According to the Framingham Heart Study, patients with chronic atrial fibrillation are approximately six times more liable to stroke than an age-matched population with normal cardiac rhythm (Wolf et al, 1983) and the risk is considerably higher if there is also rheumatic valvular disease, now far less prevalent than in the past. Furthermore, the risk for stroke conferred by the presence of atrial fibrillation varies with age, being 1 percent per year in persons younger than age 65 years, and as high as 8 percent per year in those older than age 75 years with additional risk factors. These levels of risk are of prime importance in determining the potential benefit of chronic anticoagulation, as discussed later. Embolism may also occur in cases of paroxysmal atrial fibrillation or flutter and various studies have suggested that the risk of stroke is even greater than for the chronic arrhythmia. Even more vexing, intermittent and asymptomatic atrial fibrillation is difficult to detect except with long periods of rhythm monitoring. For example, in a study of patients with implanted pacemakers or defibrillators but not known to have atrial fibrillation by Healy and colleagues, a substantial number of atrial arrhythmias were uncovered and raised the risk of stroke fivefold. Related studies by Gladstone and coworkers (2014) and by Sanna and colleagues suggest that recording heart rhythm for longer periods with various types of monitoring, not surprisingly, increases the rate of detection of episodic atrial fibrillation to approximately 15 percent, from approximately 3 percent with conventional Holter monitoring. Long-term monitoring has been adopted in routine practice in the evaluation of “cryptogenic” stroke.
Several scoring systems have been developed to gauge the future likelihood of stroke from atrial fibrillation. The CHADS2 and related systems are shorthand methods to quantitate the risk factors that modulate risk for stroke in a patient with atrial fibrillation and no valvular disease. A refinement of this system, CHA2DS2-VASc is purported to improve these predictions but the confidence intervals around the point estimates of predictive values in both scales are considerable and clinical judgment must be exercised in their use. This is reflected in part by the observation that the more extensive score does not confer increased risk of stroke in a continuous fashion with each increment in score. The scores, subject to replacement by future ones, are given in Table 33-3. Furthermore, the goal of most of these systems is to make choices regarding warfarin or similar anticoagulation for the prevention of embolic stroke from the arrhythmia as discussed later in the chapter, or as pertinently, to identify patients who have such a low risk of stroke that the risks of anticoagulation may not be justified. Epidemiologic and clinical aspects of the protective effects of anticoagulation have their own imprecisions.
The vegetations of infective and noninfective (marantic) endocarditis give rise to several different lesions in the brain as described in Chap. 31. Mural thrombus deposited on the damaged endocardium overlying a myocardial infarct in the left ventricle, particularly if there is an aneurysmal sac, is an important source of cerebral emboli, as is a thrombus associated with severe mitral stenosis without atrial fibrillation, now a far less common circumstance than when rheumatic fever was prevalent. Emboli may occur in the first few weeks after an acute myocardial infarction but Loh and colleagues found that a lesser degree of risk persists for up to 5 years. Cardiac catheterization or surgery, especially valvuloplasty, may disseminate fragments from a thrombus or a calcified valve. Mitral and aortic valve prostheses are, as mentioned, additional important sources of embolism. Subendocardial fibroelastosis, idiopathic myocardial hypertrophy, cardiac myxomas, and myocardial lesions of trichinosis are additional rare causes of embolism from a cardiac source.