Coronary Angiography For Diagnostic Purposes Research Articles

Comments on ‘Economical aspects of coronary angiography for diagnostic purposes: a Belgian perspective’

Comments on ‘Economical aspects of coronary angiography for diagnostic purposes: a Belgian perspective’

Economical aspects of coronary angiography for diagnostic purposes: a Belgian perspective

Coronary angiography (CA) is an increasing diagnostic procedure in Belgium. The aim of this analysis was to look at the financial aspects of CA in a large tertiary Belgium hospital to establish if current reimbursement is appropriate. For the analysis of costs we considered the use of the catheterisation laboratory, personnel costs and material costs during multiple weekly periods in the spring of 2023. We calculated that one cathlab needs to perform 8.21 CA's to equal incomes with costs. To allow for a small positive income (200€) for the hospital/cardiologist 9 procedures per cathlab day are required. Our hospital performs a 7 (mean) ± 0.75 (standard deviation) of CA's per cathlab day and therefore does not reach this financial break-even point. Our calculations are on the safe side, since coronary physiological interrogation with fractional flow reserve (FFR) was excluded from this analysis. Nevertheless, this is a cost-effective technique for which no extra reimbursement is foreseen in the current Belgium system.

Link between Friesinger Index and Lipid Profile in Patients Undergoing Diagnostic Coronary Angiography

Background: A strong association between abnormal lipid variables and development of atherosclerosis is widely established. However, few data exist on the association between lipid levels and the extent or severity of coronary lesions in patients with coronary artery disease. Objective: We aimed to determine the link between lipid levels and the extent or severity of coronary lesions in patients with suspected coronary artery disease using Friesinger index (FR). Methodology: In this prospective and singe-center study, consecutive patients who underwent coronary angiography for diagnostic purposes were analyzed. Each participant was evaluated for lipid levels i.e. total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, very-low-density lipoprotein (VLDL) cholesterol, non-HDL cholesterol, triglycerides/ HDL cholesterol, and triglycerides/non-HDL cholesterol. The extent of coronary disease was evaluated using FR index. Results: A total of 566 patients (mean age: 56.17 ± 9.99 years) were included in the study. The mean FR index was 5.40 ± 3.78. A significantly positive correlation was observed between FR index and total cholesterol (P = 0.002), triglycerides (P < 0.001), VLDL cholesterol (P < 0.001), non-HDL cholesterol (P = 0.006), triglycerides/HDL cholesterol ratio (P = 0.008), and triglycerides/non-HDL cholesterol ratio (P = 0.002). On the contrary, an inverse correlation was observed between FR index and HDL cholesterol (P < 0.001). Age or gender played no role in governing the FR index severity, while body-mass index, hypertension, diabetes, and smoking showed significant association with FR index (P < 0.001 for all). Conclusion: The present study demonstrates a significant link between the extent of coronary artery disease and levels of certain lipid variables.

0498: The value of image fusion in coronary angiography for the detection of coronary artery bypass graft

The coronary angiography among patients with coronary artery bypass graft (CABG) are more complex procedures with more X-ray exposure, longer compared to conventional coronary angiography. Image fusion is a new technology allowing a fusion in real-time of a 3D model obtained by reconstruction of computed tomography (CT) images with fluoroscopic images. To evaluate the contribution of image fusion in coronary angiography for the detection of CABG. A prospective study over 9 months, single center comparing the use of image fusion to conventional coronary angiography. All patients coming for angiographic control of CABG were included in the study. Patients who had previously (for another indication) a chest CT with injection of contrast media were the fusion image group, patients without prior injected chest CT constituted the control group. For patients in the fusion group, the aorta, the CABG, sternotomy sutures, the bronchi and a vertebra were reconstructed in 3D from CT acquisitions and these images were incorporated in real-time on fluoroscopic images. The following parameters were reported in both groups and compared: search time of CABG, procedure time, X-Ray exposure and the amount of contrast. 59 patients were included, 13 in the fusion image group, 46 in the control group. There were not significant differences between the 2 groups in terms of general characteristics patients and procedures. The search time of CABG was significantly shorter in the fusion group of images in the control group (16.04 min±13.2 min vs 6.4 min±4.7 min, p=0.002), as well as procedure time (31.5 min±15.2 min vs 19.4 min± 6.8 min, p = 0.007), fluoroscopy time (14.76 min±8.3 min vs 9.3 min±4.2 min, p = 0.04), Air KERMA (822.9 mGy±475.5 mGy vs 569.1 mGy±242.4 mGy, p = 0.01) and amount of iodinated contrast (121 cc ± 43.5 cc vs 88.2 cc±30.8 cc, p = 0.01). 3D reconstruction of CABG from CT with real-time fusion on coronary angiography images may shorten the search time of CABG, procedure time, X-Ray exposure and the use of iodinated contrast compared to standard coronary angiography for diagnostic purposes in patients with CABG. Abstract 0498 – Figure: 3D picture merged with the real-time fluoroscopic

