Sudden Death and Ventricular Arrhythmias in Athletes: Screening, De-Training and the Role of Catheter Ablation.

Athletes enjoy excellent health outcomes including greater longevity relative to non-athletic counterparts. Paradoxically, however, endurance athletic conditioning is associated with an increase in some arrhythmias. This review discusses the potential mechanisms for this paradox and strategies enabling early identification of potentially serious pathologies. Screening remains contentious due to the challenges of identifying relatively rare entities amongst a healthy cohort. The imperfect diagnostic accuracy of all current tests means that screening strategies have potential for harm through incorrect diagnoses as well as the potential for identification of important sub-clinical pathologies. Management of athletes at risk of ventricular arrhythmias and sudden cardiac death is similarly complex. There is much yet to learn about the specific patterns of ventricular arrhythmias in athletes, and the separation of benign from potentially life-threatening remains imperfect. There are some promising advances, however, such as specialised imaging modalities combined with improved electrophysiological diagnostics and therapeutics. Some unique clinical patterns are emerging to advance our understanding and management of athletes with ventricular arrhythmias, requiring specialised skillsets for evaluation and management.

State of the Art Review: Atrial Fibrillation in Athletes.

Exercise has substantial health benefits with pleomorphic vascular, metabolic, psychological and anti-neoplastic actions resulting in improved quality of life and longevity. Despite these many benefits, numerous studies have shown that endurance athletes are more likely to develop atrial fibrillation (AF) than non-athletes. The type, intensity and amount of sport appears to influence the risk of developing AF. Several endurance sport activities have been shown to increase the risk of developing AF but an excess in AF has not been shown in non-endurance sports. Furthermore, lifetime hours of participation appear to increase the risk of developing AF. Intriguingly, women appear relatively protected and an association between endurance sport and AF has not been clearly demonstrated amongst female endurance athletes. The mechanisms by which endurance sport promotes the development of AF are unclear. There are, however, a number of pathophysiological mechanisms which are known to increase the risk of AF in non-athletes which have correlates in athletes. These include structural remodelling of the left atrium, elevated left atrial pressure, inflammation, myocardial fibrosis, vagal tone, sinus bradycardia and genetic predisposition. In this article, we explore how some of these mechanisms may contribute to the development of AF in endurance athletes.

Protocol paper: Multi-site, cluster-randomized clinical trial for optimizing functional outcomes of older cancer survivors after chemotherapy.

BACKGROUND: Cancer survivors over the age of 65 have unique needs due to the higher prevalence of functional and cognitive impairment, comorbidities, geriatric syndromes, and greater need for social support after chemotherapy. In this study, we will evaluate whether a Geriatric Evaluation and Management-Survivorship (GEMS) intervention improves functional outcomes important to older cancer survivors following chemotherapy. METHODS: A cluster-randomized trial will be conducted in approximately 30 community oncology practices affiliated with the University of Rochester Cancer Center (URCC) National Cancer Institute Community Oncology Research Program (NCORP) Research Base. Participating sites will be randomized to the GEMS intervention, which includes Advanced Practice Practitioner (APP)-directed geriatric evaluation and management (GEM), and Survivorship Health Education (SHE) that is combined with Exercise for Cancer Patients (EXCAP©®), or usual care. Cancer survivors will be recruited from community oncology practices (of participating oncology physicians and APPs) after the enrolled clinicians have consented and completed a baseline survey. We will enroll 780 cancer survivors aged 65 years and older who have completed curative-intent chemotherapy for a solid tumor malignancy within four weeks of study enrollment. Cancer survivors will be asked to choose one caregiver to also participate for a total up to 780 caregivers. The primary aim is to compare the effectiveness of GEMS for improving patient-reported physical function at six months. The secondary aim is to compare effectiveness of GEMS for improving patient-reported cognitive function at six months. Tertiary aims include comparing the effectiveness of GEMS for improving: 1) Patient-reported physical function at twelve months; 2) objectively assessed physical function at six and twelve months; and 3) patient-reported cognitive function at twelve months and objectively assessed cognitive function at six and twelve months. Exploratory health care aims include: 1) Survivor satisfaction with care, 2) APP communication with primary care physicians (PCPs), 3) completion of referral appointments, and 4) hospitalizations at six and twelve months. Exploratory caregiver aims include: 1) Caregiver distress; 2) caregiver quality of life; 3) caregiver burden; and 4) satisfaction with patient care at six and twelve months. DISCUSSION: If successful, GEMS would be an option for a standardized APP-led survivorship care intervention. TRIAL REGISTRATION: ClinicalTrials.govNCT05006482, registered on August 9, 2021.

