Impact of donor smoking history on post heart transplant outcomes: A propensity-matched analysis of ISHLT registry.

PURPOSE: Smoking is a major public health issue, and its effect on cardiovascular outcomes is well established. This study evaluates the impact of donor smoking on heart transplant (HT) outcomes. METHODS: HT recipients between January 1, 2005, and December 31, 2016, with known donor smoking status were queried from the International Society of Heart and Lung Transplantation (ISHLT) registry. The primary outcome was all-cause mortality, and secondary endpoints were graft failure, acute rejection, and cardiac allograft vasculopathy. We utilized propensity-score matching to identify cohorts of recipients with and without a history of donor smoking. Hazard ratios for post-transplant outcomes for the matched sample were estimated from separate Cox proportional hazard models. RESULTS: Of 26 390 patients in the cohort, 18.9% had history of donor smoking. Donors with history of smoking were older, predominantly male and had higher incidence of diabetes, hypertension, cocaine use, and "high-risk" status. In propensity-matched analysis, recipients with a history of donor smoking had increased risk of death (HR 1.11, 95% CI 1.03-1.20) and higher risk of graft failure (HR 1.11, 95% CI 1.03-1.20). CONCLUSION: Donor smoking was associated with increased mortality and higher incidence of graft failure following HT. Consideration of donor smoking history is warranted while evaluating donor hearts.

Early immune biomarkers and intermediate-term outcomes after heart transplantation: Results of Clinical Trials in Organ Transplantation-18.

Clinical Trials in Organ Transplantation-18 (CTOT-18) is a follow-up analysis of the 200-subject multicenter heart transplant CTOT-05 cohort. CTOT-18 aimed to identify clinical, epidemiologic, and biologic markers associated with adverse clinical events past 1 year posttransplantation. We examined various candidate biomarkers including serum antibodies, angiogenic proteins, blood gene expression profiles, and T cell alloreactivity. The composite endpoint (CE) included death, retransplantation, coronary stent, myocardial infarction, and cardiac allograft vasculopathy. The mean follow-up was 4.5 ± SD 1.1 years. Subjects with serum anti-cardiac myosin (CM) antibody detected at transplantation and at 12 months had a higher risk of meeting the CE compared to those without anti-CM antibody (hazard ratio [HR] = 2.9, P = .046). Plasma VEGF-A and VEGF-C levels pretransplant were associated with CE (odds ratio [OR] = 13.24, P = .029; and OR = 0.13, P = .037, respectively). Early intravascular ultrasound findings or other candidate biomarkers were not associated with the study outcomes. In conclusion, anti-CM antibody and plasma levels of VEGF-A and VEGF-C were associated with an increased risk of adverse events. Although this multicenter report supports further evaluation of the mechanisms through which anti-CM antibody and plasma angiogenesis proteins lead to allograft injury, we could not identify additional markers of adverse events or potential novel therapeutic targets.

Elevated Heart Rate Following Heart Transplantation Is Associated With Increased Graft Vasculopathy and Mortality.

BACKGROUND: The effect of elevated heart rate (HR) on outcomes after heart transplantation (HT) has not been well established. The aim of this study was to assess predictors of elevated HR following HT and its impact on outcomes. METHODS AND RESULTS: We retrospectively evaluated 394 patients who underwent HT at 2 academic medical centers from 2005 to 2016. Patients were divided into 2 groups based on HR 1 year after HT: HR ≥95 beats/min (n = 162; 41%) and HR <95 beats/min (n = 232; 59%). Median follow-up time was 6.6 (interquartile range [IQR] 2.2-7.5) years. HR ≥95 beats/min 1 year after HT was associated with younger donor age, whereas HR <95 beats/min was associated with heavy donor alcohol use and African-American recipient race. Left ventricular (LV) end-diastolic dimension, mass, and ejection fraction were lower and E/E' higher in the HR ≥95 group at the time of the last follow up. HR ≥95 beats/min at 1 year after HT was independently associated with the development of cardiac allograft vasculopathy and increased mortality. CONCLUSIONS: HR ≥95 beats/min 1 year after HT is associated with a reduction in LV size and function, increased incidence of cardiac allograft vasculopathy, and reduced survival. Studies investigating the effect of medical HR reduction on post-HT outcomes are warranted.