The role of paraoxonase (PON) enzyme in the extent and severity of the coronary artery disease in type-2 diabetic patients

Increased coronary artery disease (CAD) risk is well established in diabetes mellitus (DM). Paraoxonase (PON) enzyme is known to have protective effects on lipid peroxidation. This study aimed to investigate the changes in PON activity levels with duration of DM as well as the role of PON activity in progression of CAD. Eighty-four consecutive diabetic patients (mean age 58 years, 46 men) who underwent coronary angiography for diagnostic purposes were examined. Before the angiography, fasting venous blood samples were taken for PON enzyme activity, thiobarbituric acid reactive substances (TBARS), and routine biochemical parameters. Severity and extent of coronary atherosclerosis were scored numerically using the Gensini scoring system. The population was divided into three groups according to Gensini score: Group 1, mild CAD; Group 2, moderate CAD; Group 3, severe CAD. Group 1 had higher PON levels and shorter DM duration than those of Group 3. Gensini score was significantly correlated with, PON activity (r = -0.361) and apo-AI (r = -0.375). TBARS (r = -0.290) and the duration of DM (r = -0.336) also showed a significant correlation with PON activity levels. Also, multivariate linear regression and Pearson correlation analyses showed that PON activity (P = 0.04), apo-AI levels (P = 0.01), and the duration of DM (P = 0.003) were significantly associated with Gensini score. Paraoxonase activity decreases parallel to DM duration. The lack of protective effect of PON enzyme on lipid peroxidation may be a factor in acceleration of CAD in DM.

Influence of Angiotensin Converting Enzyme Insertion/Deletion Polymorphism on Long-term Total Graft Occlusion after Coronary Artery Bypass Surgery

The renin-angiotensin system has a very important role in coronary thrombosis and restenosis. Plasma angiotensin converting enzyme (ACE) activity is associated with an insertion/deletion polymorphism in the gene coding for ACE. It is known that there is a strong correlation between ACE DD and atherosclerosis. However, little has been documented about its role in venous graft failure. The objective of this study was to investigate the relationships among the ACE gen polymorphism and long-term vein graft occlusion. The study population consisted of 87 consecutive white patients with symptomatic coronary artery disease in the previous month, who had had aorto-coronary bypass surgery (ACBS) more than 5 years back and who underwent coronary angiography for diagnostic purposes. On the same day of angiography, 10 mL whole blood was taken for ACE gene insertion/deletion (I/D) polymorphism. Mean age of the patients was 64.4 +/- 8.6 years, and 71 (82%) of the patients were men. The average ACBS time was 7.9 +/- 1.9 years. The ACE genotype was II in 15 patients (17.2%), ID in 47 patients (54.0%), and DD in 25 patients (28.7%). Thus, D allele frequency was .82. There was no significant difference between the cases with regard to age, body mass index, blood pressure status, plasma glucose level, plasma lipid profile, smoking status, average of ACBS time or family history of coronary heart disease. In ACE II group 5 patients had total venous graft occlusion, in ACE ID group 27 patients had total occlusion and in ACE DD group 20 patients had at least one graft total occlusion. The frequency of the venous graft occlusion about total venous grafts is 36% in the ACE II group, 49% in the ACE ID group, and 80% in the ACE DD group (P = .01). The ACE I/D gene polymorphism is associated with long-term survival of venous conduit. The ACE DD genotype or D allele influences the angiographic outcome of patients post-ACBS. These data suggest that routine determination of the ACE genotype may help identify patients who are at higher risk of venous graft failure after ACBS.

The stromelysin-1 5A/6A promoter polymorphism is a disease marker for the extent of coronary heart disease.

Background. Matrix metalloproteinases, such as stromelysin-1, are implicated in the pathogenesis of coronary artery disease (CAD) and acute myocardial infarction (MI). A 5A/6A promoter polymorphism can regulate the transcription of the stromelysin-1 gene in an allele-specific manner. Evidence has been presented that the 6A allele is associated with the progression of coronary heart disease (CHD). In contrast, the 5A allele may be linked to the risk of MI. Results. To analyse the relation of the 5A/6A polymorphism with the risk and severity of CHD and the risk of MI, a case-control study of 515 healthy controls and 1848 participants who underwent coronary angiography for diagnostic purposes was conducted. In the total sample, the mean CHD scores—according to Gensini—were different between 5A/6A genotypes: 5A5A homozygotes had the lowest, 6A6A genotypes the highest and 5A6A heterozygotes intermediate scores. These differences were even more pronounced when the participants were restricted to individuals with a high coronary risk profile (high apoB levels, high Lp(a) levels, high glucose levels, combinations of either high apoB and Lp(a) levels or high apoB, Lp(a) and glucose plasma levels). Mean values were used as cut points for high-risk populations, respectively. In contrast, the 5A allele was not associated with the risk of CHD or MI. Even when angiographically controlled individuals without MI were compared with MI patients in subpopulations of participants with no, single, double and triple vessel disease, the frequencies of the 5A/6A and/or the 5A5A genotypes were not higher in each subgroup, respectively. Conclusions. The present results do not confirm an association of the 5A allele with the risk of MI, observed in another investigation, but strengthen the hypothesis of earlier studies that the 6A allele is a disease marker for progression of coronary heart disease. Further investigations should evaluate whether 6A allele carriers and especially 6A homozygotes might benefit from a more aggressive therapy against CHD progression.

