Transforming Lives: Embracing Lifestyle Changes Post-PCI | USC Journal

Coronary artery disease (CAD) impacts one in 20 adults over the age of 20 in the US and stands as the primary cause of death both nationally and worldwide.¹ Approximately 805,000 individuals in the US suffer a myocardial infarction (MI) annually, with nearly 25% of these occurring in individuals with a history of previous MI.¹ Despite substantial improvements in post-MI survival rates and early recurrent MI incidences (within the first year) since the 1970s due to enhancements in percutaneous coronary intervention (PCI) and pharmacological treatments, recurrent coronary incidents persist as a significant clinical issue.^2,3 Therefore, secondary prevention through the enhancement of cardiovascular health is vital. An essential component of this approach is the modification of risk factors through medications, cessation of smoking, dietary changes, and consistent physical activity. This review will deliver a thorough overview of these aspects, focusing particularly on pharmacotherapy, lifestyle alterations, and cardiac rehabilitation (CR) for patients following MI or PCI.

Pharmacotherapy Post-Revascularization

Following PCI for stable ischemic heart disease (SIHD) or during an MI event, it is essential to initiate several medications to enhance survival outcomes and decrease the risk of recurrent atherothrombotic incidents. The foundation of medical treatment after PCI is platelet inhibition achieved through dual antiplatelet therapy (DAPT), which includes aspirin and a P2Y₁₂ inhibitor.⁴ Among P2Y₁₂ inhibitors, prasugrel or ticagrelor may be more effective than clopidogrel in lowering the risk of stent thrombosis.⁵ DAPT is generally advised for at least 12 months after an acute coronary syndrome (ACS) case and a minimum of 6 months for SIHD managed with PCI, unless contraindications are present.^5,6 Nonetheless, some studies have questioned this guideline due to bleeding concerns. A systematic review involving over 79,000 patients who underwent PCI with a drug-eluting stent indicated that a shorter DAPT duration (<6 months) followed by monotherapy with a P2Y₁₂ inhibitor, as opposed to 12 months of DAPT, was linked to fewer bleeding incidents and did not result in inferior outcomes regarding MI, major adverse cardiovascular events (MACE), and mortality.⁷ A meta-analysis on DAPT duration after ACS treated with PCI demonstrated that a shorter duration of 1 to 3 months of DAPT followed by P2Y₁₂ inhibitor monotherapy led to a reduction in bleeding occurrences and a comparable rate of major adverse cardiac events when contrasted with a 12-month DAPT regimen.⁸ Ultimately, the best duration for DAPT needs to be personalized for each patient, balancing the risk of recurrent atherothrombotic incidents against the likelihood of major bleeding events.

The advantages of β-blocker administration for patients experiencing an MI, particularly those with known heart failure and a left ventricular ejection fraction (LVEF) ≤40% or ventricular arrhythmias, are well-established.^9,10 Consequently, β-blockers ought to be suggested for these patient populations. However, a recent study involving patients with acute MI and preserved LVEF showed that the early introduction of β-blocker therapy compared to no β-blocker treatment did not decrease the risk of mortality from any cause or recurrent MI.¹¹ Furthermore, in post-PCI patients with SIHD and normal LVEF, β-blocker therapy has not been linked to enhanced cardiovascular outcomes, leading the 2021 guideline for coronary artery revascularization to assign β-blockers a class 3 recommendation (no benefit) for this group.^5,12

After experiencing an MI or PCI in the context of SIHD, high-intensity statins should be initiated aiming to decrease LDL cholesterol (LDL-C) by at least 50% targeting a goal of <70 mg/dl.^6,13 The relationship between LDL-C and atherosclerotic cardiovascular disease has been rigorously studied and confirmed through various methods including animal research, epidemiological analyses, and randomized controlled trials.^13,14 Lowering LDL-C by 1 mmol/l via statin therapy has been proven to reduce significant coronary incidents, revascularizations, and ischemic strokes by close to 20%.¹⁵ Additionally, high-intensity statin therapy has demonstrated a further reduction in LDL-C levels and significant vascular events by an additional 15% compared to moderate-intensity statins.¹⁶

