Noninvasive Assessment of Pulmonary Vascular Resistance by Doppler Echocardiography.
ABSTRACT The ratio of tricuspid regurgitation velocity (TRV) to the time-velocity integral of the right ventricular outflow tract (TVIRVOT) has been studied as a reliable measure to distinguish elevated from normal pulmonary vascular resistance (PVR). The equation TRV/TVIRVOT × 10 + 0.16 (PVRecho) has been shown to provide a good noninvasive estimate of PVR. However, its role in patients with significantly elevated PVR (> 6 Wood units [WU]) has not been conclusively evaluated. The aim of this study was to establish the validity of the TRV/TVIRVOT ratio as a correlate of PVR. The role of TRV/TVIRVOT was also compared with that of a new ratio, TRV(2)/TVIRVOT, in patients with markedly elevated PVR (>6 WU).
Data from five validation studies using TRV/TVIRVOT as an estimate of PVR were compared with invasive PVR measurements (PVRcath). Multiple linear regression analyses were generated between PVRcath and both TRV/TVIRVOT and TRV(2)/TVIRVOT. Both PVRecho and a new derived regression equation based on TRV(2)/TVIRVOT: 5.19 × TRV(2)/TVIRVOT - 0.4 (PVRecho2) were compared with PVRcath using Bland-Altman analysis. Logistic models were generated, and cutoff values for both TRV/TVIRVOT and TRV(2)/TVIRVOT were obtained to predict PVR > 6 WU.
One hundred fifty patients remained in the final analysis. Linear regression analysis between PVRcath and TRV/TVIRVOT revealed a good correlation (r = 0.76, P < .0001, Z = 0.92). There was a better correlation between PVRcath and TRV(2)/TVIRVOT (r = 0.79, P < .0001, Z = -0.01) in the entire cohort as well as in patients with PVR > 6 WU. Moreover, PVRecho2 compared better with PVRcath than PVRecho using Bland-Altman analysis in the entire cohort and in patients with PVR > 6 WU. TRV(2)/TVIRVOT and TRV/TVIRVOT both predicted PVR > 6 WU with good sensitivity and specificity.
TRV/TVIRVOT is a reliable method to identify patients with elevated PVR. In patients with TRV/TVIRVOT > 0.275, PVR is likely > 6 WU, and PVRecho2 derived from TRV(2)/TVIRVOT provides an improved noninvasive estimate of PVR compared with PVRecho.
SourceAvailable from: Miquéias Lopes-Pacheco[Show abstract] [Hide abstract]
ABSTRACT: We sought to assess whether the effects of mesenchymal stromal cells (MSC) on lung inflammation and remodeling in experimental emphysema would differ according to MSC source and administration route. Emphysema was induced in C57BL/6 mice by intratracheal (IT) administration of porcine pancreatic elastase (0.1 UI) weekly for 1 month. After the last elastase instillation, saline or MSCs (1x105), isolated from either mouse bone marrow (BM), adipose tissue (AD) or lung tissue (L), were administered intravenously (IV) or IT. After 1 week, mice were euthanized. Regardless of administration route, MSCs from each source yielded: 1) decreased mean linear intercept, neutrophil infiltration, and cell apoptosis; 2) increased elastic fiber content; 3) reduced alveolar epithelial and endothelial cell damage; and 4) decreased keratinocyte-derived chemokine (KC, a mouse analog of interleukin-8) and transforming growth factor-ß levels in lung tissue. In contrast with IV, IT MSC administration further reduced alveolar hyperinflation (BM-MSC) and collagen fiber content (BM-MSC and L-MSC). Intravenous administration of BM- and AD-MSCs reduced the number of M1 macrophages and pulmonary hypertension on echocardiography, while increasing vascular endothelial growth factor. Only BM-MSCs (IV¿>¿IT) increased the number of M2 macrophages. In conclusion, different MSC sources and administration routes variably reduced elastase-induced lung damage, but IV administration of BM-MSCs resulted in better cardiovascular function and change of the macrophage phenotype from M1 to M2.Respiratory Research 10/2014; 15(1):118. DOI:10.1186/s12931-014-0118-x · 3.13 Impact Factor
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ABSTRACT: Background The functional capacity of long-term survivors of submassive pulmonary embolism (PE) is unreported. A six-minute walk distance (6MWD) <350m and reduced heart rate recovery (HRR) indicate adverse prognosis in various chronic diseases. Methods Long-term survivors of acute PE (January 2000-June 2005) were invited to undergo prospectively planned six-minute walk test (6MWT), transthoracic echocardiogram (TTE), clinical and biochemical evaluation with cardiac biomarkers. HRR was calculated as the difference between heart rate at 6-minutes during and at 1-minute post 6MWT. Results 120 patients (52 males; mean age [±standard deviation]-65±14years) were identified 7.7±1.4years after PE. 6MWD was significantly lower than that predicted after adjustment for age, sex, and height (448±114m vs 475±89m, p=0.005), and 16% (17/104) had 6MWD <350m. Among patients with no baseline comorbidities at follow-up (Charlson comorbidity index=0), 8% (4/52) had 6MWD <350m. Resting TTE identified 29% of patients had raised right ventricular (RV) pulmonary pressure (pulmonary arterial systolic pressure [PASP]>36mmHg) and 13% had impaired RV function. Patients with 6MWD<85% predicted had significantly greater impairment of RV longitudinal function (p<0.001), higher PASP (p<0.001) and pulmonary vascular resistance (p<0.001), elevated NT-proBNP (p=0.03) and high-sensitivity troponin-T (HsTropT, p=0.03), but similar left ventricular systolic and diastolic function, to those with normal 6MWT. Conclusions Apparently well, long-term survivors of PE demonstrate impaired exercise capacity, heart rate recovery, mild pulmonary hypertension, raised PVR and right ventricular dysfunction associated with elevated NT-proBNP and HsTropT.Respiratory Medicine 08/2014; 108(10). DOI:10.1016/j.rmed.2014.08.002 · 2.92 Impact Factor
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ABSTRACT: Studies with other imaging modalities have demonstrated a relationship between contrast transit and cardiac output (CO) and pulmonary vascular resistance (PVR). We tested the hypothesis that the transit time during contrast echocardiography could accurately estimate both CO and PVR compared to right heart catheterization (RHC).Cardiovascular Ultrasound 10/2014; 12(1):44. DOI:10.1186/1476-7120-12-44 · 1.28 Impact Factor