Sandra Chaparro

Cardiac regeneration and stem cell therapy

Purpose of reviewSignificant recent developments have occurred in the field of cardiac regeneration and stem-cell therapy. Understanding the new technological advances in cell therapy will ultimate allow us to achieve a goal of cell-based cardiac repair. Recent findingsWe discuss the latest cell-based therapies (including skeletal myoblasts, bone-marrow-derived cells, stem cells), the recent clinical trials in humans and different delivery techniques. SummaryOngoing unraveling of the mechanistic and clinical complexities underlying cardiac regeneration will advance the field of regenerative medicine. Substantial progress is being made by the parallel conduct of basic science studies and clinical trials that are incorporating mechanistic evaluations.

Argatroban as novel therapy for suspected thrombosis in patients with continuous-flow left ventricle assist device and hemolysis

The growing use of left ventricular assist devices as a bridge to transplant and their increased duration as destination therapy in patients successfully treated for advance heart failure unwrap a new spectrum of complications seen in long-term use of the devices. Device thrombosis remains a therapeutic dilemma, and limited data are available for the use of direct thrombin inhibitors as a treatment option. We performed a review of literature and present a series of four patients with suspected left ventricular assist device-associated thrombosis, manifesting as hemolysis, who were treated empirically with argotraban, a direct thrombin inhibitor with the ability to interact with both free and clot-bound thrombin. In this case series, we treated four patients with argatroban for suspected device thrombosis. All showed significant improvement of hemolysis according to lactate dehydrogenase measurements, and device removal was prevented in three. Bleeding complications occurred when therapy was used closer to the operative period. Argatroban can be a viable option to treat patients with hemolysis from suspected device thrombosis in patients with HeartMate II continuous-flow left ventricular assist device. Prompt attention is needed to monitor any bleeding complications.

Combined use of Impella left ventricular assist device and extracorporeal membrane oxygenation as a bridge to recovery in fulminant myocarditis.

Myocarditis may result in cardiogenic shock, and when medical therapy is unable to maintain adequate cardiac output, mechanical circulatory support is indicated. This is the first reported case of a percutaneous left ventricular assist device being used in combination with extracorporeal membrane oxygenation in a patient with biventricular and respiratory failure, as a bridge to recovery.

Incidence of Hemolysis in Patients with Cardiogenic Shock Treated with Impella Percutaneous Left Ventricular Assist Device.

Impella assist devices have been increasingly used in cardiogenic shock (CS). This study aims to assess the incidence of hemolysis when Impella support is used longer than 6 hours in CS. We retrospectively studied all patients who required Impella between April 2009 and September 2013. Demographic data and hemolysis indicators were sampled and analyzed using paired t-test. A total of 118 devices were placed and 40 used longer than 6 hours. The average time of support was 86.63 hours, and the 30 and 90 days of survival were 65% and 60%, respectively. After 24 hours of support, the hemoglobin (Hb) decreased significantly despite 17% of patients receiving blood transfusion (p = 0.0001). By the time of removal, 65% of patients were transfused to maintain a Hb of 10 mg/dl (p = 0.0014). The lactate dehydrogenase (LDH) increased to 5,201 U/L (n = 22; p = 0.0096), the bilirubin to 5.6 mg/dl (p = 0.008), and the haptoglobin level was 15.4 mg/dl (n = 25). The cumulative incidence of hemolysis was 62.5%. Hemolysis is a common occurrence in patients with long-term Impella support for CS, evaluated by the persistent decline in Hb and haptoglobin as well as increase in LDH and bilirubin. Strict monitoring of hemolysis parameters at baseline and at frequent intervals is crucial.

Myocardial Damage Detected by Late Gadolinium Enhancement Cardiac Magnetic Resonance Is Uncommon in Peripartum Cardiomyopathy

Background In peripartum cardiomyopathy, the prevalence of focal myocardial damage detected by late gadolinium enhancement (LGE) cardiovascular magnetic resonance is important to elucidate mechanisms of myocardial injury and cardiac dysfunction. LGE equates irreversible myocardial injury, but LGE prevalence in peripartum cardiomyopathy is uncertain. Methods and Results Among 100 women enrolled within the Investigations of Pregnancy Associated Cardiomyopathy cohort, we recruited 40 women at 13 centers to undergo LGE cardiovascular magnetic resonance, enrolled within the first 13 weeks postpartum. Follow‐up scans occurred at 6 months postpartum, and death/transplant rates at 12 months. Baseline characteristics did not differ significantly in the parent cohort according to cardiovascular magnetic resonance enrollment except for mechanical circulatory support. LGE was noted only in 2 women (5%) at baseline. While left ventricular dysfunction with enlargement was prevalent at baseline cardiovascular magnetic resonance scans (eg, ejection fraction 38% [Q1–Q3 31–50%], end diastolic volume index=108 mL/m2 [Q1–Q3 83–134 mL/m2]), most women demonstrated significant improvements at 6 months, consistent with a low prevalence of LGE. LGE was not related to baseline clinical variables, ejection fraction, New York Heart Association heart failure class, or mortality. Neither of the 2 women who died exhibited LGE. LGE was inversely associated with persistent left ventricular ejection fraction at 6 months (P=0.006). Conclusions Factors other than focal myocardial damage detectable by LGE explain the initial transient depressions in baseline left ventricular ejection fraction, yet focal myocardial damage may contribute to persistent myocardial dysfunction and hinder recovery in a small minority. Most women exhibit favorable changes in ventricular function over 6 months. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT01085955.

