Recovery Of Right Ventricular Function Research Articles

Transcatheter Ductus Arteriosus Stenting for Acute Pediatric Pulmonary Arterial Hypertension is Associated with Improved Right Ventricular Echocardiography Strain.

Interventional therapies for severe pulmonary arterial hypertension (PAH) can provide right ventricular (RV) decompression and preserve cardiac output. Transcatheter stent placement in a residual ductus arteriosus (PDA) is one potentially effective option in critically ill infants and young children with PAH. We sought to assess recovery of RV function by echocardiographic strain in infants and young children following PDA stenting for acute PAH. Retrospective review of patients < 2years old who underwent PDA stenting for acute PAH. Clinical data were abstracted from the electronic medical record. RV strain (both total and free wall components) was assessed from echocardiographic images at baseline and 3, 6, and 12months post-intervention, as well as at last echocardiogram. Nine patients underwent attempted ductal stenting for PAH. The median age at intervention was 38days and median weight 3.7kg. One-third (3of 9) of patients had PAH associated with a congenital diaphragmatic hernia. PDA stents were successfully deployed in eight patients. Mean RV total strain was - 14.9 ± 5.6% at baseline and improved to - 23.8 ± 2.2% at 6 months post-procedure (p < 0.001). Mean free wall RV strain was - 19.5 ± 5.4% at baseline and improved to - 27.7 ± 4.1% at 6 months (p = 0.002). Five patients survived to discharge, and four patients survived 1 year post-discharge. PDA stenting for severe, acute PAH can improve RV function as assessed by strain echocardiography. The quantitative improvement is more prominent in the first 6 months post-procedure and stabilizes thereafter.

Long term recovery of right ventricular function after treatment of intermediate and high risk pulmonary emboli

IntroductionPulmonary embolism (PE) is a common and significant source of mortality and morbidity worldwide. A subset of patients with PE, particularly those who have intermediate and high risk events, are at increased risk for long-term right ventricular (RV) dysfunction; however, the impact of novel advanced therapies used for acute PE, including catheter-directed intervention, on long-term RV function remains uncertain. We sought to determine whether use of advanced therapies (catheter-directed intervention or systemic thrombolysis) is associated with improved long-term RV function. Materials and methodsRetrospective, single-center cohort study of adult (≥18 year old) patients admitted and discharged alive with a diagnosis of acute PE, who fell under the category of intermediate or high risk, with available follow-up echocardiograms at least 6 months after the index, seen at a single quaternary referral center in Los Angeles, CA between 2012 and 2021. ResultsThere were 113 patients in this study (58 (51.3 %) treated with anticoagulation alone, 12 (10.6 %) treated with systemic thrombolysis, and 43 (38.1 %) treated with catheter-directed intervention), with approximately equal gender and racial distribution. Patients treated with advanced therapies were significantly more likely to have moderate-severe RV dysfunction (100 % for those treated with thrombolysis, 88.3 % for those treated with catheter-directed intervention, vs 55.2 % for those treated with anticoagulation alone; p < 0.001). At a follow-up of about 1.5 years, patients treated with advanced therapy (systemic thrombolysis or catheter-directed intervention) were more likely to have normalization of RV function (93–100 % vs 81 % for anticoagulation alone, p = 0.04). The subgroup of patients with intermediate-risk PE was significantly more likely to have normalization of RV function (95.6 % vs 80.4 % for anticoagulation alone, p = 0.03). Use of advanced therapy was not associated with substantial short-term adverse events among patients who survived to hospital discharge. ConclusionPatients with intermediate and high risk PE were more likely to have recovery in RV function long-term if treated with catheter-directed intervention or systemic thrombolysis, as compared to anticoagulation alone, without substantial safety issues, despite having worse RV function at baseline. Further data is needed to verify this observation.

