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1
Tousoulis, Dimitris. Risk factors and vascular endothelium. Hauppauge, N.Y: Nova Science Publishers, 2011.
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2
Jacobsen, Sarah R. Vascular dementia: Risk factors, diagnosis, and treatment. Hauppauge, N.Y: Nova Science, 2011.
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3
Andris, Kazmers, ed. Cardiac risk assessment before vascular surgery. Armonk, NY: Futura Pub. Co., 1994.
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4
Román, Gustavo C. Managing vascular dementia: Concepts, issues, and management. London: Science Press, 2003.
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5
M, Drance Stephen, ed. Vascular risk factors and neuroprotection in glaucoma: Update 1996. Amsterdam: Kugler Publications, 1997.
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6
Boers, G. H. J. Homocysttinuria: A risk factor of premature vascular disease. Dortrecht: Foris Publications, 1986.
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7
McKinley, Michelle. B-Vitamin status and plasma homocysteine: A risk factor for vascular disease. [S.l: The Author], 1999.
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8
Drance, Stephen M. Vascular Risk Factors and Neuroprotection in Glaucoma: Update 1996. Kugler Pubns B V (Medical), 1997.
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9
M, Gotto Antonio, and International Symposium on Multiple Risk Factors in Cardiovascular Disease (3rd : 1994 : Florence, Italy), eds. Multiple risk factors in cardiovascular disease: Vascular and organ protection. Dordrecht: Kluwer Academic Publishers, 1995.
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10
Huang, Yuli, Zhen Yang, and Ji Bihl, eds. Cardiovascular Risk Factors: Related Vascular Injury and New Molecular Biomarkers. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-83250-313-3.
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Paoletti, Rodolfo, Alberico L. Catapano, Claude Lenfant, and Antonio M. Gotto Jr. Multiple Risk Factors in Cardiovascular Disease: Vascular and Organ Protection. Springer, 2012.
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12
Stewart, Robert. Vascular and mixed dementias. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0034.
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Vascular disease is the most important environmental risk factor for dementia but this research area has been hampered by inadequate outcome definitions – in particular, a diagnostic system that attempts to separate overlapping and probably interacting pathologies. There is now substantial evidence that the well-recognised risk factors for cardiovascular disease and stroke are also risk factors for dementia, including Alzheimer’s disease. However, these risk factors frequently act over several decades, meaning that the chances of definitive randomised controlled trial evidence for risk-modifying interventions are slim. This should not obscure the wide opportunity for delaying or preventing dementia through risk factor control and uncontroversial healthy lifestyles. Care should also be taken that comorbid cerebrovascular disease is not considered as excluding a diagnosis of Alzheimer’s disease, particularly now that this determines treatment eligibility.
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Landmesser, Ulf, and Wolfgang Koenig. From risk factors to plaque development and plaque destabilization. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0003.
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This chapter begins with a discussion of recent vascular research that has unveiled the complex interaction between exposure to risk factors and pathological changes at the vessel wall. Risk factors such as smoking or hyperlipidaemia first cause a pre-morbid phenotype with reversible dysfunction of flow-mediated vasodilation, known as endothelial dysfunction (ED). If exposure to risk factor(s) does not cease, ED develops into the first morphological vascular changes that finally lead to atherosclerosis. Cholesterol crystals have been shown to lead to pro-inflammatory activation of macrophages. Progression from stable coronary plaques to the plaque rupture that underlies the acute coronary syndrome is discussed in detail. The chapter provides a basic up-to-date concept of the development and progression of atherosclerosis and highlights the stages where preventive measures may still be effective.
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Swanson, Karen L. Neoplastic and Vascular Diseases. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0618.
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Neoplastic and vascular disorders are reviewed. Lung cancer is the most common malignancy and cause of cancer death in both men and women worldwide. The incidence of new lung cancers has continued to decrease in men and increase in women. The risk factors include cigarette smoking, other carcinogens, cocarcinogens, radon exposure, arsenic, asbestos, coal dust, chromium, vinyl chloride, chloromethyl ether, and chronic lung injury. Genetic and nutritional factors have been implicated. Among vascular disorders, pulmonary embolism is most common. Pulmonary embolism (PE) is the cause of death in 5% to 15% of hospitalized patients who die in the United States. In a multicenter study of PE, the mortality rate at 3 months was 15% and important prognostic factors included age older than 70 years, cancer, congestive heart failure, COPD, systolic arterial hypotension, tachypnea, and right ventricular hypokinesis.
