Continuous LVAD monitoring reveals high suction rates in clinically stable outpatients.
ABSTRACT: Suction of the left ventricle can lead to potentially life-threatening events in left ventricular assist device (LVAD) patients. With the resolution of currently available clinical LVAD monitoring healthcare professionals are unable to evaluate patients' suction occurrences in detail. This study investigates occurrences and durations of suction events and their associations with tachycardia in stable outpatients. Continuous high-resolution LVAD data from HVAD patients were analyzed in the early outpatient period for 15 days. A validated suction detection from LVAD signals was used. Suction events were evaluated as suction rates, bursts of consecutive suction beats, and clusters of suction beats. The occurrence of tachycardia was analyzed before, during, and after suction clusters. Furthermore, blood work, implant strategy, LVAD speed setting, inflow cannula position, left ventricular diameters, and adverse events were evaluated in these patients. LVAD data of 10 patients was analyzed starting at 78 ± 22 postoperative days. Individuals' highest suction rates per hour resulted in a median of 11% (range 3%-61%). Bursts categorized as consecutive suction beats with n = 2, n = 3-5, n = 6-15, and n > 15 beats were homogenously distributed with 10.3 ± 0.8% among all suction beats. Larger suction bursts were followed by shorter suction-free periods. Tachycardia during suction occurred in 12% of all suction clusters. Significant differences in clinical parameters between individuals with high and low suction rates were only observed in left ventricular end-diastolic and end-systolic diameters (P < .02). Continuous high-resolution LVAD monitoring sheds light on outpatient suction occurrences. Interindividual and intraindividual characteristics of longitudinal suction rates were observed. Longer suction clusters have higher probabilities of tachycardia within the cluster and more severe types of suction waveforms. This work shows the necessity of improved LVAD monitoring and the implementation of an LVAD speed control to reduce suction rates and their concomitant burden on the cardiovascular system.
Project description:The incidence, predictors, and impact of atrial arrhythmias along with left atrial structural changes in patients with left ventricular assist devices (LVADs) remain undetermined.All patients who underwent LVAD implantation from 2008 to 2015 at the University of Chicago Medical Center were included. Electronic medical records, electrocardiograms, echocardiograms, and cardiac electrical device interrogations were reviewed. The association of arrhythmias and clinical covariates with survival was evaluated by Kaplan-Meier and Cox proportional hazards analyses. A total of 331 patients were followed for a median of 330 days (range 0-2306 days). Mean age was 57.8±12.8 years, 256 participants (77.3%) were male, mean left ventricular ejection fraction was 20±6.6%, and 124 (37.5%) had ischemic cardiomyopathy. Atrial arrhythmias (53.8%) were highly prevalent and frequently coexisted before LVAD implantation: atrial fibrillation (AF) in 45.9%, atrial flutter in 13.9%, atrial tachycardia in 6.9%, and atrioventricular nodal reentrant tachycardia in 1.2%. New-onset AF was documented in 14 patients (7.8% of patients without prior AF) after the first 30 days with an LVAD. Increasing age, renal insufficiency, and lung disease were predictors of new-onset AF after LVAD implantation. Of patients with paroxysmal AF, 43% had no further AF after LVAD. Left atrial size and volume index improved with LVAD (P<0.005). History of persistent AF, atrial tachycardia, ventricular arrhythmia, coronary artery bypass, and low albumin were associated with decreased survival.Atrial arrhythmias are significantly prevalent in patients who require LVAD and are associated with increased mortality; however, LVADs induce favorable atrial structural and electrical remodeling.
