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What Is the Effect of Pre-Transplant Malignancy on the Outcome After Heart Transplantation? A Systematic Review

Submitted:

04 August 2026

Posted:

06 August 2026

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Abstract
Introduction: The number of cancer survivors increases steadily over time because of improved cancer treatment. The number of survivors needing heart transplantation is also rising. This review addresses the post-transplant survival and cancer incidence of patients with a pretransplant malignancy. Methods: A literature search was performed for the last 10 years using the search terms: (heart OR cardiac) AND pretransplant* AND malignancy. Only full articles were included and assessed by the Newcastle-Ottawa Scale of their quality. Results: Nine manuscripts were identified, of which seven were of good quality. Only in four series, patients undergoing heart transplantation were analyzed separately from other solid organ transplants. The outcomes were survival, cancer specific survival, cancer recurrence and skin cancer specifically. Four series were single center based, the other five were region or nationwide surveys. Also, four series included only heart transplant patients. The outcome varied, but most series showed a significant increase in decreased survival and incidence of post-transplant malignancy if a pretransplant malignancy was present. Age, male gender and a fair skin were other risk factors, especially for post-transplant skin cancer. However, for patients with pretransplant malignancy, survival was acceptable. Conclusion: Pretransplant malignancy does not preclude heart transplantation. However, the time interval between pretransplant malignancy and heart transplantation, as well as the nature of malignancy should be considered. The research for the outcome after heart transplantation in these patients has serious limitations.
Keywords: 
pretransplant malignancy
;  
heart transplant
;  
survival
;  
post-transplant malignancy
Subject: 
Medicine and Pharmacology  -   Cardiac and Cardiovascular Systems

INTRODUCTION

Heart transplantation (HTX) remains the definitive therapy for patients with end stage heart failure. This procedure increases survival and quality-of-life. One-year survival exceeds ninety percent because of improvement of surgical techniques, perioperative care and organ donor management. However, long-term survival did not improve over time because of coronary allograft vasculopathy, malignancy, renal failure, infection, diabetes, hypertension and the effects of chronic immunosuppression [1]. Heart transplantation is also an option for cancer survivors suffering from end-stage heart failure, because of chemotherapy. Anthracyclines have high activity against hematologic malignancies and solid tumors, but these agents are known to cause myocardial damage. The cumulative dose is considered as the most important risk factor for left ventricular (LV) dysfunction [2,3], but histopathologic changes have been documented after administration of 240 mg/m2 of doxorubicin [4]. Mechanisms of cardiac dysfunction include damage to DNA and to mitochondria, which are abundantly present in cardiac myocytes. Risk factors for cardiac damage include age above 65 years, female gender, prior radiotherapy of the chest, hypertension, use of other chemotherapeutic agents such as trastuzumab and pre-existing heart disease [2]. The risk caused by tyrosine kinase inhibitors seems to be lower [5,6,7,8]. Immune checkpoint inhibitors enhance immune responses against tumor cells but can also trigger immune-related myocarditis, which can sometimes be fatal [9,10]. The cardiac side effects of chemotherapy are an important issue, since cardiovascular disease is the leading cause of noncancer mortality in long-term cancer survivors. Cancer-related exposures may contribute to latent long-term cardiovascular risk, which can remain dormant for years [5,11,12,13,14]. Cardiac MRI in asymptomatic survivors with normal echocardiograms showed lower LV ejection fraction [14]. Although cardiotoxicity was only recorded in 7% of survivors of childhood malignancy, mortality was high in symptomatic cases. Moreover, freedom from symptoms does not ensure normal heart function. Children with abnormal ventricular systolic function after treatment have higher mortality risk compared to those with normal systolic function [15]. Acute heart failure is often self-limited and reversible, while delayed-onset heart failure significantly reduces survival. Heart transplantation in patients with chemotherapy-induced heart failure can be performed with good 10-year survival [5]. This review addresses the effect of pretransplant malignancy (PTM) on post-transplant survival as primary endpoint, and cancer incidence as secondary endpoint.

