الفهرس 
CARDIAC NEUROPHYSIOLOGYOnly 14 pages are availabe for public view
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Abstract
Acute cerebrovascular diseases including subarachnoid hemorrhage and other stroke syndromes can be associated with severe cardiac manifestations. The mechanism by which cardiac abnormalities occur with brain injury appears to be related to autonomic nervous system dysfunction.
As we know Nervous control of the circulation has global functions, such as redistributing blood flow to different areas of the body, increasing or decreasing pumping activity by the heart, and, providing very rapid control of systemic arterial blood pressure. The nervous system controls the circulation almost entirely through the autonomic nervous system, and By far the most important part of the autonomic nervous system for regulating the circulation is the sympathetic nervous system. One of the most important function of nervous control of the circulation is its ability to cause rapid increases in arterial blood pressure. For this purpose, the entire vasoconstrictor and cardioaccelerator functions of the sympathetic nervous system are stimulated together. At the same time, there is reciprocal inhibition of parasympathetic vagal inhibitory signals to the heart.
Definition of stroke by the World Health Organization is a ”neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours”. Strokes can be classified into two major categories: ischemic and hemorrhagic. In an Ischemic Stroke, blood supply to a part of the brain is decreased, due to Thrombosis , Embolism, Systemic hypoperfusion or Venous thrombosis .While Hemorrhagic stroke is the accumulation of blood anywhere within the skull vault. Accumulating experimental and clinical evidence suggests that stroke involving the Insular Cortex which is associated with adverse cardiac outcomes , The presumed biologic basis for this association is the role of the insular cortex in the autonomic control of cardiovascular function.
Stroke may be associated with cardiovascular changes including Acute Hypertensive Response , repolarization with ECG abnormalities, arrhythmias, neurogenic cardiac damage, Myocardial infarction with regional wall motion abnormalities, Pulmonary embolism and Venous Thromboembolism.
Acute Hypertensive Response is common in patients admitted for acute ischemic stroke, and a transient blood pressure (BP) rise can be found also in previously normotensive patients. The mechanism that raises BP at stroke onset is unknown and questions remain as to its appropriate management. Blood pressure may decline spontaneously and unpredictably, without intervening medications. The incorrect use of antihypertensive drugs in acute stroke may reduce the pressure-dependent cerebral perfusion to the ischemic penumbra and worsen cerebral damage. Conversely, poststroke hypertension could be deleterious and facilitate edema development in the ischemic tissue. Previous studies gave variable results regarding the prognostic value of high BP in acute stroke. Furthermore, little is known of the relationship between the type and site of acute stroke, rise of BP, and neurological outcome.
For the first time in 1944, Byer and colleagues described the ECG changes in sufferers of subarachnoid hemorrhage.Cardiac autonomic imbalance generated by acute cerebral lesion plays an important role, not only in producing electrocardiographic abnormalities, but also in predisposing the patients towards early mortality. Massive autonomic discharge along the sympathetic outflow tracts of the nervous system produces tachyarrhythmias which form the basis of more lethal abnormalities of heart rate and rhythm like torsade de points, ventricular fibrillation, asystole, and hence death. Sinus tachycardia is a manifestation of hypercatecholaminestate. Sinus tachycardia of higher magnitude may reflect a proportionately higher degree of autonomic discharge.
ECG changes are present in 60-90% of patients with intra-parenchymal or subarachnoid bleed and about 5-20% of patients with acute ischemic stroke. There is a relation between these changes and sudden death in sufferers of stroke. The ECG abnormalities most frequently noted are ischemic changes 35%, prolongation of QT interval 45% and disturbances in rate and rhythm 25%, which include atrial fibrillation, premature atrial and ventricular complexes, supra-ventricular and ventricular tachycardias, torasede de pointis or polymorphic ventricular tachycardias.
Cardiac arrhythmias are the most frequently found ECG abnormalities in patients with stroke. In the study by Natelson , cardiac arrhythmias were noted in 61% of patients with all types of strokes, in 78% of hemorrhagic strokes, and 51% of ischemic strokes, whereas they were observed in only 15% of the control group,(Natelson, 1985). The reported frequency of new onset cardiac arrhythmias in patients, both with ischemic and hemorrhagic stroke without underlying cardiac disease is 25-40%. (Bozluolcay et al., 2003).
One of the main diagnostic echocardiographic signs of Myocardial Infarction is regional wall motion abnormalities, but a wide spectrum of regional left ventricular wall motion abnormalities can occur with subarachnoid hemorrhage and possibly with other types of stroke. Some patients develop a pattern of transient apical left ventricular dysfunction that mimics myocardial infarction, but in the absence of significant coronary artery disease. This condition is known as Takotsubo syndrome (Yoshimura et al, 2008).
Interestingly, increased Cardiac Troponin (cTnT )was also reported to occur in 5-34% of patients with acute ischemic stroke. In several studies, the elevation of cTnT was associated with stroke severity on hospital admission, insular cortex lesions, short- and long-term clinical outcome and increased risk of mortality, indicating prognostic significance of increased cTnT in acute ischemic stroke (Kerr et al., 2009).