Ventricular Septal Shift Research Articles

Impella 5.5 Support for Delayed Surgical Ventricular Septal Defect Repair-A Paradigm Shift?

Ventricular septal defects (VSDs) remain a rare but life-threatening complication of myocardial infarction. Although the incidence has decreased due to better treatment options, the mortality rate remains high. The timing of VSD repair remains critical to outcome. The use of mechanical circulatory support is rarely described in the literature, although it may help to delay repair to allow tissue stabilization. While Impella is currently considered contraindicated due to the potential worsening of the right-to-left shunt and possible systemic embolization of necrotic debris, there is no comprehensive evidence for this. Therefore, we aimed to analyze whether the use of Impella 5.5 as a first choice for patients undergoing VSD repair should be considered for discussion. This retrospective study analyses four consecutive patients who underwent delayed ventricular septal repair after prior implantation of Impella 5.5 (Abiomed Inc., Danvers, Massachusetts, United States). A total of 75% of patients (n = 3) presented with acute right heart failure prior to implantation with a mean systolic pulmonary artery pressure of 64 ± 3.0 mmHg. Implantation was performed under local anesthesia in three cases. The mean time to surgery was 9.8 ± 3.1 days. All patients remained on the Impella 5.5 device postoperatively. Weaning from Impella 5.5 was successful in 75% (n = 3). The mean length of stay in the intensive care unit was 22.3 ± 7.5 days. Preoperative implantation of the Impella 5.5 device is a safe and feasible option for patients undergoing VSD repair. Outcomes may be improved by performing Impella implantation under local anesthesia and continuing Impella support after VSD repair. However, it is important to note that these patients represent a high-risk cohort and the mortality rate remains high.

P398 ACUTE PERICARDITIS COMPLICATED BY RAPID DEVELOPMENT OF CONSTRICTION: A CASE REPORT

Abstract A 57–years–old man with no previous cardiovascular history presented with fever, hypotension, dyspnoea at rest and chest pain. The electrocardiogram showed sinus tachycardia, PR–segment depression and diffuse concave–upwards ST–segment elevation. Elevated C–reactive protein and low pro–BNP level were found at lab tests, procalcitonin and troponin were negative. Chest X–ray showed bilateral pleural effusion. Transthoracic echocardiogram (TTE) revealed mild–to–moderate serofibrinous pericardial effusion with initial diastolic collapse of right chambers, suggesting cardiac pre–tamponade. Because of the exiguity of liquid component, pericardiocentesis was not performed, patient was stabilized by fluid–challenge with hypertonic solution. Ibuprofen and colchicine were started. Left thoracentesis was performed removing one liter of fluid overall compatible with transudate. Cytological and microbiological examinations were negative. Despite of initial clinical improvement, the patient showed kidney failure and worsening of lung failure; perianal abscess was detected causing sepsis and requiring surgical drainage and antibiotic therapy with vancomycin and piperacillin/tazobactam. Culture exams were negative. After ibuprofen replacement with indomethacin a repeated TTE showed reduced pericardial effusion, but also respiratory variation in ventricular filling with signs of interventricular dependence. Cardiac magnetic resonance showed thickening and high signal intensity of pericardial layers on T2 weighted imaging and ventricular septal shift on free–breathing cine sequences, suggesting effusive–constrictive pericarditis. Left and right cardiac catheterization demonstrated ventricular “dip and plateau” pattern and ventricular discordance. Considering the lack of clinical improvement on medical therapy, off–bypass pericardiectomy was performed. Incomplete adhesion between the two pericardial layers and thick gelatinous material were found. After surgery patient experienced rapid clinical improvement; cardiac index increased from 1.5 to 3.5 L/min/m2. Effusive–constrictive pericarditis is a rare and dreaded complication of acute pericarditis. Surgery, when appropriated, is crucial for prognosis. In our case initial response to anti–inflammatory therapy with reduced pericardial effusion unmasked constrictive physiology in an effusive–constrictive pericarditis. Clinical management was complicated by sepsis which could have played a role in constriction developing.

