LV Assist Device Research Articles

Long term outcome after septal reduction therapies in patients with hypertrophic cardiomyopathy: insights from the SHaRe registry

Abstract Background Long term outcome after septal reduction therapies SRT in HCM patients is largely unresolved, since most available studies report post-operative results up to 1 year. Purpose To evaluate the long term outcome and its predictors in patients with HCM from the SHaRe Registry (Sarcomeric Human Cardiomyopathy Registry) Registry. Methods Data from 11 high-volume HCM specialty centers from the international SHaRe Registry were used to describe the natural history of patients with SRT. Patients were followed from SRT until last follow-up or meeting the composite outcome of heart failure (cardiac transplantation, implantation of an LV assist device (LVAD), left ventricular ejection fraction (LVEF) <35%, development of NYHA class III-IV symptoms), ventricular arrhythmias (sudden cardiac death (SCD), resuscitated cardiac arrest, or appropriate implantable cardioverter-defibrillator (ICD) therapy) or HCM related death. Cox proportional hazards models were used to identify predictors of prognosis and incident development. Results Of the 10385 patients part of the ShaRe Registry, 1835 (18%, 968 (53%) males) underwent a SRT during a median follow-up of 6.8 (IQR 3.4-9.8). A total of 455 (25%) had Alcohol Septal Ablation (ASA) and 1377 (75%) had myectomy. Patients who underwent myectomy were younger (49±18 vs 56±15 years, p<0.01), more frequent with a sarcomeric mutation (396 (29%) vs 111 (24%), p<0.01), where less frequently severely symptomatic (373 (82%) vs 971 (71%) in NYHA Class III, p<0.01) and presented a more dilated left atrium (396 (29%) vs 111 (24%), p<0.01). Peri-procedural mortality was extremely low (2 (0.4%) and 4 (0.3%) in ASA and myectomy respectively). Over 6.8 years after the procedure, 77 (4%) died because of HCM (0.6%/year), 236 (13%) presented a composite HF outcome (1.9%/year) and 87 (5%) a composite VA outcome (0.7%/year). Development of the composite HF events was associated with older age at procedure (56±15 vs 49±18 years, p<0.01), the presence of a sarcomere mutation (82 (36%) vs 425 (27%), p<0.01) and a more severely dilated LA (45±10 vs 42±11 years, p<0.01). Patients who presented a composite VA event were younger at procedure (38±20 vs 54±18 years, p<0.01), developed more often a LV EF< 50% (29 (33%) vs 351 (20%), p<0.01) and a more severely dilated LA (47±7 vs 43±11 years, p<0.01) and greater LV maximal wall thickness (24±6 vs 21±6 years, p<0.01). Significant predictors of the composite HF outcome were the presence of a sarcomeric variants (hazard ratio [HR], 2.3 [95% CI, 1.3–5.6.5]) and LA diameter ≥ 45 mm (HR, 2.6 [95% CI, 1.7–3.5]). No significant difference was present between the two procedures in overall mortality, HF and VA composite outcome. Conclusions SRT were performed in 18% of patient with HCM and associated with a low peri-procedural mortality. Long term outcome was favourable but not uneventful, mainly driven by heart faluire related events.

TCTAP C-075 How a Temporary LV Assist Device Helped to Bail Out a Patient in Cardiogenic Shock with Multiple Comorbidities

TCTAP C-075 How a Temporary LV Assist Device Helped to Bail Out a Patient in Cardiogenic Shock with Multiple Comorbidities

Abstract 13532: Diastolic Function at Presentation Has Independent Prognostic Value in Patients With Peripartum Cardiomyopathy

