Oxygen In Myocardial Infarction Research Articles

Prehospital opioid dose and myocardial injury in patients with ST elevation myocardial infarction.

ObjectiveTo characterise the relationship between opioid dose and myocardial infarct size in patients with ST elevation myocardial infarction (STEMI).MethodsPatients given opioid treatment by emergency medical services with confirmed STEMI were included in this secondary, retrospective cohort analysis of the Air versus Oxygen in Myocardial Infarction (AVOID) study. Patients with cardiogenic shock were excluded. The primary endpoint was comparison of cardiac biomarkers as a measure of infarct size based on opioid dose (low ≤8.75 mg, intermediate 8.76–15 mg and high >15 mg of intravenous morphine equivalent dose).Results422 patients were included in the analysis. There was a significantly higher proportion of patients with Thrombolysis in Myocardial Infarction (TIMI) 0 or 1 flow pre-percutaneous coronary intervention (PCI) (94% vs 81%, p=0.005) and greater use of thrombus aspiration catheters (59% vs 30%, p<0.001) in the high compared with low-dose opioid group. After adjustment for potential confounders, every 1 mg of intravenous morphine equivalent dose was associated with a 1.4% (95% CI 0.2%, 2.7%, p=0.028) increase in peak creatine kinase; however, this was no longer significant after adjustment for TIMI flow pre-PCI.ConclusionsOur study suggests no benefit of higher opioid dose and a dose-dependent signal between opioid dose and increased myocardial infarct size. Prospective randomised controlled trials are required to establish causality given that this may also be explained by patients with a greater ischaemic burden requiring higher opioid doses due to more severe pain. Future research also needs to focus on strategies to mitigate the opioid–P2Y12 inhibitor interaction and non-opioid analgesia to treat ischaemic chest pain.

ROUTINE USE OF SUPPLEMENTAL OXYGEN IN PATIENTS WITH MYOCARDIAL INFARCTION WITHOUT HYPOXIA IS ASSOCIATED WITH HIGHER RATES OF RE-INFARCTION: A META-ANALYSIS

SESSION TITLE: Cardiovascular Disease SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/10/2018 01:00 PM - 02:00 PM PURPOSE: Routine use of oxygen in patients with myocardial infarction (MI) used to be the standard of practice until recently. However, recent studies have not shown any benefits in this setting. In addition, recently published AVOID study showed that routine use of oxygen is associated with a larger 6-month myocardial infarct size. At the same time, several studies published recently failed to show any harmful effect of the routine use of oxygen. We did this meta-analysis to further explore this controversial issue. We are aiming to assess whether routine use of oxygen is associated with worsened clinical outcomes. METHODS: We used the PRISMA model for our analysis. We performed a systematic search of PubMed, Scopus, Cochrane library and clinicaltrial.gov since inception till January 2017. We used following terms for the search: “infarction”, “myocardial infarction”, “acute coronary syndrome”, “ACS”, “MI”, “oxygen therapy”, “oxygen effect”, “oxygen supplementation” and “oxygen treatment”. Total of 5 studies was included in our analysis. We used RevMan 5.3 for windows (Cochrane Collaboration, Oxford, United Kingdom) for all the analysis. We used random effect model for analysis of the continuous and dichotomous variables. We used Mental-Haenszel method for the analysis. In addition, we used a confidence interval of 95% as significant and along with p-value of less than 0.5 as significant. Heterogeneity was measured using I2. The heterogeneity of <30 % was considered low, 30%-60 % was considered moderate and >60% was considered substantial. We calculated the mean difference (MD) and odds ratio (OR) for the continuous and dichotomous variables respectively RESULTS: A total of 914 patients were included in our analysis (449 in oxygen group). Infarcted myocardial mass between two groups was not significantly different (MD, 2.76-gram, 95% CI [-1.94, 7.47], a p-value 0.25; I2=67%). Similarly, we did not find a significant difference in percent infarct mass (MD, 1.48 %, CI [-1.34, 4.29], p-value 0.30; I2= 55%). We did not find any significant difference in EF between two groups (MD, -0.71, 95% CI [-3.94, 2.53], a p-value 0.67; I2= 0%). However, we found a significant increase in the incidence of re-infarction in oxygen group(4.92% vs 0.73%) (OR, 5.70, 95%, CI [1.45, 22.35], p-value 0.01; I2= 0%). There was no significant difference between two groups in in-hospital mortality (OR,1.06, 95% CI [0.30, 3.70], p-value 0.93;I2= 49%). CONCLUSIONS: Regular use of supplemental oxygen in MI without hypoxia is associated with adverse clinical outcome secondary to increased rates of re-infarction. CLINICAL IMPLICATIONS: There is uncertainty regarding the use of supplemental oxygen in patients with MI without heart failure or dyspnea in the recent guidelines. In light of our evidence of increased adverse clinical outcome, we think the guidelines should actually now recommend against the regular supplemental use of oxygen. DISCLOSURES: No relevant relationships by Ghassan Bachuwa, source=Web Response No relevant relationships by Sai Pavan Kumar Chintalapati, source=Web Response No relevant relationships by Sunil Upadhaya, source=Web Response No relevant relationships by Ravi Kanth Velagapudi, source=Web Response