Abstract 15557: Missed Diagnosis of Constrictive Pericarditis: Importance of Multimodality Imaging

Introduction: Constrictive pericarditis is a potentially reversible cause of hypotension that is diagnostically challenging. Multimodality imaging is important in the evaluation of patients for constrictive pericarditis to ensure timely management. Case Presentation: A 68-year-old female with a history of chronic hypotension controlled with midodrine and fludrocortisone, end-stage renal disease, and rheumatoid arthritis was admitted to our hospital following a ground-level fall leading to left femur fracture. At admission, her blood pressure was 100/72 mmHg and heart rate was 84 per minute. No pericardial rub, murmurs, or jugular venous distension were present. Laboratory evaluation revealed normal serum electrolytes, thyroid-stimulating hormone, and morning cortisol levels. A routine transthoracic echocardiogram was performed as part of her perioperative cardiac evaluation that demonstrated a beat-to-beat septal diastolic shudder and annulus reversus suggestive of constrictive pericarditis. These findings were confirmed with cardiac magnetic resonance imaging (CMR) that showed pericardial thickening, tubular-shaped right ventricle with impaired filling, septal bounce as well as respirophasic early diastolic septal flattening. Cardiothoracic surgery was consulted however definitive management with pericardiectomy is pending at the time of this report. Conclusion: With recent advances in tissue Doppler imaging, echocardiography can be used in clinical practice to diagnose constrictive pericarditis. Reversal of the relationship between lateral and medial e` velocities (annulus reversus) and respiration-related ventricular septal shift (septal shudder) are suggestive of constrictive pericarditis.

Characteristics and Clinical Outcomes of Cancer Patients who Developed Constrictive Physiology After Pericardiocentesis.

This study aimed to identify the characteristics and clinical outcomes of cancer patients who developed constrictive physiology (CP) after percutaneous pericardiocentesis. One-hundred thirty-three cancer patients who underwent pericardiocentesis were divided into 2 groups according to follow-up echocardiography (CP vs. non-CP). The clinical history, imaging findings, and laboratory results, and overall survival were compared. CP developed in 49 (36.8%) patients after pericardiocentesis. The CP group had a more frequent history of radiation therapy. Pericardial enhancement and malignant masses abutting the pericardium were more frequently observed in the CP group. Fever and ST segment elevation were more frequent in the CP group, with higher C-reactive protein levels (6.6±4.3mg/dL vs. 3.3±2.5mg/dL, p<0.001). Pericardial fluid leukocytes counts were significantly higher, and positive cytology was more frequent in the CP group. In baseline echocardiography before pericardiocentesis, medial e' velocity was significantly higher in the CP group (8.6±2.1cm/s vs. 6.5±2.3cm/s, p<0.001), and respirophasic ventricular septal shift, prominent expiratory hepatic venous flow reversal, pericardial adhesion, and loculated pericardial fluid were also more frequent. The risk of all-cause death was significantly high in the CP group (hazard ratio, 1.53; 95% confidence interval,1.10-2.13; p=0.005). CP frequently develops after pericardiocentesis, and it is associated with poor survival in cancer patients. Several clinical signs, imaging, and laboratory findings suggestive of pericardial inflammation and/or direct malignant pericardial invasion are frequently observed and could be used as predictors of CP development.

Abstract 16631: Predictors of Left Ventricular Dysfunction in Patients After Anatomic Repair of Congenitally Corrected Transposition of the Great Arteries

Introduction: After anatomic repair (AR) of congenitally corrected transposition of the great arteries (ccTGA), the left ventricle (LV) is re-established as the systemic ventricle. As such, LV dysfunction is an important factor in long-term patient morbidity. While predictors exist for successful AR, little is known regarding measures of LV function before and after AR, and no known predictors exist of worsening global longitudinal strain (GLS). Methods: All patients with ccTGA who survived to discharge after AR at a single institution from 2000-2018 were included. Pre-operative and discharge echocardiograms were reviewed and GLS analysis was performed. LV sphericity index was measured to determine the degree of ventricular septal shift; a lower index denotes more septal bowing into the LV. Logistic regression was used to identify factors associated with worsened GLS after AR. Results: Of 91 survivors (65% male), 51 underwent Senning/arterial switch (ASO) and 40 had Senning/Rastelli. Mean LV ejection fraction (EF) decreased from 66% to 61% after AR (p = 0.0003) with 26% having LVEF less than or equal to 55% (increased from 4% pre-op, p = 0.0003). Mean LV GLS was normal pre-op (-20.0% ± SD 4.1%) but worsened following AR (-16.5% ± 4.6%; p &lt;.0001); abnormal LV GLS (&gt; -18%) increased to 62% (vs 32% pre-op, p &lt;.0001). More patients undergoing Senning/ASO (78%) had abnormal LV GLS at discharge compared to those with a Senning/Rastelli (22%) (odds ratio [OR] 9.3, p &lt;.0001). Abnormal pre-op GLS (OR 5.8, p = 0.002) and lower LV sphericity index (OR 1.05, p = 0.01) were also significantly associated with worsening GLS at discharge. In multivariable analysis, all three remained independently associated with worsened LV GLS. Age at AR, ventricular looping, LV posterior wall thickness, and reintervention prior to discharge were not associated with changed LV GLS at discharge. Conclusions: Following AR of ccTGA, LVEF decreases but remains in the normal range, while LV GLS detects abnormalities. Risk factors for worsening GLS include abnormal pre-op LV GLS, lower LV sphericity index, and a Senning/ASO repair. Lower LV sphericity index, or more septal shift into the LV, may represent a “less trained” LV, highlighting the need for careful patient selection for AR.