Background: Peripartum cardiomyopathy (PPCM) is a rare disease with variable but potentially devastating consequences. The prognostic importance of alterations in LV diastolic function is unclear. Methods: Pregnancy Associated Cardiomyopathy cohort was a prospective study of 100 PPCM women from 30 centers presenting with LV ejection fraction (EF) < 45% within 2 months of delivery. Baseline data were mitral inflow E-wave, A-wave, E/A ratio, E deceleration time (DT), tissue Doppler septal and lateral annular velocities and biplane LA volume index. There were 90 PPCM patients and 21 female controls (8 healthy postpartum and 13 non-pregnant) with diastolic data. LV recovery was defined as LVEF ≥ 50% at 1 year. Outcome events were predefined as death, heart transplant or LV assist device (LVAD). Results: PPCM patients were aged 30±6 years with EF 35±9% at presentation. At 1 year, 84 patients had follow-up data: 63 patients (75%) had LV recovery (EF ≥50%) and 11 patients (13%) had either LVEF ≤35% or a major event (4 LVADs and 2 deaths). Elevated filling pressures (E/A≥2 and DT<150ms) were present in 57% at baseline and persisted in 11% at last echo, p<0.0001. Abnormalities in baseline diastolic function were associated with clinical outcomes and lack of LV recovery: area under the ROC curve (AUC) for E/A 0.78, p=0.0002, AUC for DT 0.82, p<0.0001, AUC for LA volume index 0.79, p<0.0001. Diastolic measures were also predictive of persistent severe LV dysfunction (EF ≤35%) or unfavorable events: E/A, p<0.0001; DT, p<0.0001, and LA volume index, p=0.0001. By multivariate analysis, baseline diastolic function was independently associated with subsequent lack of LV recovery or unfavorable events (Table). Conclusions: In PPCM patients, echo-Doppler measures of diastolic function at presentation provide important prognostic information regarding LV recovery and clinical outcomes.

Effects of small platform catheter-based left ventricular assist device support on regional myocardial signal transduction

ObjectivesLeft ventricular (LV) assist device (LVAD) support reduces pathological loading. However, load-induced adaptive responses may be suppressed. Pathological loading dysregulates cardiac G protein-coupled receptor (GPCR) signaling. Signaling through G proteins is deleterious, whereas beta (β)-arrestin-mediated signaling is cardioprotective. We examined the effects of pathological LV loading/LV dysfunction and treatment via LVAD, on β-arrestin-mediated signaling, and genetic networks downstream of load. MethodsAn ovine myocardial infarction (MI) model was used. Sheep underwent sham thoracotomy (n = 3), mid-left anterior descending coronary artery ligation to produce MI (n = 3), or MI with placement of a small-platform catheter-based LVAD (n = 3). LVAD support was continued for 2 weeks. Animals were maintained for a total of 12 weeks. Myocardial specimens were harvested and analyzed. ResultsMI induced β-arrestin activation. Increased interactions between epidermal growth factor receptor and β-arrestins were observed. LVAD support inhibited these responses to MI (P < .05). LVAD support inhibited the activation of cardioprotective signaling effectors Akt (P < .05), and, to a lesser extent, extracellular regulated kinase 1/2 (P not significant); however, MI resulted in regional activation of load-induced GPCR signaling via G proteins, as assessed by the induction of atrial natriuretic peptide mRNA expression in the MI-adjacent zone relative to the MI-remote zone (P < .05). MI-adjacent zone atrial natriuretic peptide expression was renormalized with LVAD support. ConclusionsLVAD support inhibited cardioprotective β-arrestin–mediated signaling. However, net benefits of normalization of load-induced GPCR signaling were observed in the MI-adjacent zone. These findings may have implications for the optimal extent and duration of unloading, and for the development of adjunctive medical therapies.

Mid wall fibrosis on CMR with late gadolinium enhancement may predict prognosis for LVAD and transplantation risk in patients with newly diagnosed dilated cardiomyopathy-preliminary observations from a high-volume transplant centre.

BackgroundPatients with newly diagnosed dilated cardiomyopathy (DCM) and advanced heart failure have a very high morbidity and mortality with an unpredictable clinical course. We investigated the role of cardiovascular magnetic resonance (CMR) imaging using late gadolinium enhancement (LGE) in this cohort of high‐risk patients. We hypothesized that LGE has high prognostic value in primary DCM patients referred for possible transplantation/left ventricular assist device (LVAD) consideration.MethodsOver 49 consecutive months, 61 consecutives DCM patients were referred for standard CMR(1.5T, GE) to interrogate the LV pattern, distribution, and extent of LGE (MultiHance, Princeton, NJ). Inclusion criteria for a primary non‐ischaemic DCM and EF <45% were met in 31 patients. DCM patients were categorized into: (i) presence of midwall LV stripe (+Stripe) and (ii) absence of midwall stripe (−Stripe) groups. Primary outcome was defined by the composite of death, need for LV assist device (LVAD), and urgent orthotopic cardiac transplantation (Tx) during a 12‐month follow‐up period. Kaplan–Meier survival analysis was conducted grouping patients by +Stripe and −Stripe.ResultsThere were no differences between groups for demographics, blood pressure, labs, baseline LVEF, NYHA class, or invasive haemodynamics. There were 18 patients (58%) with +Stripe. Nine events occurred: seven patients required urgent Tx and/or LVAD implantation and two patients died. The +Stripe categorization strongly predicted the need for LVAD, urgent Tx surgery, and death (log‐rank = 9, P = 0.002). All the events occurred in the +Stripe patients with no MACE experienced in the −Stripe group. The −Stripe group experienced marked signs of improvement in LVEF (P = 0.01) at follow‐up. LVEDD was predictive of need for LVAD/Tx and death by univariate analysis. Otherwise, no common clinical metric such as LVEF, LVEDV, RVEF, RVEDV, or any invasive haemodynamic parameter predicted MACE.ConclusionsThe presence of +Stripe on CMR is strongly predictive of LVAD, transplant need, and death during a 12‐month follow‐up period in DCM patients in this proof of concept study. All −Stripe patients survived without experiencing any events. Incorporating CMR imaging into routine clinical practice may have prognostic value in DCM patients; indicating conservative management in low‐risk patients while expectantly managing high‐risk patients.

