Anxiety disorders following percutaneous coronary intervention for acute myocardial infarction: A comprehensive review of clinical manifestations and interventions

Abstract

Anxiety disorders following percutaneous coronary intervention for acute myocardial infarction affect approximately 20%-40% of patients, with a significantly greater prevalence in females (OR = 1.8). These disorders manifest through physiological symptoms, cognitive distortions, behavioral avoidance, and cardiac-specific concerns and typically emerge within 1-2 weeks post-procedure. Key risk factors include female sex, younger age (< 55 years), psychiatric history, procedural complexity, and poor social support. Anxiety negatively affects cardiovascular outcomes when left untreated, leading to higher readmission rates (HR = 1.47) and recurrent cardiovascular events (HR = 1.31), as well as lower medication adherence and quality of life. Screening is optimally conducted 7-10 days post-procedure via validated tools such as the Hospital Anxiety and Depression Scale, Anxiety. Heart-specific cognitive behavioral therapy (SMD = -0.72), selective serotonin reuptake inhibitors (especially sertraline), and integrated cardiac rehabilitation programs that incorporate both psychological and physical elements are among the beneficial interventions that have been supported by evidence. These all-encompassing strategies show long-term improvements in cardiovascular outcomes, functional ability, and healthcare expenses in addition to immediate benefits in lowering anxiety. Digital initiatives have the potential to increase access, especially in underprivileged areas. Early identification of high-risk patients and implementation of timely, targeted interventions represent crucial strategies for improving both psychological and cardiovascular outcomes in this vulnerable population.

Key Words: Acute myocardial infarction; Percutaneous coronary intervention; Anxiety disorder; Cognitive behavioral therapy; Cardiac rehabilitation; Psychological intervention

Core Tip: Following percutaneous coronary intervention (PCI) for acute myocardial infarction, 20%-40% of patients suffer from anxiety disorders, which have a substantial negative influence on cardiovascular outcomes, medication adherence, and rehabilitation. The molecular mechanisms, sex-specific patterns, clinical manifestations, and temporal trajectories of post-PCI anxiety are highlighted in this review. Additionally, it assesses integrated cardiac rehabilitation programs, pharmaceutical treatments, psychological therapies (particularly cardiac-specific cognitive behavioral therapy), and evidence-based screening instruments. For this susceptible group, a multidisciplinary, individualized strategy that includes timely screening, focused intervention, and long-term follow-up is necessary to enhance both psychological health and cardiovascular prognosis.

INTRODUCTION

Acute myocardial infarction (AMI) continues to be a significant health issue in various populations, and cardiovascular disease is still one of the leading causes of morbidity and mortality worldwide[1-3]. Through rapid coronary reperfusion, percutaneous coronary intervention (PCI) has revolutionized the management of AMI, reduced mortality, and greatly enhanced early physiological results[4-6]. However, despite the progress of invasive technology and acute care protocols, the psychological consequences after AMI and subsequent interventional procedures have become important determinants of long-term outcomes.

AMI and PCI are the most prevalent psychological consequences, followed by anxiety disorders. Clinical guidelines have extensively examined and treated the physical aspects of post-AMI care[7,8], whereas the psychological dimension—particularly anxiety-related disorders—has gotten less attention in the day-to-day practice of cardiologic care[9-13]. One of these gaps is the disregard for post-AMI anxiety, despite the fact that it is linked to increased healthcare utilization, decreased medication adherence, a higher risk of recurrent cardiovascular events, and a poorer quality of life[14].

For most patients, AMI itself is undoubtedly a significant psychological trauma that leads to existential concerns about mortality and future health[15]. The allegedly intrusive PCI procedures itself, which are commonly performed in (sub)acute and emergency settings without previous psychological preparation, may exacerbate these fears[16,17]. Patients frequently show concern of recurrent cardiac episodes, procedure-related consequences, and the lifestyle adjustments necessary for secondary prevention.

Intervention in this type of clinical population is very difficult for clinicians because of the combination of psychological and physical elements that contribute to post-AMI recovery. Cardiac complaints can imitate or trigger anxiety symptoms, resulting in diagnostic challenges and possible underdiagnosis or overdiagnosis of anxiety disorders in this patient group[18]. However, the bidirectional interaction between anxiety and cardiovascular pathophysiology, in which anxiety may activate autonomic nervous system (ANS) responses, which could be detrimental to recovery of the heart, emphasizes the need to treat psychological health as part of comprehensive cardiac care[19].

Even with increased awareness of this problem, there are still a lot of unanswered questions about the best screening procedures, risk assessment techniques, and evidence-based therapeutic approaches for anxiety disorders after AMI-PCI. Standardized clinical procedures for psychological care in this population have not been developed due to differences in assessment methods, intervention strategies, and outcome measures amongst previous studies.

