessment helps to choose adequate perioperative monitoring and to indicate for an intensive care unit stay perioperatively. Chronic medications can be adjusted, according to the current knowledge on perioperative management. Drugs with the potential to reduce the incidence of post-operative cardiac events and mortality include beta-blockers, statins, and aspirin. Chronic platelet anti-aggregation and anticoagulation therapies have to be adapted by weighing the risk of bleeding against the risk of thrombotic complications.
38
Torres, Río Aguilar, Luigi P. Badano, and Dimitrios Tsiapras. Cardiac transplant patients. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0050.
Full textAbstract:
Echocardiography has a pivotal role in the care of heart transplant (HT) recipients. This chapter discusses the use of echocardiographic techniques for the assessment of HT patients. In the early post-transplant period, echocardiography has demonstrated its utility to assess the normal and abnormal structural and physiological changes of the transplanted heart, as well as to detect complications such as graft failure. During follow-up, development of acute/chronic graft rejection and cardiac allograft vasculopathy remains the leading causes of mortality in HT recipients and the role of conventional and new echocardiographic techniques in detecting these complications is discussed. Finally, the role of stress echocardiography, which provides additional functional information to the anatomical data obtained with invasive coronary angiography and intravascular ultrasound, is highlighted. The last sections of the chapter are dedicated to the echocardiographic monitoring of endomyocardial biopsies and how to schedule serial echocardiograms during the follow-up of HT recipients.
39
Frew, Anthony. Air pollution. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0341.
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Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.
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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.
Full textAbstract:
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.
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Sudden Cardiac Death and Congestive Heart Failure : Diagnosis and Treatment: Proceedings of the Symposium on New Drugs and Devices, held at Philadelphia, PA, October 26 and 27, 1982. Springer, 2011.
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Banerjee, Ashis, and Clara Oliver. Cardiac emergencies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198786870.003.0009.
Full textAbstract:
Chest pain is a common presenting complaint for patients in the emergency department. This chapter focuses on the management and recent changes to non-ST-segment elevation myocardial infarction (NSTEMI) and STEMI pathways, in keeping with national guidance. Arrhythmia management including atrial fibrillation as well as the use of scoring systems as the CHADVASC score also commonly appears in the short-answer question (SAQ) paper, which is covered in this chapter in line with current NICE guidance. In addition, there is also a section on the diagnosis and differentiation on managing a patient with a transient loss of consciousness and the associated risk factors of sudden cardiac death. This chapter also includes sections on hypertensive emergencies and the management of heart failure.
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Ruiz-Villalba, Adrián, Nikolaos Frangogiannis, and José Maria Pérez-Pomares. Origin and diversity of cardiac fibroblasts: developmental substrates of adult cardiac fibrosis. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0012.
Full textAbstract:
Cardiac connective tissues are primarily formed by cardiac fibroblasts (CF) of diverse embryonic origins. Whereas CF specific roles in cardiac morphogenesis remain under-researched, their involvement in adult cardiac fibrosis is clinically relevant. Cardiac fibrosis is a common element of several chronic cardiac conditions characterized by the loss of ventricular wall mechanical function, ultimately driving to heart failure. In the ischaemic heart early reparative fibrosis evidences the very restricted regenerative potential of the myocardium. In non-ischaemic diseases fibrosis is activated by unknown signals. We summarize current knowledge on the origin of CFs and their developmental roles, and discuss the differential disease-dependent response of different CF subpopulations to various pathological stimuli. We also describe the characteristic cell-cell and cell-matrix interactions that determine the fibrotic remodelling of the myocardium. We analyse experimental models for the study of cardiac fibrosis, and suggest future directions in the search for new markers and therapeutic targets.
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Elliott, Perry, and Alexandros Protonotarios. Arrhythmogenic right ventricular cardiomyopathy: management of symptoms and prevention of sudden cardiac death. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0361.
