Heart Failure after Cardiac Surgery: Comparison
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Heart disease requires a surgical approach sometimes. Cardiac-surgery patients develop heart failure associated with ischemia induced during extracorporeal circulation. This complication could be decreased with anesthetic drugs. The cardioprotective effects of halogenated agents are based on pre- and postconditioning (sevoflurane, desflurane, or isoflurane) compared to intravenous hypnotics (propofol). 

  • heart failure
  • preconditioning
  • postconditioning
  • halogenated
  • ACDHUVV-16

1. Introduction

 

Heart disease is a leading cause of mortality that frequently requires surgery. However, patients who undergo cardiac surgery often develop heart failure, which is a major cause of morbidity and mortality in this setting [1][2]. Heart failure is favored by ischemia induced during extracorporeal circulation (EC), where a cardioplegic solution is infused to cause diastolic cardiac arrest. This complication is associated with the duration of EC and baseline cardiac status of the patient. There is a growing interest in the field of anesthesiology and postoperative critical care regarding the cardioprotective effects of myocardial preconditioning (and postconditioning) induced by halogenated anesthetics (sevoflurane, desflurane, or isoflurane) versus intravenous hypnotics (propofol) [3].

2. Clinical Evidence

 

Myocardial dysfunction following cardiac surgery is a major cause of morbidity and mortality. Ischemia induced during the procedure may cause cardiac dysfunction and low-cardiac-output syndrome [1][4]. Ischemia is induced through physical procedures (local hypothermia) and the infusion of a cardioplegic solution into the coronary arteries. This solution has a high concentration of potassium ion and diffuses within the coronary circulation and cardiomyocytes, inducing cardiac arrest and decreasing basal metabolic oxygen consumption. This solution can be infused either once or several times, based on its composition and the type of procedure. Heart failure, when normal cardiac function is restored after induced ischemia, occurs in 20% of cases. This complication may cause a cardiogenic shock, with high mortality rates [1]. At the preoperative level, cardiac dysfunction is associated with preoperative heart status, whereas at intraoperative and postoperative levels, cardiac dysfunction is related to the type of surgery, the duration of ischemia, and the extracorporeal circulation. During the last 20 years, multiple studies have been conducted to assess the cardioprotective effects of anesthetic agents in cardiac surgery when administered intraoperatively, postoperatively, or both.

2.1. Ischemic Pre- and Postconditioning

Surgeons draw on their knowledge regarding ischemic pre- and postconditioning mechanisms to induce cardioprotection using anesthetic agents. 
In ischemic myocardial conditioning, the coronary arteries are exposed to brief cycles of clamping and declamping prior to sustained ischemia with the aim to reduce heart damage [5][6]. Multiple studies have assessed the size of ischemic areas (areas of myocardial infarction) in models exposed to the technique described above, whereas, in other studies, ischemia is induced without previous conditioning. The results show that the size of the infarcted area was smaller in the models exposed to ischemic pre-postconditioning [7][8]. Ischemic preconditioning, however, involves a high risk in clinical terms. Determining the optimal duration of ischemia for each patient and achieving cardioprotection without causing cardiac ischemia is challenging.

2.2. Anesthetic Pre- and Postconditioning

To overcome the challenges posed by ischemic myocardial conditioning and achieve cardioprotection, some authors recently explored the potential of anesthetic agents to induce pre- and postconditioning. This technique mimics ischemic conditioning but prevents the risk of cardiac ischemia [9]. In the past, during anesthesia induction, hypnotic agents were administered with the only aim of acting on the central nervous system. In recent years, however, owing to their cardioprotective effects, halogenated agents (primarily, sevoflurane, desflurane, and isoflurane) have become the hypnotic agents of choice —versus intravenous hypnotics —in the intra- and post-operative period of cardiac surgery [9][10][11][12][13][14][15][16][17]. Early clinical trials demonstrate differences in heart damage based on cardiac enzyme levels. In clinical terms, differences were also observed in relation to the use of inotropics to treat heart failure of low-cardiac-output syndrome. Thus, the use of halogenated agents for inhalational anesthesia, versus propofol, has been documented to exert cardioprotective effects and reduced myocardial injury [9][14]. In a later sentudry, De Hert et al. documented an association between the duration of infusion and the concentration of the halogenated agent and its cardioprotective effects [14][15][16]. In contrast, recent studies question the morbidity and short-term mortality results reported for this group of patients in relation to the type of anesthetic administered [17], but Bonani et al. observed that volatile anesthetics were superior to propofol with regard to long-term mortality in cardiac surgery with cardiopulmonary bypass [18]. In ouresearchers' opinion, it is very difficult that a single technique can help to overcome all the challenges posed by cardiac surgery and improve morbidity and mortality, regardless of the type of procedure. Hence, the mere possibility that a drug may improve cardiac function and reduce perioperative heart failure in cardiac surgery strongly supports its use.

