No abstract

The present study endeavored to differentiate Alzheimer's disease (AD) from vascular dementia (VaD) by comparing the metabolic and hemodynamic parameters. Positron emission tomographic (PET) studies were carried out in 13 patients with probable AD and 20 patients with VaD. PET findings were not included in the diagnostic criteria of AD or VaD. Using oxygen-15 labeled compounds, cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), oxygen extraction fraction (OEF), cerebral blood volume, and vascular transit time (VTT) were measured quantitatively during the resting state. To evaluate vascular reactivity (VR), CBF was also measured during 7% CO2 inhalation. Regional CBF from the parietal cortex positively correlated with the neuropsychological scores in both AD and VaD groups. The typical parietotemporal pattern of hypoperfusion and hypometabolism was observed in the AD group, whereas the frontal lobe including the cingulate and superior frontal gyri were predominantly affected in the VaD group. The occipital cortex was preserved in both groups. A significant increase of the OEF was found in the parietotemporal areas in the AD group. No significant prolongation was seen with VTT. There was a marked difference in VR between the two groups: VR was depleted in the VaD group, whereas VR was normal in the AD group. The increased OEF with preserved vascular reserve seen in AD may implicate participation of a vascular factor in the pathogenesis of AD, possibly at the capillary level. Thus, PET provides important functional information in discriminating AD from VaD by comparing the patterns of hypoperfusion and/or hypometabolism, and in the understanding of the underlying hemodynamic pathophysiology.

ecent clinical studies have demonstrated that longterm right ventricular apical (RVA) pacing imposes a risk of heart failure, ventricular arrhythmias, and cardiac death. 1-5 RVA pacing causes left ventricular (LV) mechanical dyssynchrony because of altered ventricular excitation that bypasses the His-Purkinje system. 6-9 Longterm RVA pacing results in LV dilatation associated with asymmetric LV hypertrophy, 10,11 regional myocardial perfusion defects 12-14 and a decrease in the LV ejection fraction (LVEF). 12,15,16 Pacing on the right ventricular (RV) septum, RV outflow tract and His or para-His bundle has been introduced as a potentially favorable alternative to RVA pacing to preserve a more physiologic ventricular activation. 8 However, previous investigations of alternative pacing sites have yielded inconsistent results, 17-23 which may be attributable, in part, to the fact that the pacing site was determined on a topological rather than functional basis. 24 Indeed, acute hemodynamic studies have demonstrated that individual optimization of the RV pacing sites could preserve LV performance in patients without LV dysfunction, and that there are substantial individual variations in the optimal pacing sites. 25,26 The paced QRS duration seems to be a practical indicator for determining the optimal RV pacing site. 14,19,22,23 However, information on the most appropriate pacing site to preserve long-term LV function is still limited.To address this issue, we investigated the effect of RV septal (RVS) pacing guided by QRS morphology on longterm LV mechanical synchronicity and function in patients with normal QRS duration and preserved LV function at baseline. Methods PatientsWe retrospectively studied 55 patients (22 men, 32 women; 70±10 years) undergoing dual-chamber pacemaker implantation for advanced atrioventricular block (AVB; n=33) or sinus node dysfunction (SND, n=22). In 40 patients (n=24 for AVB, n=16 for SND), pace mapping was carried out at the junction between the upper and middle segments of the RV septum using a hand-shaped stylet under fluoroscopy

No abstract

To elucidate the hemodynamic pathophysiology underlying Alzheimer's disease (AD), cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2) and oxygen extraction fraction (OEF) were measured with positron emission tomography in 10 patients with probable AD and in 20 age-matched normal volunteers. By the 15O intravenous bolus injection method, CBF was measured during resting state, CO2 inhalation (hypercapnia) and hyperventilation (hypocapnia), and the vascular reactivity (VR) was estimated by comparing the CBF changes (delta CBF%/PaCO2 mmHg) in the hyper- or hypocapnic to the resting state. By the 15O2 single-breath method or 15O steady-state method, CMRO2 and OEF were measured during resting state. Based on 26 regions of interest, local CBF, CMRO2 and OEF were compared statistically between the two groups. As compared with the control group, the mean CBF and CMRO2 decreased to as low as 77.0% and 88.4% of the normal values, respectively, while the mean OEF increased by 12.1% (p < 0.05) in AD patients. These changes were most pronounced in the supramarginal and superior temporal gyri. There was no focal change in VR in the AD group, and no significant difference was seen in VR to either hyper- or hypocapnia between AD and control groups. The results may suggest a vascular involvement, possibly at the capillary level, that might cause a relative misery perfusion syndrome accompanied by preserved vascular reactivity in AD.