The role of cell-substrate interaction in regulating osteoclast activation: potential implications in targeting bone loss in rheumatoid arthritis.

Analysis of tissues retrieved from the bone-pannus interface from patients with rheumatoid arthritis (RA) and studies in animal models of inflammatory arthritis provide strong evidence that osteoclasts, the cells that are essential for physiological bone resorption, are responsible for articular bone destruction in RA. However, current treatments that specifically target osteoclast-mediated bone resorption in RA have not been successful in preventing bone erosions, and new therapeutic strategies are needed. It has been noted that, although osteoclast precursors are present within the bone microenvironment at sites of pathological bone resorption, cells expressing the full morphological and functional properties of mature osteoclasts are restricted to the immediate bone surface and adjacent calcified cartilage. These findings provide evidence that, in addition to requirements for specific cytokines, interaction of osteoclast precursors with these mineralised matrices results in activation of specific signal pathways and the induction of unique gene products that are essential for terminal osteoclast differentiation and activation. These studies are designed to define the gene products and signalling pathways regulated by bone and calcified cartilage, to identify new molecular targets and novel therapeutic approaches for preventing osteoclast-mediated joint destruction in RA and related forms of pathological bone loss.

Differing mechanisms of atrial fibrillation in athletes and non-athletes: alterations in atrial structure and function.

AIMS: Atrial fibrillation (AF) is more common in athletes and may be associated with adverse left atrial (LA) remodelling. We compared LA structure and function in athletes and non-athletes with and without AF. METHODS AND RESULTS: Individuals (144) were recruited from four groups (each n = 36): (i) endurance athletes with paroxysmal AF, (ii) endurance athletes without AF, (iii) non-athletes with paroxysmal AF, and (iv) non-athletic healthy controls. Detailed echocardiograms were performed. Athletes had 35% larger LA volumes and 51% larger left ventricular (LV) volumes vs. non-athletes. Non-athletes with AF had increased LA size compared with controls. LA/LV volume ratios were similar in both athlete groups and non-athlete controls, but LA volumes were differentially increased in non-athletes with AF. Diastolic function was impaired in non-athletes with AF vs. non-athletes without, while athletes with and without AF had normal diastolic function. Compared with non-AF athletes, athletes with AF had increased LA minimum volumes (22.6 ± 5.6 vs. 19.2 ± 6.7 mL/m2, P = 0.033), with reduced LA emptying fraction (0.49 ± 0.06 vs. 0.55 ± 0.12, P = 0.02), and LA expansion index (1.0 ± 0.3 vs. 1.2 ± 0.5, P = 0.03). LA reservoir and contractile strain were decreased in athletes and similar to non-athletes with AF. CONCLUSION: Functional associations differed between athletes and non-athletes with AF, suggesting different pathophysiological mechanisms. Diastolic dysfunction and reduced strain defined non-athletes with AF. Athletes had low atrial strain and those with AF had enlarged LA volumes and reduced atrial emptying, but preserved LV diastolic parameters. Thus, AF in athletes may be triggered by an atrial myopathy from exercise-induced haemodynamic stretch consequent to increased cardiac output.