P1725 An easily dismissed suspect

Abstract Funding Acknowledgements None Introduction Constrictive pericarditis (CP) is a rare etiology of heart failure. Is a chronic inflammatory process, characterized by scarring, fibrosis and pericardial calcification. Several etiologies can be associated with CP, namely infectious, idiopathy and post-surgical. In some cases, CP can extend to the myocardium and/or lead to cardiac dysfunction. Case Report 58 years old woman, active smoking, referred to the emergency room for tachycardia on a routine electrocardiogram. History of 5 months of fatigue and dyspnea to ordinary activities, with progressive aggravation in the last month, associated with weight loss and episodic palpitations. Upon the physical examination presented jugular vein engorgement and peripheral edema. Admission electrocardiogram with atrial flutter at 150 of ventricular frequencies, without other findings. Thoracic radiography without variation (tenues pericardium enhancement), abdominal echography with moderate ascites. Blood work showed elevated liver enzymes, BNP of 230pg/ml, exclusion of infectious tuberculosis and autoimmune panel with isolated positive rheumatoid factor. Transthoracic echocardiography (TTE) at the emergency room show a non-dilated and global left ventricle hypokinesia, with reduced left ventricular ejection fraction (LVEF) and dilatation of the mitral valve ring in the genesis of moderate mitral regurgitation. Anticongestive and antiarrhythmic therapy started with rhythm conversion and clinical improve. Thoracic computed tomography scan reveals an extensive pericardial calcification. 2 months later TTE reveal a preserved LVEF, pericardial calcification, moderate mitral regurgitation, grade III diastolic dysfunction, respiration-related ventricular septal shift, increased of the mitral E-wave velocity with an E/A of 2.76, the peak mitral E-wave decreases 36% with the inspiration, dilated inferior vena cava without respiratory variation. Cardiac magnetic resonance imaging exposes a septal bounce and pericardial calcification, suggestive signs of constrictive pericarditis. The patient waits for cardiac catheterization for confirmation, being with anticoagulation, ACE inhibitors, beta-blockers and mineralocorticoid receptor antagonist medication, remaining in NYHA class I. Discussion Clinical suspicion of CP is key for its identification, since there is not a specific clinical manifestation and generally patients presented heart failure symptoms. Echocardiography is best tool for a clinical physician evaluate heart failure etiologies, and can be used with higher sensitivity and specificity associated to the correct criteria to the diagnosis of CP. Pericardiectomy is the standard treatment, however the moment of its performance is not well established, since patients can remain in NYHA class I several years and the surgical procedure have higher mortality rates.

Differentiating Constriction from Restriction (from the Mayo Clinic Echocardiographic Criteria)

Constrictive Pericarditis (CP) is a curable and reversible form of severe diastolic heart failure. We aimed to investigate the diagnostic accuracy of published echocardiographic Mayo Clinic Criteria in differentiating 107 patients with surgically proven CP from 30 patients with restrictive cardiomyopathy due to cardiac Amyloidosis. Five principal echocardiographic and Doppler variables were remeasured on preoperative transthoracic echocardiogram namely (1) respiration-related ventricular septal shift; (2) respiratory variation in mitral inflow E pulsed Doppler velocity; 3) tissue Doppler medial mitral annular e' velocity; (4) ratio of medial mitral annular e' to lateral mitral annular e' velocity; and 5) hepatic vein (HV) pulsed Doppler diastolic flow reversal ratio. Etiology of CP included viral/idiopathic or autoimmune (75%), postcardiac surgery (13%) and postradiation (7%). Univariate logistic regression analysis showed that (1) respiration related ventricular septal shift, (2) percentage change in Mitral E velocity, (3) medial e' velocity ≥9 cm/sec, (4) medial e'/lateral e' ratio ≥0.91, (5) HV diastolic reversal ratio ≥0.79 were associated with the diagnosis of CP. Multivariable logistic regression analyses showed that medial e' velocity ≥9 cm/s was independently associated with the diagnosis of CP. Respiration related ventricular septal shift had the highest sensitivity, whereas medial e' velocity ≥9 cm/s has the highest specificity to diagnose CP (Areas under curves 0.99, p 0.001). Combining respiration related ventricular septal shift with medial e' velocity ≥9 cm/s gave a desirable sensitivity (80%) and specificity (92%). Adding reversal ratio to this combination further increased the specificity (97%) but dropped the sensitivity (70%) to diagnose CP.