The effect of donor alcohol abuse on outcomes following heart transplantation.

BACKGROUND: Current guidelines recommend against the use of hearts from donors that abuse alcohol. We explored the effect of donor alcohol abuse (AA) on cardiac allograft function and outcomes in heart transplant (HTx) recipients. METHODS: Overall, 370 HTx recipients were divided into two groups: (a) the alcoholic donor group (AD, n = 58) and (b) the non-alcoholic donor group (NAD, n = 312). RESULTS: Recipients in the AD group had a slower heart rate (86 ± 13 vs 93 ± 13, P = 0.004) and an increased incidence of early atrial fibrillation (AF) (30% vs 11%, P = 0.003). Echocardiographic left ventricular mass was higher among alcoholic donors (171.7 ± 66.7 vs 151.6 ± 54.7, P = 0.02). This difference remained present 1 year following HTx (185 ± 43 vs 166 ± 42, P = 0.007). E/E' was higher in the AD group (9.5 ± 3.9 vs 8.4 ± 2.9, P = 0.04) and a larger number of AD recipients had a ventilatory equivalent for VCO2  > 34 (50% vs 31%, P = 0.04) on cardiopulmonary exercise test. There was no significant difference in rejection, cardiac allograft vasculopathy (CAV), or survival between the groups. CONCLUSIONS: Our data suggest that donor AA does not impact rejection, CAV, or intermediate-term survival, but may cause increased incidence of post-HTx AF and impaired cardiac allograft diastolic function.

The value of psychosocial factors in patient selection and outcomes after heart transplantation.

Heart transplantation remains the gold standard treatment for advanced heart failure, although its use is limited by donor organ availability. To ensure that the rare resource of a donor heart is allocated appropriately, the evaluation of the heart transplant candidates includes extensive medical and psychosocial assessments. These psychosocial factors are critically important to understand pre-heart transplant because it is known that psychosocial evaluation and psychosocial comorbidities have a strong association with post-heart transplant outcomes. The critical factors to assess are psychological functioning, adherence to medical recommendations, and social support. These factors are likely inter-related and have been shown to have an effect on the health-related quality of life and overall survival. Recently, new tools have been developed to standardize the evaluation process. In this review, we will discuss the tools available to assess psychosocial factors in the transplant candidate and discuss the role these factors have on post-heart transplant outcomes.

Regulation of connective tissue growth factor gene expression and fibrosis in human heart failure.

BACKGROUND: Heart failure (HF) is associated with excessive extracellular matrix (ECM) deposition and abnormal ECM degradation leading to cardiac fibrosis. Connective tissue growth factor (CTGF) modulates ECM production during inflammatory tissue injury, but available data on CTGF gene expression in failing human heart and its response to mechanical unloading are limited. METHODS AND RESULTS: Left ventricle (LV) tissue from patients undergoing cardiac transplantation for ischemic (ICM; n = 20) and dilated (DCM; n = 20) cardiomyopathies and from nonfailing (NF; n = 20) donor hearts were examined. Paired samples (n = 15) from patients undergoing LV assist device (LVAD) implantation as "bridge to transplant" (34-1,145 days) also were analyzed. There was more interstitial fibrosis in both ICM and DCM compared with NF hearts. Hydroxyproline concentration was also significantly increased in DCM compared with NF samples. The expression of CTGF, transforming growth factor (TGF) ß1, collagen (COL) 1-α1, COL3-α1, matrix metalloproteinase (MMP) 2, and MMP9 mRNA in ICM and DCM were also significantly elevated compared with NF samples. Although TGF-ß1, CTGF, COL1-α1, and COL3-α1 mRNA levels were reduced by unloading, there was only a modest reduction in tissue fibrosis and no difference in protein-bound hydroxyproline concentration between pre- and post-LVAD tissue samples. The persistent fibrosis may be related to a concomitant reduction in MMP9 mRNA and protein levels following unloading. CONCLUSIONS: CTGF may be a key regulator of fibrosis during maladaptive remodeling and progression to HF. Although mechanical unloading normalizes most genotypic and functional abnormalities, its effect on ECM remodeling during HF is incomplete.

Clinical characteristics and outcomes of patients with severe left ventricular dysfunction undergoing cardiac MRI viability assessment prior to revascularization.

