Ventricular Distensibility Research Articles

Incessant Malignant Ventricular Arrhythmia in a Patient with Advanced Heart Failure: A Case Report

Introduction The occurrence of refractory ventricular arrhythmia in patients with heart failure (HF) is a therapeutic dilemma. These patients, especially in the presence of advanced disease, may experience multiple triggering factors for ventricular arrhythmia, such as myocardial fibrosis, ischemia, hydroelectrolytic disorders, ventricular distention, the arrhythmogenic potential of drugs, and the underlying disease itself.– Conversely, sustained ventricular arrhythmias cause hemodynamic compromise, resulting in further ischemia and ventricular distension. This can lead to a vicious cycle of hemodynamic worsening with an increasingly [...]

Left Atrial Decompression in Pediatric Patients Supported With Extracorporeal Membrane Oxygenation for Failure to Wean From Cardiopulmonary Bypass: A Propensity-Weighted Analysis.

Background Left atrial (LA) decompression on extracorporeal membrane oxygenation (ECMO) can reduce left ventricular distension, allowing myocardial rest and recovery, and protect from lung injury secondary to cardiogenic pulmonary edema. However, clinical benefits remain unknown. We sought to evaluate the association between LA decompression and in-hospital adverse outcome (mortality, transplant on ECMO, or conversion to ventricular assist device) in patients who failed to wean from cardiopulmonary bypass using a propensity score to adjust for baseline differences. Methods and Results Children (aged <18years) with biventricular physiology supported with ECMO for failure to wean from cardiopulmonary bypass after cardiac surgery from 2000 through 2016, reported to the ELSO (Extracorporeal Life Support Organization) Registry, were included. Inverse probability of treatment weighted logistic regression was used to test the association between LA decompression and in-hospital adverse outcomes. Of the 2915 patients supported with venoarterial ECMO for failure to wean from cardiopulmonary bypass, 1508 had biventricular physiology and 279 (18%) underwent LA decompression (LA+). Genetic and congenital abnormalities (P=0.001) and pulmonary hypertension (P=0.010) were less frequent and baseline arrhythmias (P=0.022) were more frequent in LA+ patients. LA+ patients had longer pre-ECMO mechanical ventilation and CBP time (P<0.001), and used aortic cross-clamp (P=0.001) more frequently. Covariates were well balanced between the propensity-weighted cohorts. In-hospital adverse outcomes occurred in 47% of LA+ patients and 51% of the others. Weighted multivariate logistic regression showed LA decompression to be protective for in-hospital adverse outcomes (adjusted odds ratio, 0.775 [95% CI, 0.644-0.932]). Conclusions LA decompression independently decreased the risk of in-hospital adverse outcome in pediatric venoarterial ECMO patients who failed to wean from cardiopulmonary bypass, suggesting that these patients may benefit from LA decompression.

Subclavian versus femoral arterial cannulations during extracorporeal membrane oxygenation: A propensity-matched comparison.

During peripheral extracorporeal veno-arterial membrane oxygenation (VA-ECMO) support, subclavian arterial cannulation provides, in comparison to femoral arterial cannulation, an anterograde flow which may prevent from left ventricular (LV) distention and improve outcomes. We aimed to compare the effectiveness of subclavian cannulation to femoral cannulation in reducing LV overdistension consequences, hemostatic complications and mortality. This retrospective study conducted in two intensive care units of the Lille academic hospitals from January 2013 to December 2019 included 372 non-moribund adult patients supported by VA-ECMO. The primary endpoint was a new onset of pulmonary edema (PO) or LV unloading. Secondary endpoints were myocardial recovery, serious bleeding (according to Extracorporeal Life Support Organization definition), thrombotic complications (a composite of stroke, cannulated limb or mesenteric ischemia, intracardiac or aortic-root thrombosis) and 28 day mortality. Differences in outcomes were analyzed using propensity score matching (PSM) and inverse probability of treatment weighting adjustment (IPTW). As compared to femoral cannulation (n=320 patients), subclavian cannulation (n=52 patients) did not reduce the occurrence of new onset of PO or LV unloading after PSM [HR 0.99 (95% CI 0.51-1.91)]. There was no other difference in outcomes in PSM cohort. In IPTW adjustment cohort, subclavian cannulation was associated with reduced recovery and increased serious bleeding with four accidental decannulations observed. Subclavian artery cannulation was not associated with reduced LV distension related complications, thrombotic complications and 28 day mortality. Rather, it may increase serious bleeding and accidental decannulations, and reduce recovery. Therefore, subclavian cannulation should be limited to vascular accessibility issues.

