Introduction: Electrocardiographic abnormalities in obstructive hypertrophic cardiomyopathy (OHCM) can often mimic acute myocardial infarction (AMI). Is-chemia in these cases is usually induced by microvessel disease, increased oxygen demand and/or acute incre-ase in left ventricle outflow tract (LVOT) pressure gra-dient. Septal reduction therapies proved to be efficient in reducing LVOT gradient. Cases of OHCM that also need coronary revascularization for AMI are rare. Data in the literature is scarce regarding these cases and clear recommendations for their management are lacking.
Objective: Our aim is to report the case of a patient with OHCM and acute anterior MI induced by severe left anterior descendant (LAD) disease, describing the diagnostic pathway, management and patient evolution.
Methods: The 61-year-old male patient was addressed to our clinic for signs and symptoms of decompensated heart failure and worsening chest pain in the last seve-ral days. His history included hypertension and chronic kidney disease. The ECG revealed an intermittent left bundle branch block (LBBB) alternating with narrow QRS complexes associating ST segment elevation in V1-V4 with biphasic T waves in V1-V3, negative T waves in V4-V6, and left ventricular (LV) hypertrophy. Blood tests revealed a high creatinine level, elevated high sensitive I troponin and slightly elevated crea-tinkinase levels. TTE revealed an OHCM phenotype (interventricular septum-IVS of 2,1cm, LVOT gradient of 58mmHg), a LV ejection fraction of 55%, with apical hypokinesia and pulmonary hypertension.
Results: Coronary angiography revealed a 70% ste-nosis in the proximal LAD segment followed by near occlusion in the medium segment and near occlusion in the medium segment of the first diagonal branch (DI). Percutaneous transluminal coronary angioplas-ty with stent placement was performed for the LAD and DI stenosis. The first septal branch territory was proved to resume to the basal part of the IVS by myo-cardial contrast echography, without collaterals. Sep-tal reduction therapy was decided to be performed in the same session. For safety reasons, instead of alcohol instillation, a covered stent was placed in the LAD to cover the first septal branch. The evolution was good, without complications, with a significant improvement in symptomatology and a decrease in LVOT gradient to 9mmHg.
Conclusions: T he patient’s symptomatology, ECG abnormalities and high troponin level could have been secondary to the OHCM with decompensated heart failure, but coronary artery disease could not be exclu-ded. Complete investigation of OHCM cases is always mandatory, and the abnormalities should not be consi-dered to be secondary to LV hypertrophy without furt-her investigation of the coronary status. Managing both coronary artery disease by percutaneous transluminal coronary angioplasty and LVOT obstruction by septal reduction therapy in the same session is possible and effective.