Project description:Background:As survival and neuromuscular function in Duchenne Muscular Dystrophy (DMD) improve with glucocorticoid therapy and respiratory advances, the proportion of cardiac deaths is increasing. Little is known about the use and outcomes of advanced heart failure (HF) therapies in this population. Methods:A retrospective cohort study of 436 males with DMD was performed, from January 1, 2005-January 1, 2018, with the primary outcome being use of advanced HF therapies including: implantable cardioverter defibrillator (ICD), left ventricular assist device (LVAD), and heart transplantation (HTX). Results:Nine subjects had an ICD placed, 2 of whom (22.2%) had appropriate shocks for ventricular tachycardia; 1 and 968 days after implant, and all of whom were alive at last follow-up; median 18 (IQR: 12.5-25.5) months from implant. Four subjects had a LVAD implanted with post-LVAD survival of 75% at 1 year; 2 remaining on support and 1 undergoing HTX. One subject was bridged to HTX with ICD and LVAD and was alive at last follow-up, 53 months after HTX. Conclusion:Advanced HF therapies may be used effectively in select subjects with DMD. Further studies are needed to better understand risk stratification for ICD use and optimal candidacy for LVAD implantation and HTX, with hopes of improving cardiac outcomes.
Project description:Catecholaminergic polymorphic ventricular tachycardia (CPVT) is caused by mutations in cardiac ryanodine receptor (RyR2) or calsequestrin (Casq2) genes. Sinoatrial node dysfunction associated with CPVT may increase the risk for ventricular arrhythmia (VA).To test the hypothesis that CPVT is suppressed by supraventricular overdrive stimulation.Using CPVT mouse models (Casq2(-/-) and RyR2(R4496C/+) mice), the effect of increasing sinus heart rate was tested by pretreatment with atropine and by atrial overdrive pacing. Increasing intrinsic sinus rate with atropine before catecholamine challenge suppressed ventricular tachycardia in 86% of Casq2(-/-) mice (6/7) and significantly reduced the VA score (atropine: 0.6±0.2 versus vehicle: 1.7±0.3; P<0.05). Atrial overdrive pacing completely prevented VA in 16 of 19 (84%) Casq2(-/-) and in 7 of 8 (88%) RyR2(R4496C/+) mice and significantly reduced ventricular premature beats in both CPVT models (P<0.05). Rapid pacing also prevented spontaneous calcium waves and triggered beats in isolated CPVT myocytes. In humans, heart rate dependence of CPVT was evaluated by screening a CPVT patient registry for antiarrhythmic drug-naïve individuals that reached >85% of their maximum-predicted heart rate during exercise testing. All 18 CPVT patients who fulfilled the inclusion criteria exhibited VA before reaching 87% of maximum heart rate. In 6 CPVT patients (33%), VA were paradoxically suppressed as sinus heart rates increased further with continued exercise.Accelerated supraventricular rates suppress VAs in 2 CPVT mouse models and in a subset of CPVT patients. Hypothetically, atrial overdrive pacing may be a therapy for preventing exercise-induced ventricular tachycardia in treatment-refractory CPVT patients.
Project description:BACKGROUND:Characterization of right heart catheterization (RHC) waveforms provides diagnostic and clinical information in heart failure patients. We aimed to investigate the implication of RHC waveforms, specifically the y-descent, in patients with left ventricular assist device (LVAD). METHODS AND RESULTS:Patients underwent RHC and waveforms were quantified prior to and 6 months after LVAD implantation. The impact of a deep y-descent (>3 mmHg) on echocardiographic measures of right heart function and 1-year hemocompatibility-related adverse event rates were investigated. Eighty-nine patients (median 59 years old, 65 male) underwent RHC. RHC waveform showed unique changes following LVAD implantation, particularly an increase in the steepness of the y-descent. A post-LVAD deep y-descent was associated with reduced right ventricular function and enlarged right heart. Patients with post-LVAD deep y-descent had higher rates of gastrointestinal bleeding (0.866 vs 0.191 events/year) and stroke (0.199 vs 0 events/year) compared with those without (P< .05 for both). CONCLUSION:RHC waveforms characterized by deep y-descent on RHC waveform during LVAD support was associated with impaired right ventricular function and worse clinical outcomes.
