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CHAPTER SUMMARY AND CENTRAL ILLUSTRATION
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Chapter Summary
This chapter discusses the classification, pathophysiology, epidemiology, genetics, treatment, and outcomes of stroke and cerebrovascular disease, with an emphasis on cerebrovascular complications of heart disease (see Fuster and Hurst’s Central Illustration). Modifiable and nonmodifiable risk factors for stroke overlap with those for ischemic heart disease, including hypertension, diabetes, smoking, age, family history, and certain genetic factors. Heart disease can cause cerebrovascular injury due to embolism of material from the heart, embolism via a right-to-left shunt, and hypoperfusion of the brain resulting from cardiac dysfunction or arrest. The most common etiologies for cardioembolism are atrial fibrillation with thromboembolism from the left atria or left atrial appendage, intracardiac thrombus following anterior myocardial infarction or in the setting of cardiomyopathy, and valvular heart disease causing embolism of thrombotic or infective material. The diagnostic evaluation of cardioembolic stroke includes brain imaging, examination of the blood vessels supplying the brain, electrocardiogram (ECG), and echocardiography (echo). A major focus of acute ischemic stroke management is treatment with intravenous (IV) thrombolysis and the use of endovascular therapy to treat emergent large vessel occlusion stroke. The chapter also discusses secondary stroke prevention using antiplatelet medication and the management of anticoagulation in the setting of intracerebral hemorrhage.
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Cerebrovascular diseases are a group of disorders that affect the blood vessels supplying the central nervous system; they include any ischemic or hemorrhagic disease that affects the brain, retina, and spinal cord, caused typically by narrowing, occlusion, or rupture of an artery or arteriole, and less often due to capillary or venous disease. This chapter describes how cerebrovascular and cardiac diseases overlap and interact, with a focus on stroke.
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Stroke is a clinical syndrome, recognized as rapidly developing symptoms or signs of focal (at times global) central nervous system dysfunction, lasting more than 24 hours or leading to death, with vascular disease as the apparent cause; stroke may also be defined as a clinically symptomatic, persistent vascular injury to the brain, retina, or spinal cord. This definition traditionally excluded a transient ischemic attack (TIA), which is defined as a brief episode (less than 24 hours, but usually less than 1 hour) of focal brain or retinal dysfunction caused by vascular disease. Implicit in this definition was the assumption that the transient and reversible symptoms were due to reversible, rather than permanent, injury to the brain tissue. With the development of sensitive magnetic resonance imaging (MRI) methods, over half of all TIAs were found to be accompanied by evidence of infarction; hence there is now a subset of TIA with evidence of an accompanying brain infarction on imaging that is also considered a stroke. The spectrum of TIA and stroke lie on a continuum, with shared pathophysiological mechanisms and opportunities for secondary stroke prevention. As access to ...