Clinical Follow-Up of Patients after Coronary Artery Bypass Grafting

Abstract

The follow-up of patients after coronary artery bypass grafting is of paramount importance for a good control of chronic ischemic coronary disease. The non-pharmacological treatment should be approached in an assertive way with the patients, placing it at the center of the problem participating in the health process and definitely understanding the disease. Pharmacological clinical treatment involves modern drugs, widely studied, tested and available worldwide, which need to be used at the maximum tolerated dose in order to achieve the goals disseminated by the guidelines with a view to improving morbidity and mortality and quality of life of patients.

1. Introduction

Coronary heart disease is one of the main causes of mortality worldwide, and coronary artery bypass grafting is one of the forms of treatment for the disease. However, after coronary bypass surgery, the follow-up of patients is of great importance because coronary disease does not cease to exist with surgery and patients continue to fall ill in a natural process of disease evolution, the cardiovascular continuum. Such clinical follow-up should be done strictly with non-pharmacological and pharmacological measures aimed at improving the mortality of patients with chronic coronary heart disease and the morbidity involved, trying to offer the best possible quality of life. The attending cardiologist has the task of always seeking an approximation of the patient with the health-disease process, placing as the main actor of the process to actively participate in the treatment and use the best tools and therapeutic possibilities for each patient to achieve the goals guided by the guidelines.

2. Discussion

IHD (Ischemic Coronary Disease) is one of the major causes of mortality worldwide [1] and its incidence and prevalence have been increasing progressively in much of the globe [2]. This increase has occurred due to the continuous worsening of the lifestyle that we have seen adopted over the last few years by humanity, by which in the final analysis end up increasing the risks of diabetes, arterial hypertension, dyslipidemia and obesity [3], considered the great villains of IHD [4]. And an alarming finding is that this has occurred despite great efforts by various agencies around the world with campaigns of primary prevention measures and public initiatives trying to encourage lifestyle changes [5]. Even more worrisome is the fact that there has been a significant increase in young patients affected by the disease [6].

Knowledge about risk factors has improved among people and the understanding of the relationship with cardiovascular disease has also improved [1], however, it is still perceived that there is a long way to go in order to achieve a considerable significant reduction in atherosclerotic disease involvement. Guidelines from around the world recommend lifestyle changes (physical exercise, diets and smoking cessation) and control of risk factors (hypertension, diabetes and dyslipidemia) in addition to drug treatment to minimize the effects of atherosclerosis primarily, but also as a form of secondary prevention combined with some myocardial revascularization therapies in some cases for conorariopathic patients [7]. However, even when this is routinely adopted, there is still a considerable residual risk of major cardiovascular events (MACE): myocardial infarction (MI), stroke, or cardiovascular mortality (CM) [8].

IHD is a disease with typically chronic evolution, with inexorable progression over the years or decades, regardless of any type of treatment that is used [9], that is, although more modern therapies have increased the survival of patients with coronary artery disease, a significant number of them will develop Chronic Coronary Heart Disease (CCHD) at some point in the follow-up [10]. This is because the risk factors continue to overload the myocardial muscle by inflammatory oxidative stress consequent to age, diabetes, hypertension, hypercholesterolemia, sedentary lifestyle, smoking, among others, so it is present both in the genesis of atherosclerosis, as well as in the etiology of IHD and in the progression of CCHD [11]. Annually, 1 in 30 patients with IHD ends up dying due to complications related to the disease, either by Myocardial Infarction (MI), by decompensation of Heart Failure (HF) and/or by arrhythmias consequent to these conditions [12, 13], and about 5–10% of cardiac patients have some cardiovascular event per year [14]. Therefore, reducing the morbidity and mortality involved in CCHD should be our first target in the treatment of patients with this disease [15], as a form of secondary prevention, and to achieve these goals, the treatment of CCHD should be instituted in a rapid, global and rigid manner in all patients [16].

Another factor that justifies the need for assertive treatment of the disease is its important economic impact, since the need for hospital admissions, diagnostic and therapeutic procedures, medical follow-up and continued pharmacological treatment determine a significant economic impact, according to government sources [17]. In the United States, for example, the estimated annual hospital cost for the treatment of events related to ischemic heart disease was US$ 15,540,00 for non-fatal infarction, US$ 2569,00 for stable angina, and US$ 12,058,00 for unstable angina in 1998 [18], and those numbers have been increasing year after year. In Europe, the scenario is the same: in Portugal the DCCC consumed just under 2 billion euros in 2016, equivalent to 1% of that country’s GDP (Gross Domestic Product) or 11% of health expenditure at the time [19]; in Belgium in 2004 the estimated cost of the disease was more than 2 billion euros, equivalent to 4000 euros per patient that year [20].

