Severe pulmonary hypertension (PH) is prognostically highly relevant in patients with COPD. The criteria for severe PH have been defined based on hemodynamic thresholds in right heart ...catheterization.
Can noninvasive clinical tools predict severe PH in patients with COPD? How does the mortality risk change with increasing severity of airflow limitation and pulmonary vascular disease?
We retrospectively analyzed all consecutive patients with COPD with suspected PH undergoing in-depth clinical evaluation, including right heart catheterization, in our PH clinic between 2005 and 2018. Clinical variables potentially indicative of severe PH or death were analyzed using univariate and stepwise multivariate logistic regression and Cox regression analysis adjusted for age and sex.
We included 142 patients with median FEV
of 55.0% predicted (interquartile range IQR, 42.4%-69.4% predicted) and mean pulmonary arterial pressure of 35 mm Hg (IQR, 27-43 mm Hg). A multivariate model combining echocardiographic systolic pulmonary arterial pressure of ≥ 56 mm Hg, N-terminal pro-brain natriuretic peptide (NT-proBNP) plasma levels of ≥ 650 pg/mL, and pulmonary artery (PA) to ascending aorta (Ao) diameter ratio on chest CT scan of ≥ 0.93 predicted severe PH with high positive and negative predictive values (both 94%). After correction for age and sex, both airflow limitation (P = .002; Global Initiative for Chronic Obstructive Lung Disease GOLD stages 1-2 vs stage 3: hazard ratio HR, 1.56 95% CI, 0.90-2.71; GOLD stages 1-2 vs stage 4: HR, 3.45 95% CI, 1.75-6.79) and PH severity (P = .012; HR, 1.85 95% CI, 1.15-2.99) remained associated independently with survival. The combination of GOLD stages 3 and 4 airflow limitation and severe PH showed the poorest survival (HR for death, 3.26 95% CI, 1.62-6.57; P = .001 vs GOLD stages 1-2 combined with nonsevere PH).
In patients with COPD, the combination of echocardiography, NT-proBNP level, and PA to Ao diameter ratio predicts severe PH with high sensitivity and specificity. The contribution of severe PH and severe airflow limitation to impaired survival is comparable.
Aims
We examined the effectiveness of a novel cardiopulmonary management wearable sensor (worn for less than 5 mins) at measuring congestion and correlated the device findings with established ...clinical measures of congestion.
Methods and results
We enrolled three cohorts of patients: (1) patients with heart failure (HF) receiving intravenous diuretics in hospital; (2) patients established on haemodialysis, and (3) HF patients undergoing right heart catheterization (RHC). The primary outcomes in the respective cohorts were a Spearman correlation between (1) change in weight and change in thoracic impedance (TI) (from enrolment, 24 h after admission to discharge) in patients hospitalized for HF; (2) lung ultrasound B‐lines and volume removed during dialysis with device measured TI, and (3) pulmonary capillary wedge pressure (PCWP) and sub‐acoustic diastolic, third heart sound (S3) in the patients undergoing RHC. A total of 66 patients were enrolled. In HF patients (n = 25), change in weight was correlated with both change in device TI (Spearman correlation rsp = −0.64, p = 0.002) and change in device S3 (rsp = −0.53, p = 0.014). In the haemodialysis cohort (n = 21), B‐lines and TI were strongly correlated before (rsp = −0.71, p < 0.001) and after (rsp = −0.77, p < 0.001) dialysis. Volume of fluid removed by dialysis was correlated with change in device TI (rsp = 0.49, p = 0.024). In the RHC cohort (n = 20), PCWP measured at one time point and device S3 were not significantly correlated (rsp = 0.230, p = 0.204). There were no device‐related adverse events.
Conclusions
A non‐invasive device was able to detect changes in congestion in patients with HF receiving decongestion therapy and patients having fluid removed at haemodialysis. The cardiopulmonary management device, which measures multiple parameters, is a potentially useful tool to monitor patients with HF to prevent hospitalizations.
CONGEST‐HF: correlation of the cardiopulmonary monitoring (CPM) wearable device with measures of congestion. IV, intravenous; PCWP, pulmonary capillary wedge pressure.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Pulmonary hypertension (PH) is a common complication of interstitial lung disease (ILD) and is associated with worse outcomes and increased mortality. Evaluation of PH is recommended in lung ...transplant candidates, but there are currently no standardized screening approaches. Trials have identified therapies that are effective in this setting, providing another rationale to routinely screen patients with ILD for PH.
