Assessment of concomitant versus sequential trastuzumab on radiation-induced cardiovascular toxicity.

There are limited data regarding effect of trastuzumab on radiation-induced cardiovascular toxicity when used sequentially or concomitantly. This experimental study aims to investigate effect of trastuzumab on radiation-induced cardiovascular toxicity with respect to the treatment sequence. One hundred and eight female Wistar albino rats were divided into six groups (G): G1 was control, G2 was trastuzumab, and G3 was radiotherapy (RT); G4 and G6 were sequential RT and trastuzumab; and G5 was concomitant RT and trastuzumab groups, respectively. Rats were killed at 6th h, 21st and 70th days after RT; thoracic aorta and heart samples were obtained. Transthoracic echocardiography and functional studies evaluating relaxation of thoracic aorta were performed. Subendothelial edema scores of thoracic aorta samples at 21st and 70th days were higher in RT groups (G3, G4, G5, and G6) ( p < 0.001). There was a deterioration of relaxation responses of thoracic aorta samples in RT groups ( p < 0.001). Cardiac fibrosis (CF) scores revealed detrimental effect of RT beginning from 6th h and trastuzumab from 21st day. RT groups showed further deterioration of CF at 70th day. Ejection fraction, left ventricular mass, and fractional shortening were significantly decreased in G4, G5, and G6. Trastuzumab may increase pathological damage in cardiovascular structures when used with RT regardless of timing.

High-dose testosterone and dehydroepiandrosterone induce cardiotoxicity in rats: Assessment of echocardiographic, morphologic, and oxidative stress parameters.

The aim of this study is to assess cardiotoxic effect of testosterone (TES) and dehydroepiandrosterone (DHEA) in Sprague Dawley rats. We compared the impact of subacute (14 days) and subchronic (90 days) administration of suprapharmacologic doses of TES and DHEA on body weight, locomotor activity, muscle strength, echocardiographic parameters, heart histopathology, and oxidative stress markers with the control group. Testosterone (10, 30, and 100 mg/100 g body weight) and DHEA (10 mg/100 g body weight) administration decreased the body weights and locomotor activity (p < 0.05), and the combination of both increased muscle strength (p < 0.05) in rats. In our histopathological evaluation, misshapen cell nuclei, disorganized myocardial fibers, and leukocytic infiltrates were observed in high-dose TES (100 mg/100 g)-treated rats, especially on day 14. On day 90, mild changes such as misshapen cell nuclei, disorganized myocardial fibers, and leukocytic infiltrates were observed in TES and DHEA-treated groups. According to our echocardiographic study on day 14 and day 90, TES, especially at high doses, induced increase in left ventricular posterior wall diameter and ejection fraction (p < 0.05). In this study, blood oxidative stress marker malondialdehyde was increased slightly but not significantly in TES and DHEA groups. On the other hand, antioxidant enzymes such as SOD and glutathione peroxidase (GSH-Px) levels were slightly but not significantly increased in TES and DHEA groups. These data demonstrate that the potential risk to cardiac health due to exogenous androgen use may be related to oxidative stress in rats.

Thrombolytic therapy in a patient with inferolateral myocardial infarction after carbon monoxide poisoning.

INTRODUCTION: ST segment elevation myocardial infarction (STEMI) due to coronary artery occlusion caused by intracoronary thrombosis in the setting of acute carbon monoxide (CO) poisoning is a very rare presentation. We present a case of intracoronary large and mobile thrombus formation after CO poisoning. CASE PRESENTATION: A previously healthy 50-year-old woman was referred for CO poisoning. She had chest pain after exposure to CO. Her initial mental status was preoccupied with chest pain. Her initial CO fraction was 28.1%, and initial laboratory data showed creatine kinase-myocardial isoenzyme of 134 U/L (upper limit 25 U/L) and troponin I of >50 ng/mL (upper limit 0.06 ng/mL). Electrocardiography was carried out on admission, revealing an ST segment elevation in the inferolateral leads. After initial evaluation, coronary angiography was performed and an intracoronary large mobile thrombus was seen in the proximal left anterior descending (LAD) artery with no significant stenosis. We administered tenecteplase with heparin. After the thrombolytic therapy, ST elevation in the inferolateral leads resolved. Repeat angiography was performed after 24 h; the thrombus in LAD had resolved. The patient was discharged after 5 days, with persistent Q wave in the inferior leads and mild hypokinesia of the inferoposterior wall suggesting myocardial injury. CONCLUSION: We describe intracoronary thrombus formation induced by CO poisoning. Because intracoronary thrombus can result in myocardial infarction, its consideration following CO poisoning is important. Patients with CO poisoning who have symptoms of STEMI should be carefully evaluated with serial electrocardiograms, cardiac biomarkers, and an echocardiogram. When there is evidence of acute myocardial injury, a primer in coronary angiography can determine which patients could benefit from intervention.

Misuse of fentanyl transdermal patch mixed with acute coronary syndrome.

Fentanyl transdermal patches have long been used in the palliative care of patients with chronic pain with a favorable safety profile. However, intoxications secondary to intentional and unintentional misuse have been widely reported. In this study, we report an otherwise healthy woman presented to emergency department who used three patches of fentanyl to alleviate her knee pain and with a picture mimicking acute coronary syndrome.

Association between microvascular angina and erectile dsyfunction.

Although the origin of cardiac syndrome X (CSX) is still debated, endothelial dysfunction leading to reduced coronary microvascular dilatory response and increased coronary resistance is thought to have an important role in the pathogenesis. Erectile dysfunction (ED) is associated with risk factors resulting in endotelial dysfunction. Although the relationship between cardiovascular disease and ED has been well established; the relation between CSX and ED has not been extensively studied so far. We herein aimed to study ED in patients with CSX. The study was designed as a prospective case-control study. Blood samples were analyzed with respect to concentrations of low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglycerides. The subjects answered the native language five-item version of the International Index of Erectile Function Questionnaire (IIEF)-5. Each question was scored from 0 to 5 with a maximum score of 25 denoting healty subjects. We investigated the IIEF-5 score in 51 men with CSX (mean age=48.2±6.4 years), 53 men with demonstrated coronary artery disease (CAD) (mean age=48.3±4.8 years) and 52 male controls with normal coronary arteries (mean age=47.2±6.0 years). Mean IIEF-5 scores were 19.88±3.07 for CSX group, 18.83±3.31 for CAD group and 21.40±2.94 for control group. IIEF-5 scores in CSX group were found to be significantly lower than the those of control group (P<0.001). There were no significant differences in IIEF-5 scores between CSX and CAD groups (P=0.09). We have shown for the first time that patients with CSX have lower IIEF-5 scores compared with controls with normal coronary angiograms. This study suggests that ED and CSX may be different manifestations of a common underlying vascular pathology and vasculogenic ED is frequently seen in CSX at least as much as in CAD.