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The Heart and Stroke
Overview
Globally, stroke is the fifth leading cause of death in Western countries after cancer and heart disease. There are several ways in which stroke and heart disease interrelate . Cardiogenic stroke occurs when (1) clots embolize from the heart and reach the brain via the arterial circulation, or (2) as a result of severe heart failure and cerebral hypoperfusion. Medications as well as certain cardiac procedures performed to treat heart disease can lead to adverse neurological complications such as ischemic stroke. Many vascular diseases are also known to affect both the heart and the brain. For example, there is a strong correlation between cardiac disease and cerebral atherosclerosis, which escalates the risk of thrombotic stroke. Lastly, central nervous system (CNS) diseases can influence the heart and its function .
Stroke Classification
It is estimated that about 87% of strokes are ischemic and the remaining 13% are hemorrhagic. Using the Trial of Org 10172 in Acute Stroke Treatment (TOAST) criteria, ischemic strokes may be further subdivided into the following types :
- 1.
Thrombosis or embolism associated with large vessel atherosclerosis.
- 2.
Embolism of cardiac origin (cardioembolic stroke).
- 3.
Small vessel occlusion (lacunar stroke).
- 4.
Other determined cause (including hypoperfusion stroke).
- 5.
Undetermined (cryptogenic) cause (no cause identified, more than one cause, or incomplete investigation).
The incidence of each cause of ischemic stroke is variable and dependent upon patient’s age, sex, race, geographical location, risk factors, clinical history, physical findings, and the results of various tests .
Direct Cardiogenic Brain Embolism
Cardiogenic cerebral embolism is responsible for about 20% of all ischemic strokes . Cardiac sources of embolism include blood clots, tumor fragments, infected and noninfected vegetations, calcified particles, and atherosclerotic debris . As more advanced diagnostic techniques have been developed, more causative cardiac abnormalities and their association with stroke have been recognized . Conditions that are known to lead to systemic embolization may be subdivided into a high-risk and a low-risk groups based on their embolic potential ( Table 85.1 ) .
Table 85.1
Classification of Cardiac Causes of Embolism
High Potential for Embolism
|
Low Potential for Embolism
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Etiology
As seen in Table 85.1 , certain cardiac sources have much higher rates of initial and recurrent embolism. The more common sources are reviewed in the following. The risk of embolism also varies within individual cardiac abnormalities depending on many factors. For example, in patients with atrial fibrillation, the presence of associated heart disease, patient’s age, duration, chronic versus intermittent fibrillation, and atrial size, all influence embolic risk. Additionally, it is important to remember that the presence of a potential cardiac source of embolism does not definitely indicate that the stroke was caused by an embolus from the heart. Coexistent occlusive cerebrovascular disease is relatively common. In the Lausanne Stroke Registry, among patients with potential cardiac embolic sources, 11% of patients had severe cervicocranial vascular occlusive disease (>75% stenosis) and 40% had mild to moderate stenosis proximal to brain infarcts .
Common Sources of Cardiac Emboli
Intracardiac Thrombi
Atrial Fibrillation (AF) : Persistent and paroxysmal AF is a potent predictor of first and recurrent stroke, affecting more than 2.7 million Americans. The principal adverse consequence of AF is ischemic stroke, with AF patients being 3–5 times more likely to have a stroke than those without AF. In patients with brain emboli caused by a cardiac source, there is a history of nonvalvular AF in about one-half of all cases, left ventricular thrombus in almost one third, and valvular heart disease in one fourth . Patients with AF typically have more severe strokes as well as longer transient ischemic attacks (TIAs) than patients with ischemic stroke from other causes. Stroke prevention in patients with AF and other heart diseases is discussed in a separate chapter.
Ischemic Heart Disease with Intracavitary Thrombus : Patients with large anterior myocardial infarctions (MI) associated with a left ventricular (LV) ejection fraction of <40% and antero-apical wall-motion abnormalities are at increased risk for developing mural thrombus due to stasis of blood in the ventricular cavity as well as endocardial injury with associated inflammation . Ventricular thrombi can also occur in patients with chronic ventricular dysfunction caused by coronary artery disease, hypertension, and dilated cardiomyopathy. Stroke is less common among uncomplicated MI patients but can occur in up to 12% of patients with acute MI complicated by a left ventricular thrombus. The rate of stroke is higher in patients with anterior rather than inferior MI and reaches up to 20% in those with large anteroseptal involvement. The incidence of embolism is highest during the period of active thrombus formation during the first 1–3 months, with substantial risk remaining even beyond the acute phase in patients with persistent myocardial dysfunction, congestive heart failure, or AF .
