Clinical Significance of Hypoxemia without Congestive Heart Failure in Patients Presenting with Acute Myocardial Infarction

Aoki, Nobuo; Yanagisawa, Atsuo; Taniuchi, Masato; Fujita, Hiroshi; Mizuno, Haruyoshi; Yoshino, Hideaki; Ishikawa, Kinya

doi:10.1159/000006742

Cited by 5 publications

(4 citation statements)

References 29 publications

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“…Hypoxemia is a state often encountered in patients suffering from acute or chronic lung and cardiovascular diseases and may contribute to the poor, long-term outcome of patients presenting with acute myocardial infarction [10] or multiple injuries [8]. In many clinical disorders potentially complicated by hypoxemia, the severity of the disease correlates with the increased number of primed and/or activated PMN in circulation [4][5][6]28].…”

Section: Discussionmentioning

confidence: 99%

“…Hypoxemia is frequent in patients suffering from respiratory and cardiovascular diseases [7], as well as in life-threatening conditions such as following multiple injuries [8], ARDS [4], septic shock [9], and myocardial infarction [10]. However, whether moderate hypoxemia, as seen frequently in patients, contributes to sensitize the PMN to enhanced functional responses remains uncertain.…”

Section: Introductionmentioning

confidence: 99%

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Hypoxemia modifies circulating and exudate neutrophil number and functional responses in carrageenin-induced pleurisy in the rat

Tremblay

Macari

Martel

et al. 2000

Journal of Leukocyte Biology

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To assess the effect of hypoxemia on the responses of polymorphonuclear neutrophils (PMN) during an inflammatory response, rats were maintained in a low F i O 2 atmosphere (9% O 2 ) or room air for 12 h before intrathoracic injection of carrageenin or intradermal injections of agonists. After 4 h, hypoxemic rats had 50% more circulating PMN in blood and 25% less PMN in pleural exudate, whereas the number of PMN in skin biopsies did not differ from controls. Following hypoxemia, basal adhesion of blood PMN to serumcoated plastic wells was unchanged, whereas fMLPstimulated adhesion was 50% greater. In contrast, basal adhesion of exudate PMN was 72% greater. In hypoxemic rats, exudate PMN produced 64% more PMA-stimulated superoxide than blood PMN; furthermore, blood and exudate PMN produced 4.5-and 2-fold more LPS-stimulated nitric oxide than controls, respectively. These results show that a moderate level of hypoxemia may trigger mechanisms that will interfere with PMN emigration yet prime these cells for enhanced responses upon stimulation. J. Leukoc. Biol. 67: 785-792; 2000

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hypoxemia modifies circulating and exudate neutrophil number and functional responses in carrageenin-induced pleurisy in the rat

Tremblay

Macari

Martel

et al. 2000

Journal of Leukocyte Biology

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show abstract

“…Although some investigators have suggested that inducible systemic hypoxia may facilitate recovery of the infarcted myocardium [7,8], hypoxia is generally thought to aggravate hypoxemia [9]; in turn, hypoxemia is known to induce more severe cardiac dysfunction after MI [10]. Accordingly, it remains unclear whether hypoxia beneficial or detrimental to patients with MI.…”

Section: Introductionmentioning

confidence: 99%

Systematic Review and Meta-Analysis of the Impact of Hypoxia on Infarcted Myocardium: Better or Worse?

