scholarly journals Characterization of residual lipid-rich plaques despite achieving LDL-C <1.8mmol/l with a statin in patients with coronary artery disease: insights from the REASSURE-NIRS registry

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
S Kitahara ◽  
Y Kataoka ◽  
T Iwai ◽  
K Sawada ◽  
H Matama ◽  
...  

Abstract Introduction Recent studies have demonstrated favourable modification of lipidic plaque materials under achieving LDL-C &lt;1.8mmol/l with a statin, which potentially accounts for its clinical benefit. However, coronary events still occur even under optimal LDL-C management. This may suggest the presence of residual lipid-rich coronary plaque despite on-treatment LDL-C &lt;1.8mmol/l. Given that near-infrared spectroscopy (NIRS) enables quantitative evaluation of lipidic plaque in vivo, we employed this imaging modality to investigate characteristics and drivers of residual lipid-rich plaques in statin-treated patients with coronary artery disease (CAD) who achieved LDL-C &lt;1.8mmol/l. Purpose To clarify the frequency, clinical demographics and factors associated with residual lipid-rich plaques under LDL-C &lt;1.8mmol/l. Methods The REASSURE-NIRS registry is an on-going multi-center registry to enroll CAD subjects receiving NIRS/intravascular ultrasound-guided PCI. The current analysis included 133 statin-treated stable CAD patients with on-treatment LDL-C &lt;1.8mmol/l from August 2015 to December 2020. The maximum 4-mm lipid core burden index (maxLCBI4mm) at culprit lesions was measured by NIRS imaging prior to PCI. Clinical characteristics were compared in patients with and without maxLCBI4mm ≥400 at culprit lesions. Results In the current study, 45% (=58/128) of study subjects exhibited maxLCBI4mm ≥400 at culprit lesions under on-treatment LDL-C &lt;1.8 mmol/l. They were more likely to be female, whereas there were no differences in age and the frequency of risk factors. Most of study subjects received moderate to high-intensity statin (p=0.79), and over one-fourth of them were treated with ezetimibe (p=0.56). Under these lipid-lowering therapies, LDL-C level was significantly higher in patients with maxLCBI4mm ≥400 (Table). Additionally, a lower frequency of LDL-C &lt;1.4mmol/l was observed in those exhibiting maxLCBI4mm ≥400 (31.0 vs. 45.7%), but this comparison failed to meet statistical significance (p=0.09). Despite LDL-C control with a statin, deterioration of coronary flow after PCI with stent implantation more frequently occurred in patients with maxLCBI4mm ≥400 (Table). Multivariate analysis demonstrated that an independent factor associated with maxLCBI4mm ≥400 was LDL-C level (OR=1.05; 95% CI=1.00–1.10, p=0.03), but not other lipid and clinical parameters. Conclusion Almost half of CAD subjects who achieved LDL-C level &lt;1.8mmol/l still exhibited the accumulation of lipidic plaque materials within vessel wall. Given that LDL-C level was associated with this residual lipid-rich plaque features, our findings support current ESC-guideline recommended LDL-C goal (&lt;1.4mmol/l) to optimize the secondary prevention in stable CAD patients. Funding Acknowledgement Type of funding sources: None.

2021 ◽  
Vol 23 (1) ◽  
pp. 25-27
Author(s):  
Olga Iu. Mironova ◽  
◽  
Polina G. Lakotka ◽  
Viktor V. Fomin ◽  
◽  
...  

Aim. To assess the prevalence of contrast-induced acute kidney injury (CI-AKI) in patients with stable coronary artery disease (CAD) and hyperuricemia. Materials and methods. Patients with stable CAD receiving optimal medical therapy and with indications to coronary angiography and possible coronary angioplasty were included in an observational open prospective cohort study. The protocol of the study was registered in clinicaltrials.gov with ID NCT04014153. We conducted a sub-analysis of the group of patients with hyperuricemia (uric acid level >7 mg/dl). Results. We included 1023 patients with stable CAD. 32 patients suffered from hyperuricemia. The rate of CI-AKI in this group was 6.25% (2 patients), that was lower than in patients with normal levels of uric acid (13.1%). The difference was not statistically significant probably due to the small number of patients with hyperuricemia. The patients with hyperuricemia had proteinuria 3 times more frequently, than patients without, the rate of diabetes mellitus was 7% higher as well as anemia by 4.5% but didn’t reach statistical significance. Conclusion. The rate of CI-AKI in patients with hyperuricemia was twice lower than in patients with normal levels of uric acid. More research needs to be conducted in patients with metabolic syndrome in larger groups. Keywords: contrast-induced acute kidney injury, contrast-associated acute kidney injury, contrast-induced nephropathy, coronary artery disease, percutaneous coronary intervention, contrast, hyperuricemia For citation: Mironova OIu, Lakotka PG, Fomin VV. Hyperuricemia as a risk factor of contrast-induced acute kidney injury. Consilium Medicum. 2021; 23 (1): 25–27. DOI: 10.26442/20751753.2021.1.200572