Full textAbstract:
Patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) have arrhythmia-related symptoms or are identified during screening of an affected family. Heart failure symptoms occur late in the disease’s natural history. As strenuous exercise has been associated with disease acceleration and worsening of ventricular arrhythmias, lifestyle modification with restricted athletic activities is recommended upon disease diagnosis or even identification of mutation carrier status. An episode of an haemodynamically unstable, sustained ventricular tachycardia or ventricular fibrillation as well as severe systolic ventricular dysfunction constitute definitive indications for implantable cardioverter defibrillator (ICD) implantation, which should also be considered following tolerated sustained or non-sustained ventricular tachycardia episodes, syncope, or in the presence of moderate ventricular dysfunction. Antiarrhythmic medications are used as an adjunct to device therapy. Catheter ablation is recommended for incessant ventricular tachycardia or frequent appropriate ICD interventions despite maximal pharmacological therapy. Amiodarone alone or in combination with beta blockers is most effective for symptomatic ventricular arrhythmias. Beta blockers are considered for use in all patients with a definite diagnosis but evidence for their prognostic benefit is sparse. Heart failure symptoms are managed using standard protocols and heart transplantation is considered for severe ventricular dysfunction or much less commonly uncontrollable ventricular arrhythmias.
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Demetriades, Demetrios, Leslie Kobayashi, and Lydia Lam. Cardiac complications in trauma. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0062.
Full textAbstract:
Post-traumatic cardiac complications may occur after penetrating or blunt injuries to the heart or may follow severe extracardiac injuries. The majority of victims with penetrating injuries to the heart die at the scene and do not reach hospital care. For those patients who reach hospital care, an immediate operation, sometimes in the emergency room, cardiac injury repair, and cardiopulmonary resuscitation provide the only possibility of survival. Many patients develop perioperative cardiac complications such as acute cardiac failure, cardiac arrhythmias, coronary air embolism, and myocardial infarction. Some survivors develop post-operative functional abnormalities or anatomical defects, which may not manifest during the early post-operative period. It is essential that all survivors undergo detailed early and late cardiac evaluations. Blunt cardiac trauma encompasses a wide spectrum of injuries that includes asymptomatic myocardial contusion, arrhythmias, or cardiogenic shock to full-thickness cardiac rupture and death. Clinical examination, electrocardiograms, troponin measurements, and echocardiography are the cornerstone of diagnosis and monitoring of these patients. Lastly, some serious extracardiac traumatic conditions, such as traumatic pneumonectomy and severe traumatic brain injury, may result in cardiac complications. This may include tachyarrhythmias, cardiogenic shock, electrocardiographic changes, troponin elevations, heart failure, and cardiac arrest.
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Demetriades, Demetrios, Leslie Kobayashi, and Lydia Lam. Cardiac complications in trauma. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0062_update_001.
Full textAbstract:
Post-traumatic cardiac complications may occur after penetrating or blunt injuries to the heart or may follow severe extracardiac injuries. The majority of victims with penetrating injuries to the heart die at the scene and do not reach hospital care. For those patients who reach hospital care, an immediate operation, sometimes in the emergency room, cardiac injury repair, and cardiopulmonary resuscitation provide the only possibility of survival. Many patients develop perioperative cardiac complications such as acute cardiac failure, cardiac arrhythmias, coronary air embolism, and myocardial infarction. Some survivors develop post-operative functional abnormalities or anatomical defects, which may not manifest during the early post-operative period. It is essential that all survivors undergo detailed early and late cardiac evaluations. Blunt cardiac trauma encompasses a wide spectrum of injuries that includes asymptomatic myocardial contusion, arrhythmias, or cardiogenic shock to full-thickness cardiac rupture and death. Clinical examination, electrocardiograms, troponin measurements, and echocardiography are the cornerstone of diagnosis and monitoring of these patients. Lastly, some serious extracardiac traumatic conditions, such as traumatic pneumonectomy and severe traumatic brain injury, may result in cardiac complications. This may include tachyarrhythmias, cardiogenic shock, electrocardiographic changes, troponin elevations, heart failure, and cardiac arrest.
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Lam, Lydia, Leslie Kobayashi, and Demetrios Demetriades. Cardiac complications in trauma. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0062_update_002.