A new promoter polymorphism in the gene of lipopolysaccharide receptor CD14 is associated with expired myocardial infarction in patients with low atherosclerotic risk profile.

Recent findings suggest that inflammation plays a role in atherosclerosis and its acute complications. Cellular response in infections with Gram-negative bacteria is mediated by bacterial lipopolysaccharide (LPS), which activates monocytes to expression of cytokines, growth factors, and procoagulatory factors via LPS receptor CD14. Endothelial cells and smooth muscle cells are stimulated by a complex of LPS and soluble CD14. In this study, LPS receptor CD14 was analyzed to find genetic variants and check them for an association with coronary artery disease or myocardial infarction (MI). When screening the CD14 gene by single-strand conformation polymorphism analysis, a promoter polymorphism was detected and confirmed as a T-to-C exchange at position -159. We determined the genotypes of 2228 men who had undergone coronary angiography for diagnostic purposes. Within the total study group there was no significant association of either genotype with MI or coronary artery disease. However, in a subgroup with low coronary risk (normotensive nonsmokers), a relative risk for MI in probands homozygous for the T allele could be evaluated (OR, 1.6; 95% CI, 1.0 to 2.4; P<0.05). The association was even stronger in low-risk patients older than 62 years (OR, 3.8; 95% CI, 1.6 to 9.0; P<0.01). In conclusion, we describe a new CD14 promoter polymorphism that is associated with MI, especially in older patients with a low atherosclerotic risk profile.

The 4G4G Genotype of the Plasminogen Activator Inhibitor 4G/5G Gene Polymorphism Is Associated with Coronary Atherosclerosis in Patients at High Risk for this Disease

Disturbances in fibrinolytic activity, such as increase in plasminogen activator inhibitor (PAI) activity, have been linked with an increased risk for coronary artery disease (CAD) and myocardial infarction (MI). Since 4G4G homozygotes of an insertion/deletion (4G/5G) gene variation in the promoter of PAI-I have been shown to have increased levels of PAI-I, we analysed the relation of this gene polymorphism to CAD and MI in a population of 2565 participants who underwent coronary angiography for diagnostic purposes. In the total sample, the PAI-I 4G/4G genotype was associated with the presence, but not with the extent of CAD. However, in a subgroup of former and present smokers (n = 1782) or of individuals with a BMI above the mean value of 26.9 kg x m(-2) (n = 1269), the PAI-I 4G4G genotype was not only associated with the presence, but also with the extent of CAD, defined either by the number of diseased vessels or by the CHD score according to Gensini. This observation also applied to other high-risk groups of individuals with high BMI and hypertension (n = 869), of subjects with high fibrinogen plasma levels (>3.53 g x l(-1), mean value) and hypertension (n = 599) and of former and present smokers with high fibrinogen and hypertension (n = 452). An association of the gene variation with MI was not detected. The present data indicate that the 4G/4G genotype of the PAI-I gene polymorphism is an independent risk factor for coronary artery disease and that the additional presence of major cardiovascular risk factors accelerates the risk for this disease.

Positive Association of the β Fibrinogen H1/H2 Gene Variation to Basal Fibrinogen Levels and to the Increase in Fibrinogen Concentration during Acute Phase Reaction but not to Coronary Artery Disease and Myocardial Infarction

