Postoperative complications of coronary artery bypass grafting: a narrative review on pathophysiology, management strategies, and the emerging role of artificial intelligence

Introduction

Coronary artery bypass grafting (CABG) represents a cornerstone of cardiovascular medicine, providing durable revascularization for patients with complex and advanced coronary artery disease (CAD) (1,2). Since its inception, the procedure has evolved significantly, yet it remains the standard of care for specific high-risk cohorts, including those with multivessel disease, significant left main coronary artery stenosis (LMCAS), or refractory angina pectoris unresponsive to optimal medical therapy or percutaneous coronary intervention (PCI) (1-4). Landmark clinical trials have consistently demonstrated its superiority in improving long-term, event-free survival, particularly in patients with diabetes mellitus or complex anatomical disease (5,6). With nearly 400,000 procedures performed annually in the United States alone, its impact on public health is substantial (4). Despite its survival benefits, CABG remains inherently invasive, creating a physiological burden that can precipitate postoperative complications.

The profound physiological insult of CABG, often involving cardiopulmonary bypass (CPB) and cardioplegic arrest, precipitates a complex systemic inflammatory response syndrome (SIRS). This response, coupled with patient-specific comorbidities, creates a high-risk environment for a spectrum of postoperative complications that can affect nearly every organ system (7,8). These adverse events not only increase morbidity and mortality but also prolong hospitalization, escalate healthcare costs, and diminish long-term quality of life (QoL). The management of these risks has traditionally relied on population-based scoring systems and clinical experience. The sheer volume and velocity of perioperative data from genomics and comorbidities to real-time hemodynamic monitoring now present an opportunity to transcend this paradigm. Consequently, this review will also explore the burgeoning role of advanced technologies, such as artificial intelligence (AI), in revolutionizing the prediction and personalized management of these adverse outcomes.

This review provides a comprehensive, systems-based analysis of the major complications following CABG. Existing literature still lacks an integrated, system-level synthesis of post-CABG complications. Prior reviews do not clearly summarize cross-system risk factors, practical prevention strategies, or emerging tools such as AI, leaving essential gaps that this review aims to address (8). By synthesizing this evidence, we aim to highlight the critical need for a multidisciplinary, proactive approach to perioperative care and to frame the integration of advanced analytics as the next frontier in optimizing patient recovery and long-term health. We present this article in accordance with the Narrative Review reporting checklist (available at https://cdt.amegroups.com/article/view/10.21037/cdt-2025-480/rc).

Methodology

A comprehensive literature search was performed by all authors after August 6, 2025 using PubMed and Google Scholar, and articles focused on complications after CABG were selected using combinations of MeSH and free text terms related to “postoperative complications”, “coronary artery bypass grafting”, and specific complications [e.g., atrial fibrillation (AF), stroke, acute kidney injury (AKI), surgical site infection (SSI)], as well as terms related to AI in cardiac surgery. All retrieved titles and abstracts were screened independently by at least two authors, with disagreements resolved through discussion and group consensus. Full-test articles were assessed according to predefined inclusion criteria (human studies, English language, adults aged 19–80 years, CABG-specific content, published 2005–2025) and exclusion criteria (non-CABG studies, pediatric or elderly >80 years of age cohorts, non-peer-reviewed sources). A qualitative synthesis was performed to identify cross-system themes, risk factors, prevention strategies, and evidence gaps. Table 1 summarizes the search strategy. Outcome data are thoroughly presented, meeting the Scale for the Assessment of Narrative Review Articles (SANRA) standards (9).

Post-operative complications

Neurological complications

Neurological complications after CABG increase morbidity and intensive care unit (ICU) stays and affect long-term outcomes. Postoperative cognitive dysfunction (POCD) and delirium are common, with varying incidence due to different diagnostic criteria and assessment methods (10).