Coronary artery bypass grafting improves survival in patients with ischemic cardiomyopathy, however, these patients are at high risk for morbidity and mortality. The role of viability testing to guide revascularization in these patients is unclear. Cardiac magnetic resonance imaging (CMR) has not been studied adequately in this population despite being considered a reference standard for infarct imaging. We performed a multicenter retrospective analysis of patients (n = 154) with severe left ventricular systolic dysfunction [ejection fraction (EF) < 35%] on CMR who underwent CMR viability assessment prior to consideration for revascularization. Using the AHA16-segment model, percent total myocardial viability was determined depending on the degree of transmural scar thickness. Patients with or without revascularization had similar clinical characteristics and were prescribed similar medical therapy. Overall, 43% of patients (n = 66) experienced an adverse event during the median 3 years follow up. For the composite outcome (death, myocardial infarction, heart failure hospitalization, stroke, ventricular tachycardia) patients receiving revascularization were less likely to experience an adverse event compared to those without revascularization (HR 0.53, 95% CI 0.33-0.86, p = 0.01). Patients with > 50% viability on CMR had a 47% reduction in composite events when undergoing revascularization opposed to medical therapy alone (HR 0.53, p = 0.02) whereas patients with a viability < 50% were 2.7 times more likely to experience an adverse event (p = 0.01). CMR viability assessment may be an important tool in the shared decision-making process when considering revascularization options in patients with severe ischemic cardiomyopathy.

Preoperative Right Heart Dysfunction and Gastrointestinal Bleeding in Patients with Left Ventricular Assist Devices.

Gastrointestinal bleeding (GIB) is a common cause of morbidity among patients supported by left ventricular assist devices (LVADs). The aim of this study was to identify if pre-LVAD right ventricular (RV) dysfunction is associated with risk of GIB after LVAD implantation. Of 398 patients implanted with LVADs between July 2008 and July 2016, 130 (33%) developed GIB at a median of 2.6 months following LVAD implantation. Arteriovenous malformations (AVMs) were found in 42 (34%) GIB patients. Patients with GIB were older and more likely to have hypertension, diabetes, and ischemic cardiomyopathy. On pre-LVAD echocardiography, GIB patients had increased RV diastolic dimension (4.7 ± 0.8 vs. 4.4 ± 0.9 cm, p = 0.02), a higher rate of greater than mild tricuspid valve (TV) regurgitation (73 [60%] vs. 120 [47%], p = 0.006), and underwent TV repair more often (38 [30%] vs. 43 [16%], p = 0.0006) during LVAD implantation. After multivariable adjustment, preoperative greater than mild RV enlargement (hazard ratio [HR] 2.32, 95% CI 1.12-5.03; p = 0.03), TV regurgitation (HR 1.83, CI 1.02-3.44; p = 0.01), and TV repair (HR 3.76, confidence interval [CI] 1.02-4.44; p = 0.01) remained associated with risk of GIB. This finding was driven by the AVM-GIB subgroup. Preoperative RV enlargement and TV regurgitation are associated with post-LVAD AVM-related GIB.

Factors associated with non-adherence to therapy with warfarin in a population of chronic heart failure patients.

BACKGROUND: Adherence to heart failure therapy is important in reducing morbidity and mortality over the course of the disease process. The aim of this study was to examine factors associated with non-adherence to warfarin in chronic heart failure patients. METHODS: Eighty patients receiving warfarin therapy in 2002 were included. Adherence was defined as maintenance of international normalized ratio (INR) between 2 and 3.5 and keeping scheduled appointments for INR checks at least 75% of the time. Clinical variables examined included age, gender, race, insurance, left ventricular ejection fraction (LVEF), etiology, New York heart association (NYHA) class, comorbidities, smoking, and alcohol use. RESULTS: Of 80 patients studied, 59 were male with mean age ( +/- standard deviation) 52 +/- 13 years, 24 had ischemic etiology with mean LVEF of 24% +/- 9%. Non-adherence was associated with tobacco use, odds ratio of 6.5 (p <0.01). Ischemic etiology was associated with adherence, odds ratio of 4.5 (p <0.01). Non-adherent patients were more likely to be insured with Medicare/Medicaid (p = 0.04) and have better NYHA class (p = 0.04). Adherence positively correlated with older age and lower LVEF, and negatively correlated with number of hospitalizations (p<0.01 for all). In a multiple regression model, patients with improvement in LVEF had decreased adherence over the year (p<0.01). CONCLUSIONS: The profile of heart failure patients who demonstrated non-adherence to warfarin therapy included younger age, nonischemic etiology, better NYHA class, smoking, insurance with Medicare/Medicaid and improved LVEF over the study. Measures targeting these patients may result in improved adherence to other pharmacologic treatments of heart failure.