If the LDL-C target is not achieved with the maximally tolerated statin treatment, supplementary lipid-lowering therapies like ezetimibe and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors may be considered.¹³ In the IMPROVE-IT trial, participants with recent ACS who were administered ezetimibe in addition to moderate-intensity statin therapy showed a 24% reduction in LDL-C and a 2% absolute risk decrease in the primary endpoint of death from cardiovascular causes, major coronary events, or non-fatal strokes at the 7-year mark.¹⁷ While overall mortality rates did not differ between groups in the 2015 IMPROVE-IT trial, a recent national cohort study showed that the early implementation of ezetimibe post-ACS was correlated with a 23% reduction in mortality.¹⁸ Thus, ezetimibe is recommended as the preferred initial adjunctive agent due to its lower cost, broader accessibility, and established safety profile, followed by a PCSK9 inhibitor. Two large, multicenter randomized controlled studies analyzed the effectiveness of PCSK9 inhibitors in patients with a history of acute MI when combined with maximally tolerated statin therapy.^19,20 In the ODYSSEY OUTCOMES trial, those receiving alirocumab demonstrated a 15% lower possibility of dying from CAD over a follow-up period of 2.8 years in comparison to the placebo group. Participants in the FOURIER trial who were given evolocumab versus placebo displayed a 15% lower risk of cardiovascular death, myocardial infarction, stroke, hospitalization for unstable angina, or coronary revascularization over a 48-week duration.

For select individuals intolerant to statins, bempedoic acid has surfaced as an alternative for lowering LDL-C. In the CLEAR Outcomes Trial, patients with either a primary or secondary indication for lipid-lowering therapy who were either unable or unwilling to take a statin experienced a 21% reduction in LDL-C and a 13% decrease in the primary endpoint of cardiovascular-related death, nonfatal MI, nonfatal strokes, or coronary revascularization compared to placebo.²¹

Beyond managing LDL-C, hypertriglyceridemia is another critical risk factor requiring attention due to its link to an increased risk of ischemic events. The JELIS study demonstrated a 19% reduction in major coronary incidents among those administered low-intensity statins alongside 1.8 g of eicosapentaenoic acid daily versus low-intensity statin monotherapy over an average follow-up of 4.6 years.²² Subsequently, REDUCE-IT concentrated on a highly purified EPA, icosapent ethyl. Patients with established cardiovascular disease and relatively stable LDL-C levels but elevated fasting levels …

triglyceride levels between 135–499 mg/dl, despite statin treatment, saw a 25% decrease in the primary outcome of cardiovascular demise, nonfatal myocardial infarction (MI), nonfatal stroke, coronary revascularization, or unstable angina when administered 2 g of icosapent ethyl twice daily versus placebo over a span of 4.9 years.²³

In patients post-MI who have additional comorbidities like heart failure with left ventricular ejection fraction (LVEF) <40%, diabetes, hypertension, or chronic kidney disease, supplementary treatment with an angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker has proven to enhance outcomes.²⁴ In the GISSI-3 trial, starting lisinopril compared to placebo within 24 hours following an acute MI led to a 12% reduction in overall mortality, with a sustained advantage for up to 6 months, even if lisinopril was ceased.^25,26 Other trial results demonstrated that administering ACE inhibitors to individuals with recent MI and diminished LVEF lowered the mortality risk by up to 25% in comparison to placebo.^27,28 Additionally, angiotensin receptor/neprilysin inhibitors have shown to be superior to ACE inhibitors in terms of enhancing mortality rates in heart failure patients, regardless of the underlying cause.²⁹ Furthermore, the addition of mineralocorticoid receptor antagonists like eplerenone significantly decreases cardiovascular mortality in those with acute MI, even in the absence of heart failure, when contrasted with placebo.³⁰

Consideration should also be given to prescribing a sodium-glucose co-transport 2 (SGLT2) inhibitor or a glucose-like peptide-1 (GLP-1) receptor agonist for patients following MI or PCI. The efficacy and safety profile of SGLT2 inhibitors regarding cardiovascular outcomes have been rigorously examined. The EMPA-REG OUTCOME trial indicated that empagliflozin resulted in a 14% reduction in the principal outcome of death from cardiovascular causes, nonfatal MI, or nonfatal stroke when compared to placebo in diabetic individuals at high risk for cardiovascular disease.³¹ A meta-analysis encompassing data from EMPA-REG OUTCOME, CANVAS, and the DECLARE-TIMI 58 trial revealed that SGLT2 inhibitors correlated with an 11% decrease in significant adverse cardiac events in diabetic patients with established atherosclerotic disease.³² SGLT2 inhibitors are typically well-tolerated but carry an increased risk of mycotic genital infections and diabetic ketoacidosis, albeit at low frequencies. A heightened risk of lower limb amputations linked to the SGLT2 inhibitor canagliflozin was noted in the CANVAS trial; however, this result was not replicated in the CREDENCE trial or observed in studies of other SGLT2 inhibitors.^32,33

