scholarly journals Inflammatory risk factors are not associated with coronary artery calcification in patients with myeloproliferative philadelphia-negative neoplasms

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
C N Solli ◽  
S Chamat-Hedemand ◽  
H Elming ◽  
A Ngo ◽  
V Skov ◽  
...  

Abstract Background Myeloproliferative Philadelphia-negative Neoplasms (MPNs) are hematological cancers associated with chronic inflammation and endothelial dysfunction, conditions that may lead to development of premature atherosclerosis. Purpose To investigate whether biomarkers of inflammation and endothelial dysfunction are associated with the degree of atherosclerotic burden, measured by Coronary Artery Calcium Score (CACS), in patients with MPNs. Methods Patients with a validated MPN diagnosis; essential thrombocythemia (ET), polycythemia vera (PV) or myelofibrosis (MF), were recruited between 2016 and 2018 from one single specialized hematologic center. Patients filled out a standardized questionnaire on medical history, current medication, alcohol and smoking habits and family medical history. They were examined by cardiac computed tomography (CT), Endothelial Peripheral Arterial Tone (EndoPAT), and a range of blood analyses. The atherosclerotic burden was evaluated by CACS. High sensitivity C-reactive protein (hs-CRP) and Neutrophil:Lymphocyt Ratio (NLR) were used as indicators of chronic inflammation. EndoPAT was applied to evaluate endothelial dysfunction, which is linked to development of atherosclerosis. The JAK2V617F-mutation is a common gene mutation in MPN-patients. It affects the gene coding the Janus kinase 2 (JAK2) protein, and can be detected by qPCR of peripheral blood or bone marrow. The JAK2V617F-mutation is a risk factor associated with both chronic inflammation and endothelial dysfunction. Multivariable logistic regression analyses were used to identify associations between potential risk factors and a higher CACS value. Results Among 170 included patients, 161 patients completed cardiac CT (mean age 65.5 (SD 10.5), 52% men). Baseline data is presented in Table 1. JAK2V617F-mutation was found in 137 (85%) patients, 53 patients (35%, n=152) had hs-CRP>2.0 mg/L, 107 (67%, n=160) had NLR>2.15 and 32 (21%, n=154) had an abnormal EndoPAT. Overall, 66 patients (41%) had a CACS>100, with no significant difference between ET (41%), PV (42%) and MF (50%) (p=0.3). In patients with a history of ischemic heart disease (IHD), 92% had CACS>100, compared to 37% in patients without prior IHD (p=0.0003). Five independent factors associated with a CACS>100 were identified; age (OR: 1.3 [95% CI 1.1–1.4]), male sex (OR: 15.2 [95% CI 4.0–57.7]), prior IHD (OR: 15.9 [95% CI 1.2–202.4]), smoking (OR: 3.3 [95% CI 1.1–10.1]), and abnormal EndoPAT (OR: 4.8 [95% CI 1.1–20.0]) (Figure 1). Hs-CRP, NLR and JAK2V617F-mutation status were not significantly associated with CACS >100. Conclusion In this cohort of patients with MPNs, markers of chronic inflammation like hs-CRP and NLR were not associated with higher CACS, nor was the JAK2V617F-mutation. Traditional risk factors of cardiovascular disease seem to be sufficient to identify MPN patients with increased atherosclerotic burden, but measuring endothelial dysfunction provides additional information. FUNDunding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): Department of Cardiology, Zealand University Hospital, Region Zealand, Denmark Table 1. Baseline characteristics Figure 1. Odds ratio for CACS >100

2021 ◽  
Vol 8 ◽  
Author(s):  
Jun Wang ◽  
Wei Liu ◽  
Huaqiang Chen ◽  
Chengzhe Liu ◽  
Meng Wang ◽  
...  