The basis of the treatment of CCHD is the clinical medication [21], instituted years and years ago and increasingly necessary, as confirmed by the largest scientific studies available to date, with the insertion of new drugs more potent, with better results day after day, with lower incidence of undesirable effects and greater symptomatic control of patients [22]. This time, the drug therapy of CCHD has been composed of drugs that slow the progression of the disease, reduce cardiovascular events, improve symptoms and, consequently, quality of life, a fact elucidated by evidence on the reduction of angina cases [23]. This has contributed to not further worsen mortality and promote better quality of life among patients [24], since the treatment instituted prevents ventricular remodeling, preserves the myocardium and ventricular function, reduces sudden death and improves the functional class and prognosis of the sick [25].

Allied to the optimized drug treatment, the various modes of secondary prevention are already well known, as we have said, such as lifestyle changes (abandonment of sedentary lifestyle, adherence to diets known to be cardioprotective, combating obesity and smoking cessation, mainly) [26] and combating modifiable risk factors such as hypertension, diabetes and hypercholesterolemia, especially [27]. However, on the one hand, we have still noticed a very persevering therapeutic inertia among cardiologist medical professionals with little prescription of what is considered the best possible treatment [28] and on the other, little adherence on the part of patients to what has been prescribed [29]. This is an unacceptable reality since it is recognized that good adherence to optimized cardiac therapies could be associated with a 35% reduction in mortality risk from any cause in patients with CHD [30].

On the part of physicians, such inertia is erroneously justified, in part because they accept that patients being asymptomatic, for example in the postoperative period of coronary artery bypass graft surgery, are well treated, but do not pay attention to the so-called therapeutic targets already widely disseminated by international Guidelines. On the part of patients, the lack of adherence to the proposed treatment often finds justification because they do not truly know the problem they have, because often the doctors who treat it do not express themselves convincingly, they cannot make patients understand how important the subsequent treatment is. To reverse the situation, it is up to cardiologists to apply the best available evidence, which is constantly updated and widely disseminated around the world and a good persuasion training with patients and families to understand the dimension of the problem and the real benefit of the proposed treatments.

Part of the non-pharmacological treatment known to be beneficial in CCHD is the abandonment of sedentary lifestyle and stimulation of physical exercises. In fact, it has long been known that it is important that such practices are important to improve cardiovascular health in the postoperative period of Coronary Artery Bypass Graft surgery (CABG), with several studies demonstrating that patients with CCHD, who participate in regular physical training programs, and who receive guidance on the control of risk factors for cardiovascular diseases, have a lower number of postoperative events and hospital readmissions and reduced mortality [31]. However, very little is addressed in a real and practical way these orientations and the patients even understand that this conduct is really necessary, but they are not really oriented to adopt it as a daily practice or in a correct, continuous way. Thus, stimulating the practice of daily physical activities, preferably in cardiac rehabilitation programs, reduces cardiac and all-cause mortality [32].

Likewise, it is well known of all the harms of tobacco for heart health, and patients who maintain addiction after CABG surgery have a higher chance of death than those patients who do not [33]. However, it is estimated that although 70% of smokers wish at some point to stop the addiction, only 1/3 of them can actually do so [34]. This is because many of them simply do not understand the reasons why they should quit smoking or do not feel encouraged to take action since they do not have precise guidance on the risks and problems involved with addiction. It is up to the cardiologist to openly address the topic, explaining the real harms, the ways in which tobacco degrades the circulatory system and heart, but also addressing benefits that are obtained by quitting tobacco and how to proceed to achieve success in quitting smoking. Several techniques of psychotherapy or daily habits associated or not pharmacological treatments have been employed in several parts with expressive results [35]. It is essential to identify situations and strategies that can improve the effectiveness of treatments for tobacco use and in all therapeutic approaches, smoking cessation is one of the most crucial factors [36].