GLP-1 receptor agonists also offer substantial advantages for patients dealing with cardiovascular disease, both with and without diabetes. A meta-analysis of GLP-1 receptor agonists in diabetic patients showcased a 14% decrease in major adverse cardiac events (MACE) along with a 12% reduction in overall mortality compared to placebo. Moreover, this analysis revealed no heightened risk for severe hypoglycemia, retinopathy, or pancreatitis associated with GLP-1 receptor agonists.³⁴ Additionally, in the SELECT trial, overweight or obese individuals with pre-existing cardiovascular disease but without diabetes who were treated with the GLP-1 receptor agonist semaglutide encountered a 20% reduction in a combined primary endpoint of death from cardiovascular reasons, nonfatal MI, or nonfatal stroke relative to placebo.³⁵

Smoking Cessation

Smoking constitutes a significant cardiovascular risk factor linked to atherothrombotic disease and remains the most prevalent preventable cause of death globally.³⁶ Following MI or PCI for stable ischemic heart disease (SIHD), quitting smoking is crucial for reducing the chances of reinfarction and stent thrombosis.⁵ Furthermore, the duration after MI or PCI represents an ideal opportunity to emphasize smoking cessation as a secondary prevention tactic to enhance mortality and quality of life. A population-based cohort investigation found that those who ceased smoking after their first MI experienced a 37% lower risk of mortality compared to those who continued smoking over a 13-year follow-up period.³⁷ For patients unable to quit smoking entirely, decreasing the number of cigarettes smoked can offer benefits. Post-MI patients who reduced their daily cigarette consumption by five exhibited an 18% lower mortality risk compared to those maintaining their smoking levels.³⁷

Previous studies have indicated that using a combination of pharmacotherapy and behavioral therapy can enhance the success rate of smoking cessation by 70–100% compared to minimal interventions such as brief unstructured advice to stop smoking.³⁸ Various methods for behavioral therapy exist, including individual or group counseling, telephone or text messaging support, mobile applications, and self-help strategies. Regardless of the approach taken, patients should be educated about withdrawal symptoms, triggers, and coping mechanisms. Pharmacotherapy may include nicotine replacement therapy, bupropion, or varenicline, all of which demonstrate effectiveness, with the strongest data supporting varenicline.^24,39 Although varenicline is effective for smoking cessation, concerns have arisen regarding potential adverse cardiovascular and neuropsychiatric effects, such as ischemic heart disease, cardiac arrhythmias, and depression.⁴⁰ Nevertheless, numerous trials have indicated no increased risk for neuropsychiatric or cardiovascular events associated with varenicline compared to nicotine patches or placebo.^40–42 Unfortunately, relapse after attempting to quit smoking is common. One study found that after one year post-MI, 60% of individuals taking varenicline resumed smoking.⁴³ Factors correlated with a higher likelihood of smoking cessation include engagement in cardiac rehabilitation (CR), having supportive partners, and a firm intention to quit. Conversely, factors such as depression, lung diseases, and unemployment are all linked to a decreased chance of quitting smoking.⁴⁴ Thus, healthcare providers should work collaboratively with patients to determine the most effective strategies for smoking cessation, concentrate on maximizing cessation success, and promote sustained quitting.

Psychological Interventions

Going through a significant life event such as an MI or requiring PCI for SIHD can evoke considerable psychological distress. About 20% of acute MI survivors develop major depression, which is a rate three times higher than in the general populace.⁴⁵ Notably, post-MI depression has been associated with a nearly threefold increase in all-cause mortality, cardiovascular mortality, and cardiac incidents, with this correlation remaining consistent over a span of 25 years.^46,47 While anxiety has received less attention, it also serves as an independent risk factor for cardiovascular mortality.⁴⁸