Background: Heart rate variability (HRV) was proposed as a noninvasive biomarker to stratify the risk of cardiovascular disease. However, it remains to be determined if HRV can be used as a surrogate for coronary artery physiology as analyzed by quantitative flow ratio (QFR) in patients with new-onset unstable angina pectoris (UAP).Methods: A total of 129 consecutive patients with new-onset UAP who underwent 24-h long-range 12-channel electrocardiography from June 2020 to December 2020 were included in this study. HRV, coronary angiography, and QFR information was retrieved from patient medical records, the severity of coronary lesions was evaluated using the Gensini score (GS), and total atherosclerotic burden was assessed using the three-vessel contrast QFR (3V-cQFR) calculated as the sum of cQFR in three vessels.Results: Multivariate logistic analysis showed that low-frequency power (LF) and high-sensitivity C-reactive protein (hs-CRP) were directly correlated with functional ischemia of target vessel, which were inversely correlated with total atherosclerotic burden as assessed by 3V-cQFR. Moreover, incorporation of the increase in LF into the existing model that uses clinical risk factors, GS, and hs-CRP significantly increased the discriminatory ability for evaluating coronary artery physiology of target vessel.Conclusions: LF and hs-CRP are independently associated with functional ischemia in patients with new-onset UAP. The relative increase of LF and hs-CRP could add value to the use of classical cardiovascular risk factors to predict the functional severity of coronary artery stenosis. Our results suggest a potential association between the autonomic nervous system, inflammation, and coronary artery physiology.


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.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Karina P Martins ◽  
Sandhi Barreto ◽  
Daniel Bos ◽  
JESIANA PEDROSA ◽  
Douglas Mesquita ◽  
...  

Introduction: Epicardial fat has been related to coronary artery disease (CAD) independent of visceral or subcutaneous fat. The mechanism responsible for this association has not yet been elucidated. Our objective was to evaluate the association between automatically measured epicardial fat volume (EFV), cardiovascular risk factors, coronary artery calcium (CAC) and endothelial function in participants of ELSA-Brasil. Methods and Results: The sample comprised 470 (mean age 55± 8y, 52.3% men) participants from ELSA-MG, one of the Investigation Centers of the cohort, who had valid computed tomography scans and endothelial function evaluated by peripheral arterial tonometry (PAT). The mean EFV was 111 (IQ 86-144) mL. CAC=0 was detected in 55% of participants. In the multivariable analyses between cardiovascular risk factors and EFV, the following associations were observed with higher EFV: female sex; and increased age, waist circumference and triglycerides (p <0.001 for all). In multivariable analyses, higher EFV remained associated with worse endothelial function - basal pulse amplitude (q2=1.22, CI95% 1.07-1.40, p=0.004; q3=1.50, CI95% 1.30-1.74, p<0.001; q4=1.50, CI95% 1.28-1.79, p<0.001) and PAT ratio (q2=0.87, CI95% 0.81-0.95, p<0.001; q3=0.86, CI95% 0.79-0.94, p<0.001; q4=0.80, CI95% 0.73-0.89, p<0.001), but not with CAC. Conclusions: Higher EFV was associated with impaired endothelial function, but not with higher CAC. Our results suggest that the mechanism by which epicardial fat deposits relates to CAD may be different from the pathway of CAC, which relates to calcified plaques. A possible mechanism may be through the enhancement of endothelial dysfunction, microvascular disease and predominantly lipidic non-calcified plaques.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Alejandro Recio-Mayoral ◽  
Justin C Mason ◽  
Juan C Kaski ◽  
Michael B Rubens ◽  
Olivier A Harari ◽  
...  

Premature coronary atherosclerosis, which is actually seen as an active inflammatory process, is an established complication of systemic autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). We hypothesized that exposure to chronic inflammation, even in the absence of classical cardiovascular risk factors (CVRF), could result in coronary microvascular dysfunction (CMD), an early marker of coronary atherosclerosis. By means of positron emission tomography in combination with oxygen-15 labeled water, myocardial blood flow (MBF) was measured at rest and during iv adenosine infusion (140 μg/kg/min) in 13 SLE and 12 RA patients (mean [±SD] age 44±10 years) without CVRF. All patients underwent coronary angiography using multi-slice (64 slices) computed tomography and only those with none or trivial coronary artery disease (<30% luminal stenosis) were included. A group of 25 age- and gender-matched controls were also studied. There were no differences between patients and controls regarding body-mass index, blood pressure and lipid parameters. RA and SLE patients showed similar mean disease duration (16±11 and 11±7 years, respectively; p=0.12). Resting MBF was similar in patients and controls (1.25±0.27 vs 1.15±0.24 ml/min/g, p=0.15). However, during adenosine stress patients had lower MBF compared with controls (2.94±0.83 vs 4.11±0.84 ml/min/g, p<0.001). As result, coronary flow reserve (CFR; adenosine/resting MBF) was significantly reduced in patients (2.44±0.78) compared with controls (3.81±1.07; p<0.001). Seven patients showed ischemic electrocardiographic changes during adenosine and had a more severe reduction in CFR (1.76±0.81) and more years of disease (21±7 years) compared with those patients without ischemic changes (CFR 2.49±0.54; p=0.006; duration of disease 14±5 years; p=0.03). CFR was inversely correlated with years of disease (r=−0.65, p<0.001), but not with corticosteroid cumulative dose (r=0.20, p=0.39). Chronic inflammation in the absence of traditional CVRF is characterized by severe CMD. This may represent an early marker of disease which precedes and contributes to premature coronary artery disease in patients with RA and SLE.