2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Yang Ling ◽  
Shengxing Tang ◽  
Yuhan Cao ◽  
Cong Fu

Background. Increasing evidence states that the plasma lipoprotein-associated phospholipase A2 (Lp-PLA2) levels and apolipoprotein particles are regarded as the risk maker for cardiovascular heart disease. Nevertheless, the issue about whether Lp-PLA2 is associated with apolipoprotein particles in individuals who have been diagnosed as stable coronary artery disease (CAD) remains largely unexplored. Method. All 569 participants engaged in this research, who never took lipid-lowering drugs, had been divided into groups by the coronary angiography (CAG), namely, stable CAD: n=291; non-CAD: n=278. The results concerning Lp-PLA2 levels were calculated by Elisa Kit, while apolipoprotein particles were measured by the department of laboratory. Results. The plasma concentration of Lp-PLA2 was remarkably higher in stable CAD group than the non-CAD group (136.0±60.5 ng/mL vs. 113.2±65.6 ng/mL, P<0.001). Pearson correlation analyses explained the plasma Lp-PLA2 concentration was correlated with apoB (r=0.390, P<0.001) and apoB/apoA1 (r=0.450, P<0.001), not associated with apoA1 (r=−0.099, P=0.101). Conversely, the association remains unobserved among non-CAD patients except apoA1. Moreover, multiple linear regression revealed the relations between Lp-PLA2 concentrations and apoB (β=0.390, P<0.001), as well as apoB/apoA1 (β=0.450, P<0.001), but not apoA1 (β=−0.099, P=0.121). After adjustment for several risk factors regarding CAD, like hypertension, gender, smoking, age, and diabetes mellitus, there had still been positive associations between the Lp-PLA2 concentration and apoB (β=0.364, P<0.001), as well as apoB/apoA1 (β=0.390, P<0.001). Conclusion. The plasma levels of Lp-PLA2 provide positively a key link with apoB, apoB/apoA-1 among stable CAD, denoting the communication between Lp-PLA2 and apolipoprotein particles in the state of CAD.


2009 ◽  
Vol 101 (01) ◽  
pp. 157-164 ◽  
Author(s):  
Magnus Settergren ◽  
Felix Böhm ◽  
John Pernow ◽  
Paul Hjemdahl ◽  
Rickard Malmström

SummaryIn addition to lowering cholesterol, statins may reduce platelet activity and exert beneficial non-lipid (pleiotropic) effects. We evaluated the effects of two different simvastatin based treatment regimens on platelet reactivity in patients with dysglycemia and coronary artery disease (CAD). Thirty-two patients with type 2 diabetes or impaired glucose tolerance and stable CAD received six weeks of double-blind treatment with simvastatin 80 mg daily (S80; n=16) or ezetimibe 10 mg and simvastatin 10 mg daily (E10/S10; n=16). Total and low-density lipoprotein (LDL) cholesterol, and high sensitivity C-reactive protein (CRP) decreased similarly in the two groups. LDL (mM) decreased from 3.2 ± 0.6 to 1.7 ± 0.7 with E10/S10 and from 3.0 ± 1.0 to 1.4 ± 0.5 with S80 treatment. Platelet function was evaluated by whole blood flow cytometry and turbidimetric aggregometry with agonist stimulation ex vivo before and after treatment. Neither treatment affected basal or adenosine diphosphate (ADP)- or thrombin-induced platelet P-selectin expression, or fibrinogen binding, or platelet-leukocyte aggregation. Similarly, neither treatment affected ADP-induced platelet aggregation. In conclusion, lipid lowering treatment with high dose simvastatin or low dose simvastatin plus ezetimibe did not exert any substantial inhibitory effects on the basal or agonist-stimulated activity of circulating platelets in patients with stable CAD and type 2 diabetes or impaired glucose tolerance.