Another very important factor in the non-drug treatment of CCHD is diet, since it is known that diet has a key role in the progression of ischemic heart disease, since the intake of diets rich in saturated fat, calories and salt can result in greater lack of control of the main risk factors for CHCD: obesity, hypertension, diabetes and hypercholesterolemia [37]. Thus, the re-education of dietary habits represents an important intervention in the secondary prevention of ischemic heart disease and its indication is based on several clinical evidences [38]. Epidemiological, observational and intervention studies have demonstrated the positive influence of a balanced diet on the primary and secondary prevention of cardiovascular events in the postoperative period of CABG and in the follow-up of the CCHCD and dietary patterns free of trans fats reduced in saturated fats, sugars, rich in fiber, unsaturated fats and complex carbohydrates demonstrate an inverse association with the development of cardiovascular disease, presenting positive action in the control of metabolic disorders [39]. Likewise, the harmful effects of alcohol on the cardiovascular system of patients with CHCD are widely known [40], so that the consumption of alcoholic beverages should be discouraged in all patients.

In addition to these so-called conventional risk factors, some others have been cited as adjuvants in CCHD, including environmental pollution [41], stress [42], respiratory infections [43], among others, which also need to be prevented and treated. Finally, some morbidities should also be investigated and addressed, under penalty of compromising the good evolution of patients with CHCD, such as: hypothyroidism [44], chronic kidney disease [45], atrial fibrillation [46], among others.

When it comes to clinical drug treatment, as we have commented, a considerable range of drugs has been tested and approved for what is called Optimized Drug Treatment, which should be widely instituted in all patients with CHD, unless there is some important contraindication or undesirable effect limiting the use. The basis of BMT encompasses the use of prognostic-modifying and cardioprotective medications such as angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, beta-blockers (and other sinus node blockers), statins, and antiplatelet agents for all patients [25], in addition to mineracolocorticoid inhibitors in some specific situations, as well as sodium-glucose co-transporter inhibitors (SGLT2) and symptomatic medications such as nitrates and other vasodilators, diuretics, among others, as we will discuss below. Such treatment should be employed to avoid undesirable outcomes such as death, myocardial infarction and/or heart failure (HF), which is the final pathway of cardiac diseases, invariably. However, when HF is developed, other strategies are employed to reduce mortality and prevent sudden death, improve symptoms and readmissions and the prognosis of patients, such as the use of implantable cardiodefibrillator (ICD) or resynchronizer, and heart transplantation in specific cases [47].

Specifically in relation to antiplatelet agents, acetylsalicylic acid (ASA) is the first choice because it reduces, on average, by 33% the risk of cardiovascular events in patients with CCHD [48], should always be prescribed in all patients, except for rare cases of contraindication (allergy or intolerance, active bleeding, hemophilia and active peptic ulcer) or high probability of gastrointestinal or genitourinary bleeding, with degree of recommendation I, level of evidence A [49], at a dose of 75–325 mg/day [50]. Other platelet antiaggregants such as P2Y12 enzyme inhibitors (clopidogrel, prasugrel and ticagrelor) play a key role in increasing the prevention of coronary thrombogenesis, being used in association with ASA or in substitution for it when there is an absolute contraindication to its use [49], with excellent results. The Clopidogrel vs. Aspirin in Patients at Risk of Ischaemic Events (CAPRIE) study showed a slight overall benefit of clopidogrel use over ASA with a better safety profile in preventing undesirable cardiovascular outcomes [51], should be used at a dose of 75 mg/day in association with aspirin (ASA) if there is MI for 1 year and ad eternum if there is a high risk of new coronary events, and this period may be reduced depending on careful individual evaluation taking into account bleeding risk and benefit of extended antiplatelet aggregation [52]. Prasugrel, on the other hand, has a faster, more predictable onset of action and, on average, a greater antiplatelet effect than clopidogrel, with greater efficacy in aspirin patients undergoing percutaneous coronary intervention (PCI), but not in patients only clinically treated [53], however, on the other hand, it has a higher risk of bleeding and should be used with caution in patients with a history of stroke, older than 70 years and less than 60 kg of body weight [54]. Finally, Ticagrelor has a more predictable and consistent higher level of P2Y12 inhibition during maintenance treatment of patients adhering to treatment [55], and also faster onset of action than clopidogrel [56], in addition to similar efficacy and safety to aspirin when monotherapy [57], at a dose of 90 mg 2 x daily, however, more prone to bleeding [58].

