Over the past three decades, the global burden of ischemic heart disease (IHD), particularly coronary artery disease, has remained substantial despite major advances in prevention and treatment^[1-3]. In 2021, approximately 254.3 million people were living with IHD worldwide; IHD accounted for 8.99 million deaths and 188.4 million disability-adjusted life-years^[1-3]. Against this background, percutaneous coronary intervention (PCI) has expanded rapidly and continued to evolve technically^[4]. PCI can restore epicardial blood flow without open surgery and is widely used for acute coronary syndromes (ACS) and selected chronic coronary syndromes^[5-7]. More than 600,000 PCI procedures are performed annually in the United States, and procedural activity also remains high across Europe and Asia^[8,9].

Despite these advances, patients who undergo PCI remain exposed to substantial residual cardiovascular risk. Contemporary trials and registries continue to report clinically meaningful rates of major adverse cardiovascular events despite new-generation drug-eluting stents and secondary-prevention treatment^[10,11]. This persistent risk reflects progression of untreated plaques, incomplete revascularization, residual ischemia, microvascular dysfunction, inflammation, and lipid abnormalities^[12,13]. Rehospitalization, repeat revascularization, prolonged pharmacotherapy, and long-term follow-up also impose a substantial economic burden^[14-16]. Reducing recurrent events after PCI therefore remains an important clinical priority.

Lipid-lowering and antiplatelet therapy are essential after PCI, but they do not eliminate recurrent risk. Many patients remain vulnerable because medication adherence is suboptimal and atherosclerosis is a systemic disease. In a contemporary US cohort of adults with prior myocardial infarction, only 36.5% received the full combination of guideline-recommended secondary-prevention medicines for which they were eligible^[17]. Population-level data after PCI also show incomplete achievement of guideline-recommended lipid levels^[18]. Residual inflammatory and triglyceride risk may also persist despite well-controlled low-density lipoprotein cholesterol^[19]. Lifestyle factors directly shape this remaining risk through their effects on inflammation, thrombogenicity, endothelial function, metabolic health, and long-term adherence. Accordingly, guidelines from the European Society of Cardiology (ESC) and the American College of Cardiology/American Heart Association (ACC/AHA) place lifestyle modification and cardiac rehabilitation at the center of secondary prevention^[20-22]. However, those documents address broad chronic coronary disease populations and provide limited space for the post-PCI transition.

This review therefore addresses a focused question: which lifestyle recommendations are supported by direct post-PCI evidence, which rely on extrapolation from broader coronary populations? We examine diet, exercise-based cardiac rehabilitation, smoking, alcohol, medication adherence, sleep, psychological health, body weight and metabolic status, and social conditions.

We searched PubMed/MEDLINE and the reference lists of major cardiovascular guidelines and systematic reviews for English-language publications from January 2015 through July 2026. Search terms covered PCI, coronary revascularization, secondary prevention, residual risk, diet, cardiac rehabilitation, physical activity, smoking, alcohol, sleep, depression, obesity, metabolic syndrome, medication adherence, digital health, and social determinants. Earlier landmark studies were included when they remained important to current practice.

We gave priority to PCI-specific randomized trials, prospective cohorts, registries, and meta-analyses. When direct evidence was unavailable, we used studies of myocardial infarction or established coronary disease and stated that the evidence was indirect. Because this is a narrative review, we did not perform formal study selection, risk-of-bias scoring, or meta-analysis. The interpretive summaries in the table and figure are descriptive rather than formal Grading of Recommendations Assessment, Development and Evaluation (GRADE) assessment. They consider study design, risk of bias, consistency, directness to PCI, precision, effect size, and dose-response.

Diet is a key determinant of long-term prognosis after PCI, as it shapes the persistent metabolic and inflammatory milieu following revascularization. Dietary patterns are more clinically relevant than isolated nutrients because foods are consumed in combinations that jointly influence low-density lipoprotein cholesterol (LDL-C), triglycerides, blood pressure, glycemia, body weight, inflammation, and satiety^[23]. In CORonary Diet Intervention With Olive Oil and Cardiovascular PREVention (CORDIOPREV), 1,002 patients with established coronary heart disease were randomized to a Mediterranean or low-fat diet and followed for a median of 7 years; the Mediterranean strategy reduced the primary cardiovascular outcome [adjusted hazard ratio (HR), 0.72; 95% confidence interval (CI), 0.54-0.96]^[24]. This is the strongest head-to-head dietary evidence in secondary prevention, but it was a single-center, open-label study; 82.5% of participants were men, and the cohort was not restricted to recent PCI. The more direct trial enrolled only 120 patients recently treated with coronary stents and followed them for 3 months. Mediterranean and low-fat diets both improved fatty-acid profiles, with larger increases in n-3 fatty acids under the Mediterranean diet, but no clinical outcome was evaluated^[25]. Thus, PCI-specific support is biologically coherent but based on a small surrogate-endpoint trial rather than demonstrated reductions in stent thrombosis or recurrent events.