Left ventricular diastolic dysfunction in patients with chronic obstructive pulmonary disease: Impact of methods of assessment.

The prevalence of left ventricular (LV) diastolic dysfunction in patients with chronic obstructive pulmonary disease (COPD), using different echocardiographic parameters, varies widely in the literature. The highest prevalence of LV diastolic dysfunction was detected using the mitral inflow indexes that are commonly altered in these patients due to the associated tachycardia, reduced preload, and ventricular septal shift. In this study, we aimed at evaluating the impact of the used echocardiographic method of assessment on the prevalence of LV diastolic dysfunction in patients with COPD and normal LV systolic function. We studied 35 patients with COPD and 18 age-matched controls. A comprehensive approach to diagnose and grade the LV diastolic dysfunction was performed in accordance with the recommendations of the American Society of Echocardiography published in 2009. The results were compared with those of mitral inflow indexes. LV diastolic dysfunction was reported in 20 patients using the mitral inflow indexes while in only 12 patients using the comprehensive approach (P=.021). Compared to the controls, LV diastolic dysfunction was significantly more common in patients using the mitral inflow indexes (P=.001), while no statistically significant difference was detected between both groups using the comprehensive approach (P=.1). The prevalence of LV diastolic dysfunction in patients with COPD varies according to the used echocardiographic approach. Further studies are recommended to determine which approach is the most accurate in estimating the true prevalence of LV diastolic dysfunction among this group of patients.

Abstract 13989: Duration of Interventricular Septal Shift Predicts Clinical Outcome in Patients With Precapillary Pulmonary Hypertension: A CMR Study

Introduction: Right ventricular pressure overload results in interventricular septal (IVS) shift towards the left ventricle in patients with precapillary pulmonary hypertension (pPH). Hypothesis: The duration of IVS shift towards left ventricle during the cardiac cycle, as expressed by a novel marker called curvature duration index (CDi), predicts clinical outcome in pPH patients. Methods: This was a prospective study. All patients underwent cardiac magnetic resonance (CMR, Avanto Siemens 1,5T). CMR parameters of right ventricular function and dimensions were assessed. CDi (duration of IVS shift towards left ventricle x 100/cardiac cycle duration) was defined in the short-axis view at the level of papillary muscles (Figure 1). Time from enrollment to clinical failure (hospitalization due to pPH, initiation of parenteral prostanoid therapy, atrial septostomy or death) was recorded. Results: Our study included 36 consecutive patients (28 women, mean age 50.6±13.8 years) with pPH. Over a median follow-up period of 20.4 months (IQR 16.3-24.6 months) 14 clinical events were observed. In Cox proportional hazard analysis, only baseline CDi was significantly related to the composite event (HR 1.05, 95% CI 1.01-1.08, p=0.016). ROC curve analysis showed that the optimal cut-off value of CDi which predicted events was 66.7%. Kaplan-Meier survival analysis showed that CDi ≥66.7% was associated with a 9-fold increased risk for clinical failure (Figure 2). Conclusions: Ventricular septal shift towards left ventricle lasting for more than the 2/3 of the cardiac cycle is associated with worse prognosis in pPH.

Echocardiographic Diagnosis of Constrictive Pericarditis

Background— Constrictive pericarditis is a potentially reversible cause of heart failure that may be difficult to differentiate from restrictive myocardial disease and severe tricuspid regurgitation. Echocardiography provides an important opportunity to evaluate for constrictive pericarditis, and definite diagnostic criteria are needed. Methods and Results— Patients with surgically confirmed constrictive pericarditis (n=130) at Mayo Clinic (2008–2010) were compared with patients (n=36) diagnosed with restrictive myocardial disease or severe tricuspid regurgitation after constrictive pericarditis was considered but ruled out. Comprehensive echocardiograms were reviewed in blinded fashion. Five principal echocardiographic variables were selected based on prior studies and potential for clinical use: (1) respiration-related ventricular septal shift, (2) variation in mitral inflow E velocity, (3) medial mitral annular e' velocity, (4) ratio of medial mitral annular e' to lateral e', and (5) hepatic vein expiratory diastolic reversal ratio. All 5 principal variables differed significantly between the groups. In patients with atrial fibrillation or flutter (n=29), all but mitral inflow velocity remained significantly different. Three variables were independently associated with constrictive pericarditis: (1) ventricular septal shift, (2) medial mitral e', and (3) hepatic vein expiratory diastolic reversal ratio. The presence of ventricular septal shift in combination with either medial e'≥9 cm/s or hepatic vein expiratory diastolic reversal ratio ≥0.79 corresponded to a desirable combination of sensitivity (87%) and specificity (91%). The specificity increased to 97% when all 3 factors were present, but the sensitivity decreased to 64%. Conclusions— Echocardiography allows differentiation of constrictive pericarditis from restrictive myocardial disease and severe tricuspid regurgitation. Respiration-related ventricular septal shift, preserved or increased medial mitral annular e' velocity, and prominent hepatic vein expiratory diastolic flow reversals are independently associated with the diagnosis of constrictive pericarditis.