Dynamics of global and segmental strain as a marker of right ventricular contractility recovery in patients after COVID-19 pneumonia

Aim. To study the changes of morphological and functional right ventricular (RV) parameters depending on the severity of coronavirus infection 2019 (COVID-19) pneumonia over long-term follow-up.Material and methods. A total of 200 patients (men, 51,5%, mean age, 51,4±10,9 years) were examined at 2 control visits (3, 12 months after receiving two negative polymerase chain reaction tests). Patients were divided into following groups: group I (n=94) — lung tissue involvement ≥50% according to inhospital chest computed tomography (chest CT), group II (n=106) — lung tissue involvement˂50% according to chest CT.Results. The groups were comparable in key clinical and functional parameters 3 months after COVID-19 pneumonia. Speckle tracking echocardiography (STE) revealed a significant increase in following global longitudinal strain (LS) parameters: RV free wall endocardial LS (-22,7±3,2% and -24,3±3,8% in group I, p&lt;0,001; -23,2±3,5% and -24,5±3,4% in group II, p&gt;&lt;0,001), and RV endocardial LS (-21,0±3,1% and -22,5±3,7% in group I, p&gt;&lt;0,001, -21,5±3,2% and -22,6±3,3% in group II, p=0,001 ). Significant increase of segmental endocardial LS was revealed in group I in the basal segments of RV free wall (-26,2±5,1% and -28,1±5,1%, p=0,004) and interventricular septum (IVS) (-16,2 [13,9; 19,5]% and -17,5 [14,6; 21,4]%, p=0,024), IVS middle segment (-20,3±4,1% and -21,5±4,8%, p=0,030), as well as in group II in the apical segments of RV free wall (-21,9±6,7% and -24,4±5,2%, p=0,001) and IVS (-23,7±4,7% and -24,9±4,8%, p=0,014). Conclusion. Recovery of RV function during a 12-month follow-up period in patients with both severe and moderate/mild lung involvement in COVID-19 was detected using the STE method.&gt;˂0,001; -23,2±3,5% and -24,5±3,4% in group II, p˂0,001), and RV endocardial LS (-21,0±3,1% and -22,5±3,7% in group I, p˂0,001, -21,5±3,2% and -22,6±3,3% in group II, p=0,001 ). Significant increase of segmental endocardial LS was revealed in group I in the basal segments of RV free wall (-26,2±5,1% and -28,1±5,1%, p=0,004) and interventricular septum (IVS) (-16,2 [13,9; 19,5]% and -17,5 [14,6; 21,4]%, p=0,024), IVS middle segment (-20,3±4,1% and -21,5±4,8%, p=0,030), as well as in group II in the apical segments of RV free wall (-21,9±6,7% and -24,4±5,2%, p=0,001) and IVS (-23,7±4,7% and -24,9±4,8%, p=0,014).Conclusion. Recovery of RV function during a 12-month follow-up period in patients with both severe and moderate/mild lung involvement in COVID-19 was detected using the STE method.

Recovery of right ventricular function and strain in patients with ST-segment elevation myocardial infarction and concurrent chronic total occlusion

The right ventricle (RV) is frequently involved in ST-segment elevation myocardial infarction (STEMI) when the culprit or concurrent chronic total occlusion (CTO) is located in the right coronary artery (RCA). We investigated RV function recovery in STEMI-patients with concurrent CTO. In EXPLORE, STEMI-patients with concurrent CTO were randomized to CTO percutaneous coronary intervention (PCI) or no CTO-PCI. We analyzed 174 EXPLORE patients with serial cardiovascular magnetic resonance imaging RV data (baseline and 4-month follow-up), divided into three groups: CTO-RCA (CTO in RCA, culprit in non-RCA; n = 89), IRA-RCA (infarct related artery [IRA] in RCA, CTO in non-RCA; n = 56), and no-RCA (culprit and CTO not in RCA; n = 29). Tricuspid annular plane systolic excursion (TAPSE), RV ejection fraction (RVEF), RV global longitudinal strain (GLS) and free wall longitudinal strain (FWLS) were measured. We found that RV strain and TAPSE improved in IRA-RCA and CTO-RCA (irrespective of CTO-PCI) at follow-up, but not in no-RCA. Only RV FWLS was different among groups at baseline, which was lower in IRA-RCA than no-RCA (− 26.0 ± 8.3% versus − 31.0 ± 6.4%, p = 0.006). Baseline RVEF, RV end-diastolic volume and TAPSE were associated with RVEF at 4 months. RV function parameters were not predictive of 4 year mortality, although RV GLS showed additional predictive value for New York Heart Association Classification > 1 at 4 months. In conclusion, RV parameters significantly improved in patients with acute or chronic RCA occlusion, but not in no-RCA patients. RV FWLS was the only RV parameter able to discriminate between acute ischemic and non-ischemic myocardium. Moreover, RV GLS was independently predictive for functional status.

