Sudden cardiac death (SCD) remains one of the most devastating and unpredictable complications following myocardial infarction (MI), contributing significantly to global cardiovascular mortality and representing a major public health challenge even in the era of advanced reperfusion therapies [1]. Defined as a natural, unexpected fatal event due to cardiovascular causes occurring within a short time interval—usually within one hour of symptom onset, SCD is characterized by immediate loss of consciousness and the absence of premonitory signs in most individuals [2]. Though its causes are multifactorial, ventricular tachyarrhythmias, particularly ventricular tachycardia (VT) degenerating into ventricular fibrillation (VF), account for the vast majority of cases, especially in individuals with a history of MI [3]. Despite remarkable progress in acute coronary care, including more widespread use of percutaneous coronary intervention (PCI), thrombolysis, dual antiplatelet therapy, and potent lipid-lowering medications, survivors of MI continue to experience disproportionately high rates of sudden cardiac death, underscoring the persistent vulnerability of the post-infarct myocardium to lethal electrical instability [4].

Myocardial infarction triggers a cascade of structural, electrophysiological, metabolic, and molecular changes that predispose the heart to SCD. The infarcted myocardium undergoes an immediate phase of ischemia-induced electrical instability followed by long-term structural remodeling characterized by scar formation, adverse ventricular remodeling, and persistent autonomic dysregulation [5]. This evolution is neither uniform nor predictable; rather, it varies widely depending on infarct size, location, reperfusion success, underlying comorbidities, genetic predisposition, and environmental factors. Ventricular arrhythmias arising from re-entrant circuits at the borders of scarred myocardium remain the predominant mechanism of SCD in the chronic phase after MI [6]. These arrhythmogenic substrates develop as a consequence of heterogeneous conduction, altered electrical coupling, delayed depolarization, and fibrosis-related conduction block, creating conditions conducive to re-entry, which is the hallmark of sustained VT and VF [7].

Epidemiologically, numerous large-scale registries and population-based studies have demonstrated that the risk of sudden cardiac death after myocardial infarction follows a characteristic biphasic pattern, with an extremely high incidence in the early post-infarction period and a persistently elevated long-term risk in survivors [8]. The first 30 days after MI constitute the most vulnerable phase, with SCD risk increased by nearly fivefold compared to the general population, primarily due to acute ischemic arrhythmias, metabolic disturbances, and mechanical complications [9]. Although improvements in acute coronary care have reduced early mortality, they have not eliminated the early risk of SCD, particularly among individuals with large infarcts or delayed reperfusion [10]. After the first month, the risk gradually declines but remains significantly higher than that of the non-MI population, reflecting the ongoing impact of structural remodeling, electrophysiological alterations, and neurohormonal activation [11]. Even decades after an index MI, survivors continue to carry a heightened risk, especially those with impaired left ventricular function or recurrent ischemia, indicating that MI leaves a permanent arrhythmogenic scar on the myocardium [12].

Left ventricular ejection fraction LVEF has surely been recognized as the strongest clinical factor for predicting sudden cardiac death in patients after a heart attack. Moreover, this measurement remains the most reliable indicator used by doctors for assessing such risks. Basically, when the heart's pumping power drops below 35%, patients face the same high risk of dangerous heart rhythm problems and death, which is why doctors recommend ICD devices [13]. However, growing evidence surely shows that depending only on LVEF may not be enough and can sometimes give wrong information. Moreover, this approach alone is not sufficient for proper heart function assessment. As per several studies, many SCD cases happen in patients who have normal or slightly low heart pumping function, especially regarding those with heart muscle scars that can only be seen through advanced tests like CMR imaging [14]. These findings surely challenge the old ways of measuring risk and show we need better methods. Moreover, these new approaches must include structural, electrical, and nervous system markers together [15].

Scar tissue itself creates the main problem that makes heart attack survivors more likely to develop dangerous heart rhythms, which can further lead to sudden cardiac death. We are seeing that the uneven spread of scar tissue, with its complex border areas and patchy fibrosis, is the only key factor that decides how electrical circuits form again in the heart [16]. Late gadolinium enhancement LGE cardiac MRI has surely become the best non-invasive method to check heart muscle scarring and changes in heart structure. Moreover, it gives detailed information about the total scar amount, border area differences, and small structural problems [17]. Basically, many studies show the same thing - scars in the heart can cause dangerous rhythms even when the heart pumps normally, so doctors use special scans to better predict who is at risk [18]. CMR test results can actually help doctors find high-risk patients who definitely need special treatments like ICD devices or stronger medicines [19].

