Increase in local cerebral blood flow induced by circulating adrenaline: involvement of blood-brain barrier dysfunction

The influence of intravenous infusion of adrenaline (8 μg · kg^-1· min^-1) upon local cerebral blood flow (CBF) in paralyzed and artificially ventilated rats was measured autoradio-graphically with ¹⁴C-iodoantipyrine as the diffusible tracer. At this dose, adrenaline invariably increased local CBF even though blood pressure was close to normal at the time of the CBF measurement. In average, local CBF increased to 400% of control. In 6 of 9 animals the increase in flow was inhomogenous with randomingly distributed areas of very high flow rates. Experiments with i.v. administration of Evans blue prior to infusion of adrenaline showed that areas of Evans blue extravasation appeared in 3 of 4 animals. Although areas of extravasation often corresponded to areas of high flow rates the former were much more circumscribed. Furthermore, very high flow rates were found in areas showing no sign of blood-brain barrier dysfunction. It is concluded that the increase in CBF was at least partly due to a pressure-mediated passage of adrenaline across the blood-brain barrier but that such a passage can occur in the absence of macroscopically visible extravasation of protein.     

Predictors of Syncope in Patients with Hypertrophic Cardiomyopathy

Background: Approximately 30% of patients with hypertrophic cardiomyopathy (HCM) suffer syncope and syncope was the only symptom associated with sudden death. However, no systematic studies in large cohorts looking at predictors of syncope are available in the literature. Therefore, we sought to determine predictors of syncope in patients with HCM.
Methods: One hundred and seventy-three consecutive patients with HCM and a mean age of 42 ± 18 years (range 10–78) underwent extensive clinical, electrocardiographic, and echocardiographic testing to identify predictors of syncope.
Results: During the mean follow-up duration of 50 months, syncope occurred in 28% of the HCM patients. Univariate analysis showed male gender, age <40 years, family history of sudden death, PR interval, QRS width, ≥2 bursts of nonsustained ventricular tachycardia (NSVT), ≥3 bursts of nonsustained supraventricular tachycardia (NSSVT), maximum left ventricular wall thickness ≥30 mm, and abnormal blood pressure response, out of 24 demographic, clinical, hemodynamic, electrocardiographic, and echocardiographic features, to be significantly associated with syncope. Of these nine variables, the only independent predictors of syncope at multivariate analysis were age <40 years (odds ratio [OR]: 4.4, 95% confidence interval [CI]: 2.2–16, P = 0.003), ≥2 bursts of NSVT (OR: 9.9, 95% CI: 2.0–46, P = 0.0001), and ≥3 bursts of NSSVT (OR: 2.7, 95% CI: 0.38–8.25, P = 0.001). The concomitant occurrence of all three variables had a sensitivity of 87% and specificity of 73% in identifying the patients with syncopal events.
Conclusions: The results of this study showed that age <40 years, bursts of NSVT, and NSSVT were independently associated with the risk of syncope in patients with HCM. Demographic data and ambulatory ECG findings could help in risk stratification of patients with HCM.