Preoperative iodine-123 meta-iodobenzylguanidine imaging is a novel predictor of left ventricular reverse remodeling during treatment with a left ventricular assist device.

Although left ventricular reverse remodeling (LVRR) is accompanied with an improved clinical course during LV assist device (LVAD) treatment, its preoperative prediction remains uncertain. Twenty-seven heart failure patients with dilated cardiomyopathy were enrolled in this study. Patients underwent (123)I-meta-iodobenzylguanidine (MIBG) scintigraphy before LVAD implantation, and were monitored at our institute from 2010 to 2014. This study investigated the prognostic value of preoperative (123)I-MIBG parameters for predicting postoperative LVRR. Of the preoperative variables studied, including (123)I-MIBG data, washout rate (WR) ≤ 39 % was the only significant, independent predictor of LVRR (defined as LV ejection fraction ≥35 % at 6 months post-LVAD implant using univariate and multivariate logistic regression analyses) (p = 0.036, odds ratio [OR]:14.45). Improved exercise capacity and more frequent opening of the native aortic valve, as well as lower B-type natriuretic peptide plasma levels, were observed in LVRR patients (p < 0.05 for all), although β-blocker doses were comparable with those of non-LVRR patients throughout the 6-month LVAD support period. In conclusion, preoperative (123)I-MIBG is a novel predictive tool of LVRR during LVAD support.

Preoperative beta-blocker treatment is a key for deciding left ventricular assist device implantation strategy as a bridge to recovery

To date, there have been few reports demonstrating preoperative predictors for left ventricular reverse remodeling (LVRR) after LV assist device (LVAD) implantation, especially among patients with dilated cardiomyopathy (DCM). We retrospectively analyzed 60 patients with stage D heart failure due to DCM who had received LVAD treatment [pulsatile flow (PF) type, 26; continuous flow type, 34]. Data were evaluated at 6 months or just before explantation of the LVAD. We defined "LV reverse remodeling" (LVRR) by the achievement of an LV ejection fraction (LVEF) of ≥ 35 % after 6 months of LVAD support or explantation of LVAD within 6 months. LVRR occurred in 16 of our patients (26.7 %). Uni/multivariate logistic regression analyses for LVRR demonstrated that of the preoperative variables evaluated, PF LVAD usage and insufficient preoperative β-blocker treatment were independent predictors for LVRR. Patients who accomplished LVRR had a better clinical course, including lower levels of aortic valve insufficiency and lower levels of plasma B-type natriuretic peptide. Of the six patients (10.0 %) in whom LVADs were eventually explanted, all had an LVEF of ≥ 35 % before explantation or at 6 months. Based on these results, we conclude that DCM patients with insufficient preoperative β-blocker treatment have a chance to achieve LVRR under LVAD support as a bridge to recovery.

