Books on the topic 'Early heart failure'
To see the other types of publications on this topic, follow the link: Early heart failure.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 48 books for your research on the topic 'Early heart failure.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse books on a wide variety of disciplines and organise your bibliography correctly.
1
Don, Brown. Early-stage congestive heart failure. Seattle, WA: Natural Product Research Consultants, 1997.
Find full text
2
Seth, Runjan. Inotropic and lusitropic response to gbs-adrenergic stimulation, hemodynamics, and metabolic parameters in early experimental heart failure. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.
Find full text
3
Trongtō̜sak, Phētcharat. Phon rūamkan khō̜ng yātān bētā ʻǣtrīnœ̄čhik rīsēptœ̄ læ ʻǣngčhīʻōthēnsin rīsēptœ̄ tō̜ kāndamnœ̄n rōk raya rǣk nai phāwa hūačhai lomlēo =: Combined effects of ss-adrenergic blocker and angiotensin receptor blocker on the early progression of heart failure : rāingān kānwičhai. [Chonburi]: Mahāwitthayālai Būraphā, 2006.
Find full text
4
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.
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.
5
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.
6
Tragante, Vinicius, Anna Pilbrow, and Katrina Poppe, eds. Improving Early Detection and Risk Prediction in Heart Failure. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-322-1.
Full text
7
Burford, Judy. Early readmission in the elderly with congestive heart failure. 2002.
Find full text
8
Vranckx, Pascal, Wilfried Mullens, and Johan Vijgen. Non-pharmacological therapy of acute heart failure: when drugs alone are not enough. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0053.
Full textAbstract:
Acute heart failure syndrome has been defined as new-onset or a recurrence of worsening signs and symptoms of heart failure, necessitating urgent or emergency management. The management of acute heart failure syndrome is challenging, given the heterogeneity of the patient population, in terms of the clinical presentation, pathophysiology, prognosis, and therapeutic options. The management of acute heart failure syndrome is a dynamic process, requiring ongoing simultaneous diagnosis (monitoring) and treatment. Pharmacological agents remain the mainstay of therapy for acute heart failure syndrome. However, at all time, during the early diagnostic, aetiologic, and therapeutic work-up, non-pharmacologic therapy may be indicated and should be considered. The management of the complex cardiac patient with acute heart failure syndrome and/or (potential) haemodynamic compromise has become a special dimension for specialized myocardial intervention centres, providing 24 hours per day and 7 days per week state-of-the-art facilities for (primary) percutaneous coronary intervention and cardiac intensive care, including mechanical ventilation, ultrafiltration, with or without dialysis, and short-term percutaneous mechanical circulatory support. Through the understanding of the underlying pathophysiology and approaches into the problems of acute heart failure syndrome, one should be better prepared to understand and treat its many facets.
9
Plebani, Mario, Monica Maria Mion, and Martina Zaninotto. Biomarkers of renal and hepatic failure. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0039.
Full textAbstract:
In the last few years, major advances have been achieved in the understanding of the molecular and pathophysiological mechanisms which underlie the complex interactions between the heart and the kidney, as well as between the heart and the liver. According to these new insights, new biomarkers have been proposed for better evaluating and monitoring patients affected by cardiovascular diseases. In addition, some biomarkers should be used as risk factors and for an early identification and treatment of these severe diseases. This chapter reviews the most important biomarkers for evaluating the ‘cardiorenal syndrome’, in particular, the measurement of serum creatinine and its use for calculating the glomerular filtration rate which, with the new and more efficient equation, namely Chronic Kidney Disease Epidemiology Collaboration, still remains the most widely used biomarker. The role of newer biomarkers will be explored. The measurement of cystatin C, representing additional information, particularly in paediatric age groups and in the early phase of kidney disease, plays an increasing role. Neutrophil gelatinase-associated lipocalin is a recently developed and very promising new biomarker for the diagnosis of acute kidney injury, while the well-known albumin/creatinine ratio has been re-evaluated as a simple and useful tool for an early identification of kidney disease. Regarding liver diseases, a growing body of evidence demonstrates the usefulness of non-invasive makers of hepatic fibrosis that may avoid the need for a liver biopsy in most patients. A promising field of research is represented by the role of non-alcoholic fatty liver disease in the pathogenesis of cardiovascular disease.
