Hyperbaric oxygen preconditioning improves myocardial function, reduces length of intensive care stay, and limits complications post coronary artery bypass graft surgery.

OBJECTIVE: The objective of this study was to determine whether preconditioning coronary artery disease (CAD) patients with HBO(2) prior to first-time elective on-pump cardiopulmonary bypass (CPB) coronary artery bypass graft surgery (CABG) leads to improved myocardial left ventricular stroke work (LVSW) post CABG. The primary end point of this study was to demonstrate that preconditioning CAD patients with HBO(2) prior to on-pump CPB CABG leads to a statistically significant (P<.05) improvement in myocardial LVSW 24 h post CABG. METHODS: This randomised control study consisted of 81 (control group=40; HBO(2) group=41) patients who had CABG using CPB. Only the HBO(2) group received HBO(2) preconditioning for two 30-min intervals separated 5 min apart. HBO(2) treatment consisted of 100% oxygen at 2.4 ATA. Pulmonary artery catheters were used to obtain perioperative hemodynamic measurements. All routine perioperative clinical outcomes were recorded. Venous blood was taken pre HBO(2), post HBO(2) (HBO(2) group only), and during the perioperative period for analysis of troponin T. RESULTS: Prior to CPB, the HBO(2) group had significantly lower pulmonary vascular resistance (P=.03). Post CPB, the HBO(2) group had increased stroke volume (P=.01) and LVSW (P=.005). Following CABG, there was a smaller rise in troponin T in HBO(2) group suggesting that HBO(2) preconditioning prior to CABG leads to less postoperative myocardial injury. Post CABG, patients in the HBO(2) group had an 18% (P=.05) reduction in length of stay in the intensive care unit (ICU). Intraoperatively, the HBO(2) group had a 57% reduction in intraoperative blood loss (P=.02). Postoperatively, the HBO(2) group had a reduction in blood loss (11.6%), blood transfusion (34%), low cardiac output syndrome (10.4%), inotrope use (8%), atrial fibrillation (11%), pulmonary complications (12.7%), and wound infections (7.6%). Patients in the HBO(2) group saved US$116.49 per ICU hour. CONCLUSION: This study met its primary end point and demonstrated that preconditioning CAD patients with HBO(2) prior to on-pump CPB CABG was capable of improving LVSW. Additionally, this study also showed that HBO(2) preconditioning prior to CABG reduced myocardial injury, intraoperative blood loss, ICU length of stay, postoperative complications, and saved on cost, post CABG.

Pharmacological preconditioning with hyperbaric oxygen: can this therapy attenuate myocardial ischemic reperfusion injury and induce myocardial protection via nitric oxide?

Ischemic reperfusion injury (IRI) is an inevitable part cardiac surgery such as coronary artery bypass graft (CABG). While ischemic hypoxia and the ensuing normoxic or hyperoxic reperfusion are critical to the initiation and propagation of IRI, conditioning myocardial cells to an oxidative stress prior to IRI may limit the consequences of this injury. Hyperbaric oxygen (HBO2) is a modality of treatment that is known to generate an oxidative stress. Studies have shown that treatment with HBO2 postischemia and reperfusion is useful in ameliorating myocardial IRI. Moreover, preconditioning the myocardium with HBO2 before reperfusion has demonstrated a myocardial protective effect by limiting the infarct size post ischemia and reperfusion. Current evidence suggests that HBO2 preconditioning may partly attenuate IRI by stimulating the endogenous production of nitric oxide (NO). As NO has the capacity to reduce neutrophil sequestration, adhesion and associated injury, and improve vascular flow, HBO2 preconditioning induced NO may play a role in providing myocardial protection during interventions that involve an inevitable episode of IRI. This current opinion review article attempts to suggest that HBO2 may be used to pharmacologically precondition and protect the myocardium from the effects of IRI that is known to occur during cardiac surgery.

Can hyperbaric oxygen be used as adjunctive heart failure therapy through the induction of endogenous heat shock proteins?

Heart failure (HF) is a chronic condition that is expected to increase in incidence along with increased life expectancy and an aging population. As the incidence of HF increases, the cost to national healthcare budgets is expected to run into the billions. The costs of lost productivity and increased social reliance on state support must also be considered. Recently, acute myocardial infarction (AMI) has come to be seen as the major contributing factor to HF. Although thrombolysis may restore coronary perfusion after an AMI, it may also introduce ischemic reperfusion injury (IRI). In an attempt to ameliorate sustained protein damage caused by IRI, endogenous chaperone proteins known as heat shock proteins (HSPs) are induced as a consequence of the stress of IRI. Recently, hyperbaric oxygen has been shown to induce the production of HSPs in noncardiac tissue, with a resultant protective effect. This current opinion review article suggests a possible role for hyperbaric oxygen, as a technologically modern drug, in augmenting the induction of endogenous HSPs to repair and improve the function of failing hearts that have been damaged by AMI and IRI. In addition, this simple, safe, noninvasive drug may prove useful in easing the economic burden of HF on already overextended health resources.

Hyperbaric oxygen: a novel technology for modulating myocardial schemia-reperfusion via a single drug.

Over the years, the anecdotal medical use of oxygen has demonstrated, in a non-evidence-based manner, that it may have wide-ranging clinical consequences. Although oxygen is a critical substrate in the alleviation of hypoxia, anoxia, and ischemia, paradoxically, it also functions as a deleterious metabolite during the reperfusion of previously ischemic tissues. In adding to this controversy, a spate of new pioneering work has identified hyperoxygenation (hyperoxia) and its metabolites as solely and purposefully demonstrating cellular and clinical benefit,particularly in the field of ischemic reperfusion injury (IRI). Furthermore, the beneficial effects of oxygen have been technologically augmented by administration at doses above atmospheric pressure and at higher concentrations. The novel technology that involves oxygen treatment at supra-atmospheric pressures in high concentrations is known as hyperbaric oxygen (HBO). Although the concept of hyperbaric oxygen has been around since the mid 20th century, it is only during the past decade or so that its therapeutic potential as a new technology-based drug has been exploited for the purposes of cellular tolerance and protection. HBO has recently been shown to be a useful adjunct in several models of IRI, including myocardial infarction. How it does this remains to be elucidated. This article attempts to bring into the spotlight some pertinent developments regarding HBO and myocardial IRI, while simultaneously stimulating intellect, thought, and discussion as to whether this novel technology--HBO--which consists of only a singular drug--oxygen--is a therapy that warrants further laboratory and clinical investigation as a therapeutic modality that may be safe and cost-effective, without producing significant adverse effects.

Hyperbaric oxygen: a new drug in myocardial revascularization and protection?

Ischemia-reperfusion injury (IRI) occurs following coronary artery revascularization. Reactive oxygen species (ROS) were initially thought to play a role in the pathogenesis of this injury. However, the evidence for this is inconclusive. Recent studies involving ischemic preconditioning have identified ROS as potential mediators for the cardioprotective effects observed following this technique. Furthermore, cardiac studies involving IRI and the use of hyperbaric oxygen (HBO) have demonstrated the ability of HBO to induce cardioprotection and to attenuate IRI. This review suggests the possible role for HBO as a new drug in the arena of myocardial revascularization and cellular protection. While there is mounting clinical evidence for this, a methodological understanding of HBO's cellular mechanisms of actions appears to be lacking. As such, this article attempts to draw the similarity between HBO and other protective oxidative stress mechanisms and then to speculate in an evidence-based manner its possible cellular mechanistic role as a drug via the generation of ROS.