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Karamchandani, Rahul, and Nancy R. Barbas. Vascular Cognitive Impairment. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0021.
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Vascular cognitive impairment (VCI) refers to the spectrum of cognitive disturbances that result from cerebrovascular brain injury. Cerebrovascular disease is associated with multiple underlying pathologies. Risk factors, clinical features, and treatment options overlap with those associated with Alzheimer’s disease, another common cause of cognitive decline. The complexity of vascular cognitive impairment and, notably, the interplay between clinical, pathologic, genetic, and biomarker characteristics of VCI and Alzheimer’s disease are discussed. The chapter places an emphasis on vascular cognitive impairment resulting from disease affecting small vessels, in contrast to that due to disease involving large vessels, in an effort to focus on a large body of evolving work and ongoing attempts at improving understanding of this complex entity.
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Beller, Jerry, and Beller Health. 16 Dementia Types, Symptoms, and Risk Factors: Alzheimer's LBD PDD DLB FTD PPA BvFTD LATE Vascular Dementia Huntington's, Etc. Independently Published, 2019.
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Beller, Jerry, and Beller Health. Dementia Types, Risk Factors, and Symptoms: Alzheimer's Disease Vascular Lewy Body Frontotemporal Huntington's Normal Pressure Hydrocephalus Wernicke Korsakoff Dementias. Independently Published, 2019.
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Beller, Jerry, and Beller Health. Dementia Types, Risk Factors, and Symptoms 2019: Alzheimer's Disease , Vascular , Lewy Body , Frontotemporal , Huntington's , Normal Pressure Hydrocephalus , Wernicke Korsakoff Dementias. Independently Published, 2019.
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19
Ladner, Travis R., Nishant Ganesh Kumar, Lucy He, and J. Mocco. Neuroprotection for Vascular and Endovascular Neurosurgery. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0019.
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The complexity of neurovascular disease presents a challenge to the surgical and anesthesia teams managing patients with such conditions. With open or endovascular techniques, abrupt changes in hemodynamic status and intracranial pressure are an ever-present concern throughout the perioperative period. Monitoring of neurological status, hemodynamic parameters, and intracranial pressure are important adjuncts. Targeted physiologic and pharmacological interventions are critical to ensuring safe completion of complex procedures and the prevention secondary injury. This chapter reviews common complications of cerebrovascular and endovascular operations and their risk factors and summarize clinical principles, strategies, and considerations for maximizing neuroprotection in the treatment of neurovascular disease.
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Selim, Magdy. Neuroprotection for General, Orthopedic, Peripheral Vascular, and ENT Surgery. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0022.
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Unlike stroke after cardiac and carotid surgery, stroke after general; orthopedic; peripheral vascular; and ear, nose, and throat surgery has not been investigated extensively. The incidence, predisposing factors, and etiological mechanisms of stroke in patients undergoing these procedures are reviewed. Recommendations to prevent, recognize, and treat stroke following these surgical procedures are provided to minimize postoperative stroke risk and its associated morbidity and disability. Although these recommendations can help to decrease the incidence of perioperative stroke, there is an unmet need to find novel and effective neuroprotective strategies that can be used pre- or intraoperatively to minimize the effects of stroke on brain tissue and resulting disability. Future studies should evaluate the potential usefulness of neuroprotective therapies or interventions, including various anesthetic agents that can be used prophylactically in the perioperative setting.
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Raggi, Paolo, and Luis D’Marco. Imaging for detection of vascular disease in chronic kidney disease patients. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0116.
