CARDIOVASCULAR CONSEQUENCES OF CLINICAL STROKE

In clinical stroke cardiovascular abnormalities are frequently neglect ed although they occur more often than it is generally assumed. Howeve r, cardiac arrhythmias, pathological ECG findings, and changes of circ adian blood pressure patterns are significantly increased in patients with acute cerebrovascular lesions and are associated with an increase d mortality. Several clinical studies have shown that cerebral infarct ions may cause different cardiovascular abnormalities depending on the location and the size of the stroke. Hereby, the prolongation of the QT interval and the expansion of the QRS-complex as the most frequent ECG abnormalities are regarded as indicators of the electrical instabi lity of the ventricular myocardium. Furthermore, cardiac enzyme increa ses are interpreted as an indicator of myocardial damage during the ac ute phase after cerebral ischaemia. Since the autonomic nervous system plays a major role in the regulation of blood pressure, alterations o f sympatho-adrenergic activity can also affect the diurnal blood press ure profile. Some studies report frequent changes of the circadian blo od pressure patterns with a decreased night-time blood pressure declin e or a pathological night-time blood pressure elevation. Several studi es proved the importance of infarct location. The insular cortex in pa rticular has an important role in the genesis of the pathological acti vation of the sympathetic nervous system. Hence, a highly significant relationship between the extent of circadian blood pressure variation and percentage insular infarction could be found. Some findings implie d that the mechanism of cardiovascular instability following stroke re lates to the disinhibition of the insular cortex and a reacting augmen tation of the sympathetic tone. A further important aspect is given by the strong evidence that sympathetic activation is lateralized follow ing hemispheric brain infarction. Accordingly, patients with a right-s ided hemispheric infarction showed a significantly diminished circadia n blood pressure variation as compared with patients with left-sided h emispheric infarction. The results in patients with brain stem infarct ion were heterogeneous. On the one hand, patients with brain stem infa rction had substantially higher mean plasma norepinephrine levels than did patients with hemispheric infarction; on the other hand, hemisphe ric lesions were associated with a significantly higher incidence of c ardiac arrhythmias when compared to patients with brain stem infarctio n.