Decrease In Systolic Pulmonary Artery Pressure Research Articles

Decreased time constant of the pulmonary circulation in chronic thromboembolic pulmonary hypertension

This study analyzed the relationship between pulmonary vascular resistance (PVR) and pulmonary arterial compliance (Ca) in patients with idiopathic pulmonary arterial hypertension (IPAH) and proximal chronic thromboembolic pulmonary hypertension (CTEPH). It has recently been shown that the time constant of the pulmonary circulation (RC time constant), or PVR × Ca, remains unaltered in various forms and severities of pulmonary hypertension, with the exception of left heart failure. We reasoned that increased wave reflection in proximal CTEPH would be another cause of the decreased RC time constant. We conducted a retrospective analysis of invasive pulmonary hemodynamic measurements in IPAH (n = 78), proximal CTEPH (n = 91) before (pre) and after (post) pulmonary endarterectomy (PEA), and distal CTEPH (n = 53). Proximal CTEPH was defined by a postoperative mean pulmonary artery pressure (PAP) of ≤25 mmHg. Outcome measures were the RC time constant, PVR, Ca, and relationship between systolic and mean PAPs. The RC time constant for pre-PEA CTEPH was 0.49 ± 0.11 s compared with post-PEA-CTEPH (0.37 ± 0.11 s, P < 0.0001), IPAH (0.63 ± 0.14 s, P < 0.001), and distal CTEPH (0.55 ± 0.12 s, P < 0.05). A shorter RC time constant was associated with a disproportionate decrease in systolic PAP with respect to mean PAP. We concluded that the pulmonary RC time constant is decreased in proximal CTEPH compared with IPAH, pre- and post-PEA, which may be explained by increased wave reflection but also, importantly, by persistent structural changes after the removal of proximal obstructions. A reduced RC time constant in CTEPH is in accord with a wider pulse pressure and hence greater right ventricular work for a given mean PAP.

Reversal of pulmonary hypertension in children after adenoidectomy or adenotonsillectomy

IntroductionAdenotonsillar hypertrophy is a common condition in pediatric patients with upper respiratory airways complaints, and pulmonary arterial hypertension (PAH) may be one complication of that condition. ObjectivesTo study the occurrence of PAH (mean pulmonary artery pressure higher than or equal to 25mmHg) in a group of children with adenotonsillar hypertrophy and upper respiratory complaints (snoring or oral breathing), and to verify the pulmonary arterial pressure (PAP) changes after adenotonsillectomy. Study designCase–control prospective study. SettingsStudy conducted at São Lucas Hospital, approaching both public and private sector. Subject and methodsThirty-three pediatric patients with adenotonsillar hypertrophy and evidence of obstructive upper airways complaints were treated with adenotonsillectomy. All 33 patients underwent echocardiogram before and after the surgery with determination of the pulmonary arterial pressure (PAP), through either the tricuspid regurgitation or artery linear flow acceleration time estimation. Similar determinations were performed in 10 normal non operated controls. ResultsPulmonary hypertension was verified 12 (36%) of the 33 patients with adenotonsillar hypertrophy. Adenoidectomy or adenotonsillectomy was associated to a significant 27% decrease in mean PAP (27±2.8 to 20±5.1mmHg, p<0.001) and to a non significant 26% decrease in systolic PAP (35±6.2mmHg to 25±0.5mmHg, p=0.243). The PAP values in children with no pulmonary hypertension were not changed after the surgery. ConclusionsIn children with pulmonary hypertension associated to adenotonsillar hypertrophy, the adenotonsillectomy decreased PAP to normal values in all patients.