In addition to structural remodeling, autonomic nervous system dysfunction plays a crucial role in the pathogenesis of SCD after MI. Following infarction, heightened sympathetic activity and reduced parasympathetic tone contribute to increased electrical instability, facilitating the initiation and maintenance of life-threatening arrhythmias [20]. Reduced heart rate variability (HRV), impaired baroreflex sensitivity, prolonged QT variability, and abnormal cardiac sympathetic innervation assessed using I-123 MIBG scintigraphy have been associated with increased susceptibility to arrhythmic events [21]. These markers reflect a profound alteration in neurocardiac regulation, which may persist long after the acute event. As such, autonomic dysfunction represents both a mechanism and a potential biomarker for SCD risk, offering opportunities for preventive strategies including beta-blocker therapy, lifestyle modification, and emerging neuromodulation techniques such as renal denervation and vagal nerve stimulation [22].

Electrophysiological alterations following myocardial infarction further contribute to SCD risk. Abnormalities in ion-channel expression, repolarization heterogeneity, and conduction delay create a vulnerable electrical environment conducive to arrhythmogenesis. Several electrocardiographic markers have been studied as potential predictors of post-MI SCD, including QRS duration, T-wave alternans, signal-averaged ECG late potentials, frequent premature ventricular contractions, and non-sustained ventricular tachycardia (NSVT) on ambulatory Holter monitoring [23]. Although these markers provide valuable insight into electrical instability, their predictive power varies, and no single marker has demonstrated sufficient sensitivity or specificity for routine clinical use. Nevertheless, when integrated with imaging findings and autonomic parameters, such electrophysiological markers may significantly enhance risk-stratification accuracy.

Advances in acute MI management have markedly improved survival rates, but the shift in mortality patterns has led to a growing population of MI survivors with chronic structural and arrhythmic vulnerabilities. Primary PCI has dramatically reduced infarct size and improved left ventricular function in many patients, yet incomplete revascularization and microvascular obstruction remain significant contributors to long-term SCD risk [24]. Pharmacological therapies—including beta-blockers, ACE inhibitors, ARBs, mineralocorticoid receptor antagonists, statins, and more recently, SGLT2 inhibitors—have shown substantial benefits in reducing arrhythmic risk through hemodynamic stabilization, remodeling suppression, autonomic modulation, and anti-inflammatory effects. However, optimal treatment adherence, comorbidity management, and individualized therapy remain essential for maximizing long-term protective effects.

ICDs are actually the best treatment to prevent sudden cardiac death in high-risk patients after a heart attack. Further, basically, randomized trials show the same result - ICD therapy reduces death in patients with LVEF ≤35% after waiting 40-90 days post-heart attack for stabilization. Early implantation after MI itself does not improve survival and may further expose patients to unnecessary device-related complications. Most SCD cases surely happen in patients who do not meet current ICD criteria based only on LVEF. Moreover, this shows major gaps in today's risk assessment methods and an urgent need for better prediction models that include structural, electrical, autonomic, and genetic factors [25].

Sudden heart death after a heart attack surely remains a major global problem. Moreover, this continues despite significant improvements in heart care treatment. Basically, this phenomenon involves the same complex interaction between structural, autonomic, electrical, and molecular processes that change over time. As per research needs, we must understand these body processes and find exact risk signs for each person regarding better prevention methods and reducing deaths from heart rhythm problems. This review study brings together current evidence on how often sudden cardiac death happens in heart attack survivors and looks further into its causes, risk factors, new blood markers, imaging signs, heart rhythm features, and prevention methods. The study itself examines all these aspects to understand sudden cardiac death better. Also, as per available studies, this review gives complete information regarding heart rhythm problems after a heart attack that can help doctors assess patient risk, improve treatments, and guide future research.

This systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA 2020) guidelines to ensure methodological transparency and scientific rigor [26]. The protocol was designed to systematically identify, evaluate, and synthesize contemporary evidence on sudden cardiac death (SCD) after myocardial infarction (MI), including epidemiology, pathophysiological mechanisms, structural predictors, electrophysiological markers, and preventive strategies. Although meta-analysis was initially considered, considerable heterogeneity in diagnostic criteria, outcome definitions, imaging modalities, and follow-up durations precluded quantitative pooling; therefore, a qualitative synthesis approach was adopted [27]. Search Strategy A comprehensive and structured search of four major electronic databases—PubMed, Scopus, Web of Science, and Google Scholar, was conducted for studies published between January 2000 and December 2024. The search strategy integrated Medical Subject Headings (MeSH) and relevant keywords, including “sudden cardiac death,” “myocardial infarction,” “ventricular arrhythmia,” “ischemic cardiomyopathy,” “post-infarction remodeling,” “cardiac arrest,” and “ventricular tachycardia.” Boolean operators (AND/OR) were applied to optimize sensitivity and specificity. Reference lists of key articles and authoritative systematic reviews were manually screened to identify missed studies, as recommended by PRISMA and Cochrane guidelines [28]. Eligibility Criteria Studies were considered eligible for inclusion if they involved adult human participants aged 18 years or older with a confirmed diagnosis of acute or prior myocardial infarction and reported sudden cardiac death, ventricular arrhythmias, or arrhythmic mortality as primary or secondary outcomes. Only peer-reviewed observational cohorts, case–control studies, randomized clinical trials, and systematic reviews published in English between 2000 and 2024 were included. Studies were excluded if they were case reports, editorials, conference abstracts without full text, animal or in-vitro studies, or if they lacked clear definitions of myocardial infarction or sudden cardiac death. Additionally, investigations focusing on non-cardiac causes of sudden death or those with insufficient methodological clarity were removed to ensure consistency and reliability of the final synthesis. [29]. Study Selection and Data Extraction Titles and abstracts were screened independently by two reviewers. Potentially eligible articles underwent full-text evaluation to assess compliance with inclusion criteria. Disagreements were resolved through consensus or consultation with a third reviewer. Data extraction was conducted using a predefined standardized form, capturing study characteristics, population demographics, MI type (STEMI/NSTEMI), follow-up period, arrhythmic endpoints, imaging variables (e.g., scar burden), autonomic markers, electrophysiological predictors, and preventive interventions. This structured approach aligns with validated systematic review methodologies and enhances reproducibility [30]. Quality Assessment Quality appraisal was performed using the Newcastle–Ottawa Scale (NOS) for observational studies and the Cochrane Risk of Bias 2.0 tool for randomized controlled trials. Systematic reviews were assessed using the AMSTAR-2 instrument, ensuring that only moderate- and high-quality studies contributed to the core synthesis [31]. Rather than excluding lower-quality studies outright, methodological limitations were considered when interpreting results, in line with narrative synthesis principles [32]. PRISMA STUDY SELECTION SUMMARY PRISMA Stage Number of Records Records identified through database searching 1,560 Records after duplicate removal 1,350 Records screened (title/abstract) 1,350 Records excluded 1,180 Full-text articles assessed for eligibility 170 Full-text articles excluded 98 Studies included in final synthesis 72

A total of seventy-two studies met the inclusion criteria and were synthesized in the final analysis. These studies represented diverse populations from North America, Europe, East Asia, and the Middle East and collectively examined more than 1.2 million patients with documented myocardial infarction. Although the studies varied in design, follow-up duration, and risk-assessment strategies, several consistent patterns emerged regarding the epidemiology, mechanistic pathways, predictors, and clinical determinants of sudden cardiac death after myocardial infarction.

The most striking finding across the literature was the distinct temporal pattern of SCD following MI, characterized by a marked increase in arrhythmic deaths during the acute and subacute phases, followed by a persistent, though attenuated, long-term risk. Studies consistently demonstrated that the first 30 days after MI remain the period of greatest vulnerability, with a three- to five-fold increase in SCD risk compared to the general population [33]. This early risk was driven primarily by acute ischemic electrical instability, metabolic disturbances, residual ischemia, autonomic fluctuations, and, in some cases, mechanical complications such as myocardial rupture. Improvements in reperfusion therapy, particularly early percutaneous coronary intervention, have reduced—but not eliminated—early SCD incidence, suggesting that the immediate post-MI myocardium remains electrically unstable even with successful restoration of coronary flow [34].

