Neurovascular coupling in severe aortic valve stenosis.

OBJECTIVES: Aortic stenosis (AS) is characterized by obstruction of blood outflow from the left ventricle, which can impair target organ perfusion such as the brain. We hypothesized that hemodynamic changes in AS may lead to dysfunction of cerebral blood flow regulatory mechanisms. The aim of our study was to evaluate neurovascular coupling in patients with AS by Transcranial Doppler ultrasonography. METHODS: Neurovascular coupling was assessed using visually evoked cerebral blood flow velocity responses (VEFR) calculated as relative blood flow velocity changes in the posterior cerebral artery upon visual stimulation. We analyzed peak systolic, mean and end diastolic VEFR in 54 patients with severe AS and 43 controls in 10 consecutive cycles of visual stimulation. Repeated-measures ANOVA test was used to compare cerebral hemodynamic data by group. RESULTS: Patients with AS had significantly higher peak systolic (12.9% ± 5.6% and 10.5% ± 4.5%; p = .009) and mean VEFR (14.4% ± 5.8% and 12.2% ± 4.9%; p = .021) compared to controls, whereas only a tendency for higher end diastolic VEFR was observed (16.7% ± 6.9% and 14.4% ± 6.2%; p = .061). CONCLUSION: We have shown for the first time that patients with severe AS exhibit higher VEFR than controls indicating dysregulation of neurovascular coupling, which can be one of the factors contributing to development of cognitive decline.

Infectious Endocarditis of a Heterotopic Caval Valved Stent.

Right-sided infective endocarditis (IE) accounts for 5% to 10% of all IE cases. Compared with left-sided IE, it is more often associated with intravenous drug abuse and intracardiac devices, whereas the latter has become more prevalent in recent decades. The authors report the first case of IE in a heterotopic caval valved stent used for treating torrential tricuspid regurgitation. (Level of Difficulty: Advanced.).

Cerebral blood flow impairment and cognitive decline in heart failure.

BACKGROUND AND PURPOSE: Cognitive decline is an important contributor to disability in patients with chronic heart failure, affecting 25%-50% of patients. The aim of this review is to stress the importance of understanding pathophysiological mechanisms of heart failure involved in cognitive decline. METHODS: An extensive PubMed search was conducted for the literature on the basic mechanisms of cerebral blood flow regulation, the effect of cardiac dysfunction on cerebral blood flow, and possible mechanisms underlying the association between cardiac dysfunction and cognitive decline. RESULTS: Published literature supports the thesis that cardiac dysfunction leads to cerebral blood flow impairment and predisposes to cognitive decline. One of the postulated mechanisms underlying cognitive decline in chronic heart failure is chronic regional hypoperfusion of critical brain areas. Cognitive function may be further compromised by microvascular damage due to cardiovascular risk factors. Furthermore, it is implied that cerebral blood flow assessment could enable early recognition of patients at risk and help guide appropriate therapeutic strategies. CONCLUSION: Interdisciplinary knowledge in the fields of neurology and cardiology is essential to clarify heart and brain interconnections in chronic heart failure. Understanding and identifying the basic neuropathophysiological changes in chronic heart failure could help with developing methods for early recognition of patients at risk, followed by institution of therapeutic actions to prevent or decrease cognitive decline.