Left ventricular assist device-related infection: treatment and outcome.

BACKGROUND: Left ventricular assist device (LVAD) implantation has become an effective treatment option for patients with severe heart failure awaiting transplantation. Significant infection rates have been reported among LVAD recipients. However, few reports have focused specifically on device infection, its treatment, and the impact of LVAD-related infection on clinical outcome. METHODS: Forty-six LVAD-related infections were diagnosed in 38 (50%) of 76 patients who underwent LVAD implantation as a bridge to transplantation. Twenty-nine episodes of LVAD-related bloodstream infection (BSI) (including 5 that were cases of LVAD endocarditis) and 17 episodes of local LVAD infection were identified. RESULTS: Diabetes mellitus appeared to increase the risk of BSI among patients with LVAD infection. LVAD-related infection delayed transplantation, as reflected by longer device-support times (a mean duration +/- SEM of 182.8+/-31.1 days, compared with 66.3+/-8.8 days; P

The presence of HLA-directed antibodies after heart transplantation is associated with poor allograft outcome.

BACKGROUND: The clinical significance of HLA-directed antibodies newly detected after transplantation (HT) is controversial. METHODS: Seventy-one HT recipients consented to enroll. Mean follow-up time was 28 months (range 6-48). Panel reactive antibody (PRA) analysis was performed on posttransplant sera (2 weeks, 1, 2, 3, 6, and 12 months and annually thereafter) using Flow-PRA. A mean of 6.9+/-1.2 serum samples per patient were obtained. Severity of cellular rejection was measured using the ISHLT grading system. Coronary angiography and intravascular ultrasound (IVUS) studies were performed annually to evaluate severity of allograft vasculopathy. RESULTS: Twenty-five recipients had newly detected HLA-directed antibodies during the first year postHT. HLA class I antibodies were detected in 18 patients (25.4%), and class II in 11 patients (15.5%). The majority of donor recipient pairs were HLA mismatched (4.6+/-1.2 of the six major HLA antigens). Only mismatches at HLA-A locus had significant association with de novo posttransplant antibody formation. Length of ischemia time was correlated with early and sustained presence of de novo HLA-directed antibodies postheart transplant. Importantly, an association between de novo HLA-directed antibodies and cellular rejection was notes (P=0.0002). De novo HLA class II directed antibodies are also associated with IVUS documented vasculopathy (P<0.002). Finally, death due to allograft failure is associated with the presence of de novo formed HLA class II directed antibodies (P=0.008). CONCLUSIONS: Identifying the formation of de novo HLA-directed antibodies following heart transplantation may predict allograft outcome. This, in turn, may serve as a tool for individualization of immunosuppression protocols in heart transplant recipients.

Relationship between bridging with ventricular assist device on rejection after heart transplantation.