Project description:BACKGROUND:Left ventricular assist devices (LVAD) are increasingly used in patients with advanced heart failure, many of whom have been or will be implanted with an implantable cardioverter defibrillator (ICD). Interaction between both devices is a matter of concern. Subcutaneous ICD (S-ICD) obtains its signals through subcutaneous vectors, which poses special challenges with regards to adequate performance following LVAD implantation. CASE SUMMARY:We describe the case of a 24-year-old man implanted with an S-ICD because of idiopathic dilated cardiomyopathy, severe biventricular dysfunction, and self-limiting sustained ventricular tachycardias. After the implantation of a HeartMate 3™ (Left Ventricular Assist System, Abbott) several months later, the S-ICD became useless because of inappropriate sensing due to electromagnetic interference and attenuation of QRS voltage. DISCUSSION:We reviewed the reported cases in PubMed about the concomitant use of S-ICD and LVAD. Seven case reports about the performance of S-ICD in patients with an LVAD were identified, with discordant results. From these articles, we analyse the potential causes for these differing results. Pump location and operating rates in LVAD, as well as changes in the subcutaneous-electrocardiogram detected by the S-ICD after LVAD implantation are related to sensing disturbances when used in the same patient.
Project description:This paper presents a patient customised fluid-solid mechanics model of the left ventricle (LV) supported by a left ventricular assist device (LVAD). Six simulations were conducted across a range of LVAD flow protocols (constant flow, sinusoidal in-sync and sinusoidal counter-sync with respect to the cardiac cycle) at two different LVAD flow rates selected so that the aortic valve would either open (60mLs(-1)) or remain shut (80mLs(-1)). The simulation results indicate that varying LVAD flow in-sync with the cardiac cycle improves both myocardial unloading and the residence times of blood in the left ventricle. In the simulations, increasing LVAD flow during myocardial contraction and decreasing it during diastole improved the mixing of blood in the LV cavity. Additionally, this flow protocol had the effect of partly homogenising work across the myocardium when the aortic valve did not open, reducing myocardial stress and thereby improving unloading.
Project description:OBJECTIVES:This study sought to investigate the prevalence of ventricular tachycardia after percutaneous coronary intervention (PCI) of chronic total occlusion (CTO). BACKGROUND:PCI of a CTO is associated with improvement of the left ventricular ejection fraction and possibly associated with reduced mortality. However, benefits of CTO-PCI must be weighed against a higher risk of procedure-related complications. The incidence of new-onset ventricular tachycardia after a successful CTO-PCI has not been investigated so far. In this retrospective registry we seek to describe characteristics and predictors of occurrence of post-procedural ventricular tachycardias. METHODS AND RESULTS:Between 2010 and 2015, 485 patients underwent successful CTO-PCI at Heart Center Leipzig. Of them, 342 had complete follow-up and were further analyzed. Ventricular tachycardias were detected in 9 (2.6%) patients. All of them were monomorphic ventricular tachycardias occurring in median 1 day (interquartile range [IQR] 0.25-4.75 days) after PCI and caused prolongation of the hospital stay. Patients with ventricular tachycardia were older, had worse left ventricular ejection fraction (mean 33.1%, SD 5.9%) and more frequently a CTO of an infarct-related artery. The target vessel was not associated with the occurrence of ventricular arrhythmias. In multivariable analysis, only impaired left ventricular systolic function was an independent predictor for procedure-related ventricular tachycardia. Mortality rates were not different between patients with or without ventricular tachycardia. CONCLUSION:Ventricular tachycardia can occur early after CTO-PCI as possible reperfusion arrhythmia and poorer left ventricular ejection fraction is the only independent predictor for onset. Although the occurrence of ventricular tachycardia after CTO-PCI seems not to influence mortality, awareness of this possible complication and longer monitoring may be recommended.
