Reduction In Pulmonary Artery Pressure Research Articles

Impact of transcatheter mitral valve repair using MitraClip on right ventricular remodeling.

The potential of the MitraClip to prevent from right heart failure or to restore right ventricular (RV) function is still unclear. The aim of the present study was to analyze the impact of the MitraClip implantation on RV function and its association with clinical outcome. After MitraClip implantation patients underwent echocardiography follow-up scheduled between 3 and 6months after the procedure in the present single-center registry. A total of 93 patients were included. Compared to baseline, RV function declined in 20%, was unchanged in 25% and improved in 55% of the patients. Factors associated with decline in RV performance were atrial fibrillation, decrease in left ventricular function and lack of reduction in pulmonary artery pressure. Patients who experienced worsening in RV function had a significantly lower survival after mean follow-up of 11 ± 7months compared to those with preserved or improved RV function (15% vs. 83% vs. 83%; p log rank = 0.001). Furthermore, changes in TAPSE were found to be an independent predictor for all-cause mortality [HR 0.88 (0.77-0.99); p = 0.04]. The majority of patients suffering from severe MR benefited from MitraClip with respect to RV remodeling. However, 20% of the patients experienced a decline in RV function, which was associated with poor prognosis. Importantly, changes in RV function after MitraClip were identified as independent predictor for survival in contrast to baseline RV function and, therefore, should be implemented in follow-up routine for better outcome prediction.

Pulmonary Artery Denervation: Update on Clinical Studies.

Sympathetic overactivity plays an important role in the progression of pulmonary arterial hypertension (PAH). The purpose of this review is to illustrate localization of pulmonary arterial sympathetic nerves, the key steps of pulmonary artery denervation (PADN) procedure, and to highlight clinical outcomes. Sympathetic nerves mostly occurred in the posterior region of the bifurcation and pulmonary trunk. Emerging preclinical data provided the potential of PADN for PAH. PADN, produced at bifurcation area, improved a profound reduction of pulmonary arterial pressure and ameliorated clinical outcomes with an exclusive ablation catheter. The application of PADN in the patients of PAH or combined pre-capillary and post-capillary PH (CpcPH) improved the hemodynamic parameters and increased 6MWD. Sympathetic overactivity aggravates PAH. PADN is a promising interventional treatment for PAH and CpcPH. Additional clinical trials are warranted to confirm the efficacy of PADN.

Association between Arrhythmia and Pulmonary Artery Pressure in Heart Failure Patients Implanted with a Cardiac Defibrillator and Ambulatory Pulmonary Artery Pressure Sensor.

The association between ventricular arrhythmia (VA) burden or defibrillator therapy and pulmonary artery pressure (PAP) has not been characterized in an ambulatory setting; thus, we sought in the present research to determine the relationship between ambulatory PAP and VA burden. A retrospective cohort study involving patients with an implantable cardiac defibrillator and CardioMEMS™ PAP sensor (Abbott Laboratories, Chicago, IL, USA) both transmitting remotely into the Merlin.net™ patient care network (Abbott Laboratories, Chicago, IL, USA) was conducted. VA and therapy burden in the six months following sensor implant were stratified by the baseline mean PAP. Patients with PAPs of 25 mmHg to 35 mmHg and those with PAPs of 35 mmHg or more were compared with individuals with PAPs of less than 25 mmHg. The change in VA burden was reported using the averaged mean PAP reduction during the first three months. A total of 162 patients aged 69.4 years ± 10.9 years were included (74% male) with a baseline mean PAP of 36.2 mmHg ± 10.4 mmHg. Twenty patients with a baseline mean PAP of less than 25 mmHg had no VAs over six months. For 61 patients with a baseline mean PAP of between 25 mmHg and 35 mmHg, the annualized number of days with ventricular tachycardia (VT)/ventricular fibrillation (VF) was 1.65/patient-year (p < 0.001), with 8% of patients having VT/VF events. For 81 patients with a baseline mean PAP of 35 mmHg or more, 19% of patients had a VT/VF event and an annualized number of days with VT/VF events of 1.45/patient-year (p < 0.001). When analyzing the treatment effect, a reduction of 3 mmHg or more in mean PAP over three months reduced arrhythmia burden over the next three months as compared with in patients without such an improvement. In conclusion, it is indicated that VAs are associated with high PAPs, and a reduction in PAP may lead to a reduction in VAs in real-world ambulatory patients.

