Serum albumin enhances the impairment of platelet aggregation with thromboxane synthase inhibition by increasing the formation of prostaglandin D2

Gresele, Paolo; Deckmyn, Hans; Huybrechts, Erwin; Vermylen, Jos

doi:10.1016/0006-2952(84)90577-x

Cited by 109 publications

(81 citation statements)

References 28 publications

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“…Inflammation has been related to decreasing albumin synthesis rate and increasing catabolism (23,24). For these reasons, SA may be considered as a surrogate marker of what which is an important inhibitor of platelet aggregation and increases the production of the antiaggregatory PGD2 from cyclic endoperoxides as well (7). According to our findings, decreased SA level may induce noreflow phenomenon because of increased platelet activity and aggregation.…”

Section: Discussionsupporting

confidence: 51%

“…Moreover, hypoalbuminemia has been found to be a risk factor for the development of a new myocardial infarction in patients with CAD (6). Besides, serum albumin (SA) is an important inhibitor of platelet aggregation and increases the production of the antiaggregatory prostaglandin D2 (PGD2) from cyclic endoperoxides (7,8). Furthermore, hypoalbuminemia may increase blood viscosity and disrupt endothelial function on account of increased concentrations of free lysophosphatidylcholine (9).…”

Section: Abant Med J 2015;4(3):230-238 231mentioning

confidence: 99%

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The Utility of the Serum Albumin Levels on Admission for Predicting Angiographic No Reflow After Primary Percutaneous Coronary Intervention in Patients With ST-Segment Elevation Myocardial Infarction

Acet¹,

Ertaş²,

Aydın³

et al. 2015

Turk J Bioch

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Amaç: Düşük serum albümin (SA) düzeyleri artmış kardiyovasküler mortalite ile ilişkilidir. Bazal SA seviyelerinin primer perkütan koroner girişim (p-PKG) yapılan hastalarda akışsızlık fenomeni ile ilgili olup olmadığını araştırdık. Yöntem: Geriye dönük olarak p-PKG ile tedavi edilen ST yükselmeli myokard infarktüsü (STYMI)'lı 358 hasta alındı. Hasta takibi hastaneiçi dönemde yapıldı. Önceki çalışmalara uygun olarak, TIMI akım derecesi ≤2, TIMI akım derecesi >3 olanlarda ise MBG <2 olanlar akışsızlık fenomeni olarak değerlendirildi. Hastalar başvuru SA düzeylerine göre iki gruba ayrıldı. SA <3,5 g/dl olanlar hipoalbüminemik grup ve SA düzey > 3,5 g/dl yüksek albüminemik grup olarak değerlendirildi. Bulgular: PKG yapılan toplam 358 (yaş 62±14 yaş, % 72 erkek) hasta alındı. Başvuru SA düzeyleri akışsızlık fenomeni olan grupta normal akım olan gruba göre anlamlı bir şekilde daha düşüktü (p=0,021). Sonuç: Başvuru SA seviyeleri akut STYMI hastalarda p-PKG sonrası-akışsızlık fenomeninin gelişimini tahmin edebilir. Başvuru hipoalbüminemili hastalar kötü klinik ve anjiyografik sonuçları ile ilgilidir ve STYMI p-PKG ile tedavi edilen hastalarda hastane içi mortalite ve pulmoner ödem ve kardiyojenik şok gelişimi tahmin edilebilmektedir.Objective: Low serum albumin (SA) levels are associated with increased cardiovascular mortality. We investigated whether baseline SA levels are associated with no-reflow in patients undergoing primary percutaneous coronary intervention (p-PCI). Method: STEMI patients treated by p-PCI were included in the study. The patients were followed during in hospital period. We defined angiographic no-reflow phenomenon as a coronary TIMI flow grade ≤2 after vessel re-canalized or TIMI flow grade 3 together with a final MBG < 2, in the same manner as was adopted in previous studies. The patients were divided into two groups according to the SA levels on admission, that is hypoalbuminemia group was SA<3.5 g/dl and high albuminemia group SA level was >3.5 g/dl. Results: A total of 358 patients (aged 62+14 years; 72% men) who underwent p-PCI were enrolled in the study. Admission SA levels were significantly lower in the noreflow group than in the normal-reflow group (p=0.021) Conclusion: Admission SA levels may predict the development of no-reflow phenomenon after p-PCI in patients with acute STEMI. Hypoalbuminemia on admission is related to worse clinical and angiographic outcomes and predicts inhospital mortality and development of advanced pulmonary edema and cardiogenic shock (higher Killip class) in patients treated with p-PCI for STEMI.Anahtar Kelimeler: Serum albumin düzeyi, Akışsızlık fenomeni, Perkütan koroner girişim, Akut myokard infarktüsü.