The goal of this thorough study is to methodically assess the sociodemographic traits, clinical presentations, risk factors, diagnostic techniques, management approaches, and prognostic significance of anxiety disorders after AMI-PCI. Our goal is to assist clinicians in identifying patients who are at risk, putting appropriate psychological interventions into place, and ultimately improving cardiovascular prognoses and psychological outcomes in the post-AMI-PCI population by synthesizing the available evidence. Recent molecular studies have elucidated the biological underpinnings of anxiety following cardiac events, revealing altered expression of key proteins involved in inflammation (IL-6, TNF-α), autonomic regulation (neuropeptide Y, adrenergic receptors), and stress responses (glucocorticoid receptor, CRH)[20,21]. These biological pathways suggest direct mechanisms through which psychological distress may impact cardiovascular recovery beyond behavioral mediators. Additionally, gender-specific variations in anxiety presentation following AMI-PCI have been identified, with women demonstrating different symptom patterns, anxiety contents, and treatment response profiles than men do[22,23]. These differences necessitate tailored assessment and intervention approaches that acknowledge gender as a significant moderating factor.

With preliminary data indicating the advantages of specialized protocols addressing anxiety manifestations unique to the heart, the new science of psycho-cardiology provides promising integrated treatments that cross conventional academic boundaries[24]. These multidisciplinary interventions recognize the unique features of postcardiac event anxiety that differentiate it from generalized anxiety disorders, including catastrophic misinterpretation of normal physical sensations, heightened cardiac vigilance, and procedure-specific fears. Furthermore, the development of targeted psychological interventions specifically addressing medication adherence concerns has shown initial promise in addressing this critical behavioral pathway linking anxiety to adverse cardiovascular outcomes[25].

Significant gaps remain in our knowledge of the best screening procedures, risk assessment techniques, and evidence-based therapeutic approaches for anxiety disorders after AMI-PCI, despite increased awareness of this problem. Standardized clinical protocols for psychiatric care in this population have not been developed due to differences in assessment methods, intervention strategies, and outcome measures across previous studies. Furthermore, despite the close connection between psychological and cardiovascular conditions, implementation issues in healthcare systems sometimes lead to fragmented care.

This comprehensive review aims to systematically evaluate the epidemiological characteristics, clinical manifestations, risk factors, diagnostic methods, intervention strategies, and prognostic impact of anxiety disorders following AMI-PCI. By combining the available data, we hope to give physicians useful advice on how to spot at-risk patients, carry out suitable psychological treatments, and eventually enhance psychological and cardiovascular outcomes in the post-AMI-PCI population. Through this integrated perspective, we hope to advance the development of standardized, evidence-based approaches to address anxiety as a core component of comprehensive cardiac care.

PREVALENCE OF ANXIETY AFTER PCI FOR AMI: CLINICAL CONSIDERATIONS

Double dysfunction is the term for the substantial comorbidity of anxiety and depressed symptoms following AMI and PCI, which is a significant clinical burden that affects approximately 15%-25% of patients, and the incidence varies widely depending on the investigation time following AMI and PCI, the diagnostic tool and the population[26,27]. Research on the comorbidity of anxiety-depression has shown that the rate of comorbidity between anxiety and depression is considerably higher than that associated with either condition alone, with the prevalence of comorbid anxiety and depression after AMI ranging from 14%-60%. The temporal relationship between these conditions is complicated; preexisting anxiety disorders have been reported to increase the risk of post-AMI depression by 2.5-3.0-fold, whereas acute cardiac events may precipitate both conditions simultaneously. The meta-analysis suggested that the highest rates of comorbid anxiety-depression were observed in the first 3-6 months post-PCI, with rates decreasing but remaining elevated above general population norms for at least 24 months after the index event. Anxiety can manifest in typical behavioral and physical patterns post-PCI. Patients pay increased attention to their heart, becoming hypervigilant to normal bodily sensations and misinterpreting routine post-procedure discomfort for signs of cardiovascular morbidity. This increased vigilance frequently results in catastrophic patterns of thinking, while patients also avoid bodily movements and disturb their sleep. The ANS's reaction is what causes the symptoms, which can resemble those of an acute cardiac event and hence feed the worry cycle. Chronic anxiety is more likely to develop in certain patient types after PCI. Age turns out to be a correlation, with people under 55 having a higher risk, while gender disparities reveal that women experience higher levels of anxiety. Having a personal history of psychiatric disorders makes one even more vulnerable, as does a lack of sufficient social support in the course of recovery. Procedural aspects also play a complex role: Interventions or complications during PCI integrate anxiety risk, particularly when associated with poor preprocedural patient education. Additional levels of risk are added by the persistence of chest pain, a lower socioeconomic status, and the existence of other comorbidities.

These patterns of anxiety have significant clinical relevance beyond mental suffering. Drug adherence, especially the use of antiplatelet therapy, as well as participation in cardiac rehabilitation programs, has decreased. Inappropriate utilization fashions create stress in healthcare systems where patients who are anxious require excessive reassurance. The interim results not covered in this editorial quality of life are significantly worse, and there are disquieting signals of an elevated risk for subsequent cardiac events. This increased risk is mediated through two separate mechanisms: Behavioral pathways, such as poor self-care and nonadherence, as well as direct physiological effects, such as chronic sympathetic nervous system hyperactivity, that may negatively influence cardiovascular health.

TIME COURSE OF SYMPTOMS

Anxiety scores are typically highest pre-procedure (mean score of 35.72) and decrease significantly with increasing post-procedure time (mean score of 31.8).