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The well-known severity of cardiovascular disease in patients suffering from chronic kidney disease (CKD) requires an accurate risk stratification of these patients in several clinical situations. Imaging has been used successfully for such purpose in the general population and it has demonstrated excellent potential among CKD patients as well. Two main forms of arterial pathology develop in patients with CKD: atherosclerosis, with accumulation of inflammatory cells, lipids, fibrous tissue and calcium in the subintimal space, and arteriosclerosis. The latter is characterized by accumulation of deposits of hydroxyapatite and amorphous calcium crystals in the muscular media of the vessel wall, and is believed to be more closely associated with alterations of mineral metabolism than with traditional atherosclerosis risk factors. The result is the development of what appears to be premature arterial ageing, with loss of elastic properties, increased stiffness, and increased overall fragility of the arterial system. Despite intensifying research and increasing awareness of these issues, the underlying pathophysiology of the aggressive vasculopathy of CKD remains largely unknown. As a consequence, there are currently very limited pathways to prevent progression of vascular damage in CKD. The indications, strengths and weaknesses of several imaging modalities employed to evaluate vascular disease in CKD are described, focusing on coronary arterial circulation and the peripheral arteries, with the exclusion of the intracranial arteries.
22
Boers, G. H. J. Homocystinuria: A Risk Factor of Premature Vascular Disease. de Gruyter GmbH, Walter, 1986.
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23
Moulton, Calum D., and Clive Ballard. The association between depression and cognitive impairment in type 2 diabetes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0009.
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Type 2 diabetes (T2D) is an established risk factor for vascular dementia and Alzheimer’s disease, yet, the reasons are incompletely understood. To date, intervention studies targeting isolated risk factors, such as hypertension or hyperglycaemia, have proved unsuccessful. Several well-designed cohort studies have suggested that depression predicts cognitive decline in patients with T2D. However, these studies, all of later-life depression, have not fully excluded the potential for clinical overlap between depression and dementia. Mechanisms linking depression and cognitive decline may include increased vascular risk and activation of the innate inflammatory response. Future cohort studies are needed to test the effects of earlier life depression on cognitive outcomes in T2D. Mechanistic research is needed to define pathways by which depressive symptoms could lead to both vascular dementia and beta-amyloid accumulation. Finally, intervention studies should test whether depression is a potential target for the primary- or secondary prevention of cognitive decline in T2D.
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Chong, Ji Y., and Michael P. Lerario. Young Adult with Headache and Blurred Vision. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190495541.003.0018.
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Traditional vascular risk factors such as hypertension, diabetes, and high cholesterol can contribute to stroke in young adults. In the absence of typical risk factors in a young patient, a more extensive evaluation is needed. Other, more unusual causes of stroke can include autoimmune, infectious, hematological, and toxic etiologies. Often, despite an exhaustive workup, the mechanism of stroke remains cryptogenic in younger patients.
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Fratiglioni, Laura, and Chengxuan Qiu. Epidemiology of dementia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0031.
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This chapter deals with the occurrence, determinants and primary prevention of dementia. Dementia is one of the major causes of functional dependence, poor quality of life, institutionalisation and mortality among elderly people. The risk of dementia increases almost exponentially with advancing age. As the population ages, dementia poses a serious threat to public health and social welfare system of our society. Accumulating evidence suggests that cardiovascular risk factors significantly contribute to the development and expression of dementia. Thus, adequate management of vascular risk factors and related disorders can be one of the preventative strategies against cognitive ageing and dementia. In addition, psychosocial factors such as educational achievement, socially-integrated and mentally-stimulating lifestyles are critical for delaying the onset of dementia by increasing cognitive reserve. Taken together, maintaining vascular health and adopting a healthy cognitive lifestyle from a life-course perspective may be the most promising strategy to achieve late-life cognitive health.
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Qiu, Chengxuan, and Laura Fratiglioni. Epidemiology of Alzheimer’s disease. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199569854.003.0003.
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• Alzheimer’s disease is the most frequent type of dementia in elderly people. An expert panel estimates that worldwide more than 24 million people are affected by dementia, most suffering from Alzheimer’s disease• The etiological factors other than old age and genetic susceptibility for Alzheimer’s disease remain to be determined, but current evidence strongly supports the potential role of vascular risk factors and psychosocial factors in the pathogenetic process and clinical manifestation of the dementing disorders...
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Kotseva, Kornelia, Neil Oldridge, and Massimo F. Piepoli. Evaluation of preventive cardiology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0026.