Stroke

The neurological risks of CABG include stroke, which remains common and concerning despite recent declines due to new preoperative preventive strategies (11). About 53% of acute ischemic strokes happen during CABG surgery, posing a significant neurological risk with a 1.4% incidence, often in brain border zones. A history of AF is an early stroke indicator (12). The identified risks of a stroke include limited preoperative preparation time, low body surface area, prior stroke, warfarin use, and surgery performed outside North America (11,12). In diabetic patients, stroke risk factors differ by timing. Within 30 days, risks include previous stroke and warfarin use. After 30 days, risks involve renal insufficiency, high low-density lipoprotein (LDL), and lower diastolic blood pressure (DBP) (13). Stroke prevention strategies before and during CABG improve outcomes. Assessing the aorta for atherosclerosis with palpation, transesophageal echocardiogram (TEE), or endoscopic ultrasound (EUS) reduces stroke risk by enabling surgical adjustments and aiding CABG recovery (11). Off-pump CABG reduces post-op stroke by 20.7% but doesn’t significantly impact mortality in myocardial infarction (MI) (14). Additionally, the level of disability after a stroke, measured by the modified Rankin Scale (0–6), showed that patients with CABG and valve surgery or multiple bypasses experienced worse outcomes, with scores of 5 or higher, emphasizing the need to look into stroke risk in patients undergoing CABG (12).

Delirium and cognitive function

Delirium occurs in 20–52% of patients and is linked to more extended hospital and ICU stays, dementia, lower QoL, and increased mortality, highlighting the importance of early detection (15). Its pathophysiology is multifactorial, involving neuroinflammation, neurotransmitter imbalances, microvascular ischemia, and perioperative factors such as exposure to CPB (15). A randomized controlled trial shows neuroprotective agents like gastrodin safely reduce delirium and POCD, improving outcomes after CABG. A dose of 600 mg twice daily is notably effective (15). Regarding cognitive decline, donepezil shows slight promise. In post-CABG mild cognitive decline, it didn’t improve overall cognitive performance but enhanced specific memory aspects (16).

Depression

Psychological issues like depression are increasingly recognized after CABG. Statins, especially simvastatin, show better antidepressant effects than atorvastatin in patients with mild to moderate depression post-CABG, indicating neuropsychiatric benefits beyond lipid control (17).

Fatigue and pain

Fatigue and pain after CABG result from medications, morbidities, risk factors, and surgery. Postoperative pain and fatigue, which can hinder neurological recovery, are effectively managed with regional anesthesia like pectointercostal fascial block (PIFB). In elderly off-pump CABG patients, PIFB reduces pain, opioid use, and fatigue and speeds recovery, potentially improving neurological outcomes (18). A study has shown that fatigue after CABG is significantly reduced by taking vitamin C and omega-3 fatty acids (19). Aerobic training in low-risk post-CABG patients improves responses to the head-up tilt test, serving as a diagnostic for fatigue by maintaining sympathovagal balance, ensuring brain blood flow, and reducing fatigue (20).

Cardiac complications

After CABG, complications like graft failure, MI, and arrhythmias can impact patients’ health, mortality, and QoL. Robotic cardiac surgery avoids sternotomy, providing minimally invasive access that may reduce trauma and enhance recovery. Major centers like the Cleveland Clinic and Emory report feasibility, low complications, high valve repair success, and few sternotomy conversions. Meta-analyses show robotic CABG has similar mortality and adverse event rates as traditional methods, with potential benefits like fewer wound infections and shorter hospital stays (21). Table 2 highlights the cardiac complications, risks, management, and screening methods.

