Progressive Dilatation of the Main Pulmonary Artery Is a Characteristic of Pulmonary Arterial Hypertension and Is Not Related to Changes in Pressure

Assessment of Pulmonary Artery Pulsatility by Multidetector Computed Tomography in Patients Affected by Chronic Obstructive Pulmonary Disease and Pulmonary Hypertension: Preliminary Data

“…The variance observed around the slope of the relationship between diameters and PAP can be explained by several reasons: (1) differences in the amount of elastic bundles of the main pulmonary artery tissues; (2) dilation determined by previous loads, such as higher PAP peaks preceding the measures, heavier than the actual measured PAP; (3) differences in cardiac output; (4) different body surface area, since cross-sectional area of PA and left branch corrected by body surface area were significantly related to PAP; and (5) time of measurement referred to the natural history of disease, since pulmonary artery progressively increases even in case of reduction of PVR by vasodilators, due to intrinsic vessel properties independent of pressure and flow changes. Other relevant findings in the literature are the arterial/bronchial ratio > 1,1 in lobar arteries and the ratio PA/Aorta higher than 1 and close to 1.2 ± .3, as found in our patients as well [24][25][26][27][28][29].…”

“…According to preliminary reports in the literature [24][25][26][27][28][29] and our results, the diameters allow the detection of PH with fairly good sensitivity and specificity. Assuming 28 mm as the upper limit of normality (mean + 2SD) of PA, a sensitivity of 90%, a specificity of 85%, and a positive predictive value of 96% can be obtained by our study with outcomes similar to those obtained in larger series [24][25][26][27][28][29].…”

“…According to preliminary reports in the literature [24][25][26][27][28][29] and our results, the diameters allow the detection of PH with fairly good sensitivity and specificity. Assuming 28 mm as the upper limit of normality (mean + 2SD) of PA, a sensitivity of 90%, a specificity of 85%, and a positive predictive value of 96% can be obtained by our study with outcomes similar to those obtained in larger series [24][25][26][27][28][29]. The variance observed around the slope of the relationship between diameters and PAP can be explained by several reasons: (1) differences in the amount of elastic bundles of the main pulmonary artery tissues; (2) dilation determined by previous loads, such as higher PAP peaks preceding the measures, heavier than the actual measured PAP; (3) differences in cardiac output; (4) different body surface area, since cross-sectional area of PA and left branch corrected by body surface area were significantly related to PAP; and (5) time of measurement referred to the natural history of disease, since pulmonary artery progressively increases even in case of reduction of PVR by vasodilators, due to intrinsic vessel properties independent of pressure and flow changes.…”

“…Within the imaging methods, magnetic resonance imaging (MRI) is extensively studied and allows the measurement of both morphologic and functional data such as Puls and pulmonary blood flow [19][20][21], but it is not widely available. Multidetector computer Tomography (MDCT) and cardiac software imaging are diffusely employed and available; they allow the detailed examination 2 ISRN Pulmonology of heart, coronary vessels, left ventricular function, and pulmonary arteries diameters [22][23][24][25][26][27][28]. Our aims are to study whether MDCT allows the assessment of Puls in COPD, whether Puls is different between patients with and without PH, and whether it is related to hypertension.…”

Pulmonary Artery Enlargement Is Associated With Cardiac Injury During Severe Exacerbations of COPD

“…See Figure 1 and 3 legends for other abbreviations. journal.publications.chestnet.org mechanism for this change remains uncertain. As Boerrigter et al 24 reported in patients with pulmonary arterial hypertension, progressive enlargement in the pulmonary arterial diameter measured by using cardiac MRI occurs independent of changes in hemodynamics. A possible explanation for this phenomenon is that underlying pulmonary vascular disease decreases pulmonary arterial wall distensibility during stability, 25,26 but the reduced vascular distensibility is overcome during AECOPD by factors such as dynamic hyperinflation, altered gas exchange, hypoxic vasoconstriction, increased circulating volume (pulmonary edema or diastolic dysfunction), increased cardiac output, and inflammation.…”