Increase In Pulmonary Artery Systolic Pressure Research Articles

Changes in pulmonary artery systolic pressure and right ventricular function in patients with end-stage renal disease on maintenance dialysis.

Pulmonary hypertension is common in patients with end-stage renal disease, and portends a poor prognosis. There are little data in this population, and previous studies have not evaluated quantitative changes in haemodynamics over time while on maintenance dialysis. This study sought to estimate changes in pulmonary artery systolic pressure (PASP) and right ventricular function over time, and to predict PASP change using clinical variables routinely available at time of initial measurement, in patients on maintenance dialysis. We retrospectively studied patients with end-stage renal disease at a university-affiliated dialysis centre who had two separate echocardiograms 1-4 years apart. Seventy-six patients (65 haemodialysis, 11 peritoneal dialysis) were included. PASP was estimated by echocardiography. Baseline PASP was predicted by left-sided valvular disease, anaemia, COPD, left-ventricular mass index, and haemodialysis modality (P = 0.07 for modality). Average increase in PASP was 2.41 mmHg per year. Higher rates of PASP change were predicted by E/e' ratio by tissue doppler on echocardiogram, diabetes mellitus, low LV mass, and left-sided valvular heart disease (P = 0.07 for valvular disease). Patients with higher PASP had higher incidence of new-onset right ventricular dysfunction. In patients with end-stage renal disease, PASP increases over time. Changes are moderately predictable. Higher PASP predicted development of right ventricular dysfunction.

Heterogeneity of patients with arterial hypertension and heart failure with preserved left ventricular ejection fraction according to the clinical and structural-functional profile of the heart and arteries depending on the available diagnostic criteria o

The aim — to determine the frequency of different combinations of criteria of heart failure (HF) with preserved ventricular ejection fraction (EF), established by the European Society of Cardiology (ESC) in 2016, in symptomatic patients with arterial hypertension (AH) in clinical practice and to assess their relationship to the clinical profile and the structural and functional state of the heart and arteries.Materials and methods. The study included 103 patients aged 43 to 85 years, with symptoms and signs of HF, AH and LVEF ³ 50 %, which had signs of diastolic dysfunction (DD) according to Doppler EchoCG data. The level of N­terminal fragment of the brain natriuretic peptide (NT­proBNP) was assessed by an enzyme immunoassay. The pulse wave velocity (carotid­femoral) (PWVcf) was assessed using applanation tonometry. Using ECG, the back wall thickness (BWT) of the left ventricle (LV) and interventricular septal thickness (IST), end­diastolic index (EDI) and end­systolic index (ESI) of the LV, left ventricular myocardial index (LVMI), left atrium volume index (LAVI) and left ventricular ejection fraction (LVEF). Early (E) and late diastolic left ventricular filling velocity (A), E/A ratio, diastolic speed of septal and lateral motion of fibrous mitral valve ring, the mean value e¢, the relation Е/e¢, tricuspidal regurgitation velocity (TRV), the deceleration time of early diastolic filling (DT) and left ventricular isovolumic relaxation time (IVRT), and systolic pulmonary artery pressure (SPAP) — with the use of Doppler EchoCG were evaluated. Patients with ratio E/e¢ 9 — 13 at rest underwent diastolic stress test.Results and discussion. According to the ESC algorithm, HF was absent in 11 (10.6 %) patients (group 1); 28 (30.4 %) patients had structural criteria and no functional criteria (group 2); 64 (69.5 %) patients had three structural and functional criteria of HF according to ESC algorithm (group 3). High left ventricular filling pressure (LVFP) was found in all 35 (54.6 %) patients of group 3 without atrial fibrillation (AF) and in 7 (26.9 %) patients of group 3. Normal left ventricular filling pressure was found in all patients of group 1 and 7 (26.9 %) patients of group 2. Left ventricular filling pressure could not be identified in 4 (36.3 %) patients of group 1 and 12 (46.1 %) patients of group 2 (all p < 0.01). AF was present in 29 (45.3 %) patients of group 3 and in 2 patients (7.1 %) of group 2 (p < 0.01). Increase in SPAP was noted in 52 (81.2 %) patients of group 3 and 4 (14.2 %) patients of group 2 (p < 0.01). The dilatation of the right ventricle (RV) was more pronounced in group 3 than in groups 2 and 1 (p < 0.01 and p < 0.05). Patients of groups 1 and 2 were comparable according to PWVcf, patients of group 3 had higher values of this indicator than those of groups 2 and 1 (all p < 0.01). E/e¢ while exercise stress was more than 13 in 78.5 % patients of group 2 and in 18.2 % of group 1 (p < 0.01). Groups 2 and 3 had high levels of NT­proBNP — 438.4 ± 97.2 and 1057.3 ± 157.0 pg/ml, accordingly, in group 1 its level was 199.7 ± 17.2 pg/ml (all p < 0.01).Conclusions. In 70 % of patients with hypertension and clinical signs of HF, both structural and functional criteria of diagnosis of HF with preserved LV EF were defined according to the recommendations of the ESC (2016), which was associated with an increase in LV feeling pressure, AF — in 45 %, pulmonary hypertension — in 52 (81.2 %), with right ventricle dilatation — in 81 % and 27 % increase in PWVcf in compared with age and sex matched patients with AH without HF. AH patients with only two structural criteria of heart failure with a preserved LVEF in the absence of functional criteria (30 % of cases) differ from patients with AH without HF in terms of the level of NT­proBNP, an increase in E/e’ while exercise (85 % of cases) and comparable severity of clinical signs of heart failure.