MI

Post-CABG MI can occur perioperatively or postoperatively. Significant risks caused by post-CABG MI include graft occlusions, heart failure (HF), LV dysfunction, ischemia, stroke, renal dysfunction, and increased mortality (22). The development of these risks is typically characterized by an elevation of creatine kinase (CK-MB) or troponin levels (22,23). After post-CABG MI, managing ischemia may involve PCI or repeat CABG. CABG is often preferred, especially for diabetics and multivessel disease, as it offers more benefits than risks compared to PCI (24). A key management option is the modified mechanical postconditioning protocol (MMPOC), which supports myocardial protection by preserving LV function, improving reperfusion, reducing ischemia, and shortening hospital stays (23). Pharmacologic agents providing cardioprotection during ischemia-reperfusion include inhalational anesthetics like isoflurane, G-protein-coupled receptor ligands like bradykinin, adenosine, and opioids like morphine. Growth factors such as insulin and erythropoietin decrease apoptosis and enhance endothelial health, alongside statins like atorvastatin, which have pleiotropic effects (23). Typically, an electrocardiogram (ECG) and cardiac enzyme screening are recommended after CABG. No studies focus specifically on screening for post-CABG MI, but observing these factors can help detect complications and predict outcomes (22).

Arrhythmias

One of the key risks after CABG is arrhythmia abnormalities, particularly AF. The risk of post-CABG AF rises with sepsis, embolism, neurocognitive issues, CHF, and higher mortality (25). Post-CABG AF is more common in patients over 65, hypertensive, smokers, with high ejection fraction (EF), and prolonged CPB time (26). The main pathophysiological cause is vague, despite studies examining mechanisms like oxidative stress, autonomic dysfunction, inflammation, and remodeling in post-CABG AF (25,27). Several proven treatments improve post-CABG AF or its risk. Bi-atrial pacing (BIP) enhances hemodynamics by shortening inter-atrial conduction delay and boosting left atrial contraction (28). Posterior pericardiotomy (PP) effectively prevents post-CABG AF, significantly reducing risks like early and late pericardial effusion and tamponade (25). Furthermore, Tocovid, a tocotrienol-rich vitamin E isomer with antioxidant and anti-inflammatory properties, is under investigation for reducing or preventing post-CABG AF (27). Epicardial injection of botulinum toxin A better prevents AF and reduces ICU stay in CABG patients. Pre- and post-operative prophylactic amiodarone lowered post-CABG AF from 85% to 34%, shortening hospital and ICU stays (29). Magnesium supplementation can decrease post-CABG AF, reducing arrhythmias from 24% to 9% (30). Assessing for bradycardia, HF, smoking, diabetes, CHF, hypertension, renal/hepatic disease, and age over 70 is crucial to evaluate AF risk (31). Other studies recommend performing an ECG, monitoring electrolytes, and evaluating hemodynamics before and after surgery to prevent arrhythmias (32).

Low cardiac output syndrome (HF)

Ischemia significantly contributes to HF recurrence after revascularization. LV desynchrony, caused by a high-velocity electrical wave in Purkinje fibers from ischemic myocardium, reduces contractility and disrupts systolic function, promoting HF. Risk factors for HF post-CABG include acute coronary syndrome (ACS), metabolic syndrome, preoperative AF, renal insufficiency, chronic obstructive pulmonary disease (COPD), incomplete revascularization, and triple-vessel disease (33,34). Revascularization by PCI or repeat CABG is viable, with similar improvement rates for off-pump and on-pump techniques in relieving HF symptoms (35). Combining CABG with cardiac resynchronization therapy (CRT) significantly reduced hospital readmission rates (33). On discharge, patients are advised to take lipid-lowering agents, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), Ca-channel blockers, and antiplatelets for cardioprotection (34). In patients with type 2 diabetes, empagliflozin use was associated with significant risk reductions in cardiovascular death, overall mortality, and HF hospitalization (36). Perioperative glucose-insulin-potassium (GIK) infusion may reduce diastolic dysfunction after CABG by improving myocardial metabolic protection (37). Algisyl-left ventricular remodeling (LVR), an injectable hydrogel, is a feasible option that may reduce LV wall stress and improve cardiac function (38). Cardiac remodeling influences HF risk post-CABG; magnetic resonance imaging (MRI) is recommended for screening. HF assessments involve ECG, echocardiography, stress tests, and monitoring of blood sugar, blood pressure, and renal function (34,39).