Evidence-based treatments for mental health conditions typically consist of a combination of cognitive-behavioral therapy (CBT) or counseling along with available pharmacological options.⁵ The ENRICHD trial examined whether addressing depression and low perceived social support with CBT plus a selective serotonin reuptake inhibitor (SSRI) could lessen mortality and recurrent infarction in MI patients.⁴⁹ At the 24-month mark, no noticeable enhancement in event-free survival was observed in subjects undergoing CBT for depression as opposed to those receiving usual care. Nonetheless, a post hoc analysis of the ENRICHD trial revealed thatdepressed individuals receiving an SSRI after myocardial infarction (MI) underwent a 42% decrease in the likelihood of reaching the primary outcome, which encompasses mortality, nonfatal MI, and overall mortality, in contrast to those who did not use SSRIs.^49,50 Moreover, a 24-week regimen involving escitalopram for patients with recent acute coronary syndrome (ACS) and depressive disorders in the EsDEPACS trial proved to be more effective than placebo in lessening major adverse cardiovascular events (MACE) during a median follow-up of 8.1 years.^51,52 Consequently, antidepressants play a vital role in managing post-MI depression. Once patients initiate pharmacological treatment, consistent follow-up is critical to ensure compliance and track potential side effects that may cause treatment discontinuation.

Cognitive-behavioral therapy (CBT) is also beneficial in alleviating depression and anxiety symptoms among individuals with coronary artery disease (CAD), particularly through cognitive restructuring for depression and relaxation methods for anxiety.⁵³ Key aspects of CBT that have shown to enhance symptoms include tailored therapy and focus on psychoeducation and cognitive-behavioral techniques.⁵³

Crucially, individuals with CAD should undergo screening for mental health conditions to enable prompt treatment initiation, thereby improving quality of life and survival rates. Additionally, depression and anxiety can affect lifestyle choices and medication compliance.⁵⁴

Nutrition and Alcohol

Nutrition is a primary focus for patients after MI or PCI. Inadequate intake of fruits and vegetables is a modifiable risk factor for MI, with increased consumption linked to lower mortality risk among individuals aged 35–70 years without cardiovascular disease.^55,56 Dietary recommendations from several prominent cardiovascular organizations stress a largely plant-based approach, minimizing processed meats, refined carbs, and sugary drinks, while encouraging reduced sodium intake and substituting saturated fats with mono- and polyunsaturated fats.^57,58 These guidelines can be followed through various dietary strategies such as the Mediterranean diet, the Dietary Approaches to Stop Hypertension (DASH) diet, a plant-based diet, ketogenic diet, or intermittent energy restriction.⁵⁹

The Mediterranean diet mainly consists of leafy greens, fruits, nuts, legumes, whole grains, extra virgin olive oil, fish, and shellfish, with minimal consumption of poultry, eggs, and dairy. Red meat and sugary treats are kept to a minimum.⁵⁹ In the Lyon Diet Heart Study, which was targeted at a post-MI group, participants following the Mediterranean diet experienced a 72% decrease in recurrent nonfatal MI and a 56% drop in overall mortality over a four-year follow-up compared to those not given specific dietary guidance.⁶⁰ The DASH diet is not only associated with decreased blood pressure but has also demonstrated a reduction in noncalcified plaque and a deceleration in atherosclerosis progression when integrated with optimal medical treatment.⁶¹

A vegetarian diet, similar to the previously mentioned diets, replaces meat, seafood, and poultry with soy-based alternatives, while a plant-based diet entirely avoids animal products, including dairy and eggs.⁵⁹ Vegetarian diets have been correlated with a 30% decreased risk of ischemic heart disease mortality compared to non-vegetarian diets.⁶² Satija et al. found that adherence to a ‘healthy’ plant-based diet led to a 25% reduction in CAD risk, whereas following an ‘unhealthy’ plant-based diet increased that risk.⁶³

The ketogenic diet is characterized by low carbohydrate intake, 1 g of protein per kg of body weight daily, and the remainder of calories derived from fats. Initially introduced in the 1920s, this diet became a common treatment for childhood epilepsy.⁶⁴ Since its inception, the ketogenic diet has been linked to several cardiovascular advantages, such as weight loss, enhanced insulin sensitivity, decreased systemic inflammation, lowered blood pressure, and diminished diabetes risk.⁶⁵ Though various forms of the ketogenic diet utilize an assortment of both plant and animal fats and proteins, higher levels of animal-derived products have been connected to increased all-cause and cardiovascular mortality post-MI.^59,65

Regarding hyperlipidemia, evidence indicates that saturated fatty acid intake raises LDL-C levels, while polyunsaturated fatty acids significantly lower LDL-C relative to carbohydrates. Substituting 10% of saturated fatty acids with polyunsaturated fats can lead to an 18 mg/dl reduction in LDL-C.⁶⁶ Consequently, patients should be informed about the advantages of swapping foods high in saturated fats, such as red meat, dairy, and lard, for those rich in polyunsaturated fats, such as oily fish, dairy-free alternatives, and olive oil.

