Tissue Doppler echocardiography has the potential to accurately measure the different phases of the cardiac cycle which until now could only be determined invasively. It may provide a sensitive method for the assessment of changes in both cardiac contraction and relaxation in different clinical settings.

Echocardiography when combined with spectral and colour flow Doppler is well established as a safe, non-invasive, and versatile diagnostic modality in cardiology, and is now the predominant technique used for evaluation of left ventricular function and for the assessment and quantification of valvar heart lesions. When combined with physiological or pharmacological stress, echocardiography also enables the identification of reversible myocardial ischaemia and myocardial contractile reserve.

Coronary artery disease is a growing concern. Although traditional biomarkers, such as troponins and creatine kinase, play a central role in the diagnosis, risk stratification and management of coronary artery disease, they are unable to detect myocardial ischemia in the absence of necrosis. Therefore, early detection of ischemia in patients presenting with acute coronary syndrome still remains a burning question. High-sensitivity troponin is evolving as a reliable biomarker in this regard and has been absorbed into clinical practice. Biomarkers are currently the focus of immense interest as it not only helps with diagnosis and management but also helps to understand the pathophysiology of the disease process. In addition, analysis using a multimarker strategy has also proven to be a very useful tool in risk stratification. This review will focus on the biomarkers and its application in the diagnosis and risk stratification of acute coronary syndrome.

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Head-up tilt testing demonstrates vasovagal mechanisms as a cause for syncope, but the pathophysiology underlying this condition remains unclear. The aim of this study was (i) to measure plasma beta-endorphins, adrenocorticotrophic hormone, cortisol, catecholamines, and brain natriuretic peptide during head-up tilt, and (ii) to assess the effect of naloxone infusion during head-up tilt in subjects with reproducible vasovagal syncope. During the assessment of unexplained syncope, 71 subjects underwent a total of 93 tilt tests (60-70 degrees head upwards for 40-45 min or until syncope occurred) during which frequent blood sampling was performed. Subjects with a positive tilt test (n = 56) (mean duration to syncope 23.6 min) showed a larger rise in beta-endorphin levels prior to syncope (baseline 4.7 +/- 2.2 vs syncope onset 6.9 +/- 3.2 pmol.l-1, P = 0.0001) than those with a negative test (n = 37) (baseline 3.9 +/- 3.9 vs end of test 4.9 +/- 2.3 pmol.l-1, P = 0.03). During tilting, adrenocorticotrophic hormone, cortisol, and noradrenaline increased; adrenaline and brain natriuretic peptide remained unchanged; and these responses were similar in positive and negative test groups. Naloxone (2.6 mg.kg-1 i.v. bolus followed by 20 micrograms.kg-1.min-1 infusion), administered in a double-blind fashion during head-up tilt in nine subjects, failed to modify either the time to syncope or the vasodepressor response. Thus, endogenous opioids appear not to be an important trigger for vasovagal syncope, and other pathophysiological mechanisms should be considered.