Perioperative Myocardial Injury after Adult Heart Transplant: Determinants and Prognostic Value

Abstract

Background and Aim of the StudyImplications of Cardiac troponin (cTnI) release after cardiac transplantation are still unclear. This study disclosed risk factors and prognostic implication of cTnI early levels in a single centre cohort operated on between January 1999 and December 2010.MethodsData on 362 consecutive recipients (mean age: 47.8±13.7, 20.2% female, 18.2% diabetics, 22.1% with previous cardiac operations, 27.6% hospitalized, 84.9±29.4 ml/min preoperative glomerular filtration rate) were analyzed using multivariable logistic regression modeling. Target outcomes were determinants of troponin release, early graft failure (EGF), acute kidney injury (AKI) and operative death.ResultsMean cTnI release measured 24 hours after transplant was 10.9±11.6 μg/L. Overall hospital mortality was 10.8%, EGF 10.5%, and AKI was 12.2%. cTnI release>10 μg/L proved an independent predictor of EGF (OR 2.2; 95% CI, 1.06–4.6) and AKI (OR 1.031; 95% CI, 1.001-1.064). EGF, in turn, proved a determinant of hospital mortality. Risk factors for cTnI>10 μg/L release were: status 2B (OR 0.35; 95% CI, 0.18-0.69, protective), duration of the ischemic period (OR 1.006; 95% CI, 1.001-1.011), previous cardiac operation (OR 2.9; 95% CI, 1.67-5.0), and left ventricular hypertrophy (OR 3.3; 95% CI, 1.9-5.6).ConclusionsMyocardial enzyme leakage clearly emerged as an epiphenomenon of more complicated clinical course. The complex interplay between surgical procedure features, graft characteristics and recipient end-organ function highlights cTnI release as a risk marker of graft failure and acute kidney injury. The search for optimal myocardial preservation is still an issue.

Treatment with 17β‐estradiol protects donor heart against brain death effects in female rat

“…Troponin‐I is a sensitive and specific marker of slight myocardial injury. Elevated troponin‐I serum levels is related to worse prognosis after heart transplantation [21]. In line with cell death data, the level of troponin‐I was significantly increased in BD female, suggesting cardiac tissue degradation.…”

Efferocytosis and Outside-In Signaling by Cardiac Phagocytes. Links to Repair, Cellular Programming, and Intercellular Crosstalk in Heart

“…Interestingly, acute phagocytosis and innate inflammation during allograft IRI has been linked to chronic pathophysiology. For example, perioperative and acute inflammation are prognostic for worse long-term transplant outcome ( 201 , 202 ). Graft reperfusion may trigger reperfusion-associated cell death ( 38 ) and cell necrosis occurs during allograft cold storage and continues in allograft reperfusion.…”

Troponin elevations in patients with chronic cardiovascular disease: An analysis of current evidence and significance

“…Similar to troponin elevations in heart failure exacerbations, troponin elevations in heart transplant patients rarely lead to a definitive diagnosis and a successful intervention. [ 45 ] Regardless, detecting troponin elevations in the early perioperative period is distinctly different from troponin elevations in the chronic outpatient setting. Heart transplantation troponin release can be divided up into three distinct time intervals: The initial organ evaluation process, the early postoperative period, and the chronic posttransplant period.…”

“…The mechanism of troponin release is difficult to determine and is a topic of controversy. [ 45 ] Troponin elevation in the donor heart could represent thoracic trauma, intracranial pathology, or result from cardiopulmonary resuscitation. [ 46 ] A troponin elevation could delay organ selection and can lead to further invasive testing.…”

“…[ 50 ] In addition to total ischemic time, postoperative troponin elevation >10 μg/L is a marker for increased perioperative morbidity and mortality. [ 45 ]…”