Objective: The aim of the study was to test the potential role of breast arterial calcification (BAC) in the prediction of coronary artery disease (CAD) in women. The criterion standard for CAD diagnostics was coronary angiography.
Methods: This retrospective study enrolled 163 consecutive women, who underwent digital mammography and coronary angiography in our hospital. We assessed the presence and severity of BAC, and tested whether the presence and/or extent of BAC could be a predictor for CAD, quantified by Gensini score.
Results: BAC was presented in 34 patients (21%). Neither the presence of CAD (17 patients, 50%, vs 55 42.6%, P = 0.44), nor the Gensini score (20.5 ± 29.7 vs 15.4 ± 24.1, P = 0.3) differed significantly between BAC-present and BAC-absent patients.A finding of triple-vessel disease, however, more frequently occurred in the BAC-present (seven patients, 20.6%) than in the BAC-absent (nine patients, 7%) group, odds ratio (OR) 3.1, 95% CI 1-9.5, P = 0.049. The presence of BAC did not significantly increase the odds for the presence of CAD (OR = 1.29, P = 0.54). Among the subgroup of patients with CAD, BAC presence was associated with triple vessel disease (OR = 3.34, P = 0.049).
Conclusions: We did not confirm BAC as a predictor of CAD. However, BAC showed association with more severe forms of coronary atherosclerosis (triple vessel disease).
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http://dx.doi.org/10.1097/GME.0000000000001765 | DOI Listing |
Eur Heart J Cardiovasc Imaging
January 2025
Sorbonne Université, unité d'imagerie cardiovasculaire et thoracique, Hôpital La Pitié Salpêtrière (AP-HP), Laboratoire d'Imagerie Biomédicale, INSERM, CNRS, Institute of Cardiometabolism and Nutrition, ACTION Group, Paris, France.
Purpose: Epicardial adipose tissue (EAT) could contribute to the specific atherosclerosis profile observed in premature coronary artery disease (pCAD) characterized by accelerated plaque burden (calcified and non-calcified), high risk plaque features (HRP) and ischemic recurrence. Our aims were to describe EAT volume and density in pCAD compared to asymptomatic individuals matched on CV risk factors and to study their relationship with coronary plaque severity extension and vulnerability.
Materials And Methods: 208 patients who underwent coronary computed tomography angiography (CCTA) were analyzed.
Cureus
December 2024
Department of Cardiovascular Medicine, University of Texas Health Science Center at Houston, Houston, USA.
We present a case of a 52-year-old male with no known past medical history who presented to an outside hospital with acute chest pain. Initial workup revealed anteroseptal ST-elevation myocardial infarction (STEMI) for which the patient was transferred to our facility for emergent percutaneous coronary intervention (PCI). However, the patient's hospital course revealed numerous confounding pathologies that can also present as STEMI, including transthoracic echocardiogram (TTE) abnormalities consistent with takotsubo cardiomyopathy (TCM) as well as myocardial bridging presenting as post-PCI STEMI in the setting of nitroglycerin use.
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View Article and Find Full Text PDFInterv Cardiol
November 2024
Cardiology Section, Internal Medicine Department, Arab Medical Center Amman, Jordan.
Coronary artery ectasia (CAE) is an abnormal dilatation of coronary artery segments, often linked with atherosclerosis. This report discusses two cases of CAE presenting as acute coronary syndrome. A 36-year-old man had proximal blockage in the left circumflex artery (LCx) and ectasia in the obtuse marginal artery and left anterior descending artery (LAD), while a 53-year-old male smoker had an ectatic LAD with a substantial thrombus.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2025
Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, United States.
Diabetic cardiomyopathy (DMCM), defined as left ventricular dysfunction in the setting of diabetes mellitus without hypertension, coronary artery disease or valvular heart disease, is a well-recognized entity whose prevalence is certainly predicted to increase alongside the rising incidence and prevalence of diabetes mellitus. The pathophysiology of DMCM stems from hyperglycemia and insulin resistance, resulting in oxidative stress, inflammation, cardiomyocyte death, and fibrosis. These perturbations lead to left ventricular hypertrophy with associated impaired relaxation early in the course of the disease, and eventually culminating in combined systolic and diastolic heart failure.
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