Incidentally in specific cases is indicated the double antiplatelet aggregation terapy (DAPT), being always necessary the presence of aspirin associated with one of the P2Y12 inhibitors mentioned, such as: in general, infarcted patients who are submitted to CABG should receive DAPT for 1 year or in those with CCHD who were affected by AMI, as well as in those post-CABG in which a subsequent percutaneous coronary intervention (PCI) was required who should receive DAPT for at least 6 months to 1 year, depending on the type of coronary stent used and/or the benefit of maintaining therapy versus risk of bleeding, digestive, or other fatal and non-fatal [59]. In order to protect the patient from gastric bleeding, a proton pump inhibitor (PPI) such as pantoprazole at a dose of 40 mg/day for example (but not omeprazole or esomeprazole) can be used, since they reduce the risk of gastrointestinal bleeding in patients treated with DAPT and can be used with some safety [60].

In relation to other anti-thrombotic drugs, anticoagulants are currently accurately indicated if there is a rhythm of Atrial Fibrillation (AF) at any time, replacing all the antiaggregants mentioned above, and therapy is recommended in patients with CCHD and such arrhythmia to reduce the risk of ischemic events, especially cerebral, since they have been shown to be superior in this prevention in relation to monotherapy with aspirin or another P2Y12 inhibitor or DAPT [61]. On the other hand, in sinus rhythm, antiplatelet therapy associated with the use of anticoagulants, even at low doses to prevent new ischemic events, is still controversial and lacks further evidence [62].

Post-CABG dyslipidemia should be managed rigorously, following therapeutic targets already defined by guidelines based on pharmacological treatment and lifestyle change [63]. Such patients are considered to be at very high cardiovascular risk and therefore should have LDL-cholesterol reduced to less than 50 mg/dL or even lower in order to avoid further ischemic events [7]. The basis of pharmacological treatment is with statins at the maximum possible and well-tolerated dose (rosuvastatin 40 mg/day or atorvastatin 80 mg/day) and, when target LDL-cholesterol levels are not reached with statins alone, the combination of ezetimibe at a dose of 10 mg/day is indicated [64]. In recent years new antilipemics have been included in the list of treatment of dyslipidemias and in this scenario fit the molecules inhibitory of the conversion of the liver enzyme in the active metabolite PCSK9 (evolocumab and alirocumab), which guarantee an even greater reduction of LDL levels, and should be used when reaching the maximum dose of statins in association with ezetimibe and has not yet reached the recommended target level [15]. Such drugs, in robust trials, have demonstrated a great potential to reduce LDL-cholesterol levels, with interesting ischemic protection and with an equally encouraging safety and tolerability profile, being used in subcutaneous applications every 15 days. More recently, inclisiran, an inhibitor of hepatic synthesis of the enzyme PCSK9 whose LDL-cholesterol-lowering effect has been sustained in clinical studies with subcutaneous applications every 6 months, and an acceptable safety profile [65].

In addition to those already mentioned, an equally important pharmacological class for the treatment of patients after CABG and which, as we have said, is part of the basic therapeutic arsenal of these patients, are the Angiotensin-Converting Enzyme (ACEi) Inhibitors, whose main representatives are: enalapril up to 40 mg/day, captopril up to 150 mg/day, ramipril up to 10 mg/day plus lisinopril and peridonpril. They have been shown to be beneficial in the prevention of death, AMI and stroke and have an important role in minimizing the occurrence of ischemic events after CABG, and should be administered early to all patients with ventricular dysfunction, due to the advantages of these drugs in relation to cardiac remodeling and hemodynamic improvement (vasodilation and reduction of afterload) generating a decrease in mortality and acting as anti-ischemics, through its protective effects of the vascular bed (antiatherosclerotic, antithrombotic and anti-inflammatory) [66]. A not infrequent side effect of ACEi is dry cough, which can be an impediment to continuous use, and in these cases should be replaced by Angiotensin II Receptor Blockers (ARBs), whose most used representatives are: losartan up to 100 mg/day, valsartan up to 320 mg/day, candesartan up to 32 mg/day, olmesartan up to 40 mg/day. ARBs seem to be as effective as, or possibly slightly less effective than, ACEi when compared directly [67], and, therefore, although the reduction in mortality and hospitalization has been demonstrated with these drugs in some studies with patients intolerant to ACEi, due to the greater number of evidences, ACE inhibitors remain the medication of choice, ARBs being a reasonable alternative [68]. ACEi or ARBs are indicated up to the maximum tolerated dose in order to obtain maximum SBP (systolic blood pressure) below 130 mmHg and DBP (diastolic blood pressure) below 90 mmHg, and when such values are not obtained, the association with thiazide diuretics such as hydrochlorothiazide at the maximum dose of 50 mg/day should be considered, Other options being dihydropyridine calcium channel blockers as amlodipine up to 10 mg/day, levanlodipine up to 5 mg/day, nifedipine up to 60 mg/day or nitrendpine, lercanidipine, felodipine [69].