10
Fye, W. Bruce. President Roosevelt’s Secret Hypertensive Heart Disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199982356.003.0007.
Full textAbstract:
Franklin D. Roosevelt’s health was a factor in the 1944 election. Presidential press secretary Stephen Early and White House physician Ross McIntire worried that Thomas Dewey might win if voters learned that Roosevelt had severe hypertension and had an episode of congestive heart failure. Three weeks before the election, Mayo cardiologist Arlie Barnes visited the Bethesda Naval Medical Center where he learned that some physicians suspected that Roosevelt had a “serious heart ailment.” When Barnes returned to Rochester he mentioned this to a few friends. Word of this conversation reached Early, and FBI agents interrogated Barnes and other Mayo physicians two weeks before the election. During the campaign’s closing days, White House insiders orchestrated events designed to showcase a healthy commander in chief. Stifling rumors about Roosevelt’s health was part of their strategy to defeat Dewey. Less than three months into his fourth term, Roosevelt had a stroke and died.
11
Fye, W. Bruce. Pioneering Open-Heart Surgery at the University of Minnesota and the Mayo Clinic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199982356.003.0010.
Full textAbstract:
During the early 1950s, several dozen surgeons were attempting to develop technologies and techniques that would allow them to operate inside the heart. The challenge was to develop a safe way to temporarily take over the functions of the heart and lungs so the heart could be opened and drained of blood. A surgeon could then see and repair abnormal or damaged structures inside the organ. The first patients were children or adolescents with congenital heart defects that had caused heart failure. Mayo surgeon John Kirklin led a multidisciplinary team in the testing and clinical use of a heart-lung machine that had been refined in Rochester from plans provided by IBM and John Gibbon Jr. of Philadelphia. Although initial mortality was high, experience with the Mayo-Gibbon machine proved that it was possible to operate inside the hearts and save the lives of patients who were destined to die without surgery.
12
Edvardsen, Thor. Cardiomyopathies, myocarditis, and the transplanted heart. Edited by Frank Flachskampf. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0094.
Full textAbstract:
Echocardiography is an excellent tool for the diagnosis and follow-up of patients with cardiomyopathies, myocarditis, and the transplanted heart. It is the preferred method for assessment of ventricular function and valvular dysfunction and is of great value in decision-making in these patients. The different types of cardiomyopathies can usually be differentiated by echocardiography. Speckle tracking echocardiography has increased our awareness on early staging of the disease and the progress of cardiomyopathies. This chapter will explain important features of the most common cardiomyopathies and how echocardiography should be utilized. Echocardiographic findings in myocarditis include non-specific features such as decreased left ventricular function, wall motion abnormalities, and texture changes. These findings will in certain circumstances often prompt the awareness of myocarditis. Echocardiography has an important diagnostic position in patients with end-stage heart failure. The chapter will explain how echocardiography can be used in the screening period of recipients and donors, and how it can be an essential diagnostic tool in the perioperative and postoperative phases of cardiac transplantation.
13
Phon rūamkan khō̜ng yātān bētā ʻǣtrīnœ̄čhik rīsēptœ̄ læ ʻǣngčhīʻōthēnsin rīsēptœ̄ tō̜ kāndamnœ̄n rōk raya rǣk nai phāwa hūačhai lomlēo =: Combined effects of ss-adrenergic blocker and angiotensin receptor blocker on the early progression of heart failure : rāingān kānwičhai. [Chonburi]: Mahāwitthayālai Būraphā, 2006.
Find full text
14
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.
Full textAbstract:
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.
15
Serfass, Evan R., and Justin D. Ramos. Ventricular Septal Defect. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0007.
