IntroductionTrastuzumab, a recombinant humanized monoclonal antibody, is targeted against the external domain of the human epidermal growth factor receptor type 2 (HER2). It improves efficacy of HER2-positive breast cancer treatment. The authors present their experience with patients (pts) treated with trastuzumab in the aspects of cardiac complications.Material and methodsWe observed prospectively 253 women with early positive HER2 breast cancer treated with trastuzumab. Assessment of cardiovascular status, ECG and echocardiography was performed initially and every 3 months until 6th month during follow-up.ResultsCardiac complications developed in 52 pts (20.55%) and included: asymptomatic left ventricle dysfunction (43), symptomatic heart failure (6), new asymptomatic LBBB (1); new negative T-waves in ECG (2). There was a progressive decline in left ventricular ejection fraction (LVEF) during treatment. It was more enhanced in pts with cardiac complications. Following trastuzumab termination/discontinuation LVEF increased but at month 18 still remained significantly lower than initially in both groups (61.07 ±4.84 vs. 59.97 ±5.23 – no cardiac complications; p < 0.05; 58.14 ±4.08% vs. 53.08 ±5.74% – cardiac complications; p < 0.05). During 6-month follow-up 33 out of 46 pts experienced an improvement in left ventricular status. In 13 pts in whom trastuzumab was discontinued, it was restarted; 6 of them successfully completed total therapy. Univariate analysis revealed no association between any cardiovascular risk factor and the development of cardiotoxicity.ConclusionsOne out of five treated patients discontinues trastuzumab in an adjuvant setting due to cardiac complications. LV dysfunction is the most frequent. Routine cardiac monitoring should be obligatory.

In hypertensive patients, a first-ever ischemic stroke was associated with larger left atrial size, left ventricular mass index and internal carotid artery stenosis. LAVi was the left atrial measurement most closely associated with ischemic stroke.

Paraoxonases (PONs) may exert anti-atherogenic action by reducing lipid peroxidation. We evaluated the influence of 2 polymorphisms within PON1 (192 Gln/ Arg) and PON2 (311 Ser/Cys) genes in 407 young Poles: 273 patients who experienced a first myocardial infarction (MI) under the age of 45 (study group) and 134 healthy volunteers (control group) with a HEART Score < or =2 (low risk). Paraoxonase 1 polymorphism 192Gln/Arg influenced the risk of premature MI (P = .0054). A positive family history of coronary artery disease (CAD) was associated with the 192Arg allele (P = .0107). The association between PON1 genotype (192 Gln/Arg) and low-density lipoprotein cholesterol (LDL-C) (P = .036) levels was also observed. However, we did not find any relationship between polymorphism 311Ser/Cys and CAD risk (P = .418). PON1 polymorphism 192Gln/Arg influenced the risk of premature MI. The association between PON1 genotype (192 Gln/Arg) and serum LDL-C levels may be explained by PON participation in reverse cholesterol transport.

The fact that first clinical manifestation of MI occurred in G carriers when the atherosclerotic plaque was much more advanced than in T carriers may suggest that wild-type genotype provided a better compensatory mechanisms due to NO synthesis and/or release. The polymorphisms within eNOS gene G10T, 894G/T, and -786T/C were not associated with the increased risk of MI.

Perfusion abnormalities were observed in ab. 40% of patients with critical (≥ 50%) narrowing of artery affected by bridging and were mild, stress induced.