Late cardiac effect of anthracycline therapy in physically active breast cancer survivors - a prospective study.

The late-onset cardiotoxic effect of anthracycline is known, however the early detection and prevention of subclinical myocardial damage has not been fully understood yet. Besides medical therapy regular physical activities may also play a role in the prevention and reduction of side effects of chemotherapy. The aim of our present study was to detect the effect of regular physical activities on the diastolic function and on the symptoms of late heart failure in case of anthracycline chemotherapy. The prospective study included 55 female patients (age 31-65 year, average 49.5 years) with breast cancer and no cardiovascular risk factors. Proper cardiologic checkup included physical examination (blood pressure, pulse, etc.), ECG, standard echocardiography parameters (EF, LV dimensions etc.) and specific tissue Doppler (TDI) measurements. Symptoms of heart failure were also recorded. After five years of follow-up, symptoms of heart failure were evaluated again. Patients were assigned into two groups depending on their physical activity: 36 patients did perform regular physical activities (mean age 49.2 years) and 19 patients did not (average age 50.1 years). There was no significant difference between the two groups in basic physiological or standard echocardiography parameters neither at the baseline nor at the later time points. Diastolic dysfunction (decreased E/A) was detected 6 months after the beginning of the treatment (T2 time point) in both groups. In the inactive group this value fell below one however there was no significant difference (1.1±0.25 vs. 0.95±0.22). One year after the beginning of the treatment (T3) a significant difference could be detected between the two groups (1.05±0.28 vs. 0.86±0.25. P=0.038). Consistent change in diastolic function (Ea/Aa) could be detected with the more sensitive TDI (Tissue Doppler Imaging) measurements after treatments in both groups, especially in the septal segment (in the non active group the Ea/Aa decreased markedly but not significantly at T2 - 1.1±0.55 vs. 0.81±0.44, and this difference became significant at T3 and 2 years after treatment (T4), p=0.007 and p=0.065). The filling pressure (E/Ea) rose above 10 (p=0.09) in the non active group at T2; and it kept rising in both groups and became significant at T3 (p=0.012). Five years after the onset of the treatment symptoms of heart failure were less frequently reported in the physically active group than in the inactive one (19.45% vs. 68.42%). The data of our study show that the diastolic dysfunction of the left ventricle related to the anthracycline therapy became evident in the physically active group later and the symptoms of heart failure were less frequent than in the non active group after five years period. Enrollment in sport activities could be a good means for partial prevention in this group of patients. Cardiologic checkup at proper intervals plays a pivotal role in detection of possible cardiotoxicity. This is a strong indication for changes in the lifestyle of the patient and the treatment protocol alike.

Circulating endothelial cell count, plasma vWF and soluble ICAM-1 levels following primary or elective percutaneous coronary intervention.

BACKGROUND: Percutaneous coronary intervention (PCI) is an important therapeutic strategy in patients with ischaemic heart disease. Our aim was to clarify the extent of endothelial injury induced by PCI in stable angina (SA) or in acute ST-elevation myocardial infarction (STEMI). METHODS: Circulating endothelial cell (CEC) count, von Willebrand factor (vWF) and soluble intercellular adhesion molecule-1 (sICAM-1) levels were determined pre-, post-, 24 and 96h after PCI in patients with SA (n=23) and with STEMI (n=28). To provide control data regarding the effect of angiography itself stable angina patients with coronarography only (n=23) were enrolled. RESULTS: PCI and coronarography in stable angina patients caused measurable, but only non-significant elevation of CEC count and plasma vWF (p=NS). In STEMI, significantly higher baseline CEC count (p=0.019) and vWF plasma levels (p=0.046) were found compared to SA with PCI/or coronarography. After PCI, explicit increase in CEC count was observed (significant peak at 24h) (p=0.036). Positive correlation was found between baseline CKMB and CEC count at 24h (r=0.51, p<0.05). CONCLUSION: Both coronary angiography and elective PCI cause only mild endothelial injury. However, in patients with STEMI, not only the procedure itself but myocardial ischemia and the ongoing atherothrombotic process might be responsible for the prolonged and more pronounced endothelial damage.