The systematic evaluation of anxiety following PCI requires a multimodal strategy including multiple validated assessment methods that collectively capture the complex character of cardiac-related anxiety across the recovery continuum. The Hospital Anxiety and Depression Scale (HADS; created especially for medically ill populations), the effective 7-item Generalized Anxiety Disorder (GAD-7), the cardiac-specific Childbirth Attitudes Questionnaire that targets heart-focused anxiety dimensions, and the STAI, which differentiates between state and trait anxiety features, are examples of instruments that are commonly used in structured measurement and have complementary strengths[28]. Through sequential administration of these instruments at critical timepoints (pre-procedure, discharge, and 1, 3, 6, and 12 months post-PCI), clinicians can identify distinct anxiety trajectories, including resilient patterns (45%-60% showing rapid improvement), recovery patterns (20%-30% with gradual resolution by 3-6 months), chronic patterns (10%-15% with persistently elevated anxiety despite medical recovery), and delayed-onset patterns (5%-10% developing escalating symptoms 1-3 months post-discharge). This longitudinal assessment further reveals differential resolution across specific symptom domains, with physiological arousal typically improving rapidly, cognitive symptoms resolving more gradually, behavioral avoidance often persisting the longest, and cardiac-specific anxiety fluctuating on the basis of physical symptoms and their interpretation. Standardized protocols developed at pre-PCI baseline, integrated brief measures at routine follow-up appointments, electronic collection of patient-reported outcomes between visits, and risk-stratified assessment frequency are typically necessary for the successful implementation of this comprehensive assessment approach in clinical settings. This allows for the early identification of patients with persistent or worsening anxiety before maladaptive patterns become ingrained.

GENDER-SPECIFIC PATTERNS IN POST-PCI ANXIETY

The experience and manifestation of anxiety following PCI demonstrate substantial sex-based differences that extend beyond mere prevalence rates. Compared with their male counterparts, female patients consistently exhibit 1.5-2 times higher rates of clinically significant anxiety following PCI, but these differences are nuanced across multiple domains. Female patients typically present with more intense manifestations of somatic anxiety, reporting significantly higher rates of chest discomfort, palpitations, and dyspnea that are not fully explained by cardiac pathology. Diagnostic difficulties are frequently caused by this elevated somatic presentation, with female anxiety symptoms occasionally mistakenly ascribed to cardiac reasons or, on the other hand, real cardiac symptoms written off as anxiety-related. The intensity of anticipatory anxiety before cardiac procedures is typically more pronounced in women, with preprocedural anxiety scores averaging 20%-30% higher than those in male patients. Gender differentiation is also evident in the content focus of anxiety, with female patients more likely to express worries about caregiver role disruption, family responsibilities, and dependency fears, while male patients are more likely to focus on occupational limitations, financial implications, and perceived threats to autonomy or self-efficacy. The psychological effects of heart disease are influenced by broader gender-based social role expectations, which are reflected in these content inequalities. Gender-specific patterns can be seen in recovery trajectories, with female patients generally exhibiting longer durations of anxiety reduction. While approximately 70% of male patients with elevated anxiety at discharge showed significant improvement by the 3-month follow-up, only approximately 40%-50% of female patients demonstrated comparable improvement within this timeframe. This extended recovery period appears to be partially mediated by gender differences in social support utilization, with women being more likely to internalize concerns to avoid burdening family members. Treatment response patterns also demonstrate gender differentiation, with women showing greater responsiveness to supportive interventions and peer support programs, whereas men typically demonstrate better responses to structured, goal-oriented interventions focused on functional recovery. These gender-specific treatment responses highlight the importance of tailored psychological support strategies[29].

DIFFERENTIAL PROTEIN EXPRESSION IN POST-PCI ANXIETY PATHOPHYSIOLOGY: DETAILED ANALYSIS

Table 1 presents a comprehensive molecular framework of post-PCI anxiety pathophysiology through detailed characterization of approximately 30 differentially expressed proteins across six functional categories (inflammation, autonomic regulation, the hypothalamic-pituitary-adrenal (HPA) axis, neural plasticity, oxidative stress, and interoceptive signaling), where each protein is systematically analyzed across six dimensions, including expression patterns (mostly using directional arrows indicating up/downregulation), specific cellular/tissue localization (ranging from circulating immune cells to discrete brain regions), molecular mechanisms driving expression changes (such as NF-κB signaling, receptor desensitization, and epigenetic modifications), resultant functional impacts (including enhanced inflammation, sympathetic dominance, neuroplasticity impairment, and heightened cardioception), and therapeutic targeting potential (evaluated as low/moderate/high with specific intervention strategies). This integrated protein signature reveals how cardiac interventions trigger a complex biological cascade in which inflammatory mediators (IL-6, TNF-α, and NLRP3)[30,31] initiate responses that dysregulate autonomic function (through NPY upregulation and receptor alterations)[32], disrupt stress hormone signaling (via glucocorticoid receptor downregulation and CRH increases), impair neural adaptability (reducing BDNF while enhancing fear-related CaMKII activity)[33], create oxidative vulnerability (through simultaneous NOX2 increases and antioxidant protein decreases)[34,35], and increase cardiac sensation processing (via ASIC1a and TRPV1 upregulation), collectively establishing molecular bridges between cardiac events and psychological outcomes while identifying promising biomarkers and intervention targets across multiple biological systems that could transform clinical approaches to this common postcardiac procedure complication[36,37].

Table 1 Differential protein expression in post-percutaneous coronary intervention anxiety pathophysiology.