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The Joint European Societies guidelines on cardiovascular disease (CVD) prevention define lifestyle and risk factor targets for patients with coronary or other atherosclerotic disease and people at high risk of developing CVD. However, several surveys in Europe and the United States showed inadequate lifestyle and risk factor management and under-use of prophylactic drug therapies in primary and secondary CVD prevention. Various professional associations have developed core components, standards, and outcome measures to evaluate quality of care and provide guidelines for identifying opportunities for improvements. Optimal control of cardiovascular risk factors is one of the most effective methods for reducing vascular events in patients with atherosclerotic disease or high cardiovascular risk. Improving treatment adherence is also very important. Health-related quality of life (HRQL) is considered as an outcome measure in research studies and in clinical practice. HRQL measures can help in improving patient-clinician communication, screening, monitoring, and continuous assessment of quality of care.
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Kotseva, Kornelia, Neil Oldridge, and Massimo F. Piepoli. Evaluation of preventive cardiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199656653.003.0026_update_001.
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The Joint European Societies guidelines on cardiovascular disease (CVD) prevention define lifestyle and risk factor targets for patients with coronary or other atherosclerotic disease and people at high risk of developing CVD. However, several surveys in Europe and the United States showed inadequate lifestyle and risk factor management and under-use of prophylactic drug therapies in primary and secondary CVD prevention. Various professional associations have developed core components, standards, and outcome measures to evaluate quality of care and provide guidelines for identifying opportunities for improvements. Optimal control of cardiovascular risk factors is one of the most effective methods for reducing vascular events in patients with atherosclerotic disease or high cardiovascular risk. Improving treatment adherence is also very important. Health-related quality of life (HRQL) is considered as an outcome measure in research studies and in clinical practice. HRQL measures can help in improving patient-clinician communication, screening, monitoring, and continuous assessment of quality of care.
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Fromm, Annette. Vascular aetiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0004.
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Vascular aetiology of young ischaemic stroke covers a broad spectrum of causes. It includes the risk factor-mediated causes considered more common among the elderly on one hand, and a large number of rather rare disorders and conditions typical for younger ages on the other hand. This chapter is focused on atherosclerotic aetiology and comorbidity, small vessel disease and arterial dissection, which account for a majority of young ischaemic strokes worldwide, are treatable, and need to be considered as overall or contributing causes early during investigation. Specific and rare causes of young ischaemic stroke will be presented elsewhere.
30
Speer, Thimoteus, and Danilo Fliser. Abnormal endothelial vasomotor and secretory function. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0113.
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The endothelium plays a crucial role in the maintenance of vascular integrity and function. Nitric oxide produced by endothelial cells is a key player, inducing relaxation of vascular smooth muscle cells, inhibition of vascular inflammation, and prevention of coagulatory activation. Chronic kidney disease (CKD) is characterized by deterioration of different protective endothelial properties, collectively described as endothelial dysfunction. Several factors such as methylarginines, modified lipoproteins, and other substances that accumulate may be involved in the pathogenesis of endothelial dysfunction of CKD. Endothelial dysfunction is suggested to be the first critical step in the initiation of atherosclerosis. Clinical assessment of endothelial function may become important in recognition of patients with increased cardiovascular risk. Beside several invasive and non-invasive methods to assess endothelial function in vivo, measurement of circulating (bio)markers may be useful for the evaluation of endothelial dysfunction.
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Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Renal vascular disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0171.
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Renal vascular disease typically occurs with progressive narrowing of the main renal artery or smaller arterial vessels. Often, both patterns of disease coexist and result in ‘ischaemic nephropathy’ with damage to renal tissue. Much less commonly, inflammatory vasculitis can affect small or medium vessels. Ninety per cent of renal vascular disease is caused by atherosclerosis. Patients with renal vascular disease have an increased risk of cardiovascular death from associated cerebrovascular and coronary heart disease. Less than 10% of renal vascular disease is caused by fibromuscular dysplasia. The cause is unknown, but smoking is a risk factor. The disease is often bilateral and multifocal. It tends to affect the mid-portion of the renal artery, while atherosclerosis tends to occur at points of stress, especially at the junction of renal arteries with the aorta. This chapter reviews the diagnosis and management of renal vascular disease.
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Qiu, Chengxuan, and Laura Fratiglioni. Epidemiology of Alzheimer’s disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198779803.003.0003.
