Authors

• Jana Ljubas Maček — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0001-7171-2206
• Boško Skorić — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0001-5979-2346
• Marijan Pašalić — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0002-3197-2190
• Hrvoje Gašparović — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0002-2492-3702
• Jure Samardžić — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0002-9346-6402
• Ivo Planinc — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0003-0561-6704
• Maja Čikeš — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0002-4772-5549
• Daniel Lovrić — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0002-5052-6559
• Hrvoje Jurin — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0002-2599-553X
• Nina Jakuš — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0001-7304-1127
• Dora Fabijanović — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0003-2633-3439
• Davor Miličić — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0001-9101-1570

Abstract

**Introduction**: Cardiac allograft vasculopathy (CAV) is a chronic heart transplant complication (HTx) that presents a treatment challenge owing to the diffuse pattern of coronary artery involvement. Severe forms of the disease are not suitable for revascularization, which is why retransplantation often remains the only treatment option. (1-3) **Patients and Methods**: Out of a total of 176 patients following HTx, between 2001 and 2015, 129 patients were subjected to at least one coronary artery angiography by which 45 patients were CAV positive (and additionally in two patients based on clinical and autopsy findings). The mean age was 51.6±12.6 years, 78% of patients were male and the average follow-up was 3 years (IQR 2-6 years). The presence of CAV was evaluated by coronary artery angiography and analyzed with respect to the duration of ischemic time (IT), the early concentration of high-sensitive troponin T (hsTnT) and the degree of cellular graft rejection (CR). **Results:** Early hsTnT values (within 3 months after HTx) are significantly higher with prolonged IT (p=0.040) but have no predictive significance for CAV (p=0.529) or more frequent CR. IT does not correlate with the frequency of significant CR. Patients with severe CAV had significantly shorter survival than those without CAV or with mild/moderate forms of disease (p=0.016) (**Figure 1**). CR, expressed as an average patient rejection index, significantly increases the risk of CAV (p<0.001, OR 16.0), including episodes of mild CR during the first year after HTx. CAV was proven in 36% of CAV patients (N=47/131) and was the cause of direct later mortality in 10.2% of patients. Freedom from CAV at the end of the 1st year was 86%, 2nd 75%, 5th 57% and 10th 25%. FIGURE 1. Patient survival curves depending on the degree of vasculopathy: CAV-free patients or those with mild-to-moderate CAV (CAV1/CAV2) had significantly longer survival in comparison to patients with severe CAV (CAV3). **Conclusion**: More pronounced reperfusion-ischemic injury, determined by longer IT, correlated with higher concentrations of hsTnT early after HTx. The prolonged IT does not present predisposition for a stronger CR, later development of CAV or shorter survival. CAV patients have significantly shorter survival only in more severe forms of the disease, while milder and moderate forms are more effectively treated and therefore do not affect survival. Cellular rejection is associated with higher risk of CAV development, which may have important implications in clinical monitoring and treatment.

Keywords

cardiac allograft vasculopathy, heart transplantation, high-sensitive troponine, cellular rejection

DOI

Literature

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