Variation in cardiac glycoside content of monarch butterflies from natural populations in eastern North America.

A new spectrophotometric assay has been used to determine the gross concentration of cardiac glycoside in individual monarch butterflies. Adults sampled during the fall migration in four areas of eastern North America exhibited a wide variation in cardiac glycoside concentration. The correlation between spectrophotometrically measured concentrations and emetic dose determinations supports the existence of a broad palatability spectrum in wild monarch butterflies. The cardiac gylcoside concentration is greater in females than in males and is independent of the dry weight of the butterflies; contrary to prediction, both the concentration mean and variance decrease southward. The defensive advantage of incorporating cardiac glycosides may be balanced by detrimental effects on individual viability.

Mayan urbanism: impact on a tropical karst environment.

From the first millennium B.C. through the 9th-century A.D. Classic Maya collapse, nonurban populations grew exponentially, doubling every 408 years, in the twin-lake (Yaxha-Sacnab) basin that contained the Classic urban center of Yaxha. Pollen data show that forests were essentially cleared by Early Classic time. Sharply accelerated slopewash and colluviation, amplified in the Yaxha subbasin by urban construction, transferred nutrients plus calcareous, silty clay to both lakes. Except for the urban silt, colluvium appearing as lake sediments has a mean total phosphorus concentration close to that of basin soils. From this fact, from abundance and distribution of soil phosphorus, and from continuing post-Maya influxes (80 to 86 milligrams of phosphorus per square meter each year), which have no other apparent source, we conclude that riparian soils are anthrosols and that the mechanism of long-term phosphorus loading in lakes is mass transport of soil. Per capita deliveries of phosphorus match physiological outputs, approximately 0.5 kilogram of phosphorus per capita per year. Smaller apparent deliveries reflect the nonphosphatic composition of urban silt; larger societal outputs, expressing excess phosphorus from deforestation and from food waste and mortuary disposal, are probable but cannot be evaluated from our data. Eutrophication is not demonstrable and was probably impeded, even in less-impacted lakes, by suspended Maya silt. Environmental strain, the product of accelerating agroengineering demand and sequestering of nutrients in colluvium, developed too slowly to act as a servomechanism, damping population growth, at least until Late Classic time.

Expression cloning of an adenylate cyclase-coupled calcitonin receptor.

A calcitonin receptor complementary DNA (cDNA) was cloned by expression of a cDNA library from a porcine kidney epithelial cell line in COS cells. The 482-amino acid receptor has high affinity for salmon calcitonin (dissociation constant Kd approximately 6 nM) and is functionally coupled to increases in intracellular cyclic adenosine monophosphate (cAMP). The receptor shows no sequence similarity to other reported G protein-coupled receptors but is homologous to the parathyroid hormone-parathyroid hormone-related peptide (PTH-PTHrP) receptor, indicating that the receptors for these hormones, which regulate calcium homeostasis, represent a new family of G protein-coupled receptors.

Expression of two human skeletal calcitonin receptor isoforms cloned from a giant cell tumor of bone. The first intracellular domain modulates ligand binding and signal transduction.