The effect of long‐term left ventricular assist device support on myocardial sympathetic activity in patients with non‐ischaemic dilated cardiomyopathy

Dilated cardiomyopathy (DCM) patients have abundant levels of norepinephrine secondary to failure of the norepinephrine transporter uptake mechanism. Little is known about the effects of an LV assist device (LVAD) on cardiac sympathetic innervations and norepinephrine transporter dysfunction. This study examines the effects of continuous-flow HeartMate II LVAD on cardiac sympathetic innervations using [(123)I]metaiodobenzylguanidine ([(123)I]MIBG) nuclear imaging. After injecting 431 ± 21 MBq of [(123)I]MIBG, planar scintigraphy was performed at 15 min and 4 h in 14 consecutive non-diabetic non-ischaemic DCM patients. Scans were executed early post-LVAD implantation (T1) and prior to either device explantation for myocardial recovery or transplant listing (T2). [(123)I]MIBG measured parameters included early and delayed heart-mediastinum (H/M) ratios and washout rate (W/O). Catecholamine levels were measured using liquid chromatography-mass spectrometry. Following 208.4 ± 85.5 days of LVAD support, both early and delayed H/M ratios increased by 42.1% (P < 0.001) and 54.7% (P < 0.001), respectively. The W/O rate decreased by 46% (P = 0.003). Plasma norepinephrine, epinephrine, and dopamine decreased significantly in correlation with [(123)I]MIBG parameters. Ten patients had recovered and had their device explanted as they had demonstrated a higher percentage change in delayed H/M ratio, W/O rate, and norepinephrine levels. Linear regression analysis revealed a strong correlation between percentage changes in both norepinephrine and epinephrine and myocardial recovery. Combination therapy with LVAD and drug resulted in enhancement of [(123)I]MIBG uptake in DCM patients.

Regulation of Connective Tissue Growth Factor Gene Expression and Fibrosis in Human Heart Failure

BackgroundHeart failure (HF) is associated with excessive extracellular matrix (ECM) deposition and abnormal ECM degradation leading to cardiac fibrosis. Connective tissue growth factor (CTGF) modulates ECM production during inflammatory tissue injury, but available data on CTGF gene expression in failing human heart and its response to mechanical unloading are limited. Methods and ResultsLeft ventricle (LV) tissue from patients undergoing cardiac transplantation for ischemic (ICM; n = 20) and dilated (DCM; n = 20) cardiomyopathies and from nonfailing (NF; n = 20) donor hearts were examined. Paired samples (n = 15) from patients undergoing LV assist device (LVAD) implantation as “bridge to transplant” (34–1,145 days) also were analyzed. There was more interstitial fibrosis in both ICM and DCM compared with NF hearts. Hydroxyproline concentration was also significantly increased in DCM compared with NF samples. The expression of CTGF, transforming growth factor (TGF) β1, collagen (COL) 1-α1, COL3-α1, matrix metalloproteinase (MMP) 2, and MMP9 mRNA in ICM and DCM were also significantly elevated compared with NF samples. Although TGF-β1, CTGF, COL1-α1, and COL3-α1 mRNA levels were reduced by unloading, there was only a modest reduction in tissue fibrosis and no difference in protein-bound hydroxyproline concentration between pre- and post-LVAD tissue samples. The persistent fibrosis may be related to a concomitant reduction in MMP9 mRNA and protein levels following unloading. ConclusionsCTGF may be a key regulator of fibrosis during maladaptive remodeling and progression to HF. Although mechanical unloading normalizes most genotypic and functional abnormalities, its effect on ECM remodeling during HF is incomplete.

The detection of left ventricular scar by delayed enhancement-CMR in non-ischemic cardiomyopathy is a stronger predictor of cardiovascular events than left ventricular ejection fraction

Background Left ventricular ejection fraction (LVEF) is a strong predictor of subsequent cardiovascular events in patients with ischemic and non-ischemic cardiomyopathy. CMR is an excellent technique for assessment of LVEF as well as for the detection of myocardial scar. We sought to evaluate if the presence of myocardial scarring in nonischemic cardiomyopathy could be an important predictor of cardiovascular events. Methods Inclusion criteria were absence of coronary artery disease, a diagnosis of cardiomyopathy and an LVEF ≤ 45%. Patients with a diagnosis of infiltrative disorders, hypertrophic cardiomyopathy, or tachycardia-induced cardiomyopathy were excluded. A total of 132 patients (with greater than 12 months follow up) were analyzed. Imaging was performed on a 1.5 Tesla Avanto, or 3.0 Tesla Verio MRI scanner (Siemens Medical Solutions). Cine images were performed using a steady state free precession pulse sequence. Delayed enhancement (DE) CMR was performed 10 minutes after administration of 0.15 mmol/kg Gadopentetate Dimeglumine (Bayer HealthCare) with typical in-plane resolution 18 x 2.0 mm, slice thickness 6-7 mm. LV and RV volumes and EF were analyzed by manual planimetry of endocardial contours during end-diastole and end-systole. DE-CMR images were analyzed to identify hyperenhanced myocardium (> 2 SD of remote signal intensity). The primary outcome was a combination of hospitalization for heart failure, LV assist device (LVAD) implantation, cardiac transplant, or death. Adjusted Kaplan-Meier curves were constructed for groups with and without scar by CMR with p<0.05 considered significant. Multivariate logistic regression analysis was performed. Results Patient’s demographics are shown in table. All baseline demographic data were similar between patients with and without scar by CMR. The adjusted event-free survival rate was significantly lower for patients with scar compared to patients without scar by CMR at 2-years (p=0.03) (graph). Mean scar burden was 3 ± 8% of LV. On multivariable analysis, the presence of scar was an independent predictor of events, HR 2.5(CI: 0.98-6.38, p=0.04), but LVEF was not. Conclusions In non-ischemic cardiomyopathy the presence of LV scar measured by DE-CMR is a stronger predictor of cardiovascular events than LVEF.