10. Effect of pacemaker/defibrillator lead extraction on pulmonary artery systolic pressure

As the number of cardiac device implantations are on a rise, there is a parallel increase in their long-term complications including device-related infection that will require lead extraction. As the detachment of fibrosed debris reaching the pulmonary trunk can occur during the extraction, the risk of developing new-onset Pulmonary Hypertension (P. HTN) increases with every extraction. Yet, there is paucity of evidence to support such claim. Given the clinical significance of such findings, we sought to determine the risk. A chart review of 113 patients whom underwent lead extraction at Prince Sultan Cardiac Center in Saudi Arabia during the period of Jan, 2002 to Jul, 2015 was carried out. Six patients had lead extraction twice, making the total number of extractions to be 119. Of this study cohort, only 45 cases had Pulmonary Artery Systolic Pressure (PASP) measurement via Transthoracic Echocardiography (TTE) prior to and after device extraction. PASP measurements were obtained as reported whether a single measurement or a range between two readings, and an average was calculated in case of two readings. A difference of 10 mmHg or more in the PASP, whether progression or improvement, was considered clinically significant.Median follow up of TTE after lead and device extraction was 5 months. Out of 45 patients, 31 (68.9%) were males and 14 (31.1%) were females. Average age was 46.5 (SD = 17) years. Eleven patients (24.4%) experienced a significant increase of PASP after lead extraction (10 had normal pressure readings before extraction, and only one had progression to a more severe form of the disease), 9 patients (20.0%) showed improvement, and the remaining (55.6%) did not show any significant change in PASP. Average implantation-to-extraction duration of the leads was higher among those who had no pressure difference (50.6 vs. 23.3 months). When looking through potential predictors that may increase the likelihood of developing P. HTN, there was no association with a pre-existing lead-attached vegetation (2 patients only), nor the type of lead (6 high-voltage vs. 5 pacing leads across the tricuspid valve). In patients who developed P. HTN, 8 (72.7%) had their devices extracted as a result of a complicated infection (wound infections and/or infective endocarditis), as opposed to 3 (27.3%) whom underwent device extraction for other indications. Our simple descriptive study showed that the risk of developing P. HTN following lead and device extraction is negligible. However, our findings should be interpreted in the light of the limitations such as a small sample size and lack of comparable control group. Paucity of data and evidence on the long-term complications subsequent to device and lead extractions will be a subject of further exploration given the potential connection to patient outcomes and management.

Pretransplant echocardiographic parameters as markers of posttransplant outcomes in liver transplant recipients.

Despite advances in liver transplantation and preoperative risk stratification, there remains significant posttransplant morbidity and mortality from cardiovascular and renal disease. There are limited and conflicting data on the role of pretransplant echocardiography to predict these outcomes. The purpose of our study was to determine if pretransplant echocardiographic parameters were associated with posttransplant survival and the development of incident cardiovascular events and chronic kidney disease (CKD). We conducted a retrospective cohort study of 397 adult liver transplant recipients at the University of Pennsylvania from January 1, 2005 to September 30, 2014. Patients with acute liver failure, those without a diagnosis of cirrhosis (eg, polycystic liver disease without portal hypertension), retransplants, and multiorgan transplants were excluded. In multivariable Cox regression models, tricuspid regurgitation graded greater than mild was associated with significantly increased posttransplant mortality (hazard ratio, 1.68; 95% confidence interval [CI], 1.03-2.75; P = 0.04). In multivariable competing risk models, increasing pulmonary artery systolic pressure (PASP) was associated with significantly increased risk of hospitalization for myocardial infarction or heart failure (subhazard ratio per 5 mm Hg increase in PASP, 1.79; 95% CI, 1.48-2.17; P < 0.001). In multivariable competing risk models, increased left ventricular ejection fraction (LVEF) was associated with a numerical but nonsignificant increased risk of stage 4 or 5 CKD (subhazard ratio, 1.11 per 5% increase in LVEF; 95% CI, 0.99-1.24; P = 0.07). In a post hoc analysis, LVEF ≥ 65% was the best cutoff for increased risk of CKD (subhazard ratio, 1.75; 95% CI, 1.06-2.89; P = 0.03). In conclusion, several pretransplant echocardiographic parameters were associated with posttransplant morbidity and mortality, suggesting that pretransplant echocardiography may be used as a tool to risk-stratify patients for posttransplant outcomes.