Full textAbstract:
Ventricular septal defect (VSD) is the most common congenital cardiac lesion, and VSDs are found as isolated lesions in up to 20% of children with congenital heart disease. The natural history and pathophysiology of VSD varies by patient age, patient size, anatomic location, and size of the defect. Patients who have large lesions and significant left-to-right shunt resulting in heart failure symptoms, failure to thrive, pulmonary hypertension, or recurrent respiratory infections may be indicated for early surgical repair during infancy. This chapter presents a clinical scenario of a symptomatic infant undergoing primary surgical repair of a VSD to demonstrate principles of the anatomy, pathophysiology, diagnosis, and medical management of patients with VSDs. Anesthetic management is also discussed, considering the effects of left-to-right shunt, pulmonary hypertension, delayed sternal closure, and Eisenmenger’s syndrome.
16
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.
17
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.
18
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.
19
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.
20
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.
Full textAbstract:
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.
21
Sliwa, Karen, and Denise Hilfiker-Kleiner. Peripartum cardiomyopathy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0374.
Full textAbstract:
Pregnancy-related heart disease is increasing worldwide and peripartum cardiomyopathy (PPCM) is an important contributor to early (<42 days postpartum) and late (up to 1 year postpartum) maternal death. PPCM is an idiopathic form of cardiomyopathy, presenting with heart failure secondary to left ventricular dysfunction towards the end of pregnancy, or in the months following delivery, where no other cause of heart failure is identified. It is a diagnosis of exclusion. Incidence and prognosis varies according to geography and is likely due to multiple factors. The recent specific pathophysiological hypothesis which states that the oxidative stress–cathepsin D-16 kDa prolactin cascade plays a key role in the development of PPCM in experimental models and in humans suggests that a therapeutic approach involving blockade of this pathway with bromocriptine may be a novel disease-specific approach. Despite ongoing research, numerous uncertainties regarding the incidence, pathophysiology, treatment, and prognosis of PPCM patients remain, indicating the need for further investigation. The establishment of the international registry on PPCM, under the umbrella of the EuroObservational research programme, will provide novel information and address many uncertainties.
22
Golper, Thomas A., Andrew A. Udy, and Jeffrey Lipman. Drug dosing in acute kidney injury. Edited by William G. Bennett. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0364.
Full textAbstract:
Drug dosing in acute kidney injury (AKI) is one of the broadest topics in human medicine. It requires an understanding of markedly altered and constantly changing physiology under many disease situations, the use of the drugs to treat those variety of diseases, and the concept of drug removal during blood cleansing therapies. Early in AKI kidney function may be supraphysiologic, while later in the course there may be no kidney function. As function deteriorates other metabolic pathways are altered in unpredictable ways. Furthermore, the underlying disorders that lead to AKI alter metabolic pathways. Heart failure is accompanied by vasoconstriction in the muscle, skin and splanchnic beds, while brain and cardiac blood flow proportionally increase. Third spacing occurs and lungs can become congested. As either kidney or liver function deteriorates, there may be increased or decreased drug sensitivity at the receptor level. Acidosis accompanies several failing organs. Protein synthesis is qualitatively and quantitatively altered. Sepsis affects tissue permeability. All these abnormalities influence drug pharmacokinetics and dynamics. AKI is accompanied by therapeutic interventions that alter intrinsic metabolism which is in turn complicated by kidney replacement therapy (KRT). So metabolism and removal are both altered and constantly changing. Drug management in AKI is exceedingly complex and is only beginning to be understood. Thus, we approach this discussion in a physiological manner. Critically ill patients pass through phases of illness, sometimes rapidly, other times slowly. The recognition of the phases and the need to adjust medication administration strategies is crucial to improving outcomes. An early phase involving supraphysiologic kidney function may be contributory to therapeutic failures that result in the complication of later AKI and kidney function failure.
23
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.
24
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.
25
Grossman, Jonah, Tanzila Shams, and Cathy Sila. Neurological Complications of Infective Endocarditis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0167.