More recent studies have identified neprilysin, an endogenous enzyme that degrades vasoactive peptides such as bradycin and natriuretic peptides and the inhibition of this enzyme by the sacubitril-valsartan combination has shown very satisfactory results generating diuretic and natriuretic effect, myocardial relaxation anti-remodeling and reduction of renin-aldoesterone, known vasoconstrictors. Its use has been recommended in patients after CABG, especially in patients with dyspnea, in efforts to reduce cases of re-hospitalization for heart failure (HF) and death [70].

Beta-blockers (metoprolol up to 200 mg/day, atenolol up to 100 mg/day, carvedilol up to 100 mg/day, nebivolol up to 10 mg/day or bisoprolol up to 10 mg/day) also make up the basic treatment for post-CABG patients, since patients must maintain heart rate (HR) between 55 and 60 BPM at rest sinus rhythm [71], in order to ensure the best benefit, which is an important reduction in mortality and/or cardiovascular events [72]. If such a HR index cannot be achieved, the association with non-dihydropyridine calcium channel blockers (verapamil up to 480 mg/day or diltiazem up to 240 mg/day) may be necessary, although its increase in clinical benefit is uncertain and has potential undesirable effects such as bradyarrhythmias and/or atrioventricular blocks [73]. Another option to be associated with non-dihydropyridine beta-blockers and/or BCCs in the control of HR is ivabradine (at a maximum dose of 15 mg/day), which has shown good results in increasing exercise tolerance, increasing the effort-induced ischemic threshold and reducing effort-induced angina [74].

As we have already mentioned, aldosterone blockade is an important pharmacological treatment route of CCHD, especially in those patients who develop HF and/or reduced ejection fraction (EF) on echocardiogram, and this is also possible with mineralocorticoid inhibitors such as spironolactone (25–50 mg/day) and eplerenone (25–50 mg/day). The use of such medications was associated with lower mortality and hospitalization rates, as well as lower vascular and myocardial fibrosis in this type of patient [75], eplerenone, being a more selective inhibitor, has a more pronounced effect and less side effect of gynecomastia and erectile sexual dysfunction than spironolactone [76]. Similarly, patients with CCHD after CABG who develop some degree of HF should receive SGLT2 inhibitors (empaglifozine up to 25 mg/day and dapaglifozine up to 10 mg/day), which inhibit glucose reabsorption in the proximal convoluted tubule, resulting in glycosuria and reduced glycemic levels [77] and improve left ventricular parietal tension secondary to decreased pre- (effect of natriuresis and osmotic diuresis) and afterload (improvement in endothelial function and reduced blood pressure) [78], improve cardiomyocyte metabolism and bioenergetics (increased ketogenesis and increased β-hydroxybutyrate supply), inhibit the myocardial sodium-hydrogen pump (which leads to higher calcium concentration in the mitochondria), reduce cardiac necrosis and fibrosis (inhibition of collagen synthesis), and decrease cytokine production in epicardial fatty tissue [79]. Such effects guarantee in these patients a significant reduction in the main adverse cardiovascular events: cardiovascular death, AMI and stroke, and a surprising reduction in hospitalization for heart failure [80], in addition to improved quality of life and renal protection [81].