Novel control system to prevent right ventricular failure induced by rotary blood pump

Right ventricular (RV) failure is a potentially fatal complication after treatment with a left ventricular assist device (LVAD). Ventricular septal shift caused by such devices is an important factor in the progress of RV dysfunction. We developed a control system for a rotary blood pump that can change rotational speed (RS) in synchrony with the cardiac cycle. We postulated that decreasing systolic RS using this system would alter ventricular septal movement and thus prevent RV failure. We implanted the EVAHEART ventricular assist device into seven adult goats weighing 54.1 ± 2.1 kg and induced acute bi-ventricular dysfunction by coronary embolization. Left and RV pressure was monitored, and ventricular septal movement was echocardiographically determined. We evaluated circuit-clamp mode as the control condition, as well as continuous and counter-pulse modes, both with full bypass. As a result, a leftward ventricular septal shift occurred in continuous and counter-pulse modes. The septal shift was corrected as a result of decreased RS during the systolic phase in counter-pulse mode. RV fractional area change improved in counter-pulse (59.0 ± 4.6%) compared with continuous (44.7 ± 4.0%) mode. In conclusion, decreased RS delivered during the systolic phase using the counter-pulse mode of our new system holds promise for the clinical correction of ventricular septal shift resulting from a LVAD and might confer a benefit upon RV function.

How rapidly can diastolic function alter with acute afterloading: insights from a closed chest/closed pericardium acute afterload porcine model

Cardiologia CROATICA Background: The speed and timing of changes in diastolic function parameters during acute LV loading and unloading is unknown. Methods: In a closed chest, closed pericardium porcine model, LV systolic pressure was increased by 30% using a transient descending aortic partial balloon inflation. Morphology and mechanical changes were monitored in real time by echocardiography, as were changes in left and right heart diastolic pressures by 3 Millar catheters. Simultaneous blood pool and tissue Doppler data (radial and long axis) were acquired during afterload changes. Results: In 7 animals, acute loading consistently induced LV dilatation and a rightwards ventricular septal shift due to lateral LV pericardial restraint. This reduced RV volume. Afterload increase caused an immediate decrease in early diastolic filling wave (E) and lateral wall velocity (E’). This was mirrored by an immediate increase in both early diastolic LV (LVDPmin) and LA (LADPmin) pressure (Figure 1). Pulmonary vein flow gradually reduced with decreased late flow. The rightwards septal shift induced a small but significant increase in RVDPmin and an increase in mean RA pressure, but failed to increase pulmonary artery pressure. Acute afterload release immediately returned E values to baseline, but E’ showed a transient further 3 to 5 beat increase before it normalized. Conclusion: Acute afterloading variably elevates all cardiac diastolic pressures and reduces LV relaxation. These early changes in myocardial mechanics occur simultaneously with changes in LVDPmin. Right heart diastolic pressures increase due to the septal shift which both reduced RV volume and decreased LV compliance but did not elevate pulmonary pressure. E’/E recovery differed which could be attributed to transient preload changes.

Role of Radial Strain and Displacement Imaging to Quantify Wall Motion Dyssynchrony in Patients With Left Ventricular Mechanical Dyssynchrony and Chronic Right Ventricular Pressure Overload

Left ventricular (LV) deformation with ventricular septal shift is one of the most distinctive echocardiographic observations in patients with chronic right ventricular (RV) pressure overload (PO). However, little is known about the effects of RVPO on LV performance and regional synchrony. Accordingly, our objective was to test the hypothesis that chronic RVPO affects regional wall motion, synchronicity, and global LV function using a novel speckle-tracking approach to quantify and characterize regional LV wall motion dyssynchrony. Displacement and strain imaging echocardiographic studies were performed in 20 patients with RVPO from pulmonary arterial hypertension or pulmonic stenosis (mean age 53 +/- 16 years, New York Heart Association class 2.6 +/- 0.7, and peak RV systolic pressure 73 +/- 28 mm Hg) and 20 age-matched normal subjects (mean age 47 +/- 16 years). Segmental signals from 6 segments around the mid-LV short axis were defined as dyssynchronous if their changes were opposite to that of the global LV signal at each time frame, and overall LV dyssynchrony was calculated as the percentage of dyssynchrony in all 6 segments within the specified time interval from onset of QRS to the end of isovolumic relaxation. RVPO was associated with a large degree of regional dyssynchrony with paradoxical ventricular septal motion observed by displacement imaging (21 +/- 6%, p <0.05 vs control group), which was closely associated with LV eccentricity index (r = 0.79, p <0.05) and LV myocardial performance index with linear regression (r = 0.76, p <0.05). In contrast, strain imaging showed uniform segmental radial thickening in the RVPO group, which was similar to the control group, and suggests that there was no intrinsic LV contractile dyssynchrony. In conclusion, LV wall motion dyssynchrony assessed by displacement imaging, not intrinsic contractile dyssynchrony by strain imaging, coexists with LV chamber deformation with ventricular septal shift and is closely associated with impairment of LV performance.