Full textAbstract:
Infective endocarditis is the fourth leading cause of life-threatening infections, accounting for 40,000 annual U.S. hospital admissions. Due to decline in rheumatic heart disease, a shift in causative organisms from viridans streptococci to S. aureus, Group D Streptococcus, and multidrug-resistant species has been observed. The spectrum of neurological complications ranges widely from cerebrovascular pathologies-including septic embolization, mycotic aneurysms, and intracerebral hemorrhages-to seizures, meningitis, cerebritis, and abscess. Transthoracic echocardiogram remains the standard for initial investigation whereas CT scans, MRI with DWI sequence, and cerebral angiograms are useful for exploring neurological complications. Antibiotic regimens, tailored to culprit organisms, should be initiated early after obtaining blood cultures and continued for 4 to 6 weeks. Antithrombotic treatment may pose increased risk for intracerebral hemorrhage, even in the absence of mycotic aneurysms (MA). Unruptured MA must be treated according to risk of rupture and overall health of the patient. MAs either at risk or previously ruptured should be secured by neurosurgical or endovascular means. Early cardiac surgery is a viable option for prevention of septic embolization for high-risk cardiac diseases such as perivalvular abscess and infection with resistant organisms, but may increase mortality rates for those with decompensated heart failure.
26
Detering, Karen, Elizabeth Sutton, and Scott Fraser. Advance care planning in chronic disease: finding the known in the midst of the unknown. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198802136.003.0025.
Full textAbstract:
People are living longer lives with a greater burden of disease. Diseases which contribute significantly to this burden are chronic kidney disease; chronic obstructive pulmonary disease and heart failure. Technologies exist that can sustain life for patients with these disease, however patients and their families/loved ones need to know the likely outcome of their disease, its course, and all management options. Advance care planning (ACP) can assist with this process as well as ensuring that patients, families, and health care teams are aware of what treatment a patient wants—or does not want. ACP also enables the appointment of a decision maker to act on behalf of the patient should they lose capacity to make medical decisions. This chapter discusses the benefits of ACP and why it needs to be introduced early in the course of any life-limiting illness.
27
Sinagra, Gianfranco, Marco Merlo, and Davide Stolfo. Dilated cardiomyopathy: clinical diagnosis and medical management. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0356.
Full textAbstract:
Dilated cardiomyopathy (DCM) is a relatively rare primary heart muscle disease with genetic or post-inflammatory aetiology that affects relatively young patients with a low-risk co-morbidity profile. Therefore, DCM represents a particular heart failure model with specific characteristics and long-term evolution. The progressively earlier diagnosis derived from systematic familial screening programmes and the current therapeutic strategies have greatly modified the prognosis of DCM with a dramatic reduction of mortality over recent decades. A significant number of DCM patients present an impressive response to pharmacological and non-pharmacological evidence-based therapy in terms of haemodynamic improvement with subsequent left ventricular reverse remodelling, which confer a favourable long-term prognosis. However, in some DCM patients the outcome is still severe. This prognostic heterogeneity is possibly related to the aetiological variety of this disease. Maximal effort towards an early aetiological diagnosis of DCM, by using all diagnostic available tools (including cardiovascular magnetic resonance imaging, endomyocardial biopsy, and genetic testing when indicated), as well as the individualized long-term follow-up appear crucial in improving the prognostic stratification and the clinical management of these patients.
28
Gevaert, Sofie A., Eric Hoste, and John A. Kellum. Acute kidney injury. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0068.
