Dao-Yi Yu

BACKGROUND There are six different formulae for estimating mean arterial pressure (MAP) from systolic and diastolic pressure readings. This study is to determine the optimum formula for calculating MAP when compared to the gold standard approach, which is the area under the curve of an invasively measured pulse waveform divided by the cardiac cycle duration. METHODS Eight live pigs were used as the experimental model for the invasive measurement of femoral artery pressure (AP) by a fluid filled catheter connected with a pressure transducer. In addition, intraocular pressure (IOP) and jugular vein pressure (JVP) were also recorded. The mean pressure (MP) was calculated from digital waveforms sampled at 1,000 points per second with the six formulae and area method for AP, IOP and JVP. RESULTS The absolute mean difference between the area MAP and each formula’s MAP ranged from 0.98 to 3.23 mm Hg. Our study also found that even under physiological conditions, area MAP can vary between successive pulses by up to 5 mm Hg. For mean IOP and JVP, the mean difference between a formula’s MP and the area method’s was less than 1 mm Hg for most formulae. With the pooled data, there was excellent agreement amongst all formulae for MAP with the intra-class correlation coefficient (ICC) ranging from 0.97 to 0.99, while the ICC of most formulae for IOP and JVP was 1.0. CONCLUSIONS Our study suggests that all current formulae are adequate for estimating MAP, though some formulae are not suitable for mean IOP and JVP.

Microaneurysms are biomarkers of microvascular injury in diabetic retinopathy (DR). Impaired retinal capillary perfusion is a critical pathogenic mechanism in the development of microvascular abnormalities. Targeting fundamental molecular disturbances resulting from capillary nonperfusion, such as increased vascular endothelial growth factor expression, does not always reverse the anatomic complications of DR, suggesting that other pathogenic mechanisms independent of perfusion also play a role. We stratify the effects of capillary nonperfusion, inflammation, and pericyte loss on microaneurysm size and leakage in DR through three-dimensional analysis of 636 microaneurysms using high-resolution confocal scanning laser microscopy. Capillary nonperfusion, pericyte loss, and inflammatory cells were found to be independent predictors of microaneurysm size. Nonperfusion alone without pericyte loss or inflammation was not a significant predictor of microaneurysm leakage. Microaneurysms found in regions without nonperfusion were significantly smaller than those found in regions with nonperfusion, and their size was not associated with pericyte loss or inflammation. In addition, microaneurysm size was a significant predictor of leakage in regions with nonperfusion only. This report refines our understanding of the disparate pathophysiologic mechanisms in DR and provides a histologic rationale for understanding treatment failure for microvascular complications in DR.