Evidence for the Dietary Approaches to Stop Hypertension (DASH) diet, healthful plant-forward, Portfolio, and lower-carbohydrate patterns is more indirect. DASH lowers blood pressure in feeding trials, and healthful plant-based or Portfolio scores are associated with lower coronary risk, but the relevant studies largely involve general or primary-prevention populations^[26-28]. Lower-carbohydrate studies use inconsistent thresholds, frequently lack information on replacement nutrients, and show that outcomes differ when carbohydrates are replaced by unsaturated plant fats rather than saturated fat or animal foods^[29,30]. No adequately powered trial has compared Mediterranean, DASH, plant-forward, and high-quality lower-carbohydrate strategies after PCI. Accordingly, the Mediterranean pattern has the best overall secondary-prevention support, while selection among other patterns should be driven by hypertension, diabetes, hypertriglyceridemia, renal function, cultural acceptability, affordability, and food access rather than claims of equivalent post-PCI outcome benefit. Across patterns, reducing ultra-processed foods is a reasonable common target, although supporting outcome data remain observational and susceptible to residual socioeconomic and healthy-user confounding^[31,32].

Exercise-based cardiac rehabilitation (CR) has the broadest randomized evidence among the interventions reviewed. A meta-analysis of 85 randomized trials involving 23,430 patients with myocardial infarction, angina, coronary artery bypass grafting (CABG), or PCI and a median follow-up of 12 months found reductions in cardiovascular mortality [risk ratio (RR), 0.74; 95%CI, 0.64-0.86], myocardial infarction (RR, 0.82; 95%CI, 0.70-0.96), and hospitalization (RR, 0.77; 95%CI, 0.67-0.89), but not all-cause mortality (RR, 0.96; 95%CI, 0.89-1.04) or repeat PCI (RR, 0.84; 95%CI, 0.69-1.02)^[33]. The pooled population was clinically heterogeneous; many trials predated contemporary PCI and pharmacotherapy, follow-up was usually short, and low-risk men in high-income settings were overrepresented. PCI-specific cohort studies generally favor CR, but referral, socioeconomic, functional, and healthy-adherer selection can exaggerate outcome differences. Evidence is therefore more consistent for CR in coronary disease overall than for PCI-specific hard outcomes.

Aerobic activity remains the foundation of CR, with progressive resistance training added in clinically stable patients^[20,34]. Standard goals of at least 150 min of moderate aerobic activity weekly are useful long-term targets, but they should not be applied as a fixed immediate post-procedure prescription. Early planning should account for ACS versus elective PCI, radial versus femoral access, access-site complications, left ventricular function, residual or staged lesions, ischemic symptoms, frailty, and previous activity. Cardiopulmonary exercise testing is particularly valuable when symptoms, ventricular dysfunction, or residual ischemia make intensity uncertain^[34,35]. Persistent angina during rehabilitation should prompt clinical reassessment rather than automatic exercise withdrawal or escalation.

Center-based and home-based CR show broadly similar effects on exercise capacity and health-related quality of life in selected stable patients, but comparative trials are not powered to establish equivalent effects on mortality or stent-related events, and digitally enabled programs may exclude people with limited connectivity or literacy^[20,36,37]. Consequently, home or hybrid delivery should be presented as an access-enhancing alternative with risk-based supervision, not as proof that all delivery models are interchangeable. The important implementation target is automatic referral before discharge followed by documented initiation and completion, because an unacted referral does not deliver the trial-level benefit.

Smoking is consistently associated with recurrent ischemic events and stent thrombosis after PCI, although evidence for clinical outcomes is observational because smoking status cannot be randomized^[38-43]. Smokers in PCI cohorts are often younger and have fewer recorded comorbidities, which can create a misleading “smoker’s paradox” in incompletely adjusted analyses. Self-reported smoking, relapse, differences in treatment, and healthy-adherer bias further limit causal interpretation.

The biological link is well established: smoking promotes platelet activation and heightened thrombogenicity after PCI^[38]. Smokers in PCI cohorts are often younger and have fewer recorded comorbidities, which can produce an apparent “smoker’s paradox” in incompletely adjusted analyses^[39]. A Korean PCI cohort found a dose-response association between pack-years and major adverse cardiac and cerebrovascular events (MACCE)^[42]. Because exposure and later smoking behavior were measured observationally, residual confounding remains possible. The findings support early cessation but do not justify a fixed threshold beyond which vascular injury is considered irreversible.

