Research presented at EuroEcho-Imaging 2015 raises the possibility that cancer itself may damage heart muscle irrespective of exposure to cancer drug therapies.
Researchers ( Venneri L et al ) from the UK’s first dedicated cardio-oncology clinic found that both treated and untreated cancer patients had impaired heart function.
It is well known that chemotherapy is potentially toxic to the heart, making cancer patients more prone to cardiovascular complications such as heart failure, hypertension or myocardial ischaemia.
The definition of cardiotoxicity is based on a reduced ejection fraction ( less than 55% ) and symptoms of heart failure.
A study applied a more subtle measure of left ventricular function using echocardiography called strain. It indicates how well the myocardial fibres contract. Previous studies have shown that cancer patients who have had chemotherapy can have a normal ejection fraction but reduced strain and that this may predict subsequent cardiotoxicity.
The study compared myocardial strain in three groups with a normal ejection fraction ( 55% or more ): 43 patients with cancer who were currently being treated or had received treatment in the past, 36 patients with as yet untreated cancer, and 20 healthy individuals matched to the cancer groups for age and gender.
The researchers found that both groups of cancer patients had similarly reduced strain measurements, indicating impaired heart function, compared to the healthy individuals.
What was really new was the finding of reduced strain, and therefore myocardial dysfunction, in the group of patients with cancer who had not yet received treatment. This raises the possibility that the tumour itself may have a direct and deleterious effect on the function of the heart.
Patients with reduced strain before they start their cancer drug therapies may be predisposed to developing heart failure during the course of their treatment.
These patients might need closer monitoring.
This is only the second study in humans which suggests that cancer might have a direct effect on the heart.
A study published in September ( Pavo N et al, Heart 2015;101:1874-1880 ) found elevated cardiovascular biomarkers in patients with as yet untreated cancer. It could be that the tumour produces these inflammatory markers which then leads to the reduction in myocardial function.
Animal models of cancer cachexia have shown a direct deleterious effect of tumor growth on myocardial function.
In cancer patients, although cardiotoxicity is a recognized complication of chemotherapy, it is not known whether cancer per se causes myocardial dysfunction.
2D speckle tracking strain imaging is a recognized technique for detecting early left ventricular dysfunction even in the presence of a normal ejection fraction ( EF ).
The aim of this study was to compare myocardial strain in 3 groups of individuals: (i) patients receiving cancer drug therapies, (ii) patients with as yet untreated cancer and (iii) healthy controls.
Researchers evaluated 79 patients ( age 58 ± 10 years, women 62% ) with cancer referred to cardio-oncology clinic of Royal Brompton Hospital ( London - United Kingdom ) with 2D echo-derived LVEF greater than or equal to 55% and echo images amenable to speckle tracking analysis for global longitudinal ( GLS ), circumferential ( GCS ) and radial strain ( GRS ).
Seventy-one patients also underwent same day high-sensitivity troponin I and BNP assays and 66 ( 83% ) underwent CMR imaging.
Forty-three patients had current or previous exposure to cancer drug therapies ( Group 1 ) and 36 patients had not yet received treatment ( Group 2 ).
Twenty healthy age matched controls also underwent strain imaging.
CMR showed loss of torsion and/or fibrosis in 11 of the 66 cancer patients ( 17% ).
In conclusion, the findings showed that cancer patients with preserved ejection fraction, whether or not having received cancer drug therapies, had evidence of sub-clinical myocardial dysfunction manifest as reductions in GCS and GRS.
This finding raises the possibility that tumour growth per se might have an intrinsic deleterious effect on myocardial function and needs further investigation. ( Xagena )
Source: European Society of Cardiology ( ESC ), 2015