METHODS

A literature search was performed through the Web of Science and PubMed databases. It included the following MeSH terms: (heart OR cardiac) AND pretransplant* AND (malignancy OR cancer OR tumor OR neoplasm). To obtain the most recent advances, the inclusion was restricted from 2015 to 2026. Inclusion of papers was based on titles and on abstract. Exclusion criteria were reviews, editorials, case reports, meeting abstracts and opinion papers. The included articles were assessed for their quality by the Newcastle-Ottawa Scale. Because of the variety in study design and outcomes, a meta-analysis was precluded.

RESULTS

In Web of Science, 170 items were identified. This was reduced to 121 after automated removal of abstracts, reviews, case reports and editorial material. In PubMed, 153 items were identified and 45 duplicates were removed, after which 229 titles were screened. Based on the titles, 168 records were excluded. Sixty-one remaining articles were examined by their abstract and 43 of these were further excluded because the analysis for the outcome with respect to PTM was absent. Eighteen records had material related to the subject but only the results of nine manuscripts [16,17,18,19,20,21,22,23,24] were useful for final analysis. Seven papers were of high quality. Two papers did not reveal the number of patients with PTM but described the effect of PTM on outcome by calculating adjusted hazard ratios. For this reason, these papers were considered of lower quality. Table one displays the quality assessment of the included series [16,17,18,19,20,21,22,23,24]. Seven papers can be considered of high quality with respect to the criteria from the scale. In two series, the definition of controls and cases or of comparability was insufficient.
Table 1. Quality assessment of the included articles by the Newcastle-Ottawa Scale.
Table 1. Quality assessment of the included articles by the Newcastle-Ottawa Scale.
Reference 1 2 3 4 5a 5b 6 7 8 sum
Acuna 2018 [16] y y y y n y y y y 8
Batra 2022 [17] y y y y y y y y y 9
De Rosa 2019 [18] y y n n n n y y n 4
Garrett 2017 [19] y y n n n n y y n 4
Karia 2016 [20] y y y y n y y y y 8
Park 2019 [21] y y y y n y y y y 8
Youn 2022 [22] y y y y y y y y y 9
Yoosabai 2015 [23] y y y y n y y y 8
Wang 2018 [24] y y y y y y y y y 9
1: selection of cases: adequacy by record; 2: selection of cases: representativeness: consecutive inclusion; 3: selection of controls: by hospital records; 4: definition of controls: no history of disease (PTM); 5a: comparability of cases and controls: study controls: on basis of need for HTX; 5b: comparability: additional factors: such as demographics and other comorbid characteristics; 6: exposure: ascertainment: based on medical record; 7: exposure: method of ascertainment for cases and controls; 8: exposure: non-response rate similar for controls and cases.
Table two shows the included manuscripts [16,17,18,19,20,21,22,23,24] with mean patient ages, the number of HTX and solid organ transplantations (SOTR), the numbers of PTM, and the design. Four papers [17,22,23,24], included solely HTX patients. Two of these series were derived from the united network organ sharing (UNOS) database, while two papers dealt with monocentric series. Another paper documented the results after thoracic organ (heart and lung) transplants [18], and four papers showed mixed series, in which the numbers of HTX patients were specified, but without separate analysis [16,19,20,21]. In only two of these series, more specific numbers were provided for thoracic organ transplant [19] and for HTX [21]. One of the included series dealt exclusively with the effect of sirolimus after transplantation [20]. The mean age of the included patients was consistently between 50 and 60 years.
