Background: The crescent availability of high-resolution cardiac imaging allows detection of myocardial structural variations. Differentiate these entities from others with different clinical significance can be challenging. Clinicians should be familiar with myocardial clefts to avoid erroneous diagnosis.
Case Summary: A 63-year-old smoker man alerted the emergency medical system for sudden chest pain. The electrocardiogram showed Pardee wave in inferior leads. Coronary angiography evidenced a 100% occlusion of right coronary artery that was treated by angioplasty and drug-eluting stent implantation with optimal angiographic result. At ventriculography, two fissure-like protrusion were observed in the inferior wall. Urgent transthoracic echocardiogram (TTE) demonstrated two deep fissures on the mid-inferior wall, contained by a thin sub-epicardial layer, with sub-total obliteration during systole. A diagnosis of myocardial clefts was suspected and after Heart Team discussion, a conservative strategy was proposed. Early cardiac magnetic resonance (CMR) confirmed two myocardial crypts on the mid-inferior wall. Stability of myocardial fissures and absence of left ventricular remodelling was confirmed by TTE, in a 2 years of follow-up period.
Discussion: Myocardial cleft should always be considered in the differential diagnosis of myocardial wall defects. In a patient presenting with an acute myocardial infarction, the main differential diagnosis is pseudoaneurysm. In this setting modified TTE views and meticulous analysis of CMR sequences are recommended to confirm the diagnosis and estimate the risk of myocardial rupture.
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http://dx.doi.org/10.1093/ehjcr/ytaa472 | DOI Listing |
Eur J Cell Biol
December 2024
Department of Physiology and Cell Biology, Dorothy M. Davis Heart and Lung Research Institute, College of Medicine, The Ohio State University, Columbus, OH, USA. Electronic address:
Cardiac muscle α-actin is a key protein of the thin filament in the muscle sarcomere that, together with myosin thick filaments, produce force and contraction important for normal heart function. Missense mutations in cardiac muscle α-actin can cause hypertrophic cardiomyopathy, a complex disorder of the heart characterized by hypercontractility at the molecular scale that leads to diverse clinical phenotypes. While the clinical aspects of hypertrophic cardiomyopathy have been extensively studied, the molecular mechanisms of missense mutations in cardiac muscle α-actin that cause the disease remain largely elusive.
View Article and Find Full Text PDFRev Cardiovasc Med
September 2023
Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, 830011 Urumqi, Xinjiang, China.
Background: While both cystatin C and left ventricular ejection fraction (LVEF) revealed established prognostic efficacy in coronary artery disease (CAD), the relationship between cystatin C/left ventricular ejection fraction ratio (CLR) and adverse clinical outcomes among patients with CAD following percutaneous coronary intervention (PCI) remains obscure, to date. Therefore, we sought to assess the predictive efficacy of CLR among CAD patients who underwent PCI in current study.
Methods: A total of 14,733 participants, including 8622 patients with acute coronary syndrome (ACS) and 6111 patients with stable coronary artery disease (SCAD), were enrolled from a prospective cohort of 15,250 CAD patients who underwent PCI and were admitted to the First Affiliated Hospital of Xinjiang Medical University from 2016 to 2021.
Sci Rep
May 2024
Institute for Cardiogenetics, University of Luebeck, Luebeck, Germany.
A positive family history is a major independent risk factor for atherosclerosis, and genetic variation is an important aspect of cardiovascular disease research. We identified a heterozygous missense variant p.L245P in the MMP10 gene in two families with premature myocardial infarction using whole-exome sequencing.
View Article and Find Full Text PDFbioRxiv
August 2024
Department of Medicine, University of Wisconsin-Madison, Madison, WI, USA.
Radiol Case Rep
February 2024
The Division of Maternal Fetal Medicine, The Department of Obstetrics and Gynecology, State University of New York (SUNY), Downstate Health Sciences University, 450 Clarkson Ave, Box 24, Brooklyn, NY, USA.
The tricuspid valve positioned between the right atrium and right ventricle is composed of 3 leaflets (anterior, posterior, and septal) anchored by a collagenous fibrous annulus, a saddle-shaped, oval structure, providing a firm yet dynamic structural support for the tricuspid valve. The annulus is considered to separate between the right atrium and right ventricle. Structural anomalies of the fetal tricuspid valve are rare and include Ebstein's anomaly, tricuspid atresia, partial absence, unguarded tricuspid orifice (absent leaflets) cleft, double orifice, bicuspid valve and Uhl anomaly (absence of the right ventricular myocardium with an apposing endocardium and epicardium).
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