Clinical Profile, Prognostic Implication, and Response to Treatment of Pulmonary Hypertension in Patients With Severe Aortic Stenosis

The incidence, correlates, and prognostic implications of pulmonary hypertension (PH) are unclear in patients with severe aortic stenosis (AS). We studied 509 patients with severe AS evaluated for transcatheter aortic valve implantation (TAVI). Patients were divided into groups based on pulmonary artery systolic pressure (PASP): group I, 161 (31.6%) with PASP <40 mm Hg; group II, 175 (34.3%) with PASP 40 to 59 mm Hg; and group III, 173 (33.9%) with PASP ≥ 60 mm Hg. Group III patients were more symptomatic and had higher creatinine levels and higher left ventricular end-diastolic pressure. Transpulmonary gradient was >12 mm Hg in 17 patients (10.5%), 31 patients (17.7%), and 80 patients (46.2%) in groups I through III, respectively. In a median follow-up of 202 days (73 to 446) mortality rates were 35 (21.7%), 69 (39.3%), and 85 (49.1%) in groups I through III, respectively (p <0.001). Immediately after TAVI, in patients with PASP >40 mm Hg there was significant decrease in PASP (63.1 ± 16.2 to 48.8 ± 12.4 mm Hg, p <0.0001), which remained at 1 year (50.1 ± 13.1 mm Hg, p = 0.04). After surgical aortic valve replacement there was a significant immediate decrease in PASP (66.1 ± 16.3 to 44.7 ± 14.2 mm Hg, p <0.0001), which persisted at 3 to 12 months (44.8 ± 20.1 mm Hg, p <0.001). In patients who underwent balloon aortic valvuloplasty, PASP decreased immediately after the procedure (63.2 ± 14.8 to 51.8 ± 17.1 mm Hg, p <0.0001), yet at 3 to 12 months pressure returned to baseline levels (57.4 ± 17.0 mm Hg, p = 0.29). In conclusion, patients with severe AS have a high prevalence of PH, and in patients with severe AS increased PASP is associated with increased mortality. Surgical aortic valve replacement and TAVI are effective treatments for these patients and result in a significant PASP decrease.

Role of Oral Sildenafil in the Treatment of Right Ventricular Dysfunction After Heart Transplantation

Objective Right ventricular dysfunction (RVD) after heart transplantation is a major complication, especially in patients with pulmonary hypertension (PH). Herein we have presented our initial experience with oral sildenafil for RVD following heart transplantation. Materials and Methods From February 2006 to February 2008, 10 patients (7 males and 3 females) of overall mean age of 56.7 ± 9.5 years suffered from acute RVD immediately after heart transplantation. Preoperative hemodynamic data before and after a vasodilatation test (sodium nitroprusside; NTP) showed: systolic pulmonary arterial pressure (SPAP) 59.5 ± 12.9 and 44.2 ± 12.4 mm Hg; cardiac output (CO) 3.3 ± 0.9 and 3.7 ± 0.8 L/min; transpulmonary gradient (TPG) 11.7 ± 3.9 and 8.7 ± 3.6 mm Hg; and pulmonary vascular resistance (PVR) 3.9 ± 2.1 and 2.4 ± 1.3 wood units (WU), respectively. All patients required inotropes and inhaled nitric oxide (iNO) to be weaned from cardiopulmonary bypass (CPB). Results Intravenous (IV) or inhaled vasodilators could be weaned using oral sildenafil in all patients. The hemodynamic data obtained during IV or inhaled drugs (between postoperative days 5 and 10) compared with those obtained on sildenafil therapy alone (about 1 month after transplantation) showed a significant decrease in SPAP (39.0 ± 8.2 vs 32.0 ± 6.5 mm Hg; P = .049). Conclusion These data suggested that oral sildenafil may have a role in the treatment of RVD after heart transplantation.

Usefulness of Pulmonary Artery Pressure by Echocardiography to Predict Outcome in Patients Receiving Cardiac Resynchronization Therapy Heart Failure