Ultrasound-assisted catheter directed thrombolysis for pulmonary embolus during extracorporeal membrane oxygenation.

Acute pulmonary embolism (PE) is the third most common cause of cardiovascular death. For patients who are hemodynamically unstable, veno-arterial extracorporeal membrane oxygenation (VA-ECMO) support has been shown to provide hemodynamic stability, and allow time for definitive treatment and recovery. Ultrasound-assisted catheter directed thrombolysis (USAT) has the potential to be a safe adjunct and expedite right ventricular (RV) recovery for patients requiring VA-ECMO for PE. A review of all VA-ECMO patients from January 2017 to September 2019 was performed. A total of 49 of these patients were cannulated due to a PE. USAT therapy was used as an adjunct in 6 (12%) of these patients. These 6 patients were given standardized USAT therapy with EKOs catheters at 1 mg/h of tissue plasminogen activator with an unfractionated heparin infusion for additional systemic anticoagulation. Outcomes, including in-hospital death, 90-day survival, RV recovery, and complications, were examined in the cohort of patients that received USAT as an adjunct to ECMO. Median age was 54 years old. Five of the six patients presented with a massive PE and had a PE severity score of Class V. One patient presented with a submassive PE with a Bova score of 2, but was cannulated to VA-ECMO in the setting of worsening RV function. All patients demonstrated recovery of RV function, were free from in-hospital death, and were alive at 90-day follow-up. Ekosonic endovascular system therapy may be a safe and feasible adjunct for patients on VA-ECMO for PE, and allow for survival with RV recovery with minimal complications.

11C]meta-hydroxyephedrine PET evaluation in experimental pulmonary arterial hypertension: Effects of carvedilol of right ventricular sympathetic function

BackgroundLittle is known about the sequelae of chronic sympathetic nervous system (SNS) activation in patients with pulmonary arterial hypertension (PAH) and right heart failure (RHF). We aimed to, (1) validate the use of [11C]-meta-hydroxyephedrine (HED) for assessing right ventricular (RV) SNS integrity, and (2) determine the effects of β-receptor blockade on ventricular function and myocardial SNS activity in a PAH rat model. MethodsPAH was induced in male Sprague-Dawley rats (N = 36) using the Sugen+chronic hypoxia model. At week 5 post-injection, PAH rats were randomized to carvedilol (15 mg·kg−1·day−1 oral; N = 16) or vehicle (N = 16) for 4 weeks. Myocardial SNS function was assessed with HED positron emission tomography(PET). ResultsWith increasing PAH disease severity, immunohistochemistry confirmed selective sympathetic denervation within the RV and sparing of parasympathetic nerves. These findings were confirmed on PET with a significant negative relationship between HED volume of distribution(DV) and right ventricular systolic pressure (RVSP) in the RV (r = −0.90, p = 0.0003). Carvedilol did not reduce hemodynamic severity compared to vehicle. RV ejection fraction (EF) was lower in both PAH groups compared to control (p < 0.05), and was not further reduced by carvedilol. Carvedilol improved SNS function in the LV with significant increases in the HED DV, and decreased tracer washout in the LV (p < 0.05) but not RV. ConclusionsPAH disease severity correlated with a reduction in HED DV in the RV. This was associated with selective sympathetic denervation. Late carvedilol treatment did not lead to recovery of RV function. These results support the role of HED imaging in assessing SNS innervation in a failing right ventricle.

