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Background Giant cell myocarditis (GCM) is an inflammatory form of acute heart failure with high rates of cardiac transplantation or death. Standard acute treatment includes multi-drug immunosuppressive regimens. There is a small but growing number of case reports utilizing rabbit anti-thymocyte globulin in severe cases. Case summary Two cases are presented with similar presentations and clinical courses. Both are middle-aged patients with no significant past medical history, who presented with new acute decompensated heart failure that quickly progressed to cardiogenic shock requiring inotropic and mechanical circulatory support. Both underwent endomyocardial biopsies that diagnosed GCM. Both were treated with a multi-agent immunosuppressive regimen, notably including rabbit anti-thymocyte globulin, with subsequent resolution of shock and recovery of left ventricular ejection fraction. Both remain transplant-free and without ventricular arrhythmias at 7 months and 26 months, respectively. Discussion In aggregate, these cases are typical of GCM. They add to growing observational data that upfront rabbit anti-thymocyte globulin may reduce morbidity and mortality in GCM, including potentially preventing the need for complex interventions like orthotopic heart transplantation. [ABSTRACT FROM AUTHOR]

Purpose To describe a case of disseminated Verruconis gallopava infection in a cardiac transplant recipient that was successfully treated with oral posaconazole and intravenous anidulafungin. Summary A 51-year-old male initially presented with pulmonary manifestations, but subsequently developed cutaneous lesions, fungemia, osteomyelitis of the hip requiring excision, and eventually brain abscesses over the course of 3 months. The patient was successfully treated with various antifungal agents throughout his treatment course and was eventually discharged on oral posaconazole and intravenous anidulafungin. He remained on oral posaconazole suppressive therapy and had had no recurrence of fungal infection after 31 months of follow-up. Conclusion On the basis of this case report, intravenous anidulafungin and chronic suppressive therapy with oral posaconazole can successfully treat disseminated V. gallopava infections. [ABSTRACT FROM AUTHOR]

Background Myocardial bridging (MB), though typically a benign finding, may occasionally lead to syncope, myocardial infarction, arrhythmia, or sudden death. Surgical denervation of transplanted hearts complicates the management of such incidentally detected post-transplant coronary anomalies due to the lack of classic ischaemic symptoms. Case summary A middle-aged female underwent an uncomplicated cardiac transplantation from a healthy male donor in his early 20s who had suffered a cardiac arrest while using cocaine. Given the young donor age, a pre-transplant coronary angiogram (CAG) was deferred. However, 6-week post-transplant, routine CAG, and intravascular ultrasound revealed an extensive MB spanning a significant portion of the left anterior descending coronary artery with substantial myocardium at risk. A stress test with myocardial perfusion imaging performed to evaluate the functional significance of the bridge did not reveal any perfusion abnormalities in the myocardium at risk. Discussion In current practice, younger donors often do not undergo pre-transplantation CAG routinely performed in older donors given the lower prevalence of significant coronary disease. However, post-operatively this young donor was found to have passed on a potentially life-threatening MB to a denervated recipient, who cannot manifest typical anginal symptoms during ischaemia, thereby challenging providers to choose among strategies of watchful waiting, risk stratification, or pre-emptive intervention. In retrospect, the donor's mode of death may have signalled an underlying structural abnormality that warranted further pre-transplant characterization. In order to ensure optimal quality of transplanted hearts, young donors may warrant pre-transplant CAG despite their age, particularly those with a history of drug use or suspicious mode of death. [ABSTRACT FROM AUTHOR]

Aims Techniques for identifying specific microcirculatory structural changes are desirable. As such, capillary rarefaction constitutes one of the earliest changes of cardiac allograft vasculopathy (CAV) in cardiac allograft recipients, but its identification with coronary flow reserve (CFR) or intracoronary resistance measurements is hampered because of non-selective interrogation of the capillary bed. We therefore investigated the potential of wave intensity analysis (WIA) to assess capillary rarefaction and thereby predict CAV. Methods and results Fifty-two allograft patients with unobstructed coronary arteries and normal left ventricular (LV) function were assessed. Adequate aortic pressure and left anterior descending artery flow measurements at rest and with intracoronary adenosine were obtained in 46 of which 2 were lost to follow-up. In a subgroup of 15 patients, simultaneous RV biopsies were obtained and analysed for capillary density. Patients were followed up with 1-3 yearly screening angiography. A significant relationship with capillary density was noted with CFR (r =0.52, P =0.048) and the backward decompression wave (BDW) (r =-0.65, P <0.01). Over a mean follow-up of 9.3 ± 5.2 years patients with a smaller BDW had an increased risk of developing angiographic CAV (hazard ratio 2.89, 95% CI 1.12-7.39; P = 0.03). Additionally, the index BDW was lower in those who went on to have a clinical CAV-events (P =0.04) as well as more severe disease (P = 0.01). Conclusions Within cardiac transplant patients, W I A is able to quantify the earliest histological changes of CAV and can predict clinical and angiographic outcomes. This proof-of-concept for W I A also lends weight to its use in the assessment of other disease processes in which capillary rarefaction is involved. [ABSTRACT FROM AUTHOR]

