Cardiogenic shock: Basics and clinical considerations

Gowda, Ramesh M.; Fox, John; Khan, Ijaz A.

doi:10.1016/j.ijcard.2006.03.099

Cited by 27 publications

(22 citation statements)

References 69 publications

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“…Sepsis-like syndrome is characterized by elevated levels of soluble ICAM-1, VCAM-1, P-and E-selectin (32,33), and circulating cytokines including TNF-␣ and IL-8 (66). Furthermore, myocardial infarction secondary to ACSs leads to inflammatory activation, which amplifies the cardiogenic shock syndrome by releasing several cytokines including IL-6, IL-8, and TNF-␣, among others (40). High concentrations of IL-6 in patients with cardiogenic shock are an independent predictor of mortality (40).…”

Section: Hnps and Cardiovascular Diseasesmentioning

confidence: 99%

“…Furthermore, myocardial infarction secondary to ACSs leads to inflammatory activation, which amplifies the cardiogenic shock syndrome by releasing several cytokines including IL-6, IL-8, and TNF-␣, among others (40). High concentrations of IL-6 in patients with cardiogenic shock are an independent predictor of mortality (40).…”

Section: Hnps and Cardiovascular Diseasesmentioning

confidence: 99%

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Human neutrophil peptides: a novel potential mediator of inflammatory cardiovascular diseases

Quinn¹,

Henriques²,

Parker³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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The traditional view of atherosclerosis has recently been expanded from a predominantly lipid retentive disease to a coupling of inflammatory mechanisms and dyslipidemia. Studies have suggested a novel role for polymorphonuclear neutrophil (PMN)-dominant inflammation in the development of atherosclerosis. Human neutrophil peptides (HNPs), also known as alpha-defensins, are secreted and released from PMN granules upon activation and are conventionally involved in microbial killing. Current evidence suggests an important immunomodulative role for these peptides. HNP levels are markedly increased in inflammatory diseases including sepsis and acute coronary syndromes. They have been found within the intima of human atherosclerotic arteries, and their deposition in the skin correlates with the severity of coronary artery diseases. HNPs form complexes with LDL in solution and increase LDL binding to the endothelial surface. HNPs have also been shown to contribute to endothelial dysfunction, lipid metabolism disorder, and the inhibition of fibrinolysis. Given the emerging relationship between PMN-dominant inflammation and atherosclerosis, HNPs may serve as a link between them and as a biological marker and potential therapeutic target in cardiovascular diseases including coronary artery diseases and acute coronary syndromes.

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Section: Hnps and Cardiovascular Diseasesmentioning

confidence: 99%

Section: Hnps and Cardiovascular Diseasesmentioning

confidence: 99%

Human neutrophil peptides: a novel potential mediator of inflammatory cardiovascular diseases

Quinn¹,

Henriques²,

Parker³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…In cardiogenic shock, inotropic agents, but not vasopressors, are advocated [38, 39]. Intra-aortic balloon counter pulsation instantly improved sublingual microcirculatory blood flow in cardiogenic shock, but additional NE dosage was inversely correlated with microcirculatory blood flow [40].…”

Section: Resultsmentioning

confidence: 99%

The role of vasoactive agents in the resuscitation of microvascular perfusion and tissue oxygenation in critically ill patients

2010

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PurposeThe clinical use of vasoactive drugs is not only intended to improve systemic hemodynamic variables, but ultimately to attenuate derangements in organ perfusion and oxygenation during shock. This review aims (1) to discuss basic physiology with respect to manipulating vascular tone and its effect on the microcirculation, and (2) to provide an overview of available clinical data on the relation between vasoactive drugs and organ perfusion, with specific attention paid to recent developments that have enabled direct in vivo observation of the microcirculation and concepts that have originated from it.MethodsA MedLine search was conducted for clinical articles in the English language over the last 15 years pertainig to shock, sepsis, organ failure, or critically ill patients in combination with vasoactive drugs and specific variables of organ perfusion/oxygenation (e.g., tonometry, indocyanine clearance, laser Doppler, and sidestream dark field imaging).ResultsEighty original papers evaluating the specific relationship between organ perfusion/oxygenation and the use of vasoactive drugs were identified and are discussed in light of physiological theory of vasomotor tone.ConclusionsSolid clinical data in support of the idea that increasing blood pressure in shock improves microcirculatory perfusion/oxygenation seem to be lacking, and such a concept might not be in line with physiological theory of microcirculation as a low-pressure vascular compartment. In septic shock no beneficial effect on microcirculatory perfusion above a mean arterial pressure of 65 mmHg has been reported, but a wide range in inter-individual effect seems to exist. Whether improvement of microcirculatory perfusion is associated with better patient outcome remains to be elucidated.

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“…It is believed a subset of patients in these trials had the CRS averted with this approach. In the setting incipient cardiogenic shock, the risk of acute cardiorenal syndrome (type 1) is high and can be only partially managed with prompt revascularization and hemodynamic support with inotropic agents, vasopressors, and intra-aortic balloon counterpulsation [21]. Thus the primary prevention of acute cardiorenal syndrome (type 1) occurs in the outpatient realm using evidence-based approaches to avoid decompensation and hospitalization of HF and prevention of superimposed coronary ischemia through revascularization and risk factor modification [22].…”

Section: Acute Cardiorenal Syndrome Complicating Decompensated Heart mentioning

confidence: 99%

Prevention of Cardiorenal Syndromes

McCullough¹

2010

Contributions to Nephrology

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The cardiorenal syndromes (CRS) are composed of five recently defined syndromes which represent common clinical scenarios in which both the heart and the kidney are involved in a bidirectional injury process leading to dysfunction of both organs. Common to each subtype are multiple complex pathogenic factors, a precipitous decline in function and a progressive course. Most pathways that lead to CRS involve acute injury to organs which manifest evidence of chronic disease, suggesting reduced ability to sustain damage, maintain vital functions, and facilitate recovery. Prevention of CRS is an ideal clinical goal, because once initiated, CRS cannot be readily aborted, are not completely reversible, and are associated with serious consequences including hospitalization, complicated procedures, need for renal replacement therapy, and death. Principles of prevention include identification and amelioration of precipitating factors, optimal management of both chronic heart and kidney diseases, and future use of multimodality therapies for end-organ protection at the time of systemic injury. This paper will review the core concepts of prevention of CRS with practical applications to be considered in today's practice.

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Cardiogenic shock: Basics and clinical considerations

Cited by 27 publications

References 69 publications

Human neutrophil peptides: a novel potential mediator of inflammatory cardiovascular diseases

Human neutrophil peptides: a novel potential mediator of inflammatory cardiovascular diseases

The role of vasoactive agents in the resuscitation of microvascular perfusion and tissue oxygenation in critically ill patients

Prevention of Cardiorenal Syndromes

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