Acute stroke patients are at high risk for cardiac events, including myocardial infarction (MI) and dysrhythmias from autonomic derangement, particularly with strokes involving the insular cortex. Although the precise mechanisms and triggers for this have yet to be elucidated, it appears that there is a predominance of sympathetic activity associated with strokes involving the right hemisphere.115 Seizures that originate from the left temporal lobe may be more commonly associated with bradycardia and even cardiac asystole.116'117 In stroke patients, however, involvement of the right hemisphere appears to correlate most strongly with cardiac autonomic derangements. Colivicci et al.118 evaluated 103 patients with 24-hours Holter monitoring, and found a significantly higher rate of complex arrhythmias in patients with infarction of the right insular cortex. Meyer et al.119 assessed sympathetic function in acute stroke patients by measuring plasma epinephrine and norepine-phrine levels. They found that patients with involvement of the insular cortex, particularly on the right side, had significantly higher levels of plasma catechola-mines. This group also separately studied blood pressure, heart rate, cardiac output, and transcranial flow velocities in the MCAs during the first 5 days after stroke, and found strong evidence for autonomic dysfunction in patients with insular stroke, again predominantly on the right side.120 Although this remains an area of continued research, the insular cortex, particularly on the right side, may have a special association with cardiac pathology in acute stroke patients. Occasionally, these patients will have stunned myocardium, and pathology may reveal contraction band necrosis (Fig. 8.4).
MI in the setting of acute stroke is not uncommon, and may be the result of the catecholamine surge in response to the stroke. Most stroke patients are greater than 65 years of age, and intrinsic CAD is quite common in this age category. It thus becomes vital, especially in stroke patients who are unable to communicate symptoms of angina, to evaluate for the presence of MI in all acute stroke patients. Furthermore, it appears that, again, certain brain regions again appear to correlate
with the risk for developing an MI. Ay et al.121 performed a case-control study of 50 stroke patients with serum cardiac troponin T elevation, and found that patients with infarctions in the right hemisphere, specifically those with involvement of the insular cortex and inferior parietal lobule, had a troponin elevation rate of 88%, compared with 33% of patients who were without involvement of these areas (OR 15.00, 95% CI 2.65-84.79). Cardiac dysrhythmias have been noted in the acute stages of stroke, both ischemic and hemorrhagic. Orlandi et al.122 evaluated 44 acute stroke patients with 24-hour cardiac monitors, finding significant dysrhyth-mias in 75% of hemorrhage patients and 69% of ischemic stroke patients.
Interestingly, not all patients develop significant autonomic activation with stroke. Sander and Klingelhofer123 evaluated 42 stroke patients with essential hypertension and 45 normotensive patients. The normotensive patients with insular cortex stroke showed significantly reduced circadian blood pressure variations and a higher frequency of nocturnal blood pressure increases, as well as higher plasma norepinephrine levels and more frequent electrocardiographic abnormalities. Although life-threatening cardiac arrhythmias do not occur in the great majority of stroke patients in the acute setting, the clinician should be aware of the increased risk in patients with stroke involving certain brain regions.
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