Beyond the first month, a substantial proportion of surviving MI patients continued to exhibit elevated susceptibility to ventricular tachyarrhythmias and sudden cardiac death. Long-term studies with follow-ups ranging from one to ten years demonstrated that the arrhythmic risk does not normalize, particularly in individuals with impaired left ventricular function, extensive scar burden, or recurrent ischemic episodes [35]. Several investigations highlighted a “late arrhythmic plateau,” in which the risk of SCD stabilizes but remains two- to three-fold higher than in individuals without a history of MI. This observation underscores the chronic nature of electrical vulnerability created by infarcted tissue and adverse ventricular remodeling.

Structural remodeling emerged as one of the most important determinants of SCD. Cardiac magnetic resonance (CMR) imaging studies using late gadolinium enhancement consistently showed that the extent, heterogeneity, and spatial complexity of myocardial scar were strongly associated with increased risk of sustained ventricular tachycardia and sudden cardiac death [36]. In particular, patients with large infarct scars, patchy mid-myocardial fibrosis, and intricate infarct border zones were significantly more likely to experience malignant arrhythmic events. Notably, several high-quality CMR studies revealed that scar burden predicted SCD risk even in patients with preserved or mildly reduced LVEF, challenging the long-standing reliance on ejection fraction as the primary risk-stratification metric [37].

Echocardiographic parameters also contributed valuable insights, particularly left ventricular dilation, wall thinning, increased chamber sphericity, and impaired global longitudinal strain, all of which correlated with increased arrhythmic vulnerability. Although less sensitive than CMR in detecting scar morphology, echocardiography remains the most widely used imaging modality, and its findings consistently supported the role of adverse structural remodeling in predicting post-MI SCD [38].

Basically, problems with the heart's electrical activity were the same major warning sign found in multiple studies. Also, Holter monitoring showed that non-sustained ventricular tachycardia (NSVT), high premature ventricular contraction (PVC) burden, and long pauses were linked to more ventricular fibrillation and sudden cardiac death [39]. Further studies confirmed that NSVT itself increases the risk of these serious heart problems. Other heart rhythm markers like wide QRS waves, broken QRS patterns, delayed electrical signals, and tiny T-wave changes surely show problems with the heart's electrical system. Moreover, these signs reflect uneven electrical activity in the heart muscle. No single marker showed perfect accuracy, but the consistent link between electrical abnormalities and SCD further strengthened the case for combining multimodal ECG assessment with imaging-based risk stratification itself.

Autonomic dysfunction surely emerged as a strong predictor that does not require invasive methods. Moreover, this finding shows its powerful ability to predict outcomes without causing harm to patients. We are seeing that studies using heart rate tests and cardiac imaging show that increased sympathetic activity and reduced parasympathetic function are strongly linked with arrhythmia risk after MI [40]. These findings only confirm the connection between nerve system changes and heart rhythm problems. Patients with very low heart rate changes or damaged heart nerve control actually showed much higher sudden death rates. This definitely happened more during stress or physical activity. These findings supported the mechanistic model that autonomic imbalance facilitates arrhythmogenesis by altering repolarization dynamics, increasing triggered activity, and promoting dispersion of refractoriness.

In addition, several studies highlighted that incomplete revascularization and residual ischemia significantly increased SCD risk. Patients with multivessel coronary artery disease, chronic total occlusions, or inadequate revascularization following MI demonstrated substantially higher rates of late ventricular tachyarrhythmias and arrhythmic death. Conversely, early and complete revascularization led to lower scar burden, improved ventricular function, and reduced electrical instability, thereby significantly decreasing long-term arrhythmic risk [41].

Pharmacological therapy demonstrated strong protective effects. Beta-blockers substantially reduced the incidence of sudden cardiac death by attenuating sympathetic excitation and stabilizing myocardial repolarization. ACE inhibitors and ARBs reduced left ventricular dilation and adverse remodeling, leading to decreased arrhythmic vulnerability. Mineralocorticoid receptor antagonists provided additional benefits by reducing fibrosis and improving autonomic balance. Recent clinical trials suggested that SGLT2 inhibitors, originally introduced for diabetes management, may reduce arrhythmic mortality through mechanisms such as improved myocardial energy utilization, reduced intracellular sodium overload, and attenuation of cardiac inflammation. These findings represent a promising new frontier in SCD prevention among MI survivors [42].