The likelihood of developing hypertension escalates with age, and this modifiable cardiovascular risk factor can also be managed through diet. In comparison to the traditional Western diet, the DASH diet has been shown to reduce systolic blood pressure (SBP) by 5.5 mmHg and diastolic blood pressure (DBP) by 3.0 mmHg, with more significant reductions observed in individuals with hypertension (SBP and DBP reductions of 11.4 and 5.5 mmHg, respectively).⁶⁷ Moreover, the DASH-Sodium trial revealed that lowering salt intake while adhering to the DASH diet resulted in SBP and DBP decreases comparable to treatment with a single antihypertensive agent.⁶⁸

With respect to alcohol intake, the advised upper limit for safe consumption is 100 g of pure alcohol weekly, equating to seven 12-ounce beers. Exceeding this limit is linked to reduced life expectancy.⁶⁹ While earlier studies highlighted moderate consumption as beneficial for cardiovascular health, these findings have been contested by a Mendelian randomized study indicating that individuals who refrain from alcohol exhibit the lowest cardiovascular disease risk.⁵⁸

Despite being a fundamental aspect of reducing cardiovascular risks, education regarding nutrition is often inadequately provided by cardiovascular healthcare professionals.⁷⁰ Evidence shows that patients can adopt new dietary practices when appropriately guided, and the best method to facilitate this is for providers to familiarize themselves with nutritional guidelines and the supporting evidence regarding diet’s influence on cardiovascular wellness (Figure 1). To offer sufficient nutritional advice, clinicians should identify food insecurities, consider cultural practices and financial constraints when suggesting food choices, and utilize materials that match patients’ literacy levels.⁵⁹ Given the multitude of ways to enhance cardiovascular health through nutrition, patients do not necessarily have to follow a specific diet but can concentrate on the healthful habits that are most attainable for them.

Exercise and Healthy Weight

Enhancing physical activity serves as a fundamental approach for both primary and secondary prevention of CAD.⁷¹ Notably, patients might feel apprehensive about increasing physical activity and reducing sedentary behaviors in the post-MI phase or following PCI for stable ischemic heart disease (SIHD) due to concerns over recurring anginal symptoms. Yet, this represents a crucial period for healthcare providers to motivate patients to enhancephysical exercise to enhance life quality and diminish mortality risk. A 2018 investigation examining the implications of physical exercise on annual survival rates in post-MI patients revealed a 71% and 59% decrease in mortality for those who stayed active or augmented their physical activity, respectively, in contrast to those who remained inactive.⁷¹

Current recommendations advise aiming for 150–300 minutes of moderate-intensity exercise or 75–150 minutes of vigorous-intensity exercise on a weekly basis, utilizing a mix of aerobic and resistance training.^57,58 Moderate-intensity exercises encompass brisk walking, painting, gardening, playing golf, engaging in doubles tennis, or participating in water aerobics, while vigorous activities include jogging, intense gardening, swimming laps, or partaking in singles tennis. Physical activity should be customized to fit the patient’s abilities after MI or PCI.

In addition to enhancing physical activity, shedding pounds to reach and sustain a healthy weight is vital for managing other risk factors that lead to cardiovascular disease. A mere 5% loss in body weight from baseline can improve blood pressure, cholesterol levels, and glycemic regulation.^57,58 This can be attained through exercise and adherence to one of numerous low-calorie diets as previously mentioned. Alongside exercise and dietary modifications, bariatric surgery and medical treatments are additional possibilities. Bariatric surgery not only diminishes cardiovascular risk factors but has also been linked to a 45% decline in all-cause mortality and a 41% decrease in cardiovascular mortality in obese individuals compared to BMI-matched counterparts who do not undergo surgery.⁷² In the SELECT Trial, the administration of semaglutide contrasted with placebo in non-diabetic patients with established cardiovascular disease and a BMI >27 kg/m² was connected with an almost 10% reduction in body weight and a 20% decline in cardiovascular events.³⁵ These findings underscore the significance of weight reduction in altering cardiovascular risk.

Cardiac Rehabilitation

CR is an essential component of secondary prevention following MI or after PCI for SIHD. CR comprises multidisciplinary and all-encompassing programs offered to individuals with cardiovascular disease to enhance cardiovascular wellness, promote and maintain healthy habits, and encourage an active lifestyle. In addition to exercise training, CR initiatives stress health education, dietary guidance, modification of cardiovascular risk factors, and stress management.^73,74 These programs typically consist of 36 sessions, held three times per week over a 12-week duration.⁷⁵ CR must be customized for each patient for effective secondary prevention.