Two distinct calcitonin (CT) receptor (CTR)-encoding cDNAs (designated GC-2 and GC-10) were cloned and characterized from giant cell tumor of bone (GCT). Both GC-2 and GC-10 differ structurally from the human ovarian cell CTR (o-hCTR) that we cloned previously, but differ from each other only by the presence (GC-10) or absence (GC-2) of a predicted 16-amino acid insert in the putative first intracellular domain. Expression of all three CTR isoforms in COS cells demonstrated that GC-2 has a lower binding affinity for salmon (s) CT (Kd approximately 15 nM) than GC-10 or o-hCTR (Kd approximately 1.5 nM). Maximal stimulatory concentrations of CT resulted in a mean accumulation of cAMP in GC-2 transfected cells that was greater than eight times higher than in cells transfected with GC-10 after normalizing for the number of receptor-expressing cells. The marked difference in maximal cAMP response was also apparent after normalizing for receptor number. GC-2 also demonstrated a more potent ligand-mediated cAMP response compared with GC-10 for both human (h) and sCT (the EC50 values for GC-2 were approximately 0.2 nM for sCT and approximately 2 nM for hCT; EC50 values for GC-10 were approximately 6 nM for sCT and approximately 25 nM for hCT). Reverse transcriptase PCR of GCT RNA indicated that GC-2 transcripts are more abundant than those encoding for GC-10. In situ hybridization on GCT tissue sections demonstrated CTR mRNA expression in osteoclast-like cells. We localized the human CTR gene to chromosome 7 in band q22. The distinct functional characteristics of GC-2 and GC-10, which differ in structure only in the first intracellular domain, indicate that the first intracellular domain of the CTR plays a previously unidentified role in modulating ligand binding and signal transduction via the G protein/adenylate cyclase system.

Cloning, characterization, and expression of a human calcitonin receptor from an ovarian carcinoma cell line.

A human ovarian small cell carcinoma line (BIN-67) expresses abundant calcitonin (CT) receptors (CTR) (143,000 per cell) that are coupled, to adenylate cyclase. The dissociation constants (Kd) for the CTRs on these BIN-67 cells is approximately 0.42 nM for salmon CT and approximately 4.6 nM for human CT. To clone a human CTR (hCTR), a BIN-67 cDNA library was screened using a cDNA probe from a porcine renal CTR (pCTR) that we recently cloned. One positive clone of 3,588 bp was identified. Transfection of this cDNA into COS cells resulted in expression of receptors with high affinity for salmon CT (Kd = approximately 0.44 nM) and for human CT (Kd = approximately 5.4 nM). The expressed hCTR was coupled to adenylate cyclase. Northern analysis with the hCTR cDNA probe indicated a single transcript of approximately 4.2 kb. The cloned cDNA encodes a putative peptide of 490 amino acids with seven potential transmembrane domains. The amino acid sequence of the hCTR is 73% identical to the pCTR, although the hCTR contains an insert of 16 amino acids between transmembrane domain I and II. The structural differences may account for observed differences in binding affinity between the porcine renal and human ovarian CTRs. The CTRs are closely related to the receptors for parathyroid hormone-parathyroid hormone-related peptide and secretin; these receptors comprise a distinct family of G protein-coupled seven transmembrane domain receptors. Interestingly, the hCTR sequence is remotely related to the cAMP receptor of Dictyostelium discoideum (21% identical), but is not significantly related to other G protein-coupled receptor sequences now in the data bases.

Role of cell-matrix interactions in osteoclast differentiation.

Osteoclast and their mononuclear cell precursors are present within the bone microenvironment at sites of physiologic and pathologic bone resorption. Analysis of tissues from sites of bone resorption reveal that cells expressing the full morphological and functional properties of mature osteoclasts are restricted to the immediate bone surface. We hypothesize that in addition to cytokines, components of the bone matrix and specific cell surface receptors on osteoclasts and their precursors play an essential role in determining the genetic profile and functional properties of fully differentiated resorbing osteoclasts. We have employed expression profiling, with an in vitro model of matrix-dependent osteoclast differentiation, to identify the molecular pathways by which bone matrix-interactions induce terminal osteoclast differentiation and activation. In preliminary studies, we have identified unique genes and transcriptional pathways that are induced by interaction of osteoclast precursors with specific components of the mineralized bone matrix. The authenticity of the gene profiles, as markers of osteoclast differentiation and activation, have been provisionally validated using an in vivo animal bone implantation model and by examination of tissues from patients with specific forms of pathologic osteoclast-mediated bone resorption. The ultimate goal of our studies is to identify new molecular targets for inhibiting osteoclast-mediated bone loss in disorders of pathologic bone loss. The early work of Walker et al. (Walker 1972) in parabiotic animals, and the subsequent studies of Burger et al. (Burger, Van der Meer, van de Gevel, et al. 1982) using a co-culture model with fetal bone rudiments and bone marrow-derived cells, have helped to establish that osteoclasts are derived from macrophage precursors of colony forming unit-macrophage (CFU-M lineage). As such, they share a common hematopoietic origin with other CFU-M lineage cells, including tissue macrophages that populate the lung (alveolar macrophages), liver (Kupfer cells), synovium (synovial macrophages) and other organs. They also share a common lineage

