Yoshiki Motoji

Clinical Relevance of Fluid Challenge in Patients Evaluated for Pulmonary Hypertension

Background Fluid challenge may help in the differential diagnosis between pre‐ and postcapillary pulmonary hypertension (PH). However, the test is still in need of standardization and better defined clinical relevance. Methods Two hundred twelve patients referred for PH underwent a right‐sided heart catheterization with measurements before and after rapid infusion of 7 mL/kg of saline. PH was defined as mean pulmonary artery pressure ≥ 25 mm Hg, and postcapillary PH was defined as pulmonary artery wedge pressure (PAWP) > 15 mm Hg. An increase in PAWP ≥ 18 mm Hg was considered diagnostic for postcapillary PH. At baseline, 66 patients received a diagnosis of no PH; 22, of postcapillary PH; and 124, of precapillary PH (mostly pulmonary arterial hypertension). Results After fluid challenge, five of 66 patients with no PH (8%) and eight of 124 with precapillary PH (6%) had the diagnosis reclassified as postcapillary PH. Fluid challenge was associated with an increase in PAWP by 7 ± 2 mm Hg in postcapillary PH and 3 ± 1 mm Hg in both precapillary PH and no‐PH groups. Between‐group differences were significant, but there was overlap. There were no adverse events related to fluid challenge. Prediction bands calculated from quadratic fits of the PAWP responses in pooled control subjects with no PH and patients with precapillary PH helped confirm 18 mm Hg as the cutoff for diagnosing postcapillary PH. Conclusions Fluid challenge with 7 mL/kg saline increases PAWP, more in postcapillary than in precapillary PH or in control subjects with no PH. A cutoff value of 18 mm Hg allows reclassification of 6% to 8% of patients with precapillary PH or normal hemodynamic characteristics at baseline.

Effects of body position on exercise capacity and pulmonary vascular pressure-flow relationships

There has been revival of interest in exercise testing of the pulmonary circulation for the diagnosis of pulmonary vascular disease, but there still is uncertainty about body position and the most relevant measurements. Doppler echocardiography pulmonary hemodynamic measurements were performed at progressively increased workloads in 26 healthy adult volunteers in supine, semirecumbent, and upright positions that were randomly assigned at 24-h intervals. Mean pulmonary artery pressure (mPAP) was estimated from the maximum tricuspid regurgitation jet velocity. Cardiac output was calculated from the left ventricular outflow velocity-time integral. Pulmonary vascular distensibility α-index, the percent change of vessel diameter per millimeter mercury of mPAP, was calculated from multipoint mPAP-cardiac output plots. Body position did not affect maximum oxygen uptake (Vo2max), maximum respiratory exchange ratio, ventilatory equivalent for carbon dioxide, or slope of mPAP-cardiac output relationships, which was on average of 1.5 ± 0.4 mmHg·l-1·min-1 Maximum mPAP, cardiac output, and total pulmonary vascular resistance were, respectively, 34 ± 4 mmHg, 18 ± 3 l/min, and 1.9 ± 0.3 Wood units. However, the semirecumbent position was associated with a 10% decrease in maximum workload. Furthermore, cardiac output-workload or cardiac output-Vo2 relationships were nonlinear and variable. These results suggest that body position does not affect maximum exercise testing of the pulmonary circulation when results are expressed as mPAP-cardiac output or maximum total pulmonary vascular resistance. Maximum workload is decreased in semirecumbent compared with upright exercise. Workload or Vo2 cannot reliably be used as surrogates for cardiac output.

Fluid challenge predicts clinical worsening in pulmonary arterial hypertension

AIMnA fluid challenge with rapid saline infusion during right heart catheterization has been shown to be useful for the differential diagnosis between pre- and post-capillary pulmonary hypertension. The aim of this study was to evaluate the prognostic relevance of fluid challenge-induced changes in pulmonary hemodynamics in patients with pulmonary arterial hypertension (PAH).nnnMETHODSnOverall, 118 PAH patients (mean age 57u202f±u202f15u202fyears, 80 female) underwent hemodynamic measurements before and after rapid saline infusion (7u202fmL/kg in 10u202fmin) and were followed up for 19u202f±u202f4u202fmonths.nnnRESULTSnThirty-two patients (27%) had a clinical worsening event defined as the occurrence of one of the following: death, lung transplantation, initiation of parenteral prostanoids, or worsening of PAH (defined as the presence of all of the three following components: a decrease in the 6-minute walk distance of at least 15% from baseline, worsening of PAH symptoms, and need for new PAH treatment). Cardiac index (CI), stroke volume and pulmonary artery compliance were lower whereas right atrial pressure (RAP), the ratio of RAP to pulmonary artery wedge pressure (PAWP) and pulmonary vascular resistance were higher in patients with a clinical worsening event versus patients without events, both at baseline and after fluid challenge (all pu202f<u202f0.01). At multivariable Cox proportional hazards regression analysis, a post-fluid challenge CI <2.8u202fL/min/m2 (hazard ratio 0.0143; 95% confidence interval 0.006-0.3383; pu202f=u202f0.009) was the only independent predictor of outcome.nnnCONCLUSIONSnCI measured after a fluid challenge is an independent predictor of outcome in PAH.