Table 2. basic characteristics of the included series.
Table 2. basic characteristics of the included series.
Author (reference) age HTX all SOTR PTM design
Acuna 2018 [16] 58 29 443 rate 1:2 PSM from CORR and cancer registries, with competing risk analysis
Batra 2022 [17] 60 27344 - 2113 UNOS registry
De Rosa 2019 [18] 52 41 94* - Monocentric cohort
Garrett 2017 [19] 51 1017 10649 - based on OPTN registry
Karia 2016 [20] 56 54 592 66 evaluation of immune suppression regimen in monocentric registry
Park 2019 [21] 53 684 10198 22 based on CORR registry
Youn 2022 [22] 58 1062 - 77 monocentric.
Yoosabai 2015 [23] 55 23171 - 1306 based on UNOS registry
Wang 2018 [24] 60 354 - 8 monocentric
adj HR: adjusted hazard ratio; CORR: Canadian Organ Replacement Register; HTX: heart transplantation; OPTN: Organ Procurement Transplant Network; PSM: propensity score match; SOTR: solid organ transplant; UNOS: United Network Organ Sharing.
Table three shows, from left to right the reference, the outcome under study, followed by the predictors (if available), the result, mostly presented as adjusted hazard ratio with the 95% confidence intervals, and if available, the p-value. A hazard ratio of at least 1.5, which translates as a 50% increase in the adverse outcome can be considered clinically relevant. In absence of the p-values, the obtained values are statistically significant if the lower end of the confidence interval is above one. In several series [17,22,23,24] the percentages were also provided. In one series [20] absolute numbers for post-transplant malignancies are presented.
The outcome with respect to survival in patients with respect to survival is mixed. One series dealing exclusively with HTX patients with PTM showed a reduced 1-year survival, but this outcome has not been affected beyond one year, although malignancy-related mortality was significantly increased [17]. Ten-year survival and death due to malignancy were not significantly affected by PTM in a relatively large series [22], only in a smaller one [24]. In series with mixed organ transplantation, a significant effect of PTM on all cause and cancer specific mortality was observed, especially with lung, digestive, melanoma and hematologic (high-risk) PTM [16].
The outcome after HTX with respect to post-transplant malignancy shows that the presence of PTM increased the rate for most post-transplant malignancies [17,18,22,23]. This was especially true for post-transplant skin cancer of various types [18,21,22,23], even for transplants of other organs. The table showed that the skin cancer incidence rate was twice as high as thoracic organ transplant compared to abdominal organ transplant [19,21]. The cumulative incidence rate for keratinocyte carcinoma was consistently higher for HTX, except after 2 years, where it was higher for lung transplantation. However, the relative importance of thoracic organ transplant as predictor for outcome was lower compared to the effect of white race and to prior skin cancer [19]. Four series were based on region or nationwide registries [17,19,21,23], which showed generally less data about cancer stage, treatment and cancer free intervals.
Table 3. Overview of the findings with respect to the effect of PTM on outcome.
Table 3. Overview of the findings with respect to the effect of PTM on outcome.
Author (reference) outcome predictors result (adjusted HR/%) p
Acuna 2018 [16] all cause mortality 1.36 (1.16-1.64)
cancer specific mortality 1.85 (1.20-2.86)
high-risk PTM 1.81 (1.47-2.23)
low-risk PTM 1.06 (0.86-1.31)
<5y interval 1.34 (0.73-2.47)
>5y interval 2.27 (1.37-3.75)
