Oxidation Products of Nitric Oxide, NO2and NO3, in Plasma after Experimental Myocardial Infarction

Akiyama, Koichiro; Suzuki, Hiroshi; Grant, Paul; Bing, Richard J.

doi:10.1006/jmcc.1996.9998

Cited by 58 publications

(41 citation statements)

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“…36 There is growing recognition of the cytokine cascade, chemokine response, and inducible NO synthase expression associated with coronary plaque rupture. 26,[41][42][43][44][45][46] As previously described, putative mechanisms also are associated with a "wet and warm" CS presentation wherein a systemic inflammatory response syndrome and vasodilation can occur after an MI. 26,47 This phenotype is characterized by systemic inflammatory response syndrome features, lower systemic vascular resistance, and a higher risk of sepsis and mortality.…”

Section: Hemodynamic Phenotypesmentioning

confidence: 99%

Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association

Diepen¹,

Katz²,

Albert³

et al. 2017

Circulation

1,278

1,165

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Cardiogenic shock is a high-acuity, potentially complex, and hemodynamically diverse state of end-organ hypoperfusion that is frequently associated with multisystem organ failure. Despite improving survival in recent years, patient morbidity and mortality remain high, and there are few evidence-based therapeutic interventions known to clearly improve patient outcomes. This scientific statement on cardiogenic shock summarizes the epidemiology, pathophysiology, causes, and outcomes of cardiogenic shock; reviews contemporary best medical, surgical, mechanical circulatory support, and palliative care practices; advocates for the development of regionalized systems of care; and outlines future research priorities. Cardiogenic shock (CS) is a low-cardiac-output state resulting in life-threatening end-organ hypoperfusion and hypoxia.1,2 Acute myocardial infarction (MI) with left ventricular (LV) dysfunction remains the most frequent cause of CS. 1,3 Advances in reperfusion therapy have been associated with improvements in survival, but significant regional disparities in evidence-based care have been reported, and in-hospital mortality remains high (27%-51%).1,4-9 Management recommendations are distributed between disease-specific statements and guidelines, and a dedicated and comprehensive clinical resource in this area is lacking. Thus, consolidating the evidence to define contemporary best medical and surgical CS practices for both MI-associated CS and other types of CS may be an important step in knowledge translation to help attenuate disparities in evidence-based care.Regional systems of care coupled with treatment algorithms have improved survival in high-acuity time-sensitive conditions such as MI, out-of-hospital cardiac arrest (OHCA), and trauma.10-12 Applying a similar framework to CS management may lead to similar improvements in survival, and CS systems of care are emerging within existing regional cardiovascular emergency care networks; however, guidance from a national expert group on structure and systems of care has not been available. 13,14 Accordingly, the purposes of this American Heart Association (AHA) scientific statement on CS are to summarize our contemporary understanding of the epidemiology, pathophysiology, and in-hospital best care practices into a single clinical resource document; to suggest a stepwise management algorithm that integrates medical, surgical, and mechanical circulatory support (MCS) therapies; and to propose a Mission: Lifelinesupported pathway for the development of integrated regionalized CS systems of care. DEFINITION OF CSAcute cardiac hemodynamic instability may result from disorders that impair function of the myocardium, valves, conduction system, or pericardium, either in isolation HISTORICAL PERSPECTIVESBefore the routine use of early revascularization, MIassociated CS had an in-hospital mortality exceeding 80%. A registry trial of 250 patients with acute MI described the association between bedside physical examination (Killip classification) for the as...

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Section: Hemodynamic Phenotypesmentioning

confidence: 99%

Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association

Diepen¹,

Katz²,

Albert³

et al. 2017

Circulation

1,278

1,165

View full text Add to dashboard Cite

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“…Indeed, in a rabbit MI model, Akiyama et al 24 demonstrated that cardiac iNOS and plasma/ cardiac nitrite and nitrate increase early (within 3 days) after infarction and then decline rapidly over the course of 2 weeks. The source of cardiac iNOS was exclusively the infarcted or at-risk region with no expression in the contralateral normal zone.…”

Section: Echocardiographic Data and LV Weightmentioning

confidence: 99%

β-Adrenergic Blockade in Developing Heart Failure

et al. 2000

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Background-Whether ␤-adrenergic blockade modulates myocardial expression of inflammatory cytokines and nitric oxide (NO) in heart failure is unclear. Methods and Results-We administered oral metoprolol or no therapy to rats for 12 weeks after large myocardial infarction and subsequently examined left ventricular (LV) remodeling; myocardial tumor necrosis factor (TNF)-␣, interleukin (IL)-1␤, and IL-6 expression; and NO. In untreated rats, echocardiography revealed significant (PϽ0.001) LV dilatation and systolic dysfunction compared with sham. Papillary muscle studies revealed isoproterenol hyporesponsiveness to be unaltered by NO synthase (NOS) inhibition. Circulating NO metabolites were undetectable. In noninfarcted myocardium, although inducible NOS (iNOS) mRNA was absent, TNF-␣, IL-1␤, and IL-6 mRNA and protein were markedly elevated compared with sham (PϽ0.001), with 2-fold higher expression (PϽ0.025) of IL-6 compared with TNF-␣ or IL-1␤. Metoprolol administration starting 48 hours after infarction (1) attenuated (PϽ0.02) LV dilatation and systolic dysfunction, (2) preserved isoproterenol responsiveness (PϽ0.025) via NO-independent mechanisms, and (3) reduced myocardial gene expression and protein production of TNF-␣ and IL-1␤ (PϽ0.025) but not IL-6, which remained high. Conclusions-During heart failure development, adrenergic activation contributes to increased myocardial expression of TNF-␣ and IL-1␤ but not IL-6, and one mechanism underlying the beneficial effects of ␤-adrenergic blockade may involve attenuation of TNF-␣ and IL-1␤ expression independent of iNOS and NO.

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“…9 The understanding of the pathophysiology of cardiogenic shock complicating MI has recently evolved toward an appreciation of the role of systemic inflammation, including cytokine release and expression of inducible nitric oxide synthase (NOS). [10][11][12] Excessive NOS results in high levels of nitric oxide that, in turn, lead to inappropriate systemic vasodilatation, progressive systemic and coronary hypoperfusion, and myocardial depression. [10][11][12] Inhibition of NOS is a theoretically appealing approach to treatment of this high-risk population.…”

Section: The Triumph Randomized Controlled Trialmentioning

confidence: 99%

“…[10][11][12] Excessive NOS results in high levels of nitric oxide that, in turn, lead to inappropriate systemic vasodilatation, progressive systemic and coronary hypoperfusion, and myocardial depression. [10][11][12] Inhibition of NOS is a theoretically appealing approach to treatment of this high-risk population. Early singlecenter studies with isoform-nonselective NOS inhibitors were promising and suggested a substantial beneficial effect on survival.…”

Section: The Triumph Randomized Controlled Trialmentioning

confidence: 99%

Effect of Tilarginine Acetate in Patients With Acute Myocardial Infarction and Cardiogenic Shock

Investigators

Alexander²,

Reynolds³

et al. 2007

JAMA

334

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Oxidation Products of Nitric Oxide, NO2and NO3, in Plasma after Experimental Myocardial Infarction

Cited by 58 publications

References 0 publications

Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association

Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association

β-Adrenergic Blockade in Developing Heart Failure

Effect of Tilarginine Acetate in Patients With Acute Myocardial Infarction and Cardiogenic Shock

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