Monitoring Pulmonary Arterial Hypertension Using an Implantable Hemodynamic Sensor

Pulmonary arterial hypertension (PAH) is a chronic disease that ultimately progresses to right-sided heart failure (HF) and death. Close monitoring of pulmonary artery pressure (PAP) and right ventricular (RV) function allows clinicians to appropriately guide therapy. However, the burden of commonly used methods to assess RV hemodynamics, such as right heart catheterization, precludes frequent monitoring. The CardioMEMS HF System (Abbott) is an ambulatory implantable hemodynamic monitor, previously only used in patients with New York Heart Association (NYHA) class III HF. In this study, we evaluate the feasibility and early safety of monitoring patients with PAH and right-sided HF using the CardioMEMS HF System. The CardioMEMS HF sensors were implanted in 26 patients with PAH with NYHA class III or IV right-sided HF (51.3 ± 18.3 years of age, 92%women, 81%NYHA class III). PAH therapy was tracked using a minimum of weekly reviews of CardioMEMS HF daily hemodynamic measurements. Safety, functional response, and hemodynamic response were tracked up to 4 years with in-clinic follow-ups. The CardioMEMS HF System was safely used to monitor PAH therapy, with no device-related serious adverse events observed and a single preimplant serious adverse event. Significant PAP reduction and cardiac output elevation were observed as early as 1month postimplant using trends of CardioMEMS HF data, coupled with significant NYHA class and quality of life improvements within 1 year. The CardioMEMS HF System provided useful information to monitor PAH therapy, and demonstrated short- and long-term safety. Larger clinical trials are needed before its widespread use to guide therapy in patients with severe PAH with right-sided HF.

Minithoracotomy and Beating Heart Strategy for Mitral Surgery in Secondary Mitral Regurgitation.

In patients with secondary mitral regurgitation (MR) associated with low ejection fraction or previous heart surgery, minimally invasive mitral valve surgery without aortic cross-clamp (MIMVS-WAC) has shown promising results. We report our experience for this strategy in our centers. Between August 2011 and April 2017, 46 patients (mean age 69 ± 11 years, 76% males) received MIMVS-WAC. Indications for this technique were prior coronary bypass surgery (26%), severe or recent left ventricular (LV) dysfunction (30%), or both (39%). The mean EuroSCORE II was 12 ± 10. For each procedure, we conducted right minithoracotomy and hypothermic cardiopulmonary bypass (CPB) after peripheral cannulation. Mean CPB time was 159 ± 39 minutes. A mitral valve replacement (MVR) was performed in 23 cases (50%), an annuloplasty in 22 cases (48%), and a prosthesis pannus removal in 1 case (2%). Mean hospital length of stay was 12 ± 5.4 days. We report no sternotomy conversions, six reoperations for bleeding, and three deaths at 30 days. Transfusion was requested in 62% (mean infusion 2 ± 2.4 packed red blood cells). The postoperative echocardiography showed an LV function preservation in 69% of cases and a reduction of pulmonary arterial pressure in 73% of cases. Four additional deaths occurred in the long-term follow-up (mean 637 ± 381 days, median 593 days). No mitral reoperation was required, with a MR ≤ 2 in 90% of patients. In high-risk patients, the MIMVS-WAC is a safe technique. It avoids hard dissections while ensuring excellent preservation of cardiac function.

Impact of pulmonary endarterectomy on pulmonary arterial wave propagation and reservoir function.

High wave speed and large wave reflection in the pulmonary artery have previously been reported in patients with chronic thromboembolic pulmonary hypertension (CTEPH). We assessed the impact of pulmonary endarterectomy (PEA) on pulmonary arterial wave propagation and reservoir function in patients with CTEPH. Right heart catheterization was performed using a combined pressure and Doppler flow sensor-tipped guidewire to obtain simultaneous pressure and flow velocity measurements in the pulmonary artery in eight patients with CTEPH before and 3 mo after PEA. Wave intensity and reservoir-excess pressure analyses were then performed. Following PEA, mean pulmonary arterial pressure (PAPm; ∼49 vs. ∼32 mmHg), pulmonary vascular resistance (PVR; ∼11.1 vs. ∼5.1 Wood units), and wave speed (∼16.5 vs. ∼8.1 m/s), i.e., local arterial stiffness, markedly decreased. The changes in the intensity of the reflected arterial wave and wave reflection index (pre: ∼28%; post: ∼22%) were small, and patients post-PEA with and without residual pulmonary hypertension (i.e., PAPm ≥ 25 mmHg) had similar wave reflection index (∼20 vs. ∼23%). The reservoir and excess pressure decreased post-PEA, and the changes were associated with improved right ventricular afterload, function, and size. In conclusion, although PVR and arterial stiffness decreased substantially following PEA, large wave reflection persisted, even in patients without residual pulmonary hypertension, indicating lack of improvement in vascular impedance mismatch. This may continue to affect the optimal ventriculoarterial interaction, and further studies are warranted to determine whether this contributes to persistent symptoms in some patients.NEW & NOTEWORTHY We performed wave intensity analysis in the pulmonary artery in patients with chronic thromboembolic pulmonary hypertension before and 3 mo after pulmonary endarterectomy. Despite substantial reduction in pulmonary arterial pressures, vascular resistance, and arterial stiffness, large pulmonary arterial wave reflection persisted 3 mo postsurgery, even in patients without residual pulmonary hypertension, suggestive of lack of improvement in vascular impedance mismatch.

