How to protect the heart in septic shock: A hypothesis on the pathophysiology and treatment of septic heart failure

Schmittinger, Christian A.; Wurzinger, Bettina; Deutinger, Martina; Wohlmuth, Christoph; Knotzer, Hans; Torgersen, Christian; Dünser, Martin W.; Hasibeder, Walter

doi:10.1016/j.mehy.2009.10.012

Cited by 31 publications

(29 citation statements)

References 49 publications

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“…These include reversible multivessel epicardial coronary artery vasospasm secondary to sympathetic stimulation [8] , catecholamine surge especially during physical and emotional stress and acute critical illness resulting in basal hyperkinesis, myocardial stunning, and LV outflow tract obstruction eventually resulting in apical ballooning [9,10] . In our study, we observed an increased prevalence of TC in females, which is well established in the literature.…”

Section: Discussionmentioning

confidence: 99%

Gender Differences and Predictors of Mortality in Takotsubo Cardiomyopathy: Analysis from the National Inpatient Sample 2009-2010 Database

Krishnamoorthy

Garg²,

Sharma³

et al. 2015

Cardiology

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Objectives: Takotsubo cardiomyopathy (TC) is characterized by left-ventricle apical ballooning with elevated cardiac biomarkers and electrocardiographic changes similar to an acute coronary syndrome. We studied the prevalence, in-hospital mortality, and predictors of mortality in TC. Methods: All patients ≥18 years of age diagnosed with TC were identified in the Nationwide Inpatient Sample (NIS) 2009-2010 database using the 9th revision of the International Classification of Diseases (ICD) 429.83. Demographics, conventional risk factors (diabetes, hypertension, hyperlipidemia, and tobacco abuse), acute critical illnesses like sepsis, acute cerebrovascular disease (cerebrovascular accident; CVA), acute respiratory insufficiency, and acute renal failure, and chronic conditions (anxiety, depression, and malignancy) were studied. Results: The prevalence of TC was 0.02% (n = 7,510). The total in-hospital mortality rate was 2.4%, with a higher mortality in men (4.8%) than in women (2.1%). Sepsis (9 vs. 4.2%; p < 0.01) was more prevalent in men with an increased prevalence of other critical illness, although this was not statistically significant. Age (OR 1.05; 95% CI 1.01-1.09), malignancy (OR 3.38; 95% CI 1.35-8.41), acute renal failure (OR 5.4; 95% CI 2.2-13.7), acute CVA (OR 9.4; 95% CI 2.96-29.8), and acute respiratory failure (OR 11.1; 95% CI 3.9-31.1) predicted mortality in fully adjusted models. Conclusion: A higher mortality was seen in men, likely related to the increased prevalence of acute critical illnesses, ventricular arrhythmia, and sudden cardiac arrest. Acute CVA and respiratory failure were the strongest predictors of mortality.

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Section: Discussionmentioning

confidence: 99%

Gender Differences and Predictors of Mortality in Takotsubo Cardiomyopathy: Analysis from the National Inpatient Sample 2009-2010 Database

Krishnamoorthy

Garg²,

Sharma³

et al. 2015

Cardiology

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“…As adrenergic over-stimulation may contribute to the clinical deterioration and poor outcome of septic patients [61,66,137], several groups have tested β-blockers in septic animals and patients (see [30,[138][139][140] for reviews). In septic animals, β-blockers reduced heart rate though stroke volume was preserved [81,141].…”

