scholarly journals Plasma Heme Oxygenase-1 Levels in Patients with Coronary and Peripheral Artery Diseases

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Yoshimi Kishimoto ◽  
Susumu Ibe ◽  
Emi Saita ◽  
Kenji Sasaki ◽  
Hanako Niki ◽  
...  

Aims. Heme oxygenase-1 (HO-1) is an intracellular enzyme that catalyzes the oxidation of heme to generate CO, biliverdin, and iron. Since these products have antiatherogenic properties, HO-1 may play a protective role against the progression of atherosclerosis. However, plasma HO-1 levels in patients with atherosclerotic diseases, such as coronary artery disease (CAD) and peripheral artery disease (PAD), have not been clarified yet. Methods. We investigated plasma HO-1 levels by ELISA in 410 consecutive patients undergoing elective coronary angiography who also had an ankle-brachial index (ABI) test for PAD screening. Results. Of the 410 study patients, CAD was present in 225 patients (55%) (1-vessel (1-VD), n=91; 2-vessel (2-VD), n=66; 3-vessel disease (3-VD), n=68). PAD (ABI < 0.9) was found in 36 (9%) patients. Plasma HO-1 levels did not differ between 225 patients with CAD and 185 without CAD (median 0.44 versus 0.35 ng/mL), but they were significantly lower in 36 patients with PAD than in 374 without PAD (0.27 versus 0.41 ng/mL, P<0.02). After excluding the 36 patients with PAD, HO-1 levels were significantly higher in 192 patients with CAD than in 182 without CAD (0.45 versus 0.35 ng/mL, P<0.05). HO-1 levels in 4 groups of CAD(−), 1-VD, 2-VD, and 3-VD were 0.35, 0.49, 0.44, and 0.44 ng/mL, respectively, and were highest in 1-VD (P<0.05). In the multivariate analysis, HO-1 levels were inversely associated with PAD, whereas they were also associated with CAD. The odds ratios for PAD and CAD were 2.12 (95% CI = 1.03–4.37) and 0.65 (95% CI = 0.42–0.99) for the HO-1 level of <0.35 ng/mL, respectively. Conclusions. Plasma HO-1 levels were found to be low in patients with PAD, in contrast to high levels in patients with CAD.

2019 ◽  
Vol 20 (15) ◽  
pp. 3628 ◽  
Author(s):  
Yoshimi Kishimoto ◽  
Kazuo Kondo ◽  
Yukihiko Momiyama

Heme oxygenase-1 (HO-1) is an intracellular enzyme that catalyzes the oxidation of heme to generate ferrous iron, carbon monoxide (CO), and biliverdin, which is subsequently converted to bilirubin. These products have anti-inflammatory, anti-oxidant, anti-apoptotic, and anti-thrombotic properties. Although HO-1 is expressed at low levels in most tissues under basal conditions, it is highly inducible in response to various pathophysiological stresses/stimuli. HO-1 induction is thus thought to be an adaptive defense system that functions to protect cells and tissues against injury in many disease settings. In atherosclerosis, HO-1 may play a protective role against the progression of atherosclerosis, mainly due to the degradation of pro-oxidant heme, the generation of anti-oxidants biliverdin and bilirubin and the production of vasodilator CO. In animal models, a lack of HO-1 was shown to accelerate atherosclerosis, whereas HO-1 induction reduced atherosclerosis. It was also reported that HO-1 induction improved the cardiac function and postinfarction survival in animal models of heart failure or myocardial infarction. Recently, we and others examined blood HO-1 levels in patients with atherosclerotic diseases, e.g., coronary artery disease (CAD) and peripheral artery disease (PAD). Taken together, these findings to date support the notion that HO-1 plays a protective role against the progression of atherosclerotic diseases. This review summarizes the roles of HO-1 in atherosclerosis and focuses on the clinical studies that examined the relationships between HO-1 levels and atherosclerotic diseases.