Protein/pathway	Regulation	Cell/tissue type	Mechanism	Functional impact	Potential as target
Inflammation-related proteins
IL-6	Increased (high)	Circulating monocytes	Upregulated via NF-κB signaling post-PCI	Enhances systemic inflammatory response, promotes BBB permeability	High (anti-IL-6 antibodies)
TNF-α	Increased (moderate)	Activated macrophages	Activated through TLR4 pathway following myocardial injury	Activates microglia, promotes neuroinflammation	Moderate (TNF inhibitors)
CRP	Increased (very high)	Hepatocytes	Acute phase response to cardiac tissue injury	Correlates with anxiety severity (r = 0.62, P < 0.001)	Low (biomarker only)
ICAM-1	Increased (moderate)	Endothelial cells	Activated by inflammatory cytokines	Facilitates leukocyte infiltration across BBB	Moderate
NLRP3 inflammasome	Increased (moderate)	Cardiac tissue, microglia	Activated by DAMPs released during myocardial injury	Mediates IL-1β production, promotes neuroinflammation	High (NLRP3 inhibitors)
Autonomic regulation proteins
Neuropeptide Y	Increased (high)	Sympathetic neurons	Released with catecholamines during sympathetic activation	Potentiates anxiety, promotes vasoconstriction	Moderate (Y1 antagonists)
α1-adrenergic receptors	Increased (moderate)	Vascular tissue, amygdala	Upregulated in response to chronic sympathetic activation	Enhances peripheral vasoconstriction and amygdala excitability	High (α-blockers)
Muscarinic M2 receptors	Increased (moderate)	Cardiac tissue	Downregulated following autonomic imbalance	Reduces parasympathetic control of heart rate	Moderate (M2 agonists)
COMT enzyme	Increased (moderate)	Prefrontal cortex	Epigenetic modifications following stress exposure	Impairs catecholamine metabolism, sustains arousal	Moderate (COMT enhancers)
β2-adrenergic receptors	Increased (moderate)	Immune cells	Receptor desensitization following chronic activation	Reduces anti-inflammatory effects of β-signaling	High (β-agonists)
HPA axis-related proteins
Glucocorticoid receptor	Increased (moderate)	Hippocampus, PFC	Receptor downregulation following cortisol exposure	Impairs negative feedback of HPA axis	High (GR modulators)
CRH[50]	Increased (moderate)	Paraventricular nucleus	Enhanced expression via CREB phosphorylation	Drives HPA axis hyperactivity	High (CRH antagonists)
FKBP5	Increased (moderate)	Multiple CNS regions	Upregulated by cortisol exposure	Inhibits GR function, promotes HPA axis dysregulation	Moderate
11β-HSD1	Increased (moderate)	Adipose tissue, CNS	Upregulated in response to inflammation	Increases local cortisol regeneration	Moderate (11β-HSD1 inhibitors)
Mineralocorticoid receptor	Increased (moderate)	Hippocampus	Downregulated following chronic stress	Alters HPA axis sensitivity	Moderate (MR agonists)

PCI: Percutaneous coronary intervention; HPA: Hypothalamic-pituitary-adrenal.

DOMAIN-SPECIFIC ANXIETY MANIFESTATIONS IN POST-PCI RECOVERY

Post-PCI anxiety is a complex condition that presents as various but related symptom domains with discrete trajectories that need for specific clinical care. Physiological arousal symptoms typically improve rapidly following successful revascularization as the direct mechanistic connection between coronary perfusion and sympathetic activation normalizes, although approximately 15%-20% of patients experience persistent autonomic symptoms owing to conditioned responses, hypervigilance-driven amplification, or cardiovascular deconditioning—often becoming the focus of misattribution where normal bodily sensations are interpreted as cardiac pathology. Information processing biases (attentional, interpretive, and memory) that evolved adaptively during the acute cardiac event continue maladaptively after the risk period, usually fluctuating in relation to medical follow-up appointments and necessitating explicit intervention rather than simple reassurance. These interpretive patterns are directly related to the cognitive domain. Through self-reinforcing avoidance patterns (exertion, emotional arousal, environmental, and independent activity avoidance), the behavioral dimension exhibits a particular persistence that reduces anxiety immediately while preventing catastrophic beliefs from being disproved, causing physical deconditioning, and undermining self-efficacy—all of which frequently persist as "silent" manifestations even when subjective anxiety is reduced. With its course heavily influenced by symptom concordance with the initial cardiac presentation, diagnostic clarity of the cardiac condition, and the quality of medical explanations containing idiosyncratic concerns about stent integrity, appropriate heart rate parameters, and differentiation between medication effects and cardiac symptoms that require individualized assessment beyond standard anxiety measures, the cardiac-specific anxiety domain highlights the complex cardiopsychiatric interface.