Implantable cardioverter-defibrillators (ICDs) were consistently shown to reduce sudden cardiac death in high-risk individuals with LVEF ≤35%. Studies demonstrated clear survival benefits when ICD implantation occurred after the ventricular remodeling period, typically 40–90 days after MI. However, early implantation immediately after MI did not reduce all-cause mortality, highlighting the importance of patient selection and timing. Subgroup analyses further revealed that ICD benefits were greatest among patients with extensive scar burden, inducible VT on electrophysiological studies, recurrent NSVT, or abnormalities on advanced imaging.

Genetic and molecular studies, though fewer in number, identified several polymorphisms associated with increased arrhythmic risk. These included variants affecting ion-channel function, fibrotic pathways, mitochondrial metabolism, and autonomic regulation. While still exploratory, such findings suggest that genetic predisposition may play a meaningful role in determining post-MI arrhythmogenic susceptibility.

Taken together, the results of this systematic review demonstrate that sudden cardiac death after myocardial infarction arises from a multifaceted interplay among structural, electrophysiological, autonomic, ischemic, and genetic factors. The evidence strongly indicates that risk stratification should move beyond LVEF alone and incorporate multimodal assessment—including advanced imaging, ECG markers, autonomic testing, clinical risk scoring, revascularization status, and pharmacological response—to more accurately identify individuals at the highest risk of SCD.

The findings of this systematic review demonstrate that sudden cardiac death (SCD) following myocardial infarction (MI) is a multifactorial, time-dependent, and pathophysiologically complex phenomenon that continues to pose a major global clinical challenge despite significant advancements in the diagnosis and management of coronary artery disease. Although immediate survival following MI has improved substantially due to enhanced reperfusion strategies, antithrombotic therapy, high-sensitivity diagnostics, and improved critical care pathways, the persistent risk of lethal ventricular arrhythmias remains a defining and unresolved component of long-term post-MI morbidity and mortality [43]. This underscores the importance of understanding the evolving arrhythmogenic substrate formed after MI, as well as the need for more refined risk-stratification strategies.

One of the most significant observations across the included studies was the dynamic and biphasic nature of arrhythmic risk after MI. In the early phase, typically within the first 30 days, SCD is predominantly driven by acute ischemia, metabolic disarray, autonomic fluctuations, reperfusion injury, and transient left ventricular dysfunction. As described in earlier results, this early phase is marked by profound heterogeneity in myocardial repolarization and heightened electrical instability, making it particularly vulnerable to polymorphic ventricular tachycardia and ventricular fibrillation [44]. While early revascularization reduces infarct size and electrical instability, it cannot completely eliminate early SCD risk. Patients with delayed presentation, suboptimal reperfusion, or mechanical complications remain especially vulnerable.

Beyond the acute phase, the long-term risk of SCD arises from persistent structural and electrophysiological remodeling of the myocardium. Fibrotic scar formation and border-zone heterogeneity are central to the arrhythmogenic substrate. Multiple studies highlighted that the scar’s spatial complexity, tissue heterogeneity, and conduction-delay pathways create the ideal conditions for re-entrant ventricular tachycardia circuits [45]. Importantly, late gadolinium enhancement (LGE) cardiac MRI consistently emerged as the most powerful imaging modality for predicting arrhythmic events, outperforming traditional metrics such as left ventricular ejection fraction (LVEF). Scar burden, interstitial fibrosis, and infarct border-zone complexity have all been strongly associated with increased risk of sustained VT and SCD in long-term survivors of MI [46].

This developing body of evidence underscores a major limitation of current guideline-directed risk stratification: LVEF alone is not sufficient for identifying patients at highest risk. While LVEF <35% remains a strong predictor and the threshold for implantable cardioverter-defibrillator (ICD) therapy, several studies have reported that up to 70% of SCD events occur in patients with LVEF >35%, many of whom exhibit significant myocardial fibrosis detectable only by advanced imaging [47]. These findings challenge the historical reliance on LVEF as the sole risk discriminator and highlight the need to incorporate multimodal metrics—including MRI-based scar quantification, electrocardiographic abnormalities, autonomic markers, and electrophysiological characteristics—to better identify at-risk individuals.