Full textAbstract:
Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as sepsis). Acute kidney injury replaced the previously used term ‘acute renal failure’ and comprises the entire spectrum of the disease, from small changes in function to the requirement of renal replacement therapy. Not only failure, but also minor and less severe decreases, in kidney function are of clinical significance both in the short and long-term. The most recent definition for acute kidney injury is proposed by the Kidney Disease: Improving Global Outcomes clinical practice guidelines workgroup. This definition is a modification of the RIFLE and AKIN definitions and staging criteria, and it stages patients according to changes in the urine output and serum creatinine (see Tables 68.1 and 68.2). Acute kidney injury is a heterogeneous syndrome with different and multiple aetiologies, often with several insults occurring in the same individual. The underlying processes include nephrotoxicity, and neurohormonal, haemodynamic, autoimmune, and inflammatory abnormalities. The most frequent cause for acute kidney injury in intensive cardiac care patients are low cardiac output with an impaired kidney perfusion (cardiogenic shock) and/or a marked increase in venous pressure (acute decompensated heart failure). Predictors for acute kidney injury in these patients include: baseline renal dysfunction, diabetes, anaemia, and hypertension, as well as the administration of high doses of diuretics. In the intensive cardiac care unit, attention must be paid to the prevention of acute kidney injury: monitoring of high-risk patients, prompt resuscitation, maintenance of an adequate mean arterial pressure, cardiac output, and intravascular volume (avoidance of both fluid overload and hypovolaemia), as well as the avoidance or protection against nephrotoxic agents. The treatment of acute kidney injury focuses on the treatment of the underlying aetiology, supportive care, and avoiding further injury from nephrotoxic agents. More specific therapies have not yet demonstrated efficacy. Renal replacement therapy is indicated in life-threatening changes in fluid, electrolyte, and acid-base balance, but there are also arguments for more early initiation.
29
Gevaert, Sofie A., Eric Hoste, and John A. Kellum. Acute kidney injury. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0068_update_001.
Full textAbstract:
Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as sepsis). Acute kidney injury replaced the previously used term ‘acute renal failure’ and comprises the entire spectrum of the disease, from small changes in function to the requirement of renal replacement therapy. Not only failure, but also minor and less severe decreases, in kidney function are of clinical significance both in the short and long-term. The most recent definition for acute kidney injury is proposed by the Kidney Disease: Improving Global Outcomes clinical practice guidelines workgroup. This definition is a modification of the RIFLE and AKIN definitions and staging criteria, and it stages patients according to changes in the urine output and serum creatinine (see Tables 68.1 and 68.2). Acute kidney injury is a heterogeneous syndrome with different and multiple aetiologies, often with several insults occurring in the same individual. The underlying processes include nephrotoxicity, and neurohormonal, haemodynamic, autoimmune, and inflammatory abnormalities. The most frequent cause for acute kidney injury in intensive cardiac care patients are low cardiac output with an impaired kidney perfusion (cardiogenic shock) and/or a marked increase in venous pressure (acute decompensated heart failure). Predictors for acute kidney injury in these patients include: baseline renal dysfunction, diabetes, anaemia, and hypertension, as well as the administration of high doses of diuretics. In the intensive cardiac care unit, attention must be paid to the prevention of acute kidney injury: monitoring of high-risk patients, prompt resuscitation, maintenance of an adequate mean arterial pressure, cardiac output, and intravascular volume (avoidance of both fluid overload and hypovolaemia), as well as the avoidance or protection against nephrotoxic agents. The treatment of acute kidney injury focuses on the treatment of the underlying aetiology, supportive care, and avoiding further injury from nephrotoxic agents. More specific therapies have not yet demonstrated efficacy. Renal replacement therapy is indicated in life-threatening changes in fluid, electrolyte, and acid-base balance, but there are also arguments for more early initiation.
30
Ritchie, James, Darren Green, Constantina Chrysochou, and Philip A. Kalra. Renal artery stenosis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0213.
Full textAbstract:
Renovascular disease refers to a narrowing of a main or branch renal artery. Consequences include loss of functional renal tissue and renovascular hypertension, with other manifestations depending on the underlying cause. Worldwide the most common cause is atherosclerotic narrowing, with other causal pathologies including fibromuscular disease (FMD) and inflammatory conditions. FMD occurs much more frequently in women than in men, and is associated with smoking but genetic predisposing factors are also suspected. In South East Asia, Takayasu arteritis is an important cause.Takayasu disease often presents in a non-specific syndromic manner with fatigue and malaise. FMD often presents with early-onset hypertension. Atherosclerotic renal artery stenosis is often clinically silent with suspicion raised due to the existence of other cardiovascular pathology with the more dramatic presentations of acute decompensated heart failure or acute kidney injury less common. Clinical criteria can identify patients at risk.