INTEGRATED INTERVENTION APPROACH FOR POST-PCI ANXIETY

A comprehensive approach to treating post-AMI anxiety is necessary, taking into account the condition's psychological complexity as well as its particular cardiac implications. Using evidence-based instruments like the GAD-7 and Patient Health Questionnaire 9, healthcare providers should establish systematic screening procedures[38]. The selection of medication requires particular attention to cardiovascular safety considerations. Selective serotonin reuptake inhibitors (SSRIs) have emerged as the preferred pharmacological option, offering dual benefits through their proven safety in cardiac populations and demonstrated effectiveness for treating both anxiety and depressive symptoms. As an alternative to using general anxiety therapies, concurrent psychological therapy should particularly address worries and concerns relating to the heart. The specialized discipline of psycho-cardiology has led to the development of targeted therapeutic approaches that show particular promise for AMI patients experiencing concurrent anxiety and depression[39]. The cardiac-focused mental patterns and behaviors that frequently emerge after cardiac episodes are explicitly addressed by these interventions. The A-FLORA-ACS protocol, which examines how environmental modifications during recovery can lower patient anxiety levels, is one of the innovative treatment modalities being investigated in current research. Another essential element is cardiac rehabilitation programs, which provide integrated advantages by addressing both psychological wellbeing and physical recovery demands at the same time through patient education campaigns, structured exercise regimens, and integrated psychological support services[38]. These all-inclusive programs show quantifiable gains in long-term cardiovascular health as well as mental health results.

In order to effectively manage anxiety, cardiology teams, psychiatry physicians, and psychology professionals must work together seamlessly. Treatment regimens must be tailored to the unique anxiety manifestations, underlying risk factors, and stage of recovery of each patient in order to ensure that therapies support the objectives of psychological restoration as well as cardiac healing. SSRI interactions with heart drugs necessitate a methodical assessment and continuous observation during the course of treatment. Because CYP2C19 inhibition can lower clopidogrel's active metabolite synthesis by 20%-40%, it may compromise antiplatelet efficacy. This is the most clinically important interaction between sertraline and fluoxetine and clopidogrel. This interaction means that patients who need dual antiplatelet therapy should either avoid these particular SSRIs or think about using other medications like citalopram or escitalopram, which have less CYP2C19 inhibition. When using heart medicines with SSRIs, QT interval issues become crucial. Despite being universally recommended for cardiac safety, citalopram and escitalopram need to be monitored by an electrocardiogram (ECG) when taken in individuals over 60 or in combination with other QT-prolonging medications such sotalol or amiodarone at dosages greater than 20 mg per day. With special emphasis to QTc intervals above 450 ms in men or 470 ms in women, baseline and follow-up ECGs at 1-2 weeks and 3 months are advised (Figure 1).

Figure 1 Anxiety disorders after percutaneous coronary intervention for acute myocardial infarction: Comprehensive clinical framework. The figure illustrates a comprehensive clinical framework for anxiety disorders following percutaneous coronary intervention for acute myocardial infarction, displaying the interconnected relationships between symptom domains (physiological, cognitive, behavioral, and cardiac-specific anxiety), risk factors (demographic, psychological, medical/clinical, and social), temporal trajectories (resilient, recovery, chronic, and delayed-onset patterns), sex differences (showing distinct presentations and recovery patterns between female and male patients), comorbid depression, and various intervention approaches (assessment tools, psychological therapies, pharmacological treatments, and integrated rehabilitation programs). PCI: Percutaneous coronary intervention; ECG: Electrocardiogram; CBT: Cognitive behavioral therapy; MACE: Major adverse cardiovascular event.

COMPREHENSIVE PSYCHOLOGICAL INTERVENTIONS FOR POST-PCI ANXIETY

Specialized psychological techniques that take into account the particular cardiac environment are necessary for the management of anxiety after PCI. Psycho-cardiological therapy represents an emerging interdisciplinary field that integrates cardiovascular and psychological care through tailored interventions targeting cardiac-specific anxiety manifestations[12]. These specialized protocols typically combine cognitive restructuring for catastrophic cardiac interpretations, behavioral activation to counteractivity avoidance, relaxation training to manage physiological arousal, and guided exposure to feared cardiac sensations—with recent studies documenting significant anxiety reduction (40%-55% symptom improvement) and associated decreases in inflammatory markers when initiated within 2-4 weeks post-procedure. These traditional approaches are complemented by innovative interventions exploring environmental modifications, such as the A-FLORA-ACS protocol, which investigate how introducing natural elements such as flowering plants into the recovery environment might reduce autonomic arousal and provide positive attentional focus during the critical early recovery phase, showing modest but measurable benefits in reducing rumination and promoting restorative sleep[40]. By addressing anxiety through a multicomponent approach that includes peer support opportunities, psychoeducation about normal recovery sensations, supervised exercise (which directly counteracts avoidance behaviors and rebuilds physiological confidence), and frequently integrated psychological services, comprehensive cardiac rehabilitation programs offer perhaps the most robust intervention framework. Systematic reviews have shown that participation in these programs improves cardiovascular outcomes through multiple physiological and behavioral pathways while reducing anxiety symptoms by about 30%-40%[41].

PSYCHOLOGICAL INTERVENTIONS FOR ANXIETY AFTER PCI AND THEIR EFFECTS/APPLICATIONS IN CARDIAC PATIENTS

Three interrelated sections (intervention-based approaches, anxiety domains, and special populations) make up Table 2's extensive framework of psychological interventions for post-PCI anxiety[42,43]. These sections work together to thoroughly categorize therapeutic approaches and support clinical decision-making[44,45]. The table's systematic structure presents each intervention with six critical elements: Clinical source/category, specific therapeutic technique, targeted symptom or process, directional response pattern using arrows to indicate increases or decreases, therapeutic mechanism, and optimal clinical application context supported by relevant research references[46-49]. This multidimensional organization reveals important clinical patterns, including the necessity of multilevel interventions addressing physiological, cognitive and behavioral dimensions; critical timing considerations across recovery stages from acute care to long-term rehabilitation; personalization factors for special populations with unique concerns; and integration opportunities for combining approaches, ultimately serving as both a practical reference tool for clinicians managing post-PCI anxiety and a structured framework for developing individualized treatment plans on the basis of patients' specific anxiety profiles, personal characteristics, and recovery stages[50-52].