In addition to structural factors, autonomic nervous system dysregulation emerged as a significant contributor to arrhythmic vulnerability. Post-MI patients commonly experience heightened sympathetic activation and blunted parasympathetic tone, processes that significantly increase the likelihood of ventricular arrhythmias. Markers such as reduced heart rate variability (HRV), impaired baroreflex sensitivity, prolonged QT variability, and abnormalities in cardiac sympathetic innervation (evidenced by I-123 MIBG scintigraphy) demonstrated strong and consistent associations with SCD risk across multiple studies [48]. The mechanism appears to reflect a synergistic interaction between autonomic imbalance and scar-mediated conduction abnormalities, amplifying the arrhythmogenic potential of the post-infarct myocardium. The potential role of neuromodulation therapies, including vagal nerve stimulation, stellate ganglion blockade, and renal sympathetic denervation, is being explored in emerging studies and may offer novel long-term strategies for arrhythmia control [49].

We are seeing that heart rhythm problems on ECG tests - like wide QRS waves, broken QRS patterns, late signals, and changing T-waves - are only markers that show risk for dangerous heart rhythms. These indicators show the same electrical delays and abnormal heart rhythm patterns that happen in damaged heart muscle after a heart attack. We are seeing that these methods give different results in different studies, but when we use them together with imaging results, they only help to make better predictions about risk [50]. Holter monitoring detects non-sustained ventricular tachycardia and high PVC burdens, which further supports using multiple assessment methods rather than depending on one parameter itself [51].

Revascularization, both in the acute and chronic setting, plays a crucial role in modifying arrhythmic risk. Early PCI surely reduces the size of heart damage and scar tissue formation. Moreover, this approach lowers the chances of dangerous heart rhythm problems. Basically, studies show that incomplete heart vessel repair, blocked arteries, and ongoing blood supply problems increase the same long-term risk of sudden heart death [52]. Moreover, this actually shows that doctors should definitely focus on the best way to restore blood flow to the heart, especially in patients who have blockages in multiple heart vessels. Functional tests like fractional flow reserve (FFR) and noninvasive ischemia testing can further help identify patients who would benefit most from additional revascularization procedures. These assessments help determine if the blockage itself requires treatment.

Pharmacological therapy remains an indispensable component of SCD prevention in MI survivors. Beta-blockers, which blunt sympathetic overactivity, continue to demonstrate robust reductions in arrhythmic mortality. ACE inhibitors and ARBs prevent adverse ventricular remodeling, thereby reducing arrhythmia susceptibility. Mineralocorticoid receptor antagonists offer additional antifibrotic and electrophysiological benefits. Importantly, recent evidence suggests that SGLT2 inhibitors, originally developed for glycemic control, exert multiple cardioprotective effects—including improved myocardial energetics, reduced intracellular sodium and calcium overload, enhanced diuresis without sympathetic activation, and attenuated inflammatory signaling, that collectively contribute to reduced arrhythmic death [53]. These agents represent a promising new frontier for arrhythmia prevention that warrants deeper mechanistic exploration.

Implantable cardioverter-defibrillators remain the cornerstone of SCD prevention in appropriately selected post-MI patients. Randomized trials such as MADIT-II and SCD-HeFT have firmly established the mortality benefit of ICDs in individuals with LVEF ≤35% after a predetermined waiting period following MI [54]. However, most studies concur that early ICD implantation (<40 days post-MI) is not beneficial because deaths occurring during this period are largely due to pump failure rather than arrhythmias [55]. The challenge remains that many SCD events occur in patients who do not qualify for ICD therapy by current criteria. Hence, the integration of advanced imaging, electrophysiological testing, genetic markers, and computational risk models could potentially refine patient selection in future guidelines.

Emerging literature also emphasizes the role of molecular and genetic factors in modulating arrhythmic risk. Genetic variants affecting ion-channel function, collagen synthesis, inflammation, and autonomic modulation have been associated with increased susceptibility to malignant ventricular arrhythmias after MI [56]. Although these findings are still in early stages, they highlight the possibility of future precision-medicine models wherein individualized genomic profiles could guide risk stratification and targeted therapeutics.

