Introduction: Dilated cardiomyopathy (DCM) is an important cause of heart failure (HF) and remains a challenge for the clinician in terms of therapeutical approach and identifying the underlying causes. Coronary artery disease (CAD) and subsequent myocardial ischemia are a common cause for DCM. Mitral regur-gitation (MR) can be a consequence of DCM and/or myocardial ischemia, but it can also induce DCM. MR is also a well known complication of weightlifting.
Case presentation: We would like to bring to your at-tention the case of a 61-year-old caucasian male and former body-builder who was reffered to our Cardi-ology clinic for DCM (EF of 15%). The patient has a history of mitral valve replacement (2017: St Jude 31, mechanical prosthesis) due to severe MR, CAD (2016: a total of 5 drug- elluting stents as following: 2 of them placed on the anterior descending artery and 3 of them on the right coronary artery) with silent ischemia and HF with reduced EF (30-35%), NYHA class II. The patient was receiving optimal medical therapy, in accor-dance with the HF stage and current ESC guidelines. In the month before the current hospitalization, the symptoms progressively worsened with paroxysmal dyspnea episodes, marked fatigue, palpitations and inability to achieve small efforts (NYHA class III-IV). On admission, the ECG revealed a new onset left bundle branch block (QRS of 130ms) while the cardiac ultra-sound showed a dramatically altered EF of 10-15%. The Holter recording revealed a grade 1 AV block (PR 220ms) and ventricular arrhythmias (premature ven-tricular contractions, bigeminy). Coronary angiography was performed, however it did not detect any new coronary lesions and the stents were patent. Given the context, an ICD is implanted and cardiac resynchronization therapy is attempted. Four days after the procedure, the EF increased to 25-30%.
Particularity of the case: The etiology of the DCM in this case is a mixed one, with more factors concurring. Mitral regurgitation was the first to occur as a result of repeated isometric exertion. Later, the ischemic component was added, perpetuating both the MR and the left ventricular dilation. Moreover, despite the mul-tiple coronary lesions which required dilatation and stenting, the patient never described angina. In this situation, the diagnosis and treatment of CAD occu-red later than usual because of the silent ischemia. This condition allowed the perpetuation of myocardial is-chemia, which in turn contributed to the dilatation of the left ventricle. In this case, the sudden deterioration of the ejection fraction is indisputably the consequen-ce of the newly onset LBBB. In addition, the patient’s risk of sudden cardiac death (SCD) became very high, given the results of the Holter recording. For these reasons, the ideal treatment must address the following issues: the primary prevention of SCD and restoring the synchronized contraction of the left ventricle. Both were successfully achieved. This case and its positive outcome clearly show that addressing the etiologies of DCM (mitral valve replacement and the interventional treatment of CAD) is a necessary condition in order to succesfully manage these patients, but it is not always sufficient. This prompts the clinicians to think of the dynamics between the EF and the „status quo“ of the myocardium and to use the adequate methods in order to achieve the balance between them.