English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Background Apical hyperthrophic cardiomyopathy (AHCM) is an uncommon form of hyperthrophic cardiomyopathy (HCM) with less prevalent detection of gene mutations and sudden cardiac death compared with other types of HCM. Purpose We present the case of a 76 years old patient with multiple cardiovascular risk factors (hypertension, dyslipidemia, obesity, former smoker) with history of unprovoked pulmonary embolism - PE (2018), without evidence of deep venous thrombosis, in treatment with rivaroxaban, who presented with worsening severe dyspnea at effort and peripheral edemas, symptoms started a few days before admission. He denied angina or palpitations. Methods On clinical examination we identified obesity grade II and bilateral leg edema and routine laboratory tests revealed controlled dyslipidemia. The electrocardiogram (ECG) showed atrial flutter (AF) with block 5:1, heart rate 50/min, with negative T waves in DI, aVL and V2-V6. Transthoracic echocardiography with contrast was performed showing no wall motion abnormalities otherwise with a mild concentric left ventricle hypertrophy (LVH) except for the apex where there was severe LVH suggestive for AHCM; there was an increased aortic velocity with an aortic valve with degenerative changes. We thought that the changes on the ECG were most likely due to AHCM. A thoracic tomography scan with contrast was also performed because of associated dyspnea which excluded an acute recurrence of PE. The next day the T waves on ECG normalized, putting forward for consideration an acute coronary syndrome. We performed a coronarography which confirmed a 80% stenosis of proximal left anterior descending (LAD) artery with subsequent placement of a drug eluting stent. We also did a transesophageal echocardiography (noncompliant patient) for exclusion of intracardiac thrombi (which also showed bicuspid aortic valve) and then we performed radiofrequency ablation of the cavotricuspid isthmus followed by atrial overdrive pacing for typical AF, but unsuccessful, with degeneration into atrial fibrillation. Results Sometimes heart failure might occur due to multiple etiological factors and mechanisms of decompensation. We had a patient with AHCM with an ECG that could be interpreted as typical for this pathology but with concomitent severely affected LAD coronary artery, with AF and high grade atrioventricular block plus mild aortic stenosis with a bicuspid aortic valve with indication for strict follow up. Conclusions AHCM was first described in Japan where has the highest prevalence, but is also documented in other countries (rare in Caucasian population). Note that AHCM often mimic acute coronary syndromes through clinical manifestations and electrocardiographic aspects. Our case report showed a Caucasian patient with AHCM with concomitent severe atherosclerotic desease and aortic stenosis on a bicuspid valve.

P888 How many diagnoses can one heart gather?