Cardiovascular Diseases Poster Session
An autoregulatory mechanism maintains cerebral blood flow at constant levels over a blood pressure range of 60 to 150 mmHg (1) . This control system becomes compromised by the progression of angiopathy derived from conditions such as hypertension and / or diabetes mellitus, which in turn narrows the range of autoregulation. Thereafter, changes in blood pressure will affect the cerebral blood flow. Postural cerebral hypoperfusion is a phenomenon that can lead to transient neurologic deficits during postural change (2). Postural hypoperfusion has been visualized by brain Tc-99m hexamethyl-propyleneamine oxime (HMPAO) SPECT in which Tc-99m HMPAO deposits in the brain revealing the frozen cerebral perfusion images (3) of patients with Takayasu's arteritis (4), cerebrovascular disease (5) and orthostatic hypotension (6) due to the dysfunctional autoregulation of cerebral blood flow.
We investigated whether or not postural cerebral hypoperfusion is involved in causing cerebral infarction compared with diabetic or hypertensive factors.
Materials and Methods
Upright test with Tc-99m HMPAO brain SPECT (Fig.1)Fig.1: Procedure for upright stress test.
After inserting a plastic flexible needle into the antecubital vein, a patient lay on a couch in a quiet and dim room with the legs elevated for 30 min. During this period, Tc-99m HMPAO was labeled by adding Tc-99m pertechnetate to a non-radioactive kit (Cerebrotec, Nihon Medipysics, Nishinomiya). The patient was then was instructed to move from the supine, to a standing position within about three seconds, with assistance if necessary. As soon as the patient was fully upright, a bolus injection of 400 MBq of Tc-99m HMPAO was administered, followed by a flush with 20 ml of saline. The patient remained standing for 5 min to complete Tc-99m HMPAO fixation in the brain, then was moved to the SPECT room. The first SPECT was initiated, then another 500 MBq of Tc-99m HMPAO was administered while the patient remained in the SPECT bed. Blood pressure was measured using a sphygmomanometer before and immediately after the upright test.
CRITERIA FOR RISK FACTORS
Carotid stenosis, cerebral infarction and orthostatic hypotension were scored as follows.
Stenosis and infarct scores are shown in Fig. 2 and 3, respectively.Fig.2: Stenosis score in groups A to D.
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Fig.3: Infarct score in groups A to D.
We classified into PCH (+) (n=19) and PCH(-) (n=13). In PCH (-), t-value by $B&V(J 2 analysis between Groups A and B, A and C, A and D significantly differed at 0.030, 0.042 and 0.006, respectively. However, in PCH(+) that did not reveal significant differences in PCH (+) values of 0.533, 0.702 and 0.152, respectively (Fig.4).
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Fig.4: Rates of cerebral infarction in groups A to D with and without postural cerebral infarction.
Representative case of PCH(+) was shown in Fig. 5.
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Fig.5: Patient in Group C shows postural cerebral hypoperfusion in the bilateral front-parietal area. Upright Tc-99m HMPAO brain SPECT shows decreased activity in bilateral front-parietal areas (arrow). Subsequent supine Tc-99m HMPAO brain SPECT shows filling in the bilateral frontal areas (R, Right; Raise-up, upright Tc-99m HMPAO brain SPECT; Supine, Supine Tc-99m HMPAO brain SPECT.)
Discussion and Conclusion
Frontal susceptibility to changes in blood flow might be due to a "functional" hemodynamic mechanism that induces orthostatic stress, namely maladapted autoregulation. Postural cerebral hypoperfusion with upright Tc-99m HMPAO brain SPECT would be a transient abnormality in the CBF which would be undetectable if the CBF was assessed only in the supine position. Lesions in cerebrovascular disease initially involve the frontal area of the brain as evidenced by CT scans showing abnormal features such as areas of low density and periventricular hyperlucency. From a statistical viewpoint, the number of elderly patients with orthostatic hypotension has increased (7). This may be derived from a delayed autonomic nervous response to restore blood pressure according to postural changes. Maladaptation in the frontal area might play a role in the progression of cerebral ischemia or infarction.
The risk factor of cerebral hypoperfusion indicating the occurrence of cerebral infarction was equivalent to that of hypertension or/and diabetes mellitus. It is therefore crucial that postural hypoperfusion is controlled as well as hypertension and diabetes mellitus, to prevent cerebral infarction from progressing.
|Hayashida, K.; Kume, N.; Nishiooeda, Y.; Fukuchi, K.; (1998). Postural Cerebral Hypoperfusion Could Be The Risk Factor For Cerebral Infarction. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Available at URL http://www.mcmaster.ca/inabis98/cvdisease/hayashida0420/index.html|
|© 1998 Author(s) Hold Copyright|