Pang¹,

Zhao²,

Zhou³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Patients with myocardial infarction and hypoxemia require supplemental oxygen. However, the current therapeutic paradigm is contradicted by several recent studies in which the post-infarcted heart appears to benefit from systemic hypoxia. With this systematic review and meta-analysis, we aimed to discover whether systemic hypoxia is beneficial or detrimental to the infarcted myocardium. Methods: We conducted an electronic search of the PubMed, EMBASE, and Web of Science databases and extracted the outcomes of cardiac function, geometry, and hemodynamics. A random-effect model was applied when the I² value of greater than 50%. The sensitivity analysis was performed by omitting one study at a time, and publication bias was assessed using Egger’s test. In addition, the quality of studies was evaluated using the risk of bias tool devised by the Systematic Review Centre for Laboratory Animal Experimentation. Results: Six reports comprising 14 experiments were ultimately screened from among 10,323 initially identified preclinical studies. Few studies reported the method of randomization and none described allocation concealment, random outcome assessment or blinding. Overall, chronic hypoxia was found to have a beneficial effect on the ejection fraction (standard mean difference [SMD] = 5.39; 95% confidence interval [CI], 3.83 to 6.95; P < 0.001) of the infarcted heart, whereas acute hypoxia significantly improved hemodynamics, as indicated by an increase in the maximal rate of rise of left ventricular pressure (SMD = 1.27; 95% CI, 0.27 to 2.28; P = 0.013) and cardiac output (SMD = 1.26; 95% CI, 0.34 to 2.18; P = 0.007) and a decrease in total systematic vascular resistance (SMD = –0.89; 95% CI, –1.24 to –0.53; P < 0.001). Furthermore, a reduced oxygen content increased the stroke volume (P = 0.010). However, hypoxia reduced the end-systolic (SMD = –2.67; 95% CI, –4.09 to –1.26; P < 0.001) and end-diastolic (SMD = –3.61; 95% CI, –4.65 to –2.57; P < 0.001) left ventricular diameters and increased the total pulmonary resistance (SMD = 0.76; 95% CI, 0.20 to 1.33; P = 0.008), pulmonary arterial mean pressure (SMD = 2.02; 95% CI, 0.23 to 3.81; P = 0.027), and left atrial pressure (SMD = 1.20; 95% CI, 0.57 to 1.82; P < 0.001). Conclusion: Hypoxia significantly improved heart function after infarction, with particular beneficial effects on systolic function and hemodynamics. However, it had slightly adverse effects on pulmonary circulation and left ventricular geometry. A lower inspired oxygen concentration may improve cardiac function, although further research is needed to determine the optimum level of hypoxia. Finally, more studies of hypoxia and myocardial infarction in larger species are required before these findings can be incorporated into therapeutic guidelines.

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“…Heart failure and mortality is significantly increased by tissue necrosis from hypoxia. Myocardial injury can result from hypoxemia, where a decrease in oxygen partial pressure (pO2) is observed (103,104). Under normal physiological conditions, hypoxia induces gene expressions that initiate erythropoiesis, activating the maturation and proliferation of hematopoietic progenitor cells (hematopoietic stem cells) present in peripheral blood and bone marrow (105).…”

Section: Refractory Hypoxemia and Hypoxiamentioning

confidence: 99%

The potential of melatonin in the prevention and attenuation of oxidative hemolysis and myocardial injury from cd147 SARS-CoV-2 spike protein receptor binding

Loh¹

2020

Melatonin Res.

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The rapid escalation of pandemic health threats associated with the novel, pathogenic SARS-CoV-2 coronavirus poses unprecedented challenges as proven effective vaccines and drugs have yet to be produced. Refractory hypoxemia and myocardial injury have been observed as two of the major causes of fatality in COVID-19 patients. SARS-CoV-2 spike (S) protein binding to broadly expressed CD147 receptors on erythrocytes causes oxidative hemolysis that may result in refractory hypoxemia and myocardial injury. Both of these life-threatening conditions are further exacerbated by imbalance in ACE2 from spike (S) protein receptor binding. Dysregulation in the CD147-cyclophilin A signaling pathway, together with altered calcium signaling from SARS-CoV-2 ion channel activities, may contribute to hypercoagulation, thrombosis, and cardiac remodeling resulting in heart failure. Melatonin is an ancient pleiotropic molecule with recognized antioxidant properties that is essential for the protection of erythrocytes from oxidative hemolysis. Found in erythrocytes, melatonin can reverse hemolytic anemia, normalize heme synthesis, restore lymphocytes and platelet counts, and reduce vessel permeability during an acute hemolytic crisis by maintaining intracellular calcium homeostasis and reduction of oxidative stress. In acute hypoxic conditions, melatonin is cardioprotective via blunting of cardiopulmonary response to hypoxia and suppressing hypoxia pathways. Melatonin normalizes endothelial-dependent nitric oxide production to prevent multiple organ damage from hypercoagulability, thrombosis, and hypertension associated with oxidative hemolysis and ACE2 deficiency, protecting cardiomyocytes from hypertrophy. This review discusses the full potential of melatonin as a safe and effective therapeutic intervention for the prevention and attenuation of hemoglobinopathies, refractory hypoxemia and myocardial injury during critical COVID-19 infections.

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Clinical Significance of Hypoxemia without Congestive Heart Failure in Patients Presenting with Acute Myocardial Infarction

Cited by 5 publications

References 29 publications

Hypoxemia modifies circulating and exudate neutrophil number and functional responses in carrageenin-induced pleurisy in the rat

Hypoxemia modifies circulating and exudate neutrophil number and functional responses in carrageenin-induced pleurisy in the rat

Systematic Review and Meta-Analysis of the Impact of Hypoxia on Infarcted Myocardium: Better or Worse?

The potential of melatonin in the prevention and attenuation of oxidative hemolysis and myocardial injury from cd147 SARS-CoV-2 spike protein receptor binding

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