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This chapter provides a brief overview concerning the global epidemic, risk and protective factors, and possible intervention strategies of Alzheimer’s disease, the most common type of dementia. Alzheimer’s disease, which is projected to reach global epidemic level in three to four decades, already has a huge economic and societal impact. Epidemiologic research has provided sufficient evidence supporting that lifestyle or cardiovascular risk factors in middle-aged and older adults play a critical role in the onset and progression of late-life dementia and Alzheimer’s disease, whereas active engagement in mental, social, and physical activities may postpone the onset of the dementing disorders. The community intervention studies are warranted to determine to what extent intervention strategies towards control of major lifestyle and cardiovascular risk factors and related vascular disorders as well as maintenance of an active lifestyle may help delay the onset of Alzheimer’s disease and dementia syndrome.
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Guzik, Tomasz J., and Rhian M. Touyz. Vascular pathophysiology of hypertension. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0019.
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Hypertension is a multifactorial disease, in which vascular dysfunction plays a prominent role. It occurs in over 30% of adults worldwide and an additional 30% are at high risk of developing the disease. Vascular pathology is both a cause of the disease and a key manifestation of hypertension-associated target-organ damage. It leads to clinical symptoms and is a key risk factor for cardiovascular disease. All layers of the vascular wall and the endothelium are involved in the pathogenesis of hypertension. Pathogenetic mechanisms, whereby vascular damage contributes to hypertension, are linked to increased peripheral vascular resistance. At the vascular level, processes leading to change sin peripheral resistance include hyper-contractility of vascular smooth muscle cells, endothelial dysfunction, and structural remodelling, due to aberrant vascular signalling, oxidative and inflammatory responses. Increased vascular stiffness due to vascular remodelling, adventitial fibrosis, and inflammation are key processes involved in sustained and established hypertension. These mechanisms are linked to vascular smooth muscle and fibroblast proliferation, migration, extracellular matrix remodelling, calcification, and inflammation. Apart from the key role in the pathogenesis of hypertension, hypertensive vasculopathy also predisposes to atherosclerosis, another risk factor for cardiovascular disease. This is linked to increased transmural pressure, blood flow, and shear stress alterations in hypertension, as well as endothelial dysfunction and vascular stiffness. Therefore, understanding the mechanisms and identifying potential novel treatments targeting hypertensive vasculopathy are of primary importance in vascular medicine.
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Chong, Ji Y., and Michael P. Lerario. Seeing Jellyfish. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190495541.003.0021.
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Migraine may mimic stroke, but acute migraine can also be a (rare) cause of stroke, particularly in the posterior circulation. This risk is particularly high in patients who experience migraine aura, or in those who are smokers or who take oral contraceptives. Because this is a diagnosis of exclusion, other etiologies of stroke need to be investigated. Although there are no high-level clinical trial data, it is advised to control vascular risk factors and avoid medications that can potentially induce vasoconstriction in patients with migraine-related stroke.
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.
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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.
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Pruthi, Rajiv K. Coagulation (Hemostasis and Thrombosis). Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0295.
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The coagulation system has 2 essential functions: to maintain hemostasis and to prevent and limit thrombosis. The procoagulant component of the hemostatic system prevents and controls hemorrhage. Vascular injury results in activation of hemostasis, which consists of vasospasm, platelet plug formation (platelet activation, adhesion, and aggregation), and fibrin clot formation (by activation of coagulation factors in the procoagulant system). The anticoagulant system prevents excessive formation of blood clots, and the fibrinolytic system breaks down and remodels blood clots. Quantitative abnormalities (deficiencies) and qualitative abnormalities of platelets and coagulation factors lead to bleeding disorders, whereas deficiencies of the anticoagulant system are risk factors for thrombosis. Common disorders of hemostasis and thrombosis are reviewed.
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Morris, Rhiain. Psychological management of coronary heart disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0123.
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Both anxiety and depression have been found to increase the risk of developing coronary heart disease (CHD) and lead to exacerbation of cardiac symptoms, with the latter subsequently impacting recovery/rehabilitation (e.g. leading to an increased number of readmissions to hospital, and an increased mortality risk following myocardial infarction (MI)). This may be due to pathophysiologic effects, such as vascular inflammation and autonomic dysfunction, and poor lifestyle/behavioural patterns, including non-attendance at cardiac rehabilitation classes; and/or poor treatment adherence. Psychosocial factors such as stress, hostility, social isolation, socio-economic status, and psychological defensiveness can also affect the course of cardiac illness.