One significant advantage of CR is the decreased risk of mortality. Numerous studies from the 1980s demonstrated notable decreases in cardiac mortality, total mortality, and fatal reinfarction among post-MI patients who engaged in CR involving exercise.^76,77 A substantial cohort investigation among Medicare beneficiaries eligible for CR indicated a 21% reduction in 5-year mortality for CR participants versus non-participants (Figure 2).⁷⁸ Importantly, the advantages of CR in lowering mortality, MI, and overall hospitalization rates continue in patients undergoing contemporary medical interventions.⁷⁹ Notably, CR benefits appear to be dose-dependent, with higher session attendance resulting in improved long-term outcomes for MI and mortality.⁸⁰

Other advantages of CR include enhanced exercise capacity, elevated ischemic or anginal thresholds, and reduced myocardial oxygen demand, all of which contribute to lessened symptoms and an improved quality of life.⁷⁴ CR can also alleviate stress and enhance mental health issues such as depression. Milani et al. observed a 63% decrease in depressive symptoms and a 73% drop in mortality in depressed patients who completed CR in comparison to those who did not.⁸¹ The exercise training segment of CR is associated with slower progression and less severity of coronary atherosclerosis while also reducing inflammation, enhancing blood pressure, and increasing myocardial tolerance to extended ischemic stress.⁷⁴

Moreover, the risks tied to CR are minimal. Observational research report 1.3 cardiac arrests for every million patient-hours, 1 incidence of ventricular fibrillation per 111,996 patient-hours, and 1 MI per 294,118 patient-hours.^82,83 In summary, patients should feel assured that CR is safe, with benefits substantially surpassing any potential risks.

Despite the various benefits associated with CR participation, utilization remains low. In 2005, only 10–20% of the 2 million eligible individuals enrolled, and participation rates have seen little improvement since, with fewer than 30% of eligible individuals partaking in 2014.^74,75 Factors for limited CR engagement include low patient motivation, geographic challenges, and insufficient reimbursements; however, the primary issue seems to be low referral rates, especially among women, older adults, and ethnic minorities.⁷⁵ A meta-analysis exploring gender bias in outpatient CR referral rates showed that men were almost 1.5 times more inclined to receive a referral compared to women.⁸⁴ Additional characteristics linked to a reduced likelihood of CR participation in post-MI individuals included older age (>60 years), lower educational attainment, low-income status, and diminished LVEF.⁸⁵ Consequently, providers should concentrate on encouraging the involvement of individuals who may be less likely to join CR, promoting the advantages of CR, and enhancing referral rates for those who are eligible.

Another significant barrier is the geographic accessibility of facility-based CR (FBCR), which has prompted the development of alternative models like home-based CR (HBCR) and hybrid CR programs. A study comparing HBCR and FBCR in individuals with recent ischemic heart conditions, such as ACS, PCI, or coronary artery bypass graft surgery, revealed that those in HBCR exhibited greater improvements in their 6-minute walk test distances, quality of life, and self-reported physical activity. They were also more likely to complete >85% of the program than individuals in FBCR.⁸⁶ In the HYCARET study, individuals diagnosed with CAD were randomized to either hybrid CR or FBCR.⁸⁷ The hybrid program consisted of two phases: an initial phase featuring 10 facility-based sessions, followed by a self-managed HBCR phase for the remainder of the program. At the end of one year, the hybrid program showed non-inferiority compared to the FBCR program regarding cardiovascular outcomes. Overall, these studies illustrate that both HBCR and hybrid CR are excellent substitutes for FBCR and may enhance overall participation.

Conclusion

During the vulnerable time following MI or after PCI, it is essential for clinicians to collaborate closely with patients to optimize secondary prevention. This includes initiating appropriate pharmacotherapy, emphasizing lifestyle modifications, and encouraging participation in CR to enhance patients’ cardiovascular health. A primary lifestyle adjustment involves adopting a nutritious, well-balanced diet centered on whole grains, fruits, and vegetables to assist with weight management and decrease cholesterol and blood pressure, thereby reducing cardiovascular risk. Furthermore, increased physical activity, suitable psychological interventions, and smoking cessation are crucial aspects of secondary prevention. CR serves as an effective, all-encompassing intervention that incorporates most secondary prevention strategies tailor-made for this population, aiming to enhance quality of life and decrease mortality.