Selective Reductions in Pulmonary Artery Pressure Lowers Sympathetic Neural Activity in Healthy Humans at High Altitude

Chronically elevated sympathetic neural activity is a characteristic of many disease states. Tonic chemoreflex activation has been implicated in the development of sympathetic overactivity; however, other reflexes may also contribute. For example, in an animal model, stimulation of pulmonary baroreceptors induces a reflex increase in sympathetic neural activity. In humans, pulmonary pressure has been shown to be related to basal sympathetic activity in pulmonary hypertension; however a critical step in determining a causal link is to establish whether changing pulmonary pressure alters sympathetic outflow. In this pilot study, we exposed thirteen healthy humans (5 females, 28 [ ± 7] years) to high altitude hypoxia (HA; 4383m), a setting known to increase both pulmonary pressure and sympathetic activation, before selectively lowering pulmonary pressure via inhalation of the pulmonary vasodilator nitric oxide. Muscle sympathetic nerve activity (MSNA; Microneurography), blood pressure (BP; Photoplethysmography), heart rate (HR; Electrocardiogram), and peripheral oxygen saturation (SPO2; Pulse oximetry) were continually measured during ambient air breathing (Amb) and during a 6‐minute inhalation of nitric oxide (iNO; 40ppm in 21% O2). Pulmonary artery systolic pressure (PASP), pulmonary vascular resistance (PVR) and stroke volume (SV) were determined via cardiac ultrasound. iNO reduced PASP (−23 ± 12%) and PVR (−21 ± 16%) compared to Amb (Table 1). iNO also reduced MSNA burst frequency (−18 ± 18%), burst incidence (−16 ± 17%) and total activity (−21 ± 20%) compared to Amb. MSNA changes during iNO were not related to changes in SPO2 (r = −0.16, P = 0.61) or MAP (r = −0.28, P = 0.35). Our data demonstrate that selectively reducing pulmonary pressure reduces sympathetic nerve activity in healthy humans; therefore, this provides evidence for a causal link in the relationship between pulmonary pressure and basal sympathetic activity. Further investigation is warranted to establish whether elevated pulmonary pressure is a mechanism contributing to chronically elevated sympathetic outflow in disease.Support or Funding InformationThis study was supported by the Natural Sciences and Engineering Research Council of Canada and a Canada Research Chair in Cerebrovascular Physiology grant.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The Utility of CardioMEMS Implantable Hemodynamic Monitoring Device in Heartware HVAD Patient with Recurrent Gastrointestinal Bleeding

Introduction CardioMEMS heart sensor is a wireless implantable hemodynamic monitoring system that can guide the management of heart failure (HF). Its role in HF patients with left-ventricular assist device (LVAD) is undetermined. Gastrointestinal (GI) bleeding is a common complication in the LVAD population. Severe GI bleeding can lead to a hypovolemic state which results in decreased pulmonary artery pressure (PAP). In this case, we report the changes in PAP recorded by CardioMEMS in an LVAD patient with recurrent GI bleeding. Case Report A 66 year-old man with Heartware HVAD implantation for ischemic cardiomyopathy, atrial fibrillation, diabetes and CardioMEMS device implantation presented to the emergency department (ED) on 6/8 due to black stools for 4 days. He was hospitalized 3 times in the preceding 2 months for GI bleeding of unclear etiology requiring blood transfusions and monthly octreotide. In the ED, he was stable and LVAD interrogation did not show any events. However, he had a drop in hemoglobin (Hb) from a baseline of 8.9 g/dL to 6.9 g/dL. He underwent push enteroscopy during this hospital stay which demonstrated bleeding jejunal angioplastic lesions. The PAP readings during the episodes of GI bleeding were reviewed. There was a significant reduction in PAP at the date of symptom onset from one day prior; from 57/26 mmHg (mPAP 38 mmHg) on 6/3 to 48/24 mmHg (mPAP 34 mmHg) on 6/4 corresponding with 2 g/dL drop in Hb level (See figure). This phenomenon was seen in a prior episode of GI bleeding 2 months prior. The PAP numbers dropped considerably to 39/18 mmHg (mPAP 27 mmHg) at the onset of symptoms compared with 49/22 mmHg (mPAP 33 mmHg) 1 day prior associated with 2.9 g/dL decline in Hb level. During the time PAP changes were observed, diuretic therapy was not modified. Summary In patients implanted with CardioMEMS device, a sudden drop in PAP can herald a GI bleeding episode. Monitoring PAP trends can be helpful in LVAD patients who are at higher risk for GI bleeding.

