The assessment of endothelial function in the cardiac catheterization laboratory in patients with risk factors for atherosclerotic coronary artery disease

Herz ◽  
1999 ◽  
Vol 24 (7) ◽  
pp. 544-547 ◽  
Author(s):  
David Hasdai ◽  
Amir Lerman
Circulation ◽  
2006 ◽  
Vol 114 (12) ◽  
pp. 1321-1341 ◽  
Author(s):  
Morton J. Kern ◽  
Amir Lerman ◽  
Jan-Willen Bech ◽  
Bernard De Bruyne ◽  
Eric Eeckhout ◽  
...  

Author(s):  
Lucas H. Timmins ◽  
Jonathan D. Suever ◽  
Parham Eshtehardi ◽  
Michael C. McDaniel ◽  
Habib Samady ◽  
...  

Virtual histology-intravascular ultrasound (VH-IVUS) has gained increasing utility in the cardiac catheterization laboratory, not only in determining underlying atherosclerotic lesion composition prior to stent placement, but also in clinical studies assessing the natural history of coronary artery disease (CAD) [1]. Furthermore, VH-IVUS has provided an excellent means of quantifying disease progression by comparing data sets collected over time (i.e., longitudinal studies) and potentially identifying rapidly progressing and potentially vulnerable plaques. One difficulty, however, in analyzing VH-IVUS derived CAD progression is the accurate co-registration of image sets collected over a period of time. Commonly, an expert VH-IVUS image reader reviews these image sets side-by-side on a display and co-registers images along the vessel main axis, herein axially co-registered, by identifying image locations relative to fiduciary anatomical markers (e.g., branches). Despite this method being the standard for analyzing CAD progression, it is limited by the inability to accurately co-register VH-IVUS data in the circumferential direction (i.e., rotating images such that their cylindrical coordinate bases coincide; herein circumferentially co-registered). Thus, a significant amount of information on focal plaque progression is lost that could provide a greater understanding of the natural evolution of CAD, the effects of various pharmaceutical agents (e.g., statins) on lesion composition changes, and the impact of local mechanical factors that induce plaque progression/regression and transformation.


2007 ◽  
Vol 71 (5) ◽  
pp. 698-702 ◽  
Author(s):  
Cevat Kirma ◽  
Mustafa Akcakoyun ◽  
Ali Metin Esen ◽  
Irfan Barutcu ◽  
Osman Karakaya ◽  
...  

2019 ◽  
Vol 8 (2) ◽  
pp. 255 ◽  
Author(s):  
Samit Shah ◽  
Steven Pfau

Coronary angiography has been the principle modality for assessing the severity of atherosclerotic coronary artery disease for several decades. However, there is a complex relationship between angiographic coronary stenosis and the presence or absence of myocardial ischemia. Recent technological advances now allow for the assessment of coronary physiology in the catheterization laboratory at the time of diagnostic coronary angiography. Early studies focused on coronary flow reserve (CFR) but more recent work has demonstrated the physiologic accuracy and prognostic value of the fractional flow reserve (FFR) and instantaneous wave free ratio (iFR) for the assessment of coronary artery disease. These measurements have been validated in large multi-center clinical trials and have become indispensable tools for guiding revascularization in the cardiac catheterization laboratory. The physiological assessment of chest pain in the absence of epicardial coronary artery disease involves coronary thermodilution to obtain the index of microcirculatory resistance (IMR) or Doppler velocity measurement to determine the coronary flow velocity reserve (CFVR). Physiology-based coronary artery assessment brings “personalized medicine” to the catheterization laboratory and allows cardiologists and referring providers to make decisions based on objective findings and evidence-based treatment algorithms. The purpose of this review is to describe the theory, technical aspects, and relevant clinical trials related to coronary physiology assessment for an intended audience of general medical practitioners.


Author(s):  
Manjunath G Raju ◽  
Srikar Sidini ◽  
Joseph Gardiner ◽  
Ameeth Vedre ◽  
George S Abela

Background: Guidelines for triaging patients for cardiac catheterization recommend a risk assessment and noninvasive testing. We determined patterns of noninvasive testing and the diagnostic yield of catheterization among patients with suspected coronary artery disease in our outpatient clinical center at Michigan State University. Methods: We conducted a retrospective cohort study of 133 consecutive patients who underwent elective cardiac catheterization from July 2008 through August 2010. Demographic characteristics, risk factors, symptoms and the results of noninvasive testing were correlated with the presence of obstructive coronary artery disease, which was defined as 50% or more of coronary artery stenosis. Results: The median age was 62 years with 71% men. Risk factors included diabetes 39%; hypertension 77 %; prior CAD 44% and dyslipidemia 79 %. Angina/chest pain was present in 62 % and atrial fibrillation in 7%. Patients with prior CAD receiving percutaneous coronary intervention were 34 % (20/58) as compared to 27% (20/75) without prior CAD. Noninvasive testing was performed in 78 % (104/133) of the patients. Among patients undergoing heart catheterization 53% (71/133) had obstructive coronary artery disease. A total of 97 patients had an abnormal stress test and 52% (50/97) had obstructive CAD. Associations with obstructive coronary artery disease were: male sex (odds ratio [OR], 1.51; 95% confidence interval [CI], 0.71, 3.19), older age (OR per 5-year increment, 1.21; 95% CI, 1.03, 1.42), presence of diabetes (OR= 1.51; 95% CI, 0.75, 3.06), and presence of dyslipidemia (OR=1.42; 95% CI, 0.62 to 3.29). Conclusions: Patients with a positive result on a noninvasive test were more likely to have obstructive coronary artery disease than those who did not undergo any testing but this did not achieve significance (52% vs. 48%; P=.76). A larger patient group may be required to confirm this observation. However, improved strategies for risk stratification could help increase the diagnostic yield of cardiac catheterization in routine clinical practice.


2018 ◽  
Vol 33 (7) ◽  
pp. 706-712 ◽  
Author(s):  
Jeehoon Kang ◽  
Hack-Lyoung Kim ◽  
Jae-Bin Seo ◽  
Jin-Yong Lee ◽  
Min-Kyong Moon ◽  
...  

2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.


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