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Section: Discussionsupporting

confidence: 51%

Section: Abant Med J 2015;4(3):230-238 231mentioning

confidence: 99%

The Utility of the Serum Albumin Levels on Admission for Predicting Angiographic No Reflow After Primary Percutaneous Coronary Intervention in Patients With ST-Segment Elevation Myocardial Infarction

Acet¹,

Ertaş²,

Aydın³

et al. 2015

Turk J Bioch

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“…15) Albumin is an important inhibitor of platelet aggregation and increases the production of the antiaggregatory prostaglandin PGD2 from cyclic endoperoxides as well. 16,17) Hypoalbuminemia may increase blood viscosity and disrupt endothelial function because of increased concentrations of free lysophosphatidyl choline. 18) It is unclear whether the deleterious impact of low serum albumin levels in the early phase of acute coronary syndrome reflects the state of inflammation or an independent effect of albumin itself, given its numerous roles.…”

Section: Discussionmentioning

confidence: 99%

Low Serum Albumin Levels and In-Hospital Adverse Outcomes in Acute Coronary Syndrome

2010

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SummaryEpidemiological studies have demonstrated an association between low serum albumin levels and coronary heart disease and mortality. Nevertheless, the impact of a low serum albumin level during acute coronary syndrome has not yet been established. The aim of the present study was to investigate whether low serum albumin levels are associated with adverse outcomes in acute coronary syndrome. We enrolled 82 consecutive patients with acute coronary syndrome from whom venous blood for serum albumin measurement was drawn immediately upon hospital admission. Thirty-five patients had a low albumin level (hypoalbuminemia) and 47 had a normal albumin level (normoalbuminemia). In-hospital adverse outcomes (death, acute heart failure, cardiogenic shock, and reinfarction) were recorded during hospitalization in the intensive coronary care unit. The results of our study showed that the incidence of in-hospital adverse outcomes was 43%, with death occurring in 8 patients (10%). In-hospital adverse outcomes occurred more frequently in patients presenting with hypoalbuminemia, whereas mortality did not differ significantly. Univariate analysis showed that hypoalbuminemia was associated with a 2.8-fold greater risk of developing adverse outcomes. This risk was greater in the subgroup of NSTEACS (5.4-fold increased risk), but not in those with STEMI. Adjustment with other covariates revealed that hypoalbuminemia did not predict independently in-hospital adverse outcomes. It interacted with other predictors, especially Killip class II-IV, which was consistently an independent predictor of in-hospital adverse outcomes. (Int Heart J 2010; 51: 221-226)

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“…Albumin binds to endothelial glycocalyx and maintains the normal permeability of microvessel walls, serving as a carrier for various molecules through its capability of transcytosis across endothelium [59,61,62]. Tang et al [63] demonstrated significantly reduced blood brain barrier permeability in a transient focal ischemia rat model when treated with rt-PA along with albumin, and hence significantly attenuating deleterious effects of rt-PA. Albumin is also an important inhibitor of platelet aggregation [64][65][66]. Albumin also increases the production of the anti-aggregatory prostaglandin (PGD2) from cyclic endoperoxides [65].…”

Section: Albuminmentioning

confidence: 99%

“…Tang et al [63] demonstrated significantly reduced blood brain barrier permeability in a transient focal ischemia rat model when treated with rt-PA along with albumin, and hence significantly attenuating deleterious effects of rt-PA. Albumin is also an important inhibitor of platelet aggregation [64][65][66]. Albumin also increases the production of the anti-aggregatory prostaglandin (PGD2) from cyclic endoperoxides [65]. The use of albumin also binds plateletactivating factor with high affinity [66,67], and decreases platelet-activating factor induced responses in platelets [68].…”

Section: Albuminmentioning

confidence: 99%

Investigational Therapies for Ischemic Stroke: Neuroprotection and Neurorecovery

2011

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Stroke is one of the leading causes of death and disability worldwide. Current treatment strategies for ischemic stroke primarily focus on reducing the size of ischemic damage and rescuing dying cells early after occurrence. To date, intravenous recombinant tissue plasminogen activator is the only United States Food and Drug Administration approved therapy for acute ischemic stroke, but its use is limited by a narrow therapeutic window. The pathophysiology of stroke is complex and it involves excitotoxicity mechanisms, inflammatory pathways, oxidative damage, ionic imbalances, apoptosis, angiogenesis, neuroprotection, and neurorestoration. Regeneration of the brain after damage is still active days and even weeks after a stroke occurs, which might provide a second window for treatment. A huge number of neuroprotective agents have been designed to interrupt the ischemic cascade, but therapeutic trials of these agents have yet to show consistent benefit, despite successful preceding animal studies. Several agents of great promise are currently in the middle to late stages of the clinical trial setting and may emerge in routine practice in the near future. In this review, we highlight select pharmacologic and cell-based therapies that are currently in the clinical trial stage for stroke.

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Serum albumin enhances the impairment of platelet aggregation with thromboxane synthase inhibition by increasing the formation of prostaglandin D2

Cited by 109 publications

References 28 publications

The Utility of the Serum Albumin Levels on Admission for Predicting Angiographic No Reflow After Primary Percutaneous Coronary Intervention in Patients With ST-Segment Elevation Myocardial Infarction

The Utility of the Serum Albumin Levels on Admission for Predicting Angiographic No Reflow After Primary Percutaneous Coronary Intervention in Patients With ST-Segment Elevation Myocardial Infarction

Low Serum Albumin Levels and In-Hospital Adverse Outcomes in Acute Coronary Syndrome

Investigational Therapies for Ischemic Stroke: Neuroprotection and Neurorecovery

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