Project description:Atrial fibrillation (AF) tachycardia causes heart failure and requires more attention. The genetic background of individual heart rate (HR) variations during AF are unclear. We hypothesized that HR-associated single nucleotide polymorphisms (SNPs) reported in Genome-Wide Association Studies (GWAS) are also associated with HR during AF. We enrolled patients with persistent AF (311 for screening and 146 for replication) who underwent AF ablation and were genotyped for the 21 h-associated SNPs reported in GWAS. The patients underwent 24-h Holter monitoring before AF ablation and electrophysiological study after AF ablation during sinus rhythm. Only the GJA1 SNP rs1015451 (T>C) was significantly associated with total HR (TT 110,643?±?17,542 beats/day, TC 116,350?±?19,060 beats/day, CC 122,163?±?25,684 beats/day, P?=?8.5?×?10<sup>-4</sup>). We also confirmed this significant association in the replication set. The intra-atrial conduction was faster in AF patients with the GJA1 minor allele than in those without it. Multivariate analysis revealed the presence of a GJA1 SNP rs1015451 additive model, female gender, lower left ventricular ejection fraction, and higher 1:1 atrioventricular nodal conduction were independently associated with higher HR during AF. The GJA1 SNP might be a new genetic marker for AF tachycardia.
Project description:For almost half a century, cardiac transplant has been the only long-term treatment for patients with end-stage heart failure. Implantable left ventricular assist devices (LVADs) have emerged as a new treatment option for advanced heart failure as destination therapy for patients either too old or not suitable for transplant. A meta-analysis presenting head-to-head comparisons of cardiac transplant versus LVAD as destination therapy (LVAD-DT) found no difference in 1-year mortality rates between LVAD-DT and cardiac transplant (OR 1.49; 95% CI [0.48-4.66]; I2=82.8%). Moreover, a recent subanalysis from the Interagency Registry for Mechanically Assisted Circulatory Support found similar outcomes after LVAD-DT implantation in both transplant and non-transplant centres. The time is right for LVAD-DT in non-transplant centres, provided multidisciplinary heart failure teams and expertise are in place.
Project description:BACKGROUND:Cardiac recovery in response to mechanical unloading by left ventricular assist devices (LVADs) has been demonstrated in subgroups of patients with chronic heart failure (HF). Hallmarks of HF are depletion and disorganization of the transverse tubular system (t-system) in cardiomyocytes. Here, we investigated remodeling of the t-system in human end-stage HF and its role in cardiac recovery. METHODS:Left ventricular biopsies were obtained from 5 donors and 26 patients with chronic HF undergoing implantation of LVADs. Three-dimensional confocal microscopy and computational image analysis were applied to assess t-system structure, density, and distance of ryanodine receptor clusters to the sarcolemma, including the t-system. Recovery of cardiac function in response to mechanical unloading was assessed by echocardiography during turndown of the LVAD. RESULTS:The majority of HF myocytes showed remarkable t-system remodeling, particularly sheet-like invaginations of the sarcolemma. Circularity of t-system components was decreased in HF versus controls (0.37±0.01 versus 0.46±0.02; P<0.01), and the volume/length ratio was increased in HF (0.36±0.01 versus 0.25±0.02 µm2; P<0.0001). T-system density was reduced in HF, leading to increased ryanodine receptor-sarcolemma distances (0.96±0.05 versus 0.64±0.1 µm; P<0.01). Low ryanodine receptor-sarcolemma distances at the time of LVAD implantation predicted high post-LVAD left ventricular ejection fractions (P<0.01) and ejection fraction increases during unloading (P<0.01). Ejection fraction in patients with pre-LVAD ryanodine receptor-sarcolemma distances >1 µm did not improve after mechanical unloading. In addition, calcium transients were recorded in field-stimulated isolated human cardiomyocytes and analyzed with respect to local t-system density. Calcium release in HF myocytes was restricted to regions proximal to the sarcolemma. Local calcium upstroke was delayed (23.9±4.9 versus 10.3±1.7 milliseconds; P<0.05) and more asynchronous (18.1±1.5 versus 8.9±2.2 milliseconds; P<0.01) in HF cells with low t-system density versus cells with high t-system density. CONCLUSIONS:The t-system in end-stage human HF presents a characteristic novel phenotype consisting of sheet-like invaginations of the sarcolemma. Our results suggest that the remodeled t-system impairs excitation-contraction coupling and functional recovery during chronic LVAD unloading. An intact t-system at the time of LVAD implantation may constitute a precondition and predictor for functional cardiac recovery after mechanical unloading.