Intra‐Aortic Balloon Pump for Left Ventricular Unloading in Veno‐Arterial Extracorporeal Membrane Oxygenation: The Last Remaining Indication in Cardiogenic Shock

Intra‐Aortic Balloon Pump for Left Ventricular Unloading in Veno‐Arterial Extracorporeal Membrane Oxygenation: The Last Remaining Indication in Cardiogenic Shock

Contribution of Cardiac Magnetic Resonance to Hematochromatosis

Hemochromatosis is a disease characterized by the progressive accumulation of iron in the body. It can be primitive or secondary. It affects several organs including the heart, liver, pancreas and pituitary gland. The preponderant cardiac involvement is myocardial, related to the iron myocyte overload, causing a decrease in left ventricular distensibility. Echocardiography is the first-line examination, showing an abnormality of left ventricular filling and, later, cavitary dilatation with left ventricular systolic dysfunction. Cardiac MRI is the gold standard for measuring excess iron in the myocardium in the context of hemochromatosis using the T2 * technique. It plays a major role for the diagnosis of cardiac involvement and for monitoring the chelation treatment. In this study, we report three cases of patients with hemochromatosis whose cardiac localization was confirmed or eliminated using cardiac MRI. Cardiovascular magnetic resonance has been used to assess myocardial iron deposition using the relaxation parameters T2*. Heart T2* falls with increasing iron loading. One patient had a myocardial T2* below 20 ms indicating myocardial siderosis. The others patients had a T2 *&gt; 20 ms. The late enhancement was absent in all our patients. This study aims at detecting the myocardial iron overload using cardiac MRI. The treatment is based on bleeding in primary hemochromatosis while in secondary hemochromatosis, it is based on excretion of iron by chemical chelation.

Right Ventricular Diastolic Performance in Patients With Chronic Thromboembolic Pulmonary Hypertension Assessed by Echocardiography.

Background: There have been no systemic studies about right heart filling pressure and right ventricular (RV) distensibility in patients with chronic thromboembolic pulmonary hypertension (CTEPH). Therefore, we aimed to explore combinations of echocardiographic indices to assess the stages of RV diastolic dysfunction.Methods and Results: We recruited 32 healthy volunteers and 71 patients with CTEPH. All participants underwent echocardiography, cardiac catheterization (in patients with CTEPH), and a 6-min walk test (6MWT). The right atrial (RA) end-systolic area was adjusted for body surface area (BSA) (indexed RA area). RV global longitudinal diastolic strain rates (SRs) and RV ejection fraction (EF) were measured by speckle tracking and three-dimensional echocardiography (3D echo), respectively. All 71 patients with CTEPH underwent pulmonary endarterectomy. Of the 71 patients, 52 (73%) had decreased RV systolic function; 12 (16.9%), 26 (36.6%), and 33 (46.5%) patients had normal RV diastolic pattern, abnormal relaxation (stage 1), and pseudo-normal patterns (stage 2), respectively. The receiver operating characteristic curve analysis showed that the optimal cut-off values of early diastolic SR <0.8 s−1 and indexed RA area > 8.8 cm2/BSA had the best accuracy in identifying patients with RV diastolic dysfunction, with 87% sensitivity and 82% specificity. During a mean follow-up of 25.2 months after pulmonary endarterectomy, the preoperative indexed RA area was shown as an independent risk factor of the decreased 6MWT distance.Conclusions: Measuring early diastolic SR and indexed RA area would be useful in stratifying RV diastolic function.