Total Anomalous Pulmonary Venous Connection Beyond the First Decade of Life.

We report our experience with surgery for total anomalous pulmonary venous connection (TAPVC) beyond first decade of life. Between January 1987 and July 2017, 98 patients ≥ten years underwent TAPVC repair. Their detailed case-records were analyzed. Mean age was 19.05 (± 12.8; median 18) years. Anatomic subtypes were supracardiac (n = 62), cardiac (n = 20), and mixed (n = 16). An atrial septal defect (ASD) was present in all. Severe tricuspid valve regurgitation was present in four patients and severe rheumatic mitral regurgitation was present in one. On preoperative cardiac catheterization, mean pulmonary artery pressure was 67 ± 15.6 mm Hg (median 58; range 37-96). Mean pulmonary vascular resistance was 5.6 ± 3.9 Woods units·m2 (median 4.7, range 2.9-11.8). Twenty-five patients had moderate and eight had severe pulmonary arterial hypertension. Right ventricular dysfunction was present in eight patients. At repair, a small ASD was left open in 87 patients while in 11 patients, the ASD was closed using a unidirectional valved patch. Follow-up was available for 90 (92%) patients. There were no late deaths over a mean follow-up of 163 ± 103.98 months (median 163, range 1-362). Eighty-two patients were in NYHA class I and eight were in class II. Right ventricular function normalized in 82 patients while 80 patients had reduction in pulmonary artery pressure. Event-free survival was 94.2% at 5 years, 92.3% at 10 years, and 90% at 20 and 30 years. Outcomes of surgical repair for TAPVC beyond first decade of life are satisfactory. Close follow-up, however, is necessary for possible persistence of pulmonary arterial hypertension.

Per-operative Changes of Pulmonary Artery Pressure following Closed Mitral Commissurotomy

Background: Mitral stenosis is often present with pulmonary hypertension. Closed Mitral Commissurotomy (CMC) is a treatment of choice for severe mitral stenosis. In this study, we examined the per-operative changes of pulmonary artery pressure following opening of stenosed mitral valve.&#x0D; Methods: All these CMCs were performed routinely through the left antero-lateral thoracotomy (4th intercostal space) and dilatation was done by metallic Tubb’s Dilator. Peroperative left atrial and Pulminary Arterial pressures were measured before and after dilatation.&#x0D; Results: 15 patients had undergone CMC. Following CMC, per-operative mean Pulmonary artery pressure was reduced from 45.5±7.1 mm of Hg to 39.0±8.8 mm of Hg (p=0.043). Mean left atrial pressure reduced from 35.9±5.6 mm of Hg to 30.0±9.1 mm of Hg (p = 0.049). At three months follow up after closed mitral commissurotomy mitral valve area at echocardiography was found 2.29±0.18 cm2. There was no case of death after closed mitral commissurotomy. Mild mitral regurgitation occurred in 1 patient.&#x0D; Conclusion: We conclude that there is immediate significant reduction of pulmonary Artery pressure following closed mitral commissurotomy. This reduction is apparently comparable with a similar reduction of left atrial pressure.&#x0D; Cardiovasc. j. 2019; 11(2): 147-151

Tissue plasminogen activator dose and pulmonary artery pressure reduction in catheter directed thrombolysis of submassive pulmonary embolism.