Infections during left ventricular assist device support do not affect posttransplant outcomes.

BACKGROUND: Although infections acquired during ventricular assist device support may increase the risk of infection and have an impact on transplant survival, their true posttransplant consequences remain to be determined. This study evaluates the impact of an outpatient program, newer devices, and an updated infection management protocol on infection-related patient outcomes after transplant. METHODS AND RESULTS: Eighty-six patients received a left ventricular assist device (LVAD) between June 1996 and June 1999. Fifty patients transplanted during the same period, without prior device support, were used as controls; they were matched to transplanted LVAD recipients by age, sex, diagnosis, and transplant date. The nature of and actuarial freedom from peritransplant and posttransplant infections were compared at 6 months after transplant; actuarial patient survival was compared at 3 years. Infection was defined as leukocytosis or leukopenia, with a positive culture requiring either medical or surgical intervention. Forty-four patients (51%) were successfully discharged home on LVAD support, and 61 (71%) were transplanted. A high incidence of infection during device support did not have an impact on pretransplant or posttransplant mortality, posttransplant infectious rate, or overall patient survival. Active infections at transplant also did not significantly influence 6-month mortality. In comparison, LVAD recipients had a lower freedom from infection than did controls (P:<0.05); however, 3-year survival did not differ: 79% and 87% for the LVAD and control groups, respectively. CONCLUSIONS: Although LVADs increase the risk of infection in the early posttransplant period, this appears not to have an impact on transplantability or patient survival and likely reflects effective infection control in both inpatient and outpatient settings.

Improved survival rates support left ventricular assist device implantation early after myocardial infarction.

OBJECTIVES: Implantation of left ventricular assist devices (LVADs) early after acute myocardial infarction (MI) has traditionally been thought to be associated with high mortality rates due to technical limitations and severe end-organ dysfunction. At some experienced centers, doctors have refrained from earlier operation after MI to allow for a period of hemodynamic and end-organ stabilization. METHODS: We retrospectively investigated the effect of preoperative MI on the survival rates of 25 patients who received a Thermocardiosystems Incorporated LVAD either <2 weeks (Early) (n = 15) or >2 weeks (Late) (n = 10) after MI. Outcome variables included perioperative right ventricular assistance (and right-sided circulatory failure), hemodynamic indexes, percent transplanted or explanted, and mortality. RESULTS: No statistically significant differences were demonstrated between demographic, perioperative or hemodynamic variables between the Early and Late groups. Patients in the Early group demonstrated a lower rate of perioperative mechanical right ventricular assistance, but had a higher rate of perioperative inhaled nitric oxide use. In addition, 67% of patients in the Early group survived to transplantation and 7% to explantation, findings comparable to those in the Late group (60% and 0% respectively). CONCLUSIONS: This clinical experience suggests that patients may have comparable outcomes whether implanted early or late after acute MI. These data therefore support the early identification and timely application of this modality in post-MI LVAD candidates, as this strategy may also reveal a subgroup of patients for whom post-MI temporary LVAD insertion may allow for full ventricular recovery.

Implantable left ventricular assist devices provide an excellent outpatient bridge to transplantation and recovery.