Smoking cessation is associated with lower long-term risk after PCI. In the Korean cohort, people who quit after smoking < 20 pack-years had risks close to persistent non-smokers, whereas heavier former smokers retained greater residual risk^[42]. Another contemporary stenting cohort linked sustained cessation with lower 10-year all-cause and cardiovascular mortality^[43]. These studies support quitting as early as possible, but the size of benefit should not be read as a randomized treatment effect because relapse and healthy-adherer bias cannot be excluded.

Effective cessation usually requires repeated behavioral support and, when appropriate, medication. In the 302-patient Evaluation of Varenicline (Champix) in Smoking Cessation for Patients Post-Acute Coronary Syndrome (EVITA) trial, varenicline increased 24-week abstinence from 32.5% to 47.3%, although the trial was not restricted to PCI and was not powered for cardiovascular events^[44]. In a cohort of more than 27,000 hospitalized patients with coronary disease, early nicotine replacement therapy was not associated with higher short-term mortality or a longer hospital stay^[45]. Mobile interventions may help with abstinence and adherence, but they have generally not been tested for their effects on post-PCI clinical events^[46,47]. Treatment should begin during hospitalization when possible and should include early follow-up for relapse^[48,49].

Alcohol is the area in which observational and other evidence conflict most clearly. In a Korean insurance cohort of 77,409 PCI recipients followed for 4.0 years, both within-guideline and above-guideline drinkers had lower recorded MACCE risks than non-drinkers (adjusted HRs, 0.84 and 0.83)^[50]. However, intake was self-reported during a health examination within 1 year after PCI. Patients who were too ill or disadvantaged to attend were less likely to be included, and the non-drinker group may have included former drinkers who stopped because of illness.

The apparent J-shaped association should not be interpreted as proof that alcohol is protective. People who continue to drink may differ from abstainers in health, diet, income, and treatment adherence. Sick-quitter bias, healthy-user bias, changes in intake, reverse causation, and residual confounding are difficult to remove. Mendelian-randomization studies found no protective threshold for blood pressure or coronary disease^[51,52], and a meta-analysis designed to reduce former-drinker and study-quality bias found no significant mortality benefit with low-volume intake^[53]. No randomized trial has assigned alcohol consumption after PCI.

Patients who do not drink should not be advised to start for cardiovascular protection. Those who drink should avoid binge drinking and should consider reduction or abstinence, especially when they have atrial fibrillation, hypertension, cardiomyopathy, liver disease, problematic use, or important bleeding risk^[54-58]. Current evidence does not identify a dose that improves prognosis after PCI. Alcohol use should be reviewed again during follow-up because intake may change after discharge.

The long-term benefit of PCI also depends on adherence to indicated guideline-directed medical therapy (GDMT), particularly antiplatelet and lipid-lowering treatment and, when clinically indicated, renin-angiotensin-system inhibitors, beta-blockers, and other cardioprotective medicines^[20,59]. Medication adherence is not a lifestyle factor in the usual sense, but it is a modifiable behavior with immediate importance after stent implantation.

Adherence declines over time, even in clinical trials. In contemporary revascularization trials, use of an antiplatelet agent, beta-blocker, and statin fell from 67% at 1 year to 53% at 5 years. Fewer than 40% remained on all three drugs plus an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker^[60].

Common barriers include limited health literacy, the belief that PCI has cured the disease, polypharmacy, complex dosing, adverse effects, medication cost, limited insurance coverage, fragmented follow-up, and poor communication^[59,60]. These barriers often cluster with social disadvantage. As a result, observational links between adherence and outcomes may partly reflect healthy-adherer bias or differences in contraindications.

In the functionally complete revascularization cohort, adherence to GDMT declined from 61.2% at 1 month to 35.3% at 3 years. After propensity-score matching, sustained GDMT was associated with lower risks of 3-year MACCE (adjusted HR, 0.52; 95%CI, 0.36-0.75) and ischemia-driven revascularization (adjusted HR, 0.14; 95%CI, 0.07-0.28)^[61]. Because treatment was not randomized and adherence changed over time, these results cannot be interpreted as purely causal. Even so, uninterrupted antiplatelet therapy during stent healing has a clear procedure-specific role. Medication access, understanding of missed doses, and a plan for bleeding should therefore be confirmed before discharge.

The appropriate combination and duration of medication should be reviewed over time. Recent evidence questions routine long-term beta-blocker therapy after myocardial infarction when left ventricular ejection fraction is preserved and there is no other indication; benefit is clearer when systolic function is reduced or mildly reduced^[59,62]. Adherence should therefore mean taking medicines that remain indicated, not continuing every discharge medicine indefinitely without review.