31
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0045.
Full textAbstract:
Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
32
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_001.
Full textAbstract:
Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
33
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_002.
Full textAbstract:
Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
34
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_003.
Full textAbstract:
Mechanical complications after an acute infarction involve different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies occurring in <1% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment (Ibanez et al, 2017). Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
35
Gerovasili, Vasiliki, and Serafim N. Nanas. Neuromuscular Electrical Stimulation: A New Therapeutic and Rehabilitation Strategy in the ICU. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0044.
Full textAbstract:
Many critically ill patients undergo a period of immobilization with detrimental effects on skeletal muscle, effects which seem most pronounced in the first days of critical illness. Diagnosis of intensive care unit muscle weakness (ICUAW) is often made after discontinuation of sedation when significant nerve and/or muscle damage may already have occurred. Recently, there has been interest in early mobilization during the acute phase of critical illness, with the goal of preventing ICUAW. Neuromuscular electrical stimulation (NEMS) is an alternative form of exercise that has been successfully used in patients with advanced chronic obstructive pulmonary disease (COPD) and chronic heart failure. NEMS is a rehabilitation tool that can be used in critically ill, sedated patients, does not require patient cooperation, and is therefore a promising intervention to prevent muscle dysfunction in the critically ill. When applied early during the course of critical illness, NEMS can preserve muscle morphology and function. Available evidence suggests that NEMS may have a preventive role in the development of ICUAW and could even contribute to a shorter duration of weaning from mechanical ventilation. Studies are needed to evaluate the long-term effect of NEMS and to explore NEMS settings and delivery characteristics most appropriate for different subgroups of critically ill patients.
36
Eisler, Garrett. “Nothing More than Just a Game”. Edited by Robert Gordon. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780195391374.013.0010.
Full textAbstract:
Stephen Sondheim’s most recent musical was based on one of his oldest ideas. As early as 1952 the composer-lyricist became fixated on the real-life misadventures of Addison and Wilson Mizner, misfit brothers who became legendary for their colossal business failures in the early twentieth century.Road Show, the musical Sondheim and librettist John Weidman finally wrote about the Mizners, underwent many transformations between 1999 and 2008 (including the adoption of two other titles:Wise GuysandBounce). But the most significant changes were tonal, from an initially vaudevillian travelogue comedy to an antiromantic one-act chamber musical. This final, now authoritative version delivered an emotional impact exceeding most previous works by this notoriously “all head, no heart” dramatist and offered a harsh vision of the materialist mania of the American Dream.
37
Odeberg-Wernerman, Suzanne, and Margareta Mure. Anaesthesia for urological surgery and for robotic surgery in urology and gynaecology. Edited by Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0062.
Full textAbstract:
Laparoscopic and robot-assisted laparoscopic surgical procedures are commonly used in both urology and gynaecology. These minimally invasive techniques result in early mobilization and short hospital stay and robot-assisted operations are increasingly favoured by patients and surgeons. A complex physiological response is created by the combined effects of carbon dioxide pneumoperitoneum, elevated intra-abdominal pressure, and sometimes a profound Trendelenburg position. Healthy patients tolerate this situation well, but compromised patients are at risk of developing heart failure, ischaemia, or both. Correct interpretation of vital signs can be challenging in this situation. This chapter gives an overview of the physiology during laparoscopic and robot-assisted laparoscopic surgery and gives recommendations for anaesthesia and monitoring. The field of urology and gynaecology also includes major open surgery as well as transurethral surgery and techniques for the management of urinary tract stones. The anaesthetic management and perioperative care of major open surgery, including the increasingly adopted ‘enhanced recovery after surgery’ concept, are also covered. The syndrome of transurethral resection of the prostate can still place patients at risk despite increased knowledge and improved selection of irrigation fluid.
38
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.
Full textAbstract:
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.
39
Karatasakis, G., and G. D. Athanassopoulos. Cardiomyopathies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199599639.003.0019.