Secondary pulmonary hypertension is a marker of advanced heart failure (HF) that confers a poor prognosis. Consecutive patients from 2004 through 2005 who underwent echocardiographic assessments of systolic pulmonary arterial pressure (SPAP) before the implantation of cardiac resynchronization therapy defibrillators were included. Patients were divided into tertiles according to baseline SPAP. Patients in the lowest (group I, 20 to 29 mm Hg) and highest (group III, 45 to 88 mm Hg) tertiles were compared for the end points or death or transplantation and for HF hospital admission. Two hundred seventy patients were evaluated, of whom 95% were Caucasians and 91% men. The mean age was 66.5 +/- 11.6 years, the mean QRS duration was 155 +/- 30 ms, the mean left ventricular ejection fraction was 22.6 +/- 9.7%, and the mean New York Heart Association functional class was 3.0 +/- 0.4. In a multivariate model, death or transplantation was significantly more likely in group III (hazard ratio 2.62, 95% confidence interval 1.1 to 6.4, p = 0.036), as was HF admission (hazard ratio 6.35, 95% confidence interval 2.6 to 15.8, p <0.001). In patients with follow-up echocardiographic assessments, a reduction in SPAP was a significant predictor of freedom from the combined end point (hazard ratio 0.29, 95% confidence interval 0.12 to 0.76, p = 0.011). In conclusion, elevated baseline SPAP in patients who underwent cardiac resynchronization therapy is an independent predictor of all-cause mortality or transplantation and HF admission. A decrease in SPAP on follow-up echocardiography is an independent positive prognostic marker.

Effect of levosimendan on right ventricular systolic and diastolic functions in patients with ischaemic heart failure

Levosimendan is a novel positive inotropic calcium sensitiser agent used in acute left heart failure. In this study, the effect of levosimendan on the right ventricular systolic and diastolic functions was evaluated by tissue Doppler comparing them with dobutamine in patients with ischaemic heart failure. Patients having an acute decompensated heart failure with ischaemic cardiomyopathy and left ventricular ejection fraction <40% were included in the study. Before and 24-h after treatment, peak systolic (Sa), peak early (Ea), peak late (Aa) diastolic annular velocities and Ea/Aa ratio from tricuspid lateral annulus by tissue Doppler and systolic pulmonary artery pressure (SPAP) were measured. Sa, Ea and the Ea/Aa ratio were significantly increased in the levosimendan group whereas SPAP was significantly reduced. In the dobutamine group, no significant differences were observed in the Sa, Ea, Aa and Ea/Aa ratio in spite of a significant reduction in SPAP. Decrease in SPAP was greater in the levosimendan group (p=0.002). Levosimendan improves right ventricular systolic and diastolic functions.

Estudio observacional sobre la efectividad y tolerabilidad del bosentán en el tratamiento de la hipertensión pulmonar en un hospital general de tercer nivel

The pathogenesis of pulmonary hypertension (PHT) involves elevated levels of endothelin. Bosentan is a receptor antagonist used for the treatment of this disease. The purpose of the study is to assess the efficacy and tolerability of this drug in clinical practice. A retrospective observational study of 10 patients with primary pulmonary hypertension (seven) and secondary to pulmonary thromboembolism (PTE), treated with bosentan. The decrease in systolic pulmonary artery pressure (SPAP) and the New York Heart Association (NYHA) functional classification were measured, together with treatment safety based on transaminase levels in the mid term and long term until the treatment period of two years was completed. The decrease in SPAP between the beginning and the end of the treatment was not significant. Three of the ten patients began treatment in class II, five in class III and two in class IV. After 12 months of treatment, six patients were in class II, two in class IV, one patient died and another stopped the treatment due to toxicity. Four patients continued the treatment for 24 months, and the results were compared with those obtained during the first year: Two patients remained in class II, one patient deteriorated to class III and the four died. Bosentan is shown to be effective after six months of treatment, losing efficacy after two years. Bosentan gave satisfactory results in PHT secondary to PTE.

Pulmonary embolism: a follow-up study of the relation between the degree of right ventricle overload and the extent of perfusion defects.