Serial Echocardiographic Assessment of Patients (Pts) with Relapsed Multiple Myeloma (RMM) Receiving Carfilzomib and Dexamethasone (Kd) Vs Bortezomib and Dexamethasone (Vd): A Substudy of the Phase 3 Endeavor Trial (NCT01568866)

Serial Echocardiographic Assessment of Patients (Pts) with Relapsed Multiple Myeloma (RMM) Receiving Carfilzomib and Dexamethasone (Kd) Vs Bortezomib and Dexamethasone (Vd): A Substudy of the Phase 3 Endeavor Trial (NCT01568866)

Possibilities of electrocardiographic and decartographic parametersin the diagnosis of right ventricular overload in patients with pulmonary arterial hypertension

Aim: to study the possibilities of electrocardiographic and decartographic parameters to identify and assess the severity of overload of the right ventricle in pulmonary arterial hypertension (PAH) patients. Material and methods. Decartographic parameters of the activation duration and repolarization acceleration were studied in 120 patients with PAH and 120 healthy individuals compared to traditional ECG criteria of right ventricular hypertrophy. Moderate increase in systolic pulmonary artery pressure (SPAP) was determined as SPAP 30-50 mm Hg; severe as SPAP greater than 50 mm Hg. Results. The most informative decartographic indicators for the separation of the PAH group as a whole, and the subgroup with moderate increase in SPAP and normal group were the X and Z components of the repolarization acceleration vector and the index of activation duration, and for the separation of subgroups with moderate and severe increase in SPAP - Y component of the repolarization acceleration vector and index of activation duration. Decartographic parameters were more informative as compared with ECG criteria. Conclusion. In patients with PAH decartographic parameters can be useful for detecting the overload of the right ventricle and the assessment of its severity.

Возможности электрокардиографических и дэкартографических параметров в диагностике перегрузки правого желудочка у больных артериальной легочной гипертензией

Aim: to study the possibilities of electrocardiographic and decartographic parameters to identify and assess the severity of overload of the right ventricle in pulmonary arterial hypertension (PAH) patients. Material and methods. Decartographic parameters of the activation duration and repolarization acceleration were studied in 120 patients with PAH and 120 healthy individuals compared to traditional ECG criteria of right ventricular hypertrophy. Moderate increase in systolic pulmonary artery pressure (SPAP) was determined as SPAP 30-50 mm Hg; severe as SPAP greater than 50 mm Hg. Results. The most informative decartographic indicators for the separation of the PAH group as a whole, and the subgroup with moderate increase in SPAP and normal group were the X and Z components of the repolarization acceleration vector and the index of activation duration, and for the separation of subgroups with moderate and severe increase in SPAP - Y component of the repolarization acceleration vector and index of activation duration. Decartographic parameters were more informative as compared with ECG criteria. Conclusion. In patients with PAH decartographic parameters can be useful for detecting the overload of the right ventricle and the assessment of its severity.

Hypoxia, not pulmonary vascular pressure, induces blood flow through intrapulmonary arteriovenous anastomoses.

Blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) is increased by acute hypoxia during rest by unknown mechanisms. Oral administration of acetazolamide blunts the pulmonary vascular pressure response to acute hypoxia, thus permitting the observation of IPAVA blood flow with minimal pulmonary pressure change. Hypoxic pulmonary vasoconstriction was attenuated in humans following acetazolamide administration and partially restored with bicarbonate infusion, indicating that the effects of acetazolamide on hypoxic pulmonary vasoconstriction may involve an interaction between arterial pH and PCO2. We observed that IPAVA blood flow during hypoxia was similar before and after acetazolamide administration, even after acid-base status correction, indicating that pulmonary pressure, pH and PCO2 are unlikely regulators of IPAVA blood flow. Blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) is increased with exposure to acute hypoxia and has been associated with pulmonary artery systolic pressure (PASP). We aimed to determine the direct relationship between blood flow through IPAVA and PASP in 10 participants with no detectable intracardiac shunt by comparing: (1) isocapnic hypoxia (control); (2) isocapnic hypoxia with oral administration of acetazolamide (AZ; 250 mg, three times a day for 48 h) to prevent increases in PASP; and (3) isocapnic hypoxia with AZ and 8.4% NaHCO3 infusion (AZ + HCO3 (-) ) to control for AZ-induced acidosis. Isocapnic hypoxia (20 min) was maintained by end-tidal forcing, blood flow through IPAVA was determined by agitated saline contrast echocardiography and PASP was estimated by Doppler ultrasound. Arterial blood samples were collected at rest before each isocapnic-hypoxia condition to determine pH, [HCO3(-)] and Pa,CO2. AZ decreased pH (-0.08 ± 0.01), [HCO3(-)] (-7.1 ± 0.7 mmol l(-1)) and Pa,CO2 (-4.5 ± 1.4 mmHg; P < 0.01), while intravenous NaHCO3 restored arterial blood gas parameters to control levels. Although PASP increased from baseline in all three hypoxic conditions (P < 0.05), a main effect of condition expressed an 11 ± 2% reduction in PASP from control (P < 0.001) following AZ administration while intravenous NaHCO3 partially restored the PASP response to isocapnic hypoxia. Blood flow through IPAVA increased during exposure to isocapnic hypoxia (P < 0.01) and was unrelated to PASP, cardiac output and pulmonary vascular resistance for all conditions. In conclusion, isocapnic hypoxia induces blood flow through IPAVA independent of changes in PASP and the influence of AZ on the PASP response to isocapnic hypoxia is dependent upon the H(+) concentration or Pa,CO2.

Exercise-Induced Abnormal Increase of Systolic Pulmonary Artery Pressure in Adult Patients With Sickle Cell Anemia: An Exercise Stress Echocardiography Study.

Pulmonary hypertension (PH) at rest is a risk factor for death in patients with sickle cell anemia (SCA). Exercise echocardiography (EE) can detect latent PH. We sought to investigate the occurrence of exercise-induced abnormal response of systolic pulmonary artery pressure (SPAP) in adult patients with SCA and normal SPAP at rest, and to identify the independent predictors of this abnormal response. Forty-four adult patients with SCA and normal SPAP at rest (tricuspid regurgitant jet flow velocity [TRV] <2.5m/sec) were studied and divided into 2 groups: exhibiting normal SPAP after treadmill EE (TRV≤2.7m/sec) (G1), and exhibiting abnormal exercise-induced increase of SPAP (TRV>2.7m/sec) (G2). TRV cutoff points at rest and during EE were based on data from healthy-matched control subjects. Abnormal response of SPAP with exercise occurred in 57% of the sample (G2), with mean TRV level of 3.39±0.41m/sec (range 2.8-4.5m/sec), significantly higher than those of G1 (2.29±0.25m/sec, range 2.0-2.7m/sec; P<0.001). Multivariate analysis identified TRV value in resting conditions ≥2.25m/sec (P<0.05), left atrial volume index ≥41mL/m2 (P<0.05), and a E/e'-waves ratio ≥6.3 (P<0.05) as independent predictors of exercise-induced increase of SPAP. We concluded that adult patients with SCA and normal SPAP at rest may exhibit abnormal exercise-induced increase in SPAP, which was independently related to resting TRV levels, and indices of diastolic impairment and left ventricular filling pressure.

Elevated pulmonary artery systolic pressure predicts heart failure admissions in African Americans: Jackson Heart Study.