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Ferro, José M., and Ana Catarina Fonseca. Secondary prevention. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0015.
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There are no specific guidelines regarding secondary stroke prevention in young adult stroke patients. Recommendations for secondary prevention are mainly extrapolated from data obtained from older individuals, because young adults were excluded or under-represented in most secondary stroke prevention clinical trials. Secondary stroke prevention includes (a) screening and control of vascular risk factors, that is, hypertension, diabetes mellitus, hyperlipidaemia, atrial fibrillation, hormonal contraception, infections, trauma, physical inactivity, obesity, poor nutrition, smoking, alcohol, and illicit drug use; and (b) identification and treatment of specific causes of ischaemic stroke, that is, cardioembolism, large vessel extra- and intracranial atherosclerotic disease, small vessel disease, dissection, antiphospholipid syndrome, moyamoya disease, sickle cell disease, and some rare diseases. There is then an opportunity for lifelong prevention of vascular events after stroke in a young adult.
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Hayhow, Bradleigh, and Sergio Starkstein. Biological Effects of Depression. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0005.
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This chapter examines the bidirectional relationship between depression and stroke. It is now clearly established that depression is a significant risk factor for stroke, and vice-versa. We review the main biological and demographic factors underlying the association between stroke and depression, the predicted mortality, the mechanism of post-stroke depression, and recent findings on its pharmacological prevention. We conclude by stressing the need for developing effective strategies to manage the burden of illness associated with these interacting conditions. As with the cardiovascular system depression has major effects on the occurrence of stroke. Morbidity and mortality are increased for patients with cerebral vascular accidents (CVA) who are depressed and is seen even in a 10-year follow-up. Depression should be treated concurrently with the management of the acute phase of a CVA.
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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.
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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.
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Delcourt, Candice, and Craig Anderson. Epidemiology of stroke. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0234.
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Approximately 20 million strokes occur in the world each year and over one-quarter of these are fatal. This makes stroke the second most common cause of death, after ischaemic heart disease, and strokes are responsible for 6 million deaths (almost 10% of all deaths) annually. Stroke has major consequences in terms of residual physical disability, depression, dementia, epilepsy, and carer burden. Moreover, around 20% of survivors experience a further stroke or serious vascular event within a few years of the index event. The economic and societal costs of stroke are enormous. With ongoing demographic changes, including the ageing and urbanization of populations, and persistence of highly prevalent risk factors related to adverse lifestyles, the global burden of disease related to stroke is predicted to rise substantially by 2030.
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Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Screening for kidney disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0353.
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Renal disease is common and, with routine reporting of estimated glomerular filtration rates, impairment of renal function is increasingly being recognized. As renal impairment is usually asymptomatic until very advanced, chronic kidney disease (CKD) guidelines have been developed to improve the identification and screening of at-risk populations. Target groups include patients with vascular risk factors (e.g. diabetes mellitus and hypertension); patients with certain multisystem diseases which can cause renal impairment; patients with urological conditions; patients on nephrotoxic medication; and immediate relatives of patients with established renal disease. Kidney function should also be checked during intercurrent illness and perioperatively in all patients with CKD or suspected CKD. The frequency of screening is dictated by the CKD stage.
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Banerjee, Amitava, and Kaleab Asrress. Screening for cardiovascular disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0351.