To describe the course of changes in perfusion lung scintigraphy (LS) after acute pulmonary embolism (PE) and test the hypothesis that patients with persistent pulmonary hypertension (PH)/right ventricle (RV) dysfunction after acute PE can be differentiated from those without through larger perfusion defects (PDf) on LS. Design. Prospective, one-year follow-up study with repeated LS and echocardiography-Doppler investigations. Single centre, University Hospital. Patients with clinical suspicion of acute PE with a diagnosis confirmed by LS and/or pulmonary angiography and able to undergo repeated investigations. Of the 78 patients included, a six-week follow-up was completed in 67 and a one-year follow-up in 64. Time course of PDf in relation to time course of pulmonary artery systolic pressure (PAsP) and RV function. Initially, PDf decreased exponentially, until the beginning of a stable phase, which was achieved within 54 days for 90% of the patients and within 148 days for all. The temporal relation for the regress of PDf and decrease in PAsP was loose. Patients with persistent PDf suffered PH/RV dysfunction more often than those without. However, the variability in the degree of haemodynamic changes for a given extent of PDf was large. After acute PE, LS is of use for the identification of the group of patients that may have persistent PH/RV dysfunction. However. since the identification of individual patients is uncertain, LS cannot replace echocardiography-Doppler in the identification of persistent PH/RV dysfunction after acute PE.

Nitric oxide inhalation as a chemical assist for circulation in patients after cardiovascular surgery.

The objective of this study was to investigate whether nitric oxide (NO) inhalation might be an alternative strategy as a chemical assist for the circulation in patients showing a deterioration in oxygen delivery. Twelve adult patients whose oxygen delivery indices (DO2I) were less than 400 ml/min/m2 after cardiovascular surgery were included in this study. NO was administered via a premixing system or a side stream system at doses between 1 and 10 (5.1+/-2.4) ppm. Data obtained before and during a 120 min NO inhalation were compared using the paired Student's t-test. The increase in PaO2/FiO2 resulting from NO inhalation was significant (from 162 to 251 mm Hg). DO2I increased significantly from 326 to 417 ml/min/m2 concomitantly with significant increases in both arterial oxygen content (CaO2) and cardiac index (CI) (from 14.1 to 15.4 vol% and from 2.31 to 2.71 L/min/m2 , respectively). The increase in SvO2 during NO inhalation was significant (from 55.2 to 62.6%). Among the other hemodynamic parameters, both total pulmonary resistance and systolic pulmonary arterial pressure (SPAP) showed significant decreases during NO inhalation, but right atrial pressure did not change significantly. There was a close relationship between the baseline SPAP level (bSPAP) and the decrease in SPAP during NO inhalation (dSPAP) (r = -0.88). However, negative correlations were observed between bSPAP and percentage increase in CI (%CI) (r = -0.61) and between bSPAP and percentage increase in DO2I (%DO2I) (r = -0.48). Moreover, positive relationships were observed between dSPAP and %CI (r = 0.62) and between dSPAP and %DO2I (r = 0.45). Hemoglobin (Hb) increased significantly from 11.0 to 11.4 g/dl. There were no significant changes in Fio2, pH, PacO2, or base excess (BE) during NO inhalation. The level of methemoglobin measured during the study period remained within the normal range (0.86+/-0.23%). In conclusion, NO inhalation could be an efficient and alternative assist for the circulation in patients whose oxygen delivery deteriorates after cardiovascular surgery.

Inhaled Nitric Oxide Selectively Decreases Pulmonary Artery Pressure and Pulmonary Vascular Resistance Following Acute Massive Pulmonary Microembolism in Piglets

Acute massive pulmonary embolism increases pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR), which may lead to early right ventricular failure and subsequent cardiocirculatory deterioration. Inhaled nitric oxide (NO) selectively dilates pulmonary vessels in vivo. Thus, inhaled NO may be useful in preventing cardiocirculatory deterioration following pulmonary embolism. We investigated the effects of inhaled NO in the acute phase of massive pulmonary microembolism in 10 anesthetized and mechanically ventilated piglets (body weight, 18 +/- 2 kg). Microspheres of 300-microns diameter were injected i.v. in an amount sufficient to initially increase mean PAP to 45 mm Hg. Forty-five minutes after pulmonary embolization, the pretreatment control values were recorded. Thereafter, the piglets inhaled 40 ppm NO, and subsequently 80 ppm NO. When 40 ppm NO was inhaled, there was a significant decrease in systolic PAP (-10.3%; 44.5 +/- 2.2 to 39.9 +/- 2.4 mm Hg; p < 0.05) and mean PAP (-9.4%; 32.9 +/- 1.3 to 29.8 +/- 1.3 mm Hg; p < 0.05). PVR was changed by -13.6% (p = 0.07). Administration of 80 ppm NO resulted in a significant decrease in systolic PAP (-12.6%; to 38.9 +/- 1.9 mm Hg; p < 0.05), mean PAP (-11.9%; to 29.0 +/- 1.4 mm Hg; p < 0.05), and PVR (-19.4%; p < 0.05) compared with pretreatment values. Discontinuation of NO inhalation was associated with an immediate return to pretreatment values. Systemic hemodynamics and the arterial and mixed venous oxygen concentrations remained unchanged. We conclude that inhaled NO following acute massive pulmonary microembolism selectively decreases PAP and PVR without influencing systemic hemodynamics in piglets.

