Is an Automatic Control Algorithm Necessary for Centrifugal Pumps?

In order to meet physiologic changes in LVAD patients, VAD manufacturers have been developing automatic control algorithms for rotary blood pumps. However, whether an automatic control algorithm is required for normal physiological functioning is unknown. Physiological patterns may be monitored by analyzing daily VAD parameter data (Speed, Power, and Estimated Flow) as acquired by the HeartWare® LVAS Controller. Experiment: Log files from patients supported on the HeartWare® LVAS which contained VAD parameter data (logged at 15minute intervals) were analyzed for daily performance under various physiological conditions while a constant VAD Speed was maintained. A 12-point moving average of Estimated Flow was calculated to eliminate erratic deviation in flow and provide a visual reference of circadian rhythm. Resulting data was analyzed and presented in a weekly viewable time frame. O\u27Driscoll, G., Tamez, D., & Voskoboynikov, N. (2008). Is an automatic control algorithm necessary for centrifugal pumps? Journal of Cardiac Failure, 14(6), S53. doi:10.1016/j.cardfail.2008.06.167 ISSN: 1532-841

Treatment of Later Humoral Rejection with Anti-CD20 Monoclonal Antibody Rituximab: A Single Centre Experience

Humoral or vascular rejection is a B cell-mediated production of immunoglobulin (Ig) G antibody against a transplanted organ that results in immune complex deposition on the vascular endothelium, activation of the complement cascade, production of endothelial dysfunction and regional ischaemic injury

Treatment of parainfluenza virus 3 pneumonia in a cardiac transplant recipient with intravenous ribavirin and methylprednisolone

A 59-year-old man developed a lower respiratory tract infection 10 years after orthotopic cardiac transplantation. He did not respond to broad-spectrum antibiotic and antifungal treatment. Parainfluenza virus type 3 was the causative organism, and he was successfully treated with intravenous ribavirin and methylprednisolone

Strategy of aggressive steroid weaning and routine alendronate therapy to reduce bone loss after cardiac transplantation

Objective: Osteoporosis is common after cardiac transplantation. The routine use of prednisolone posttransplantation is a major contributor to bone mineral loss. We sought to study the effectiveness of a strategy combining aggressive steroid weaning and routine prophylaxis with alendronate to reduce bone loss without adversely affecting posttransplantation survival. Patients and Methods: This retrospective clinical study compared 2 cohorts of patients. Group A included 28 patients who had undergone transplantation since June 1999, all of whom were prescribed alendronate (10 mg daily or 70 mg weekly). All were aggressively weaned off prednisolone with the aim of being steroid-free by 9 months posttransplantation. Only 10 of the 28 patients were on prednisolone at the time of the study. Group B was an historical control cohort of 28 posttransplant patients reviewed in a cross-sectional study in 1995. Only 2 patients were on osteoporosis prophylaxis with estrogen or vitamin D; 26 patients were on prednisolone at the time of the study. The groups were compared by dual-energy X-ray absorptiometry (DEXA) bone mineral densitometry at the femoral neck and lumbar spine at a mean of 3 years after transplantation. We compared the cumulative survival of the 2 groups. Results: Cumulative survival posttransplantation was similar in both groups. Compared with group B, group A showed a significantly higher mean femoral Z-score (+0.3 vs −0.5, P = .01) and lumbar spine Z-score (0.0 vs −0.9, P \u3c .02). The incidence of osteoporosis (defined by WHO criteria as T-score ≤ −2.5) was lower in group A compared with group B (18% vs 29%, P = NS). Conclusions: A strategy of aggressive weaning of prednisolone postcardiac transplantation coupled with routine osteoporosis prophylaxis using alendronate was associated with significantly higher bone mass and a trend toward a reduced incidence of osteoporosis. This strategy was successful to reduce the use of steroid without any adverse effect on cumulative survival posttransplantation