PurposeThe purpose of this study is to assess the incremental effect of tissue plasminogen activator (t-PA) dose on pulmonary artery pressure (PAP) and bleeding during catheter directed thrombolysis (CDT) of submassive pulmonary embolism (PE).Materials and methodsRecords of 46 consecutive patients (25 men, 21 women, mean age 55±14 y) who underwent CDT for submassive PE between September 2009 and February 2017 were retrospectively reviewed. Mean t-PA rate was 0.7±0.3 mg/h. PAP was measured at baseline and daily until CDT termination. Mixed-effects regression modeling was performed of repeated PAP measures in individual patients. Bleeding events were classified by Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO) and t-PA dose at onset.ResultsMean t-PA dose was 43.0±30.0 mg over 61.9± 28.8 h. Mean systolic PAP decreased from 51.7±15.5 mmHg at baseline to 35.6±12.7 mmHg at CDT termination (p<0.001). Mixed-effects regression revealed a linear decrease in systolic PAP over time (β = -0.37 (SE = 0.05), p<0.001) with reduction in mean systolic PAP to 44.8±1.9 mmHg at 12 mg t-PA/20 h, 39.5±2.0 mmHg at 24 mg t-PA/40 h, and 34.9±2.1 mmHg at 36 mg/60 h. No severe, one moderate, and 8 mild bleeding events occurred; bleeding onset was more frequent at ≤24 mg t-PA (p <0.001). One patient expired from cardiopulmonary arrest after 16 h of CDT (15.4 mg t-PA); no additional intra-procedural fatalities occurred.ConclusionIncreased total t-PA dose and CDT duration were associated with greater PAP reduction without increased bleeding events.

AEROSOLIZED EPOPROSTENOL TO TREAT PULMONARY HYPERTENSION SECONDARY TO MASSIVE PULMONARY EMBOLISM

SESSION TITLE: Critical Care 2 SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Prostacyclins are potent systemic and pulmonary vasodilators that reduce pulmonary arterial pressure and pulmonary vascular resistance when administered intravenously in pulmonary arterial hypertension, resulting in increased cardiac index and oxygen delivery. Aerosolized prostacyclins are used to treat acute pulmonary hypertension (pHTN) from the acute respiratory distress syndrome and post-cardiac surgery while minimizing systemic hypotension. Very little data exists on the use of aerosolized prostacyclins from another cause of acute pHTN: acute pulmonary embolism (PE). CASE PRESENTATION: A 78 year-old Caucasian male presented to our institution with massive bilateral PE with complete occlusion of his right main pulmonary artery. Bedside transthoracic echocardiogram (TTE) demonstrated right ventricular dilation with moderately reduced function. Immediately following the placement of an ultrasonic thrombolytic catheter system into the right main pulmonary artery, he suffered a cardiac arrest. Aerosolized epoprostenol was administered as salvage therapy via the inspiratory limb of the ventilation circuit at a fixed dose of 160,000 ng/hr. Within 30 minutes of administration, the patient’s oxygen saturation and blood pressure increased from 72% to 91% and 92/59 mmHg to 159/85 mmHg, respectively. The patient’s condition stabilized, and the medication was titrated off 48 hours later. After 6 weeks of hospitalization and inpatient rehabilitation the patient was discharged home. Repeat TTE 2 months post discharge revealed normal right ventricular size and function. DISCUSSION: PE is a common cause of acute pHTN in the critical care setting. Acute right heart failure develops secondary to increased right ventricular filling pressures and stroke work, often leading to obstructive shock and death. In these patients, preserving right heart function via immediate reduction in pulmonary arterial pressures is desired. Embolectomy or thrombolysis are often successful in reducing right ventricular afterload. Aerosolized prostacyclin has been shown in a case report to be transiently beneficial for acute pHTN from PE following systemic thrombolysis. Aerosolized epoprostenol may improve right ventricular function through targeted vasodilation in the pulmonary vasculature and alveolar gas exchange due to increased surface area. In patients with extensive clot burden, there is a theoretical risk of worsening V:Q mismatch by dilating pulmonary capillary beds with proximal emboli. CONCLUSIONS: We present a case of massive PE with cardiac arrest in which the addition of aerosolized epoprostenol following catheter-directed thrombolysis resulted in rapid improvement in pulmonary hemodynamics and gas exchange. Our hope is to establish the potential benefits of aerosolized epoprostenol for patients with refractory right heart failure from PE, although proper patient selection and timing of therapy remains unknown. Reference #1: Webb SA, Stott S, van Heerden PV. The use of inhaled aerosolized prostacyclin in the treatment of pulmonary hypertension secondary to pulmonary embolism. Intensive Care Med. 1996; 22:353-355. Reference #2: Kooter, et al. No effect of epoprostenol on right ventricular diameter in patients with acute pulmonary embolism: a randomized controlled trial. BMC Pulmonary Medicine. 2010; 10:18 DISCLOSURES: No relevant relationships by Tufik Assad, source=Web Response No relevant relationships by Mary Bourget, source=Web Response No relevant relationships by Aaron Milstone, source=Admin input No relevant relationships by Michael Wright, source=Web Response

Daily non-invasive haemodynamic telemonitoring for efficacy evaluation of MitraClip® implantation in patients with advanced systolic heart failure.