Impact of Medical Therapy on Pulmonary Hypertension in Patients With Congestive Heart Failure Awaiting Cardiac Transplantation

Pulmonary artery (PA) hypertension in transplant recipients increases mortality from right heart failure following heart transplantation. We examined the impact of long-term medical therapy on the severity of PA hypertension in patients with end-stage congestive heart failure on a transplant waiting list. The initial and final, quarterly right heart catheterization data on 60 patients (50 men, aged 50 ± 9 years, New York Heart Association class III to IV) awaiting heart transplantation were analyzed and the patients divided into 2 groups: group A, those with persistent elevated systolic PA pressures throughout the 10-month follow-up (n = 31 of 60), and group B, those who had any decrease in systolic PA pressure during that period (n = 29 of 60). Group A had no change in hemodynamics. Group B had a significant decrease (± SD) in right atrial (11 ± 7 to 5 ± 4 mm Hg), PA (57 ± 11 to 37 ± 11 mm Hg), and PA wedge (25 ± 9 to 14 ± 7 mm Hg) pressures, with increases in cardiac output (3.8 ± 0.9 to 4.7 ± 1.1 L/min) and ejection fraction (18 ± 6% to 27 ± 11%) (p <0.05). The combined end point of transplant or death occurred in 28 of 31 patients (90%) in group A versus 14 of 29 (50%) in group B (p = 0.0004). Ischemic etiology was present in 71% of patients in group A versus 68% with idiopathic dilated cardiomyopathy in group B (p = 0.003). The reversibility of PA hypertension rather than its initial severity is predictive of patient clinical outcome. Idiopathic, as opposed to ischemic, cardiomyopathy responds better to medical therapy. (Am J Cardiol 1996;78:440–443)

159 CLOSED VERSUS OPEN MITRAL COMMISSUROTOMY IN CHILD REN WITH RHEUMATIC MITRAL STENOSIS

There has been controversy about the relative merits of closed mitral commissurotomy (CMC) versus open mitral commissurotomy (OMC) in younger patients with rheumatic mitral stenosis (RMS). In an attempt to resolve this uncertainty, 23 patients (pts) aged 10-15 years, consecutively admitted with RMS and pulmonary hypertension (PH) were randomly assigned to OMC (12 pts) and CMC (11 pts). All had cardiac catheterization and left ventricular angiography prior to surgery and again 3-73 wks (x=18) after operation. All pts had RMS either alone or associated with insignificant mitral regurgitation (MR). All pts had PH [pulmonary artery systolic pressure (PASP) 92.5 ± 16.5 mmHg]. In CMC group, 3 pts (27%) had poor results: one died 3 days after surgery, 2 required mitral valve replacement shortly afterwards due to massive MR, whereas only 1 pt (8%) in OMC group developed severe MR. All remaining pts have had significant clinical improvement. Although decrease in PASP was similar in both groups (OMC=36%, CMC=37%), pts in OMC group had greater decrease in pulmonary wedge pressure (PWP) than CMC group (48% vs 33%, p < 0.01). After commissurotomy, only 2 of 10 pts (20%) in CMC group had normal PWP, (≤13 mm Hg) whereas 6 of 12 pts (50%) in OMC group had normal PWP, indicating residual MS in a large number of pts in CMC group. It is concluded that in a center where large numbers of OMC and CMC are performed routinely, OMC should be the preferred method in children with RMS