Congestive Heart Failure : Current data indicates that congestive heart failure affects an estimated 5.1 million Americans. Patients with ischemic and nonischemic dilated cardiomyopathy have a similarly increased stroke risk by a factor of 2 to 3, accounting for an estimated 10% of ischemic strokes . Stroke rates may be higher in certain subgroups, including patients with prior stroke or TIA, lower ejection fraction, LV noncompaction, peripartum cardiomyopathy, and Chagas heart disease . The 5-year recurrent stroke rate in patients with cardiac failure has been reported to be as high as 45% .
Prosthetic Valves and Devices : The magnitude of risk for brain embolism from a diseased heart valve depends on the nature and severity of the disease, as well as the surgical procedure performed. Notably, atrial fibrillation often coexists with valve disease.
Intracardiac Vegetation
Emboli, including ischemic strokes, are common in patients with infective endocarditis . Specific vegetation characteristics, such as large size, mobility, and location on the mitral valve, as well as vegetations related to a Staphylococcus aureus infection, are associated with an increased risk of symptomatic embolism . Cerebral complications are the most severe and frequent extracardiac sequelae of infective endocarditis, occurring in an estimated 15–20% of patients. These complications include ischemic and hemorrhagic stroke (preceding the diagnosis of infective endocarditis in 60% of patients), TIA, silent cerebral embolism, mycotic aneurysm, brain abscess, and meningitis . Unfortunately, these patients can develop multiple neurological complications ( Figs. 85.1–85.3 ). Intracranial hemorrhage (ICH) occurs in about 5% of patients with infective endocarditis . The ICH is typically attributed to ruptured mycotic aneurysms, which can cause fatal subarachnoid bleeding. However, ICH in these patients can also result from septic erosion of the arterial wall causing rupture, without the presence of a well-delineated aneurysm. An infected embolus can also cause a hemorrhagic infarction with massive bleeding in patients who are on anticoagulation at the time of the event . Embolization usually stops when the infection is controlled. Warfarin does not prevent embolization and is contraindicated in patients with endocarditis and known cerebral embolism, unless indicated in patients with prosthetic valves or pulmonary embolism .
Intracardiac Tumors
Primary cardiac tumors, which can be associated with cerebral embolism and stroke, are extremely rare with atrial myxomas constituting over half of the cases. Papillary fibroelastoma is another histologically benign tumor associated with embolism. Embolic events have long been thought to occur in patients with cardiac tumors secondary to embolization of tumor fragments . Aortic valve and left atrial tumors pose the greatest anatomical risk for embolism. Furthermore, patients with smaller tumors, minimal symptomatology, and no evidence of mitral regurgitation also have a high risk of embolism. The presence of mitral regurgitation and decreased functional status (New York Heart Association III/IV) are actually protective against the occurrence of embolism in patients with intracardiac masses. Cardiac tumors can be resected with low early mortality, and late survival after operation in the context of an embolic stroke is similar to patients with cardiac tumors who undergo resection for other indications .
Aortic Atheroma
Emboli can also arise from the aorta . Ulcerated atheromatous plaques are often found at necropsy in patients with ischemic strokes, particularly in patient with cryptogenic stroke . Transesophageal echocardiography (TEE) often shows aortic atheromas, but technical factors can limit visualization of the entire arch. Large (>4 mm), protruding mobile aortic atheromas are especially likely to cause embolic strokes and are associated with a higher rate of stroke recurrence . For this subgroup of patients, the optimal treatment–antiplatelet monotherapy versus anticoagulation for the prevention of ischemic stroke and TIA due to aortic disease is not clear. Other recommended therapies include lipid-lowering therapy (e.g., statins), blood pressure control, smoking cessation, and, in patients with diabetes, glycemic control. In the setting of nonmobile protruding aortic arch atheroma, antiplatelet agents are the treatment regimen of choice for stroke prevention in patients with aortic arch disease .
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