The Incidence of Right Ventricular Dysfunction Is Similar in Pulsatile and Continuous-Flow Left Ventricular Assist Devices

Introduction: Continuous-flow left ventricular assist devices (LVADs) augment cardiac output without the degree of left ventricular decompression and septal shift seen with pulsatile LVADs. Rotor speed is adjusted based on hemodynamic, echocardiographic and clinical data to optimize output and ventricular interaction. For these reasons, we theorized that the incidence of right ventricular dysfunction (RVD) may be reduced in patients implanted with continuous-flow LVADs. Methods: We retrospectively compared the incidence of RVD in patients implanted with pulsatile (Thoratec, Novacor or Heartmate XVE) and continuous-flow (Jarvik, Ventrassist or Heartmate II) LVADs.

Biventricular assistance with the Jarvik FlowMaker: A case report

After implantation of a left ventricular assist device (LVAD), right ventricular dysfunction and elevated peripheral vascular resistance may result in right ventricular failure and increased mortality. Right ventricular support may become necessary, as in the following case in which two Jarvik FlowMakers (Jarvik Heart, Inc, New York, NY) provided biventricular assistance. A 21-year-old man with end-stage idiopathic cardiomyopathy was referred to our hospital and approved for heart transplantation. He had a left ventricular ejection fraction lower than 20% with mitral and tricuspid regurgitation. Despite maximal medical therapy and balloon counterpulsation, LVAD support became necessary as a lifesaving measure. A Jarvik FlowMaker was implanted in the left ventricle through a midline sternotomy with outflow graft anastomosis to the ascending aorta.1Westaby S. Frazier O.H. Pigott D.W. Saito S. Jarvik R.K. Implant technique for the Jarvik 2000 Heart.Ann Thorac Surg. 2002; 73: 1337-1340Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar On postoperative day 1, the cardiac index increased by 60%, from 1.5 to 2.3 L/(min · m2). The patient was extubated on day 3. Two days later, he had ventricular tachycardia that responded to drug therapy and cardioversion. Sepsis supervened, hepatic function deteriorated, and the white blood cell count rose to 28.2 × 103 cells/μL. On postoperative day 12, respiratory failure and bradycardia necessitated resuscitation and reintubation. Right ventricular function worsened, and tricuspid regurgitation became severe. A right atrial pressure greater than 20 mm Hg was required for adequate cardiac output. Hepatic function further deteriorated, and right ventricular support was clinically necessary. Because of the FlowMaker's unique suitability for intracardiac placement and its ease of implantation without cardiopulmonary bypass, this device was implanted for right ventricular support on postoperative day 15. A purse-string suture was placed on the upper lateral wall of the right atrium, and the pump was inserted into the atrium (Figure 1). The cardiac index increased to greater than 3.0 L/(min · m2), maintaining the central venous pressure at 5 to 10 cm H2O. Unfortunately, because of progressive sepsis and hepatic failure, the patient died after 27 days of LVAD support and 12 days of biventricular support. Both pumps had a typical appearance at removal, and autopsy findings were unremarkable. Although implantable pulsatile LVADs can save patients with end-stage heart failure, these devices may impair right ventricular function. This problem is usually overcome by relieving the high left-sided pressures typical of severe heart failure. However, when left ventricular filling remains inadequate despite pharmacotherapy to enhance right ventricular function and lower pulmonary vascular resistance, a right ventricular assist device may be required. Unfortunately, implantation is invariably delayed until end-organ failure is irreversible, and the mortality remains high even when a physiologic cardiac output is achieved. Implantable pulsatile LVADs may decrease the left atrial and left ventricular pressures below normal physiologic levels. Pulsatility is generated as in the normal heart, with a systolic duration equivalent to about 33% of the cardiac cycle and a diastolic filling time like that of the normal heart. However, the pump's cycle is not synchronized with the patient's cardiac cycle. This lack of synchrony, along with subphysiologic left-sided pressures and a resultant ventricular and atrial septal shift (Figure 2), may impair natural right ventricular function. If left-sided filling is inadequate, the septal shift is accentuated. Attempts to enhance left-sided output by increasing device speed (in hopes of increasing flow) only worsen the situation.2Santamore W.P. Gray L.A. Left ventricular contributions to right ventricular systolic function during LVAD support.Ann Thorac Surg. 1996; 61: 350-356Abstract Full Text PDF PubMed Scopus (94) Google Scholar Implantable LVADs are not designed for right-sided support. However, the FlowMaker's intracardiac placement makes it uniquely suitable as an implantable support device for either the pulmonary or systemic circulation. Device placement in the right atrium appears superior to right ventricular placement. By directing the inlet toward the inferior vena caval–right atrial junction and keeping right atrial pressures at 5 to 10 cm H2O, we were able to achieve reliable right ventricular unloading and deliver satisfactory blood flow to the left-sided pump. This therapy failed to save our critically ill patient. More timely implantation of a FlowMaker right ventricular assist device, along with a pulsatile or nonpulsatile LVAD, may be lifesaving in future cases. A FlowMaker right ventricular assist device alone may also be appropriate for long-term or destination therapy for isolated right ventricular failure or for congenital heart disease involving compromised or absent right ventricular function.