BACKGROUND: Ventricular assist devices (VADs) are commonly used to bridge patients to heart transplantation. Recipients of VADs may develop anti-human histocompatibility leukocyte antigen antibodies, as reflected by elevated panel-reactive antibodies (PRA). The purpose of this study was to evaluate the relationship between bridging with VAD before heart transplantation and development of cellular rejection, humoral rejection, and allograft vasculopathy after transplantation. METHODS: Data on all patients who underwent cardiac transplantation between July 1994 and February 2001 at Rush Presbyterian St Luke's Medical Center were retrospectively reviewed. Data collected included sex, age, etiology of cardiomyopathy, percentage panel reactive antibodies (by cytotoxic method), type and duration of mechanical circulatory support, transfusion history, rejection history (both cellular and humoral) after cardiac transplantation, and development of allograft vasculopathy. Cellular rejection was treated when International Society of Heart and Lung and Transplantation Grade 2 or greater in the first 12 months after transplant and Grade 3 or greater after 12 months and treated with intensification of immunosuppression. Humoral rejection was defined clinically as allograft dysfunction by echocardiography without evidence of cellular rejection on endomyocardial biopsy or allograft vasculopathy. Allograft vasculopathy was defined by presence of any degree of luminal narrowing or pruning of distal vessels by coronary arteriography. Statistical analyses were performed by chi-square test, Fisher's exact test, and Wilcoxon rank sum test, as appropriate. RESULTS: Ninety-eight patients underwent cardiac transplantation during the study period (87 men, mean age 49 years, 46 ischemic etiology). Of these, 48 were bridged with HeartMate VAD (20 patients received vented electric device, 28 received pneumatic device). Nineteen percent of VAD patients had a peak pretransplant PRA > or =10% vs 2% of patients without VAD (p = 0.014). PRA > or =10%, use of VAD, or duration of VAD support did not predict development of humoral rejection. Use of VAD did not predict development of cellular rejection or allograft vasculopathy. VAD use was not associated with sudden death after heart transplantation. In the entire group of 98 patients, neither humoral nor cellular rejection predicted development of allograft vasculopathy. Longer ischemic time correlated with increased cellular rejection and humoral rejection after transplantation (p = 0.01). CONCLUSIONS: Some patients bridged to cardiac transplantation with VADs have increased PRA before heart transplantation, but this does not appear to translate into increased risk of either humoral or cellular rejection after transplantation or development of allograft vasculopathy as detected by coronary angiography.

Sideroblastic anemia due to linezolid in a patient with a left ventricular assist device.

An acquired form of sideroblastic anemia has been described in association with several drugs, especially anti-microbial agents. A case of sideroblastic anemia is presented in a patient with a left ventricular assist device drive-line infection who was receiving linezolid, an antibiotic used for serious infections with gram-positive organisms. This patient's anemia resolved after discontinuation of the drug; he subsequently underwent an uncomplicated orthotopic heart transplant with no recurrence of anemia. As linezolid has been shown to have hematologic side effects, blood count monitoring is recommended in patients receiving this drug for long-term therapy.

Neurologic aspects of heart transplantation.

Cardiac transplantation remains the best treatment option for patients with end-stage, NYHA class IV heart failure who have failed conventional therapy. However, transplant rates have remained static largely due to limited organ donor supplies. Therefore, appropriate allocation of this precious resource is critical to maximize benefit, both at a patient level and at a societal level. Neurologic diseases, such as cerebrovascular disease and peripheral neuropathy, are prevalent in this patient population, as the major risk factors for heart disease place patients at risk for neurologic disease as well. Examples include hypertension, smoking, hypercholesterolemia, obesity, and diabetes. Pretransplant neurologic evaluation is very important to identify conditions that may limit survival after cardiac transplantation. In general, systemic diseases exacerbated by immunosuppression, conditions limiting ability to rehabilitate, and dementias are considered contraindications. Post-transplant neurologic complications are divided into central versus peripheral, and early versus late. The most common early complication is ischemic stroke. Other serious complications include hemorrhagic stroke, encephalopathy, and critical illness neuropathy. Over the long term, post-transplant immunosuppressive regimens are considered "a double edged sword." Although immunosuppressive medications are critical to preventing rejection and allograft dysfunction, they do have significant risk of morbidity and mortality associated with them, including neurologic side-effects. These include: (1) drug toxicities, such as lowering of seizure thresholds; (2) encephalopathy, such as posterior reversible encephalopathy syndrome (PRES); (3) infections; (4) malignancies, such as post-transplant lymphoproliferative disorder (PTLD). Many of the same considerations discussed in adult heart transplant recipients apply to pediatric heart transplant recipients as well. In children, seizures are the most common neurologic complication, although other neurologic complication rates are comparable.

Incidence of fractures after cardiac and lung transplantation: a single center experience.

