An unusual association of hypertrophic obstructive cardiomyopathy Translated title: Asociación inusual de la miocardiopatía hipertrófica obstructiva

Mitral annulus calcification (MAC) is a chronic, degenerative process in the fibrous base of the mitral valve. Although MAC was initially thought to be an age-related degenerative process, there is accumulating evidence that other mechanisms, such as atherosclerosis and abnormal calcium-phosphorus metabolism, also contribute to the development of MAC. Despite its frequency, the clinical relevance of MAC is grossly underappreciated. Indeed, MAC is associated with an increased incidence of cardiovascular disease, mitral valve disease, arrhythmias, and mortality. MAC also influences the outcomes of cardiac surgery and interventions, and its clinical relevance may well increase substantially in the forthcoming era of transcatheter mitral valve replacement. In this paper, we review the available published data to provide a consistent, clinically relevant description of MAC on the basis of contemporary imaging. We describe the pathophysiological mechanisms contributing to the formation of MAC and the clinical implications of this disease entity.

Patent foramen ovale (PFO) is growing in clinical interest because of a renewed focus on embolic stroke of undetermined source (ESUS), the PFO attributable fraction (the 10-point Risk of Paradoxical Embolism score), technical advances in PFO diagnosis, and the emergence of endovascular device closure as a treatment option. However, recent randomized controlled trials of the management of patients with ESUS and PFO failed to demonstrate the superiority of closure over medical treatment. The mechanisms of stroke other than paradoxical embolism may be important in patients with ESUS and PFO. This paper reviews the current understanding of the pathophysiology of stroke and therapeutic options in patients with PFO and ESUS.

Background This study assessed the echocardiographic predictors of sudden cardiac death (SCD) within two population-based cohorts. Methods and Results Echocardiograms were obtained on 2383 participants (1993–95) from the Atherosclerosis Risk in Communities (ARIC) Study (100% African-American) and 5366 participants (1987–89 and 1994–95) from the Cardiovascular Health Study (CHS). The main outcome was physician-adjudicated SCD. We used Cox proportional hazards models with incident coronary heart disease (CHD) and heart failure as time-dependent covariates to assess the association between echocardiographic variables and SCD, adjusting for Framingham risk score (FRS) variables, CHD, and renal function. Cohort-specific results were meta-analyzed. During a median follow-up of 7.3 years and 13.1 years, 44 ARIC Study and 275 CHS participants had SCD, respectively. In the meta-analyzed results, the adjusted hazard ratios (95% confidence intervals) for predictors of SCD were 3.07 (2.29–4.11) for reduced left ventricular ejection fraction (LVEF); 1.85 (1.36–2.52) for mitral annular calcification; 1.64 (1.07–2.51) for mitral E/A >1.5 and 1.52 (1.14–2.02) for mitral E/A <0.7 (vs mitral E/A 0.7–1.5); 1.30 (1.15–1.48) per one standard deviation (SD) increase in left ventricular mass; and 1.15 (1.02–1.30) per one SD increase in left atrial diameter. A receiver-operating characteristic model for prediction of SCD using FRS variables had a c-statistic of 0.61 for ARIC and 0.67 for CHS; the full multivariable model including all echocardiographic variables had a c-statistic of 0.76 for ARIC and 0.74 for CHS. Conclusions In addition to reduced LVEF, we identified other echocardiographic-derived variables predictive for SCD that provided incremental value over clinical risk factors.