Practical measures include medication reconciliation, plain-language counseling, simpler regimens, review of affordability, pharmacist support, nurse-led follow-up, and digital reminders suited to the patient’s access and literacy^[59,63]. Evidence for individual implementation strategies is heterogeneous, and nurse-led post-PCI studies remain few^[63]. Programs should measure access, persistence, bleeding, adverse effects, and clinical outcomes rather than app use alone.

Medication adherence should be managed together with lifestyle care. The immediate priorities are uninterrupted antiplatelet treatment and reliable access to prescribed medicines. Later visits should address adverse effects, regimen complexity, cost, and whether each medicine remains indicated.

Residual risk after PCI has several components. Lipid-related risk includes LDL-C, lipoprotein(a), and plaque progression. Inflammatory risk may persist despite lipid control. Thrombotic risk depends on the stent, lesion, and patient. Ischemic risk includes incomplete revascularization, untreated epicardial disease, vasomotor abnormalities, and coronary microvascular dysfunction. Cardiometabolic risk includes obesity, diabetes, hypertension, and kidney disease^{[12,13,77-81]}. Lifestyle care can improve several of these areas, but it cannot replace targeted medication or investigation of recurrent symptoms.

Modern secondary prevention combines lifestyle and adherence support with treatment directed at the patient’s remaining risks. In the Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk (FOURIER) trial, adding evolocumab to statin therapy reduced cardiovascular events (HR, 0.85; 95%CI, 0.79-0.92)^[82]. Low-dose colchicine reduced events after myocardial infarction in the Colchicine Cardiovascular Outcomes Trial (COLCOT) and in chronic coronary disease in LoDoCo2 (HRs, 0.77 and 0.69)^[83,84]. Semaglutide reduced MACE in SELECT (HR, 0.80)^[71]. These trials support treatment of lipid, inflammatory, and cardiometabolic risk, but none tested a complete post-PCI lifestyle program.

Antithrombotic treatment is especially important after PCI. Dual antiplatelet therapy (DAPT) intensity and duration should balance ischemic and bleeding risks, particularly after complex PCI. Depending on the patient, options may include prolonged DAPT, P2Y12-inhibitor monotherapy, or dual-pathway inhibition^[59,79,85]. Lifestyle counseling should reinforce adherence and bleeding surveillance but should not replace an individualized antithrombotic plan.

Delivery also matters. Automatic CR referral, early follow-up, multidisciplinary care, and home-based or hybrid programs may improve access. However, CR capacity remains limited in many countries, and digital programs may widen inequalities unless telephone and other low-technology options are retained^{[72-74,76,86]}. The proposed phase-specific lifestyle and secondary-prevention framework is summarized in Table 2^[87]. The relationships among residual-risk pathways, evidence across domains, and the phased management approach are summarized in Figure 1.

Future studies should test a clear post-PCI care pathway rather than another general education program. One practical design would start before discharge with confirmation of DAPT access and smoking treatment, provide follow-up at 7-14 days, begin CR and dietary support within 2-4 weeks, review cardiometabolic targets at 3 months, and reassess symptoms, bleeding, relapse, and social barriers through 12 months. Studies should distinguish ACS from elective PCI, radial from femoral access, complete from incomplete revascularization, and center-based from home-based care. Outcomes should include MACE, bleeding, angina, physical function, medication adherence, CR completion, cost, and equity.

Artificial intelligence (AI)-supported coaching, wearable-guided rehabilitation, digital monitoring, and remote follow-up should be tested prospectively before routine use. Studies should define how data will change care and should address privacy, safety, and unequal digital access. Economic analyses should include staff time, devices, travel, patient time, readmissions, and quality-adjusted life-years. In low- and middle-income settings, research should prioritize feasible approaches such as automatic referral, task sharing, culturally appropriate diets, telephone support, and non-digital options^{[72-74,76,86,88]}.

PCI restores coronary blood flow but does not cure systemic atherosclerosis or remove the risks from untreated lesions, residual ischemia, medication non-adherence, and adverse health behaviors. A PCI-focused approach is useful because early recovery involves access-site healing, time-sensitive DAPT adherence, possible staged or incomplete revascularization, and a risk that symptom relief will be mistaken for cure.

The strength of evidence varies across lifestyle domains. Exercise-based CR and smoking cessation have the most consistent support. A Mediterranean diet has randomized secondary-prevention evidence, but direct post-PCI outcome data are limited. Evidence for other dietary patterns, alcohol, sleep, psychological interventions, weight loss, and digital care is less certain. The best post-PCI care combines realistic lifestyle support with individualized management of lipid, inflammatory, thrombotic, ischemic, and cardiometabolic risk.