Associazione Nazionale Medici Cardiologi Ospedalieri

CONGRESS ABSTRACT

CONGRESS ABSTRACT

STRESS ANGINA IN A PATIENT WITH ANOMALOUS ORIGIN OF THE LEFT CORONARY ARTERY AND INTRAMYOCARDIAL COURSE: A RARE DANGER

Fiorella Annalisa Taranto(Taranto) – Cardiologia P.O. Santissima Annunziata | Burattini Osvaldo Taranto(Taranto) – Cardiologia P.O. Santissima Annnunziata | Ganimede Maria Porzia Taranto(Taranto) – Radiologia P.O. Santissima Annunziata

Background

The anomalous origin of coronary artery (AOC) still represents one of the most intriguing conundrumsin cardiology. It is generally diagnosed during coronary angiography performed for other reasons and 85% of the cases are benign. Nonetheless, they can sometimes cause angina, coronary syndrome, and sudden cardiac death.

Clinical case

We describe a rare case of a 50-year-old dyslipidemic man, overweight, with arterial hypertension (AH) reporting episodes of stable angina when performing physical activities for several months. On the EKG a negative T wave in the lateral site was noticed, therefore an echocardiogram was ordered, which showed heart disease with moderate left ventricular hypertrophy, without obstruction of the left ventricular outflow tract. Notably, the patient already underwent cardiac magnetic resonance imaging (CMR) in another center, in the suspicion of initial hypertrophic cardiomyopathy. However, to us, the hypertrophy seemed to be rather related to the previously unknown AH, which probably remained undiagnosed for years. Coronary angiography showed an anomalous origin of the left coronary artery from the right sinus of Valsalva. On CT coronary angiogram the anterior descending artery (ADA), after its anomalous origin, described an interventricular, subpulmonary course, becoming intramyocardial for a stretch of approximately 39 mm, consequently undergoing a severe narrowing of caliber. Hence, stress CMR was performed with dobutamine and resulted positive for inducible ischemia. We proceed with interseptal cardiac surgical correction, cautiously releasing the ADA from the endocardium and overlying myocardium (coronary debridging).

Discussion and Conclusions

In clinical practice, it is difficult to establish a causal relationship between symptoms and AOC, as this represents a rare finding. In our case, an intramyocardial course was also identifiedand was responsible for both systolic and diastolic compression by the hypertrophic myocardium. The symptoms had begun to appear when myocardial hypertrophy due to untreated AH had become significant. Following the European guidelines, the treatment of AOC with evidence of ischemia should be surgical. We believe it is of fundamental importance in the presence of AOC to always suspect and exclude the presence of any coronary compressions, responsible for ischemia and arrhythmic events.