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Cardiovascular consequences of clinical stroke
1Department of Neurology, Technical University of Munich, Germany.
Insights
Cardiovascular abnormalities, including arrhythmias and blood pressure changes, are common after stroke and linked to higher mortality. Stroke location, especially in the insular cortex, influences these cardiac issues and sympathetic nervous system activation.
Area of Science:
- Neurology
- Cardiology
- Autonomic Nervous System
Background:
- Cardiovascular abnormalities are frequently observed in stroke patients but often overlooked.
- Cardiac arrhythmias, abnormal ECG findings, and altered circadian blood pressure patterns are significantly increased in acute cerebrovascular lesions, correlating with higher mortality.
- Cerebral infarctions can induce diverse cardiovascular abnormalities based on stroke location and size.
Purpose of the Study:
- To investigate the relationship between stroke location and cardiovascular abnormalities.
- To explore the role of the autonomic nervous system in stroke-related cardiovascular changes.
- To analyze the impact of hemispheric lateralization on circadian blood pressure variation post-stroke.
Main Methods:
- Analysis of clinical data from stroke patients.
- Electrocardiogram (ECG) interpretation to identify arrhythmias and electrical instability.
- Monitoring of circadian blood pressure patterns and plasma norepinephrine levels.
- Correlation of cardiovascular findings with stroke location (e.g., insular cortex, brain stem, cerebral hemispheres).
Main Results:
- Prolongation of the QT interval and QRS complex expansion are frequent ECG abnormalities indicating ventricular myocardial electrical instability.
- Cardiac enzyme elevations suggest myocardial damage post-cerebral ischemia.
- Insular cortex lesions are significantly associated with altered circadian blood pressure variation due to sympathetic nervous system activation.
- Right-sided hemispheric infarction correlates with diminished circadian blood pressure variation compared to left-sided infarction.
- Brain stem infarction shows higher norepinephrine levels but a lower incidence of cardiac arrhythmias than hemispheric infarction.
Conclusions:
- Stroke significantly impacts cardiovascular function, with specific locations influencing the type and severity of abnormalities.
- The insular cortex plays a critical role in mediating stroke-induced cardiovascular instability via sympathetic nervous system pathways.
- Hemispheric lateralization of stroke affects circadian blood pressure regulation, highlighting the brain's influence on autonomic cardiovascular control.
Abstract:
In clinical stroke cardiovascular abnormalities are frequently neglected although they occur more often than it is generally assumed. However, cardiac arrhythmias, pathological ECG findings, and changes of circadian blood pressure patterns are significantly increased in patients with acute cerebrovascular lesions and are associated with an increased mortality. Several clinical studies have shown that cerebral infarctions 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 instability of the ventricular myocardium. Furthermore, cardiac enzyme increases are interpreted as an indicator of myocardial damage during the acute phase after cerebral ischaemia. Since the autonomic nervous system plays a major role in the regulation of blood pressure, alterations of sympatho-adrenergic activity can also affect the diurnal blood pressure profile. Some studies report frequent changes of the circadian blood pressure patterns with a decreased night-time blood pressure decline or a pathological night-time blood pressure elevation. Several studies proved the importance of infarct location. The insular cortex in particular has an important role in the genesis of the pathological activation 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 implied that the mechanism of cardiovascular instability following stroke relates to the disinhibition of the insular cortex and a reacting augmentation of the sympathetic tone. A further important aspect is given by the strong evidence that sympathetic activation ] is lateralized following hemispheric brain infarction. Accordingly, patients with a right-sided hemispheric infarction showed a significantly diminished circadian blood pressure variation as compared with patients with left-sided hemispheric infarction. The results in patients with brain stem infarction were heterogeneous. On the one hand, patients with brain stem infarction had substantially higher mean plasma norepinephrine levels than did patients with hemispheric infarction; on the other hand, hemispheric lesions were associated with a significantly higher incidence of cardiac arrhythmias when compared to patients with brain stem infarction.