Systemic Inflammatory Response Syndrome After Acute Myocardial Infarction Complicated by Cardiogenic Shock

Kohsaka, Shun; Menon, Venu; Lowe, April M.; Lange, Michael; Džavík, Vladimir; Sleeper, Lynn A.; Hochman, Judith S.

doi:10.1001/archinte.165.14.1643

Cited by 292 publications

(174 citation statements)

References 22 publications

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“…In fact, sepsis was suspected in 18% of the SHOCK trial cohort, 74% of whom developed positive bacterial cultures. 29 SVR was lower in these patients, and low SVR preceded the clinical diagnosis of infection and culture positivity by days.…”

Section: Peripheral Vasculature Neurohormones and Inflammationmentioning

confidence: 74%

“…The reflex mechanism of increased systemic vascular resistance (SVR) is not fully effective, as demonstrated by variable SVR, with median SVR during CS in the normal range despite vasopressor therapy in the SHOCK Trial. 29 In some patients, SVR may be low, similar to septic shock. In fact, sepsis was suspected in 18% of the SHOCK trial cohort, 74% of whom developed positive bacterial cultures.…”

Section: Peripheral Vasculature Neurohormones and Inflammationmentioning

confidence: 99%

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Cardiogenic Shock

2008

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ardiogenic shock (CS) occurs in Ϸ5% to 8% of patients hospitalized with ST-elevation myocardial infarction (STEMI). Recent research has suggested that the peripheral vasculature and neurohormonal and cytokine systems play a role in the pathogenesis and persistence of CS. Early revascularization for CS improves survival substantially. New mechanical approaches to treatment are available, and clinical trials are feasible even in this high-risk population. Most importantly, hospital survivors have an excellent chance for long-term survival with good quality of life. This review will outline the causes, pathophysiology, and treatment of CS with a focus on CS complicating myocardial infarction (MI.) The case will be made for viewing CS as a serious disorder with a high early death rate, but one that is treatable and that, if approached aggressively, can result in full recovery. The diagnosis is usually made with the help of pulmonary artery (PA) catheterization; however, Doppler echocardiography may also be used to confirm elevation of LV filling pressures. 1 Hypoperfusion may be manifest clinically by cool extremities, decreased urine output, and/or alteration in mental status. Hemodynamic abnormalities form a spectrum that ranges from mild hypoperfusion to profound shock, and the short-term outcome is directly related to the severity of hemodynamic derangement. MI with LV failure remains the most common cause of CS. It is critical to exclude complicating factors that may cause shock in MI patients. Chief among these are the mechanical complications: ventricular septal rupture, contained free wall rupture, and papillary muscle rupture. Mechanical complications must be strongly suspected in patients with CS complicating nonanterior MI, particularly a first MI. Echocardiography is the technique of choice to rule out these entities and should be performed early unless the diagnosis is extensive anterior MI and the patient is undergoing prompt percutaneous coronary intervention (PCI). In addition, the detection of valvular disease before angiography may alter the revascularization approach. Diagnosis and CausesHemorrhage, infection, and/or bowel ischemia may contribute to shock in the setting of MI. As with mechanical complications, a high index of suspicion is required to make these diagnoses in MI patients, and survival may depend on timely recognition and treatment.Any cause of acute, severe LV or RV dysfunction may lead to CS. Acute myopericarditis, tako-tsubo cardiomyopathy, and hypertrophic cardiomyopathy may all present with ST elevation, release of cardiac markers, and shock in the absence of significant coronary artery disease. Stress-induced cardiomyopathy, also known as apical ballooning or takotsubo cardiomyopathy, is a syndrome of acute LV dysfunction after emotional or respiratory distress that leads to CS in 4.2% of cases. 2 Acute valvular regurgitation, typically caused by endocarditis or chordal rupture due to trauma or degenerative disease, may also cause CS. Aortic dissection may lead to CS via acute,...

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Section: Peripheral Vasculature Neurohormones and Inflammationmentioning

confidence: 74%

Section: Peripheral Vasculature Neurohormones and Inflammationmentioning

confidence: 99%

Cardiogenic Shock

2008

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“…MI вызывает развитие острофазного асепти-ческого воспалительного ответа, который в тяже-лых случаях приводит к системному воспалитель-ному ответу [14]. У больных с MI наблюдается многократное увеличение концентрации CRP, особенно выраженное у пациентов с ВО (табл.…”

Section: Discussionunclassified

Cytokine Profile in Visceral Obesity and Adverse Cardiovascular Prognosis of Myocardial Infarction

Gruzdeva¹,

Акбашева²,

Матвеева³

et al. 2015

Med. immunol.

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“…[1][2][3][4] The current understanding of the underlying pathophysiology that marks patients with an unfavorable course and lack of response to treatment is limited. This was evident in the recently published Triumph trial that addressed the possible adverse effects of a presumed excessive nitric oxide (NO) production secondary to inflammation in CS.…”

mentioning

confidence: 99%

“…However, observational studies have suggested that systemic inflammation and neurohormonal activation plays an important role in the pathogenesis of CS. 3,[6][7][8][9][10] The naturally occurring NO-inhibitor asymmetrical dimethylarginine (ADMA) has been implicated in the pathogenesis of endothelial dysfunction and several chronic cardiovascular disorders. [11][12][13][14] In contrast to its increasing recognition as a risk marker in cardiovascular disease, little is known about ADMA's role in the acute setting.…”

mentioning

confidence: 99%