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Clinical symptoms of acute or chronic myocardial ischemia due to congenital coronary anomalies occasionally develop during adult life. While several types of coronary anomalies have been already reported, origin of the coronary arteries outside of the ascending aorta and pulmonary trunk is exceedingly rare, and has indeed been described to date only in a 6-day-old newborn. We hereby report to the best of our knowledge the first and unique case of an adult patient with ischemic cardiomyopathy, in whom coronary angiography and aortography disclosed both left main trunk hypoplasia and subsidiary left coronary supply provided by an ectopic artery arising from the descending thoracic aorta.

The "apical ballooning" is a cardiac syndrome characterized by acute extensive but reversible akinesia of the apex and mid part of the left ventricle (LV), without obstructive coronary artery disease (CAD), triggered by emotional or physical stress, accompanied by chest pain and/or dyspnoea, electrocardiographic changes mimicking acute coronary syndromes (ACS), and minimal but, to date, obligatory release of cardiac enzymes. Today the precise aetiology remains unknown, but prognosis is generally excellent. We hereby report a unique case of a 60-year-old woman presenting with transient wide anterolateral akinesia and severe LV dysfunction with persistently normal myocardial markers, despite the extent of wall motion abnormalities. This clinical vignette is the first proof of the concept that timely recognition and management may be able to prevent myocardial necrosis in patients with apical ballooning syndrome.

We recently observed a family with tall R waves from V1 to V3 in different relatives, regardless of the actual presence and localization of idiopathic left ventricular hypertrophy.

during atria1 pacing at a rate just in excess of the sinus rate. Wellens and Durrer [I] found a strong correlation between the antegrade effective refractory period of the accessory pathway and the cycle length of the ventricular response during atria1 fibrillation. Kanakis et al. [2] found, however, that the effective refractory period depends upon the cycle length of the driving stimuli. At shorter cycle lengths the effective refractory period decreased, with a maximum decrease of 40 msec. Gallagher et al [3] confirmed this observation. The maximum decrease of the effective refractory period in their patients was 45 msec. In our case, the variability of the effective refractory period, measured at different cycle lengths, exceeded all known maximum values. Neither the effective refractory period, measured by programmed atria1 stimulation, nor the pre-Wenckebach cycle length, determined by incremental atria1 pacing, yielded values similar to the cycle length during atria1 fibrillation. Substantially shorter cycle lengths during atria1 fibrillation than the effective refractory period of the accessory pathway have not been described till now. The explanation for this phenomenon in our patient could be an unusual variability in the dependence of the effective refractory period on the driving rate. Changes in sympathetic tone could possibly cause this. We conclude that induction of atria1 fibrillation is the only reliable way of assessing those patients with Wolff-Parkinson-White syndrome who are at risk of developing fast ventricular rates during atria1 fibrillation.