2018 ◽  
Vol 32 ◽  
pp. 71
Author(s):  
Yoshimi Kishimoto ◽  
Susumu Ibe ◽  
Emi Saita ◽  
Kenji Sasaki ◽  
Hanako Niki ◽  
...  

2020 ◽  
Vol 189 (9) ◽  
pp. 951-962 ◽  
Author(s):  
Jonathan T Unkart ◽  
Matthew A Allison ◽  
Maria Rosario G Araneta ◽  
Joachim H Ix ◽  
Kunihiro Matsushita ◽  
...  

Abstract Using data from the Multi-Ethnic Study of Atherosclerosis (United States, 2000–2015), 6,527 racially/ethnically diverse adults (mean age, 62 (standard deviation, 10) years) free of known cardiovascular (CVD) had ankle brachial index (ABI) assessment of their bilateral dorsalis pedis/posterior tibial arteries (4 vessels total) and were followed for total mortality and incident CVD events/mortality. Individuals were classified into categories of 0-, 1-, 2-, 3- or 4-vessel peripheral artery disease (PAD) (ABI of ≤0.9). There were 1,202 deaths (18%), 656 incident CVD events (10%), and 282 CVD deaths (4.3%). Of the 6,527 individuals, 5,711 (87.5%) had 0-, 460 (7.0%) had 1-, 218 (3.3%) had 2-, 69 (1.1%) had 3-, and 69 (1.1%) had 4-vessel PAD, respectively. In multivariable Cox models, higher number of vessels with PAD was associated with higher risk of mortality (P for trend &lt;0.001), CVD events (P for trend = 0.002), and CVD mortality (P for trend = 0.001). Compared with individuals who had 0-vessel disease, hazard ratios for mortality were 1.29 (95% confidence interval (CI): 1.06, 1.59) for 1-, 1.45 (95% CI: 1.14, 1.86) for 2-, 1.58 (95% CI: 1.13, 2.21) for 3-, and 2.15 (95% CI: 1.58, 2.94) for 4-vessel disease. A similar pattern was seen for CVD events/mortality. These results suggest the importance of accounting for ABI values of all 4 leg arteries in clinical practice and research.


2016 ◽  
Vol 14 (4) ◽  
pp. 3459-3463 ◽  
Author(s):  
Salvatore Santo Signorelli ◽  
Guido Li Volsi ◽  
Valerio Fiore ◽  
Marco Mangiafico ◽  
Ignazio Barbagallo ◽  
...  

Author(s):  
Muriel Sprynger ◽  
Iana Simova ◽  
Scipione Carerj

Arterial diseases are heavily intertwined with atherosclerosis and coronary artery disease and the presence of both symptomatic and asymptomatic peripheral artery diseases is known to affect the rate of cardiovascular events and deaths. Screening for abdominal aortic aneurysm (AAA) in selected populations is also a major issue for the cardiologist. Additionally, intima-media thickness and ankle-brachial index (ABI) measurements, screening for carotid or femoral plaques, and new techniques looking at the rigidity and elasticity of arteries may further help with risk stratification, especially in intermediary risk populations. Cardiologists may also encounter other conditions such as subclavian artery disease, arterial dissection, arterial entrapment, and arteritis (e.g. giant cell or Takayasu’s arteritis). Even if they don’t undertake imaging themselves, they should know about these diseases and when to refer patients. Although cardiac and vascular ultrasounds are complementary, they require a completely different skill set and formal training. The ultimate goal of this chapter is to define the basic principles that any cardiologist should know, and also provide guidance to cardiologists more interested in vascular diseases. For the benefit of the patient there is a need for collaboration between the different disciplines involved in vascular diseases according to local medical availability and skill.