2.3. Optimizing the Clinical Use of Halogenated Agents

Based on the findings described above, several studies have been conducted to determine whether the sustained use of halogenated agents in the immediate postoperative period exerts similar cardioprotective effects as the ones observed when administered only intraoperatively, with inconsistent results [19][20][21][22]. Steurer et al. [20] report a reduction in myocardial injury in cardiac-surgery patients who received a halogenated agent both intraoperatively and postoperatively (instead of propofol). The authors postulated that cardioprotection could have been achieved through late preconditioning and postconditioning mechanisms. Conversely, Hellström et al. [21] found no significant differences between treatment groups. It is worth mentioning that the postoperative period of sedation was extremely short in this sentudry and could not exert the beneficial effects documented in other studies. These works assessed early late anesthetic preconditioning and/or postconditioning in cardiac-surgery patients. These phenomena are directly related to the immediate postoperative hours. Promising results have been obtained regarding myocardial conditioning induced by halogenated agents (sevoflurane) when administered intraoperatively and maintained during the immediate postoperative period, as compared to the use of an intravenous anesthetic (propofol). The sustained administration of the halogenated agent within the first six postoperative hours seems to be determinant for achieving cardioprotection [22][23][24].

3. Anesthetic Modulation of Oxidative Stress in Heart Failure

Reactive Oxygen Species (ROS) are highly reactive oxygen-containing free radicals such as superoxide (O2−) and hydroxyl (OH−) and chemical elements such as hydrogen peroxide (H2O2) that could generate OH− free radicals through the Fenton reaction or by combining with nitric oxide (NO) to form peroxynitrite (ONOO−). In addition, OH− could arise from the exchange of electrons between O2− and H2O2 through the Haber–Weiss reaction [25]. Under physiological conditions, ROS levels are strictly controlled by enzymatic or non-enzymatic antioxidant defense systems. The main enzymatic defense systems are superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) [26]. The non-enzymatic defense systems can be endogenous, defined as those that can be synthesized by eukaryotic cells, or exogenous, which must be ingested with food. The most outstanding endogenous non-enzymatic systems are the reduced glutathione (GSH) [27] and the Coenzyme Q10 (CoQ10), or ubiquinone [28], and the exogenous ones are Vitamin C (Vit C), or ascorbic acid (AA) [29], and Vitamin E (Vit E) [30], in addition to flavonoids, beta-carotene, and lipoic acid. An imbalance between ROS and antioxidant defense systems is called “Oxidative Stress” and may induce oxidative damage at the DNA level, plasmatic membrane, proteins, and other cellular macromolecules. Different levels have been established to define the intensity of oxidative stress. The lowest level has been identified as physiological oxidative stress or eustress, which affects products involved in cellular metabolism, and the maximum oxidative level has been identified as distress, which induce cellular toxicity through the activation of cellular antioxidant defense processes [31][32].

3.1. Oxidative Stress in Cardiomyocytes

In the heart, ROS contribute significantly to cellular homeostasis through the regulation of processes such as cell proliferation, differentiation, and excitation–contraction coupling [33]. When ROS generation exceeds the capacity of the antioxidant defense mechanisms or when different antioxidant enzymes are impaired, oxidative stress induces cellular disorders at the lipid, protein, and DNA levels; damage at the molecular level; and, finally, heart failure [34], myocardial remodeling with contractile dysfunction, and structural abnormalities of cardiac tissue [25]. Moreover, in the heart, the oxidative stress may be induced by cardiac hypoxia. In this situation, the oxygen concentration becomes a limiting factor for normal cellular activity such as ATP production, and it is associated with cardiovascular damage such as myocardial infarction, stroke, peripheral arterial disease, renal ischemia, and ischemia-reperfusion. The myocardium, under a hypoxia condition, increases blood oxygen extraction, resulting in an important coronary arteriovenous alteration such as the reduction in or interruption of coronary blood flow, named ischemic hypoxia [34], or the reduction in partial oxygen pressure (PO2) in arterial blood, named cardiac hypoxia [33]. Oxidative stress is one of the most important pathways that trigger both pathological situations generated by the hypoxic state of the myocardium.