Although elevated pulmonary artery systolic pressure (PASP) is associated with heart failure (HF), whether PASP measurement can help predict future HF admissions is not known, especially in African Americans who are at increased risk for HF. We hypothesized that elevated PASP is associated with increased risk of HF admission and improves HF prediction in African American population. We conducted a longitudinal analysis using the Jackson Heart Study cohort (n=3125; 32.2% men) with baseline echocardiography-derived PASP and follow-up for HF admissions. Hazard ratio for HF admission was estimated using Cox proportional hazard model adjusted for variables in the Atherosclerosis Risk in Community (ARIC) HF prediction model. During a median follow-up of 3.46 years, 3.42% of the cohort was admitted for HF. Subjects with HF had a higher PASP (35.6±11.4 versus 27.6±6.9 mm Hg; P<0.001). The hazard of HF admission increased with higher baseline PASP (adjusted hazard ratio per 10 mm Hg increase in PASP: 2.03; 95% confidence interval, 1.67-2.48; adjusted hazard ratio for highest [≥33 mm Hg] versus lowest quartile [<24 mm Hg] of PASP: 2.69; 95% confidence interval, 1.43-5.06) and remained significant irrespective of history of HF or preserved/reduced ejection fraction. Addition of PASP to the ARIC model resulted in a significant improvement in model discrimination (area under the curve=0.82 before versus 0.84 after; P=0.03) and improved net reclassification index (11-15%) using PASP as a continuous or dichotomous (cutoff=33 mm Hg) variable. Elevated PASP predicts HF admissions in African Americans and may aid in early identification of at-risk subjects for aggressive risk factor modification.

Risk Factors for Progression of Functional Tricuspid Regurgitation

The aim of this study was to determine the risk factors for tricuspid regurgitation (TR) progression in a contemporary population of patients referred for echocardiography. In a case-control study, we compared 100 consecutive patients with TR progression on serial echocardiograms (trivial or mild TR on the first echocardiogram and moderate or severe functional TR on a follow-up echocardiogram) with 100 patients matched for age and gender, having mild TR at baseline and no TR progression. Mean age was 72 ± 10 years, 55% were males, and time to TR progression was 5.3 ± 2.9 years. Less than 10% had rheumatic heart disease. Left ventricular ejection fraction was preserved (≥50%) in 85% of the TR progression group and in 74% of the control group (p = 0.06). Pulmonary artery systolic pressure increased from 41 ± 16 to 56 ± 18 mm Hg in the TR progression group and decreased from 44 ± 13 to 41 ± 11 mm Hg in the control group (p <0.0001). Independent risk factors for TR progression were pulmonary artery systolic pressure change during follow-up (odds ratio per 1 mm Hg 1.14, 95% confidence interval 1.06 to 1.23, p <0.0001), permanent atrial fibrillation (odds ratio 14.3, 95% confidence interval 4.6 to 44.2, p <0.0001), and coronary artery disease (odds ratio 5.7, 95% confidence interval 1.4 to 22.8, p = 0.015). All-cause mortality at 3 years was 20% for patients without TR progression, 42% for moderate TR, and 63% for severe TR, p <0.0001. Progression-to-severe TR independently predicted subsequent mortality. In conclusion, in patients with low prevalence of rheumatic heart disease and preserved left ventricular ejection fraction, pulmonary artery systolic pressure increase and permanent atrial fibrillation were the most powerful risk factors for TR progression. Progression-to-severe TR was an independent predictor of subsequent mortality.

Abstract 18738: Pulmonary Artery Systolic Pressures Increase With Aging: A Longitudinal, Population Based Study

Background: A community based, cross-sectional echo survey demonstrated that pulmonary artery systolic pressure (PASP) increases with age and that PASP is associated with systemic arterial stiffness, Doppler estimated left ventricular (LV) filling pressures and lung function. Longitudinal assessment of PASP is needed to confirm cross-sectional observations. Objectives: To assess the whether PASP changes over time in longitudinally studied subjects and determine whether changes in PASP are associated with changes in systemic vascular stiffness, LV filling pressures or lung function. Methods: A random sample (n=2042) of the Olmsted County, MN population over age 40 underwent echo, record review and spirometry between 1997-2000 (Exam 1). A subset (n=1402) underwent repeat studies four years later (2001-2004; Exam 2). The current analysis includes the 723 subjects with paired PASP measurements. Changes ([[Unable to Display Character: ▵]]) in PASP, systemic arterial stiffness (pulse pressure; PP), LV filling pressure (E/e’) and lung function (% age/sex expected forced expiratory volume, %FEV1) were assessed. Results: At Exam 1, the median (interquartile range) age was 62 (69-70) years (62% female). Median time between exams was 48 (47-49) months. PASP increased from 26.1 (24.4-30.0) mmHg at Exam 1 to 28.0 (24.4-32.0) mmHg at Exam 2 (p&lt;0.0001 by paired t test) for an average (SD) [[Unable to Display Character: ▵]] of 1.2 ± 5.5 mmHg. Adjusting for age and PASP at Exam 1, [[Unable to Display Character: ▵]]PASP was associated with [[Unable to Display Character: ▵]] age with an increase (parameter estimate (pe) ± standard error (se)) of 1.4±0.7 mmHg per year increase in age (p=0.046). [[Unable to Display Character: ▵]]PASP was not associated with sex and there was no age-sex interaction. Adjusting for age and PASP at Exam 1, [[Unable to Display Character: ▵]] age and Exam 1 values for PP, E/e or %FEV1 as appropriate, [[Unable to Display Character: ▵]]PASP was associated with [[Unable to Display Character: ▵]] PP (pe±se = 0.03±0.01 mmHg; p=0.01) [[Unable to Display Character: ▵]]E/e’ (pe±se = 0.21±0.06 mmHg, p=0.001) and [[Unable to Display Character: ▵]]%FEV1 (-0.09±0.02 mmHg, p&lt;0.0001) suggesting that increases in PASP were related to increases in vascular stiffening, increases in LV filling pressures and declining lung function. Conclusions: In this longitudinal, population based study we find that PASP increases with aging and that increases in PASP over time are related to increases in systemic vascular stiffness and LV filling pressures and decreases in lung function.

