The main underlying mechanism of cardiac abnormalities in cerebrovascular (CV) disease is an abnormal autonomic nervous system function with altered sympathetic and parasympathetic output. The ECG abnormalities in CV diseases are ST elevation or depression, prolonged QT interval, T wave inversion and pathologic Q waves (1).
Hypothalamic stimulation can reproduce the ECG changes that are seen in acute CV disease (2).
The rhythm disturbances that might be seen are torsade de pointes, and other life-threatening arrhythmias, atrial fibrillation, SVT and bradycardia due to sinoatrial block, sinus arrest and AV-Block (3). Other cardiac manifestations are neurogenic pulmonary edema, myocardial damage with cardiac enzymes and troponin elevation -at autopsy, subendocardial hemorrhage and fibrosis have been described.
Subarachnoid hemorrhage
Patients with subarachnoid hemorrhage suffering from life-threatening arrhythmia (VT/VF) have high concentrations of plasma catecholamine, serum CK-MB, myosin light chain and troponin T (4). Fifty percent of patients with subarachnoid hemorrhage have hypokalemia that can lead to arrhythmias.
Stroke
The control sites of the autonomic function are the insular cortex, amygdala and the lateral hypothalamus. Patients with brain stem infarctions have higher mean plasma NE levels compared to patients with hemispheric infarctions. On the other hand, patients with hemispheric lesions have a higher incidence of cardiac arrhythmias compared to patients with brain stem infarction (5).
There is a cortical asymmetry in the regulation of cardiovascular functions. Animal studies demonstrated a higher sympathetic discharge in the right hemispheric stroke compared to left-sided strokes. Strokes in the region of the insula - especially the right one - are associated with a low heart rate variability and a high incidence of sudden death (6,7).
Other manifestations of insular involvement are nocturnal increases in blood pressure, high NE levels, QT prolongations and low sympathetic and parasympathetic activities (6,7).
High risk patients who need arrhythmia monitoring in the intensive care unit are those with insular involvement, right-sided stroke, advanced age, coexisting hypertensive or coronary heart disease and those expressing intense emotional stress (3).
Mental stress
Mental stress triggers ischemia in 40 to 70% of stable coronary patients with positive exercise tests. Mental stress induced ischemia is independently associated with a higher rate of fatal and nonfatal cardiac events. It predicts events over and above exercise-induced ischemia (8).
Another entity is transient LV apical ballooning (tako-tsubo-like left ventricular dysfunction) in the absence of CAD. It occurs predominantly in women after acute emotional or physical stress. The underlying etiology is not clear, but it can be myocardial stunning due to high level of catacholamines, coronary vasospasm, plaque ruptures, and myocarditis in genetically prone patients. The treatment is mainly beta blockers and the prognosis is good (9).
Brain death
Systolic myocardial dysfunction - segmental or global - is seen in 42% of patients with brain death and it is not predicted by clinical, ECG or brain CT characteristics. Ventricular arrhythmias are more common (32% more) in patients with myocardial dysfunction (7). In spontaneous subarachnoid hemorrhages, there is a segmental myocardial dysfunction, but in head trauma there might be a segmental or global dysfunction.
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