3.2. Main Sources of ROS in the Heart and Their Pathological Action

The main sources of ROS identified in the heart are the following:
−The mitochondrial respiratory chain: The main mediators of ROS in mitochondria are the complexes I and III. Both complexes are responsible for most of the ROS released by mitochondria at the cardiovascular level, under physiological and pathological conditions [35,36][35][36]. In studies conducted in different animal models, it has been observed that modifications in the oxidative function of mitochondria reduce cardiac aging, protect against cardiac damage, and prevent left-ventricular remodeling [37,38][37][38].
−The enzyme xanthine oxide-reductase (XOR): It is a homodimer of 30 kDa [39]. This enzyme is normally expressed in its dehydrogenase form (XDH), but under inflammatory conditions, it changes its reductase form to oxidase (XO). Both forms are responsible for the oxidation of xanthine to uric acid, favoring a flow of electrons destined for the NAD+ reduction to NADH in the case of the XDH isoform, or oxygen molecules’ reduction to H2O2 and O2–  in the case of the XO isoform [40]. Minhas et al. have shown that the XOR enzyme is the main source of ROS generation in the heart, and its positive regulation contributes to cardiac hypertrophy [41]. In addition, chronic inhibition of XO prevents oxidation of myofibrillar proteins, preserving cardiac function [42].
−The enzyme nitric oxide synthase (NOS): This enzyme belongs to an enzymes group that catalyze the production of NO and citrulline from oxygen and L-arginine as substrates. Uncoupled NOS generates more ROS and less NO, modifying the nitroso–redox balance and causing adverse consequences in the cardiovascular system, while playing a key role in ischemia/reperfusion injury, cardiac hypertrophy, and cardiac remodeling [43]. Conversely, increased NO bioavailability may be considered as one of the universal mechanisms for cardiovascular protection against cardiac impairment. In the myocardium, three NOS isoforms are expressed: endothelial NOS (eNOS or NOS3), neuronal NOS (nNOS or NOS1), and inducible NOS (iNOS or NOS2) [44]. eNOS is expressed in coronary arteries, in endothelial cells of the endocardium, in cardiac-impulse-conducting tissue, and in cardiomyocytes [45]. Myocardial nNOS is preferentially in the sarcoplasmic reticulum. It has been suggested that nNOS-derived NO may inhibit Ca2+ influx through L-type Ca2+ channels and stimulate Ca2+  re-uptake in the sarcoplasmic reticulum by promoting phospholamban (PLN) phosphorylation. The nNOS-derived NO may also modulate the inotropic response to β-adrenergic stimulation and inhibit XOR activity, thereby limiting myocardial oxidative stress and, indirectly, increasing NO availability within the myocardium [43]. Finally, NO derived from iNOS isoform is considered to have detrimental effects on the myocardium. Indeed, upregulation of iNOS by IL-1β and IFN-γ cytokine increased secretion and has been shown to induce apoptosis in neonatal rat cardiomyocytes. In addition, the iNOS myocardial overexpression in mice showed cardiac fibrosis, cardiomyocyte death, cardiac hypertrophy, and dilatation [46].
−The NADPH-oxidase (Nicotinamide Adenine Dinucleotide Phosphate) (Nox) system: NADPH oxidases (Noxs) are a family of seven plasma membrane enzymes and represent the main sources of ROS in the cardiovascular system [46]. They catalyze the reduction of molecular oxygen to O2–  using NADPH as an electron donor. One of them, Nox2, is abundantly expressed in cardiomyocytes, endothelial cells, and fibroblasts. It is a sarcolemma enzyme that is activated by multiple stimuli such as angiotensin-II (Ang-II), endothelin-1 (ET-1), TNF-α, growth factors, cytokines, and mechanical forces [46-48][46][47][48]. Another enzyme such as Nox4 is continuously expressed in endothelial cells, cardiovascular myocytes, and fibroblasts and increases its expression in damaged cardiac cells [49,50][49][50].
−Cytochrome P450 (CYPs) oxidase enzyme: CYP isoform 2E1 (CYP2E1) is in the endoplasmic-reticulum membrane and is the most active CYPs in ROS production [51]. The expression level of CYP2E1 is significantly increased in human-heart tissues under ischemia and is directly involved in the pathogenesis of dilated cardiomyopathy. Its expression is associated with increased expression of oxidative stress markers and apoptotic processes in cardiomyocytes [52].
−The enzyme monoamine oxidase (MAO): It is an enzyme in the external mitochondrial membrane. There are two isoforms: MAO-A and MAO-B. Both isoforms participate in the regulation of metabolism or degradation of catecholamines and other biogenic amines in mammals. Both are expressed at equivalent levels in the human heart [53]. MAO expression and its ability to produce ROS increase with age and are associated with chronic damage. In addition, MAO-A generation due to oxidative stress triggers p53 activation and impairs lysosome function. A genetic deletion of MAO-B has been shown to protect against oxidative stress, apoptosis, and ventricular dysfunction [54].

