Nuclear medicine in the assessment and prevention of cancer therapy-related cardiotoxicity: prospects and proposal of use by the European Association of Nuclear Medicine (EANM).

Cardiotoxicity may present as (pulmonary) hypertension, acute and chronic coronary syndromes, venous thromboembolism, cardiomyopathies/heart failure, arrhythmia, valvular heart disease, peripheral arterial disease, and myocarditis. Many of these disease entities can be diagnosed by established cardiovascular diagnostic pathways. Nuclear medicine, however, has proven promising in the diagnosis of cardiomyopathies/heart failure, and peri- and myocarditis as well as arterial inflammation. This article first outlines the spectrum of cardiotoxic cancer therapies and the potential side effects. This will be complemented by the definition of cardiotoxicity using non-nuclear cardiovascular imaging (echocardiography, CMR) and biomarkers. Available nuclear imaging techniques are then presented and specific suggestions are made for their application and potential role in the diagnosis of cardiotoxicity.

Assessment of coronary artery disease during hospitalization for cancer treatment.

BACKGROUND: With improvement of cancer-specific survival, comorbidities and treatment-related side effects, particularly cardiovascular toxicities, need close attention. The aim of the present study was to evaluate clinical characteristics and outcomes of cancer patients requiring coronary angiography during inpatient care. METHODS: We performed a retrospective analysis of patients hospitalized between 02/2011 and 02/2018 in our two university hospital cancer centers. From a cohort of 60,676 cancer patients, we identified 153 patients (65.7 ± 11.6 years, 73.2% male), who underwent coronary angiography and were eligible for analysis. These were compared to a control group of 153 non-cancer patients pair-matched with respect to age, sex, and indication for catheterization. RESULTS: Cancer patients presented in 66% with an acute coronary syndrome (ACS). The most prevalent cancer entities were lymphoma (19%) and lung cancer (18.3%). The rate of primary percutaneous coronary interventions (PCI) was significantly lower in the cancer cohort (40.5% vs. 53.6%, p = 0.029), although manifestation of coronary artery disease (CAD) and PCI results were comparable (SYNergy between PCI with TAXus and cardiac surgery (SYNTAX)-score, delta pre- and post-PCI - 9.8 vs. - 8.0, p = 0.2). Mortality was remarkably high in cancer patients (1-year mortality 46% vs. 8% in non-cancer patients, p < 0.001), particularly with troponin-positive ACS (5-year mortality 71%). CONCLUSION: Strategies to effectively control cardiovascular risks in cancer patients are needed. Additionally, suspected CAD in cancer patients should not prevent prompt diagnostic clarification and optimal revascularization as PCI results in cancer patients are comparable to non-cancer patients and occurrence of troponin-positive ACS leads to a significantly increased risk of mortality.

Risk Assessment of Patients Undergoing Transfemoral Aortic Valve Implantation upon Admission for Post-Interventional Intensive Care and Surveillance: Implications on Short- and Midterm Outcomes.

BACKGROUND: Several studies have found that standard risk scores inaccurately reflect risk in TAVI cohorts. The assessment of mortality risk upon post-interventional ICU admission is important to optimizing clinical management. This study sought to determine outcomes and factors affecting mortality in patients admitted to the intensive care unit (ICU) after transcatheter aortic valve implantation (TAVI), and to analyze and compare the predictive values of SAPS II and EuroSCORE. METHODS AND FINDINGS: 214 consecutive patients treated with transfemoral TAVI (2006-2012) admitted to the ICU in an academic tertiary-care university hospital, were included in this retrospective data analysis. The overall 30-day mortality rate was 7%. Non-survivors at 30-days and survivors showed differences in the rates of catecholamine therapy upon ICU admission (93 vs. 29%; p<0.001), stroke (20 vs. 1%;p<0.001), sepsis (27 vs. 2%;p<0.001), kidney injury (83 vs. 56%; log-rank p<0.001), catecholamine therapy (88 vs. 61%;log-rank p<0.001) and vascular complications (60 vs. 17%; p<0.001). Mean SAPS II score and predicted mortality were higher in non-survivors (38.1±7.0 vs. 29.9±6.2;p<0.001 and 23.1±11.7 vs. 10.5±8.2;p<0.001, retrospectively), whereas the logistic EuroSCORE could not discriminate between the groups (p = 0.555). Among the biochemical parameters, the maximum values of creatinine, procalcitonin, and troponin I during the first 48 h after ICU admission were significantly higher in non-survivors. Multivariate analysis of baseline characteristics and complications associated with two-year mortality showed no significant results. CONCLUSIONS: The SAPS II is a good tool for estimating ICU mortality immediately after performing the TAVI procedure and provides valuable information for other known predictors of mortality.

Assessment of the functional diversity of human myoglobin.

Myoglobin is presumably the most studied protein in biology. Its functional properties as a dioxygen storage and facilitator of dioxygen transport are widely acknowledged. Experimental evidence also implicates an essential role for myoglobin in the heart in regulating nitric oxide homeostasis. Under normoxia, oxygenated myoglobin can scavenge excessive nitric oxide, while under hypoxia, deoxygenated myoglobin can reduce nitrite, an oxidative product of nitric oxide, to bioactive nitric oxide. Myoglobin-driven nitrite reduction can protect the heart from ischemia and reperfusion injury. While horse and mouse myoglobin have been previously described to reduce nitrite under these conditions, a comparable activity has not been detected in human myoglobin. We here show that human myoglobin is a fully functional nitrite reductase. To study the role of human myoglobin for nitric oxide homeostasis we used repeated photometric wavelength scans and chemiluminescence based experiments. The results revealed that oxygenated human myoglobin reacts with nitrite-derived nitric oxide to form ferric myoglobin and that deoxygenated human myoglobin acts as a nitrite reductase in vitro and in situ. Rates of both nitric oxide scavenging and nitrite reduction were significantly higher in human compared to horse myoglobin. These data extend the existing knowledge about the functional properties of human myoglobin and are the basis for further translational studies towards the importance of myoglobin for nitric oxide metabolism in humans.