AimPatients with advanced systolic chronic heart failure frequently suffer from progressive functional mitral regurgitation. We report our initial experience in patients with an implanted pulmonary artery pressure (PAP) sensor, who developed severe mitral regurgitation, which was treated with the MitraClip system. We non‐invasively compared changes in PAP values in patients after MitraClip with PAP changes in patients without MitraClip.Methods and resultsAmong 28 patients with New York Heart Association III heart failure with implanted PAP sensor for haemodynamic telemonitoring from a single centre, four patients (age 66 ± 6 years, left ventricular ejection fraction 21 ± 3%, and cardiac index 1.8 ± 0.3) received a MitraClip procedure and were compared with 24 patients (age 72 ± 8 years, left ventricular ejection fraction 26 ± 9.9%, and cardiac index 2.0 ± 1.0) without MitraClip procedure in a descriptive manner. Ambulatory PAP values were followed for 90 days in both groups. In comparison with the PAP values 4 weeks before MitraClip procedure, PAP was profoundly reduced in all four patients after 30 days (ΔPAPmean −11 ± 5, ΔPAPdiast −7 ± 3 mmHg, P < 0.02) as well as after 90 days (ΔPAPmean −6.3 ± 6, ΔPAPdiast −1 ± 3 mmHg). Reductions in PAP were accompanied by a profound reduction in N terminal pro brain natriuretic peptide as well as clinical and echocardiographic improvement. When analysing the dynamics with a regression model, reductions in all PAP values were significantly greater after MitraClip compared with conservative haemodynamic monitoring (P < 0.001).ConclusionsThe efficacy of the interventional MitraClip procedure on clinical symptoms can be confirmed by haemodynamic telemonitoring. Thus, daily non‐invasive haemodynamic telemonitoring allows, for the first time, for a continuous assessment of the haemodynamic efficacy of novel therapies in patients with chronic heart failure.

Intravenous anesthesia with nitroglycerin inhalation for surgical abortion in a patient with severe congenital heart disease and low oxygen saturation

Introduction:Congenital heart disease and pulmonary arterial hypertension are perilous to a gravida for the high morbidity and mortality.Case presentation:We report an extremely rare case of a 27-year-old gravida with congenital heart disease and severe pulmonary arterial hypertension of 115 mmHg. Arterial blood gas analysis revealed her oxygen saturation (SpO2) of 67.8% and oxygen partial pressure of 40.0 mmHg, which were severely low. The patient was diagnosed as having gestation combined with congenital heart disease, severe pulmonary arterial hypertension, and hypoxemia.Interventions: The patient was treated with surgical abortion. The patient was monitored with invasive blood pressure (BP), electrocardiogram (ECG), heart rate, SpO2, and arterial gas analysis as from entry into the operation suite. We performed total intravenous anesthesia with nitroglycerin inhalation. She was returned to the ward at the end of surgery.Conclusion:To our knowledge, this is the first reported case in a gravida with severe heart disease and very low SpO2. Nitroglycerin inhalation may provide dilation of the pulmonary artery, reduction of pulmonary artery pressure, and improvement of oxygenation. Our case report may provide alternative regimen to anesthesia practitioners in similar circumstances.

Carbonic anhydrase is not a relevant nitrite reductase or nitrous anhydrase in the lung.