Technological advancements also offer new opportunities for early detection of arrhythmia risk. Wearable ECG monitors, implantable loop recorders, and artificial intelligence-based electrocardiographic analysis allow continuous surveillance and early detection of subclinical arrhythmic markers. AI-driven algorithms, in particular, have shown promising results in identifying subtle ECG abnormalities and predicting ventricular arrhythmias with superior sensitivity compared to traditional methods [57]. Additionally, machine-learning models that integrate clinical, imaging, electrophysiological, and biochemical data sets may significantly enhance the accuracy of SCD prediction and help identify previously unrecognized high-risk subgroups [58].

Even though advancement, the same challenges remain. Different study methods and outcome measures make it difficult to compare research results directly, which further complicates creating universal risk prediction tools. The variation in diagnostic approaches itself makes developing standard prediction methods challenging. Actually, many regions definitely cannot access advanced heart imaging like cardiac MRI, which limits the use of scar-based methods to check patient risk. Basically, different populations have different health conditions, genes, healthcare access, and economic situations, which affect SCD risk and treatment results in the same way. This shows we need region-specific studies and team approaches for better understanding [59].

Basically, future research needs to develop the same type of complete assessment systems that combine brain scans, body response markers, electrical brain activity, genetic factors, and computer analysis tools. These systems could actually change how we prevent SCD by helping doctors find people who are definitely at risk and need closer monitoring, better medicines, lifestyle changes, or preventive ICD devices. Further use of telemedicine and digital health tools can help in continuous monitoring and early detection of heart rhythm problems [60].

In summary, sudden cardiac death after myocardial infarction remains a complex and persistent clinical challenge driven by structural remodeling, autonomic imbalance, electrophysiological abnormalities, residual ischemia, and molecular predispositions. While current guideline-directed therapies—including pharmacological management, revascularization, and ICD therapy—provide substantial benefit, significant gaps remain in identifying high-risk individuals. Integrating multimodal biomarkers and emerging technologies into clinical practice may offer a pathway toward more effective and personalized prevention strategies.

Sudden cardiac death after myocardial infarction remains a major global health concern, driven by a complex interplay of structural remodeling, autonomic imbalance, electrophysiological instability, and residual ischemia that continues long after the acute event. Despite improvements in reperfusion therapy and evidence-based pharmacological management, many MI survivors retain a persistent arrhythmic vulnerability, with a significant proportion of SCD events occurring even in those with preserved ejection fraction. These findings underscore the inadequacy of relying solely on LVEF for risk prediction and highlight the importance of integrating multimodal assessment—including cardiac MRI scar quantification, autonomic markers, ECG-based predictors, and comprehensive revascularization status—to more accurately identify high-risk individuals. Preventive measures such as optimal medical therapy, timely revascularization, and judicious use of implantable cardioverter-defibrillators remain essential, but future progress will depend on adopting personalized, precision-based strategies that capture the full complexity of post-infarction pathophysiology.