Abstract 13331: Case Report Of Transient Right Bundle Branch Block With S1q3t3 Pattern In Acute Pulmonary Embolism

69 year old woman with hypertension, sleep apnea and who had a recent knee replacement, was brought in to the emergency room (ER) for syncope. She had her physiotherapy session earlier in the day and became symptomatic with dizziness and shortness of breath and passed out. In the ER she had a systolic blood pressure (SBP) of 90mmHg and an oxygen saturation (O2 sat) of 80% on room air. She was given fluid bolus with improvement of SBP to 110mmHg. O2 sat improved to 99% with 10L of oxygen. Treatment was started with full dose of Enoxaparin subcutaneously. A 12-lead electrocardiogram (EKG) showed sinus tachycardia (ST) at 117 beats per minute (BPM), right bundle branch block (RBBB) and S1Q3T3 pattern. A bedside echocardiogram showed right ventricular (RV) distension. A CT-angiogram showed bilateral main stem pulmonary emboli (PE) with signs of RV strain. Patient was admitted and remained hemodynamically stable. A repeat EKG done the following day showed ST at 110 BPM with resolution of RBBB. An echocardiogram done now showed normal RV size and function. Patent was eventually discharged home on full dose apixaban. Q3S1T3 Figure 1 - ST, RBBB, S1Q3T3 pattern Figure 2 - ST Discussion: The patient presented with new RBBB (Figure 1) due to RV strain from acute PE as shown by the CT-angiogram and bedside echocardiogram. The EKG also showed S1Q3T3 pattern. With the resolution of the RV strain the following day, as noted on the subsequent echocardiogram, the 12 lead EKG showed the resolution of the RBBB and the QRS complex became narrow (Figure 2). RBBB is thought to be caused by acute RV overload and dilatation, accompanied by subendocardial ischemia in the right bundle. The S1Q3T3 pattern is historically considered as a “classic” EKG pattern associated with acute PE, even though it is neither sensitive nor specific for acute PE. Conclusion: The RBBB along with the S1Q3T3 pattern and its resolution with improvement of RV hemodynamics, is the first reported case in the literature.

Abstract 13889: Impact Of Acute Hypoxia On Left Ventricular Relaxation Time In Healthy Men

Introduction: The oxygen-dependence of myocardial contractility is known but it is not the case for ventricular distension in humans. It has been shown that acute ischemia causes incomplete and retarded relaxation through the decrease in intracellular pH and ATP content. Purpose: to verify whether hypoxemia changes the left ventricular relaxation time (LVRT). Methods: Overall, 37 physically active normotensive men (age 19-42 years, 20.4±2.3 yrs., M±SD) constituted the study sample. The LVRT was derived from aortic pulse wave analysis (SphygmoCor) and measured as difference between the end of systole (ejection duration point, ED, corresponding to the closure of aortic valve) and the time of peak pressure (T1), generated by LV in the aortic root and corresponding to the first incisura [LVRT,%=(ED-T1)/length of cardiac cycle*100]. Subjects inhaled hypoxic mixture with 10%O2 over 10 min for mean blood SpO2 of 80%. Associations were assessed by partial correlation (age, SBP=const.), multiple linear regression analyses (GLM option in SPSS), and t-test for dependent samples. Results: At baseline, the longer length of LVR was associated with lower end systolic blood pressure (r=-0.56, p&lt;0.001). The regression model combining heart rate, augmentation pressure, and aortic-to-radial pulse pressure amplification explained 98.6% of total LVRT variation with significant effects of all covariates. Hypoxia increased LVRT from 19.0±2.8% to 23.1±4.2%, p&lt;0.001. The response of LVRT to hypoxic exposure (range for Δ, -0.7%, +9.1%) was directly correlated with the extent of blood oxygen desaturation (r=0.53, p=0.016). Conclusion: The results show that cardiomyocytes retard their relaxation in hypoxic conditions. Cardiomyocytes happened to be quite sensitive to hypoxemia since even 10-min hypoxia was sufficient for elongation of the ventricular relaxation.