Late humoral rejection in a cardiac transplant recipient treated with the anti-CD20 Monoclonal Antibody Rituximab

Humoral or vascular rejection results from a B cell-mediated production of immunoglobulin (Ig) G antibody against a transplanted organ, producing immune complex deposition on the vascular endothelium, activation of the complement cascade, generation of endothelial dysfunction, and regional ischemic injury. Antibody-mediated rejection, which may be accompanied by hemodynamic compromise, is associated with reduced long-term graft survival.1 Patients believed to be at an increased risk of developing humoral rejection include women,2 particularly those with high levels of panel reactive antibodies,3 cytomegalovirus seropositivity,4 and 5 and positive cross matches,3 and 6 and subjects with prior sensitization to OKT3.7 Treatment options for humoral rejection include plasmapheresis to lower the circulating immunoglobulin levels followed by high-dose cyclophosphamide to reduce the B-cell population. Other modalities include total lymphoid irradiation, photophoresis, splenectomy, and, for treatment failures, retransplantation.8 Rituximab is a chimeric humanized monoclonal antibody directed against the pan B-cell surface molecule, CD20. It is approved for the treatment of low-grade B-cell non-Hodgkin’s lymphoma. It has also been used successfully for the treatment of posttransplant B-cell lymphoproliferative disease.9 We report a case of late humoral rejection successfully treated with rituximab

Anti-thymocyte globulin as an adjunct to treatment of fulminant lymphocytic myocarditis

There is much debate over the role of immunosuppression in the treatment of acute and fulminant myocarditis. The low incidence of the condition prevents large numbers of cases for study, and treatment protocols vary greatly between institutions. In this study we add our experience with anti-thymocyte globulin as an adjunct to standard medical therapy for 5 patients presenting with cardiogenic shock due to fulminant myocarditis. All cases were associated with rapid and dramatic improvement in hemodynamic and electrophysiologic abnormalities, returning patients to NYHA Class I and cardiac function to normal or near normal by discharge

Successful treatment of ventricular assist device associated ventricular thrombus with systemic tenecteplase

The Jarvik 2000 Flowmaker® is an implantable left-ventricular assist device (LVAD) that produces axial-flow by means of a single, rotating, vaned impeller which eliminates the need for valves, an internal compliance chamber, or an externalised vent.1 A known complication of continuous, axial-flow LVADs is thrombosis within the left ventricle, adjacent to the device\u27s inflow conduit with subsequent inflow obstruction manifesting as recurrent heart failure. Delgado et al. reported two cases in which a catheter was used to continuously infuse recombinant tissue plasminogen activator (tPA) into the left ventricle until signs of successful thrombolysis was achieved.2 We report a case of intracardiac thrombus successfully treated with a single dose of peripherally administered thrombolytic

Ventricular Assist Device – How to Obtain Optimal Benefits?

Heart failure is now acknowledged to be the most common malignant disease in industrialized countries, with advanced heart failure having a worse prognosis than most forms of cancer (Garg, Yusuf 1993). Advances in pharmacological treatment have helped patients in all stages of systolic dysfunction, even those with NYHA IV symptoms (the Captopril-Digoxin Multicenter Research Group 1988, Packer et al. 1996, the RALES Investigators 1996). The Working Group on Heart Failure of the European Society of Cardiology has promoted a number of initiatives aimed at improving the treatment of heart failure (ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2008). Despite advances in pharmacological treatments aimed at a neurohormonal blockade for heart failure, there is still a growing number of patients with advanced symptoms who suffer significant morbidity and mortality. Mechanical stresses on the myocardium (increased preload and afterload) and chronic neurohormonal activation conspire to propagate the maladaptive ventricular remodeling responsible for the insidious nature of heart failure. Recent studies suggest that further pharmacological neurohormonal blockade may be neither safe nor effective (Mann 2004). This finding has led to the concept that the limit to which neurohormonal and cytokine mechanisms can be blocked in heart failure patients has already been reached (Cohn, Tognoni 2001). The problem of how to treat patients worldwide who develop advanced heart failure despite optimal medical therapy has not yet been resolved (Gronda, Vitali 1999)

