Mechanisms underlying the J-curve for diastolic blood pressure: Subclinical myocardial injury and immune activation

Topel, Matthew; Sandesara, Pratik B.; Stahl, Eric; Hayek, Salim S.; Tahhan, Ayman Samman; O’Neal, Wesley T.; Ko, Yi‐An; Alkhoder, Ayman; Gafeer, Mohamad Mazen; Kim, Jonathan H.; Wilson, Peter W.F.; Shaw, Leslee J.; Epstein, Stephen E.; Vaccarino, Viola; Sperling, Laurence; Quyyumi, Arshed A.

doi:10.1016/j.ijcard.2018.09.028

Cited by 7 publications

(4 citation statements)

References 46 publications

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“…However, our data revealed a robust negative correlation between immune activation and diastolic blood pressure (r ϭ Ϫ0.33; P ϭ 0.002) and likewise for coagulation and diastolic blood pressure (r ϭ Ϫ0.22; P ϭ 0.04). This is supported by a recent study showing that diastolic blood pressure (Ͻ60 mmHg) is associated with subclinical myocardial injury and immune activation (32). Thus we conclude that cART intervention in our study most likely elicits detrimental effects, including higher CVD risk, via dysregulated immune responses coupled with lower diastolic blood pressure and perturbations of lipoprotein subclasses to a greater extent than the traditional CVD risk factors.…”

Section: Limitationssupporting

confidence: 88%

HIV and cardiovascular diseases risk: exploring the interplay between T-cell activation, coagulation, monocyte subsets, and lipid subclass alterations

Teer

Joseph

Driescher

et al. 2019

American Journal of Physiology-Heart and Circulatory Physiology

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Although rollout of combined antiretroviral treatment (cART) has blunted human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS) onset, there is increased development of cardiovascular diseases (CVDs) in HIV-infected individuals. While most HIV-infected individuals on cART achieve viral suppression, this may not necessarily result in complete immunological recovery. This study therefore evaluated T-cell-mediated changes and coagulation markers in HIV-positive individuals to ascertain their potential to increase CVD risk. Eighty participants were recruited (Worcester, South Africa), and fasted blood was collected to evaluate: 1) immune activation (CD38 expression on CD4+ and CD8+ T cells) and thrombus formation [tissue factor (CD142)] on CD4+ and CD8+ T cells; 2) monocyte subpopulations (nonclassical, intermediate, and classical); and 3) classical regulatory T (Treg) cells with activation markers [glycoprotein A repetitions predominant (GARP) and special AT-rich sequence-binding protein 1 (SATB-1)]. High- and low-density lipoprotein subclasses (Lipoprint) were also determined. This study revealed four key findings for HIV-positive patients: 1) coexpression of the CD142 coagulation marker together with immune activation on both CD4+ and CD8+ T cells during chronic infection stages; 2) Treg cell activation and upregulated GARP and SATB-1 contributing to Treg dysfunction in chronic HIV; 3) proatherogenic monocyte subset expansion with significant correlation between T-cell activation and macrophage activation (marker: CD163); and 4) significant correlation between immune activation and lipid subclasses, revealing crucial changes that can be missed by traditional lipid marker assessments (LDL and HDL). These data also implicate lipopolysaccharide-binding protein as a crucial link between immune activation, lipid alterations, and increased CVD risk. NEW & NOTEWORTHY With combined antiretroviral treatment rollout, HIV-AIDS patients are increasingly associated with cardiovascular diseases onset. This study demonstrated the significant interplay between adaptive immune cell activation and monocyte/macrophage markers in especially HIV-positive individuals with virological failure and on second line treatment. Our data also show a unique link between immune activation and lipid subclass alterations, revealing important changes that can be missed by traditional lipid marker assessments (e.g., LDL and HDL).

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Section: Limitationssupporting

confidence: 88%

HIV and cardiovascular diseases risk: exploring the interplay between T-cell activation, coagulation, monocyte subsets, and lipid subclass alterations

Teer

Joseph

Driescher

et al. 2019

American Journal of Physiology-Heart and Circulatory Physiology

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“…It is worth mentioning that suPAR retains its prognostic value even at low glomerular filtration rates, indicating that it is not just a marker of kidney function [4]. Furthermore, an inverse correlation between preoperative suPAR levels and intraoperative sublingual microcirculatory perfusion may exist in patients undergoing major noncardiac surgery [26, 27]. All these may explain the positive correlation of suPAR with the ASA score, the CCI, and the POSSUM scoring system in our study.…”