Section: Beta-blockers In Sepsismentioning

confidence: 99%

The Heart in Sepsis: From Basic Mechanisms to Clinical Management

Rudiger¹,

Singer

2013

CVP

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Septic shock is characterized by circulatory compromise, microcirculatory alterations and mitochondrial damage, which all reduce cellular energy production. In order to reduce the risk of major cell death and a diminished likelihood of recovery, adaptive changes appear to be activated. As a result, cells and organs may survive in a non-functioning hibernation-like condition. Sepsis-induced cardiac dysfunction may represent an example of such functional shutdown. Sepsis-induced myocardial dysfunction is common, corresponds to the severity of sepsis, and is reversible in survivors. Its mechanisms include the attenuation of the adrenergic response at the cardiomyocyte level, alterations of intracellular calcium trafficking and blunted calcium sensitivity of contractile proteins. All these changes are mediated by cytokines. Treatment includes preload optimization with sufficient fluids. However, excessive volume loading is harmful. The first line vasopressor recommended at present is norepinephrine, while vasopressin can be started as a salvage therapy for those not responding to catecholamines. During early sepsis, cardiac output can be increased by dobutamine. While early administration of catecholamines might be necessary to restore adequate organ perfusion, prolonged administration might be harmful. Novel therapies for sepsis-induced cardiac dysfunction are discussed in this article. Cardiac inotropy can be increased by levosimendan, istaroxime or omecamtiv mecarbil without greatly increasing cellular oxygen demands. Heart rate reduction with ivabradine reduces myocardial oxygen expenditure and ameliorates diastolic filling. Beta-blockers additionally reduce local and systemic inflammation. Advances may also come from metabolic interventions such as pyruvate, succinate or high dose insulin substitutions. All these potentially advantageous concepts require rigorous testing before implementation in routine clinical practice. While early administration of catecholamines might be necessary to restore adequate organ perfusion and pressure, prolonged administration might be harmful.Novel therapies for sepsis-induced cardiac dysfunction are discussed in this article. Cardiac inotropy can be increased by levosimendan, istaroxime or omecamtiv mecarbil without greatly increasing cellular oxygen demands. Heart rate reduction with ivabradine will reduce myocardial oxygen expenditure and ameliorate diastolic filling. Beta-blockers additionally reduce local and systemic inflammation. Advances may also come from metabolic interventions such as pyruvate, succinate or high dose insulin substitutions. However, all these potentially advantageous concepts require rigorous testing before implementation in routine clinical practice.-3 -Alain Rudiger & Mervyn Singer: The heart in sepsis

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“…[1][2][3] During sepsis secretion of excessive pro-inflammatory mediators, such as cytokines, has been established. 4 Among these cytokines, tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 (which respectively activate and regulate the inflammatory system in response to infectious stimuli) are released in large quantities by various immune cell types in the early stage of sepsis.…”

Section: Introductionmentioning

confidence: 99%

Effect of induced mild hypothermia on two pro-inflammatory cytokines and oxidative parameters during experimental acute sepsis

et al. 2013

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This study aimed to determine the effect of induced mild hypothermia (34°C) on the production of two cytokines (interleukin (IL-6) and tumor necrosis factor (TNF)alpha) and reactive nitrogen and oxygen species in plasma and the heart of acutely septic rats. After anesthesia and in conditions of normothermia (38°C) or mild hypothermia (34°C), acute sepsis was induced by cecal ligation and perforation. For each temperature three groups were formed: (1) baseline (blood sample collected at T0 hour), (2) sham (blood sample at T4 hours) and (3) septic (blood sample at T4 hours). At either temperature sepsis induced a significant increase in plasma IL-6, TNF-alpha and HO• concentration, compared with the sham groups (P ≤ 0.016). Compared with the normothermic septic group, septic rats exposed to mild hypothermia showed a mild decrease in TNF-alpha concentration (104 ± 50 pg/ml vs. 215 ± 114 pg/ml; P > 0.05) and a significant decrease in IL-6 (1131 ± 402 pg/ml vs. 2494 ± 691 pg/ml, P = 0.038). At either temperature sepsis induced no enhancement within the heart of lipoperoxidation (malondialdehyde content) or antioxidant activities (superoxide dismutase and catalase). In conclusion, during acute sepsis, induced mild hypothermia appears to reduce some pro-inflammatory and oxidative responses. This may, in part, explain the beneficial effect of hypothermia on survival duration of septic rats.

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How to protect the heart in septic shock: A hypothesis on the pathophysiology and treatment of septic heart failure

Cited by 31 publications

References 49 publications

Gender Differences and Predictors of Mortality in Takotsubo Cardiomyopathy: Analysis from the National Inpatient Sample 2009-2010 Database

Gender Differences and Predictors of Mortality in Takotsubo Cardiomyopathy: Analysis from the National Inpatient Sample 2009-2010 Database

The Heart in Sepsis: From Basic Mechanisms to Clinical Management

Effect of induced mild hypothermia on two pro-inflammatory cytokines and oxidative parameters during experimental acute sepsis

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