E3-ligase knock down revealed differential titin degradation by autophagy and the ubiquitin proteasome system

The sarcomere protein titin is a major determinant of cardiomyocyte stiffness and ventricular distensibility. The constant mechanical stress on titin requires well-controlled protein quality control, the exact mechanisms of which have not yet been fully elucidated. Here, we analyzed E3-ligases potentially responsible for cardiac titin ubiquitination and specifically studied the involvement of the autophagosomal system in titin degradation. Pharmacological inhibition of autophagy and the proteasome in cultured primary rat cardiomyocytes significantly elevated titin ubiquitination and increased titin degradation. Using in-vitro pull down assays we identified binding of E3-ligases MuRF1-3, CHIP and Fbx32 to several titin domains. Immunofluorescence analysis showed sarcomeric localization of the E3-ligases. siRNA-mediated knock-down of the E3-ligases MuRF-1, -3 and a combination of CHIP/Fbx32 significantly reduced autophagy-related titin ubiquitination, whereas knock-down of MuRF-2 and -3 reduced proteasome-related titin ubiquitination. We demonstrated that the proteasomal and the autophagosomal-lysosomal system participate in degradation of the titin filament. We found that ubiquitination and degradation of titin are partially regulated by E3-ligases of the MuRF family. We further identified CHIP and Fbx32 as E3-ligases involved in titin ubiquitination.

1547 An Alternative Approach to High-Risk Resternotomy

Abstract Introduction Resternotomies are associated with substantial perioperative morbidity and mortality. Strategies described in literature mostly involve peripheral cannulation pre-sternotomy. Disadvantages of this technique relate to prolonged systemic heparinisation and cardiopulmonary bypass (CPB) time and the sequelae of hypothermic circulatory arrest. We describe a two-stage approach that potentially reduces the complications associated with high-risk resternotomy. Method 3 high-risk patients (from pre-operative CT images) were referred for redo complex aortic surgery. A right mini-thoracotomy incision was first made in the 4th or 5th intercostal space. The right lung was isolated and careful blunt dissection was carried out to mobilise the heart and great vessels attached to the sternum. Once these structures were free, thoracotomy incision was closed. A standard median sternotomy was then performed and central cannulation carried out after systemic heparinisation. Rest of the surgery was performed routinely. In one patient, aortic aneurysm was heavily adherent and attempts to mobilise it fully proved impossible. Resultantly, systemic heparinisation was administered and the patient was cannulated in the right superficial femoral artery and right atrium (via mini-thoracotomy). CPB was instituted and the patient cooled to 28 °C. Right superior pulmonary vein vent was introduced to prevent left ventricular distension from hypothermic ventricular fibrillation. Once the heart and aneurysm were decompressed on full CPB, complete mobilisation was performed safely. All 3 patients survived surgery without major complications. Conclusions Meticulous preoperative planning is key to management of high-risk resternotomy. We describe a novel technique which we believe minimises risk of morbidity and mortality in these complex cases.

Aquaporin-4 Mediates Permanent Brain Alterations in a Mouse Model of Hypoxia-Aged Hydrocephalus.

Aquaporin-4 (AQP4) is the principal water channel in the brain being expressed in astrocytes and ependymal cells. AQP4 plays an important role in cerebrospinal fluid (CSF) homeostasis, and alterations in its expression have been associated with hydrocephalus. AQP4 contributes to the development of hydrocephalus by hypoxia in aged mice, reproducing such principal characteristics of the disease. Here, we explore whether these alterations associated with the hydrocephalic state are permanent or can be reverted by reexposure to normoxia. Alterations such as ventriculomegaly, elevated intracranial pressure, and cognitive deficits were reversed, whereas deficits in CSF outflow and ventricular distensibility were not recovered, remaining impaired even one month after reestablishment of normoxia. Interestingly, in AQP4−/− mice, the impairment in CSF drainage and ventricular distensibility was completely reverted by re-normoxia, indicating that AQP4 has a structural role in the chronification of those alterations. Finally, we show that aged mice subjected to two hypoxic episodes experience permanent ventriculomegaly. These data reveal that repetitive hypoxic events in aged cerebral tissue promote the permanent alterations involved in hydrocephalic pathophysiology, which are dependent on AQP4 expression.