Angiology ◽  
2021 ◽  
pp. 000331972110043
Author(s):  
Clemens Höbaus ◽  
Gerfried Pesau ◽  
Bernhard Zierfuss ◽  
Renate Koppensteiner ◽  
Gerit-Holger Schernthaner

We evaluated angiogenin as a prospective biomarker in peripheral artery disease (PAD) patients with and without claudication symptoms. A pilot study suggested an elevation of angiogenin in critical limb ischemia. However, in PAD patients, the predictive value of angiogenin has not yet been evaluated. For this purpose, 342 patients with PAD (age: 69 ± 10 years, 34.5% women) were followed-up for 7 years in a cross-sectional study. Angiogenin was measured by enzyme-linked immunosorbent assay. All-cause and cardiovascular mortality were analyzed by Cox regression. Angiogenin levels were higher in men ( P = .001) and were associated with patient waist-to-hip ratio ( P < .001), fasting triglycerides ( P = .011), and inversely with estimated glomerular filtration rate ( P = .009). However, angiogenin showed no association with age, characteristics of diabetes, markers of lipid metabolism, or C-reactive protein. Angiogenin did not correlate with markers of angiogenesis such as vascular endothelial growth factor, angiopoietin-2, or tie-2. Furthermore, angiogenin was not associated with PAD Fontaine stages or with patient ankle-brachial index in addition to all-cause mortality (hazard ratio [HR] = 1.09 [95% CI: 0.89-1.34]) or cardiovascular morality (HR = 1.05 [0.82-1.35]). These results suggest that angiogenin does not provide further information regarding outcome prediction in patients with PAD.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Yu ◽  
J Teliewubai ◽  
X Fan ◽  
C Chi ◽  
H Ji ◽  
...  

Abstract Background Peripheral artery disease (PAD) is prevalent and substantially contributes to cardiovascular mortality particularly in the elderly, although the pathophysiological impact of PAD on heart itself still needs further investigation. In theory, PAD can increase pulse wave reflection which is an important determinant of subendocardial viability ratio (SEVR), a valuable estimate of myocardial perfusion as indicated by previous invasive studies. Thus, we hypothesize that PAD impairs myocardial perfusion through increasing pulse wave reflection. In this study, we aim to test this hypothesis in a large cohort from the Northern Shanghai Study. Methods A total of 2947 community-dwelling elderly Chinese (43.6% male, mean age: 71.3±5.9 years) were recruited. Ankle-brachial index were measured with the VP1000 device and used to diagnose PAD. Pulse wave reflection was estimated as aortic augmentation pressure (AP). Aortic BP, AP and SEVR were assessed by radial applanation tonometry. Multiple linear regression with SEVR and AP as dependent variable and PAD as independent variable, meanwhile adjusted for other covariates, were performed, respectively. Results 375 (12.7%) participants presented PAD. Compared to subjects without PAD, those with PAD showed significantly lower SEVR (126 vs. 132, P&lt;0.001) but higher AP (19 vs. 17 mmHg, P&lt;0.001). Multiple regression analysis revealed that both SEVR (regression coefficient [B] = −1.69, P=0.04, R2=0.61) and AP (B=1.19, P=0.04, R2=0.56) significantly associated with PAD, respectively. However, the association between SEVR and PAD was abolished when further adjusted for AP (B=−0.49, P=0.52). Similar results were obtained when inter-leg systolic BP difference was used to diagnose PAD. Conclusions PAD significantly and independently associates with myocardial perfusion; moreover, this association is mediated by increased pulse wave reflection. These findings provide a new dimension for understanding the pathophysiological mechanisms of cardiac damage of PAD. Funding Acknowledgement Type of funding source: None


Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 419
Author(s):  
Yohei Sanada ◽  
Sho Joseph Ozaki Tan ◽  
Nobuo Adachi ◽  
Shigeru Miyaki