Full textAbstract:
Post-traumatic cardiac complications may occur after penetrating or blunt injuries to the heart or may follow severe extracardiac injuries. The majority of victims with penetrating injuries to the heart die at the scene and do not reach hospital care. For those patients who reach hospital care, an immediate operation, sometimes in the emergency room, cardiac injury repair, and cardiopulmonary resuscitation provide the only possibility of survival. Many patients develop perioperative cardiac complications such as acute cardiac failure, cardiac arrhythmias, coronary air embolism, and myocardial infarction. Some survivors develop post-operative functional abnormalities or anatomical defects, which may not manifest during the early post-operative period. It is essential that all survivors undergo detailed early and late cardiac evaluations. Blunt cardiac trauma encompasses a wide spectrum of injuries that includes asymptomatic myocardial contusion, arrhythmias, or cardiogenic shock to full-thickness cardiac rupture and death. Clinical examination, electrocardiograms, troponin measurements, and echocardiography are the cornerstone of diagnosis and monitoring of these patients. Lastly, some serious extracardiac traumatic conditions, such as traumatic pneumonectomy and severe traumatic brain injury, may result in cardiac complications. This may include tachyarrhythmias, cardiogenic shock, electrocardiographic changes, troponin elevations, heart failure, and cardiac arrest.
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Lam, Lydia, Leslie Kobayashi, and Demetrios Demetriades. Cardiac complications in trauma. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0062_update_003.
Full textAbstract:
Post-traumatic cardiac complications may occur after penetrating or blunt injuries to the heart or may follow severe extracardiac injuries. The majority of victims with penetrating injuries to the heart die at the scene and do not reach hospital care. For those patients who reach hospital care, an immediate operation, sometimes in the emergency room, cardiac injury repair, and cardiopulmonary resuscitation provide the only possibility of survival. Many patients develop perioperative cardiac complications such as acute cardiac failure, cardiac arrhythmias, coronary air embolism, and myocardial infarction. Some survivors develop post-operative functional abnormalities or anatomical defects, which may not manifest during the early post-operative period. It is essential that all survivors undergo detailed early and late cardiac evaluations. Blunt cardiac trauma encompasses a wide spectrum of injuries that includes asymptomatic myocardial contusion, arrhythmias, or cardiogenic shock to full-thickness cardiac rupture and death. Clinical examination, electrocardiograms, troponin measurements, and echocardiography are the cornerstone of diagnosis and monitoring of these patients. Lastly, some serious extracardiac traumatic conditions, such as traumatic pneumonectomy and severe traumatic brain injury, may result in cardiac complications. This may include tachyarrhythmias, cardiogenic shock, electrocardiographic changes, troponin elevations, heart failure, and cardiac arrest.
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Hagendorff, Andreas. Cardiac involvement in systemic diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199599639.003.0020.
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Systemic diseases are generally an interdisciplinary challenge in clinical practice. Systemic diseases are able to induce tissue damage in different organs with ongoing duration of the illness. The heart and the circulation are important targets in systemic diseases. The cardiac involvement in systemic diseases normally introduces a chronic process of alterations in cardiac tissue, which causes cardiac failure in the end stage of the diseases or causes dangerous and life-threatening problems by induced acute cardiac events, such as myocardial infarction due to coronary thrombosis. Thus, diagnostic methods—especially imaging techniques—are required, which can be used for screening as well as for the detection of early stages of the diseases. Two-dimensional echocardiography is the predominant diagnostic technique in cardiology for the detection of injuries in cardiac tissue—e.g. the myocardium, endocardium, and the pericardium—due to the overall availability of the non-invasive procedure.The quality of the echocardiography and the success rate of detecting cardiac pathologies in patients with primary non-cardiac problems depend on the competence and expertise of the investigator. Especially in this scenario clinical knowledge about the influence of the systemic disease on cardiac anatomy and physiology is essential for central diagnostic problem. Therefore the primary echocardiography in these patients should be performed by an experienced clinician or investigator. It is possible to detect changes of cardiac morphology and function at different stages of systemic diseases as well as complications of the systemic diseases by echocardiography.The different parts of this chapter will show proposals for qualified transthoracic echocardiography focusing on cardiac structures which are mainly involved in different systemic diseases.
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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.
Full textAbstract:
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.