Intra-aortic Balloon Pump Use With Extra Corporeal Membrane Oxygenation-A Mock Circulation Loop Study.

Venoarterial extracorporeal membrane oxygenation (ECMO) is used in cardiogenic shock refractory to inotropic support and intra-aortic balloon pump (IABP) support. Peripheral ECMO can lead to ventricular distention, and IABP can be used to mitigate these effects. The aim of this study was to quantify the effects of IABP concomitant with ECMO, under different simulated hemodynamic conditions in a mock circulatory loop. Different simulated states of isolated left ventricular (LV) failure and biventricular failure with graded LV failure severities were supported with ECMO and ECMO with IABP. The impact on left ventricular end-diastolic pressure (LVEDP), volume (LVEDV), coronary flow rate, and cerebral flow rate were evaluated. Left ventricular volumes and pressures increased from the heart failure states with the addition of ECMO. The IABP provided between 3% and 7% reductions in LVEDP and between 1% and 10% reductions in LVEDV. The addition of IABP had minimal effect on cerebral blood flow (0% to 7%), but the variable impact on coronary blood flow with increased diastolic coronary flow of 23% to 50%, but the reduction in mean coronary flow by up to 30%. The efficacy of the IABP was strongly related to ventricular contractility. This study demonstrates the need for careful IABP selection concomitant with ECMO.

Clinical efficacy of direct or indirect left ventricular unloading during venoarterial extracorporeal membrane oxygenation for primary cardiogenic shock

ObjectiveLeft ventricular (LV) distention is a feared complication in patients receiving venoarterial (VA) extracorporeal membrane oxygenation (ECMO). LV unloading can be achieved indirectly with intra-aortic balloon pump (IABP) or directly with an Impella device (Abiomed, Danvers, Mass). We sought to assess the clinical and hemodynamic effects of IABP and Impella devices on patients supported with VA ECMO. MethodsWe conducted a retrospective review of VA ECMO patients at our institution from January 2015 to June 2020. Patients were categorized as either ECMO alone or ECMO with LV unloading. LV unloading was characterized as either ECMO with IABP or ECMO with Impella. We recorded baseline characteristics, survival, complications, and hemodynamic changes associated with device initiation. ResultsDuring the study, 143 patients received ECMO alone whereas 140 received ECMO with LV unloading (68 ECMO with IABP, 72 ECMO with Impella). ECMO with Impella patients had a higher incidence of bleeding events compared with ECMO alone or ECMO with IABP (52.8% vs 37.1% vs 17.7%; P < .0001). Compared with ECMO alone, ECMO with IABP patients had better survival at 180 days (log rank P = .005) whereas survival in ECMO with Impella patients was not different (log rank P = .66). In a multivariable Cox hazard analysis, age (hazard ratio [HR], 1.02; 95% confidence interval [CI], 1.00-1.03; P = .015), male sex (HR, 0.54; 95% CI, 0.38-0.80; P = .002), baseline lactate (HR, 1.06; 95% CI, 1.02-1.11; P = .004), baseline creatinine (HR, 1.06; 95% CI, 1.00-1.11; P = .032), need for extracorporeal membrane oxygenation-cardiopulmonary resuscitation (HR, 2.09; 95% CI, 1.40-3.39; P = .001), and presence of pre-ECMO IABP (HR, 0.45; 95% CI, 0.25-0.83; P = .010) were associated with reduced mortality. There was no significant difference in hemodynamic changes in the ECMO with IABP versus ECMO with Impella cohorts. ConclusionsConcomitant support with IABP might help reduce morbidity and improve 180-day survival in patients receiving VA ECMO for cardiogenic shock.

Electrocardiogram Findings Associated With Malignant Pericardial Effusion and Cardiac Tamponade.