Diagnosis of pulmonary embolism by acute right heart morphologic and hemodynamic changes observed during exercise stress echocardiography

In addition to the conventional means of diagnosing pulmonary embolism, resting echocardiography has sometimes been useful. We describe the case of a patient with a normal resting transthoracic echocardiogram, but with a markedly abnormal posttreadmill exercise echocardiogram revealing acute right ventricular dilatation, marked ventricular septal shift, and acute pulmonary hypertension. Pulmonary embolism was suspected and subsequently confirmed by chest computed tomographic angiography.

Pressure and Volume Loading of the Right Ventricle Have Opposite Effects on Left Ventricular Ejection Fraction

Left ventricular ejection fraction has been reported to be depressed in patients with right ventricular volume overload (RVVO) due to Ebstein's anomaly and uncomplicated atrial septal defect, whereas it is usually preserved in right ventricular pressure overload (RVPO) due to congenital pulmonic stenosis. In the present study, we examined the hypothesis that the differential timing of active displacement of the ventricular septum into the left ventricle in RVPO (end systole) and RVVO (end diastole) results in opposite effects of RVPO and RVVO on left ventricular ejection fraction. Ten patients with severe tricuspid regurgitation after tricuspid valve resection for endocarditis and 10 patients with primary pulmonary hypertension were studied as models of isolated RVVO and RVPO, respectively. Left ventricular ejection fraction, end-diastolic volume, and regional systolic shortening were measured with the use of echocardiographic techniques in these 20 patients and 10 healthy control subjects. In RVPO, despite marked underfilling of the left ventricle relative to the healthy control subjects (end-diastolic volume, 48 +/- 26 versus 77 +/- 20 mL; P < .02), left ventricular ejection fraction was similar to that of the control subjects (56 +/- 5% versus 60 +/- 4%; P = .07) and only 1 of 10 RVPO patients had an ejection fraction of less than 50%. In contrast, in RVVO the left ventricle was volume replete (end-diastolic volume, 84 +/- 26 versus 77 +/- 20 mL; P = NS), but left ventricular ejection fraction was significantly depressed (51 +/- 4% versus 60 +/- 4%, P < .001) compared with the control subjects, and 4 of 10 RVVO patients had an ejection fraction of less than 50%. Analysis of systolic fractional shortening along two perpendicular short-axis diameters and the mutually orthogonal long axis demonstrated isolated augmentation of fractional shortening in the ventricular septal-to-posterolateral free wall dimension in RVPO (47.4 +/- 13.7% versus 34.2 +/- 13.1%, P < .05) and isolated depression of fractional shortening along that same dimension in RVVO (13.7 +/- 11.8% versus 34.2 +/- 13.1%, P < .001) compared with the control subjects. End-systolic leftward ventricular septal shift in RVPO results in isolated augmentation of systolic shortening in the septal-to-free wall dimension, whereas end-diastolic leftward ventricular septal shift in RVVO results in isolated reduction in systolic shortening in the septal-to-free wall dimension. As a result, despite relative underfilling of the left ventricle in RVPO, resting left ventricular ejection fraction is preserved, whereas ejection fraction is depressed for the volume-replete left ventricle of patients with RVVO.

Altered left ventricular chamber stiffness and isovolumic relaxation in dogs with chronic pulmonary hypertension caused by emphysema.