Acute coronary syndromes: Supplemental oxygen in myocardial infarction.

Acute coronary syndromes: Supplemental oxygen in myocardial infarction.

Air versus oxygen in myocardial infarction (AVOID) trial sub-study: time-dependent effect of oxygen administration on myocardial injury

Background: Routine oxygen therapy has been associated with increased myocardial injury following acute myocardial infarction, although the time-dependent effect of oxygen administration on myocardial infarct size has not been evaluated. Methods: This was a planned sub-study of the Australian multicentre, prospective, randomised, controlled AVOID trial, of 441 STEMI patients who were allocated to routine oxygen therapy (8L/min via facemask) or no supplemental oxygen. The primary endpoint was myocardial infarct size as assessed by cardiac enzymes, troponin (cTnI) and creatine kinase (CK). Allocated treatment was commenced by paramedics after randomisation, and continued for up to 12 hours post procedural intervention in hospital. Peak and are under the curve for cTnI and CK and were assessed using linear regression models adjusted for age, gender, pre-intervention TIMI flow, Killip class, culprit artery, and symptom-to-intervention time. Results: Pre-intervention oxygen administration was not associated with peak cTnI or peak CK release. After adjustment, when compared to no oxygen administration, longer durations of post-intervention oxygen therapy were associatedwithhigher ratiosofmeanpeakcTnI (≤2hours: 1.43 [95% CI: 0.99 to 2.08, p=0.059]; 2-6 hours: 1.67 [95% CI: 1.14 to 2.44, p=0.009]; 6-12 hours: 2.05 [95% CI: 1.30 to 3.24, p=0.002] and mean peak CK (≤2 hours: 1.22 [95% CI: 0.95 to 1.78, p=0.120]; 2-6 hours: 1.31 [95% CI: 1.01 to 1.71, p=0.043]; 6-12 hours: 1.62 [95% CI: 1.19 to 2.22, p=0.002]. Conclusion: In patients with STEMI, longer durations of oxygen therapy post-procedural intervention may be associated with increased myocardial injury.

Oxygen therapy in acute coronary syndrome: are the benefits worth the risk?

Oxygen supplementation is a standard treatment for all patients who present with acute coronary syndrome, regardless of oxygen saturation levels. Most of the data regarding the function of oxygen in myocardial infarction is based on a limited number of basic and clinical studies. We performed a systematic literature review that explores the basic and clinical data on the function of oxygen in ischaemic heart disease and myocardial infarction. This review discusses many aspects of oxygen treatment: (i) basic studies on the effects of oxygen in ischaemia and the potential cardiovascular effects of oxygen metabolites; (ii) clinical trials that have assessed the value of inhaled oxygen, supersaturated oxygen, and intracoronary injection of hyperoxaemic solutions in myocardial infarction; and (iii) the haemodynamic effects of oxygen in various clinical scenarios and its direct effects on the coronary vasculature. Our findings suggest that there are conflicting data on the effects of oxygen treatment. Further, the potential harmful effects of oxygen must be considered, particularly in myocardial infarction. These findings question the current guidelines and recommendations and emphasize the need for large clinical trials.