A case report: biventricular takotsubo cardiomyopathy with sequential ventricular recovery due to pulmonary hypertension

BackgroundBiventricular Takotsubo cardiomyopathy (BTC) is estimated to occur in 25–42% of those with Takotsubo cardiomyopathy (TC). Little is known about which subset of patients are predisposed to having concomitant right ventricular (RV) involvement, or the pattern of recovery in BTC.Case summaryWe describe a 69-year-old woman who presented with dyspnoea and was subsequently diagnosed with BTC. We propose that this was triggered by an exacerbation of chronic obstructive pulmonary disease on a background of multiple predisposing factors including recent bereavement, previous excessive alcohol use, status as a current smoker, and anxiety. During her admission, she required non-invasive ventilation and inotropic support to manage her type two respiratory failure and acute heart failure. Serial echocardiograms during the admission allowed us to capture and present the sequential recovery of ventricular systolic function, with the left ventricular (LV) recovery preceding the right ventricle.DiscussionOur patient fulfils the International Takotsubo Diagnostic criteria of transient LV dysfunction, emotional and physical triggers, electrocardiogram abnormalities, raised troponin and brain natriuretic peptide and no occlusive coronary artery disease. We hypothesize that pulmonary hypertension-related strain on the right ventricle due to lung disease, may have led to the observed delay in the recovery of RV function, despite the full recovery of LV function.

Impact on clinical outcomes of right ventricular response to percutaneous correction of secondary mitral regurgitation

Abstract Funding Acknowledgements Type of funding sources: None. Background. Right ventricular function (RVF) is a strong determinant of prognosis in patients with reduced ejection fraction heart failure (HFrEF) and secondary mitral regurgitation (SMR). Percutaneous mitral valve repair (pMVR) can promote the recovery of RVF. Purpose. We sought to characterize the RV response to pMVR in HFrEF with SMR and to assess the influence of improved RVF after pMVR in this specific setting of patients. Methods. We included all the patients with HFrEF and SMR≥3+ successfully treated with pMVR between April 2012 and January 2020 in two tertiary care centers for HF. Improved RVF was defined as DRVFAC≥5% at early follow-up (median time 4 months). The primary endpoint was a composite of death/heart transplant (D/HT). Results. In total, 110 patients were included. Mean age was 67 ± 12 years, mean LVEF was 31 ± 8% and mean RVFAC was 31 ± 10%. DRVFAC≥5% occurred in 54 (49%) patients and was independent from the measures of left ventricle recovery. During a median follow-up of 36 months (IQR 19-52), 40 patients (36%) died or were transplanted. After adjustment for other significant covariates, DRVFAC≥5% was significantly associated with lower risk of D/HT (HR 0.49, 95% CI 0.24 – 0.98 p &amp;lt; 0.042) along with M2+ at follow-up (HR 0.36; 95% CI 0.17-0.74 p 0.005). Conclusions. In patients with HFrEF and SMR, the improvement of RVF is frequent after pMVR and is associated with better long-term survival free from HT. Abstract Figure.

Case of recurrent pulmonary thromboembolism due to therapeutic non-compliance

Pulmonary embolism occurs when thrombi enter the pulmonary arterial circulation. Most pulmonary embolisms are the result of deep venous thrombosis of the pelvic limbs, chest or pelvis, and, less commonly, the jugular veins or inferior vena cava. Venous thromboembolism includes deep vein thrombosis and pulmonary embolism. It is the third most common cardiovascular disease, with a total annual incidence of 100-200 per 100 000 population. INTRODUCTION: Acute pulmonary embolism is the most serious clinical presentation of venous thromboembolism. Overall, pulmonary embolism is a major cause of mortality, morbidity and hospitalization. Mortality in pulmonary embolism depends on haemodynamic impairment, age and co morbidities. The prognosis of patients with pulmonary embolism depends on two factors : underlying disease state plus diagnosis, and appropriate treatment. Approximately 10% of patients who develop pulmonary embolism die within the first hour, and 30% subsequently die of recurrent embolism. CASE PRESENTATION: In this presentation we present the case of a 49-year-old male patient without co morbidities, presented repeatedly to the Emergency Room for symptoms suggestive of pulmonary thromboembolism, who benefited from life-saving therapies due to timely diagnosis and appropriate treatment, with subsequent favorable outcome. CONCLUSIONS: The particularity of the case is that, on the one hand, the thromboembolic event recurred in a short time, on the other hand, the evolution was favorable in both cases, with complete recovery of right ventricular function and disappearance of pulmonary hypertension, despite the fact that the patient was non-compliant with initial anticoagulation therapy. This was due to both early diagnosis and timely administration of appropriate treatment.