2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Benjamin Valente-Acosta ◽  
Manuel Alfonso Baños-González ◽  
Marco Antonio Peña-Duque ◽  
Marco Antonio Martínez-Ríos ◽  
Leslie Quintanar-Trejo ◽  
...  

Background. Thrombin has been implicated as a key molecule in atherosclerotic progression. Clinical evidence shows that thrombin generation is enhanced in atherosclerosis, but its role as a risk factor for coronary atherosclerotic burden has not been proven in coronary artery disease (CAD) stable patients.Objectives. To evaluate the association between TAT levels and homocysteine levels and the presence of coronary artery disease diagnosed by coronary angiography in patients with stable CAD.Methods and Results. We included 95 stable patients admitted to the Haemodynamics Department, including 63 patients with significant CAD and 32 patients without. We measured the thrombin-antithrombin complex (TAT) and homocysteine concentrations in all the patients. The CAD patients exhibited higher concentrations of TAT (40.76 μg/L versus 20.81 μg/L,p=0.002) and homocysteine (11.36μmol/L versus 8.81μmol/L,p<0.01) compared to the patients without significant CAD. Specifically, in patients with CAD+ the level of TAT level was associated with the severity of CAD being 36.17 ± 24.48 μg/L in the patients with bivascular obstruction and 42.77 ± 31.81 μg/L in trivascular coronary obstruction,p=0.002.Conclusions. The level of in vivo thrombin generation, quantified as TAT complexes, is associated with the presence and severity of CAD assessed by coronary angiography in stable CAD patients.


2006 ◽  
Vol 91 (7) ◽  
pp. 2542-2547 ◽  
Author(s):  
Stefan Pilz ◽  
Hubert Scharnagl ◽  
Beate Tiran ◽  
Ursula Seelhorst ◽  
Britta Wellnitz ◽  
...  

Abstract Context: Free fatty acids (FFAs) are associated with several cardiovascular risk factors and exert harmful effects on the myocardium. Objective: The aim of our study was to elucidate the relationship between FFAs and mortality in subjects who underwent coronary angiography. Design, Setting, and Participants: Ludwigshafen Risk and Cardiovascular Health is a prospective cohort study of Caucasians who had undergone coronary angiography at baseline (1997–2000). During a median time of follow-up of 5.38 yr, 513 deaths had occurred among 3315 study participants with measured FFAs. Main Outcome Measure: Hazard ratios for mortality according to FFA levels were measured. Results: At the fourth quartile of FFAs, fully adjusted hazard ratios for death from any cause and cardiovascular causes were 1.58 (P = 0.002) and 1.83 (P = 0.001), respectively. In persons with angiographic coronary artery disease (CAD), stable CAD, and unstable CAD, the predictive value of FFAs was similar to that in the entire cohort, but the association did not attain statistical significance in persons without CAD analyzed separately. FFA levels were not related to the presence of angiographic CAD but were elevated in subjects with unstable CAD, compared with probands with stable CAD. Furthermore, FFAs increased with the severity of heart failure and were positively correlated with N-terminal pro-B-type natriuretic peptide (P &lt; 0.001). Conclusions: FFA levels independently predict all-cause and cardiovascular mortality in subjects with angiographic CAD. A possible diagnostic use of FFAs warrants further studies, but our results may underline the importance of therapeutic approaches to influence FFA metabolism.


2020 ◽  
Vol 18 (5) ◽  
pp. 523-530 ◽  
Author(s):  
Konstantinos Maniatis ◽  
Gerasimos Siasos ◽  
Evangelos Oikonomou ◽  
Manolis Vavuranakis ◽  
Marina Zaromytidou ◽  
...  

