chest pain syndrome
Recently Published Documents


TOTAL DOCUMENTS

50
(FIVE YEARS 5)

H-INDEX

13
(FIVE YEARS 0)

Radiology ◽  
2021 ◽  
Author(s):  
Anna Palmisano ◽  
Davide Vignale ◽  
Marijana Tadic ◽  
Francesco Moroni ◽  
Domenico De Stefano ◽  
...  

2021 ◽  
Vol 73 (1) ◽  
Author(s):  
Mahfouz El Shahawy ◽  
Susan Tucker ◽  
Lillee Izadi ◽  
Antonella Sabatini ◽  
Sukanya Mohan

Abstract Background Excess epicardial fat volume (EFV) has been recently implicated in cardiovascular structural and functional abnormalities. It has been associated with abnormal microvascular stiffness (as reflected by radial artery waveform; C2), which may result in microvascular dysfunction and contribute to the atypical chest pain syndrome without obstructive coronary artery disease (CAD). Women have been statistically shown to present with atypical chest pain more often than men and specifically without obstructive CAD. The aim of this study is to assess whether excess EFV in female subjects is associated with significant microvascular dysfunction (i.e., C2), in subjects without obstructive CAD. Results We screened 596 asymptomatic subjects, ages 20–79, using the Early Cardiovascular Health Risk Scoring System (ECVHRS), which has been reported. Out of the 596 total subjects, 230 subjects had a CACS. Out of these 230 subjects, 77 subjects (45 females; 32 males) had a 0 CACS. The 45 females from this cohort were the subjects of this study, and they were further categorized into 3 groups: group 1 (normal EFV, non-obese female subjects; n=16), females with ECVHRS < 3 and ACC/AHA risk score < 5%; group 2 (n = 9), females with elevated EFV and no abdominal visceral obesity; and group 3 (n=20), females with elevated EFV and abdominal visceral obesity. The average EFV was determined to be 72±20 cm3 among group 1, which indicates the values for normal EFV. The results in group 2 indicate that excess EFV is contributing to the development of microvascular dysfunction, resulting in abnormal micro-arterial (C2) elasticity (p< 0.00001), increase in resting blood pressure (p =0.0001), an abnormal rise in blood pressure (BP) at rest and post-mild protocol exercise (PME) (p = < 0.00001), and abnormal increase in carotid intima-media thickness (CIMT) (p = 0.000164). Conclusion Excess EFV appears to be not only a novel cardiovascular risk marker, but also the culprit for other cardiovascular risk markers. Based on these findings, elevated EFV may contribute to the development of the atypical chest pain syndrome in females without obstructive CAD. Additionally, EFV is emerging as a potential clinically relevant significant cardiovascular risk biomarker and may become a target to reduce cardiovascular morbidity and mortality.


2021 ◽  
Vol 14 (3) ◽  
pp. e242425
Author(s):  
Love Shah ◽  
Deeksha Kundapur ◽  
Shravan Nosib

We present the case of a 61-year-old woman with chest pain syndrome. Cardiac catheterisation did not reveal atherosclerotic coronary disease. However, a haemodynamically significant fistula connecting the left coronary artery to the left atrial appendage was found to be the culprit through a left-to-left shunting mechanism. In this report, we review the pathophysiology of coronary artery fistulas and the mechanism by which these fistulas may lead to ‘coronary steal syndrome’. Indications for interventional and surgical management are outlined. Ultimately, we suggest the consideration of coronary artery fistulas in the differential diagnosis of patients presenting with chest pain.


2016 ◽  
Vol 43 (6) ◽  
pp. 537-540 ◽  
Author(s):  
Robert A. Aertker ◽  
Benjamin Y.C. Cheong ◽  
Roberto Lufschanowski

We present the case of a 63-year-old woman with a remote history of supraventricular tachycardia and hyperlipidemia, who presented with recurrent episodes of acute-onset chest pain. An electrocardiogram showed no evidence of acute coronary syndrome. A chest radiograph revealed a prominent right-sided heart border. A suspected congenital pericardial cyst was identified on a computed tomographic chest scan, and stranding was noted around the cyst. The patient was treated with nonsteroidal anti-inflammatory drugs, and the pain initially abated. Another flare-up was treated similarly. Cardiac magnetic resonance imaging was then performed after symptoms had resolved, and no evidence of the cyst was seen. The suspected cause of the patient's chest pain was acute inflammation of a congenital pericardial cyst with subsequent rupture and resolution of symptoms.


Sign in / Sign up

Export Citation Format

Share Document