![]() Moreover, the significant increase of cardiac enzymes following acute stroke enhances the evidence of an interplay between stroke and cardiac muscle disturbances 11. The sympathetic and parasympathetic imbalance after stroke is documented by impairment of heart rate and blood pressure regulation 9 and by an increased catecholamine release 10, which mediates beta-adrenergic effects on the myocardium. ![]() As cardioembolism is a common cause of stroke, acute cerebral ischemia itself seems to induce an imbalance of central autonomic control, leading then to cardiac dysfunctions. AF represents a major cause of approximately 30% of strokes 6 and, because of its possible paroxysmal pattern, it could be underdiagnosed 7.Ī strict interaction between cardiovascular and neurological systems is well known 8. However, rhythmic disturbances may also lead to brain ischemia. Although preexisting cardiac pathologies may worsen clinical outcomes 4, arrhythmias are common in stroke patients even in the absence of previous heart diseases, suggesting also a role for central nervous system (CNS) in these abnormalities 2, 5. New-onset arrhythmias, including supraventricular tachycardia, supraventricular extrasystole (SVEB), ventricular extrasystole (VEB), bradycardia, atrial fibrillation (AF) and QT interval prolongation, tend to occur often during the first few hours after stroke 3. Therefore, 7-day Holter ECG should be required as an effective first-line approach to improve both diagnosis and therapeutic management after stroke.Ĭardiac complications, such as arrhythmias, congestive heart failure, and myocardial injuries, are fairly frequent after acute stroke 1, 2. 7-day Holter ECG monitoring proved to be superior as compared to 24-h recording for the detection of all arrhythmias, some of which (SVEB and VEB) were associated with specific brain areas involvement. An association was found between SVEB and parietal (p = 0.013) and temporal (p = 0.013) lobe lesions, whereas VEB correlated with insular involvement (p = 0.002). Patients with SVRs and bradycardia were older (p = 0.0001 p = 0.035) and had higher CHA 2DS 2VASc scores (p = 0.004 p = 0.026) respectively, in the comparison with patients without these two arrhythmias. Compared to the first 24 h of monitoring, 7-Holter ECG showed a significant higher detection for all arrhythmias (AF p = 0.02 bradycardia p = 0.03 tachycardia p = 0.0001 SVEB p = 0.0002 VEB p = 0.0001 SVRs p = 0.0001). 7-day Holter ECG detected AF in 4% of patients, supraventricular extrasystole (SVEB) in 94%, ventricular extrasystole (VEB) in 88%, short supraventricular runs (SVRs) in 54%, supraventricular tachycardia in 20%, and bradycardia in 6%. Analysis of the rhythm recorded over 7 days was compared to analysis limited at the first 24 h of monitoring. One hundred and twenty patients with cryptogenic ischemic stroke underwent clinical and neuroimaging assessment and were monitored with a 7-day Holter ECG. The aims of the study were to detect the rate of atrial fibrillation (AF) and other cardiac arrhythmias after acute ischemic stroke, by using a 7-day Holter ECG which has proved to be superior to the standard 24-h recording, and to evaluate the possible association between brain lesions and arrhythmias. Post-stroke arrhythmias represent a risk factor for complications and worse prognosis after cerebrovascular events.
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