Osteoporotic fractures are well-known complications of organ transplantation. Fracture rates up to 35% have been previously reported following heart and lung transplantations. Our institutional pretransplant protocols include DXA scans, vitamin D screening, and appropriate antiresorptive therapy. We aimed to assess the incidence of fragility fractures following cardiac or lung transplantation. In a retrospective study 210 electronic medical records of patients who underwent LT (110 men, 100 women) and 105 HT (88 men, 17 women) between 2005 and 2010 were analyzed. Both clinical and radiographic fractures were recorded. DXA scans were obtained immediately after transplant. 17 out of 210 LT patients (8.0%) had fractures after transplantation and 9 out of 105 HT patients (8.6%) had fractures. The median time to the first fracture was 12 months and the mean time was 18 months for both LT and HT. In the HT recipients, the median femoral neck T score was statistically lower in the fracture group versus the nonfracture group. Similar results were seen in the LT patients. Conclusion. Our findings demonstrate a much lower incidence of fractures in heart and lung transplant recipients in comparison with earlier reports. Comprehensive bone care and early initiation of antiresorptive therapy are possible contributors to these improved outcomes.

Left ventricular assist device-induced coagulation and platelet activation and effect of the current anticoagulant therapy regimen.

Left ventricular assist devices (LVADs) are mechanical pumps that enhance cardiac function in patients with heart failure. In all, 7 patients with an LVADs (1.8 international normalized ratio warfarin, 81 mg aspirin) were evaluated monthly for 3 months for platelet and coagulation activation (controls: 5 healthy adults and 5 patients having warfarin). Platelet works revealed greater inhibition of collagen (31.8% vs 7.9%; P = .004), arachidonate- (30.9% vs 8.2%; P = .001), and adenosine diphosphate- (10.9% vs 6.1%; P = .004)-induced platelet aggregation for LVADs. Thrombelastography (recalcified whole blood) showed inhibition of clot initiation time (R; 8.81 vs 6.02 min; P = .001) and stronger clot formation (maximum amplitude; 69.1 vs 64.9 mm; P = .016). Platelet function determined by plateletMapping and flow cytometry was within the normal range. The LVADs had increased ratio of von Willebrand Factor (vWF) antigen and vWF propeptide, indicating increased degradation of vWF (2.04 vs 1.44; P = .144). Coagulation and platelet activation caused by LVAD is suppressed by pharmacotherapy, yielding a profile similar to that of patients on warfarin alone.

Variations in institutional staffing and clinical practice are predictive of center-specific 1-year survival post-transplant.

BACKGROUND: The accuracy of various risk models to predict early post-transplant mortality is limited by the type, quality, and era of the data collected. Most models incorporate a large number of recipient-derived and donor-derived variables; however, other factors related to specific institutional practices likely influence early mortality. The goal of this study was to determine if the addition of institutional practice variables would improve the predictive accuracy of a recipient/donor risk model in a modern cohort of heart transplant recipients. METHODS: Between 1999 and 2007, 3,591 primary heart transplants were performed at the 26 institutions participating in the Cardiac Transplant Research Database. Multivariable regression analysis in the hazard domain was used to identify recipient, donor, and institutional practice variables that were predictive of 1-year mortality. The derived model was used to predict institutional outcomes and compare them with observed outcomes first without and then with the inclusion of the institutional practice variables. RESULTS: Eleven individual plus 2 interaction recipient variables and 2 individual plus 2 interaction donor variables were predictive of increased mortality. The addition of institutional practice variables to the model identified 4 variables associated with decreased mortality: greater number of transplant cardiologists, a thoracic surgery fellowship, a surgery or cardiology attending taking donor call, and routine surveillance for antibody-mediated rejection. By using a p-value > 0.10 as a robust measure of similarity, the addition of institutional practice variables increased the number of institutions with similar predicted vs. observed mortality from 18 of 26 institutions (69%) to 26 of 26 (100%), demonstrating improved predictive accuracy of the model. CONCLUSIONS: Multiple recipient and donor variables influence early survival but do not fully explain the difference in predicted and observed outcomes at the institutional level. Variations in staffing and clinical practice contribute to risk, and the addition of these variables to our risk model improved predictive accuracy.

Factors associated with stress and coping at 5 and 10 years after heart transplantation.