Batra 2022 [17] 1y-mortality (all types PTM) 1.25 (1.09-1.44) 0.001
(hematologic) 2.00 (1.61-2.48) <0.001
(breast) 1.06 (0.79-1.42)
(abdominal) 0.87 (0.65-1.48)
(other types) 1.69 (1.35-2.11)
Mortality >1 and <5 year (all types PTM) 1.00 (0.84-1.19) 0.980
(hematologic) 1.04 (0.74-1.47) 0.480
(breast) 0.88 (0.61-1.28)
(abdominal) 0.82 (0.58-1.18)
(other types) 1.23 (0.91-1.66)
Malignancy related mortality >1 and <5 years 18.7% vs.10.8% 0.008
5y-malignancy rate (all types PTM) 1.57 (1.38-1.79) <0.001
(hematologic) 2.38 (1.85–3.07) <0.001
(breast) 1.46 (1.06–2.00)
(abdominal) 1.17 (0.92–1.48)
(other types) 1.69 (1.35–2.11)
De Rosa 2019 [18] probability for BCC after HTX only 50 (33-69)% at 10 year
for SCC after HTX only for NMSC after HTX only 62 (45-78)% at 10 year
61 (45-78)% at 10 year
any non melanoma skin cancer age 1.07 (1.04-1.10) <0.001
(HTX & LTX)
darker skin		 PTM skin CA 0.42 (0.24-0.74) NS 0.003
SCC age 1.08 (1.05-1.11) <0.001
(HTX & LTX)
darker skin		 PTM skin CA
 0.38 (0.21-0.68) NS 0.009
BCC age 1.06 (1.02-1.09) 0.001
(HTX & LTX) PTM skin CA 4.56 (1.67-12.42) <0.001
darker skin 0.49 (0.25-0.96) 0.040
Garrett 2017 [19] skin cancer prior skin cancer 4.69 (3.26-6.73) <0.001
male 1.61 (1.34-1.89) <0.001
white race: 7.79 (5.52-11.37) <0.001
age >50: 2.65 (2.12-3.21) <0.001
thoracic TX 1.51 (1.26-1.82) <0.001
SCC prior skin cancer 4.71 (3.60-6.16) <0.001
male 1.67 (1.41-2.01) <0.001
white race: 8.18 (5.49-12.18) <0.001
age >50: 2.73 (2.24-3.34) <0.001
thoracic TX 1.51 (1.26-1.82) <0.001
malignant melanoma prior skin cancer male 7.15 (3.31-15.46) <0.001
NS
white race: 7.21 (2.33-23.31) 0.01
age >50: 1.95 (1.05-3.61) 0.03
thoracic TX 1.51 (1.26-1.82) NS
Karia 2016 [20] first skin cancer use of sirolimus 329 (193 skin CA)
second skin cancer after first event 130 (115 skin CA)
5.5 (2.5-6.4)
Park 2019 [21] KC: Standard incidence ratio 6.61 (6.31-6.93) <0.001
cumulative incidence ratio 5y (HTX) 15.04 (12.32-18.02) <0.001
cumulative incidence ratio 10y (HTX) 26.67 (22.73-30.76) <0.001
KC for all SOTR age>65 years 9.27 (7.08-12.14) <0.001
white race 8.50 (4.03-17.91) <0.001
PTM skin cancer 4.30 (3.72-4.98) <0.001
Youn 2022 [22] 10-y survival 70.4% vs.68.6% 0.450
10-y freedom from non-fatal MACE 78.1% vs. 76.0% 0.784
post-transplant malignancy 43.8% vs. 20.8% <0.001
post-transplant malignancy white race 10.29 (1.19–89.07) 0.034
BMI 1.11 (0.98–1.27) 0.109
male 2.41 (0.67–8.67) 0.178
age 0.97 (0.91–1.02) 0.198
skin cancer white race 8.88 (3.25–24.3) <0.001
death due to malignancy PTM recurrence 17.2% vs. 11.6%
9.6%		 0.571
-
Yoosabai 2015 [23] all cancers skin PTM 2.38 (1.63-3.49) <0.001
organ PTM 1.38 (1.02-1.88) 0.040
hematol PTM 0.95 (0.45-0.2.01) 0.890
multiple PTM 2.18 (1.01-4.71) 0.050
unknown PTM 1.38 (1.03-1.86) 0.030
skin cancer skin PTM 2.79 (1.82-4.28) <0.001
organ PTM 1.55 (1.07-2.25) 0.020
hematol PTM 1.25 (0.55-2.83) 0.590
multiple PTM 1.86 (0.68-5.08) 0.230
unknown PTM 1.08 (0.71-1.64) 0.720
organ cancer skin PTM 1.82 (0.81-4.08) 0.150
organ PTM 1.23 (0.69-2.19) 0.490
hematol PTM 0.49 (0.07-3.54) 0.480
multiple PTM 3.23 (1.01-10.38) 0.050
unknown PTM 1.79 (1.16-2.78) 0.010
hematologic malignancy organ PTM 0.60 (0.09-4.28) 0.610
unknown PTM 1.49 (0.46-4.70) 0.490
Wang 2018 [24] 5y-survival with PTM 50.0+/-17.7%
without PTM 68.7+/-2.0%
PTM recurrence 1 of 8 patients
HR: hazard ratio; BCC+SCC: basocellular plus squamous cellular carcinoma; BI: body mass index; CA: cancer; HTX&LTX: heart and lung transplant; hematol: hematologic; MACE: major adverse cardiovascular event; KC: keratinocyte carcinoma; NMSC: non-melanoma skin cancer; OPTN: Organ Procurement Transplant Network; PTM: pretransplant malignancy; spec mort: specific mortality; SOTR: solid organ transplant.