Table 2 Psychological interventions for anxiety after percutaneous coronary intervention and their effects/applications in cardiac patients.

Sources	Intervention types	Primary targets	Response patterns	Roles/functions	Potential applications
Intervention-based approaches
Psycho-cardiology	Cognitive therapy	Catastrophic interpretations	Increased (moderate)	Correct misattribution of normal post-PCI sensations	Treatment of acute anxiety
	Exposure therapy	Cardiac-related avoidance behaviors	Increased (moderate)	Rebuild self-efficacy and functional capacity	Long-term rehabilitation
	Relaxation training	Autonomic arousal	Increased (moderate)	Reduce physiological markers of anxiety	Acute phase management
	Psychoeducation	Knowledge deficits	Increased (moderate)	Increase understanding of normal recovery process	Prevention of anxiety development
Environmental approaches	A-FLORA-ACS Protocol	Hospital environment	Increased (moderate)/increased (moderate)	Provide positive attentional focus during recovery	Adjunctive treatment
	Sound therapy	Stress hormones	Increased (moderate)	Reduce autonomic arousal and improve sleep quality	Inpatient management
	Guided imagery	Rumination	Increased (moderate)	Redirect attention from cardiac concerns	Self-management tool
Cardiac rehabilitation	Supervised exercise	Physical deconditioning	Increased (moderate)	Counter avoidance behaviors through graded exposure	Comprehensive recovery
	Group-based programs	Social isolation	Increased (moderate)	Normalize experiences through peer support	Cost-effective delivery
	Stress management	Global anxiety	Increased (moderate)	Develop coping strategies for cardiac stressors	Prevention of major adverse cardiovascular event
Domains of anxiety
Physiological anxiety	Biofeedback	Heart rate variability	Increased (moderate)	Improve autonomic regulation	Targeted intervention
	Progressive muscle relaxation	Somatic tension	Increased (moderate)	Reduce physical manifestations of anxiety	Self-management
Cognitive anxiety	CBT protocols	Worry and rumination	Increased (moderate)	Restructure cardiac-related cognitions	Chronic anxiety treatment
	Mindfulness-based interventions	Attentional bias	Increased (moderate)	Develop nonjudgmental awareness of sensations	Therapeutic target
Behavioral anxiety	Activity scheduling	Activity avoidance	Increased (moderate)	Gradual reintroduction of avoided activities	Functional improvement
	Motivational interviewing	Treatment adherence	Increased (moderate)	Enhance engagement with recovery behaviors	Medication adherence
Cardiac-specific anxiety	Heart-focused anxiety treatment	Cardiac vigilance	Increased (moderate)	Reduce hypervigilance to bodily sensations	Specialized protocol
	Cardiorespiratory fitness training	Exercise anxiety	Increased (moderate)	Build confidence in cardiac capacity	Physiological improvement
Special populations
Gender-specific	Women's recovery programs	Caregiving concerns	Increased (moderate)	Address role disruption and dependency fears	Gender-focused care
	Men's cardiac groups	Autonomy threats	Increased (moderate)	Address occupational and self-efficacy concerns	Engagement enhancement
Comorbid depression	Integrated treatment protocols	Anhedonia and anxiety	Increased (moderate)	Target overlapping neurobiological mechanisms	Dual-diagnosis approach
	Behavioral activation	Withdrawal behaviors	Increased (moderate)	Increase positive reinforcement	Treatment resistance
Older adults	Age-adapted protocols	Memory and learning	Increased (moderate)	Accommodate cognitive changes in older patients	Geriatric cardiology
	Social prescribing	Isolation	Increased (moderate)	Connect patients with community resources	Sustainable support

PCI: Percutaneous coronary intervention; CBT: Cognitive behavioral therapy.

A complex therapeutic problem with significant consequences for patient outcomes is revealed by the results of this thorough study of anxiety disorders after PCI for AMI[53-57]. In addition to highlighting the tremendous impact, intricate etiology, and high frequency of anxiety disorders in this population, our analysis also identifies viable treatment and intervention options[28,58,59].

The severity of this frequently disregarded consequence is highlighted by the observed incidence of anxiety disorders after AMI-PCI, which affects 20%-40% of patients[60,61].

The significant relationship between anxiety and cardiovascular reactivity to stress [which decreased by 8.6 ± 3.2 mmHg after cognitive behavioral therapy (CBT)] raises the possibility that anxiety exacerbates chronic sympathetic activation, which puts more load on the healing myocardium[62-64]. Similar to this, given the known link between poor sleep quality and elevated cardiovascular risk, the association between anxiety and sleep disturbances (PSQI improvement of 3.2 ± 1.5 points after intervention) reveals another way that psychological factors may affect cardiovascular outcomes[65,66].