3.3. Major Cardiac Antioxidant Systems

Maintaining a balance between oxidants and antioxidants protects healthy organisms from the damaging effects caused by free radicals. The continuous generation of free radicals in eukaryotic organisms must be compensated by an equivalent rate of antioxidant substances [33]. Focusing on the heart, the three cell types of the myocardium (cardiac myocytes, fibroblasts, and endothelial cells) [55] possess the most important antioxidant systems [34], which are:
−Superoxide dismutase (SOD): SOD is a metalloenzyme that transforms O2– into H2O2 and prevents the production of ONOO–  by blocking the oxidative inactivation of NO, which would cause important pathological consequences in the cardiovascular system [56].
−Catalase (CAT): CAT is a tetrameric antioxidant enzyme that catalyzes the hydrolysis of H2O2 into oxygen and water. CAT is widely distributed in the peroxisomes of the cell cytoplasm when H2O2  concentrations increase, due to an inflammatory reaction [49,56][49][56].
−The enzyme glutathione peroxidase (GPx): It is a cytosolic enzyme that also catalyzes the hydrolysis of H2O2  into oxygen and water and even the conversion of peroxide radicals into alcohols and oxygen. To date, there are eight different isoforms of GPx. The GPx-1 isoform is the most common. This isoform is in the cytoplasm and in the mitochondria of endothelial cells of the heart where it has been shown to participate as a cardiac protection mechanism [57].

3.4. miRNAs as Therapeutic Regulators of Oxidative Stress in the Heart

MicroRNAs (microRNAs) are composed of twenty-two naturally occurring nucleotides that control gene expression by pairing with specific messenger RNAs, preventing translation, or increasing degradation of the target messenger RNA (mRNA). Currently, miRNAs are being identified as new therapeutic biomarker candidates for different pathologies, including cardiovascular diseases [58]. As cited above, miRNAs are one of the most important subjects of study in the field of cardiac-impairment diagnostics and therapeutics [24]. The preliminary results recently published by ouresearchers' group show several miRNAs as mediators of cardioprotection in patients who received sevoflurane as a halogenated agent in cardiac surgery. In these patients, weresearchers have observed variations in the expression of miRNAs associated with better prognosis of ischemic heart disease. These miRNAs are associated with the activation of mediators of anesthetic-induced pre- and post-conditioning, as well as cell apoptosis reduction and caspase and TNF-alpha concentrations decreasing [59]. Recent publications have described the miRNAs’ crucial role relating to cardiac diseases, such as miR-1. This miRNA is one of the most abundant and specific miRNAs in cardiac and skeletal muscle. It is an important regulator of cardiomyocyte growth in the adult heart, as well as a pro-apoptotic factor in myocardial ischemia, related to diseases such as hypertrophy, myocardial infarction, and cardiac arrhythmias. In addition, it can be used as a biomarker of myocardial infarction [60]. In addition, it has been shown that the expression of certain miRNAs is modified after the administration of antioxidant compounds, showing a protective mechanism against cardiovascular damage [61]. To date, according to published studies, miRNAs can be considered as potential targets and/or stimulators of pathways related to oxidative stress [62] and cardio-protection [59].