Do the remodeling effects of sacubitril/valsartan treatment depend upon heart failure duration?

The angiotensin receptor and neprilysin inhibitor (ARNI) sacubitril/valsartan (LCZ696) is recommended for the treatment of patients with heart failure in New York Heart Association (NYHA) class II-III and left ventricular ejection fraction (LVEF) 35% or less. We examined the effects of sacubitril/valsartan on cardiac remodeling and their correlation with heart failure duration in patients enrolled in our heart failure clinic from March 2017 to December 2019. Echocardiographic and clinical/laboratory data were collected at baseline and at 6-month and 12-month follow-up visits in 69 patients (age 67 ± 12 years, disease duration 8.4 ± 5.8 years, 93% men). At both time points, mean NYHA class, NT-proBNP level, LVEF, LV end-systolic volume, and estimated systolic pulmonary pressure significantly (P < 0.05) improved versus baseline, as did the proportion of patients with diastolic dysfunction grade 3 or functional mitral regurgitation grade 3-4. In the subgroup with mean disease duration less than 8.5 years (n = 40), there was a significant improvement in all variables at both time points; in this group, a recovery of right ventricular function was also seen at the 12-month follow-up. On the contrary, patients with heart failure duration of at least 8.5 years (n = 29) showed only a slight improvement in LVEF and mitral regurgitation at 12 months. There were no significant changes in renal function and/or potassium levels in all patients. In patients with a relatively short disease duration, sacubitril/valsartan was associated with a strong favorable remodeling of the left ventricle and improvement in pulmonary circulation.

Pulmonary Hypertension and Right Ventricular Failure: Lung Transplant Versus Heart-Lung Transplant.

Pulmonary arterial hypertension is a highly morbid disease with limited treatment options that improve survival and currently the only curative treatment is transplantation. There is a small body of literature comparing the efficacy of lung and heart-lung transplantation in this population. The bulk of evidence suggests that most patients with severe right ventricular failure undergoing transplant will have recovery of right ventricular function after lung transplantation. Existing data suggest that, in the absence of complex congenital heart disease or significant left ventricular dysfunction, double-lung transplant is the surgical procedure of choice.

Delineating the molecular and histological events that govern right ventricular recovery using a novel mouse model of pulmonary artery de-banding.

The temporal sequence of events underlying functional right ventricular (RV) recovery after improvement of pulmonary hypertension-associated pressure overload is unknown. We sought to establish a novel mouse model of gradual RV recovery from pressure overload and use it to delineate RV reverse-remodelling events. Surgical pulmonary artery banding (PAB) around a 26-G needle induced RV dysfunction with increased RV pressures, reduced exercise capacity and caused liver congestion, hypertrophic, fibrotic, and vascular myocardial remodelling within 5 weeks of chronic RV pressure overload in mice. Gradual reduction of the afterload burden through PA band absorption (de-PAB)-after RV dysfunction and structural remodelling were established-initiated recovery of RV function (cardiac output and exercise capacity) along with rapid normalization in RV hypertrophy (RV/left ventricular + S and cardiomyocyte area) and RV pressures (right ventricular systolic pressure). RV fibrotic (collagen, elastic fibres, and vimentin+ fibroblasts) and vascular (capillary density) remodelling were equally reversible; however, reversal occurred at a later timepoint after de-PAB, when RV function was already completely restored. Microarray gene expression (ClariomS, Thermo Fisher Scientific, Waltham, MA, USA) along with gene ontology analyses in RV tissues revealed growth factors, immune modulators, and apoptosis mediators as major cellular components underlying functional RV recovery. We established a novel gradual de-PAB mouse model and used it to demonstrate that established pulmonary hypertension-associated RV dysfunction is fully reversible. Mechanistically, we link functional RV improvement to hypertrophic normalization that precedes fibrotic and vascular reverse-remodelling events.

Evaluation and Management of Right-Sided Heart Failure: A Scientific Statement From the American Heart Association.