In patients who still remain symptomatic for angina after CABG, it is crucial to identify if there is no de novo obstructive coronary disease by means of follow-up exams such as cineangiochonariography and/or myocardial scintigraphy/echostress for example and once the presence of arterial obstruction is excluded, improve the antianginal treatment, which can be done with short-acting nitrates (such as isosorbide dinitrate 5 mg) or long-acting (such as isosorbide mononitrate up to 60 mg) mg/day, and other medications, which have adjuvant power and should be used when the patient is on the maximum tolerated dose of beta-blockers [7]. Trimetazidine (35 mg 12/12 h or 80 mg single daily dose) is an antianginal with neutral hemodynamic effect that in addition to beta-blocker improves effort-induced myocardial ischemia more than other antianginal drugs [82], which supports the indication of its use as a second line of medications in patients with BMT and still persistently anginal [7]. Other available options of anti-anginal drugs such as nicorandil and ranolazine are also possible but with fewer indications for the treatment of patients with CCHD and have use considered an exception by the largest studies carried out, since although they reasonably improve angina have possible undesirable effects that discourage the use such as nausea, increased QT interval, gastrointestinal ulcerations, constipation, among others [7], moreover, the studies revealed that such medications did not interfere, in a statistically justifiable way, in the reduction of the compound of hard events (AMI, cardiac death and stroke) [83].

It is perceived that the range of treatment for CCHD is immense, however, a major obstacle, as has been said, to achieve goals and the maximum benefit that the treatment can offer is adherence to treatment by patients. Studies have emphasized that low adherence to treatment, both pharmacological and non-pharmacological, is among the main destabilizing factors of CCHD [84] and because of this, readmission rates remain high [85]. Several studies have shown that low adherence to treatment would be related to risk factors involving socioeconomic problems, psychological disorders and cognitive impairments, added to the characteristics of the disease and the complexity of the treatment. In addition, the costs of medications, the quantities and their effects, the relationship between health professional and patient and the various types of support given are factors that contribute to influence treatment adherence [86]. Alarming numbers, such as 50% adherence to optimized pharmacological treatment and only 20% adherence to non-pharmacological guidelines, have been found in studies with CCHD [86], a frightening scenario that needs to be urgently reversed with systematic education of patients and more frequent follow-up by attending physicians, in search of the best for each patient.

Special attention deserves some questions and doubts brought by patients in relation to some factors in the post-CABG such as hormone replacement for example, use of medications for erectile dysfunction and testosterone replacement, consent to sexual activities, vitamin replacement and vaccination in general.

Regarding hormone replacement, some controversies are old, but the current trend is towards non-indication for cardiovascular protection, since the results of large randomized studies have shown that replacement does not improve cardiac prognosis and increases the risk of more severe cardiovascular disease in women after 60 years of age [7]. In addition, smokers and obese women should be encouraged to lose weight and stop the addiction and if it is not possible, hormone replacement is even more preventive, despite greatly increasing the risk of thromboembolic phenomena.

In the case of erectile dysfunction it is known that such a condition is an important predictor for more serious cardiovascular diseases in post-CABG patients and a high percentage of patients after CABG have some erectile disorder. Even the association with coronary artery disease is the cause of erectile dysfunction, in general, especially if the patient is diabetic, and not the use of medications (such as beta-blockers, ACE inhibitors, statins, etc.) to treat CHCD as is thought, although the evidence is limited and conflicting. Usually if erectile symptoms occurred within 4 weeks of starting treatment for CCHD the cause may actually be medications and other therapeutic options may be tried, but if they occur after 4 weeks of use, other causes should be investigated. On the other hand, drug therapies for erectile dysfunction do not increase the cardiovascular risk in patients with CHCD after CABG and can be indicated in stable patients, if necessary, as long as they are not using nitrates and do not use doses higher than the maximum recommended as safe, and special attention should be paid to more hypotensive patients [87].

Incidentally a frequent doubt in the follow-up of post-CABG patients is the return to sexual activities. The fear of the occurrence of cardiac complications during sexual intercourse is responsible for most of the changes in sexual dysfunction that occurs in patients with heart disease after CABG, and it is reported that 17% of patients and 35% of their spouses are afraid to resume sexual activities and 39% of patients reduce their practice after having undergone this type of treatment. However since the creation of man sexual activity is part of our day-to-day and it has light metabolic expenditure, because the maximum cardiac effort does not exceed more than 10–15 seconds, reaching maximum heart rate between 90 and 144 bpm, and similar to climbing two flights of stairs, walking hurriedly or performing common tasks in various occupations [88], so that the cardiac patient after CABG, as he feels safe, less symptomatic, and after 3–4 weeks which is the approximate time of bone healing of the sternotomy, you can be released to practice your sexual activities normally.