OBJECTIVES: Our recent experience with outpatient left ventricular assist device (LVAD) support is presented to demonstrate the possibilities and limitations of long-term outpatient mechanical circulatory assistance. BACKGROUND: The experience with inpatient LVAD support as a bridge to transplantation has proved the efficacy of such therapy in improving circulatory hemodynamic status, restoring normal end-organ function and facilitating patient rehabilitation. With miniaturization of the power supplies and controllers, such mechanical circulatory support can now be accomplished in an outpatient setting. METHODS: Between March 1993 and February 1997, 32 patients (26 male, 6 female, mean [+/-SEM] age 49 +/- 15 years) underwent implantation of the ThermoCardiosystems (TCI) Heartmate vented electric (VE) LVAD. The VE LVAD is powered by batteries worn on shoulder holsters and is operated by a belt-mounted system controller, allowing unrestricted patient ambulation and hospital discharge. RESULTS: Mean duration of support was 122 +/- 26 days (range 3 to 605), with a survival rate to transplantation or explantation of 78%. Nineteen patients were discharged from the hospital on mean postoperative day 41 +/- 4 (range 17 to 68), for an outpatient support time of 108 +/- 30 days (range 2 to 466). Four patients underwent early transplantation and could not participate in the discharge program, and three patients currently await discharge. The complication rate was not statistically different from that encountered in our previous 52 patients with a pneumatic LVAD. CONCLUSIONS: Outpatient LVAD support is safe and provides improved quality of life for patients awaiting transplantation. Wearable and totally implantable LVADs should be studied as permanent treatment options for patients who are not candidates for heart transplantation.

The Ides of March. The match 1993 in perspective.

BACKGROUND: The total number of US medical school graduates who selected categorical programs in internal medicine in this year's match fell by 7.9%. Consequently, the program fill rate for US graduates declined for the eighth consecutive year, from 55.9% to 53.1%. Preliminary positions and international graduates continue to increase, though questions remain whether these residents serve as good role models to encourage student interest in internal medicine. METHODS: We reviewed the 1993 National Resident Matching Program data and several curricular reforms implemented in our internal medicine clerkship and residency program to evaluate whether such reform might enhance interest in general internal medicine. RESULTS: Reform in our internal medicine clerkship curriculum included increased emphasis on problem-based learning and exposure to generalist role models. This resulted in substantial increases on the average miniboard examination and a 22% increase in the number of students pursuing residency in internal medicine from the previous year. Residency curricular reform centered around enhanced ambulatory care teaching along with improved exposure to generalist role models. This resulted in a gradual increase in the number of residency graduates who were staying in general internal medicine from 21% in 1991 to 40% in 1993. CONCLUSIONS: Innovative curricular changes in our internal medicine clerkship and residency programs have led to enhanced interest in general internal medicine. Although our results are preliminary, such change is necessary, not only to continue program excellence, but for simple survival.

Fluconazole in the treatment of hepatosplenic candidiasis.

Hepatosplenic candidiasis has increased in frequency among immunocompromised hosts. Risk factors include hematologic malignancy, intensive chemotherapy, prolonged neutropenia, and treatment with broad-spectrum antibiotics. Patients most commonly present with abdominal pain, persistent fevers despite antibiotic therapy, and an elevated alkaline phosphatase level that is out of proportion to other hepatic enzyme levels. Gastrointestinal mucosal damage secondary to intensive chemotherapy may allow colonization with Candida species and subsequent seeding of the portal vein. Treatment has consisted of prolonged courses of amphotericin B, with mortality rates approaching 50%. We report a case of hepatosplenic candidiasis in a patient with acute myelogenous leukemia who had clinical and radiographic improvement during fluconazole therapy. Fluconazole may be an efficacious and less toxic alternative to amphotericin B.

Hematopoietic microenvironment transfer by stromal fibroblasts derived from bone marrow varying in cellularity.