Electrocardiogram Findings Associated With Malignant Pericardial Effusion and Cardiac Tamponade.

Anesthetic management of a patient with severe aortic regurgitation undergoing reoperation for ascending aorta false aneurysm using hypothermia: prevention of ventricular fibrillation by nifekalant

BackgroundTo prevent cardiac collapse and to protect cerebral function, hypothermic cardiopulmonary bypass is established before resternotomy. However, ventricular fibrillation under hypothermia facilitates left ventricular distension, which causes irreversible myocardial damage when the patient has aortic regurgitation. We report a case of successful management in preventing ventricular fibrillation under hypothermia by using nifekalant.Case presentationA 56-year-old male, who had been performed a David operation, was scheduled for a Bentall operation for a pseudo aortic aneurysm with severe aortic regurgitation. After inducing anesthesia, we administered intravenous nifekalant and a vent tube was inserted into the left ventricle under one-lung ventilation. Extracorporeal circulation was established and resternotomy started after cooling to 27 °C. Although severe bradycardia and QT prolongation were observed, ventricular fibrillation did not occur until aortic cross-clamping.ConclusionCombining maintaining cerebral perfusion and avoiding left ventricle distension during hypothermia was successfully managed with nifekalant in our redo cardiac patient with aortic regurgitation.

RA pressure waveforms as a means for describing right ventricular diastolic stiffness

Introduction Exercise-induced changes in right atrial (RA) pressure associates with morality in patients with pulmonary hypertension (PH). Increased right ventricular (RV) diastolic stiffness impairs right ventricular filling during atrial contraction. Right atrial waveforms consist of the a-wave (atrial contraction) and v-wave (RA passive filling), as well as x and y descents representing atrial relaxation and ventricular filling, respectively. Ventricular distensibility has been associated with the difference between the x- and y-descents (x-y difference) in RA pressure. A positive x-y difference correlates with increased ventricular stiffness. The study aim was to investigate the relationship between RA pressure waveforms and RV diastolic function in patients with pulmonary arterial hypertension (PAH). We hypothesized that exercise-induced increases in RA pressure associate with increased RV diastolic stiffness and a positive x-y difference. Methods Participants (n = 52) with a right heart catheterization (RHC) and invasive cardiopulmonary exercise test were selected from the University of Arizona Pulmonary Hypertension Registry. Resting (REST) and peak exercise (EX) measurements of RA pressure (RAP), pulmonary artery pressure (PAP), cardiac output (CO), and heart rate (HR) were analyzed. Raw RA waveforms were analyzed to identify the a-wave, v-wave, and x- and y-descents using a custom MATLAB program. Single-beat methods were used to calculate end-diastolic elastance (Eed) a measure of RV stiffness. Wilcoxon signed-rank test was used test differences between rest and exercise conditions (R version 4.0.3). Data is presented as mean ± standard deviation or median [IQR]. A p< 0.05 is considered significant. Results Forty-three participants with pulmonary arterial hypertension diagnosis (age: 53 ± 13, sex: 73% female) and 9 participants without PH (age: 61 ± 13 years, sex: 100% female) were included. At rest, patients with pulmonary hypertension have increased PAP (37 ± 11 vs 16 ± 5 mmHg, p < 0.001) but no significant differences in RAP (2.7 [0.5-4.7] vs 0.1 [-0.1 – 3.0] mmHg, p = 0.4). There is a non-significant increase in Eed (0.61 [0.34-0.93] vs. 0.31 [0.26-0.53] mmHg/ml, p = 0.07) compared to controls. At peak exercise (PAH: 20 [10-50] W and controls: 30 [10-60] W), RA pressure significantly increased (Figure 1A). Participants with PAH had an exercise-induced increase in RA x-descent (Figure 1B) and y-descent (Figure 1C). There was an exercise-induced decrease in the x-y descent in participants with PAH but not Controls (Figure 1D). The x-y difference did not correlate with resting Eed at rest (p = 0.58) or peak exercise (p = 0.22). Discussion/Conclusion Exercise significantly increased average RA, x-descent, and y-descent pressure. The RA x-y difference did not correlate with end-diastolic elastance, another measure of ventricular stiffness. Overall, exercise decreased the x-y difference in participants with PAH that suggests an exercise-induced increase in ventricular distensibility. Further investigations are needed to determine if exercise-induced changes in RA pressure can unmask structural or pressure induced changes in RV diastolic function.

