Effect of hypertension on development of cerebral infarction

Comparison of embolic with nonembolic cerebral artery occlusion

Abstract

We reported earlier that bilateral carotid ligation in hyprertensive rats caused much more pronounced ischemia than in normotensive rats. Results of the study suggested that hypertension may predispose to production of larger cerebral infarcts when the main cerebral arteries are occluded.
In order to elucidate the role of hypertension in production of cerebral infarcts in humans, 80 patients with definite embolic cerebral infarction (ECI) and 69 with nonembolic cerebral infarction (NECI) admitted within two weeks after onset were analyzed in the present study. Diagnosis of ECI was made only when the patient met at least two of the following criteria; 1) abrupt onset and completion of focal cerebral symptoms and signs, 2) presence of embolic source, and 3) evidence of systemic embolism. Arterial occlusion and/or reopening of occluded artery were confirmed by cerebral angiography in the majority of cases. The ratio of the largest low Vat area to the largest hemispheric area in CT films (expressed in %) was used to represent the size of the infarct (Infarct-Index).
When the Infarct-Index in the ECI-group was plotted against the mean arterial blood pressure (MABP) at 0, 7, 28 and 60 days after the onset, a significant positive correlation was obtained at each stage. In the NECI-group, no correlation was present at all.
When the ECI-group was further divided according to the site of occlusion, i.e. the internal carotid, the middle cerebral artery (MCA) stem and MCA branch occlusion, significant positive correlations were obtained only in patients with embolic occlusion of MCA stem and branch at the chronic stage (28 and 60 days after the onset). As blood pressure is unlikely to be modified by an event that occurred in the brain one or two months before, the level of blood pressure in the chronic stage may well reflect the habitual blood pressure before the stroke. Thus, the above evidence that the correlation was highly significant 60 days after the onset of ECI, strongly suggests the importance of longstanding hypertension in production of larger infarct when the main cerebral artery is abruptly occluded.
To clarify the speculation mentioned above, Infarct-Index was related to MABP before the onset of stroke in patients whose blood pressure had been periodically checked at the outpatient clinic. The correlation was again significant at 5% level in the ECI-group.
Further, patients with history of hypertension showed a higher mean Infarct-Index, and worse outcome than those without history of hypertension. Those differences were significant only in the ECI-group, but not in the NECI-group.
From the result of the present study, it is concluded that longstanding hypertension may not only be the most important risk factor of stroke, but also play an imprtant role in production of more severe and larger ischemia especially when the main cerebral artery is abruptly occluded.