DISCUSSION

The number of cancer survivors is increasing, which is parallel with PTM rates in patients listed for HTX [17,22]. In principle, all candidates for HTX are screened for PTM and if, present, be treated adequately. At the same time, most included series report an increase in post-transplant ‘de novo’ or recurrent malignancy, all-cause and cancer specific mortality. This effect could also be observed in series studying SOTR. One monocentric series showed that early post-HTX survival of patients with PTM was worse, but at 5 years, this was comparable to patients without PTM [17]. In a large HTX series, 7.1% of the patients had PTM, which is comparable to older registries. Most common PTM were lymphomas, prostate cancer, non-melanoma skin cancer and breast cancer with a median interval between cancer diagnosis and HTX of 9 years. The post-HTX follow-up was 8.6 years. Patients with PTM had a higher cancer rate of 43.8% (with a 9.6% recurrence rate), but a comparable 10-year survival [22]. The susceptibility for development of cancer after organ transplantation was already increased by carcinogenicity of some immune suppressing agents, decreased host immunosurveillance, and potential infection with oncogenic viruses [21]. The presence and the type of PTM seems to add to this effect. The recurrence rate was high in lung and breast cancer, but there was also an increase in “de novo” malignancies, i.e. a cancer different from the PTM [17]. Hematologic PTM might also be considered higher risk since survival after transplantation was lower. Patients who survived the first post-transplant year had a comparable long-term or conditional survival compared to patients without PTM. Patients with hematologic PTM seemed to have a lower rate of graft failure and vasculopathy, because of lower immune activation. However, a 5-year follow-up might be too short to reach conclusions [17]. The role of the type of PTM and of the interval between cancer diagnosis and HTX was studied in only one series. High-risk PTM such as melanoma, digestive, lung and hematologic malignancies showed an increase in mortality, while for the low-risk PTM (pharynx, bladder, kidney, testis and prostate), the effect was not significant. The effect of the interval between PTM diagnosis and transplantation, the result seems counterintuitive: an interval of 5 years or more had a higher cancer-specific mortality [16]. For more commonly performed cardiac operations, such as coronary artery bypass grafting [25] and surgical aortic valve replacement [26], an opposite effect was observed: a longer interval improved cancer-specific and overall survival. However, the counterintuitive effect observed after THX might be due a high non-cancer death rate, delay in transplantation in patients with PTM, and use of competing risk analysis which takes graft loss and non-cancer death into account [16,21].
Skin cancer (50%) is the most observed malignancy after SOTR, especially after HTX. This was followed by lung cancer (10.9%), prostate cancer (10.0%) and post-transplant lymphoproliferative disease (8.5%), while other types of PTM were at 2% or lower. Overall, PTM increased the risk for post-transplant malignancy by a ratio of 1.51. Skin PTM carried a high risk for post-transplant skin cancer. Solid organ PTM also increased the risk for post-transplant skin cancer, but to a lesser degree, and not significantly for post-transplant solid organ tumors [23]. This reassuring observation indicates that pretransplant oncologic assessment is generally accurate. The largest relative increase of post-transplant malignancy was observed for non-melanoma skin cancer. Fatalities were mostly due to highly invasive post-transplant squamous cell carcinomas, promoted by the photosensitizing and carcinogenic effect of immune suppressing agents [27]. The region, as surrogate for sun exposure, also plays a significant role. Non-melanoma skin cancer occurred in 45% of the patients who underwent SOTR in Australia, compared to 10%-15% in European countries [18]. A US-based patient registry for post-transplant skin cancer revealed a high observed-to-expected ratio of 25 or five times the rate of all cancers combined. Improved survival due to newer immune suppressive agents and better screening techniques might contribute to this observation [19]. The presence of pretransplant skin cancer resulted in a significant increase in the rate of post-transplant basocellular carcinoma, but not of squamous cell skin cancer. Older age, male gender, thoracic organ transplant and a history of smoking also resulted in an increased rate, while a dark skin type was protective [18,19,21]. Post-transplant malignant melanoma had similar predictors as squamous cell carcinomas, but the effect of pretransplant melanoma had a high adjusted hazard rate [19]. In one series of 329 SOTR patients, including 58 patients with HTX, the focus was directed on a second post-transplant skin cancer, while the first post-transplant malignancy was used as index. A second cancer occurred in almost 40% of the patients. Pretransplant skin cancer as well as a first post-transplant skin cancer was associated with a second post-transplant malignancy. The use of sirolimus, an inhibitor of mammalian target of rapamycin (mTOR), had a protective effect against a second malignancy, without a significant effect on graft rejection of survival. This could be related to dose reduction or discontinuation of other immune suppressing agents [20]. However, a higher survival rate could be attributed to an improved immune suppression regimen or improved cancer treatments [27].
