Cerebrovascular reactivity in patients with a recent lacunar infarction.

Abstract

Sirs: There are contradictory findings on the relation between cerebrovascular reactivity and the presence of a lacunar infarction [4–6]. This may be caused by methodological shortcomings as, for example, studying patients with other risk factors for a reduced cerebrovascular reactivity such as carotid or middle cerebral artery stenosis or by the inclusion of patients who also had asymptomatic large vessel infarctions [7].We studied the cerebrovascular reactivity in twelve consecutive patients with a single symptomatic lacunar infarction in the middle cerebral artery territory who did not suffer from the earlier mentioned risk factors for a reduced cerebrovascular reactivity. Patients were examined within one week after the infarction by means of CO2 enhanced transcranial Doppler. Lacunar infarction was defined as the sudden onset of clinical features corresponding with one of the classic lacunar syndromes accompanied by an ischemic lesion on a conventional cerebral CT – or MRI scan smaller than 15 mm in diameter [1]. Twelve controls were randomly selected from healthy individuals who underwent MRI to serve as controls for a study on cognition and lacunar infarction [8]. Participants gave informed consent before the study. The study was approved by the local medical ethics committee. Cerebrovascular reactivity was defined as the percentage increase in blood flow velocity in the middle cerebral artery on both sides, during inspiration of 5 % CO2 divided by the absolute increase in end-tidal CO2 (mm Hg) in the same period of time (%/mm Hg CO2 increase) [3]. Possible confounders in the relation between cerebrovascular reactivity and a lacunar infarction including hypertension, diabetes or smoking were considered present whenever diagnosed in the medical history or when the patient used antihypertensive drugs, oral anti-diabetics or insulin, respectively. Statistical analysis was performed by means of age and sex adjusted analysis of covariance. Mean age was 52.0 years (SD 12.1) in the controls and 58.2 years (SD 16.8) in patients, respectively (p = 0.31). There were 3 women in the control and 2 in the patient group (p = 0.5). None of the patients suffered from diabetes. Five patients and two controls had hypertension (p = 0.23). Among both groups there were 5 smokers. Mean cerebrovascular reactivity was significantly lower among individuals with a lacunar infarction than in those without (3.0 (SD 1.3) versus 4.8 (SD 1.9) %/mm Hg; p = 0.01, figure). The mean cerebrovascular reactivity in the symptomatic hemisphere was 3.1 (SD 1.4) %/mm Hg compared with 3.2 (SD 1.2) in the asymptomatic hemisphere (p = 0.77). Adjustment for possible confounding vascular factors did not alter the magnitude of the association. Since we studied only twelve patients the estimation of the mean cerebrovascular reactivity may have been influenced by chance and may potentially have a low precision, as is reflected by the standard deviation of these measurements. Owing to the cross-sectional design it is impossible to establish a causal relationship between cerebrovascular reactivity and the occurrence of a lacunar infarction. Since we excluded individuals with other risk factors for a reduced cerebrovascular reactivity our finding may be considered as a marker for generalised small vessel disease, not seen on imaging [2, 3]. Our observation of an impaired cerebrovascular reactivity in both hemispheres in patients with a one-sided lacunar infarction supports this. The occurrence of a lacunar infarction at any specific moment and location is probably a random process that is more likely to occur in persons with general small vessel disease in the brain. Theoretically, destruction of brain tissue caused by the infarction also could have led to a reduced cerebrovascular reactivity. However, this explanation seems less likely since the cerebrovascular reactivity in the asymptomatic hemisphere was also reduced. Future studies should be large and prospective in order to unravel the chain of events from a reduction in vasomotor reactivity to the occurrence of a lacunar infarct. Follow up is needed in order to investigate whether a reduced cerebrovascular reactivity is predictive for the occurrence of future infarction. LETTER TO THE EDITORS