Objectives: The role of routine C4d staining in endomyocardial biopsy specimens is uncertain. The implications of a diagnosis of acute cellular rejection (ACR) with a positive C4d with or without any evidence of antibody-mediated rejection (AMR) are unclear. This study sought to evaluate a distinct phenotype of ACR+/C4d+ in AMR- patients.Methods: Data on C4d, ACR, and AMR were collected. Donor-specific antibody (DSA), panel-reactive antibody (PRA), flow crossmatch, and data on ACR and AMR episodes were also reviewed.Results: Thirty-five patients were followed. Group I with C4d+ biopsy specimens was compared with group II with C4d- biopsy specimens. ACR greater than 1R was higher in group I compared with group II (50% vs 7.4%; P = .01). Clinical suspicion of AMR, positive retrospective crossmatches, and detection of de novo DSA were also higher in group I.Conclusions: Our result indicate that C4d and ACR positivity in posttransplant patients may be a harbinger of a subclinical form of asymptomatic AMR. [ABSTRACT FROM AUTHOR]

OBJECTIVE The aim of the study was to show the effect of heart transplant donor-recipient weight mismatch on mortality, right-ventricular (RV) failure, and medium-term control of systemic blood pressure. METHODS From 2000 to 2008 inclusive, 161 patients undergoing orthotopic heart transplantation at our unit were retrospectively analyzed. The cohort was divided into three groups of similar size depending on the tertile ranges of the donor-recipient weight ratio. Median follow-up was 4.81 years. Donor-recipient body weight ratio was analyzed with respect to intubation time, time in intensive care unit (ITU), development of RV failure, medium-term survival, and freedom from medium-term hypertension. RESULTS The median age was 115 months (23 days to 18 years), at a median weight of 26.9 kg (3-88 kg) at transplant. Median donor-recipient weight ratio was 1.61 (0.62-3.25). Mean intubation time was 448 h (SD 749.2), mean timein the ITU 302.7 h (SD 617.8). On linear regression, these were not related to donor-recipient weight ratio. A total of 38 patients (23.6%) developed postoperative RV failure. Nearly one-fifth (18.9) of patients in the lowest tertile group developed RV failure. In the middle tertile group, 24.5% developed RV failure and 28.8% in the upper tertile of weight mismatch, although this was not statistically significant (p = 0.48). On survival analysis, there was a higher mortality among those with the lowest tertile of mismatch (log-rank p = 0.04), but there was no difference in midterm survival on condition of survival to discharge (log-rank p = 0.14). There was also no association between weight ratio and freedom from medium-term hypertension as measured on serial 24-h ambulatory blood pressure monitoring (log-rank p = 0.39). There were nine patients in whom the weight mismatch was 3 or greater. There was no association between this ‘extreme’ mismatch group and either midterm mortality (p = 0.76) or freedom from hypertension (p = 0.62), but this was associated with the need for postoperative extracorporeal membrane oxygenator (ECMO) support (p < 0.01). CONCLUSIONS Our current policy involves accepting a maximum donor-recipient weight ratio of 3. These encouraging findings cautiously justify this policy, in an era when marginal donors are increasingly sought. [ABSTRACT FROM AUTHOR]

Aims: Hypertrophic cardiomyopathy (HCM) is an important cause of heart failure-related disability over a wide range of ages. Profiles of severe progressive heart failure symptoms and death, or heart transplantation deserve more complete definition within large patient cohorts. [ABSTRACT FROM PUBLISHER]

Abstract: Ischemic heart disease is the leading cause of morbidity and mortality in the western world. Ischemic damage can occur by acute myocardial infarction, stable angina, cardiac stunning, and myocardial hibernation. In addition, ‘scheduled’ ischemic events, occurring during cardiac surgery, heart transplantation, and elective angioplasty, can also result in cardiac damage. Ischemic or pharmacological preconditioning can decrease the extent of damage to the myocardium. Although the mechanism of preconditioning-mediated cardioprotection is not fully understood, εPKC has been implicated as a critical mediator of this process in animal studies. The use of isozyme-specific pharmacological tools has permitted a better elucidation of the upstream stimuli and the downstream transducers of εPKC in the pathways leading to cardioprotection. While little is known about the role of εPKC in these pathways in humans, animal studies suggest a potential therapeutic role of εPKC. This review will focus on the role of εPKC in cardiac protection and on the signal transduction cascades that have been implicated in this protection. [Copyright &y& Elsevier]

Primary cutaneous T-cell lymphoproliferative disorders (PCTCLDs) are uncommon in organ transplant recipients. CD30+ PCTCLDs are rare in children and have not previously been reported following organ transplantation. We report a 15-year-old boy with Netherton's syndrome who developed CD30+ PCTCLD 6 years following a cardiac transplantation. [ABSTRACT FROM AUTHOR]

We evaluated the role of percutaneous transluminal coronary angioplasty (PTCA) in a series of orthotopic cardiac transplant recipients with severe epicardial coronary occlusive disease. Ten ortho topic cardiac transplant patients treated by PTCA up to March 1990 were reviewed. All had significant epicardial coronary artery lesions (>70% stenosis compared with the adjacent healthy artery) and exercise electrocardiogram or isotope perfusion evidence of myocardial ischaemia in the relevant region. Primary angiographic PTCA success was achieved in 12 of the 16 lesions attempted (75%). Mean stenosis improvement was from 80% of adjacent healthy artery (range 70–90%) to 12% (range 0–20%). Median angiographic follow-up of 9 months (2–25 months) is available for all patients. The mean recurrence rate is 33% (4 of 12 successfully treated lesions) defined as >50% reduction in the original gain at the PTCA. We have shown that PTCA is technically possible in a series of cardiac transplant recipients. The primary success and recurrence rates are comparable to the use of PTCA in conventional atherosclerotic coronary disease. [ABSTRACT FROM PUBLISHER]