Our results support the hypothesis that carriers of the PlA2 allele might have an increased risk for ACS. PlA2 homozygosity was associated with an inadequate response to aspirin therapy. Our data further suggest that patients with PlA2 allele homozygosity might benefit from antiplatelet therapy based on adenosine diphosphate antagonists throughout secondary treatment for prevention of ACS.

Platelets have a central role in the development of arterial thrombosis and subsequent cardiovascular events. An appreciation of this complex process has made antiplatelet therapy the cornerstone of cardiovascular disease management. However, numerous patients will experience a recurrent atherothrombotic vascular event despite adequate antiplatelet therapy. Individual differences in the rate of platelet activation and reactivity markedly influence normal hemostasis and the pathological outcome of thrombosis. Such an individual variability is largely determined by environmental and genetic factors. These are known to either hamper platelets' response to agonists, and thereby mimic the pharmacological modulation of platelet function or mask therapy effect and sensitize platelets. In this article, we reviewed the antiplatelet mechanisms of aspirin and clopidogrel and the possible role of different polymorphisms, which may affect the efficacy of antiplatelet therapy. Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.

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Analyzing the data of different laboratory methods aspirin resistance seems to be associated with poor clinical outcome, although currently no standardized or widely accepted definition of aspirin resistance exists. The widely used laboratory methods might not be comparable with each other; therefore, specific treatment recommendations for patients who exhibit high platelet reactivity during aspirin therapy or who have poor platelet inhibition by aspirin are not established.

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Intracardiac manifestation of hepatocellular carcinoma (HCC) is a rare condition and an uncommon finding even at autopsy. Pulmonary tumor embolism as a presenting feature of HCC has been published only twice previously. In our case report, a 63-year-old man presented with high fever and six episodes of recurrent pneumonias during the last half year. Echocardiography was performed, a solid mass was found in the right atrium. Transesophageal echocardiography proved a tumor mass in the inferior vena cava (IVC) extending into the right atrium, abdominal ultrasound revealed tumor mass in the IVC and a solid tumor in the liver. Combined liver and heart surgery was attempted in order to remove the tumor mass from both the liver and the right atrium. Acute cor pulmonale occurred during tumor removal from the right atrium and the patient expired. In addition to local factors the possibility of embolization should arise in the background of recurrent pneumonia. Occult carcinoma must be included in possible causes of recurrent pulmonary embolism. Searching for primary malignancy should include HCC as frequent cause of hypercoagulability. In case of HCC, echocardiography is suggested because of the possibility of expansion in IVC or right atrium and tumor-embolization.

Retinoids (as environmental factors) are decreased significantly with increased prevalence of Leiden mutation (as a genetic factor) in patients before the clinical manifestation of histologically different (planocellular and hepatocellular carcinoma, and adenocarcinoma) GI cancer.