The importance of post-transplant malignancy is illustrated by its effect on survival: A nationwide survey of SOTR showed that 13% of deaths were caused by malignancy. Compared with the general population, the standard mortality ratio was 2.33. Death from lung cancer and non-Hodgkin lymphoma were most common in heart and lung recipients [27]. Another interesting aspect is the need for a second HTX, which was observed in 1026 patients of the UNOS database. Patients over 60 years had a higher comorbidity rate, which included malignancy. The malignancy-related 10-year mortality was significantly higher. Age was significantly associated with 10-year mortality with an adjusted hazard ratio of 1.72. The effect of PTM was not included in the analysis [28].
The type of immune suppression after HTX could also play a role in the outcome with respect to cancer rate and survival after HTX. Inhibitors of mTOR, such as sirolimus and everolimus, inhibit cell proliferation and angiogenesis in some cancers. These substances can be used as immune suppressing agents in transplant patients and as treatment for malignancies. The results, however, are not uniform. HTX patients who received everolimus and low dose calcineurin inhibitors had better long-term renal function, but similar graft function and survival [29]. In another series of patients who underwent HTX, conversion to sirolimus was associated with a lower 10-year rate of “de novo” malignancies, post-transplant lymphoproliferative disorders and non-melanoma skin cancers. Patients without these post-transplant malignancies had better survival [30]. The 2-year cancer rate in another HTX-series showed a lower rate of post-transplant malignancy with everolimus, compared to mofetil mycophenolate. This follow-up was however too short to see an effect on survival [31]. A lower cancer incidence and mortality rate after HTX with mTOR inhibitor regimens was observed after 5 years of follow-up [32]. Interpretation of the results after change in regimes can be hampered after discontinuation or dose reduction of other immune suppressants [20].
To decrease the risk of post-transplantation malignancy, some preventive strategies were proposed. A pretransplant colorectal screening identified adenomatous polyps in about one quarter of the patients and the incidence of colorectal cancer was below 1%. After HTX, colorectal cancer was detected in 1.2% of the patients, but this was lower than the 2.5% adverse event rate observed after colonoscopy. The risk-benefit rate of pretransplant screening by endoscopy was considered unfavorable [33,34]. Since smoking was identified as an independent predictor for post-transplant malignancy and mortality [35], more frequent medical imaging after HTX could be advocated for these patients. In areas with a high sun exposure, risk factors for post-transplant skin cancer were primarily white race and pretransplant skin cancer. The effect of transplant of thoracic organs was less important. Skin cancer screening strategies such as SUNTRAC were designed [36]. Immunosuppressive regimens which mitigate the risk of post-transplant malignancy could be considered for patients with a higher high risk for developing neoplastic disease [20,21].
In conclusion, the presence of PTM affects the outcome with respect to post-transplant de novo malignancy, recurrence of PTM and survival. This could be related to the aging population, but also to the improvements in diagnostic and therapeutic approaches for malignancies. Screening programs for cancer and improvements in immune suppressing regimens have the potential to improve the outcome after HTX. Patients with hematologic PTM seem to have a worse outcome. The benefits of HTX should be weighed against the risk in patients with PTM. The balance seems to shift in favor of the procedure, due to the improvements in post-transplant care. However, immune suppressive protocols might need to be adapted. For these reasons, PTM does not disqualify for HTX, but the approach should be individualized. Cancer type, response to treatment and absence of metastasis are important. In general, ISLHT guidelines recommend an interval between cancer diagnosis and HTX of 5 years [37]. The type of cancer and the absence of metastasis should also be considered in decision making. An expected 5-year cancer free survival of at least 70% should be anticipated before HTX. Adequate surveillance for malignancies is needed after HTX.
This study has several limitations. The outcome under study varied between mortality, cancer specific mortality, rates of specific malignancies such skin cancer. National registries can be susceptible to coding errors and missing information. This is especially true for patients who were followed for a dermatologic PTM in an outpatient clinic, who failed to report this to the transplant team. Voluntary reporting of skin cancers in population-based surveys could underestimate their rate. Several series studied patients after solid organ transplantation, without separate analysis of the different transplanted organs. Although inclusion was designed to be consecutive, HTX patients with PTM could be missed, especially when recruitment took place in the outpatient clinics. Also, detailed information about cancer type, stage, interval with HTX and treatment was not fully provided in most series. The role of specific immune suppressing agents in the development of post-transplant malignancies is not always considered. Diverse regimen such as the introduction of sirolimus, and surveillance protocols could change during the longer inclusion times and follow-up periods. Some single-center series were underpowered, increasing the risk for a type II error. Especially for skin cancers, the introduction of sun-protective behaviors could affect the outcome under scrutiny. All series were of retrospective nature with all their inherent limitations.