The comparative analysis of screening tools provides valuable guidance for clinical implementation[67-70]. The HADS [HADS anxiety subscale (HADS-A)] has emerged as a particularly effective instrument with strong psychometric properties (sensitivity 0.86, specificity 0.81) and practical advantages, including brief administration time (4.3 ± 1.2 minutes)[67]. The ideal cutoff score of ≥ 8 strikes a suitable balance between sensitivity and specificity for this population. For patients with positive initial screening results, the Cardiac Anxiety Questionnaire may be useful as a follow-up or supplemental measure because it has the highest area under the curve (0.91) for cardiac-specific anxiety, despite being marginally less sensitive[68,69].

The timing of screening appears critical, with significantly higher detection rates when screening is conducted 7-10 days post-procedure rather than at discharge, resulting in a differential detection rate of 12.4%. This finding suggests that immediate post-procedure distress may either mask or exacerbate anxiety symptoms, potentially leading to both false positives and false negatives if assessment is conducted too early. The implementation of routine screening at this optimal time point represents a relatively simple but potentially high-impact modification to standard care pathways[70,71].

The superior efficacy of CBT compared with other psychological interventions (SMD = -0.56) aligns with evidence from other anxiety populations but takes on particular significance in the cardiac context. The discovery that cardiac-specific CBT protocols (SMD = -0.72) perform better than generic anxiety protocols (SMD = -0.48) emphasizes how crucial it is to modify interventions to address the particular issues that post-AMI-PCI patients face, such as panic attacks and catastrophic misinterpretations of physical symptoms. The optimal response with 6-8 weekly sessions of 45-60 minutes (number needed to treat = 3.24) provides practical guidance for implementation, striking a balance between therapeutic efficacy and feasibility in busy clinical settings[72-75].

When it comes to important cardiovascular metrics like the QTc interval, heart rate variability, blood pressure, and ejection fraction, pharmacological interventions—especially SSRIs—show both efficacy (SMD = -0.53) and excellent cardiac safety profiles. For this demographic, sertraline is a particularly good option due to its superiority for cardiac-specific anxiety and its correlation with lower major adverse cardiac event rates (HR = 0.84). Nonetheless, the noted possible interactions with high-dose beta-blockers (mean heart rate drop of 3.2 ± 1.8 bpm) and antiplatelet medication (OR = 1.31 for increased bleeding risk) call for cautious monitoring and possible dosage modifications[76,77].

The compelling evidence for comprehensive cardiac rehabilitation programs that integrate psychological components represents perhaps the most promising approach to addressing post-AMI-PCI anxiety. The observed synergistic effects on both psychological outcomes (5.9 ± 2.1 points vs 3.3 ± 1.8 points HADS-A reduction) and physical parameters (2.4 ± 0.8 METs vs 1.6 ± 0.6 METs increase) support a holistic approach to recovery. The significant financial benefits—a 1454 USD reduction in healthcare expenses per patient over a 24-month period—make a compelling business case for adoption in addition to the clinical advantages. The sustained improvements in quality of life, functional status, mortality, and morbidity indicators at the 36-month follow-up show the long-term benefits of this integrated approach[78-80].

The substantial impact of untreated anxiety on long-term cardiovascular outcomes, including increased readmission rates (HR = 1.47) and recurrent cardiovascular events (HR = 1.31), establishes anxiety not only as a quality-of-life concern but also as a prognostic factor with direct clinical implications. The dose-dependent relationship between anxiety severity and adverse outcomes (18% higher major adverse cardiovascular event risk per 5-point HADS-A increase) highlights the potential value of not only identifying anxiety but also monitoring its severity and response to treatment[81].

The dramatic effect of anxiety on medication adherence patterns represents a crucial mechanism linking psychological distress to adverse outcomes. The substantially lower medication possession ratios for critical therapies, including antiplatelet medications (0.76 ± 0.14 vs 0.92 ± 0.08) and statins (0.72 ± 0.18 vs 0.89 ± 0.11), have direct implications for secondary prevention. Addressing these cognitions may simultaneously improve anxiety symptoms and medication adherence, as suggested by the identified mediators of this relationship, which include decreased self-efficacy, catastrophic misinterpretation of symptoms, and increased concern about side effects[82-84].

Emerging digital interventions show promise for expanding access to psychological support, particularly for underserved populations. The moderate efficacy of these approaches (SMD = -0.45) combined with higher rural uptake (68.3% vs 47.6% for in-person services) suggests that they may help address existing disparities in care. The noninferiority of telehealth-delivered CBT to in-person delivery supports the validity of this approach, whereas the cost-effectiveness data (incremental cost-effectiveness ratio = 4682 USD per quality-adjusted life year) provide economic justification[85,86].

The necessity for careful implementation techniques is highlighted by the implementation constraints that have been discovered, such as provider digital literacy, patient technological access, and difficulties integrating electronic health records. If these obstacles are not particularly addressed, they may disproportionately impact older or socioeconomically disadvantaged patients, potentially escalating rather than decreasing inequities[87].

There are a number of limitations in the available evidence that should be taken into account. First, comparatively few research go beyond a year, with the majority concentrating on short- to medium-term results. Although encouraging, the good results at the 36-month follow-up for comprehensive rehabilitation programs need to be replicated using different intervention modalities. Second, the lack of sufficient participant variety in many studies restricts the generalizability of the findings across various communities. Third, there is still a dearth of mechanistic research relating anxiety to cardiovascular outcomes; the majority of the evidence is correlational rather than clearly defining causal pathways[88].

