Excerpt

Numerous evidences support obesity as both an independent risk factor and a risk marker for the development of asymptomatic and symptomatic coronary artery disease (CAD), heart failure, and atrial fibrillation.1 Diagnosis and risk stratification of cardiovascular impairment in obese population are important to identify those subjects who might benefit from more straight therapeutic strategies. Yet, noninvasive cardiac imaging techniques have restraints in obese subjects and the diagnostic accuracy is often limited. When physical exercise is used as stressor, the poor exercise tolerance leads to underestimation of inducible ischemia. The poor acoustic window for ultrasound in patients with obesity affects the performance of echocardiography in depiction of global and regional motion, thickness, and function of left ventricle. The excess soft tissue attenuation of radioactivity frequently produces artifactual myocardial perfusion defects and poor signal-to-noise ratios for single-photon emission computed tomography (SPECT) imaging.2 The value of attenuation correction is easy to accept, and it is generally recognized that it is important to discern if a tracer deficit is due to diminished myocardial perfusion or if it is an attenuation or motion artifact. Another problem is to establish whether the defect is really reversible or represents a result of scatter and interference from extracardiac tracer activity. It seems conceivable that attenuation correction should at least improve the problems related with an attenuation artifact. However, the question of whether attenuation correction is needed is still unsolved and it has been debated for a long time.3 Gantry bore and table weight limits also affect the ability to accommodate high grade obese on conventional SPECT or positron emission tomography (PET). Hence, it is critical to identify noninvasive imaging modalities with preserved diagnostic and prognostic values irrespective of inpatients’ body mass index (BMI). …