What screening strategies for identifying PH in patients with ILD are supported by expert consensus?
The study convened a panel of 16 pulmonologists with expertise in PH and ILD, and used a modified Delphi consensus process with three surveys to identify PH screening strategies. Survey 1 consisted primarily of open-ended questions. Surveys 2 and 3 were developed from responses to survey 1 and contained statements about PH screening that panelists rated from -5 (strongly disagree) to 5 (strongly agree).
Panelists reached consensus on several triggers for suspicion of PH including the following: symptoms, clinical signs, findings on chest CT scan or other imaging, abnormalities in pulse oximetry, elevations in brain natriuretic peptide (BNP) or N-terminal pro-brain natriuretic peptide (NT-proBNP), and unexplained worsening in pulmonary function tests or 6-min walk distance. Echocardiography and BNP/NT-proBNP were identified as screening tools for PH. Right heart catheterization was deemed essential for confirming PH.
Many patients with ILD may benefit from early evaluation of PH now that an approved therapy is available. Protocols to evaluate patients with ILD often overlap with evaluations for pulmonary hypertension-interstitial lung disease and can be used to assess the risk of PH. Because standardized approaches are lacking, this consensus statement is intended to aid physicians in the identification of patients with ILD and possible PH, and provide guidance for timely right heart catheterization.
•Right atrial pressure during exercise should not exceed 12 mm Hg (absolute values) or 1.3 mm Hg/L/min (cardiac output–normalized values).•Patients with pulmonary hypertension frequently display an ...abnormal increase in right atrial pressure during exercise, which may be more frequent and severe in pulmonary hypertension owing to heart failure with preserved ejection fraction than in pulmonary arterial hypertension, implying an exhausted Frank–Starling reserve in the former group.•Preload-related factors (including stressed blood volume and tricuspid regurgitation) may underlie right heart maladaptation to exercise in patients with pulmonary hypertension.
Right heart failure (RHF) is associated with a dismal prognosis in patients with pulmonary hypertension (PH). Exercise right heart catheterization may unmask right heart maladaptation as a sign of RHF. We sought to (1) define the normal limits of right atrial pressure (RAP) increase during exercise; (2) describe the right heart adaptation to exercise in PH owing to heart failure with preserved ejection fraction (PH-HFpEF) and in pulmonary arterial hypertension (PAH); and (3) identify the factors associated with right heart maladaptation during exercise.
We analyzed rest and exercise right heart catheterization from patients with PH-HFpEF and PAH. Right heart adaptation was described by absolute or cardiac output (CO)-normalized changes of RAP during exercise. Individuals with noncardiac dyspnea (NCD) served to define abnormal RAP responses (>97.5th percentile). Thirty patients with PH-HFpEF, 30 patients with PAH, and 21 patients with NCD were included. PH-HFpEF were older than PAH, with more cardiovascular comorbidities, and a higher prevalence of severe tricuspid regurgitation (P < .05). The upper limit of normal for peak RAP and RAP/CO slope in NCD were >12 mm Hg and ≥1.30 mm Hg/L/min, respectively. PH-HFpEF had higher peak RAP and RAP/CO slope than PAH (20 mm Hg 16–24 mm Hg vs 12 mm Hg 9–19 mm Hg and 3.47 mm Hg/L/min 2.02–6.19 mm Hg/L/min vs 1.90 mm Hg/L/min 1.01–4.29 mm Hg/L/min, P < .05). A higher proportion of PH-HFpEF had RAP/CO slope and peak RAP above normal (P < .001). Estimated stressed blood volume at peak exercise was higher in PH-HFpEF than PAH (P < .05). In the whole PH cohort, the RAP/CO slope was associated with age, the rate of increase in estimated stressed blood volume during exercise, severe tricuspid regurgitation, and right atrial dilation.
Patients with PH-HFpEF display a steeper increase of RAP during exercise than those with PAH. Preload-mediated mechanisms may play a role in the development of exercise-induced RHF.