Section: Discussionmentioning

confidence: 75%

Soluble Urokinase Receptor Levels Are Not Affected by the Systemic Inflammatory Response to Anesthesia and Operative Trauma

et al. 2022

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Introduction: Soluble urokinase plasminogen activator receptor (suPAR) is an emerging biomarker of the level of chronic systemic inflammation and the general condition of the patient. We aimed to investigate the impact of general anesthesia and major surgery on suPAR and C-reactive protein (CRP) levels in patients undergoing elective major non-cardiac surgery. Methods: The study included patients undergoing elective major non-cardiac surgery with an expected duration of ≥2 hours under general anesthesia. Inclusion criteria were: age ≥18 years and American Society of Anesthesiologists’ physical status I to IV. Blood was drawn 30 minutes prior to anesthesia and surgery (preoperatively), as well as 30 minutes after emergence from anesthesia (postoperatively). Plasma suPAR levels were determined using the suPARnostic® quick triage lateral flow assay. CRP measurements were performed by particle-enhanced immunoturbidimetric assay. Results: Preoperative and postoperative suPAR levels were similar and not statistically significant [7.7 (5.28-10.4) ng/mL vs. 7.15 (5.68-9.8) ng/mL, p=0.462]. CRP levels increased significantly during surgery [from 0.81 (0.24-2.1) mg/dL to 5.76 (2.2-8.75) mg/dL, p<0.001]. However, no correlation was found between CRP and suPAR levels, both preoperatively (rho=0.127; p=0.208) and postoperatively (rho=0.017; p=0.87). A statistically significant increase was also observed in white blood cell count postoperatively (7.576 vs. 10.711, p<0.001). Conclusion: General anesthesia and operative trauma did not influence the perioperative suPAR levels despite the activation of systemic inflammatory reaction.

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“…Already in 2000, Smulyan and Safar [14] published a recommendation to avoid a marked decrease in dBP while treating (I)SH. The problem arises because sBP and dBP are "inextricably married" [15] and it is very difficult to decrease sBP (aiming to improve prognosis) without reducing dBP at the same time [15][16][17][18].…”

Section: Resultsmentioning

confidence: 99%

Unsolved Problem: (Isolated) Systolic Hypertension with Diastolic Blood Pressure below the Safety Margin

Koraćević

Stojanović²,

Kostić

et al. 2020

Med Princ Pract

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The problem of high systolic blood pressure (sBP) combined with low diastolic blood pressure (dBP) requires attention because sBP is directly and continuously related to the most important criterion, i.e., all-cause mortality, whereas dBP becomes inversely related to it after the age of 50–60 years. The European Society of Cardiology and European Society of Hypertension (ESC/ESH) 2018 guidelines for hypertension (HTN) are helpful because they recommend a lower safety cut-off for in-treatment dBP. To prevent tissue hypoperfusion, these guidelines recommend that dBP should be ≥70 mm Hg during treatment. A patient with very elevated sBP (e.g., 220 mm Hg) and low dBP (e.g., 65 mm Hg) is difficult to treat if one strictly follows the guidelines. In this situation, the sBP is a clear indication for antihypertensive treatment, but the dBP is a relative contraindication (as it is <70 mm Hg, a safety margin recognized by the 2018 ESC/ESH guidelines). The dilemma about whether or not to treat isolated systolic hypertension (SH) patients with low dBP (<70 mm Hg) is evident from the fact that almost half (45%) remain untreated. This is a common occurrence and identifying this problem is the first step to solving it. We suggest that an adequate search and analysis should be performed, starting from the exploration of the prognosis of the isolated (I)SH subset of patients with a very low dBP (<70 mm Hg) at the beginning of already performed randomized clinical trials.

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Mechanisms underlying the J-curve for diastolic blood pressure: Subclinical myocardial injury and immune activation

Cited by 7 publications

References 46 publications

HIV and cardiovascular diseases risk: exploring the interplay between T-cell activation, coagulation, monocyte subsets, and lipid subclass alterations

HIV and cardiovascular diseases risk: exploring the interplay between T-cell activation, coagulation, monocyte subsets, and lipid subclass alterations

Soluble Urokinase Receptor Levels Are Not Affected by the Systemic Inflammatory Response to Anesthesia and Operative Trauma

Unsolved Problem: (Isolated) Systolic Hypertension with Diastolic Blood Pressure below the Safety Margin

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