2017 ◽  
Vol 2017 ◽  
pp. 1-7
Author(s):  
Da Shang ◽  
Qionghong Xie ◽  
Bin Shang ◽  
Min Zhang ◽  
Li You ◽  
...  

Background.Coronary artery calcification (CAC) contributes to high risk of cardiocerebrovascular diseases in dialysis patients. However, the risk factors for CAC initiation in peritoneal dialysis (PD) patients are not known clearly.Methods.Adult patients with baseline CaCS = 0 and who were followed up for at least 3 years or until the conversion from absent to any measurable CAC detected were included in this observational cohort study. Binary logistic regression was performed to identify the risk factors for CAC initiation in PD patients.Results.70 patients recruited to our study were split into a noninitiation group (n=37) and an initiation group (n=33) according to the conversion of any measurable CAC during their follow-up or not. In univariate analysis, systolic blood pressure, serum phosphorus, fibrinogen, hs-CRP, serum creatinine, and triglycerides were positively associated with the initiation of CAC, while the high density lipoprotein and nPCR did the opposite function. Multivariate analysis revealed that hyperphosphatemia and hs-CRP were the independent risk factors for CAC initiation after adjustments.Conclusions.Hyperphosphatemia and hs-CRP were the independent risk factors for CAC initiation in PD patients. These results suggested potential clinical strategies to prevent the initiation of CAC in PD patients.


Author(s):  
Charalambos Vlachopoulos ◽  
Nikolaos Ioakeimidis

Erectile dysfunction (ED) is defined as the inability to obtain or maintain a penile erection to support satisfactory sexual performance. It is considered an early manifestation of generalized vascular disease and recognized as a marker of increased cardiovascular risk both acutely and chronically by predicting all-cause mortality, cardiovascular mortality, coronary events, stroke, and peripheral artery disease in men with and without known coronary artery disease. The link between ED and cardiovascular disease might reside in the interaction between androgen level, chronic inflammation, and cardiovascular risk factors that determine endothelial dysfunction and atherosclerosis both in the penile and coronary circulation. Because penile artery size is smaller compared with coronary arteries, the same degree of endothelial dysfunction and atherosclerotic burden causes a more significant reduction of blood flow in erectile tissues compared with that in coronary circulation. From a clinical standpoint, because ED may precede cardiovascular disease, it can be used as an early marker to identify men at higher risk of cardiovascular events. The average 3-year time period between the onset of ED symptoms and a cardiovascular event offers the opportunity for detailed cardiological assessment and intensive treatment of risk factors.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Caselli ◽  
S Rocchiccioli ◽  
A Rosendael ◽  
R Buechel ◽  
A Teresinska ◽  
...  

