Metabolic syndrome (Mets) is a clinical condition characterized by a cluster of major risk factors for cardiovascular disease (CVD) and type 2 diabetes: proatherogenic dyslipidemia, elevated blood pressure, dysglycemia, and abdominal obesity. Each risk factor has an independent effect, but, when aggregated, they become synergistic, doubling the risk of developing cardiovascular diseases and causing a 1.5-fold increase in all-cause mortality. We will highlight gender differences in the epidemiology, etiology, pathophysiology, and clinical expression of the aforementioned Mets components. Moreover, we will discuss gender differences in new biochemical markers of metabolic syndrome and cardiovascular risk.

Summary: A 52-year-old man presented after one episode of effort angina, normal treadmill electrocardiogram (ECG), and clearly positive adenosine cardiac magnetic resonance (aCMR) for reversible perfusion defects in the left anterior descending (LAD) coronary artery territory. Contrast high-dose dipyridamole (0.84 mg/kg per 6 min) stress echocardiography (cSE) demonstrated normal myocardial perfusion (MP) and wall motion at rest, while perfusion defects were shown in the lateral and apical segments after dipyridamole. Wall motion at stress was completely normal and stress/rest Doppler diastolic velocity ratio on the LAD demonstrated reduced flow reserve. In this case, cSE was the provocative test detecting both the LAD and circumflex obstructive lesions, thanks to MP analysis, while wall motion assessment was negative, not different from treadmill ECG, and aCMR highlighted only the LAD disease.Learning points: In spite of the low sensitivity of wall motion assessment during stress-echocardiography to detect coronary artery disease (CAD) in patients with multivessel disease and balanced ischemia, the addition of cSE with myocardial perfusion assessment, is not only able to overcome this limitation of false negative rate on a per-patient basis, but may also depict multivessel myocardial perfusion defects more efficiently than aCMR, as in the reported case, thanks to high spatial resolution. Myocardial perfusion assessment during cSE, although not always technically feasible, has a very high spatial and temporal resolution which can easily demonstrate multivessel subendocardial perfusion defects during maximal vasodilation, which is often the only detectable marker of multivessel, balanced CAD. It is known that wall motion analysis during pharmacologic stress may result in falsely negative multivessel disease; in these cases perfusion imaging or Doppler measurement of coronary flow reserve may be helpful to detect multivessel obstructive CAD, which is a significant and dismal prognostic finding. aCMR is assumed as the perfect imaging modality for CAD detection, but in selected cases, such as the one presented, an advanced echocardiographic method in experienced hands can provide even more comprehensive results.