Carbonic anhydrase (CA) inhibitors such as acetazolamide inhibit hypoxic pulmonary vasoconstriction (HPV) in humans and other mammals, but the mechanism of this action remains unknown. It has been postulated that carbonic anhydrase may act as a nitrous anhydrase in vivo to generate nitric oxide (NO) from nitrite and that this formation is increased in the presence of acetazolamide. Acetazolamide reduces HPV in pigs without evidence of any NO generation, whereas nebulized sodium nitrite reduces HPV by NO formation; however; combined infusion of acetazolamide with sodium nitrite inhalation did not further increase exhaled NO concentration over inhaled nitrite alone in pigs exposed to alveolar hypoxia. We conclude that acetazolamide does not function as either a nitrous anhydrase or a nitrite reductase in the lungs of pigs, and probably other mammals, to explain its vasodilating actions in the pulmonary or systemic circulations. The carbonic anhydrase (CA) inhibitors acetazolamide and its structurally similar analogue methazolamide prevent or reduce hypoxic pulmonary vasoconstriction (HPV) in dogs and humans in vivo, by a mechanism unrelated to CA inhibition. In rodent blood and isolated blood vessels, it has been reported that inhibition of CA leads to increased generation of nitric oxide (NO) from nitrite and vascular relaxation in vitro. We tested the physiological relevance of augmented NO generation by CA from nitrite with acetazolamide in anaesthetized pigs during alveolar hypoxia in vivo. We found that acetazolamide prevents HPV in anaesthetized pigs, as in other mammalian species. A single nebulization of sodium nitrite reduces HPV, but this action wanes in the succeeding 3h of hypoxia as nitrite is metabolized and excreted. Pulmonary artery pressure reduction and NO formation as measured by exhaled gas concentration from inhaled sodium nitrite were not increased by acetazolamide during alveolar hypoxia. Thus, our data argue against a physiological role of carbonic anhydrase as a nitrous anhydrase or nitrite reductase as a mechanism for its inhibition of HPV in the lung and blood in vivo.

Predictors of Persistent Tricuspid Regurgitation After Transcatheter Aortic Valve Replacement in Patients With Baseline Tricuspid Regurgitation.

This study sought to analyze outcomes in patients with moderate-severe tricuspid regurgitation (TR) undergoing transcatheter aortic valve replacement (TAVR). The consequences of uncorrected significant TR in patients undergoing TAVR remain undefined. Between 2009 and 2014, 369 patients underwent TAVR at our institution, and 58 of these had baseline moderate-severe TR. Preoperative, 30-day, and 1-year transthoracic echocardiograms were analyzed. Predictors of persistent TR at 30 days and survival were assessed. Fifty-eight patients with baseline moderate-severe TR underwent TAVR. Transcatheter aortic valve replacement resulted in significant reductions in pulmonary artery pressures and TR severity (100% vs 64%; P < 0.001) at 30 days. This was sustained at 1 year and was associated with significant improvements in stroke volume index and New York Heart Association functional class. No changes in right ventricular function or size were noted. The only independent predictor of persistent moderate-severe TR at 30 days was preoperative atrial fibrillation [AF; odds ratio (OR), 4.56; 95% confidence interval, 1.1-18.3; P = 0.033]. Independent predictors of overall long-term survival included AF (OR, 0.41; P = 0.001) and chronic lung disease (OR, 0.47; P = 0.011), but not baseline moderate-severe TR. In patients with baseline moderate-severe TR, persistent moderate-severe TR at 30 days was associated with worsened overall survival (log-rank P = 0.02). Baseline moderate-severe TR is not uncommon in patients undergoing TAVR, and frequently improves. However, the presence of AF suggests that that TR is likely to persist after TAVR and is also indicative of a poor long-term outcome. Whether redirecting such patients to surgery for concomitant tricuspid valve repair will further improve outcomes requires further study.

Dobutamine and Nitroglycerin Versus Milrinone for Perioperative Management of Pulmonary Hypertension in Mitral Valve Surgery. A Randomized Controlled Study

To compare the effects of dobutamine and nitroglycerin to milrinone in young patients with severe pulmonary hypertension undergoing mitral valve replacement. A prospective randomized, double-blinded, controlled study. Single university hospital. Forty patients had systolic pulmonary arterial pressure ≥60 mmHg and were scheduled for elective mitral valve replacement. The patients were divided randomly into 2 equal groups according to the drugs given during the study. The patients in group I received 5 to 20 µg/kg/min of dobutamine and 0.5 to 3 µg/kg/min of nitroglycerin, and patients in group II received a loading dose of milrinone, 50 µg/kg over 10 minutes, followed by a maintenance dose of 0.25 to 0.75 µg/kg/min. The primary outcome was the effects of interventional drugs on mean pulmonary artery pressure. The secondary outcomes were the effects of interventional drugs on systemic and pulmonary hemodynamic parameters measured from induction of anesthesia until the first 12 hours in the intensive care unit stay. There was a more significant decrease in mean pulmonary artery pressure, pulmonary capillary wedge pressure, and central venous pressure in group II than group I at all time points after cardiopulmonary bypass. There were more significant increases in heart rate, mean arterial pressure, cardiac output, and mixed venous oxygen tension in group I than group II, which became more obvious in time. In both groups, there was a significant decrease in systemic vascular resistance and pulmonary vascular resistance at all times. Milrinone provides adequate cardiac performance, causing a greater reduction in pulmonary artery pressure and pulmonary capillary wedge pressure.