Full textAbstract:
Echocardiography is a key diagnostic method in the management of patients with cardiomyopathies.The main echocardiographic findings of hypertrophic cardiomyopathy are asymmetric hypertrophy of the septum, increased echogenicity of the myocardium, systolic anterior motion, turbulent left ventricular (LV) outflow tract blood flow, intracavitary gradient of dynamic nature, mid-systolic closure of the aortic valve and mitral regurgitation. The degree of hypertrophy and the magnitude of the obstruction have prognostic meaning. Echocardiography plays a fundamental role not only in diagnostic process, but also in management of patients, prognostic stratification, and evaluation of therapeutic intervention effects.In idiopathic dilated cardiomyopathy, echocardiography reveals dilation and impaired contraction of the LV or both ventricles. The biplane Simpson’s method incorporates much of the shape of the LV in calculation of volume; currently, three-dimensional echocardiography accurately evaluates LV volumes. Deformation parameters might be used for detection of early ventricular involvement. Stress echocardiography using dobutamine or dipyridamole may contribute to risk stratification, evaluating contractile reserve and left anterior descending flow reserve. LV dyssynchrony assessment is challenging and in patients with biventricular pacing already applied, optimization of atrio-interventricular delays should be done. Specific characteristics of right ventricular dysplasia and isolated LV non-compaction can be recognized, resulting in an increasing frequency of their prevalence. Rare forms of cardiomyopathy related with neuromuscular disorders can be studied at an earlier stage of ventricular involvement.Restrictive and infiltrative cardiomyopathies are characterized by an increase in ventricular stiffness with ensuing diastolic dysfunction and heart failure. A variety of entities may produce this pathological disturbance with amyloidosis being the most prevalent. Storage diseases (Fabry, Gaucher, Hurler) are currently treatable and early detection of ventricular involvement is of paramount importance for successful treatment. Traditional differentiation between constrictive pericarditis (surgically manageable) and the rare cases of restrictive cardiomyopathy should be properly performed.
40
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.
Full textAbstract:
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.
41
Barnard, Matthew, and Nicola Jones. Intensive care management after cardiothoracic surgery. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0368.
Full textAbstract:
Management of the post-cardiothoracic surgical patient follows general principles of intensive care, but incorporates certain unique considerations. In cardiac surgical patients peri-operative ischaemia, arrhythmias and ventricular dysfunction mandate specific monitoring requirements, and individual pharmacological and mechanical support. Suspicion of myocardial ischaemia should not only lead to pharmacological treatment, but also consideration of urgent angiography to exclude coronary graft occlusion. Ventricular dysfunction may be pre-existing or attributable to intra-operative myocardial ‘stunning’. Catecholamines and phosphodiesterase inhibitors are the mainstay of therapy. Rarely, intra-aortic balloon pumping or ventricular assist devices are required. Significant bleeding (with potential cardiac tamponade), respiratory compromise, acute kidney injury, neurological injury, and deep sternal wound infection each occur in ~2–3% of cardiac surgical patients. Each of these has individual risk factors and specific management considerations. General guidelines for patients who have undergone thoracic surgery include early extubation, fluid restriction, effective analgesia, and protective lung ventilation. Thoracic patients are at risk of atelectasis, respiratory infection, bronchial air leak, and right ventricular failure. Positive pressure ventilation is avoided whenever possible particularly after pneumonectomy, but is sometimes necessary in compromised patients. Air leaks are common. Alveolopleural fistulae usually improve with conservative management,whereas bronchopleural fistulae are more likely to require surgical intervention. Lung surgery is high risk for patients with ischaemic heart disease. Patients with pre-existing elevated pulmonary vascular resistance may exhibit right ventricular dysfunction and may fail to cope with a further increase in pulmonary vascular resistance consequent to lung resection. Lung collapse and infection are constant risks throughout the entire post-operative period.
42
Hagendorff, Andreas. Cardiac involvement in systemic diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199599639.003.0020.
Full textAbstract:
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.
43
Cohen, Samy. Doves Among Hawks. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780190947903.001.0001.