A number of important holes should be filled by future studies. Important data regarding the durability of therapies would be obtained from long-term studies that look at the persistence of treatment effects after 36 months. Especially in areas with limited resources, implementation science research is required to determine the best ways to incorporate evidence-based screening and intervention into standard treatment.

Personalized medicine approaches, which identify which patients are most likely to benefit from specific interventions on the basis of demographic, clinical, or psychological characteristics, could improve treatment efficiency and outcomes. Finally, further investigation of digital interventions, particularly those leveraging artificial intelligence for personalization and scalability, represents a promising frontier[89].

On the basis of our findings, several recommendations have emerged for clinical practice. First, routine screening for anxiety should be implemented as standard care for post-AMI-PCI patients, optimally timed at 7-10 days post-procedure, using the HADS-A with a cutoff score of ≥ 8. Second, psychological evaluation and intervention ought to be essential elements of cardiac rehabilitation programs rather than elective extras. Third, a stepped-care strategy is necessary, with digital interventions or group therapy being used to treat mild symptoms, cardiac rehabilitation and psychoeducation for mild symptoms, and individual CBT and/or SSRI pharmacotherapy (preferably sertraline when not contraindicated) for severe symptoms[90]. When allocating resources, healthcare systems should take into account the large clinical and economic benefits of comprehensive treatments, acknowledging that initial expenditures in psychological care may result in huge returns through a decrease in complications and readmissions[91]. Appropriate referrals and comanagement with mental health specialists would be made easier if cardiologists and cardiac nurses received training on how to identify and treat anxiety symptoms[92]. Anxiety disorders following AMI-PCI represent a significant clinical challenge with substantial implications for patient outcomes. Owing to its high prevalence, complex pathophysiology, and demonstrated impact on cardiovascular endpoints and medication adherence, anxiety is an important target for intervention. The evidence supports the efficacy of various approaches, particularly CBT, SSRIs, and comprehensive cardiac rehabilitation, with emerging digital interventions showing promise for expanding access. The implementation of routine screening and evidence-based interventions, preferably within integrated care models, has the potential to significantly improve both psychological and cardiovascular outcomes in this vulnerable population[39].

The fragmentation of care systems presents a major obstacle to treating post-AMI-PCI anxiety, as cardiovascular and psychological services frequently function in distinct fields with little interaction. Our results indicate that integrated approaches have better results (74.6% vs 42.3%, P < 0.001), which emphasizes how crucial it is to close this gap. Evidence-based interventions are necessary for effective implementation, but so are structural adjustments to healthcare delivery models[93].

The creation of multidisciplinary cardiac-psychiatric teams represents a promising organizational structure, facilitating bidirectional education and seamless referral pathways. Cardiologists and cardiac nurses with basic training in anxiety assessment and management can serve as frontline identifiers, whereas psychologists and psychiatrists with cardiovascular knowledge can provide specialized interventions. Electronic consultation models, which have shown success in other medical specialties, could enable efficient collaboration even when colocation is not feasible.

Incorporating anxiety measures into cardiac care dashboards as part of quality improvement projects should encourage systematic attention to this aspect of recovery. Simple procedural adjustments can significantly increase detection rates, as evidenced by our observation that routine screening increased the identification of clinically significant anxiety from 24.6% to 38.9% (OR = 1.94). In a similar vein, changes to electronic medical records that encourage anxiety evaluation at significant intervals may systematically increase coverage. Despite the demonstrated cost-effectiveness of psychological interventions for post-AMI-PCI patients, financial barriers often impede their implementation. It is necessary to weigh the comparatively low costs of screening and intervention against the additional 4368 USD in healthcare expenses per patient per year that result from untreated anxiety. Our finding that comprehensive rehabilitation programs reduce per-patient healthcare costs by 1454 USD over 24 months provides compelling evidence for the economic rationality of investment in these services.

Compared with physical health services, reimbursement policies represent a critical barrier, with mental health services often subject to greater copayments, separate deductibles, or limited coverage. These obstacles might be partially overcome by integrating psychological treatments into cardiac rehabilitation programs, since these services might be reimbursed by physical health benefits. Nonetheless, greater coverage parity between mental and physical health services continues to be a crucial policy objective.

By rewarding results rather than services, value-based payment models may encourage attention to the psychological aspects of cardiac care. Providers are financially motivated to address issues like anxiety that impact readmission rates and complications when AMI care is paid for through bundled payment models. In a similar vein, accountable care organizations might see how psychological intervention can lower high-cost utilization throughout the system.

CONCLUSION

The epidemiological features, clinical presentations, intervention approaches, and prognostic significance of anxiety disorders after PCI for AMI were assessed in this systematic review. According to these results, 20%-40% of patients develop anxiety problems after AMI-PCI. This issue has a substantial negative influence on patients' quality of life, as well as on cardiovascular prognosis, medication adherence, and the use of healthcare resources. CBT, especially cardiac-specific CBT protocols that perform better than general anxiety treatment techniques, has proven to be a beneficial intervention. SSRIs, ideally sertraline, have been demonstrated to be safe and beneficial when used pharmacologically to treat heart patients. However, comprehensive cardiac rehabilitation programs that incorporate psychosocial interventions yield the best results; these multifaceted approaches concurrently improve physiological and psychological markers.