A multidisciplinary team-based process improves outpatient anticoagulation quality with continuous-flow left-ventricular assist devices

a Department of Pharmacy, Jackson Memorial Hospital, Jackson Health System, Miami, FL, United States b Miami Transplant Institute, Miami, FL, United States c Department of Medicine, University of Miami, Miami, FL, United States d Department of Pharmacy Practice, University of Connecticut School of Pharmacy, Storrs, CT, United States e Department of Pharmacy, New York Presbyterian Columbia University Medical Center, New York, NY, United States

Mannose binding lectin (mbl2) haplotype frequencies in solid organ transplant patients and correlation with MBL protein levels — Evaluation of complement-mediated effector pathway deficiency

Mannose-binding lectin (MBL) is a protein critical in activating complement. Patients with wild-type and variant mbl2 genotypes have high or low concentrations of MBL protein, which is known to increase susceptibility to transplant rejection or infection, respectively. Our objective was to determine mbl2 genotype frequencies in future solid organ transplant recipients in order to optimize their induction and maintenance immunosuppressive therapies, and to provide MBL reference data for this unique population. We genotyped 1687 patients, and concurrently measured protein in 807 of them, during 2010-2011. Frequencies of the structural allele SNPs in our population were similar to those of other studied populations; however, Black patients with the same intermediate and deficient mbl2 genotypes as Caucasians produced significantly lower levels of MBL protein; therefore, within this population more genotypes should be considered MBL-deficient. Overall, the most critical parameter in determining serum MBL protein concentration was genotype, which was independent of other factors including ethnicity, gender, or diseased native organ type.

An unexpected cause of massive hemolysis in percutaneous left ventricular assist device

We present the case of a 24 year-old patient that developed massive hemolysis shortly after percutaneous left ventricular assist device, Impella 2.5, was placed. The hemolysis occurred without device alarm while the device was in the correct position. Further investigation of the device revealed fiber wrapped around the tip of the device, as a culprit. This case emphasizes on the special caution applied during device preparation to minimize the possible adverse events.

Severe Hemolytic Anemia and Acute Kidney Injury After Percutaneous Continuous-Flow Ventricular Assistance

The incidence of hemolysis after ventricular assist device implantation is low and has been estimated at ≈3%.1 The Impella 2.5 (Abiomed; Danvers, MA) continuous-flow left ventricular assist device uses a microaxial pump that draws blood from the left ventricular cavity and expels it into the ascending aorta. The device is percutaneously inserted via the femoral artery and used as temporary circulatory support. In this case, we describe a patient who developed severe hemolytic anemia and acute kidney injury shortly after insertion of an Impella 2.5 ventricular assist device. A 50-year-old male patient with idiopathic dilated cardiomyopathy and an ejection fraction of 15%, receiving home dobutamine infusion therapy, presented to the emergency department with multiple firings of his biventricular automatic implantable cardioverter defibrillator. The night before admission, the patient felt 2 shocks from his device. Interrogation of his automatic implantable cardioverter defibrillator revealed ventricular fibrillation before each firing. He …

Methylene blue-induced serotonin syndrome after left ventricular assist device implantation: A case report and literature review

From the University of Miami Miller School of Medicine; Internal Medicine Department, Jackson Memorial Hospital, University of Miami; and Division of Cardiovascular Medicine, University of Miami Hospital, Miami, Fla. Disclosures: Dr Chaparro is a consultant for Abbott and received research support fromMedtronic on an unrelated project. All other authors have nothing to disclose with regard to commercial support. The authors attest to having full freedom to explore data, analyze results independently, and had sole authority in deciding to submit the material for publication. Received for publication Feb 15, 2017; revisions received April 21, 2017; accepted for publication May 17, 2017; available ahead of print June 24, 2017. Address for reprints: Sandra V. Chaparro, MD, Cardiovascular Medicine, University of Miami Miller School of Medicine, Clinical Research Building, Room 1110, 1120 NW 14th St, Miami, FL 33136 (E-mail: schaparro@ miami.edu). J Thorac Cardiovasc Surg 2017;154:e39-43 0022-5223/