Introduction: Although its existence has been suspec-ted since 1869, being described as a separate clinical entity in 1960 by Braunwald et al., the hypertrophic car-diomyopathy by its various forms of presentation often remains a difficult diagnosis, hiding under the mask of other cardiac pathologies. Being the most widespread genetic disease of the heart, hypertrophic cardiomyo-pathy can embrace any cardiac clinical symptomato-logy from completely asymptomatic to sudden cardiac death. The diagnosis of this disease can be challenging and it can be unmasked by the appearance of an acute coronary syndrome.
Methods: A 78-year-old female without a known car-dio-vascular history is referred to our department for the suspicion of an antero-extensive ST-elevation myo-cardial infarction (STEMI), due to precordial pain of underlying character. We mention that the patient re-ceived in pre-hospital dual platelet therapy, statin, he-parin bolus and amiodarone. The clinical exam showed arrhythmic cardiac noises, intense systolic murmur in the aortic area with associated friction, and myocardi-al cytolysis syndrome. The ECG showed atrial fibrilla-tion 100 a/ minute and an aspect of antero-extensive STEMI. The echocardiographic evaluation presents an obstructive hypertrophic cardiomyopathy with a 20 telediastolic diameter of the left ventricle, with a moderately diminished ejection fraction.
Results: T he coronary angiography, ventriculography and left cardiac catheterization documented normal coronary arteries, major left ventricular hypertrophy with an intraventricular gradient of 90-150 mmHg with almost complete obstruction at the medioventri-cular level, anatomy of the first septal artery allowing embolization as a method of treatment. At discharge, the patient was in sinus rhythm under anticoagulant therapy, antiarrhythmic, and is to return for septal em-bolization. We mention that the subsequent ultrasound evaluation of the patient’s daughter has showed a non-obstructive hypertrophic cardiomyopathy.
Conclusions: The particularity of this case consists of the complete asymptomatic evolution of a major gene-tic cardiac pathology. It was accidentally discovered at the age of 78 due to the occurrence of an acute coronary syndrome possibly by embolic mechanism given the presence of non-anticoagulated atrial fibrillation or the imbalance between increased demand at tissular level. It should also be stressed the importance of in-terventional treatment in this patient, but also the early diagnosis of the disease for other family members with the possibility of subsequent monitoring and preventi-on of complications.