The results show that chronic cigarette smoking is associated with a prolonged Tp-e interval, increased Tp-e/QT ratio and Tp-e/QTc ratio. These observations may indicate that there may be a relationship between smoking and altered ventricular repolarization. Abnormal ventricular repolarization values on an ECG may explain the increased cardiovascular event risk in long-term heavy cigarette smokers.

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.

Among childhood psychiatric disorders, attention deficit hyperactivity disorder (ADHD) is of greatest interest to practitioners. Methylphenidate (MPH) is a drug that is widely used in the treatment of children in whom ADHD has been diagnosed. Although this treatment has been used for years, its effects on the heart remain the subject of debate. The QT interval comprises the ventricular activation and recovery periods as seen on electrocardiogram (ECG). The acute effect of MPH on QT interval dispersion is unknown. Researchers in the present study sought to investigate the acute effects of MPH on QT interval as seen on ECG. A total of 25 patients with ADHD (mean age, 9.4+/-2.1 y) who were treated with MPH were enrolled in the study. Twelve-lead derivation ECGs were taken before and 2 h after administration of 10 mg of MPH. Maximum QT interval, minimum QT interval, and interval durations were measured, and QT dispersion was calculated, for each ECG. QT dispersion measured after medication administration decreased significantly from 59.6+/-16.3 ms to 50.8+/-10.9 ms (P=.016); corrected QT dispersion decreased significantly from 70.9+/-17.6 ms to 61.3+/-13.3 ms (P=.011). Maximum QT interval duration decreased from 73.7+/-21.8 ms to 361.8+/-29.0 ms (P=.006); minimum QT interval duration rose from 317.0+/-23.3 ms to 322.3+/-21.6 ms (P=.312). In conclusion, the findings of this study show that MPH reduces QT dispersion during the acute period shortly after its administration.

Left ventricular (LV) diastolic dysfunction (LVD) is a common complication secondary to hypertension. It has been reported that bisoprolol is effective in reducing blood pressure and has beneficial cardiac effects in patients with hypertension. However, its effect on LV diastolic function has not been studied in detail. In this study, we sought to determine bisoprolol’s effect on left ventricle diastolic function. Data from 25 patients were statistically analyzed. Peaks E and A wave, E/A ratio, isovolumetric relaxation time and E wave deceleration time were measured echocardiographically. Doppler echocardiography measurements after bisoprolol treatment revealed an improvement in LV diastolic function. In conclusion, our results show that treatment with bisoprolol, improves echocardiographic parameters of LV diastolic function after 3 months of treatment.

We describe live three-dimensional transthoracic echocardiographic (3DTTE) findings in a 52-year-old female who had previously undergone an aortopulmonary tunnel operation for anomalous origin of the left coronary artery (ACA) from the pulmonary artery. Three-dimensional transthoracic echocardiography clearly delineated the origin of the ACA from the posterolateral aspect of the main pulmonary artery just above the pulmonary valve, the surgically created tunnel, as well as a small defect in the tunnel near the aortic end communicating with the pulmonary artery.