Resistive or dynamic exercise stress testing of the pulmonary circulation and the right heart

There has been recent revival of interest in exercise stress testing of the pulmonary circulation and the right ventricle (RV) for the differential diagnosis of dyspnoea or latent pre- or post-capillary pulmonary hypertension [1–3]. However, guidelines remain cautious because of persistent uncertainties about protocols and the limits of normal [4]. In fact, exercise protocols still vary, with either cycling [3, 6–8], weight lifting [5, 6] or even handgrip [9] modalities, with invasive [3, 5–7, 9] or non-invasive [7, 8, 10] measurements either during [3, 6–10] or after [5] the exercise stress. Furthermore, pulmonary artery pressure (PAP) has been reported either alone [5, 8] or as a function of either cardiac output (CO) [1–3, 7, 10], workload [7, 11] or oxygen uptake (V′O2) [12]. In the meantime, flow-corrected PAP during exercise emerges as the measurement of choice for pulmonary vascular function [1–3], and body position may not matter provided a sufficient number of exercise pressure-flow coordinates is generated to smoothen out higher baseline pulmonary vascular resistance (PVR) in the upright position [10], but there remains uncertainty about the most relevant measurements of RV function [7, 13, 14]. Although there is a rationale in favour of incremental dynamic exercise, there is currently no consensus about the optimal exercise modality. We therefore compared the cardiovascular and gas exchange effects of resistive (handgrip), mixed resistive/dynamic (weight lifting) or dynamic (cycling) exercise on the pulmonary circulation and the RV in healthy volunteers. Exercise stress testing of the pulmonary circulation and the right heart should be dynamic, not resistive http://ow.ly/ZEyF30c9RlP

Lung diffusing capacity in sub-Saharan Africans versus European Caucasians

Single breath measurements of lung diffusing capacity (DL) for carbon monoxide (CO) and nitric oxide (NO) were performed in age-, sex-, weight- and height-matched 32 sub-Saharan Africans (13 women) and 32 Caucasian Europeans, and repeated in 14 of each group at 80% of maximum exercise capacity. In Africans versus Caucasians respectively, DLNO was 153±31 vs 176±38ml/mmHg/min at rest (P<0.001) and 210±48 vs 241±52ml/mmHg/min at exercise (P<0.01) while hemoglobin-adjusted DLCO was 29±6 vs 34±6ml/mmHg/min at rest (P<0.001), and 46±11 vs 51±13ml/mmHg/min at exercise (P<0.01). However there were no differences in DLCO/alveolar volume(VA) (KCO) and DLNO/VA(KNO). The sitting-to-standing height ratio was lower in the Africans. Differences in lung volume with respect to body height explain lower DLNO and DLCO in sub-Saharan Africans as compared to Caucasian Europeans.

The Right Heart-Pulmonary Circulation Unit in Systemic Hypertension

Systemic hypertension is a risk factor for left heart failure, mostly with preserved ejection fraction. Left heart failure is a cause of pulmonary hypertension and eventual right ventricular (RV) failure. There has been report of altered RV function in mild to moderate hypertension with preserved systolic as well as diastolic function of the left ventricle. The pathophysiology of this complication of hypertension is unclear. Preserving the RV and preventing the development of pulmonary vascular disease may be considered among the targets of optimized therapy for systemic hypertension.

Right ventricular dyssynchrony during hypoxic breathing but not during exercise in healthy subjects: a speckle tracking echocardiography study

What is the central question of this study? Right ventricular dyssynchrony in severe pulmonary hypertension is associated with a poor prognosis. However, it has recently been observed in patients with lung or connective tissue disease and pulmonary artery pressure at the upper limits of normal. The mechanisms of right ventricular dyssynchrony in pulmonary hypertension remain uncertain. What is the main finding and its importance? Acute hypoxic breathing, but not normoxic exercise, induces an increase in right ventricular dyssynchrony detected by speckle tracking echocardiography in healthy subjects. These results add new insights into the determinants of right ventricular dyssynchrony, suggesting a role for systemic factors added to afterload in the pathophysiology of right ventricular inhomogeneity of contraction.