In chronic obstructive lung disease, a right to left ventricular septal shift that occurs as a consequence of right ventricular pressure overload is the usual mechanism given to explain a decrease in left ventricular (LV) diastolic performance. The purpose of the present study was to examine the extent to which this mechanism could account for a decrease in LV diastolic function in a canine model in which pulmonary artery pressure was elevated to a level found in human disease. Severe emphysema was produced in dogs by repeated instillations of the enzyme papain into the lung. To assess LV diastolic function, we used sonomicrometry, in which three pairs of subendocardial crystal transducers were implanted along the three orthogonal axes of the LV. LV end-diastolic dimensions and pressure-strain relations along the three axes, as well as the time constant of LV isovolumic relaxation (T), were measured before (baseline) and after 1 year of emphysema (post-1-year study). The results showed that after 1 year of pulmonary hypertension, LV pressure-strain relations were decreased along the septal-lateral and anterior-posterior axes, but a right to left ventricular septal shift was not detected. The relation of average midwall circumferential stress to midwall circumferential strain was used to describe the intrinsic compliance of the LV. The results showed that myocardial stiffness increased in emphysema but that chamber volume was not reduced. At the post-1-year study, T was abnormally increased in the emphysema group in response to augmented preload and afterload compared with preemphysema measurements. We conclude that mechanisms other than ventricular interdependence may be operative in leading to altered LV diastolic filling in chronic emphysema.

Interaction between effects of hypoxia and hypercapnia on altering left ventricular relaxation and chamber stiffness in dogs.

Left ventricular (LV) isovolumic relaxation and chamber stiffness were examined in dogs to see how hypoxemia and hypercapnia occurring during an acute exacerbation of chronic obstructive lung disease could directly affect diastolic performance. Measurements were obtained during baseline (arterial PO2 approximately 200 mm Hg; PCO2 approximately 35 mm Hg; pH approximately 7.35), hypoxia (PO2 approximately 35 mm Hg; PCO2 approximately 35 mm Hg; pH approximately 7.35), and hypoxia-hypercapnia (PO2 approximately 35 mm Hg; PCO2 approximately 60 mm Hg; pH approximately 7.15) in an open-chest, open-pericardium preparation. Changes in LV diastolic performance during hypoxic and hypercapnic interventions were contrasted with those caused by ventricular interdependence in which pulmonary artery occlusion was used to produce a right to left ventricular septal shift. Subendocardial ultrasonic crystal transducers were placed along the three orthogonal axes of the left ventricle to measure dimensions by sonomicrometry. Along each axis, LV end-diastolic dimension-pressure relations were constructed in the various conditions; the slope of this relationship, obtained over a linear portion of the curve, was used as an index of diastolic dimensional distensibility (DD). The results showed that during hypoxia, DD appeared decreased along the three axes, with a reduction in filling primarily along the anterior-posterior and apex-base axes. The addition of hypercapnia to hypoxia completely abolished the hypoxic effect. On the other hand, during pulmonary artery occlusion, LV DD were not changed along the latter two dimensions. We conclude that during respiratory failure, LV diastolic performance may be directly affected by arterial blood gas tensions, which by altering the interaction between the contractile filaments modulate LV filling.

Doppler echocardiographic demonstration of the differential effects of right ventricular pressure and volume overload on left ventricular geometry and filling

To compare the effects of isolated right ventricular pressure and volume overload on left ventricular diastolic geometry and filling, 11 patients with primary pulmonary hypertension, 11 patients with severe tricuspid regurgitation due to tricuspid valve resection and 11 normal subjects were studied with use of Doppler echocardiography techniques. Right ventricular systolic overload in primary pulmonary hypertension resulted in substantial leftword ventricular septal shift that was most marked at end-systole and early diastole and decreased substantially by end-diastole. Right ventricular diastolic overload after tricuspid valve resection resulted in maximal leftward ventricular septal shift at end-diastole sparing end-systole and early diastole. The early diastolic distortion of left ventricular geometry associated with right ventricular pressure overload resulted in prolongation of isovolumetric relaxation of the left ventricle (129 ± 39 ms) and a reduction in early diastolic finding compared with values in normal subjects.Late diastolic distortion of left ventricular geometry associated with right ventricular volume overload had no influence on the duration of left ventricular isovolumetric relaxatoon (52 ± 32 ms) but caused a reduction in the atrial systolic contribution to late distolic filling of the left ventricle compared with values in normal sujects. In patients with right ventricular pressure overload, 52 ± 16% of left ventricular filling occurred in early diastole compared with 78 ± 11% in patients with right ventricular volume overload (p < 0.001). The differential effects of systolic and diastolic right ventricular overload on the pattern of left ventricular filling appear to bt related to the timing of leftward ventricular septal displacement.