Pulmonary complications

Postoperative pulmonary complications (PPCs) are common after cardiac surgery, contributing to higher morbidity, mortality, longer hospital stays, and increased healthcare costs. Their clinical signs range from mild to severe (40).

Pneumonia, atelectasis, COPD, obstructive sleep apnea (OSA), pleural effusion, and respiratory failure

Atelectasis, pleural effusion, and pneumonia are the most common PPCs after CABG. Age ≥65 years was linked to atelectasis, along with diabetes. Pneumonia was associated with prior MI and prolonged ventilation. A history of bronchitis and COPD was linked to pneumothorax, while HF was related to pulmonary edema (41). Additionally, COPD is associated with higher postoperative pneumonia and respiratory failure but does not appear to increase 30-day mortality (42). Patients with a history of COVID-19 pneumonia show increased pleural effusions and pneumonia post-CABG, but mortality rates are similar to those without prior infection (43). OSA is linked to an increased risk of major cardiac and cerebrovascular events after CABG (44).

CPB causes systemic inflammation, increasing lung damage and leading to pulmonary edema. Patients experience dyspnea, crackles, and bilateral infiltrates. Failure to wean from ventilation after 48–72 hours often results from poor respiratory drive or severe lung injury (45,46). Postoperative pain often limits deep inspiration, leading to atelectasis. A preoperative ultrasound-guided pectoral-intercostal fascial block (PIFB) demonstrated sustained improvement in ventilation (47). Aprotinin, an antifibrinolytic, reduces pulmonary injury after CABG by maintaining nitric oxide and reducing leukocyte activation (48). High-dose melatonin reduced inflammatory markers and led to shorter intubation times (49).

Patients with postoperative complications may have reduced functional performance and pulmonary function at discharge and after six months, indicating that early intervention can improve outcomes (50). Preventive strategies like incentive spirometry, combined with deep-breathing exercises, significantly reduce pulmonary complications and improve lung function (51,52). Preoperative inspiratory muscle training also reduces PPCs and postoperative stay in high-risk patients (53). Detecting early signs and identifying risk factors are essential to prevent respiratory failure (40).

Gastrointestinal (GI)/hepatobiliary (HB) complications

While severe GI and HB complications are rare after CABG, they can significantly increase in-hospital mortality if they occur (54). A study using esophagogastroduodenoscopy (EGD) found that 28 of 231 patients on antiplatelet therapy had ulcers, and 10.4% had reflux esophagitis (55). Severe complications include ischemic bowel, perforated ulcers, and pancreatitis. A predictive model indicated over a 50% chance of serious issues in high-risk patients (European System for Cardiac Operative Risk Evaluation i.e., EuroSCORE >8) (54). Subclinical liver fibrosis, assessed by the Fibrosis-4 Index FIB-4 score, may also be linked to increased surgical risk (56). To prevent GI lesions, more frequent use of proton pump inhibitors is recommended for patients on antiplatelet therapy (55).

Renal complications

The spectrum of renal dysfunction after CABG relates to ischemia-reperfusion injury during CPB, oxidative stress, and hemodynamic changes (57-59).

AKI

AKI is a common complication after CABG, affecting up to 30% of patients and is linked to higher morbidity, mortality, and longer hospital stays (57,59). Renal dysfunction after cardiac surgery is multifactorial. Factors include pre-existing cardiovascular issues, prolonged CPB, hypothermia, and renal hypoperfusion, which cause renal hypoxia and damage tubular cells (57). Additionally, CPB often leads to severe hemodilution, impairing microcirculatory function and oxygen delivery (58). Patient-related risks include advanced age, pre-existing renal impairment, low EF, poorly controlled diabetes, female gender, and peripheral vascular disease (36,57,59). Surgical risk factors include surgery duration, cross-clamp time, and hemolysis (59). Chronic kidney disease (CKD) significantly increases the risk (60). Rare complications like graft avulsion can also lead to renal malperfusion (61,62).

