Late ventricular remodeling in non-reperfused acute myocardial infarction in humans is predicted by angiotensin II type 1 receptor density on blood platelets

Mączewski, Michał; Borys, Marcin; Kacprzak, Pawel; Gdowski, Tomasz; Kowalewski, Marek; Wojciechowski, Dariusz

doi:10.1016/j.ijcard.2007.04.074

Cited by 6 publications

(4 citation statements)

References 28 publications

(41 reference statements)

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“…Ang II is associated with an increase in the production and secretion of plasminogen activatorinhibitor type 1 from endothelial and smooth muscle cells and an augmentation of tissue factor expression, thereby enhancing the activity of the coagulation system (19,20). Moreover, it is well established from previous studies that platelets express the AT 1 receptor and its activation by Ang II potentiates platelet activation and aggregation (21)(22)(23). On the other hand, Ang-(1-7) has been described as an antithrombotic peptide (24).…”

Section: Discussionmentioning

confidence: 99%

ACE2 Activation Promotes Antithrombotic Activity

Fraga‐Silva

Sorg

Wankhede

et al. 2010

Mol Med

129

122

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Hyperactivity of the axis ACE/AngII/AT1R of the renin‐angiotensin system is associated with occurrence of acute thrombotic event. Recently a novel concept of a counterrugulatory axis, ACE2/Ang‐(1‐7)/Mas, has emerged. We hypothesized that ACE2 would be protective against thrombosis. Thrombus was induced in the vena cava of SHR and WKY rats by FeCl3 solution. ACE2 and ACE protein expression and activities in the thrombus were determined by Western blot and fluorogenic kinetic assays, respectively. Real time thrombus formation was visualized by intravital microscopy of the vessels of nude mice. Ferric chloride‐induced thrombus weight was 40% higher in the SHR compared to WKY rats. This was associated with a 20% decreased in ACE2 activity in the thrombus of the SHR. In contrast, ACE2 protein expression and ACE activity did not differ between the thrombus of WKY rats and SHR. Inhibition of ACE2 by DX600 increased the thrombus weight by 30%, preferentially in the SHR. Furthermore, treatment with XNT resulted in a 30% attenuation of thrombus formation in both the SHR and WKY. In addition, XNT treatment prolonged the time for complete vessel occlusion and reduced thrombus size when observed under real‐time intravital microscopy. Our data demonstrated that a decrease in ACE2 activity is associated with increased thrombus formation in the SHR. Furthermore, activation of ACE2 attenuates thrombus formation.

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Section: Discussionmentioning

confidence: 99%

ACE2 Activation Promotes Antithrombotic Activity

Fraga‐Silva

Sorg

Wankhede

et al. 2010

Mol Med

129

122

View full text Add to dashboard Cite

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“…Angiotensin II receptor 2 (AT-2R) is thought to cause the opposite effects of AT-1R. A higher density of AT-1 receptors, as detected on blood platelets, may confer a greater risk of undergoing LVR for up to six months after an AMI [144,145]. Moreover, angiotensin converting enzyme (ACE) is implied in the degradation of bradykinin (Bk), which is a biomolecule that plays a protective role in endothelial cells [146] and induces reparative processes in the myocardium [147] against hypoxic injury.…”

Section: Raas Antagonistsmentioning

confidence: 99%

Reducing Cardiac Injury during ST-Elevation Myocardial Infarction: A Reasoned Approach to a Multitarget Therapeutic Strategy

Bellis

Gioia²,

Mauro

et al. 2021

JCM

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The significant reduction in ‘ischemic time’ through capillary diffusion of primary percutaneous intervention (pPCI) has rendered myocardial-ischemia reperfusion injury (MIRI) prevention a major issue in order to improve the prognosis of ST elevation myocardial infarction (STEMI) patients. In fact, while the ischemic damage increases with the severity and the duration of blood flow reduction, reperfusion injury reaches its maximum with a moderate amount of ischemic injury. MIRI leads to the development of post-STEMI left ventricular remodeling (post-STEMI LVR), thereby increasing the risk of arrhythmias and heart failure. Single pharmacological and mechanical interventions have shown some benefits, but have not satisfactorily reduced mortality. Therefore, a multitarget therapeutic strategy is needed, but no univocal indications have come from the clinical trials performed so far. On the basis of the results of the consistent clinical studies analyzed in this review, we try to design a randomized clinical trial aimed at evaluating the effects of a reasoned multitarget therapeutic strategy on the prevention of post-STEMI LVR. In fact, we believe that the correct timing of pharmacological and mechanical intervention application, according to their specific ability to interfere with survival pathways, may significantly reduce the incidence of post-STEMI LVR and thus improve patient prognosis.

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“…Angiotensin II receptor 2 (AT2R) is thought to cause opposite effects of AT1R. In post-myocardial infarction patients, a higher density of AT-1 receptor density, as detected on blood platelets, may confer a greater risk of undergoing ventricular remodeling for up to 6 months after an infarction [17,18].…”

Section: B Renin-angiotensin-aldosterone System Regulationmentioning

confidence: 99%

Left ventricular remodeling in the post-infarction heart: a review of cellular, molecular mechanisms, and therapeutic modalities

2010

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As more patients survive myocardial infarctions, the incidence of heart failure increases. After an infarction, the human heart undergoes a series of structural changes, which are governed by cellular and molecular mechanisms in a pathological metamorphosis termed "remodeling." This review will discuss the current developments in our understanding of these molecular and cellular events in remodeling and the various pharmacological, cellular and device therapies used to treat, and potentially retard, this condition. Specifically, this paper will examine the neurohormonal activity of the renin-angiotensin-aldosterone axis and its molecular effects on the heart. The emerging understanding of the extra-cellular matrix and the various active molecules within it, such as the matrix metalloproteinases, elicits new appreciation for their role in cardiac remodeling and as possible future therapeutic targets. Cell therapy with stem cells is another recent therapy with great potential in improving post-infarcted hearts. Lastly, the cellular and molecular effects of left ventricular assist devices on remodeling will be reviewed. Our increasing knowledge of the cellular and molecular mechanisms underlying cardiac remodeling enables us not only to better understand how our more successful therapies, like angiotensin-converting enzyme inhibitors, work, but also to explore new therapies of the future.

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Late ventricular remodeling in non-reperfused acute myocardial infarction in humans is predicted by angiotensin II type 1 receptor density on blood platelets

Cited by 6 publications

References 28 publications

ACE2 Activation Promotes Antithrombotic Activity

ACE2 Activation Promotes Antithrombotic Activity

Reducing Cardiac Injury during ST-Elevation Myocardial Infarction: A Reasoned Approach to a Multitarget Therapeutic Strategy

Left ventricular remodeling in the post-infarction heart: a review of cellular, molecular mechanisms, and therapeutic modalities

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