RV Contractility and Exercise-Induced Pulmonary Hypertension in Chronic Mountain Sickness: A Stress Echocardiographic and Tissue Doppler Imaging Study

The aim of this study was to evaluate right ventricular (RV) and left ventricular function and pulmonary circulation in chronic mountain sickness (CMS) patients with rest and stress echocardiography compared with healthy high-altitude (HA) dwellers. CMS or Monge's disease is defined by excessive erythrocytosis (hemoglobin >21 g/dl in males, 19 g/dl in females) and severe hypoxemia. In some cases, a moderate or severe increase in pulmonarypressure is present, suggesting a similar pathogenesis of pulmonary hypertension. In La Paz (Bolivia, 3,600 m sea level), 46 CMS patients and 40 HA dwellers of similar age were evaluated at rest and during semisupine bicycle exercise. Pulmonary artery pressure (PAP), pulmonary vascular resistance, and cardiac function were estimated by Doppler echocardiography. Compared with HA dwellers, CMS patients showed RV dilation at rest (RV mid diameter: 36±5 mmvs. 32 ± 4 mm, CMS vs. HA, p= 0.001) and reduced RV fractional area change both at rest (35± 9% vs. 43±9%, p= 0.002) and during exercise (36 ± 9% vs. 43 ± 8%, CMS vs. HA, p= 0.005). The RV systolic longitudinal function (RV-S') decreased in CMS patients, whereas it increased in the control patients (p<0.0001) at peak stress. The RV end-systolic pressure-area relationship, a load independent surrogate of RV contractility, was similar in CMS patients and HA dwellers with a significant increase in systolic PAP and pulmonary vascular resistance in CMS patients (systolic PAP: 50 ± 12 mm Hg vs. 38 ± 8 mm Hg, CMS vs. HA, p < 0.0001; pulmonary vascular resistance: 2.9 ± 1 mm Hg/min/l vs.2.2 ± 1 mm Hg/min/l, p= 0.03). Both groups showed comparable systolic and diastolic left ventricular function both at rest and during stress. Comparable RV contractile reserve in CMS and HA suggests that the lower resting values of RV function in CMS may represent a physiological adaptation to chronic hypoxic conditions rather than impaired RV function. (Chronic Mountain Sickness, Systemic Vascular Function [CMS]; NCT01182792).

Assessment and Prognostic Relevance of Right Ventricular Contractile Reserve in Patients With Severe Pulmonary Hypertension

This study sought to analyze a new approach to assess exercise-induced pulmonary artery systolic pressure (PASP) increase by means of stress Doppler echocardiography as a possible measure of right ventricular contractile reserve in patients with severe pulmonary hypertension and right heart failure. In this prospective study, patients with invasively diagnosed pulmonary arterial hypertension or inoperable chronic thromboembolic pulmonary hypertension and impaired right ventricular pump function despite a stable targeted pulmonary arterial hypertension medication underwent a broad panel of noninvasive assessments, including stress echocardiography and cardiopulmonary exercise testing. On the basis of the assumption that exercise-induced PASP is a measure of right ventricular contractile reserve, patients were classified into 2 groups according to an exercise-induced PASP increase above or below the median. Patients were followed up for 3.0 ± 1.8 years. Univariate and multivariate analyses were used for factors predicting survival. Of 124 patients, 66 were below the median exercise-induced PASP increase of 30 mm Hg (low PASP), and 58 patients were above the median (high PASP). These groups were not significantly different in terms of medication and resting hemodynamics. Low PASP was associated with a significantly lower 6-minute walking distance, peak o2 per kilogram, and 1-, 3-, and 4-year survival rates (92%, 69%, and 48%, respectively, versus 96%, 92%, and 89%). In the multivariate Cox model analysis adjusted for age and sex, PASP increase during exercise and peak o2 per kilogram remained independent prognostic markers (hazard ratio, 2.56 for peak o2 per kilogram and 2.84 for PASP increase). Exercise-induced PASP increase is of high clinical and prognostic relevance in pulmonary hypertension patients and may indicate right ventricular contractile reserve. Stress Doppler echocardiography may be a useful tool for prognostic assessment in pulmonary hypertension patients.

