Background And Objectives: The absence of obstructive coronary artery disease (CAD) in patients with angina is common, but its prognosis is debated. We investigated outcomes of such patients to identify predictors of cardiovascular events.
Methods: We selected 1014 patients with angina, evidence of myocardial ischemia at the electrocardiogram (ECG) exercise test or imaging stress tests, and nonobstructive CAD (absence of lumen diameter reduction ≥50%) at coronary angiography between 1999 and 2015. Note that, 1905 age- and risk factors-matched asymptomatic subjects served as "real-world" comparators. The primary endpoint was the occurrence of all-cause death or myocardial infarction.
Results: At 6-years median follow-up (interquartile range, 3-9 years), the primary endpoint occurred in 53 patients (5.5%, 0.92/100 person-years). Besides similar event rates compared with asymptomatic subjects (hazard ratio [HR] 0.85, 95% confidence interval [CI] 0.62-1.15, p = 0.28), the index population showed a very heterogeneous prognosis. Patients with nonobstructive CAD (HR 1.85, 95% CI 1.02-3.37, p = 0.04, compared with "normal" coronary arteries) and ischemia at imaging tests (HR 2.11, 95% CI 1.07-4.14, p = 0.03, compared with ischemia detected only at the ECG exercise test) were at higher risk and those with both these components showing even >10-fold event rates as compared with the absence of both. Three-hundred and twenty-five patients (34%) continued to experience angina, 69 (7.2%) underwent repeat coronary angiography, and 14 (1.5%) had consequent coronary revascularization for atherosclerosis progression.
Conclusion: Apart from the impaired quality of life, angina without obstructive CAD has an overall benign but very heterogeneous prognosis. Nonobstructive CAD and myocardial ischemia at imaging tests both confer a higher risk.
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http://dx.doi.org/10.1111/joim.13390 | 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 PDFFront Endocrinol (Lausanne)
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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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