Autologous fibroblast derivatives of red and yellow marrow of rabbits were shown to differ in their capability to transfer a hematopoietic microenvironment upon implantation under the renal capsule. Although a heterotopic ossicle formed in each instance, the quality of the associated medullary tissue mirrored the quality of the bone marrow used to generate the stromal fibroblasts. Thus, fibroblasts cultured from a cellular marrow produced a stroma with numerous hematopoietic foci whereas those cultured from a severely hypocellular marrow produced a stroma with mainly fat cells. The results with 21 implants point to a transmittable regulatory role of a class of stromal fibroblasts.

Cloning and characterization of a mouse brain calcitonin receptor complementary deoxyribonucleic acid and mapping of the calcitonin receptor gene.

We have identified and characterized a mouse brain calcitonin receptor (CTR) complementary DNA (cDNA). This cDNA encodes a receptor protein that, after expression, has high affinity binding for salmon calcitonin (Kd approximately, 12.5 nM) and is coupled to adenylate cyclase. The binding affinity of this expressed receptor for salmon calcitonin is lower than that described for the previously cloned porcine renal and human ovarian CTRs, but is similar to that of the recently described rat brain CTR, designated the C1b form of the receptor. Analysis of the deduced structure of the mouse brain CTR reveals that it is highly related to the other CTR cDNAs that belong to a distinct family of G-protein-coupled receptors with seven transmembrane-spanning domains. The major structural feature that distinguishes the mouse cDNA clone from the other CTRs is the presence of a consecutive 111-basepair nucleotide sequence that encodes a 37-amino acid sequence which is predicted to localize to the first extracellular loop between the second and third transmembrane-spanning domains. We have mapped the CTR gene in the mouse to the proximal region of chromosome 6, which is homologous to the 7q region of human chromosome 7; only a single CTR gene was identified. Preliminary analysis of the mouse CTR gene reveals that it is complex, consisting of multiple exons separated by lengthy introns that would allow for splice variants consistent with the existence of multiple CTR isoforms predicted from the CTR cDNA clones. The differential cellular and tissue distribution of these functionally distinct CTR isoforms provides the molecular basis for the previously reported widespread distribution and functional heterogeneity of the CTR.

Improved survival in patients with acute myocarditis using external pulsatile mechanical ventricular assistance.

BACKGROUND: Acute myocarditis remains a disease with a variable clinical course, from full ventricular recovery to complete heart failure; to date, few cases have been reported that describe the efficacy of temporary mechanical ventricular assistance for its treatment. METHODS: We evaluated the voluntary world registry with the use of an external pulsatile ventricular assist device (the ABIOMED BVS 5000 [BVS]) for acute myocarditis to determine the impact of mechanical ventricular assistance on outcome. Variables analyzed included patient demographics, serum chemistries, and overall hemodynamics prior to BVS, while on BVS support, and after BVS explanation. Postoperative parameters included re-operation, bleeding, respiratory failure, renal failure, and infections, neurologic, or embolic events. RESULTS: Eighteen patients in the ABIOMED world registry underwent BVS implantation for myocarditis; 11 (61.1%) had complete pre-operative and hemodynamic data for analysis. Patients were supported for 13.2 +/- 17.0 days, after which time 7 (63.6%) patients survived to explanation of the device and 2 (18.2%) underwent transplantation. Elevated admission serum chemistries (blood ureanitrogen [BUN], creatinine, transaminases) and hemodynamics (central venous pressure [CVP], mean pulmonary arterial pressure [PAP], pulmonary capillary wedge pressure [PCW], cardiac index [CI], all normalized during the period of device support. Estimated ejection fractions in the 7 explanted patients ranged between 50 to 60% at routine evaluation 3 years after device removal. CONCLUSIONS: Temporary mechanical ventricular assistance represents an efficacious therapy for acute myocarditis in patients with hemodynamic decompensation despite maximal medical therapy. Failure to achieve full ventricular recovery while on device support still allows for other surgical alternatives, including implantation of a long-term implantable ventricular assist device, or cardiac transplantation.