Effect of Acetazolamide and Gingko Biloba on the Human Pulmonary Vascular Response to an Acute Altitude Ascent

Acetazolamide and gingko biloba are the two most investigated drugs for the prevention of acute mountain sickness (AMS). Evidence suggests that they may also reduce pulmonary artery systolic pressure (PASP). To investigate whether these two drugs for AMS prevention also reduce PASP with rapid airlift ascent to high altitude, a randomized controlled trial was conducted on 28 healthy young men with acetazolamide (125 mg bid), gingko biloba (120 mg bid), or placebo for 3 days prior to airlift ascent (397 m) and for the first 3 days at high altitude (3658 m). PASP, AMS, arterial oxygen saturation (Sao2), mean arterial pressure (MAP), heart rate (HR), forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), and peak expiratory flow (PEF) were assessed both at 397 m and 3658 m. HR, PEF, and PASP increased with altitude exposure (p<0.05), and SaO2 decreased (p<0.05). PASP with acetazolamide (mean at 3658 m, 26.2 mm Hg; incremental change, 4.7 mm Hg, 95% CI., 2.6-6.9 mm Hg) was lower than that with ginkgo biloba (mean at 3658 m, 33.7 mm Hg, p=0.001; incremental change, 13.1 mm Hg, 95%CI., 9.6-16.5 mm Hg, p=0.002), and with placebo (mean at 3658 m, 34.7 mm Hg, p<0.001; 14.4 mm Hg, 95% CI., 8.8-20.0 mm Hg, p=0.001). The data show that a low prophylactic dosage of acetazolamide, but not gingko biloba, mitigates the early increase of PASP in a quick ascent profile.

Impaired right ventricular function and elevated pulmonary artery pressure: a lethal combination

Impaired right ventricular function and elevated pulmonary artery pressure: a lethal combination

The pulmonary vascular response to combined activation of the muscle metaboreflex and mechanoreflex

Muscle metabo- and mechanoreflexes are known to influence systemic cardiovascular responses to exercise. Whether interplay between these reflexes is operant in the control of the pulmonary vascular response to exercise is unknown. The aim of this study was to assess the pulmonary vascular response to the combined activation of the two muscle reflexes. Nine healthy subjects performed a bout of isometric calf plantarflexion exercise during local circulatory occlusion, which was continued for 9 min postexercise (PECO). At 5 min into PECO the calf muscle was passively stretched for 180 s. A control (no exercise) protocol was also undertaken. Heart rate, blood pressure measurements and echocardiographically determined estimates of systolic pulmonary artery pressure (SPAP) and cardiac output ( ) were obtained at intervals throughout the two protocols. Elevations in SPAP (by 22.51 ± 2.61%), (by 26.92 ± 2.99%) and mean arterial pressure (by 15.38 ± 2.29%) were noted during isometric exercise in comparison to baseline (all P < 0.05). Increases in SPAP and mean arterial pressure persisted during PECO (All P < 0.05), whereas returned to resting levels. These increases in mean arterial pressure and SPAP were sustained during stretch which significantly elevated (All P < 0.05). These data suggest that activation of the muscle mechanoreflex attenuated the increases in pulmonary vascular resistance caused by metaboreflex activation. This finding has important implications for the regulation of pulmonary haemodynamics during human exercise.