Full textAbstract:
What has become of Israel's peace movement? In the early 1980s, it was a major political force, bringing hundreds of thousands onto the streets; but since then, its importance has declined amid spiralling violence. Now, and especially since the second Intifada of 2000–5, the “doves” of the Israel/Palestine conflict struggle to be heard over its 'hawks', and the days of mass mobilization are over. "Doves Among” Hawks charts the successes and failures of a beleaguered peace movement, from its formation after the Six-Day War to the current security-obsessed climate, where Israel's “doves” seem to be fighting a lost and outdated battle. Samy Cohen's history of a peace process that once took on the Israeli settler movements exposes how that cause has been derailed and demoralized by suicide attacks. But the peace movement is not dead—it has simply transformed. From human rights monitors to lobbies of the bereaved, Cohen reveals a multitude of smaller, grassroots organizations that have emerged with unexpected energy. These lawyers, doctors, army reservists, former diplomats and senior security personnel are the unsung heroes of his story.
44
Lameire, Norbert, Raymond Vanholder, and Wim Van Biesen. Clinical approach to the patient with acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0222_update_001.
Full textAbstract:
The prognosis of acute kidney injury (AKI) depends on early diagnosis and therapy. A multitude of causes are classified according to their origin as prerenal, intrinsic (intrarenal), and post-renal.Prerenal AKI means a loss of renal function despite intact nephrons, for example, because of volume depletion and/or hypotension.There is a broad spectrum of intrinsic causes of AKI including acute tubular necrosis (ATN), interstitial nephritis, glomerulonephritis, and vasculitis. Evaluation includes careful review of the patient’s history, physical examination, urinalysis, selected urine chemistries, imaging of the urinary tree, and eventual kidney biopsy. The history should focus on the tempo of loss of function (if known), associated systemic diseases, and symptoms related to the urinary tract (especially those that suggest obstruction). In addition, a review of the medications looking for potentially nephrotoxic drugs is essential. The physical examination is directed towards the identification of findings of a systemic disease and a detailed assessment of the patient’s haemodynamic status. This latter goal may require invasive monitoring, especially in the oliguric patient with conflicting clinical findings, where the physical examination has limited accuracy.Excluding urinary tract obstruction is necessary in all cases and may be established easily by renal ultrasound.Distinction between the two most common causes of AKI (prerenal AKI and ATN) is sometimes difficult, especially because the clinical examination is often misleading in the setting of mild volume depletion or overload. Urinary chemistries, like calculation of the fractional excretion of sodium (FENa), may be used to help in this distinction. In contrast to FENa, the fractional excretion of urea has the advantage of being rather independent of diuretic therapy. Response to fluid repletion is still regarded as the gold standard in the differentiation between prerenal and intrinsic AKI. Return of renal function to baseline or resuming of diuresis within 24 to 72 hours is considered to indicate ‘transient, mostly prerenal AKI’, whereas persistent renal failure usually indicates intrinsic disease. Transient AKI may, however, also occur in short-lived ATN. Furthermore, rapid fluid application is contraindicated in a substantial number of patients, such as those with congestive heart failure.‘Muddy brown’ casts and/or tubular epithelial cell casts in the urine sediment are typically seen in patients with ATN. Their presence is an important tool in the distinction between ATN and prerenal AKI, which is characterized by a normal sediment, or by occasional hyaline casts. There is a possible role for new serum and/or urinary biomarkers in the diagnosis and prognosis of the patient with AKI, including the differential diagnosis between pre-renal AKI and ATN. Further studies are needed before their routine determination can be recommended.When a diagnosis cannot be made with reasonable certainty through this evaluation, renal biopsy should be considered; when intrarenal causes such as crescentic glomerulonephritis or vasculitis are suspected, immediate biopsy to avoid delay in the initiation of therapy is mandatory.
45
Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0036.
Full textAbstract:
Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among troponin-negative subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
46
Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0036_update_001.
Full textAbstract:
Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among normal-troponin subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
47
Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0036_update_002.
Full textAbstract:
Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among normal-troponin subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
48
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.
Full textAbstract:
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.