Osteoarthritis (OA) is a common aging-associated disease that clinically manifests as joint pain, mobility limitations, and compromised quality of life. Today, OA treatment is limited to pain management and joint arthroplasty at the later stages of disease progression. OA pathogenesis is predominantly mediated by oxidative damage to joint cartilage extracellular matrix and local cells such as chondrocytes, osteoclasts, osteoblasts, and synovial fibroblasts. Under normal conditions, cells prevent the accumulation of reactive oxygen species (ROS) under oxidatively stressful conditions through their adaptive cytoprotective mechanisms. Heme oxygenase-1 (HO-1) is an iron-dependent cytoprotective enzyme that functions as the inducible form of HO. HO-1 and its metabolites carbon monoxide and biliverdin contribute towards the maintenance of redox homeostasis. HO-1 expression is primarily regulated at the transcriptional level through transcriptional factor nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2), specificity protein 1 (Sp1), transcriptional repressor BTB-and-CNC homology 1 (Bach1), and epigenetic regulation. Several studies report that HO-1 expression can be regulated using various antioxidative factors and chemical compounds, suggesting therapeutic implications in OA pathogenesis as well as in the wider context of joint disease. Here, we review the protective role of HO-1 in OA with a focus on the regulatory mechanisms that mediate HO-1 activity.


Diagnostics ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1407
Author(s):  
Robert K. Clemens ◽  
Monika Hunjadi ◽  
Andreas Ritsch ◽  
Lucia Rohrer ◽  
Thomas O. Meier ◽  
...  

Background: Cholesterol efflux is an important mechanism by which high-density lipoproteins (HDLs) protect against cardiovascular disease. As peripheral artery disease (PAD) is associated with high mortality rates, mainly due to cardiovascular causes, we investigated whether cholesterol efflux capacity (CEC) of apolipoprotein B (apoB)-depleted plasma, a widely used surrogate of HDL function, may serve as a predictive marker for mortality in this patient population. Methods: In this prospective single-center study (median follow-up time: 9.3 years), apoB-containing lipoproteins were precipitated from plasma of 95 patients with PAD and incubated with J744-macrophages, which were loaded with radiolabeled cholesterol. CEC was defined as the fractional radiolabel released during 4 h of incubation. Results: Baseline CEC was lower in PAD patients that currently smoked (p = 0.015) and had a history of myocardial infarction (p = 0.011). Moreover, CEC showed a significant correlation with HDL-cholesterol (p = 0.003) and apolipoprotein A-I levels (p = 0.001) as well as the ankle-brachial index (ABI, p = 0.018). However, CEC did not differ between survivors and non-survivors. Neither revealed Kaplan–Meier and Cox regression analyses any significant association of CEC with all-cause mortality rates. Conclusion: Taken together, CEC is associated with ABI but does not predict all-cause mortality in patients with PAD.


Angiology ◽  
2019 ◽  
Vol 71 (4) ◽  
pp. 303-314
Author(s):  
Rupert Bauersachs ◽  
Sebastian Debus ◽  
Mark Nehler ◽  
Maria Huelsebeck ◽  
Janita Balradj ◽  
...  

Patients with peripheral artery disease (PAD) have an increased risk of cardiovascular (CV) and limb events, but the disease is frequently underdiagnosed and treatment options are limited. This review examines the disease burden of symptomatic PAD as well as key guideline recommendations. Publications were identified using the ProQuest portal to access the Medline, Medline In-Process, and Embase databases. Search terms for symptomatic PAD were combined with terms relevant to epidemiology, burden, treatment practice, and physiopathology. Articles in English published between January 2001 and September 2016 were screened according to the population, interventions, comparator, outcomes, and study design criteria. Relevant publications (n = 200) were identified. The reported incidence and prevalence of PAD varied depending on the definitions used and the study populations. Patients generally had a poor prognosis, with an increased risk of mortality, CV, and limb events and decreased quality of life. Guideline recommendations included ankle–brachial index measurements, exercise testing, and angiography for diagnosis and risk factor modification, antiplatelets, cilostazol, exercise therapy, or surgical interventions for treatment, depending on the patient profile. The clinical, humanistic, and economic burden of disease in patients with symptomatic PAD is substantial and needs to be reduced through improved PAD management.


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