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We report a 57-year-old patient with acute anterior wall infarction with a history of a coronary baypass graft operation in 2007. He also had concurrent left arm cyanosis and severe pain. He had received diagnosis of pancreatic adenocarcinoma one month previously and had had his first chemotherapy in the previous week with gemcitabine and 5-fluorouracil. After the angiography, a giant thrombus was detected in the proximal left subclavian artery, deteriorating the flows of both left internal mammarian artery (LIMA) to left anterior descending (LAD) coronary artery graft, as well as the left brachial artery. The proximal subclavian artery was stented and good flow was achieved. Through the LIMA, the distal part of LAD, which was totally obstructed with probable distal thrombus embolization, was reached and a percutaneous balloon angioplasty performed. However, the no-reflow phenomenon was observed in distal LAD. A Fogarty traction of thrombus was performed successfully for the revascularization of the left arm. Approximately 30 minutes after the procedure, both angina and ST segment elevation in ECG were resolved under unfractioned heparin and nitroglycerin infusion. However, the patient died due to sepsis seven days after admission to hospital. In the literature, there are only a few previous reports on this rare clinical entity. The eitology, presentation, and the possible management strategies of this clinical entity is presented in this report.

A 41-year-old female was admitted to our hospital with an unidentified source of fever, dyspnea and dizziness. Transthoracic echocardiography demonstrated severe mitral valve regurgitation, and further examination with transesophageal echocardiography (TEE) revealed a 7 mm vegetation on the anterior mitral leaflet. Blood cultures were negative, and after 45 days of empiric 12 g/day ampicillin-sulbactam therapy, the vegetation was shown to have disappeared. However, due to ongoing severe mitral regurgitation and valve deformity, a prosthetic metallic mitral valve replacement was performed. After the operation, TEE was performed again due to subfebrile fever; however, the valve was normal and blood cultures were negative. Because of the probable relapse risk of infective endocarditis, the preoperative intravenous antibiotherapy was continued for 21 days and then orally for one week. Then, she was placed on follow-up by our outpatient clinic. As her INR was highly unstable during this period and she developed newonset subfebrile fever, she was hospitalized again, and the TEE demonstrated vegetation. Blood cultures were still negative, and a combination of vancomycin-rifampicin-gentamicin was started. While under that therapy, first stroke and after a few days recurrent trans-ischemic attack developed, and the vegetation was seen to have enlarged. Urgent valve operation was performed with a bioprosthetic mitral valve, and ampicillinsulbactam therapy was added to her previous antibiotherapy at the suggestion of the Microbiology Department. Oral anticoagulant therapy was planned for three months; however, during the postoperative period, her INR levels were highly unstable and could not be maintained in therapeutic ranges for even two consecutive days. Adjusted dosage of dabigatran to 110 mg/bid according to renal clearance in combination with 150 mg/day aspirin was started. However, valve thrombosis and a massive stroke developed under this therapy. The thrombosis disappeared after continuous heparin infusion, and she was discharged with neurological sequelae on 150 mg/day aspirin 55 days after her last operation. During the follow-up period of four months, no other clinical events occurred.

A 23-year-old male who had a VDDR pacemaker implanted seven years ago due to sick sinus syndrome and recurrent syncope episodes was admitted with symptoms of dyspnea, fever, and tachycardia, which were present for a few days. He was suspected to be suffering from pneumonia and underwent computed tomography scanning of the thorax, which revealed widespread infiltration in the lung parenchyma and pulmonary emboli. Transthoracic echocardiography revealed an extremely mobile echogenic structure in the right atrium, which was determined to be the free portion of a ruptured pacemaker lead. There was an overlying thrombus and/or vegetation-like organized soft tissue within the right ventricle around the lead component. In this article, the rupture of a permanent pacemaker lead, which complicated the course of infective endocarditis associated with pulmonary embolism and pneumonia is reported. We hypothesize that the underlying mechanism for the rupture is soft tissue entrapment within the right ventricle. Unfortunately, this rare and life-threatening situation led to the death of our patient after the surgical removal of the device and its components.