Testosterone, in turn, as we know, has androgenic and anabolic effects, but also exerts an effect on the vascular bed, promoting vasodilation through the release of nitric oxide and modulation of calcium channels, which impacts endothelial function. In patients with coronary artery disease (CAD) and heart failure (HF), reductions in total testosterone concentrations are related to higher mortality and severity of these diseases, however, although the effects of testosterone on the increase of muscle mass and muscle strength are well established in the literature, the effects of this substance on the cardiovascular system need to be better elucidated [89], studies have shown that exogenous replacement is related to changes in the lipid profile (reduction of HDL and increase in LDL), morphological and functional changes of the left ventricle, hemodynamic changes and autonomic alterations [90], which makes it still not well regarded and controversial for the treatment of patients with CCHD after CABG [87].

Vitamins and supplements have emerged in droves these days with promises of improving cardiac performance. The association between hypovitaminosis and inflammatory markers and subclinical atherosclerosis has been reported in several studies, generally cross-sectional and small and deficiency of some vitamins has been associated with both endothelial dysfunction, reflected by lower brachial artery flow-mediated dilation as to the greater carotid intima-medial thickness in different patient profiles [91]. Still some studies have even shown that the status of vitamin D for example can also influence the prognosis of individuals already affected by AMI and in elderly with stable HF have significantly lower concentrations of 25(OH)D, verifying among these a prevalence of hypovitaminosis D of almost 100% [92]. However, a recent population survey in the United States showed that the prevalence of hypovitaminosis D has been increasing in recent years, currently affecting up to 90.0% of pigmented populations (black, Hispanic and Asian) and around 3/4 of the white population, especially in older patients [93]. Therefore, it is not yet clear whether hypovitaminosis D is an important risk factor for heart disease or occurs at random due to the age of those affected with the disease and data from randomized studies to evaluate the impact of vitamin D supplementation in patients with coronary artery disease after CABG on their cardiovascular risk are limited, especially in relation to hard outcomes, and have sometimes reported conflicting results [92]. As seen, some hypovitaminosis is an emerging public health problem in the world, with important implications for cardiovascular morbidity and mortality, but there is still a lack of sufficient evidence, based on large randomized and placebo-controlled studies, with long-term follow-up and with adequate statistical power to evaluate hard outcomes in patients with coronary artery disease after CABGV and only in this way can the role of vitamin supplementation in the prevention and treatment of these patients be definitively established.

Finally, the need for influenza vaccination in patients with heart disease was determined first by historical reports of increased mortality in epidemics and, later, by epidemiological studies and today, it is known that annual vaccination is an effective measure in secondary prevention, as it reduces hospital admissions for HF, stroke and AMI in post-CABG patients, in addition to reducing overall mortality more significantly than many drugs or interventions [93]. On the other hand, since the first series published from China and Italy, the severity of COVID-19 has stood out in the carriers of chronic non-communicable diseases such as those with CHD after CABG, most likely taken in common by chronic systemic inflammation, so that currently this group of patients must also be vaccinated against COVID, In the light of current knowledge [94], however, it remains to better define the periodicity of vaccination indication or vaccination schedule. In addition, it is known that patients with post-CABG CHCD have an increased chance of presenting decompensation of the disease at some point and hospitalization for HF and, in a nosocomial environment, patients with HF have an increased risk of pulmonary infections, especially pneumonia, thus, vaccination against respiratory infections by pneumococci is also cost-effective as a public health measure [95].

The clinical evolution of coronary patients after CABG tends to be benign, but some cases may present complications in the follow-up, and therefore this should be done often, with routine consultations every 6 months in the first year after surgery, at most, because the chance of developing exacerbations of the disease and the appearance of HF is great due to systolic and/or diastolic dysfunction due to myocardial injury caused by chonaropathy [7]. And it is recognized that there is a risk of more evident complications in symptomatic patients but also in oligo or asymptomatic patients, so that in the consultations an active search for HF symptoms should be made, with special attention to the search for exercise intolerance and dyspnea to exertion in addition to the search for associated angina or equivalent, assessment of adherence to recommended therapy, physical activities and diet [7]. In the clinical examination it is necessary to check the nutritional status and make active research for signs of HF such as leg edema, presence of signs of HF such as jugular stasis, hepatomegaly, sacral edema/anasarca, pulmonary crepitation, among others, and also evaluate heart rate and blood pressure and know how the pressure levels are outside the office environment for therapeutic optimization in addition to cardiac auscultation in order to search for heart murmurs and/or muffling of sounds [7].