Preventive treatments aim to reduce ischemic and inflammatory insults using antioxidants and anti-inflammatory agents like N-acetylcysteine, empagliflozin in diabetics, recombinant human atrial natriuretic peptide (HANP) in CKD patients, and minocycline (36,57,59,60,63). In a trial, perioperative empagliflozin safely reduced AKI risk in diabetic patients (63). Empagliflozin also reduced cardiovascular mortality and HF hospitalization (36). Carperitide (HANP) improves renal function in preoperative CKD patients undergoing CABG, offering long-term benefits (60). Early initiation of ACE inhibitors postoperatively may also improve cardiovascular and renal outcomes (64). Coronary computed tomography angiography (CCTA)-guided approaches are associated with lower rates of contrast-induced nephropathy compared to conventional angiography (65). Management focuses on early detection of AKI by monitoring creatinine, urine output, and estimated glomerular filtration rate (eGFR), with careful fluid management to preserve renal circulation (57,59,60,64). Table 3 outlines the strategies to prevent and manage AKI post-CABG.

Endocrine complications

Diabetes

Diabetes is linked to an increased risk of post-CABG mortality and sternal wound infections (66). In diabetic patients, post-CABG grafts often fail due to atherosclerosis, especially in the saphenous vein (67). For diabetic patients with cardiovascular issues, CABG generally has better outcomes than PCI, with fewer cardiovascular deaths (68).

To reduce AKI risk in diabetic post-CABG patients, empagliflozin is recommended. Given before surgery, it also lowers MI risk (63). Rosiglitazone, a peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist, slows atherosclerosis progression after CABG in Type 2 diabetes mellitus (T2DM) patients by inhibiting pro-inflammatory genes and exerting antithrombotic effects (67). A yearly stress myocardial perfusion SPECT (MPS) scan can provide crucial information on myocardial irritation and ischemia in stable diabetic patients after CABG (69). Other screening methods include angiography, intravascular ultrasound, and assessment of athero-thrombo-inflammatory markers to evaluate plasma glucose, lipids, and inflammation (67).

Hematologic complications

CABG procedures can lead to hematological imbalances. Reactive thrombocytosis occurs in about 20% of patients, possibly increasing thrombotic complications (70). CABG with CPB triggers blood clotting and inflammation, leading to complications like deep vein thrombosis (DVT) (71).

DVT/pulmonary embolism (PE)/coagulopathy & bleeding

DVT is a common cause of illness and death after CABG, occurring in 70–80% of patients, though detectable PE is rare (<1%) (72). Grafted veins may promote atherosclerotic plaque development, but aggressive lipid-lowering medication can help reduce this risk (73). Patients on aspirin or clopidogrel before CABG are at a higher risk of bleeding (74,75).

Post-surgically, higher coagulation risk is linked to oxidative stress. The optimal time to give aspirin is within 6 hours post-op to reduce vein graft occlusion and other adverse events (76,77). For reactive thrombocytosis, combining aspirin with clopidogrel is more effective than aspirin alone (70). Ticagrelor showed no significant difference in benefits compared to aspirin (78), while another study found lower overall mortality with clopidogrel compared to ticagrelor (79). Using both heparin and aspirin reduces DVT risk more effectively than heparin alone (72). Enoxaparin is a safe alternative to unfractionated heparin (UFH) preoperatively (80). Keeping LDL below 100 mg/dL with statins after CABG significantly improves graft patency (81). Using a mini-CPB system during CABG reduces blood coagulation activation (71). Figure 1 outlines the prevention, management, and outcomes of hematological complications post-CABG.