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Visual Take Home Graphic. Right heart maladaptation to exercise in PH-HFpEF and in PAH. Patients with PH-HFpEF presented more frequently with right heart maladaptation, with higher RAP and RAP/CO slope and a flatter Frank–Starling curve, despite lower right ventricular afterload than PAH. Preload-dependent mechanisms (higher increase in eSBV and tricuspid regurgitation) were associated with right heart maladaptation to exercise in PH. Exemplificative pressure traces from patients from both groups are reported, with overt sign of tricuspid regurgitation in PH-HFpEF (which was extremely frequent in this cohort), including tall V waves in the right atrium. CO, cardiac output; eSBV, estimated stressed blood volume, PH, pulmonary hypertension; PH-HFpEF, pulmonary hypertension owing to heart failure with preserved ejection fraction; RAP, right atrial pressure.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
The measurements used to define pulmonary hypertension (PH) etiology, pulmonary arterial wedge pressure (PAWP), and left ventricular end-diastolic pressure (LVEDP) vary in clinical practice. We aimed ...to identify clinical features associated with measurement discrepancy between PAWP and LVEDP in patients with PH.
We extracted clinical data and invasive hemodynamics from consecutive patients undergoing concurrent right and left heart catheterization at Vanderbilt University between 1998 and 2014. The primary outcome was discordance between PAWP and LVEDP in patients with PH in a logistic regression model.
We identified 2,270 study subjects (median age, 63 years; 53% men). The mean difference between PAWP and LVEDP was -1.6 mm Hg (interquartile range, -15 to 12 mm Hg). The two measurements were moderately correlated by linear regression (R = 0.6, P < .001). Results were similar when restricted to patients with PH. Among patients with PH (n = 1,331), older age (OR, 1.77; 95% CI, 1.23-2.45) was associated with PAWP underestimation in multivariate models, whereas atrial fibrillation (OR, 1.75; 95% CI, 1.08-2.84), a history of rheumatic valve disease (OR, 2.2; 95% CI, 1.36-3.52), and larger left atrial diameter (OR, 1.70; 95% CI, 1.24-2.32) were associated with PAWP overestimation of LVEDP. Results were similar in sensitivity analyses.
Clinically meaningful disagreement between PAWP and LVEDP is common. Atrial fibrillation, rheumatic valve disease, and larger left atrial diameter are associated with misclassification of PH etiology when relying on PAWP alone. These findings are important because of the fundamental differences in the treatment of precapillary and postcapillary PH.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
The impact of exercise training on the right heart and pulmonary circulation has not yet been invasively assessed in patients with pulmonary hypertension (PH) and right heart failure. This ...prospective randomized controlled study investigates the effects of exercise training on peak VO2/kg, haemodynamics, and further clinically relevant parameters in PH patients.
Eighty-seven patients with pulmonary arterial hypertension and inoperable chronic thrombo-embolic PH (54% female, 56 ± 15 years, 84% World Health Organization functional class III/IV, 53% combination therapy) on stable disease-targeted medication were randomly assigned to a control and training group. Medication remained unchanged during the study period. Non-invasive assessments and right heart catheterization at rest and during exercise were performed at baseline and after 15 weeks. Primary endpoint was the change in peak VO2/kg. Secondary endpoints included changes in haemodynamics. For missing data, multiple imputation and responder analyses were performed. The study results showed a significant improvement of peak VO2/kg in the training group (difference from baseline to 15 weeks: training +3.1 ± 2.7 mL/min/kg equals +24.3% vs. control -0.2 ± 2.3 mL/min/kg equals +0.9%, P < 0.001). Cardiac index (CI) at rest and during exercise, mean pulmonary arterial pressure, pulmonary vascular resistance, 6 min walking distance, quality of life, and exercise capacity significantly improved by exercise training.
Low-dose exercise training at 4-7 days/week significantly improved peak VO2/kg, haemodynamics, and further clinically relevant parameters. The improvements of CI at rest and during exercise indicate that exercise training may improve the right ventricular function. Further, large multicentre trials are necessary to confirm these results.
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.
A physiological approach to the analysis of hemodynamic data in pulmonary hypertension (PH) has the advantage of reducing the large number (well over 100) of potential causal illnesses into four ...simple mechanisms. A fifth condition is composed of mixtures of the four basic mechanisms. This approach was beautifully described by Paul Wood, the great cardiologist whose name is given to the units of pulmonary vascular resistance (PVR), Wood units. This approach uses well understood physiological contributions to pulmonary vascular pressure. It is powerful, the major uncertainty being in determination of the magnitude of each mechanism in patients that have mixed PH of several causes. It also makes sense of the occasionally awkward clustering of conditions in the clinical classification of the World Symposium, which omits pulmonary vasoconstriction, hyperkinetic states, and the highly prevalent condition of “mixed” PH. This method of analysis is described and demonstrated, much as Wood did in his writings. The method is useful in the office, the ICU, and in consultation. A basic message from this approach is that correct assessment requires measurement of each of the three major inputs, pulmonary arterial pressure (Ppa), pulmonary artery wedge pressure (Pwedge) and cardiac output (CO). Some cases also need left ventricular end diastolic pressure (LVEDP). Other data contributing to analysis will be discussed in each condition. A key to avoiding mistakes is to always remember that PH is simply an elevation in pressure and is not inherently diagnostic of cause.