Fibrinogen has been demonstrated to be an independent risk factor of cardiovascular disease. The absence of the HaeIII cutting site (H2 allele) of an H1/H2 gene variation in the promoter region of the beta fibrinogen gene was associated with increased levels of fibrinogen. In the present study, the effects of the H1/H2 gene variation not only on plasma fibrinogen concentrations but also on coronary artery disease (CAD) and myocardial infarction (MI) were investigated in 923 individuals who underwent coronary angiography for diagnostic purposes. Relation of the H1/H2 genotype to fibrinogen plasma levels: A strong association was observed between the H1/H2 gene variation and fibrinogen levels. The differences in fibrinogen plasma levels between H2H2 and H1H1 homozygotes were almost threefold more pronounced within subjects with clinical chemical signs of an acute phase reaction (CRP > or = 7.5 mg/l) than within a subgroup of subjects without these signs (CRP < 7.5 mg/l) (median of CRP distribution: 7.5 mg/l). In 207 patients who underwent aortocoronary bypass surgery plasma fibrinogen levels were almost identical directly after surgery. Two days after operation fibrinogen increased to clearly higher levels in H2H2 homozygotes than in H1H2 and H1H1 genotypes, whereas almost the same maximal increases in fibrinogen concentrations were reached 3-4 days after surgery in all individuals. Relation of the H1/H2 genotype to CAD and MI. Whereas in the total population the plasma fibrinogen concentrations were strongly associated with smoking, CAD and MI, an association of the H1/H2 gene variation to CAD and MI was not detected. However, mean age at first MI of H2H2 individuals (62.9 years) was clearly higher than of H1H2 genotypes (56.9 years) and of H1H1 subjects (56.4 years). In addition, in a subgroup of individuals with a higher risk of MI by either high apoB and/or low apoA1 plasma levels the portion of MI patients was clearly smaller within H2H2 homozygotes than within H1H2 or H1H1 genotypes, although-also in these high risk groups-mean age at first MI of H2H2 individuals were higher than of the other two genotypes. Obviously, the H2 allele of the fibrinogen H1/H2 genotype does not only influence basal fibrinogen concentrations, but particularly also the extent of fibrinogen level increase during acute phase reaction. Whereas the fibrinogen plasma level is positively associated with coronary artery disease and myocardial infarction, the H2 allele-although exhibiting an association with elevated fibrinogen levels-was not positively associated with CAD and MI.

Evidence for the existence of a functional cardiac renin-angiotensin system in humans.

The presence of mRNA for the essential components of the renin-angiotensin system (RAS) has been found in animal and human hearts. The present study was designed to provide evidence for the existence of a (functional) cardiac RAS. Twenty-four patients with atypical chest pain undergoing coronary angiography for diagnostic purposes were investigated. The cardiac production rate of angiotensins was estimated by measurement of the cardiac extraction of 125I-angiotensin I and 125I-angiotensin II associated with the determination of endogenous angiotensins in aortic and coronary sinus blood in normal, low, or high sodium diets. In a normal sodium diet, angiotensin I and II aorta-coronary sinus gradients were tendentially negative (-1.8 +/- 2.5 and -0.9 +/- 1.7 pg/mL, respectively), and the amounts of angiotensin I and II added by cardiac tissues were 6.5 +/- 3.1 and 2.7 +/- 1.3 pg/mL, respectively. The low sodium diet caused a significant increase in both plasma renin activity (PRA) and angiotensin I concentration in aortic but not in coronary sinus blood, resulting in a more negative aorta-coronary sinus gradient (-9.7 +/- 3.1 pg/mL, P < .01). Angiotensin formation by PRA in blood during transcardiac passage increased (P < .001), whereas angiotensin I formed by cardiac tissues decreased dramatically. Accordingly, in the low sodium diet, 125I-angiotensin II extraction did not change, the cardiac fractional conversion rate of 125I-angiotensin I to 125I-angiotensin II notably decreased (P < .01), and angiotensin II formation by cardiac tissues was undetectable. The high sodium diet caused a decrease in PRA and no changes in cardiac extraction of radiolabeled angiotensins; conversely, angiotensin I formed by cardiac tissues, cardiac Ang I fractional conversion rate, and angiotensin II formed during transcardiac passage significantly (P < .01 for all) increased. These results provide evidence for the existence of a functional cardiac RAS independent of but related to the circulating RAS.

Gene Polymorphism but not Catalytic Activity of Angiotensin I–Converting Enzyme Is Associated With Coronary Artery Disease and Myocardial Infarction in Low-Risk Patients

An insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene has been postulated to be associated with an increased risk of coronary artery disease (CAD) and myocardial infarction (MI). In the present study, the effects of I/D gene polymorphism and of ACE activity on CAD and MI were investigated in 920 individuals who underwent coronary angiography for diagnostic purposes. In the total population and in all CAD and MI groups, a strong association was observed between the gene polymorphism and ACE activities; DD genotypes had approximately twofold higher ACE activities than II genotypes. Although classic risk and protective factors of CAD and MI were identified, associations of ACE genotype and of ACE activity to CAD and MI were not detected in the total population. Among subjects defined to be at lower risk of MI by low body mass index and low cigarette consumption, however, an association of the DD genotype with MI was found. Exclusion of individuals with triglyceride levels > 140 mg/dL and cholesterol levels > 180 mg/dL revealed an association of the DD genotype with CAD. An association of the ACE activity with CAD or MI could not be demonstrated in any of the low-risk populations. Increased ACE activity obviously is not a risk factor of CAD or MI. The importance of the deletion polymorphism for the development of CAD and MI may be restricted to individuals without classic risk factors.