Figure 1 Prevention, Management, and Outcomes of Hematological Complications Post CABG. *, prescription of anticoagulants is given in specific cases; for instance, when patients have previous history of atrial fibrillation. At the same time, careful hematological laboratory monitoring are important to ensure no hemorrhage. The figure is created via BioRender with credit. ASA, acetylsalicylic acid; DVT, deep vein thrombosis; PE, pulmonary embolism; Pre-op, pre-operative.

Infectious complications

SSIs/sepsis

Infections are a leading cause of complications after major heart surgery, with an incidence of 5.9% to 16.5% (82). SSIs after sternotomy are more common in low- and middle-income countries (83). The main complications include pneumonia, SSIs, and bloodstream infections (82).

Patients undergoing CABG are often older adults with risk factors like age-related immune decline and comorbidities such as diabetes, COPD, and renal dysfunction (82). Other modifiable risk factors include smoking, hyperglycemia, and Staphylococcus aureus colonization (84). SSIs include superficial and deep postsurgical mediastinitis, primarily caused by Gram-positive bacteria (85). Lower Human Development Index (HDI) is associated with higher SSI rates, likely due to limited resources and poor infection control (83). A trial found that vacuum-assisted negative-pressure wound therapy (NPWT) significantly reduced mediastinitis in patients who received an internal mammary artery graft (85). Insulin-dependent diabetics face more sternal wound complications, regardless of obesity (66).

Preventing SSIs involves optimizing glycemic control, intranasal S. aureus decolonization, and preoperative intravenous cephalosporin (84). When prevention fails, vacuum dressings can reduce post-surgical mediastinitis (85), although evidence for NPWT in preventing all SSIs is limited (86).

Psychosocial and rehabilitation aspects

Psychosocial recovery

Psychological distress, mainly depression and anxiety, is common after CABG. Depression occurs in 20–40% of patients and is linked to higher morbidity and poorer adherence to treatments (87-89). Anxiety often co-occurs with depression and can worsen cardiac symptoms (90). Cognitive dysfunction in older adults is another concern, affecting self-care and rehabilitation participation (91). Early screening is crucial for timely intervention.

Cardiac rehabilitation (CR) and functional recovery

Structured CR is linked to better physical and mental function, fewer hospitalizations, and lower mortality after CABG (16,92,93). Supervised exercise training, including aerobic activities and deep breathing, enhances cardiopulmonary fitness and supports reintegration into daily life (20,94-97).

QoL and social support

QoL after CABG typically improves within 6–12 months. However, patients with ongoing psychological distress or poor social support, especially women, may experience a blunted recovery (98). Table 4 summarizes the sources and levels of evidence regarding key findings in the post-operative complications.

Advancing post-CABG care: future perspectives and innovations

Future protocols should include neurologic risk assessments prior to surgery to personalize care. The positive effects of simvastatin and gastrodin on post-CABG depression and delirium warrant larger trials. Intraoperative monitoring with cerebral oximetry and serum biomarkers could guide interventions to prevent POCD and stroke (99). Future research should optimize hematologic management through trials on platelet testing and biomarker-guided therapy. Multicenter studies should assess the link between early hematological risk factors and late complications (100). Emerging surgical techniques, such as mini-CPB, should be researched in large-scale trials to determine their long-term benefits. Further research into the complex mechanisms of AKI is vital to enhance long-term outcomes. Future studies should develop predictive models using non-invasive liver fibrosis markers, such as FIB-4, to inform surgical decisions. Lastly, exploring long-term PPC outcomes and tailored prehabilitation strategies offers valuable clinical insights. Utilizing machine learning (ML) for early risk assessment may further enhance postoperative outcomes.

Emerging role of AI in post-CABG care

The management of post-CABG complications, which span multiple physiological systems, presents a significant challenge in data integration. AI, particularly ML, offers a transformative approach to synthesize vast and heterogeneous patient data from preoperative risk factors to real-time intraoperative and postoperative monitoring, to create a more predictive, personalized, and proactive care paradigm (101-104).