Pulmonary hemodynamics during exercise may reveal early pulmonary vascular disease and may be of clinical and prognostic relevance in systemic sclerosis (SSc). We aimed to assess the prognostic ...relevance of exercise pulmonary resistances in patients with SSc with no or mildly increased mean pulmonary arterial pressure (mPAP).
Are pulmonary resistances at peak exercise independent predictors of mortality in systemic sclerosis?
All SSc patients with resting mPAP < 25 mm Hg and at least one year of follow-up data who underwent symptom-limited exercise right heart catheterization between April 2005 and December 2018 were analyzed retrospectively. Age-adjusted Cox regression analysis was used to evaluate the association between pulmonary resistances and all-cause mortality.
The cohort consisted of 80 patients: 73 women and 7 men with a mean age of 57 years (interquartile range IQR, 47-67 years) and a mean follow-up time of 10.4 years (IQR, 8.5-11.8 years). At baseline, resting mPAP of ≤ 20 mm Hg and 21 to 24 mm Hg was found in 68 and 12 patients, respectively. Pulmonary vascular resistance (PVR) and total pulmonary resistance (TPR) at peak exercise were associated significantly with mortality (P = .006 hazard ratio (HR), 2.20; 95% CI, 1.26-3.87 and P = .026 HR, 1.56; 95% CI, 1.06-2.29), whereas resting PVR and TPR were not (P = .087 HR, 2.27; 95% CI, 0.89-5.83 and P = .079 HR, 1.88; 95% CI, 0.93-3.80). The mPAP per cardiac output (CO) and transpulmonary gradient (TPG) per CO slopes were associated significantly with mortality (P = .047 HR, 1.14; 95% CI, 1.002-1.286 and P = .034 HR, 1.34; 95% CI, 1.02-1.76) as well. The area under the receiver operating characteristic curve for exercise PVR to predict 10-year mortality was 0.917 (95% CI, 0.797-1.000).
PVR and TPR at peak exercise, mPAP/CO slope, and TPG/CO slope are predictors of age-adjusted long-term mortality in SSc patients with no or mildly increased pulmonary arterial pressure.
Patients with chronic thromboembolic disease (CTED) may suffer from exercise intolerance without pulmonary hypertension at rest. Pulmonary endarterectomy (PEA) for symptomatic CTED results in ...improvement of symptoms and quality of life. Neither the pathophysiology of the exercise limitation nor the underlying mechanisms of the PEA-induced improvement have been studied previously.
We studied hemodynamic and ventilatory responses upon exercise in 14 patients with CTED. After 1 year, we studied the underlying physiologic mechanisms of the PEA-induced symptomatic improvement.
Cardiopulmonary exercise testing (CPET) was performed during right heart catheterization, and noninvasive CPET was performed 1 year postoperatively.
During exercise, we observed abnormal pulmonary vascular responses, that is, a steep mean pulmonary artery pressure/cardiac output (2.7 ± 1.2 mm Hg·min·L−1), and low pulmonary vascular compliance (2.8 ± 1.1 mL·mm Hg−1); mean pulmonary artery pressure/cardiac output slope correlated with dead-space ventilation (r = 0.586; P = .028) and ventilatory equivalents for carbon dioxide slope (r = .580; P = .030). Postoperatively, the improvement observed in exercise capacity was related to improvements in CPET-derived parameters pointing to restoration of right ventricle stroke volume response (oxygen pulse: 11.7 ± 3.1 to 13.3 ± 3.3; P = .027; heart rate response: 80.9 ± 12.4 to 72.0 ± 5.7; P = .003); and, indicating improved ventilatory efficiency, the ventilatory equivalents for carbon dioxide slope decreased from 38.2 ± 3.6 to 32.8 ± 7.0 (P = .014).
Patients with CTED showed an abnormal pulmonary vascular response to exercise and a decreased ventilatory efficiency. Responses after PEA point to restoration of right ventricle stroke volume response and ventilatory efficiency.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
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