Severe cardiac insufficiency as a result of complicated myocardial infarction - Choice of therapy

On 28th January 2004 patient P.T., aged 56, suffered an extensive and complicated anterolateral myocardial infarction with low output syndrome and double ventricular tachycardia interrupted by electrical cardioversion. Emergency coronary angiography and percutaneous coronary intervention of the left anterior descending artery with a result of 100%→5% and left circumflex with a result of 99%→% were performed with simultaneous implantation of stents at the Royal Perth Hospital in Australia. The patient required intubation, intra-aortal counterpulsatio, ECG assessment, blood pressure measurement and invasive haemodynamic monitoring (CI, CO, PAWP, PAP). On the fifth day, in the face of lack of haemodynamic improvement, an additional infusion of levosimendan was added to the infusion of noradrenalin and dobutamine, which resulted in a slight transient improvement in the clinical status of the patient. In view of the unsatisfactory haemodynamic parameters and following a preliminary qualification for cardiac transplant (OHTx), a mechanical device supporting the function of the left ventricle was implanted without complications into the abdominal cavity on the 30th day of hospitalisation. On 15th April 2005 OHTx was performed with good clinical results

The athlete\u27s heart: A contemporary appraisal of the \u27Morganroth Hypothesis\u27

As early as 1975, Morganroth and colleagues hypothesized that the cardiac morphological adaptation observed in athletes corresponded with the nature of the haemodynamic stimulus imposed on the ventricles during repeated exercise bouts. Endurance training purportedly leads to an eccentric form of cardiac hypertrophy, principally characterized by increased left ventricular (LV) cavity dimension, and thus LV mass (LVM), as a consequence of prolonged repetitive volume overload. In contrast, strength training is supposedly associated with a concentric form of hypertrophy where increased ventricular wall thickness, with no change in cavity size, underpins the elevated LVM as a consequence of the pressure overload produced during strenuous resistive exercise. The \u27Morganroth hypothesis\u27 has been broadly adopted in the scientific and medical literature, partly as a consequence of a large body of cross-sectional evidence suggesting that endurance athletes have greater cavity dimensions than control subjects or resistance athletes. However, in conflict with the \u27Morganroth hypothesis\u27, several studies suggest that LV wall thickness is increased more in endurance-, than strengthtrained athletes and others have reported no morphological changes in resistancetrained athletes. Such controversial data may reflect variability in the training stimuli, with little obvious attempt to quantify these issues in previous research. Further reflection on the \u27Morganroth hypothesis\u27 may also be pertinent as more sensitive technologies, such as magnetic resonance imaging, are now being employed for the assessment of cardiac morphology. Finally, the process of scaling (or normalizing) cardiac size for between-subject differences in body size and composition has further complicated the description and understanding of cardiac morphology in athletes. Specifically, it is possible that the increased LVM observed in some athletes may merely reflect a \u27larger than normal\u27 body size. These considerations emphasise the limitations of the predominance of crosssectional comparisons in the available literature, which assume that differences between groups are due to a training effect per se rather than other betweensubject differences. The small number of longitudinal training studies undertaken in athletes suggest that individuals with athlete\u27s heart can exhibit further cardiac adaptation in response to training resumption. Longitudinal training studies undertaken in previously sedentary subjects generally indicate that exercise results in enlargement of LV cavity size, increases in wall thickness or LVM following training. However, there are currently limited longitudinal data available to comment on the effects of different modalities of exercise training on LV cavity dimension and wall thickness. In summary, significant caveats related to cross-sectional literature, the relative insensitivity of echocardiographic measurements and the paucity of evidence from longitudinal exercise training studies, warrant ongoing research to verify the \u27Morganroth hypothesis\u27