The prognostic impact of dynamic ventricular dyssynchrony in patients with idiopathic dilated cardiomyopathy and narrow QRS

Asynchronous myocardial contraction adversely influences left ventricular (LV) function and is therefore associated with a poor prognosis in heart failure. Exercise-induced change in ventricular dyssynchrony may be an important determinant of dynamic changes in cardiac output and mitral regurgitation. A prospective, longitudinal study was designed with pre-defined dyssynchrony index and outcome variables to test the hypothesis that dynamic dyssynchrony is associated with worse long-term event-free survival in patients with dilated cardiomyopathy (DCM) and 'narrow' QRS complex. One-hundred eighty patients (62 ± 8 years; 110 males) with NYHA class II-III, idiopathic DCM, ejection fraction ≤35%, and QRS duration <120 ms were selected. All the patients underwent standard Doppler echo, colour tissue velocity imaging (DTI), and supine bicycle exercise stress echocardiography. Cardiac synchronicity was defined, at rest and at peak exercise, as DTI velocity opposing-wall delay (significant if ≥65 ms). Outcome was defined as freedom from death, heart transplantation, or LV-assist device implantation, over a median follow-up of 48 months, and a Cox proportional hazards model was used for survival analysis. At baseline examination, DCM patients showed a reduced LV ejection fraction (31 + 4%). A significant electromechanical delay in 58 patients (32%). At the peak of physical exercise, a significant electromechanical delay was detected in 103 patients (57%). There were 41 events during the follow-up (23%): 28 cardiac deaths, 8 heart transplantations, and 5 LV-assist device implantations over 4 years. When adjusted for confounding baseline variables, LV end-diastolic volume, restrictive mitral flow pattern, severity of mitral regurgitation, and the presence of exercise-induced intraventricular dyssynchrony were the only independent determinants of an adverse outcome. In patients with idiopathic DCM and narrow QRS, the increase in echocardiographic dyssynchrony during exercise was the strongest predictor of less favourable event-free survival.

Study Results Demonstrate Feasibility of a Continuous-Flow LV Assist Device

The continuous-flow pump, a new type of surgically implanted LV assist device, is designed to improve upon the undesirable size, noise, and limited

Does the β 2 -Agonist Clenbuterol Help to Maintain Myocardial Potential to Recover During Mechanical Unloading?

Chronic mechanical unloading induces left ventricular (LV) atrophy, which may impair functional recovery during support with an LV-assist device. Clenbuterol, a beta2-adrenergic receptor (AR) agonist, is known to induce myocardial hypertrophy and might prevent LV atrophy during LV unloading. Furthermore, beta2-AR stimulation is reported to improve Ca2+ handling and contribute to antiapoptosis. However, there is little information on the effects of clenbuterol during LV unloading. We investigated LV atrophy and function after LV unloading produced by heterotopic heart transplantation in isogenic rats. After transplantation, rats were randomized to 1 of 2 groups (n=10 each). The clenbuterol group received 2 mg.kg(-1).d(-1) of the drug for 2 weeks; the control group received normal saline. The weight of unloaded control hearts was 48% less than that of host hearts after 2 weeks of unloading. Clenbuterol significantly increased the weight of the host hearts but did not prevent unloading-induced LV atrophy. Papillary muscles were isolated and stimulated, and there was no difference in developed tension between the 2 groups. However, the inotropic response to the beta-AR agonist isoproterenol significantly improved in the clenbuterol group. The mRNA expression of myocardial sarco(endo)plasmic reticulum Ca2+-ATPase 2a (SERCA2a) and fetal gene shift (myosin heavy chain [MHC] mRNA isozyme) was also significantly improved by clenbuterol treatment. There was no difference in beta1-AR mRNA expression between the 2 groups. In contrast, beta2-AR mRNA was significantly decreased in the clenbuterol-treated, unloaded heart. This indicates that clenbuterol may downregulate beta2-ARs. In the evaluation of apoptosis, mRNA expression of caspase-3, which is the central pathway for apoptosis, tended to be better in the clenbuterol group. During complete LV unloading, clenbuterol did not prevent myocardial atrophy but improved gene expression (SERCA2a, beta-MHC) and beta-adrenergic responsiveness and potentially prevented myocardial apoptosis. However, chronic administration of clenbuterol may be associated with downregulation of beta2-ARs.