The diverse causes of right-sided heart failure (RHF) include, among others, primary cardiomyopathies with right ventricular (RV) involvement, RV ischemia and infarction, volume loading caused by cardiac lesions associated with congenital heart disease and valvular pathologies, and pressure loading resulting from pulmonic stenosis or pulmonary hypertension from a variety of causes, including left-sided heart disease. Progressive RV dysfunction in these disease states is associated with increased morbidity and mortality. The purpose of this scientific statement is to provide guidance on the assessment and management of RHF. The writing group used systematic literature reviews, published translational and clinical studies, clinical practice guidelines, and expert opinion/statements to summarize existing evidence and to identify areas of inadequacy requiring future research. The panel reviewed the most relevant adult medical literature excluding routine laboratory tests using MEDLINE, EMBASE, and Web of Science through September 2017. The document is organized and classified according to the American Heart Association to provide specific suggestions, considerations, or reference to contemporary clinical practice recommendations. Chronic RHF is associated with decreased exercise tolerance, poor functional capacity, decreased cardiac output and progressive end-organ damage (caused by a combination of end-organ venous congestion and underperfusion), and cachexia resulting from poor absorption of nutrients, as well as a systemic proinflammatory state. It is the principal cause of death in patients with pulmonary arterial hypertension. Similarly, acute RHF is associated with hemodynamic instability and is the primary cause of death in patients presenting with massive pulmonary embolism, RV myocardial infarction, and postcardiotomy shock associated with cardiac surgery. Functional assessment of the right side of the heart can be hindered by its complex geometry. Multiple hemodynamic and biochemical markers are associated with worsening RHF and can serve to guide clinical assessment and therapeutic decision making. Pharmacological and mechanical interventions targeting isolated acute and chronic RHF have not been well investigated. Specific therapies promoting stabilization and recovery of RV function are lacking. RHF is a complex syndrome including diverse causes, pathways, and pathological processes. In this scientific statement, we review the causes and epidemiology of RV dysfunction and the pathophysiology of acute and chronic RHF and provide guidance for the management of the associated conditions leading to and caused by RHF.

Catheter-directed interventions compared with systemic thrombolysis achieve improved ventricular function recovery at a potentially lower complication rate for acute pulmonary embolism

ObjectiveCatheter-directed interventions (CDIs) are increasingly performed for acute pulmonary embolism (PE) as they are presumed to provide similar therapeutic benefits to systemic thrombolysis (ST) while decreasing the associated complications. The purpose of this study was to compare outcomes between CDI and ST. MethodsConsecutive patients who underwent CDIs or ST for massive or submassive PE between 2006 and 2016 were identified. Clinical and echocardiographic parameters at baseline and after treatment were recorded. Clinical success was defined as decompensation resolution (or prevention) without major bleeding, stroke, other major treatment-related event, or in-hospital death. The χ2 test and t-test were used for between-groups comparisons. ResultsThere were 213 patients who received CDIs (standard catheter thrombolysis in 56, ultrasound-assisted thrombolysis in 146, suction thrombectomies in 10, and pharmacomechanical thrombolysis in 1) and 104 patients who received ST (94 high dose [100 mg], 10 low dose [50 mg]). At baseline, CDI and ST groups had comparable echocardiographic parameters, demographics, and comorbidities, except for PE type (massive PE, 8.5% for CDIs vs 69.2% for ST; P < .001), age (60.2 ± 14.9 years for CDIs vs 55.9 ± 17.3 years for ST; P = .023), and renal function (glomerular filtration rate, 78.1 ± 33.7 mL/min/1.73 m2 for CDIs vs 64.1 ± 35.2 mL/min/1.73 m2 for ST; P = .001). Without stratifying per PE type, CDIs had a higher clinical success rate (87.8% vs 66.3%; P < .001) and a lower rate of major bleed (8.0% vs 19.2%; P = .003), stroke (1.4% vs 4.8%; P = .120), and death (1.4% vs 13.5%; P < .001). On stratifying by PE type, there was no difference in clinical success between groups. The mean reduction in right ventricular/left ventricular diameter ratio between baseline and the first post-treatment echocardiographic examination (within 30 days) was significantly higher for CDI (0.27 ± 0.20 vs 0.18 ± 0.15; P = .037). Beyond 30 days, there was no echocardiographic difference between groups. There was no significant difference in clinical outcomes and echocardiographic parameters between standard and ultrasound-assisted CDIs. ConclusionsCDIs provide improved recovery of right ventricular function compared with ST. Major bleeding and stroke complications may be lower, but larger studies are needed to validate this. CDIs are complementary to ST, and their use should be individualized on the basis of the patients' clinical presentation, risk profile, and local resources.