In the periodic evaluation of complementary exams, the routine electrocardiogram, which provides information on heart rate and rhythm, as well as possible identification of arrhythmias and conduction disorders and signs of overload of cardiac chambers, and echocardiogram for evaluation of cardiac chambers, systolic and/or diastolic dysfunction, of the ejection fraction, appear as crucial options. The presence of cavitary thrombi and other complications as indirect signs of pulmonary hypertension and valve dysfunction, among others [7]. The chest X-ray, in turn, is useful for identifying signs of pulmonary congestion, interstitial edema and investigation of pleural effusions7 and blood laboratory tests serve for the objective evaluation of nitrogenous slags and subjective renal function, investigation of electrolyte disturbances and evaluation/follow-up/treatment of metabolic diseases such as thyroidopathy, diabetes and hypercholesterolemia in addition to the identification of possible complicating factors such as hyperuricemia, liver diseases, among others [7]. It should be noted, however, that although there is some additional prognostic value in the use of several serological biomarkers (such as BNP, CRP, among others) individually or in association with each other, there is currently no evidence that routine use ensures better evaluation and care [7].

All this evaluation is of paramount importance because post-CABG patients are recognized as having very high cardiovascular risk and as such should have the laboratory and hemodynamic targets sought at all times, in order to minimize the risk of secondary HF, need for new revascularization (percutaneous or surgical), death or other complications, which may be more impactful in the first year after surgery. After 1 year of CABG, annual consultations are sufficient in patients with good evolution and in patients with some complication identified by complementary tests, or in those at high risk for them, or who have symptoms at some point again a more rigorous follow-up is necessary [7].

Other equally important tests for follow-up are the 24-hour holter and 7–20 day lopper, which can help in the search for arrhythmias and/or evaluation of symptoms such as dizziness, palpitation, among others and signs such as syncope or pre-syncope, for example. Similarly, a TILT-test may be indicated in special situations and carotid and lower extremity Doppler if concomitant vascular obstruction at other arterial sites is suspected. In cases where the echocardiogram is not elucidative or if there is the intention to investigate the presence of myocardial fibrosis or infiltrative myocardial diseases, magnetic resonance imaging is highly indicated. If the idea is functional evaluation of the patient with a view to release for physical activity practices and/or research of stress-induced signs/symptoms, the treadmill exercise test is highly indicated.

Finally, in patients with unequivocal persistent symptoms of de novo coronary obstruction, such as angina on exertion, for example despite the optimized drug treatment and the recommended therapeutic goals have been achieved, a new evaluation for the investigation of metabolic alterations and myocardial ischemic suffering can be used as scintigraphy or other imaging tests with stress such as echocardiography, for example [96]. If there is indeed ischemia demonstrated by such tests and/or the patient remains symptomatic, a new coronary angiography may be more elucidative and define better forms of treatment.

It is noticed, therefore, that the prognosis of post-CABG patients will depend on a number of factors such as the presence of comorbidities such as diabetes, dyslipidemias, advanced age, obesity, smoking, degree of physical activity and adherence to healthy living practices (diet, etc.) prior to surgery, in addition to the concomitant presence of cancer, arterial obstructions in other arterial sites, hepato or nephropathies or other systemic diseases. It is also recognized that the presence of symptoms of angina and/or dyspnea after CABG or equivalent also mean a worse prognosis of patients with CHCD, as well as arrhythmias on exertion or at rest and especially adherence to the proposed drug therapy. They also have a considerable influence on the anatomical-morphological-functional aspects of the cardiac chambers seen by echocardiogram and/or resonance imaging and the presence of new coronary obstructions after CABG with or without the need for new revascularization.

3. Conclusion

As seen, the post-CABG treatment is extremely important and follow-up of patients of paramount necessity, since the disease has a progressive character and the evolution to hard outcomes seems inexorable. The attending cardiologist takes a broad, rigorous and continuous approach placing the patient in the center of attention with an understanding of the disease, clear and objective explanations. Always attentive to the recommended goals and adopting the best available evidence with the most cost-effective treatment to achieve them and with great empathy with the patient in order to provide improvement in overall mortality, morbidity and quality of life.

Conflict of interest

The author has no conflict of interest.