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Effect of Stroke on Heart, Diabetes and Hypertension 139

possible mechanisms for this are not yet very clear
and needs further research.

Effect of stroke on hypertension
Hypertension is one of the modifiable risk factors
for stroke and stroke in turn can affect pre-exist-
ing hypertension or produce an acute hypertensive
response due to various factors. Both low and high
blood pressure values are detrimental to the outcome
of stroke as shown in the International stroke trial,
which suggests a ‘U’-shaped relationship between
systolic blood pressure and stroke outcome in terms
of both morbidity and mortality. Hence, a detailed un-
derstanding of the pathophysiology of acute hyper-
tensive response is absolutely essential for an appro-
priate management. Even though stroke can affect
blood pressure in either way, the acute hypertensive
response is more common than the other, seen ap-
proximately in 50% of stroke patients according to
international studies. Acute hypertensive response Figure 5. Differential Influence of The Two
of stroke is defined as “Elevation of blood pressure Hemispheres On Vasomotor Centre
above normal or premorbid values within 24 hours In most strokes one or the other structures are af-
(5)
of stroke onset” . fected because of widespread nature of these control
In few patients it may be because of undiagnosed systems resulting in altered autonomic balance and
or undertreated chronic hypertension but in most pa- hence the blood pressure. This is the most import-
tients it is because of stroke specific and stroke re- ant mechanism underlying blood pressure changes
lated causes as evidenced by normalization of blood following stroke. Other less important mechanisms
pressure over few days and early spontaneous de- or causes that might contribute to blood pressure
cline in blood pressure following thrombolytic ther- changes following stroke includes increased serum
apy. levels of cathecholamine and cortisol secondary to
release of inflammatory mediators from infracted tis-
In human brain the parasympathetic system is later- sue, infection, urinary retention .
(5)
alised to left cerebral hemisphere with inhibitor inputs
from the prefrontal region and excitatory inputs from Few studies have shown that the pattern and course
the insular cortex. Similarly the sympathetic system of blood pressure changes following stroke are sub-
is lateralized to right cerebral hemisphere with similar type specific, with lacunar infarcts showing high-
excitatory and inhibitory inputs. These two systems er blood pressure at the time of admission and 24
are further modulated by amygdala, hypothalamus hours later when compared to cardio-embolic and
(5)
and cingulate cortex. The final outputs from these large vessel atherothrombotic strokes .
two systems are through the brainstem structures( Post thrombolysis hypertension is associated with
poor outcome at 90 days which is probably relat-
ed to failure of recanalisation,( as recanaliastion is
associated with early spontaneous decline in blood
pressure )or reperfusion injury resulting in release of
inflammatory cytokines from the infarcted tissue and
thereby resulting in hypertension.

On the converse
The pathophysiology of stroke is influenced by (Ta-
ble:1)

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