Aims Ischaemic but viable myocardium may exhibit prolongation of contraction and QT interval duration, but it is largely unknown whether non-invasive assessment of regional heterogeneities of myocardial deformation and QT interval duration could identify patients with significant coronary artery disease (CAD). Methods and results We retrospectively studied 205 patients with suspected CAD who underwent coronary angiography. QTc dispersion was assessed from a 12-lead electrocardiogram (ECG) as the difference between the longest and shortest QTc intervals. Contraction duration was assessed as time from the ECG R-(Q-)wave to peak longitudinal strain in each of 18 left ventricular segments. Mechanical dispersion was defined as either the standard deviation of 18 time intervals (dispersionSD18) or as the difference between the longest and shortest time intervals (dispersiondelta). Longitudinal strain was measured by speckle tracking echocardiography. Mean contraction duration was longer in patients with significant CAD compared with control subjects (428 ± 51 vs. 410 ± 40 ms; P = 0.032), and it was correlated to QTc interval duration ( r = 0.47; P < 0.001). In contrast to QTc interval duration and dispersion, both parameters of mechanical dispersion were independently associated with CAD ( P < 0.001) and had incremental value over traditional risk factors, wall motion abnormalities, and global longitudinal strain (GLS) for the detection of significant CAD. Conclusion The QTc interval and myocardial contraction duration are related to the presence of significant CAD in patients without a history of previous myocardial infarction. Myocardial mechanical dispersion has an incremental value to GLS for identifying patients with significant CAD.

Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome that is often overlooked, misdiagnosed, and maltreated. Medical treatment poses a significant challenge because of the lack of randomized studies to guide treatment. The initial clinical presentation should guide medical and interventional management. Fibrinolytic agents and anticoagulants should be avoided because they could favor hematoma propagation. In patients with SCAD, antiplatelet therapy should be prescribed especially dual antiplatelet therapy (DAPT) consisting of aspirin and clopidogrel, whereas potent P2Y12 inhibitors, e.g., ticagrelor and prasugrel, should be avoided. If a stent was used, DAPT should be continued for 12 months. Aspirin only can be an option for patients without “high-risk” angiographic features—thrombus burden, critical stenosis, and decreased coronary flow. Beta-blocking (BB) agents should be used to prevent recurrence of SCAD. There is a general agreement that angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, mineralocorticoid antagonists, and loop diuretics should be used in patients with SCAD experiencing the symptoms of heart failure and a decrease in left ventricular ejection fraction below 50%. Although without firm evidence, statins can be used in SCAD due to their pleiotropic properties. The results of a randomized trial on the use of BB and statins are awaited. Aggregation of data from national registries might point out truly beneficial medications for patients with SCAD.