Clinical and Hemodynamic Efficacy of Left Ventricular Unloading during Venoarterial Extracorporeal Membrane Oxygenation

<h3>Purpose</h3> Left ventricular (LV) distention is a feared complication in patients on venoarterial extracorporeal membrane oxygenation (VA-ECMO) for cardiogenic shock. LV unloading could be achieved with concomitant intra-aortic balloon pump (IABP) or Impella. We sought to assess the clinical and hemodynamic effects of IABP and Impella on patients supported with VA-ECMO <h3>Methods</h3> We conducted a retrospective review of patients who received VA-ECMO at our institution between January 2015 and June 2020. Patients with post-cardiotomy shock were excluded. Patients were categorized as having received either ECMO alone or ECMO+LV unloading. LV unloading was further characterized as either ECMO+IABP, or ECMO+Impella. We recorded baseline characteristics, post-operative complications, and hemodynamic changes associated with device initiation. <h3>Results</h3> During the study period, 142 patients received ECMO alone, 76 received ECMO+IABP, and 76 received ECMO+Impella. The ECMO+LV unloading group had more male patients compared to ECMO alone (70.4% vs 57.5%, p=0.026). 39.4% of ECMO alone patients survived to discharge, compared to 44.4% of ECMO+LV unloading patients (p=0.12). The ECMO+LV unloading group showed a greater decrease in mean pulmonary diastolic pressures compared to ECMO alone after 24 hours of support (-6.0 ± 8.4 mmHg vs -0.1 ± 10.8 mmHg, p = 0.032). ECMO+Impella patients had a higher incidence of bleeding events compared to ECMO alone or ECMO+IABP (52.6% vs 37.3% vs 20.8%, p = 0.0003). Kaplan Meier analysis revealed that ECMO+IABP had better survival compared to ECMO alone and ECMO+Impella (Figure 1). In a multivariable Cox-hazard analysis, age (HR= 1.02), male sex (HR=0.57), baseline lactate (HR =1.05), baseline creatinine (HR=1.06), need for ECPR (HR=2.21) and presence of IABP (HR=0.48) were independent predictors for mortality. <h3>Conclusion</h3> Concomitant support with IABP may help to reduce morbidity in patients on VA-ECMO for cardiogenic shock.

Left Atrial Veno-Arterial Extracorporeal Membrane Oxygenation (LAVA-ECMO) is a Feasible Option for Patients in Cardiogenic Shock for Whom Impella Offloading is Contraindicated

Introduction Left ventricular thrombus is a potentially life-threatening condition with significant risk of catastrophic embolic events. We present a case of a young patient with cardiogenic shock and biventricular thrombi salvaged by utilizing left atrial veno-arterial extracorporeal membrane oxygenation (LAVA-ECMO). Case Report A 20-year-old male presented with acute biventricular cardiogenic shock with progressive end organ injury. An echocardiogram revealed a left ventricular ejection fraction of 10% with biventricular apical thrombi. The multidisciplinary Shock Team recommended further support with VA-ECMO. However, VA-ECMO alone increases afterload and possibly worsens ventricular distention, potentially leading to stasis, thrombus development, and pulmonary edema. An Impella device is often used to decompress the ventricle; however, it was contraindicated in this patient due to the left ventricular thrombus. Therefore, the decision was made to offload the left ventricle using a left atrial catheter placed percutaneously via the common femoral vein, with transseptal access to the left atrium for cannulation of LAVA-ECMO. This multistage catheter allowed both atria to be drained simultaneously, unloading both ventricles of the heart. Ultimately, the patient was deemed not to be a candidate for transplant due to obesity. He was transitioned to a Heartmate 3 durable left ventricular assist device (LVAD) on hospital day 6, with concurrent insertion of a Sentinel embolic protection device—with multiple captured debris upon removal— and surgical removal of the thrombi. He remained neurologically intact postoperatively and was discharged home after 21 days in the hospital. He was diagnosed with a familial cardiomyopathy with plans for weight loss and cardiac transplantation. Summary Biventricular thrombosis is a rare finding in a patient with profound cardiogenic shock, which complicates treatment options. LAVA-ECMO can provide biventricular support without the need for intraventricular device placement and should be considered early in the course of this disease.