Background/Aims Most important cause of mortality in chronic obstructive pulmonary disease (COPD) patients is known to be cardiovascular disease (CVD). The objective of the present study was to evaluate the echocardiographic parameters in COPD patients with or without pre-diagnosed CVD and to investigate the relationship between echocardiographic parameters and systemic inflammation markers. Methods A total of 60 stable COPD patients (23 patients with CVD, group 1; 37 patients without CVD, group 2) and 21 healthy controls (group 3) were included in the study. Six-minute walking test (6MWT), COPD assessment test (CAT), and Body mass index, airflow Obstruction, Dyspnea, and Exercise (BODE) index results were recorded. High-sensitivity C-reactive protein (HsCRP), interleukin 8 (IL-8), fetuin-A, Clara cell protein (CCL-16), N-terminal pro-brain natriuretic peptide levels were studied in serum. Parameters of left and right ventricular systolic and diastolic function were measured by echocardiography. Results Patients with COPD had higher levels of systemic inflammation markers and lower level of inflammation inhibitor fetuin-A. When three groups were compared, group 1 had lower 6MWT result. HsCRP was highest in group 2 while other inflammatory markers were similar in groups 1 and 2. Regarding echocardiographic parameters, left ventricular ejection fraction (LVEF) was lower and left ventricle end-diastolic diameter (LVED), left ventricle end-systolic diameter (LVES) diameters were higher in group 1. The aortic diameter was higher in COPD patients. Fetuin-A was correlated with diameter of aorta and LVES. LVEF, LVED, and LVES were found to be correlated with functional parameters of COPD cases. Conclusions In COPD, left ventricular functions are affected as well as right ventricle before prominent clinical findings of cardiac disease and these echocardiographic parameters correlate with functional parameters of COPD patients.

Aims. Cardiovascular diseases are the primary cause of premature morbidity and mortality in early breast cancer patients after treatment with cardiotoxic chemotherapeutic agents. Arterial stiffness is an independent risk factor for future cardiovascular diseases and can be used as a predictive marker of subclinical cardiac damage. The aim of this study is to analyze the arterial stiffness in breast cancer patients who are in the follow-up period after receiving anthracycline-based chemotherapy regimens with trastuzumab. Methods and Material. We enrolled 45 HER2-positive breast cancer patients who are on follow-up at least for six months after completion of adjuvant chemotherapy with trastuzumab, and cardiovascular risk matched 30 control volunteers. The measurements were done with pulse wave analyzing machine. Results. Mean pulse wave velocity was higher in breast cancer patients compared to controls. The pulse wave velocity was significantly higher in patients receiving aromatase inhibitors compared to patients under tamoxifen. It was also significantly higher in postmenopausal breast cancer patients than postmenopausal controls. Conclusions. Arterial stiffness measurements may predict the breast cancer survivors with higher risk for cardiovascular events earlier in the follow-up period, and necessary preventive approaches and/or treatments can be applied.

This study examined the value of blood marker S100A1 in detecting cardiotoxicity induced by chemotherapy agents; trastuzumab and lapatinib, in normal rat heart. The rats were divided into three groups: control (n = 8, no treatment), T (n = 8, one time ip treatment with 10 mg/kg trastuzumab) and L (n = 8, oral treatment with 100 mg/kg/day lapatinib for 7 days). The activities of oxidative stress parameters Malondialdehyde (MDA), Superoxide dismutase (SOD), Catalase (CAT) and Glutathione (GSH) were measured from the extracted cardiac tissues. The levels of troponinI and S100A1 expressions were measured from blood samples. All biomarkers responded to the treatments as they exhibited alterations from their normative values, validating the chemically induced cardiotoxicity. S100A1 expression attenuated significantly (75%), which made the sensitive detection of cardiotoxicity feasible. Assessment of cardiotoxicity with S100A1 may be a valuable alternative in clinical oncology of cancers in some organs such as breast and prostate, as they do not overexpress it to compete against.