Utilization of Veno-Arterial Extracorporeal Membrane Oxygenation for Massive Pulmonary Embolism

The management of massive pulmonary embolism remains challenging, with a considerable mortality rate. Although veno-arterial extracorporeal membrane oxygenation (VA-ECMO) for massive pulmonary embolism has been reported, its use as salvage therapy has been associated with poor outcomes. We reviewed our experience utilizing an aggressive, protocolized approach of VA-ECMO to triage, optimize, and treat these patients. All patients with a massive pulmonary embolism who were placed on VA-ECMO, as an initial intervention determined by protocol, were retrospectively reviewed. ECMO support was continued until organ optimization was achieved or neurologic status was determined. At that time, if the thrombus burden resolved, decannulation was performed. If substantial clot burden was still present with evidence of right ventricular (RV) strain, operative therapy was undertaken. Twenty patients were identified. Before cannulation, all patients had an RV-to-left ventricular ratio greater than 1.0 and severe RV dysfunction. The median duration of ECMO support was 5.1 days, with significant improvement in end-organ function. Ultimately, 40% received anticoagulation alone, 5% underwent catheter-directed therapy, and 55% underwent surgical pulmonary embolectomy. Care was withdrawn in 1 patient with a prolonged pre-cannulation cardiac arrest after confirmation of neurologic death. In-hospital and 90-day survival was 95%. At discharge, 18 of 19 patients had normal RV function, and 1 patient, who received catheter-directed therapy, had mild dysfunction. VA-ECMO appears to be an effective tool to optimize end-organ function as a bridge to recovery or intervention, with excellent outcomes. This approach may allow clinicians to better triage patients with massive pulmonary embolism to the appropriate therapy on the basis of recovery of RV function, residual thrombus burden, operative risk, and neurologic status.

Use of low-dose thrombolytics for treatment of intracardiac thrombus and massive pulmonary embolus after aborted liver transplant leads to recovery of right ventricular function and redo liver transplantation

This is a 61-year-old man with end-stage liver disease who experienced cardiac arrest secondary to a massive pulmonary embolus and intracardiac thrombus during cannulation for veno-venous extracorporeal membrane oxygenation (ECMO)...

Tunneling a Pulmonary Artery Graft: A Simplified Way to Insert and Remove a Temporary Right Ventricular Assist Device.

Right ventricular failure can occur early or late after left ventricular assist device implantation. Support with a right ventricular assist device is needed in patients whose right ventricular failure does not respond to conservative management. The use of a temporary right ventricular assist device can enable the recovery of right ventricular function and avoid the use of a more permanent biventricular assist device, which is associated with complications and higher costs. We present our technique of instituting temporary right ventricular assist device support in patients who have undergone left ventricular assist device implantation.

Impact of Concomitant Tricuspid Annuloplasty on Tricuspid Regurgitation, Right Ventricular Function, and Pulmonary Artery Hypertension After Repair of Mitral Valve Prolapse