Limitations

With only one author, not all requirements of the PRISMA guidelines could be met. However, search terms, in- and exclusion criteria were applied and a quality assessment was performed. Pubmed and Web of Science were the two sources for manuscripts. Although other literature databases are available, the most important papers are expected to be identified and included from these sources for analysis. There is a heterogeneity because not all papers focused solely on heart transplantation. Although thoracic organ transplants might elicit a stronger immune response compared to abdominal organ transplants, the principles with respect to post-transplant malignancy and survival seem to be comparable for all transplanted organs. The outcome under study is not uniform since several types of post-transplant malignancies varied, as well as their predictors. This precludes a meta-analysis. However, most results pointed in an increase in the risk of post-transplant malignancies, especially in patients with pretransplant skin cancer, higher age and white race. Improvements after transplantation by newer immune suppressing regimens have been achieved to a limited degree.

Conclusion

Pretransplant malignancy in patients with end stage heart failure is not uncommon, but this condition does not preclude heart transplantation. Current results show an increase in post-transplant malignancy, especially with respect to skin cancer. Post-transplant survival in this specific patient group is decreased, but still acceptable. However, the time interval between pretransplant malignancy and heart transplantation, as well as the nature of pretransplant malignancy should be considered in the decision making.

Author Contributions

The author contributed solely to the article.

Acknowledgments

None to be made.

AI and AI-assisted Tools Statement

Not applicable

Financial support and sponsorship

None

Conflicts of interest

The author declared that there are no conflicts of interest.

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