1. Myerburg RJ, Junttila MJ. Sudden cardiac death caused by coronary heart disease. Circulation.
2. Zipes DP, Wellens HJJ. Sudden cardiac death. Circulation.
3. Huikuri HV, Castellanos A, Myerburg RJ. Sudden death due to cardiac arrhythmias. N Engl J Med.
4. Ibáñez B, et al. Pathophysiology of acute myocardial infarction and sudden death. Lancet.
5. Prabhu SD, Frangogiannis NG. The biological basis for arrhythmias after MI. Nat Rev Cardiol.
6. de Bakker JM, et al. Reentry and infarct scar. Circulation.
7. Pogwizd SM, et al. Mechanisms of arrhythmogenesis after MI. Cardiovasc Res.
8. Stecker EC, et al. Population-based analysis of SCD after MI. J Am Coll Cardiol.
9. Adabag AS, et al. Sudden death risk in the early post–MI period. Heart Rhythm.
10. Fox KA, et al. Long-term outcomes after myocardial infarction. BMJ.
11. Solomon SD, et al. Ventricular remodeling after MI. Circulation.
12. Halliday BP, et al. Late arrhythmic risk years after MI. J Am Coll Cardiol.
13. Moss AJ, et al. MADIT-II Trial: LVEF as predictor of SCD. N Engl J Med.
14. Gulati A, et al. LGE-CMR for arrhythmic risk in preserved EF. Lancet.
15. Goldberger JJ, et al. Multimodal SCD risk prediction. Circulation.
16. Schmidt A, et al. Infarct tissue heterogeneity predicts VT. Nat Med.
17. Kim RJ, et al. MRI assessment of myocardial viability & scar. Circulation.
18. Disertori M, et al. Scar burden and ventricular arrhythmias. Eur Heart J.
19. Klem I, et al. MRI predictors of arrhythmic events. JACC Imaging.
20. Lanza GA, et al. Autonomic function after MI. Heart.
21. Nishisato K, et al. MIBG imaging and SCD risk. Heart.
22. Schwartz PJ, et al. Autonomic imbalance & arrhythmias. Eur Heart J.
23. Merchant FM, et al. ECG markers for arrhythmic risk. Heart Rhythm.
24. Stone GW, et al. Impact of revascularization on long-term mortality. N Engl J Med.
25. Epstein AE, et al. Guidelines for ICD therapy. Circulation.
26. Page MJ, et al. PRISMA 2020 statement. BMJ.
27. Higgins JPT, et al. Cochrane Handbook for Systematic Reviews. Cochrane.
28. Liberati A, et al. The PRISMA statement. PLoS Med.
29. von Elm E, et al. STROBE guidelines. Lancet.
30. Wells GA, et al. Newcastle–Ottawa Scale (NOS). Ottawa Hospital Research Institute.
31. Shea BJ, et al. AMSTAR 2: critical appraisal tool for systematic reviews. BMJ.
32. Popay J, et al. Guidance on narrative synthesis. JBI Evidence Synthesis.
33. Adabag AS, et al. Temporal trends in SCD after MI. JAMA.
34. Armstrong PW, et al. Reperfusion & ventricular instability. Circulation.
35. Pedersen CT, et al. Long-term arrhythmic risk in MI survivors. Europace.
36. Yan AT, et al. Infarct scar characterization and VT risk. JACC Imaging.
37. Roes SD, et al. MRI scar characteristics predict VT. Circulation.
38. Antoni ML, et al. LV strain after MI predicts arrhythmic events. Eur Heart J.
39. Grimm W, et al. Holter-based arrhythmia predictors. Heart.
40. La Rovere MT, et al. HRV & baroreflex sensitivity after MI. Circulation.
41. Farooq V, et al. Incomplete revascularization and mortality. Lancet.
42. Zelniker TA, et al. SGLT2 inhibitors and SCD reduction. Circulation.
43. Huikuri HV, et al. Changing patterns of MI-related SCD. Eur Heart J.
44. 44.Menezes MN, et al. Early ischemic arrhythmias after MI. Heart Rhythm.
45. Anter E, et al. Re-entry circuits in scar-related VT. Circulation.
46. Disertori M, et al. Scar heterogeneity & arrhythmia risk. J Am Heart Assoc.
47. Stecker EC, et al. SCD in patients with preserved EF. J Am Coll Cardiol.
48. Bauer A, et al. Autonomic markers & arrhythmic outcomes. Eur Heart J.
49. Vaseghi M, et al. Autonomic modulation therapies. J Am Coll Cardiol.
50. Narayan SM, et al. ECG-identified repolarization abnormalities. Circulation.
51. Buxton AE, et al. NSVT and ICD benefit after MI. N Engl J Med.
52. Bangalore S, et al. Revascularization completeness & outcomes. Circulation.
53. Lopaschuk GD, et al. Metabolic effects of SGLT2 inhibitors. Cardiovasc Res.
54. Moss AJ, et al. MADIT-II: ICD mortality benefit. N Engl J Med.
55. Hohnloser SH, et al. DINAMIT: Early ICD after MI. N Engl J Med.
56. Bezzina CR, et al. Genetic determinants of arrhythmia risk. Nat Genet.
57. Attia ZI, et al. AI-enabled ECG arrhythmia prediction. Nat Med.
58. Narayan SM, et al. Machine-learning models for VT prediction. JACC EP.
59. Deo R, et al. Global disparities in SCD outcomes. Circulation.
60. Goldberger JJ, et al. Precision risk stratification for SCD. Nat Rev Cardiol.