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Screening involves testing asymptomatic individuals who have risk factors, or individuals who are in the early stages of a disease, in order to decide whether further investigation, clinical intervention, or treatment is warranted. Therefore, screening is classically a primary prevention strategy which aims to capture disease early in its course, but it can also involve secondary prevention in individuals with established disease. In the words of Geoffrey Rose, screening is a ‘population’ strategy. Examples of screening programmes are blood pressure monitoring in primary care to screen for hypertension, and ultrasound examination to screen for abdominal aortic aneurysm. The effectiveness and feasibility of screening are influenced by several factors. First, the diagnostic accuracy of the screening test in question is crucial. For example, exercise ECG testing, although widely used, is not recommended in investigation of chest pain in current National Institute for Health and Care Excellence guidelines, due to its low sensitivity and specificity in the detection of coronary artery disease. Moreover, exercise ECG testing has even lower diagnostic accuracy in asymptomatic patients with coronary artery disease. Second, physical and financial resources influence the decision to screen. For example, the cost and the effectiveness of CT coronary angiography and other new imaging modalities to assess coronary vasculature must be weighed against the cost of existing investigations (e.g. coronary angiography) and the need for new equipment and staff training and recruitment. Finally, the safety of the investigation is an important factor, and patient preferences and physician preferences should be taken into consideration. However, while non-invasive screening examinations are preferable from the point of view of patients and clinicians, sometimes invasive screening tests may be required at a later stage in order to give a definitive diagnosis (e.g. pressure wire studies to measure fractional flow reserve in a coronary artery). The WHO’s principles of screening, first formulated in 1968, are still very relevant today. Decision analysis has led to ‘pathways’ which guide investigation and treatment within screening programmes. There is increasing recognition that there are shared risk factors and shared preventive and treatment strategies for vascular disease, regardless of arterial territory. The concept of ‘vascular medicine’ has gained credence, leading to opportunistic screening in other vascular territories if an individual presents with disease in one territory. For example, post-myocardial infarction patients have higher incidence of cerebrovascular and peripheral arterial disease, so carotid duplex scanning and measurement of the ankle–brachial pressure index may be valid screening approaches for arterial disease in other territories.
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Vlachopoulos, Charalambos, and Nikolaos Ioakeimidis. Erectile dysfunction as a marker and predictor of cardiovascular disease. Edited by Charalambos Vlachopoulos. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0245.
Full textAbstract:
Erectile dysfunction (ED) is defined as the inability to obtain or maintain a penile erection to support satisfactory sexual performance. It is considered an early manifestation of generalized vascular disease and recognized as a marker of increased cardiovascular risk both acutely and chronically by predicting all-cause mortality, cardiovascular mortality, coronary events, stroke, and peripheral artery disease in men with and without known coronary artery disease. The link between ED and cardiovascular disease might reside in the interaction between androgen level, chronic inflammation, and cardiovascular risk factors that determine endothelial dysfunction and atherosclerosis both in the penile and coronary circulation. Because penile artery size is smaller compared with coronary arteries, the same degree of endothelial dysfunction and atherosclerotic burden causes a more significant reduction of blood flow in erectile tissues compared with that in coronary circulation. From a clinical standpoint, because ED may precede cardiovascular disease, it can be used as an early marker to identify men at higher risk of cardiovascular events. The average 3-year time period between the onset of ED symptoms and a cardiovascular event offers the opportunity for detailed cardiological assessment and intensive treatment of risk factors.
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Madl, Ulrike. Pathophysiology of glucose control. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0258.
Full textAbstract:
Hyperglycaemia is a frequent phenomenon in critically-ill patients, associated with increased morbidity and mortality. Hyperglycaemia results in cellular glucose overload and toxic adverse effects of glycolysis and oxidative phosphorylation, especially in tissues with insulin-independent glucose uptake, and acute hyperglycaemia can exert a variety of negative effects. It is the main side effect of intensive insulin therapy. Both severe and moderate hypoglycaemia are independent risk factors of mortality in critically-ill patients. Prolonged hypoglycaemia induces neuronal damage, but may also have adverse cardiovascular effects. Several risk factors predispose critically-ill patients to hypoglycaemic events. Rapid glucose fluctuations may induce oxidative stress and lead to vascular damage. Glucose complexity is a marker of endogenous glucose regulation. Association between hyperglycaemia and outcome is weaker in diabetic critically-ill patients than in non-diabetic patients. Pre-admission glucose control in diabetic critically-ill patients plays a role in the response to glucose control and mortality.
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Noori, Muna, and Catherine Nelson-Piercy. Pathophysiology and management of pre-eclampsia, eclampsia, and HELLP syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0366.
Full textAbstract:
Pre-eclampsia is a multisystem disorder of pregnancy, characterized by the gestational onset of hypertension and proteinuria, which presents as part of a spectrum of disease with potentially serious consequences for both mother and foetus. Pre-eclampsia is a syndrome with multiple aetiologies, which has made it difficult to develop adequate screening tests and treatments. Pre-eclampsia is likely to develop only in vulnerable women with a mix of genetic susceptibility, vascular, metabolic, and inflammatory dysfunction. A number of prepregnancy risk factors for pre-eclampsia have been identified. However, not all women with risk factors develop pre-eclampsia, while many women without do, making it a challenging condition to predict. As pre-eclampsia cannot be prevented, its management remains supportive, with close monitoring of clinical signs and symptoms, antihypertensive therapy, seizure prophylaxis, and ultimately delivery when necessary. This chapter outlines the pathophysiology, diagnosis, and sequelae of pre-eclampsia, and provides an overview of antenatal, intrapartum, and post-natal management of women with pre-eclampsia.