A key opportunity for AI lies in developing robust predictive models. By analyzing thousands of data points from electronic health records, AI algorithms can identify patients at the highest risk for specific complications before surgery. AI models can integrate preoperative factors (age, renal function, diabetes) with intraoperative variables (CPB time, hemodynamic shifts) to generate a real-time risk score for the development of AKI (105). This would allow clinicians to implement targeted preventive strategies for the most vulnerable patients. Similarly, AI can help predict the likelihood of postoperative delirium (106) or stroke by analyzing a combination of risk factors, triggering enhanced neurological monitoring and early intervention protocols. For SSIs, ML can identify non-obvious patterns among patient comorbidities and procedural details to predict risk, enabling targeted antimicrobial stewardship (107).

Postoperatively, AI can analyze complex data streams in real-time to detect subtle signs of deterioration far earlier than human observation alone. AI-powered algorithms can monitor ECGs and arterial pressure waveforms to predict the onset of arrhythmias or Low Cardiac Output Syndrome, enabling preemptive intervention (108,109). By integrating ventilator data with blood gas analysis, AI tools could predict the likelihood of failure to wean from mechanical ventilation, allowing for earlier adjustments to respiratory support (110).

Beyond prediction, AI can guide clinical decision-making by recommending personalized interventions. By learning from the outcomes of thousands of previous patients, AI-driven decision support systems could suggest optimal antiplatelet strategies tailored to an individual’s risk profile or personalized rehabilitation protocols based on a patient’s functional capacity and recovery trajectory.

However, integration of AI into post-CABG care presents challenges. The development of effective models requires large, high-quality, and diverse datasets. Furthermore, these models must be rigorously validated in real-world clinical settings to ensure they are accurate, unbiased, and generalizable. Ethical considerations regarding data privacy and algorithmic transparency must also be addressed (111). Future research should focus on prospective clinical trials to confirm whether AI-guided interventions truly improve patient outcomes, reduce complications, and enhance the QoL after CABG.

Limitations

The primary limitation of this review is its underrepresentation of specific high-risk subgroups. There is limited evaluation of integrated preventive strategies. Variations in study design, sample sizes, and endpoints result in heterogeneity, complicating the identification of universal best practices. The scarcity of endocrine-related papers led to insufficient information on certain complications. Furthermore, many studies focus on short-term issues, while long-term hematological problems are less understood. The narrative review methodology risks publication or selection bias. The literature on GI and HB complications is limited. Many studies on pulmonary complications are small-scale or single-center, limiting their broader applicability. Research on infectious complications faces methodological challenges, including geographic and economic differences. Definitions of SSIs are inconsistent, reducing data reliability. These issues highlight the need for standardized, multicenter, prospective studies.

Conclusions

CABG is a landmark treatment for complex CAD. However, it carries serious postoperative risks. The multisystem nature of post-CABG complications—covering neurological, cardiac, pulmonary, renal, GI, endocrine, hematological, infectious, and psychosocial issues—makes it essential to have a comprehensive, multidisciplinary approach to perioperative care. Common complications like AF, AKI, and delirium remain prevalent. New strategies like SGLT2 inhibitors, neuroprotection, and advanced monitoring could reduce adverse outcomes. Future research should aim to improve predictive models and tailor therapies to individual risk factors. A standardized, system-based approach to surveillance and management is urgently needed to optimize recovery, long-term outcomes, and QoL after CABG.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://cdt.amegroups.com/article/view/10.21037/cdt-2025-480/rc

Peer Review File: Available at https://cdt.amegroups.com/article/view/10.21037/cdt-2025-480/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://cdt.amegroups.com/article/view/10.21037/cdt-2025-480/coif). M.M. serves as an unpaid editorial board member of Cardiovascular Diagnosis and Therapy from September 2025 to December 2027. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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