Clinical and echocardiographic correlations of exercise-induced pulmonary hypertension in systemic sclerosis: A multicenter study

Patients with systemic sclerosis (SSc) are at risk for developing pulmonary hypertension, which is associated with a poor prognosis. Exercise Doppler echocardiography enables the identification of exercise-induced increase in pulmonary artery systolic pressure (PASP) and may provide a thorough noninvasive hemodynamic evaluation. The aim of this study was to evaluate the clinical and echocardiographic determinants of exercise-induced increase in PASP in a large population of patients with SSc. We selected 164 patients with SSc (age 58 ± 13 years, 91% female) with normal resting PASP (<40 mm Hg) who underwent a comprehensive 2-dimensional and Doppler echocardiography and graded bicycle semisupine exercise Doppler echocardiography. Pulmonary artery systolic pressure, cardiac output, and pulmonary vascular resistance (PVR) were estimated noninvasively. Cutoff values of PASP ≥50 mm Hg and PVR ≥3.0 Wood Units at peak exercise were considered a significant exercise-induced increase in PASP and PVR, respectively. Sixty-nine (42%) patients showed a significant exercise-induced increase in PASP. Among them, peak PVR ≥3 Wood Units was present only in 11% of patients, about 5% of the total population. Univariate analysis showed that age, presence of interstitial lung disease, and both right and left diastolic dysfunction are predictors of peak PASP ≥50 mm Hg, but none of these parameters predict elevated peak PVR. Exercise-induced increase in PASP occurs in almost one-half of patients with SSc with normal resting PASP. Peak exercise PASP is affected by age, interstitial lung disease, and right and left ventricular diastolic dysfunction and, only in 5% of the patients, is associated with an increase in PVR during exercise, suggesting heterogeneity of the mechanisms underlying exercise-induced pulmonary hypertension in SSc.

Prognostic Value of Pulmonary Hypertension in Patients Undergoing Surgery for Degenerative Mitral Valve Disease with Leaflet Prolapse

The aim of this study was to evaluate the impact of pulmonary hypertension (PH) on early and late outcomes following surgery in patients with degenerative mitral regurgitation. The study included 270 patients who had undergone isolated mitral valve surgery (MVS) for leaflet prolapse during 1998 to 2010. Pulmonary artery systolic pressure (PASP) was measured with Doppler echocardiography pre- and postoperatively. The impact of PH (PASP > 50 mmHg) on mortality and the potential for postoperative resolution of preoperatively elevated PASP was retrospectively analyzed. The incidence of PH was 27% (n = 74/270). Postoperative normalization, or reduction of preoperative PASP, was demonstrated in 87% of the patients with PH at a median of two months (interquartile range 1 to 19). Absent improvement or a postoperative increase in PASP was independently predicted by age (OR 1.08, 95% CI 1.02-1.14, p = 0.010). Preoperative PH resulted in a fourfold higher risk of postoperative mortality (HR 4.3, 95% CI 1.1-17.4, p = 0.039) during the first three years of follow-up. PH is an independent predictor of mortality during the initial three years following MVS. The majority of patients with PH demonstrated a reduction of preoperatively elevated PASP following surgery and the increased risk of mortality gradually decreased after three years. Our findings support early admission for mitral valve surgery before the occurrence of PH.

Catecholamine-induced opening of intrapulmonary arteriovenous anastomoses in healthy humans at rest

The mechanism or mechanisms that cause intrapulmonary arteriovenous anastomoses (IPAVA) to either open during exercise in subjects breathing room air and at rest when breathing hypoxic gas mixtures, or to close during exercise while breathing 100% oxygen, remain unknown. During conditions when IPAVA are open, plasma epinephrine (EPI) and dopamine (DA) concentrations both increase, potentially representing a common mechanism. The purpose of this study was to determine whether EPI or DA infusions open IPAVA in resting subjects breathing room air and, subsequently, 100% oxygen. We hypothesized that these catecholamine infusions would open IPAVA. We performed saline-contrast echocardiography in nine subjects without a patent foramen ovale before and during serial EPI and DA infusions while breathing room air and then while breathing 100% oxygen. Bubble scores (0-5) were assigned based on the number and spatial distribution of bubbles in the left ventricle. Pulmonary artery systolic pressure (PASP) was estimated using Doppler ultrasound, while cardiac output (Q(C)) was measured using echocardiography. Bubble scores were significantly greater during EPI infusions of 80-320 ng·kg(-1)·min(-1) compared with baseline when subjects breathed room air; however, bubble scores did not increase when they breathed 100% oxygen. At comparable Q(C) and PASP, intravenous DA (16 μg·kg(-1)·min(-1)) and EPI (40 ng·kg(-1)·min(-1)) resulted in identical bubble scores. Subsequent studies revealed that β-blockade did not prevent hypoxia-induced opening of IPAVA. We suggest that increases in Q(C) or PASP (or both) secondary to EPI or DA infusions open IPAVA in normoxia. The closing mechanism associated with breathing 100% oxygen is independent from the opening mechanisms.