Background: Osteoprotegerin and osteopontin have recently emerged as key factors in both vascular remodelling and atherosclerosis progression. Interleukin-6 (IL-6) is an inflammatory cytokine with a key role in atherosclerosis. The relationship of osteoprotegerin, osteopontin, and IL-6 serum levels with endothelial function and arterial stiffness was evaluated in patients with coronary artery disease (CAD). Methods: We enrolled 219 patients with stable CAD and 112 control subjects. Osteoprotegerin, osteopontin and IL-6 serum levels were measured using an ELISA assay. Endothelial function was evaluated by flow-mediated dilation (FMD) in the brachial artery and carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness. Results: There was no significant difference between control subjects and CAD patients according to age and sex. Compared with control subjects, CAD patients had significantly impaired FMD (p<0.001) and increased PWV (p=0.009). CAD patients also had significantly higher levels of osteoprotegerin (p<0.001), osteopontin (p<0.001) and IL-6 (p=0.03), compared with control subjects. Moreover, IL-6 levels were correlated with osteoprotegerin (r=0.17, p=0.01) and osteopontin (r=0.30, p<0.001) levels. FMD was correlated with osteoprotegerin levels independent of possible confounders [b coefficient= - 0.79, 95% CI (-1.54, -0.05), p=0.04]. Conclusion: CAD patients have increased osteoprotegerin, osteopontin and IL-6 levels. Moreover, there is a consistent association between osteoprotegerin and osteopontin serum levels, vascular function and inflammation in CAD patients. These findings suggest another possible mechanism linking osteoprotegerin and osteopontin serum levels with CAD progression through arterial wall stiffening and inflammation.


2021 ◽  
Vol 10 (13) ◽  
pp. 2759
Author(s):  
Krzysztof Bryniarski ◽  
Pawel Gasior ◽  
Jacek Legutko ◽  
Dawid Makowicz ◽  
Anna Kedziora ◽  
...  

Myocardial infarction with non-obstructive coronary artery disease (MINOCA) is a working diagnosis for patients presenting with acute myocardial infarction without obstructive coronary artery disease on coronary angiography. It is a heterogenous entity with a number of possible etiologies that can be determined through the use of appropriate diagnostic algorithms. Common causes of a MINOCA may include plaque disruption, spontaneous coronary artery dissection, coronary artery spasm, and coronary thromboembolism. Optical coherence tomography (OCT) is an intravascular imaging modality which allows the differentiation of coronary tissue morphological characteristics including the identification of thin cap fibroatheroma and the differentiation between plaque rupture or erosion, due to its high resolution. In this narrative review we will discuss the role of OCT in patients presenting with MINOCA. In this group of patients OCT has been shown to reveal abnormal findings in almost half of the cases. Moreover, combining OCT with cardiac magnetic resonance (CMR) was shown to allow the identification of most of the underlying mechanisms of MINOCA. Hence, it is recommended that both OCT and CMR can be used in patients with a working diagnosis of MINOCA. Well-designed prospective studies are needed in order to gain a better understanding of this condition and to provide optimal management while reducing morbidity and mortality in that subset patients.


2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
KA Krychtiuk ◽  
M Lenz ◽  
P Hohensinner ◽  
K Distelmaier ◽  
L Schrutka ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): FWF Background and aims Proprotein convertase subtilisin/kexin type-9 (PCSK9) is an enzyme promoting the degradation of low-density lipoprotein receptors (LDL-R) in hepatocytes. Inhibition of PCSK9 has emerged as a novel target for lipid-lowering therapy. Monocytes are crucially involved in the pathogenesis of atherosclerosis and can be divided into three subsets. The aim of this study was to examine whether circulating levels of PCSK9 are associated with monocyte subsets. Methods We included 69 patients with stable coronary artery disease. PCSK9 levels were measured and monocyte subsets were assessed by flow cytometry and divided into classical monocytes (CD14++CD16-; CM), intermediate monocytes (CD14++CD16+; IM) and non-classical monocytes (CD14 + CD16++; NCM). Results Mean age was 64 years and 80% of patients were male. Patients on statin treatment (n = 55) showed higher PCSK9-levels (245.4 (206.0-305.5) ng/mL) as opposed to those without statin treatment (186.1 (162.3-275.4) ng/mL; p = 0.05). In patients on statin treatment, CM correlated with circulating PCSK9 levels (R = 0.29; p = 0.04), while NCM showed an inverse correlation with PCSK9 levels (R=-0.33; p = 0.02). Patients with PCSK9 levels above the median showed a significantly higher proportion of CM as compared to patients with PCSK-9 below the median (83.5 IQR 79.2-86.7 vs. 80.4, IQR 76.5-85.2%; p = 0.05). Conversely, PCSK9 levels &gt;median were associated with a significantly lower proportion of NCM as compared to those with PCSK9 &lt;median (10.2, IQR 7.3-14.6 vs. 14.3, IQR 10.9-18.7%; p = 0.02). In contrast, IM showed no association with PCSK-9 levels. Conclusions We hereby provide a novel link between PCSK9 regulation, innate immunity and atherosclerotic disease in statin-treated patients.


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