Abstract Background Leptin is an adipokine involved in energy homeostasis and has been related with established vascular risk factors. However, studies on the association of leptin plasma levels with coronary artery disease (CAD) have yielded conflicting results. Purpose Aim of the present study was to evaluate the association between leptin plasma levels and presence, severity and progression of coronary atherosclerosis in patients with suspected stable CAD. Methods In a cohort of 257 patients with symptoms of stable CAD enrolled in the SMARTool study, coronary computed tomography angiography (CTA), plasma leptin levels and clinical and bio-humoral CAD risk profile (including glucose, lipid and inflammation variables) were obtained at enrolment and after 6±1yrs of follow-up. Sixty-four patients were revascularized and the remaining 193 represent the population for the present study. CTA findings were categorised as no-minimal CAD (<30% stenosis), non-obstructive CAD (30%-50% stenosis) and obstructive CAD (≥50% stenosis in at least one major coronary vessel). A CTA risk score (based on plaque extent, severity, composition, and location) was calculated at baseline and at follow-up to assess coronary atherosclerotic burden and its progression (Δ CTA score≥5). Results CTA findings showed obstructive CAD in 11% of patients at baseline and in 15% at follow-up (p<0.0001). CTA risk score, was 8.03±7.80 at baseline and increased to 10.33±8.17 at follow-up (p<0.0001) with CAD progression in 20% of patients. Leptin plasma levels were inversely related with CTA findings both at baseline and follow-up (Figure). In a Cox model, baseline plasma leptin was an independent predictor of CAD progression, after adjustment for clinical risk factors, biomarkers, and treatment (HR 0.572, 95% CI 0.393–0.834, P=0.0037). Figure 1 Conclusion Plasma leptin is inversely associated with coronary atherosclerotic burden and disease progression in patients with stable CAD. This association is independent of known factors affecting leptin levels. These results could prompt further investigations on the pathophysiological mechanisms of this association. Acknowledgement/Funding EU H2020 research and innovation program under grant agreement No 689068


ESC CardioMed ◽  
2018 ◽  
pp. 1016-1019
Author(s):  
Charalambos Vlachopoulos ◽  
Nikolaos Ioakeimidis

Erectile dysfunction (ED) is defined as the inability to obtain or maintain a penile erection to support satisfactory sexual performance. It is considered an early manifestation of generalized vascular disease and recognized as a marker of increased cardiovascular risk both acutely and chronically by predicting all-cause mortality, cardiovascular mortality, coronary events, stroke, and peripheral artery disease in men with and without known coronary artery disease. The link between ED and cardiovascular disease might reside in the interaction between androgen level, chronic inflammation, and cardiovascular risk factors that determine endothelial dysfunction and atherosclerosis both in the penile and coronary circulation. Because penile artery size is smaller compared with coronary arteries, the same degree of endothelial dysfunction and atherosclerotic burden causes a more significant reduction of blood flow in erectile tissues compared with that in coronary circulation. From a clinical standpoint, because ED may precede cardiovascular disease, it can be used as an early marker to identify men at higher risk of cardiovascular events. The average 3-year time period between the onset of ED symptoms and a cardiovascular event offers the opportunity for detailed cardiological assessment and intensive treatment of risk factors.


2018 ◽  
pp. bjsports-2018-099840 ◽  
Author(s):  
Hélder Dores ◽  
Pedro de Araújo Gonçalves ◽  
José Monge ◽  
Rogério Costa ◽  
Luis Tátá ◽  
...  

ObjectivePreparticipation evaluation of veteran athletes should focus on accurate cardiovascular (CV) risk stratification and subclinical detection of coronary artery disease (CAD), which is the main cause of sudden cardiac death in this population. We aimed to investigate the effectiveness of current preparticipation methodology used to identify veteran athletes with high coronary atherosclerotic burden.MethodsA total of 105 asymptomatic male athletes aged ≥40 years old, with low to moderate CV risk (Systematic Coronary Risk Estimation <5%) who trained ≥4 hours/week for at least 5 years, were studied. The screening protocol included clinical evaluation, ECG, transthoracic echocardiogram and exercise testing. Cardiac CT was performed to detect CAD, defined as a high atherosclerotic burden according to coronary artery calcium score and coronary CT angiography.ResultsThe majority of the athletes (n=88) engaged in endurance sports, with a median volume of exercise of 66 (44; 103) metabolic equivalent task score/hour/week. Exercise testing was abnormal in 13 (12.4%) athletes, 6 (5.7%) with electrocardiographic criteria for myocardial ischaemia and 7 (6.7%) with exercise-induced ventricular arrhythmias. A high coronary atherosclerotic burden was present in 27 (25.7%) athletes, of whom 11 (40.7%) had CV risk factors and 6 had abnormal exercise tests, including 3 who were positive for myocardial ischaemia.ConclusionsConventional methodology used in preparticipation evaluation of veteran athletes, based on clinical CV risk factors and exercise testing, was poor at identifying significant subclinical CAD. The inclusion of more objective markers, particularly data derived from cardiac CT, is promising for more accurate CV risk stratification of these athletes.


Sign in / Sign up

Export Citation Format

Share Document