Modalities of Left Ventricle Decompression during VA-ECMO Therapy.

Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is used to sustain circulatory and respiratory support in patients with severe cardiogenic shock or refractory cardiac arrest. Although VA-ECMO allows adequate perfusion of end-organs, it may have detrimental effects on myocardial recovery. Hemodynamic consequences on the left ventricle, such as the increase of afterload, end-diastolic pressure and volume, can lead to left ventricular (LV) distention, increase of myocardial oxygen consumption and delayed LV function recovery. LV distention occurs in almost 50% of patients supported with VA-ECMO and is associated with an increase in morbidity and mortality. Thus, recognizing, preventing and treating LV distention is key in the management of these patients. In this review, we aim to discuss the pathophysiology of LV distention and to describe the strategies to unload the LV in patients supported with VA-ECMO.

The heart as a spring, the measurement of myocardial bounce to assess left ventricular function on cardiac MR.

Little has been reported on the left ventricular myocardial distension (bounce) and its utility to assess cardiac function. The purpose of this study is to determine whether myocardial bounce at end diastole is reproducibly visualized by blinded observers and to determine whether it corresponds to systolic and diastolic function. 144 Consecutive cardiac MR exams between September and December 2017 were selected for analysis. The bounce was graded by two blinded observers, and the change in LV diameter pre and post bounce was measured. The bounce was defined as the rapid change in LV volume that occurs at the end of diastole during atrial contraction just prior to systolic ejection. Inter-reader agreement was summarized using Cohen's kappa. Spearman's rank correlation coefficient was used to evaluate associations between bounce grade and cardiac physiology parameters. Overall agreement was good with unweighted kappa = 0.69 (95% CI 0.60-0.79). Bounce grade was significantly correlated with the average change in LV diameter before and after the bounce (Spearman's rho = 0.76, p < 0.001). Median diameter changes were 0.0, 1.9, and 4.2mm in grades 0 (no bounce), 1 (small bounce), and 2 (normal), respectively. The bounce lasted 8 to 12ms in all patients. Bounce grade was significantly correlated with LV EF (Spearman's rho = 0.43, p < 0.001). Median EF was 44%, 51%, and 58% in grades 0, 1, and 2, respectively. Of the 87 patients who had E/A ratio or E/e' ratio measured, bounce grade was also significantly correlated with E/A ratio (r = - 0.24, p = 0.034) and E/e' ratio (r = - 0.24, p = 0.022), with lower grades having higher ratio values on average (Table 4). Of the 15 patients with a bounce grade of 0 by one or both readers and EF ≥ 50%, 8 had E/A ratio measurements and 7 had E/e' ratio measurements. The E/A ratio values ranged from 1 to 2.7 (median 1.5). The E/e' ratio values ranged from 4.8 to 9.6 (median 7.7). The simple observation of a normal myocardial bounce during cine loop review of cardiac MR exams was predictive of normal diastolic and systolic cardiac function. Lack of myocardial bounce was highly associated with both systolic and diastolic dysfunction. The subpopulation of patients with loss of myocardial bounce and normal ejection fraction appear to represent patients with early diastolic dysfunction. Further studies with more diastolic dysfunction MRs are needed to examine this relationship. This study suggests changes to the myocardial bounce seen on cardiac MR may be a simple useful tool for detecting cardiac dysfunction. This study is not to replace, but rather aid the clinical diagnosis and management of both diastolic and systolic dysfunction.