Carotid artery stenting and endarterectomy have different effects on heart rate variability.

OBJECTIVE: Due to their close proximity to the carotid sinus baroreceptor region, carotid endarterectomy (CEA) and carotid angioplasty/stenting (CAS) carry an inherent risk of affecting baroreflex-mediated regulation of the heart rate. Variations in the heart rate can be studied by measuring heart rate variability (HRV), in which distinct frequency bands in the power spectrum represent sympathetic and parasympathetic modulations on sinus node pacemaker activity. We aimed to investigate the influence of CEA and CAS on HRV. METHODS: One-hour recordings of R-R intervals on ECG were obtained before and after CEA (10 patients) or CAS (12 patients). The power spectrum of the R-R time series was estimated using the FFT technique. The power in low frequency (LF) and high frequency (HF) bands were computed and normalized to their total power (TP). The LF/HF ratio, an index of sympathovagal balance, was calculated. RESULTS: Compared to preoperative levels, LF/HF exhibited 85%, 96%, and 70% increase on the second, third, and fourth days after CEA, respectively. In contrast, LF/HF decreased by 26%, 32%, and 26% on the respective days following CAS; the difference between groups was significant (p=0.0069). Normalized LF increased after CEA and decreased after CAS, while the opposite was observed for normalized HF (p=0.0217). There was no significant change in TP. CONCLUSIONS: CEA and CAS have differential effects on the sympathovagal balance on the heart. The relative increase in sympathetic modulation after CEA and parasympathetic modulation after CAS are likely mediated by alterations in the sensitivity of carotid sinus baroreceptors. Altered cardiac autonomic modulation may play a role in the occurrence of cardiac disturbances following carotid interventions.

Hyperhomocysteinemia is associated with the presence of left atrial thrombus in stroke patients with nonvalvular atrial fibrillation.

BACKGROUND AND PURPOSE: Blood stasis is the fundamental mechanism leading to thrombus formation in the venous system. Homocysteine also poses a significant risk for venous thrombosis through its endothelial toxic and prothrombotic properties. In the present study, we hypothesized that high homocysteine might be associated with thrombus formation in another stasis-related condition, atrial fibrillation. METHODS: Forty-two consecutive patients with ischemic stroke caused by nonvalvular atrial fibrillation and admitted within the first day of symptom onset were included. Total fasting plasma homocysteine, serum folic acid, and vitamin B12 levels were measured. All patients were evaluated by transesophageal echocardiography for the presence of a left atrial (LA) thrombus. Homocysteine and vitamin levels were compared between groups with or without LA thrombus. RESULTS: Transesophageal echocardiography revealed LA thrombus in 20 patients. Mean homocysteine levels were significantly higher in patients with LA thrombus (20.75 versus 13.34 micromol/L, P<0.001). Multivariate logistic regression analysis showed that the effect of high homocysteine was independent of other clinical or echocardiographic variables known to increase LA thrombus (P=0.017). There was no difference in vitamin B12 levels between groups (P=0.118), whereas the mean folic acid level was significantly lower in patients with LA thrombus (P=0.004). CONCLUSIONS: High plasma homocysteine conveys an independent risk for LA thrombus formation in patients with stroke caused by nonvalvular atrial fibrillation. This finding further supports the thrombogenic role of high homocysteine in conditions associated with blood stasis.

Primary angiitis of the central nervous system and silent cortical hemorrhages.

Primary angiitis of the CNS is histopathologically characterized by ischemic lesions and small petechial hemorrhages. Unlike CT or conventional MR imaging, gradient-echo MR imaging depicts these chronic petechial hemorrhages. We herein report the case of biopsy-proved primary angiitis of the CNS in a 42-year-old man; whom gradient-echo MR imaging revealed multiple petechial hemorrhages in the cortical-subcortical brain regions. The identification of petechial hemorrhages by gradient-echo MR imaging promises to be a valuable surrogate marker supporting the diagnosis of primary angiitis of the CNS.

Involvement of the central nervous system in Miller Fisher syndrome: a case report.

Miller Fisher syndrome (MFS) is characterised by ophthalmoplegia, ataxia and areflexia. Reports on cerebellar ataxia and supranuclear oculomotor derangement in MFS suggested an additional involvement of the central nervous system (CNS), resembling Bickerstaff's brainstem encephalitis (BBE). In the present report, a patient with a monophasic acute illness, early recovery and specific clinical-laboratory findings suggested both intrinsic brainstem and peripheral nerve disease (MFS and BBE). In pons and medulla oblangata, blurred to discrete T2-lesions were revealed by cranial MRI, while involvement of peripheral nerves was detected with EMG. The CSF showed no increase in protein or cell content, such as occurs in brainstem encephalitis.

Unusually prolonged progressing stroke: an expanding anterior cerebral artery infarction.

Progressive clinical deterioration over a period of weeks coupled with MRI evidence of infarction growth is quite uncommon. In this report, we describe a patient with an occluded left anterior cerebral artery (ACA) at the origin of the A2 segment. His symptoms attributable to a posteriorly located small infarction within the ACA territory slowly progressed during the following 8 weeks. A follow-up MRI revealed that the infarction had expanded to involve the whole region of the left ACA. Occasional patients like ours indicate that stroke is a dynamic disorder with an extremely variable clinical course and state of tissue injury.

Creatine kinase-MB elevation after stroke is not cardiac in origin: comparison with troponin T levels.

BACKGROUND AND PURPOSE: Creatine kinase-MB (CK-MB) increases in some patients with stroke, with no clear evidence of an acute coronary syndrome. Its elevations have been suggested to represent a biological marker for stroke-related myocardial injury. Troponin T has superior sensitivity and specificity to CK-MB in revealing minor myocardial injury. Therefore, we studied troponin T levels after stroke to determine whether troponin T increases in parallel to CK-MB. METHODS: We made daily measurements of CK-MB, myoglobin, total creatine kinase (total CK), and troponin T levels up to day 5 in 32 patients with large hemispheric infarction and with no history of coronary heart disease. The daily enzyme levels were compared with those of a control group of 22 patients with neurological diseases other than stroke. RESULTS: Serum CK-MB, myoglobin, and total CK levels were elevated above the cutoff value in 11, 26, and 20 patients with stroke, respectively. These enzyme levels gradually increased within the first 3 days and declined afterward. Troponin T did not exceed the reference range in any patients. One patient had elevated myoglobin and 3 had elevated total CK in the control group. The difference between groups was significant for CK-MB, myoglobin, and total CK at various time points. CONCLUSIONS: Troponin T, a more specific biochemical marker of myocardial injury, does not increase after stroke. Normal troponin T along with elevated CK-MB signifies that CK-MB is not the biological marker for myocytolysis. CK-MB elevations in stroke patients are likely to be noncardiac in origin.