LV Assist Device Bridges Transplant Eligibility Gap

LV Assist Device Bridges Transplant Eligibility Gap

Quantitative Myocardial Cytokine Expression and Activation of the Apoptotic Pathway in Patients Who Require Left Ventricular Assist Devices

Background Molecular mechanisms underlying the deterioration of patients undergoing LV assist device (LVAD) implantation remain poorly understood. We studied the cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-1β and IL-6 and the terminal stage of the apoptotic pathway in patients with decompensating heart failure who required LVAD support and compared them with patients with less severe heart failure undergoing elective heart transplantation. Methods and Results Myocardial and serum samples from 23 patients undergoing LVAD implantation were compared with those from 36 patients undergoing elective heart transplantation. Myocardial TNF-α mRNA (1.71-fold; P &lt;0.05) and protein (3.43±0.19 versus 2.95±0.10 pg/mg protein; P &lt;0.05) were elevated in the LVAD patients. Immunocytochemistry demonstrated TNF expression in the myocytes. Serum TNF-α was also elevated (12.5±1.9 versus 4.0±0.4 pg/mL; P &lt;0.0001) in the LVAD patients. IL-6 mRNA (2.57-fold higher; P &lt;0.005) and protein (27.83±9.35 versus 4.26±1.24 pg/mg protein; P &lt;0.001) were higher in the LVAD candidates, as was serum IL-6 (79.3±23.6 versus 7.1±1.6 pg/mL; P &lt;0.0001). Interleukin-1β mRNA expression was 9.78-fold higher in the LVAD patients ( P &lt;0.001). iNOS mRNA expression was similar to that in advanced heart failure patients and was not further elevated in the LVAD patients. Levels of procaspase-9 (8.02±0.91 versus 6.16±0.43 oligodeoxynucleotide [OD] units; P &lt;0.01), cleaved caspase-9 (10.02±1.0 versus 7.34±0.40 OD units; P &lt;0.05), intact and spliced DFF-45 (4.58±0.75 versus 2.84±0.23 OD units; P &lt;0.05) were raised in LVAD patients, but caspase-3 and human nuclease CPAN were not. Conclusions Elevated TNF-α, IL-1β, and IL-6 and alterations in the apoptotic pathway were found in the myocardium and elevated TNF-α and IL-6 in serum of deteriorating patients who required LVAD support. These occurrences may have therapeutic implications and influence the timing of LVAD insertion.

Quantitation of right ventricular shape changes after left ventricular assist device implantation.

Complex effects of left (LV) and right ventricular (RV) interaction account for changes in RV function during LV assist device (LVAD) support. It has been hypothesized that changes in RV cross-sectional shape (RVS) may be a contributing factor in the development of RV dysfunction during LVAD support. To test the hypothesis that the RVS would become more circular as a result of septal shift during LVAD support, 13 patients were studied before and after LVAD implantation. The shape of the RV was quantified using a shape factor (SF) that was equal to (4 x pi x area)/P2, where P is the perimeter of RVS. The RV area and perimeter were measured from digitized images of the RV obtained by transesophageal echocardiography in patients before and after LVAD implantation. The group SF increased considerably after LVAD (SFpre = 0.78 +/- 0.12 versus SFpost = 0.88 +/- 0.07, p < 0.05). Patients were divided into three groups: 1) patients whose RV exhibited a low SF pre-LVAD that increased significantly, 2) those with a moderate SF pre-LVAD that increased slightly, and 3) those who had high pre-LVAD SF (< 0.90) that did not change. The decompression of the LV caused by LVAD implantation results in a shift of the septum from right to left, increasing SF. This increase is more pronounced in some patients. Quantitation of the degree of RV SF change may help predict the development of RV failure during LVAD support.