BackgroundFor patients undergoing mitral valve (MV) repair, the indications for and results of concomitant tricuspid annuloplasty remain controversial. ObjectivesThis study was designed to compare a strategy of routine concomitant tricuspid annuloplasty for moderate tricuspid regurgitation (TR) or tricuspid annular dilation in patients undergoing degenerative MV surgery. MethodsOf 645 consecutive patients (mean age 57 ± 13 years) undergoing primary repair of degenerative mitral regurgitation between 2003 and 2011, 419 (65%) underwent concomitant tricuspid annuloplasty for moderate TR and/or tricuspid annular dilation. These patients were retrospectively analyzed with longitudinal echocardiographic follow-up. ResultsPatients undergoing tricuspid valve repair were older (mean age 59.2 years vs. 52.3 years), had worse right and left ventricular function and higher pulmonary artery pressures, and were more likely to have had atrial fibrillation than patients undergoing isolated MV repair (all p < 0.05). No significant difference in 30-day mortality, morbidity, or permanent pacemaker requirement was seen between treatment groups. Freedom from moderate TR at 7 years was not significantly different in the 2 groups, but multivariate analysis showed that tricuspid annuloplasty was independently associated with freedom from late moderate TR (p = 0.04), and was an independent predictor of recovery of right ventricular function (p = 0.02). ConclusionsIn patients with moderate TR or tricuspid annular dilation who were undergoing degenerative mitral repair, concomitant tricuspid annuloplasty is safe, effective, and associated with improved long-term right-sided remodeling. Routine treatment of moderate TR or tricuspid annular dilation at the time of MV repair appears to be beneficial.

Assessment of right ventricular function by isovolumic contraction acceleration before and after percutaneous closure of atrial septal defects: a preliminary study.

The main purpose of present study was to investigate the impact of percutaneous closure of atrial septal defect (ASD) on right ventricular (RV) systolic function assessed by tricuspid annular isovolumic myocardial acceleration (IVA) that is independent of preload and afterload changes. A prospective cohort study was designed involving twenty five patients with secundum type ASD whom were successfully closed percutaneously between 2009 and 2011. Standard transthoracic echocardiography and tissue Doppler imaging were performed in all patients 12 to 24 hours before and one month after closure. Paired t test was performed to determine the statistical significance of variables before and after closure. Significant decreases were observed in RV end-diastolic diameter, RV/left ventricular (LV) end-diastolic diameter ratio, right ventricular systolic myocardial velocity (Sm), right ventricular early myocardial velocity (Em) and right ventricular late myocardial velocity (Am) in the control echocardiography in the first month when compared with pre-procedure values. While significant increase was observed after procedure in right ventricular IVA (3.4 ± 1.3 m/sec2 vs. 4.2 ± 1.8 m/sec2, p=0.001), no significant change was observed in right ventricular global performance index, in right ventricular Em/Am ratio and left ventricular ejection fraction. Percutaneous closure of ASD resulted in recovery of right ventricular function as early as 1 month after closure.

Intravenous Sildenafil in Right Ventricular Dysfunction with Pulmonary Hypertension following a Heart Transplant

The objective of the present work is to describe the experience with intravenous (IV) sildenafil in heart transplant (HT) patients with reactive pulmonary hypertension (PH) who developed right ventricular dysfunction (RVD) in the immediate postoperative period. The first 5 patients who received IV sildenafil followinga HT are presented. The HTs took place between March 2011 and September 2012 in patients aged 37 to 64 years; all patients were male. Prior to the HT, mean pulmonary artery pressure (mPAP) was 32-56 mmHg. In all cases, the hemodynamic study demonstrated PH reactivity (positive vasodilator test with nitric oxide). All 5 patients developed RVD with hemodynamic instability immediately after the HT, despite the administration of nitric oxide from the time of intubation prior to the implant, optimal medical treatment in all cases, and a ventricular assist in 2 cases. In all patients, IV sildenafil was initiated at 10 mg/8 h for 48 h and was subsequently increased to 20 mg/8 h. in its oral formulation until discharge from the hospital. The change in pulmonary pressure was assessed using a Swan-Ganz catheter. Ventricular function was assessed using echocardiography. Length of stay in the Resuscitation Unit and mid-term survival were also assessed. Average time of extracorporeal circulation was 200 ± 110 min and organ ischemic time was 210 ± 95 min. All of the patients demonstrated pulmonary and systemic hemodynamic improvement, as well as recovery of right ventricular function after completing the treatment with IV sildenafil. The stay in the Resuscitation Unit lasted 3-25 days. All the patients were discharged from hospital with no mortality to date. Intravenous sildenafil improves right ventricle hemodynamics associated with pulmonary hypertension post-HT. Prophylactic prevention with this drug could be indicated for patients with reactive PH who are about to receive a transplant.