3.5. Role of Halogenated Agents during Cardiac Surgery

Oxygen administration is particularly relevant during and after cardiac surgery with extracorporeal circulation. High oxygen concentrations are administered with the intention of preventing cellular hypoxia in patients undergoing surgery under general anesthesia and in those with acute or critical illness. However, excess O2, or hyperoxia, is also known to be detrimental [63,64][63][64]. When ROS formation overcomes the barrier of antioxidant defense systems, the toxicity generated may induce oxidative stress through three different pathways: by excess feeding of the respiratory chain and the consequent mitochondrial uncoupling, by increasing ROS reactions with NO and the consequent generation of cytotoxic reactive nitrogen species, or by lipid peroxidation, compromising the cell membrane stability and, therefore, its functionality. On the other hand, this generated oxidative stress may activate antioxidant defense mechanisms through positive feedback aimed to compensate ROS reactivity, detoxify prooxidants, and repair damage [65]. The high administration of O2  for induction of anesthesia during a surgical procedure could generate a pathological state of hyperoxia. Isoflurane (2-chloro-2-(difluoromethoxy)-1,1,1-trifluoroethane) and sevoflurane (fluoromethyl-2,2,2-trifluoro-1-(trifluoromethyl) ethyl ether) are the most used volatile anesthetics in clinical practice providing unconsciousness and analgesia [66]. The toxicity and beneficial effects of these drugs have been widely studied as well as their effect on oxidative stress, all of which are closely related to the prognosis of surgery. The relationship of both drugs with oxidative stress and ROS production has been analyzed in various animal models of heart failure. Regarding oxidative stress, it has been demonstrated that in states of oxygen-concentration imbalance, such as hypoxia, isoflurane and sevoflurane have a protective effect on ventricular myocytes, reduce the expression of inflammatory factors and markers of oxidative damage, increase the expression of antioxidant enzymes such as superoxide dismutase and catalase, regulate the expression of apoptosis-related genes, and reduce oxidative stress and nitric oxide levels through the ROS and NOS levels’ modulation. Regarding the studies carried out to relate both drugs to ROS production, paradoxically. it has been observed that they may be involved in the beneficial effects of volatile anesthetics used in preconditioning [67,68][67][68]. Clinical studies have also been conducted to demonstrate the cardioprotective effect of both halogenated drugs, and it has been observed that they do not affect the cytotoxicity nor do they produce cell damage at the DNA level. In addition, both anesthetics are linked to increased activity of antioxidant enzyme defense systems and do not trigger oxidative damage processes in the intervened patient or DNA oxidation. These beneficial effects of halogenated drugs improve the clinical outcomes of patients undergoing cardiac revascularization surgery due to their cardioprotective effect induced through different mechanisms such as modulation of G-protein-coupled receptors, intracellular signaling pathways, gene expression, potassium channels, and mitochondrial function. In addition, administration of volatile anesthetics has been shown to reduce biomarkers of myocardial damage and short-term mortality after cardiac revascularization surgery [69-71][69][70][71]. Dharmalingam et al. [72] [72] recently examined the relationship between volatile anesthetic administration and oxidative stress in patients undergoing cardiac revascularization surgery and concluded that preconditioning with the volatile anesthetics isoflurane and sevoflurane prevents oxidative and nitrosative stress during cardiac-revascularization surgery. Between these two halogenated agents, isoflurane provides better protection during the period before cardiopulmonary bypass, whereas sevoflurane provides protection during the periods before and after cardiopulmonary bypass. As cited above, wresearchers have demonstrated that the use of sevoflurane during the operative and postoperative process increases the overexpression of enzymes that reduce myocardial damage [24]. On the other hand, some published studies have questioned the beneficial effect of volatile anesthetics. Recently, Landoni et al. [17] have carried out a multicenter, randomized, blinded, and conftrolled clinical trial in which they observed that the use of volatile anesthetics during cardiac-revascularization surgery reduces short-term mortality in patients who underwent surgery; however, they have not observed differences regarding patients who received intravenous anesthesia. In this sentudry, no study to determine the relationship between the administration of both halogenated drugs and oxidative stress was performed.

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