Dosage is important when using oxygen for patients with myocardial infarction

In questioning the use of oxygen supplementation for patients with myocardial infarction, Beasley and colleagues1 failed to discuss the importance of the plasma tension and the relevant science (JRSM 2007;100:130-133). Cardiac output is tailored to oxygen demand and vascular tone relates to the plasma oxygen tension because it determines the oxygen saturation of haemoglobin. The calibre of vessels is determined by the degree of binding of the vasodilator nitric oxide (NO) by oxygenated haemoglobin in forming S-nitrosohaemoglobin.2 In the presence of a coronary artery occlusion, upstream vasoconstriction by oxygen reduces blood flow, limiting the delivery of erythrocytes and hence oxygen availability. However, this only applies over the small range of inspired oxygen concentrations used in oxygen supplementation, because the vasoconstriction is limited by the sites available for NO binding by oxyhaemoglobin. Using 100% oxygen under hyperbaric conditions, plasma oxygen levels may be increased to more than compensate for the loss of oxygen transport by erythrocytes. Boerema et al.3 demonstrated this experimentally in 1960, showing that life is possible without blood when breathing oxygen under hyperbaric conditions. Higher plasma oxygen concentrations greatly increase the concentration gradient for the transport of oxygen to tissues; at two atmospheres absolute breathing 100% oxygen the concentration gradient is increased ten-fold. This explains the reduction of myocardial infarct size demonstrated experimentally using hyperbaric oxygenation. Beasley et al. do not reference the controlled trials of oxygen treatment under hyperbaric conditions. A controlled study of hyperbaric oxygen in myocardial infarction published in 19734 demonstrated benefit, especially in cardiogenic shock, and the paper includes ECG tracings showing abnormalities improving as the patients were pressurized. More recently, a controlled trial has shown the benefit of combining hyperbaric oxygen treatment with thrombolysis.5

The utility of oxygen in myocardial infarction

A 50-year-old female called for an ambulance 30 min after the onset of a “squeezing” sensation in the substernal region of her chest. Paramedics found her to be in moderate distress due to the pain. She was immediately placed on 15 liters of oxygen by non-rebreather mask (NRBM). En route to the hospital, a peripheral intravenous (i.v.) line was placed, and the patient was given one spray of sublingual nitroglycerin every 5 min (for a total of three sprays), 4 mg of morphine sulfate i.v., and 81 mg of aspirin p.o. Upon arrival in the Emergency Department (ED), the patient’s chest pain was still present without improvement. The vital signs were: temperature 36.7°C, heart rate 86 beats/min, respiratory rate 20 breaths/min, and blood pressure 148/72 torr. The oxygen saturation was 99% while on oxygen. A 12-lead electrocardiogram (EKG) was performed (Figure 1). Pulmonary embolism was considered to be in the differential diagnosis. Approximately 5 min after the first EKG, the patient’s oxygen was discontinued to obtain a room air arterial blood gas sample. Eight minutes later, a second 12-lead EKG (Figure 2) was performed; it showed evidence of an acute inferior wall infarction. Immediately after the second EKG was performed and approximately 9 min after the oxygen was removed, it was replaced (15 L by NRBM). Precisely 3 min after the oxygen was replaced, a third 12-lead EKG was performed (Figure 3) showing near elimination of the ST segment elevations. Other than oxygen, the patient received only morphine sulfate (4 mg i.v.) between the second and third EKGs. The patient’s chest pain persisted. Approximately 45 min after this patient’s arrival in the ED, she was given thrombolytic therapy. Complete relief of her chest pain occurred shortly thereafter (Figure 4). The cardiac enzyme studies later confirmed that she had suffered an acute myocardial infarction. This set of EKGs illustrates the importance of providing oxygen to all patients who suffer from acute chest pain that might be due to acute myocardial infarction. The literature supports the use of oxygen in this setting, but the benefit of 100% versus 40% inspired oxygen has not been proven. (1–6)

Circulatory and metabolic effects of oxygen in myocardial infarction.

The circulatory and metabolic effects of inhalation of oxygen in high concentration were investigated in 50 patients with acute myocardial infarction. The heart rate, arterial blood pressure, cardiac out-put, blood gas tensions, pH, and lactate and pyruvate levels were measured. In general, oxygen inhalation produced a fall in cardiac output and stroke volume and a rise in blood pressure and systemic vascular resistance. In a small number of patients with very low cardiac out-puts there was a rise in output. A substantial rise in arterial oxygen tension was obtained even in patients with low initial values. The raised arterial blood lactate levels which were frequently present were reduced after oxygen. The therapeutic implications of these effects are discussed.

HÆMODYNAMIC AND METABOLIC EFFECTS OF HYPERBARIC OXYGEN IN MYOCARDIAL INFARCTION

HÆMODYNAMIC AND METABOLIC EFFECTS OF HYPERBARIC OXYGEN IN MYOCARDIAL INFARCTION