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Connolly, Susan, and Margaret E. Cupples. Community-based prevention centres. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0025.
Full textAbstract:
The need for a new approach to cardiovascular disease prevention, both secondary and primary, that is different from traditional health service provision through hospital cardiac rehabilitation services and general practice is evident. The targets set in the cardiovascular prevention guidelines for modifiable cardiovascular risk factors-smoking, diet and physical activity, weight and its distribution, blood pressure, lipids, and diabetes-are not being adequately achieved for either coronary or other vascular patients or for those at high multifactorial risk of developing CVD. There is also evidence of an increasing disparity in levels of risk between different community groups, largely attributable to social determinants of health. Community-based prevention centres provide a novel approach to reducing cardiovascular risk, in which there is shared working between professionals and the public and a shared understanding of the barriers that individuals experience in their attempts to engage in effective measures for both secondary and primary prevention.
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Chapman, Rachel, and Stefano Sabato. Massive Transfusion in a Child. Edited by Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel, and Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0020.
Full textAbstract:
Massive transfusion in a child is likely to occur in cases of trauma or during surgeries that are at risk for severe blood loss such as liver transplantation and craniofacial procedures. It may also occur when least expected, if inadvertent injury to a vascular structure occurs during surgery. Ability to enlist assistance with administration of the various blood products required and also with checking frequent laboratory results will facilitate the process. Knowledge of the different factors that rapidly become depleted as well as lab values that need to be closely monitored is necessary to avoid further complications during massive blood transfusion.
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Tatlisumak, Turgut, and Lars Thomassen, eds. Ischaemic Stroke in the Young. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.001.0001.
Full textAbstract:
Stroke in the young is different, complex, and challenging. This book delivers a comprehensive review of the different aspects of young ischaemic stroke. Incidence, risk factors, and aetiology differ notably from those seen in the elderly. There is an increased prevalence of traditional risk factors already at a young age, but the book also focuses on special risk factors in young stroke patients. In many young stroke patients, aetiology remains unclear. The book outlines an extensive diagnostic workup and a stroke subtype classification adapted for young strokes. Gender differences are prevalent in young stroke. The book describes risk factors that are either unique or more prevalent in women and the importance of treating them aggressively. Stroke symptoms in children are comparable to those in adults, but there is a dramatic bystander delay in diagnosing the stroke. The text therefore also deals with rapid stroke recognition and adaption to the special needs in children. Young stroke patients are under-represented in randomized controlled treatment trials. In the emergency setting, unusual clinical findings and off-label situations may be faced and the decision-making process may be challenging. Recommendations for secondary prevention are also mainly extrapolated from studies in older individuals. The authors extrapolate data and draw conclusions on the acute and prophylactic treatment of young stroke. Prognosis after young stroke is poor. Even minor stroke may have devastating life-long consequences for quality of life, education, and working capacity. The book points to the opportunity for lifelong prevention of vascular events.
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Metzner, Julia I., and Deepak Sharma. Venous Air Embolism. Edited by David E. Traul and Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0025.
Full textAbstract:
Venous air embolism (VAE) is typically the entrainment of air from the surgical field into the vascular system producing adverse systemic effects based on the severity of embolism. Historically, VAE has most often been associated with sitting position craniotomies. However, there is now a clear recognition of the potential risk of this complication during craniotomy in any position, albeit with lesser incidence and severity. VAE can also occur during cervical spine surgery in the sitting position, although less often. While in many circumstances VAE may be subclinical and even undetected, it has the potential to lead to significant cardiovascular compromise during surgery, with the risk of adverse outcomes. Hence, it is imperative for anesthesiologists to be aware of the causes of and risk factors for VAE, its clinical presentation, diagnostic options, and treatment strategies to effectively prevent and intervene early in this potentially fatal condition.