Evaluation of Liver Graft Recipient Workup in Predicting of Early Cardiovascular Events During Liver Transplantation: A Single-Center Experience.

BACKGROUND: Cardiovascular events (CVE) contribute to serious complications and death after liver transplantation (LT). Troponin I (TnI) level >0.07 mg/L and prior cardiac disease are known to be the independent predictors for posttransplant CVE. We evaluated single-center cardiac workup to predict early cardiovascular morbidity and mortality after LT. PATIENTS AND METHODS: We recruited 105 consecutive liver transplant recipients (male/female, 59/46; mean age, 51.66 ± 11.67 years). The cardiological assessment at evaluation for LT included medical history, electrocardiogram, echocardiography, Holter monitoring, and exercise test. We collected data regarding CVE including hypotonia with catecholamine usage, arrhythmia, sudden cardiac death, pulmonary edema, and myocardial infarction within 7 days after LT. RESULTS: CVE during LT occurred in 42 recipients (40%) and after LT in 9 patients (8.57%). Proposed cutoff level of TnI >0.07 mg/L did not correlate with CVE during operation (P = .73) or after LT (P = .47). CVE during LT was associated with arterial hypertension in medical history (P <.001), right ventricular systolic pressure (P< .05), and clinical scores: Child-Pugh (P = .04), Model for End-Stage Liver Disease (MELD) (P = .04), MELD incorporating serum sodium (P<.03), and integrated MELD score (P = .01). CVE after LT correlated only with arrhythmia (P<.001) and catecholamine usage (P < .05) perioperatively. Of interest, catecholamine usage during LT was associated with prolonged stay at the intensive care unit (P < .05). CONCLUSION: The single-center algorithm with noninvasive cardiac procedures without TnI assessment is optimal in evaluation before LT; however, medical history and severity of the liver disease are crucial for short-term cardiovascular morbidity after LT.

Risk Factors of Prolonged ICU Stay in Liver Transplant Recipients in a Single-Center Experience.

BACKGROUND: Prolonged initial intensive care unit (ICU) stay after liver transplantation (LT) is associated with prolonged total hospitalization, increased hospital mortality, and impaired patient and graft survival. Recent data suggested that model for end-stage liver disease (MELD) score at the time of LT and the length of surgery were the two independent risk factors for an ICU stay longer than 3 days after LT. We further identified factors influencing prolonged ICU stay in single-center liver graft recipients. PATIENTS AND METHODS: One hundred fifty consecutive LT recipients (M/F 94/56, median age 55 (range, 39-60), 36% with viral hepatitis, were prospectively enrolled into the study. Associations between clinical factors and prolonged ICU stay were evaluated using logistic regression models. Receiver operating characteristic curves were analyzed to determine the appropriate cutoffs for continuous variables. Threshold for significance was P ≤ .05. RESULTS: Highly prolonged (≥8 days) and moderately prolonged (≥6 days) postoperative ICU stay was noted in 19 (12.7%) and 59 (39.3%) patients, respectively. Serum bilirubin (P = .001) and creatinine concentrations (P = .011), international normalized ratio (P = .004), and sodium-MELD (P < .001) were all significantly associated with postoperative intensive care unit stay over or equal to 75th percentile (6 days). Sodium-MELD was significantly associated with postoperative care unit stay greater or equal to the 90th percentile (8 days; P = .018). CONCLUSIONS: Sodium-MELD might be a novel risk factor of prolonged ICU stay in this single-center experience.

Troponin I Is Not a Predictor of Early Cardiovascular Morbidity in Liver Transplant Recipients.

BACKGROUND: Cardiovascular events (CVE) might occur in 20% to 70% of liver transplant recipients, and major CVE are associated with poor long-term survival. Overall, the ability to identify patients at the highest risk of death after liver transplantation (LT) has been improved. Abnormal pretransplant troponin I (TnI) level is regarded as one of predictors of postoperative CVE. We evaluated the number of early CVE after LT and the impact of pretransplant TnI on cardiovascular morbidity. PATIENTS AND METHODS: We prospectively enrolled 110 consecutive liver transplant recipients (M/F 67/43, age 53.3 ± 10.4 years, 32.7% with hepatitis C virus). Seven of them (6.4%) were on urgent protocol and 3 patients (2.7%) had re-LT. TnI level was measured at listing for LT and directly after LT; clinical outcomes were observed within the first 7 days after LT. RESULTS: CVE during LT occurred in 51 recipients (46.4%). CVE after LT at the intensive care unit were noticed in 13 patients (11.8%). One patient (0.9%) died in the first 7 days after LT. The level of TnI >0.07 did not correlate with CVE during operation and 7 days after LT (P > .05), but the subgroup with TnI >0.07 before LT had a trend with higher TnI after LT (P = .065). Recipients with hepatitis C virus had a trend for higher TnI after LT (P = .061). CVE directly after LT correlated significantly with Child-Pugh (P = .01), Model for End-Stage Liver Disease (MELD), MELD incorporating serum sodium, and integrated MELD scales (P < .001). CONCLUSION: In our single-center algorithm, TnI with canonical cutoff value of 0.07 was not an effective predictor for cardiac outcomes shortly after LT in our population.

Gene expression profiling in peripheral blood nuclear cells in patients with refractory ischaemic end-stage heart failure.

Functional analysis of up- and down-regulated genes might reveal whether peripheral blood cells may be considered as a material of diagnostic or prognostic value in patients with end-stage heart failure (HF). The aim of the present study was to compare the transcriptomic profile of peripheral blood nuclear cells from 6 male patients with ischaemic end-stage HF with those of 6 male patients with asymptomatic cardiac dysfunction. The expression of genes in peripheral blood nuclear cells in both groups of patients was measured using whole-genome oligonucleotide microarrays utilizing 35 035 oligonucleotide probes. Microarray analyses revealed 130 down-regulated genes and 15 up-regulated genes in the patients with end-stage HF. Some of the down-regulated genes belonged to the pathways that other studies have shown to be down-regulated in cardiomyopathy. We also identified up-regulated genes that have been correlated with HF severity (CXCL16) and genes involved in the regulation of expression of platelet activation factor receptor (PTAFR, RBPSUH, MCC, and PSMA7). In conclusion, the identification of genes that are differentially expressed in peripheral blood nuclear cells of patients with HF supports the suggestion that this diagnostic approach may be useful in searching for the molecular predisposition for development of severe refractory HF in patients with post-infarction asymptomatic abnormalities and remodelling of the left ventricle. These results need further investigation and validation.