Hypertrophic cardiomyopathy (HCM) is a common (\> 1/500 in the general adult population) genetically transmitted disease impacting markedly patients' lives from the early ages to the latest. The phenotype as the prognosis of HCM may greatly differ from one patient to another: most patients present no or few symptoms and a near-normal lifespan, while others are severely symptomatic. Paroxysmal, persistent or permanent atrial fibrillation (AF) is frequent in HCM, occurring in more than 20%-25% of patients and is often considered as an important turning point for the quality of life of these patients. AF decreases cardiac output and exercise tolerance, increases hospitalization rate, and markedly increase the risk of embolic stroke with the need for life-anticoagulation. It has been shown that stroke may precede AF discovery and that it may occur at young ages with devastation consequences. AF also may trigger sudden cardiac death.
Observational studies have been conducted to search for parameters which correlate with the risk of AF (P wave duration and supra-ventricular burst on the Holter-ECG monitoring, L-wave morphology, degree of hypertrophy, clinical parameters-comorbidities, and size of the left atrium) with no real impact on clinical management. Left Atrial strain (LA-strain) has been recently demonstrated relevant (for instance our pilot work (for predicting stroke and/or AF (a cut-off of 15% is highly specific, 20% being the optimal cut-off). LA-strain (cut-off 20%) could be used for defining the patients that might require preventive anticoagulation therapy.
A randomized clinical trial is needed to extend the use of anticoagulation therapy to patients in sinus rhythm but identified to be at risk for AF.
Of note, it has been demonstrated that in this population, stroke occurred in 67% of the patients without any clinical atrial arrhythmia.
40 - 80 years of age
50 and 120 kg of weight
In sinus rhythm
Prior confirmed diagnosis of "primary" hypertrophic cardiomyopathy
Secondary hypertrophic cardiomyopathy (aortic stenosis, hypertension, amyloidosis and all phenocopies…)
Signs of heart failure
Hospitalization
Uncontrolled blood pressure
Parallel
Anticoagulant treatment Rivaroxaban
DrugAnticoagulant treatment Rivaroxaban in addition to best medical therapy
Best medical therapy
Other interventionBest medical therapy alone
all-cause death, myocardial infarction, stroke and systemic embolism
Bleeding
Number of observed bleeding divided by the sum of person-time at risk
Ischemic endpoints and bleeding to estimate the net clinical benefit
The net clinical benefit is calculated by subtracting the rate of excess bleeding events attributable to the experimental arm from the rate of excess ischemic events possibly prevented by the experimental arm
Atrial arrhythmias
Left Atrial reservoir strain
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