Acute Reduction in Pulmonary Artery Pressures with Sacubitril-Valsartan Measured by the CardioMEMS HF Device

The combination drug sacubitril-valsartan induces known vasodilatory hemodynamic effects; however, hemodynamic effects on pulmonary artery pressure have yet to be described. In this case-series, we evaluate the effect of sacubitril-valsartan on pulmonary artery pressures (PAPs) in patients diagnosed with heart failure with reduced ejection fraction (HFrEF) and a previously implanted CardioMEMS device.

Impact of Practice-Based Management of Pulmonary Artery Pressures in 2000 Patients Implanted With the CardioMEMS Sensor.

Elevated pulmonary artery (PA) pressures in patients with heart failure are associated with a high risk for hospitalization and mortality. Recent clinical trial evidence demonstrated a direct relationship between lowering remotely monitored PA pressures and heart failure hospitalization risk reduction with a novel implantable PA pressure monitoring system (CardioMEMS HF System, St. Jude Medical). This study examines PA pressure changes in the first 2000 US patients implanted in general practice use. Deidentified data from the remote monitoring Merlin.net (St. Jude Medical) database were used to examine PA pressure trends from the first consecutive 2000 patients with at least 6 months of follow-up. Changes in PA pressures were evaluated with an area under the curve methodology to estimate the total sum increase or decrease in pressures (mm Hg-day) during the follow-up period relative to the baseline pressure. As a reference, the PA pressure trends were compared with the historic CHAMPION clinical trial (CardioMEMS Heart Sensor Allows Monitoring of Pressure to Improve Outcomes in New York Heart Association [NYHA] Functional Class III Heart Failure Patients). The area under the curve results are presented as mean±2 SE, and P values comparing the area under the curve of the general-use cohort with outcomes in the CHAMPION trial were computed by the t test with equal variance. Patients were on average 70±12 years old; 60% were male; 34% had preserved ejection fraction; and patients were followed up for an average of 333±125 days. At implantation, the mean PA pressure for the general-use patients was 34.9±10.2 mm Hg compared with 31.3±10.9 mm Hg for CHAMPION treatment and 32.0±10.5 mm Hg for CHAMPION control groups. The general-use patients had an area under the curve of -32.8 mm Hg-day at the 1-month time mark, -156.2 mm Hg-day at the 3-month time mark, and -434.0 mm Hg-day after 6 months of hemodynamic guided care, which was significantly lower than the treatment group in the CHAMPION trial. Patients consistently transmitted pressure information with a median of 1.27 days between transmissions after 6 months. The first 2000 general-use patients managed with hemodynamic-guided heart failure care had higher PA pressures at baseline and experienced greater reduction in PA pressure over time compared with the pivotal CHAMPION clinical trial. These data demonstrate that general use of implantable hemodynamic technology in a nontrial setting leads to significant lowering of PA pressures.

Nitrite Prevents Right Ventricular Failure and Remodeling Induced by Pulmonary Artery Banding.

Nitrite has been shown to reduce right ventricle (RV) remodeling in experimental pulmonary hypertension. However, whether this effect is due to a reduction in RV afterload (ie, reduction in pulmonary artery pressure) or a direct effect on the RV itself remains unanswered. We hypothesize that nitrite has direct effects on RV remodeling and studied its effects in mice with pulmonary artery banding (PAB). PAB decreased exercise tolerance and reduced RV systolic and diastolic function. Nitrite treatment attenuated the decrease in RV systolic function and improved the RV diastolic function. Nitrite-treated mice with PAB had similar exercise tolerance compared with a control group. PAB induced RV hypertrophy and fibrosis which were associated with increased expression of phospho-Akt. Interestingly, nitrite treatment attenuated PAB-induced RV hypertrophy and reduced the expression of phospho-Akt in RV tissue from mice with PAB. In neonatal rat cardiac fibroblast, nitrite also attenuated hypoxia-induced increase in expression of phospho-Akt. Our study indicates that nitrite treatment has direct beneficial effects on RV and improves function and attenuates remodeling in RV exposed to chronic pressure overload. These beneficial effects, at least in part, could be due to the inhibition of the phospho-Akt (p-Akt) pathway activation.