BACKGROUND: Heart transplant-related stressors and coping are related to poor outcomes early after transplant. The purposes of our study were to (1) identify the most frequent and bothersome stressors and most used and effective coping strategies and (2) compare the most frequent and bothersome stresses and most used and effective coping styles between patients at 5 and 10 years after heart transplantation. We also examined differences in coping styles by patient characteristics and factors associated with frequency and intensity of stress at 5 and 10 years after heart transplantation. METHODS: This report is a secondary analysis of data from a prospective, multisite study of quality of life outcomes. Data are from separate cohorts of 199 patients at 5 years after transplant and 98 patients at 10 years. Patients completed the Heart Transplant Stressor Scale and Jalowiec Coping Scale. Statistical analyses included frequencies, measures of central tendency, t-tests, chi-square, and generalized linear models. RESULTS: At 5 and 10 years after heart transplantation, the most bothersome stressors were regarding work, school, and financial issues. Patients who were 10 years after transplant reported less stress, similar stress intensity, and less use and perceived effectiveness of negative coping than patients who were 5 years after transplant. Long-term after transplant, demographic characteristics, psychologic problems, negative coping, and clinical factors were related to stress frequency and/or intensity. CONCLUSIONS: Heart transplant-related stress occurs long-term after surgery. Types of transplant-related stress and factors related to stress confirm the importance of ongoing psychologic and clinical support after heart transplantation.

Single photon emission computed tomography myocardial perfusion imaging to detect cardiac allograft vasculopathy.

AIMS: Cardiac allograft vasculopathy (CAV) is a major cause of morbidity and mortality in cardiac transplant recipients. This study evaluates the usefulness of single photon emission computed tomography (SPECT) and various SPECT-derived diastolic variables to detect CAV in heart transplant patients. METHODS AND RESULTS: A retrospective review of 141 SPECT studies with corresponding coronary angiograms within 12 months was performed on 99 transplant recipients. Diastolic function was assessed using computer-derived measures of peak filling rate (PFR), time to peak filling rate (TPFR), and mean first one-third filling rate (MFR/3). Angiography identified CAV in 53 of the 141 studies (38%). Of the 53, SPECT identified 7 with reversible myocardial defects (sensitivity 13%) and stress-induced electrocardiographic evidence of ischaemia was seen in one patient (sensitivity 2%). SPECT imaging was negative in 86 of the 88 negative coronary angiograms (specificity 98%). The positive predictive value and negative predictive value were 78 and 65%, respectively. If a more stringent definition of CAV was used (≥70% stenosis), the sensitivity and specificity were unchanged (14 and 98%, respectively). There was no statistical difference in diastolic variables between patients with or without angiographic evidence of CAV in regard to PFR (3.57 ± 1.14 vs. 3.18 ± 1.21 EDV/s, P = 0.90), TPFR (149 ± 32 vs. 153 ± 43 ms, P = 0.33), or MFR/3 (1.37 ± 0.43 vs. 1.27 ± 0.42 EDV/s, P = 0.94). CONCLUSION: Adenosine stress/rest technetium-99m tetrofosmin-gated SPECT is not a sensitive test for detection of CAV in heart transplant recipients. Diastolic dysfunction, as assessed by SPECT, was not shown to be associated with development of CAV.

Abdominal aortic aneurysms (AAA) post heart transplantation: a systematic review of literature.

Peripheral vascular disease is highly prevalent post heart transplantation (HTx). The prevalence of abdominal aortic aneurysms (AAA) post HTx ranges from 1.1-10%. We performed a Pub Med, EMBASE and Cochrane review search to identify articles on AAA post HTx. Data gathered from published data included: risk factors, progression of the aneurysm and clinical outcomes. Five studies were included in the systematic review. Baseline demographic data, clinical characteristics, data on AAA prevalence and characteristics, the treatment strategies and follow up were extracted from each of these studies. Our systematic review showed that the prevalence of AAA post HTx ranged from 2-10% in the retrospective studies and 6.5% in a single prospective study. Rupture rates during a follow up period ranged from 11-38% and during that time period the mean aneurysmal expansion rate ranged from 0.78±0.41 cm/yr to 1.2±0.4 cm/yr. Male gender, ischemic heart disease, corticosteroid use, smoking and improved hemodynamics and ejection fraction post HTx were reported as possible associated risk factors in the development of AAA. Open surgical management was the treatment of choice although endovascular treatment was used in a minority of patients. AAA is increasingly prevalent post HTx and may be associated with greater rupture and expansion rates. Meticulous follow up and further prospective clinical studies are warranted to determine risk factors, expansion rates and clinical outcomes.