Myocardial Revascularization in Heart Failure With Reduced Ejection Fraction

Background: Heart failure (HF) patients with reduced ejection fraction (HFrEF) now more commonly die of non-cardiovascular causes than they did in the past. In patients with both HFrEF and ischemic cardiomyopathy (as the cause of HFrEF or as an accompanying condition), the effect of myocardial revascularization—i.e. percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG)—on long-term outcome is unclear.

Methods: This review is based on publications that were retrieved by a selective search of the literature for pertinent clinical studies and current guidelines.

Results: Drug treatment for HFrEF has markedly prolonged these patients’ survival. In a comparative study, HF pharmacotherapy was found to add an average of 8.3 years to the lifespan of a 55-year-old patient with HFrEF. Three of the four randomized controlled trials on revascularization procedures were conducted prior to the major pharmacotherapy improvements leading to better outcomes in HF patients over the past decade. These trial data indicate a long-term benefit from CABG compared to medical treatment alone in patients with HFrEF and severe coronary heart disease. For example, in the STICH trial, the hazard ratio for death from any cause after a follow-up time of nearly 10 years was 0.84 (95% confidence interval, [0.73; 0.97]). The role of pre-procedural myocardial viability and ischemia testing remains to be fully determined. The choice of method for myocardial revascularization should be discussed within an interdisciplinary cardiac team in consideration of the patient’s symptoms and ischemic burden, the complexity of the coronary findings, as well as the patient’s perioperative risk and current medical HF therapy. No RCTs comparing CABG to PCI are yet available.

Conclusion: Optimal guideline-directed medical therapy is a key determinant of long-term survival in patients with HFrEF.

Cite this as: Haring B, Bauersachs J, Frey N, Hoppe UC, Doenst T, Böhm M: Myocardial revascularization in heart failure with reduced ejection fraction. Dtsch Arztebl Int 2025; 122: 103–8. DOI: 10.3238/arztebl.m2024.0249

Ischemic cardiomyopathy (ICM) resulting from coronary heart disease is the principal cause of heart failure (HF) with reduced ejection fraction (HFrEF) (1). Pathophysiologically, ICM is responsible for the development of left ventricular (LV) dysfunction, either abruptly, through the occurrence of myocardial infarction, or gradually, owing to progressive deterioration of systolic function with no detectable acute coronary events. The decline in contractile function is accompanied by increases in myocardial fibrosis (scar burden) and in regions of dysfunctional yet vital myocardium (hibernating myocardium) (Figure 1).

Figure 1

Likelihood of myocardial recovery following ischemia

Cause of death and cardiovascular prognosis in HFrEF

The main cause of death for patients with HFrEF has changed over the past 20 years (2). Causes unrelated to the cardiovascular system, e.g., cancers, have become more common than cardiovascular causes (Figure 2). The extent of contractile dysfunction, valvular dysfunction, and coronary vessel disease determines the cardiovascular prognosis of HFrEF patients (3, 4, 5). In patients with a left ventricular ejection fraction (LVEF) below 45%, a 10% fall in LVEF is associated with a 39% increase in overall mortality (hazard ratio [HR] 1.39, 95% confidence interval [1.32; 1.46]) (3). On the other hand, the contractile reserve of the myocardium during drug treatment is an important predictor of survival for patients with HFrEF (6). In recent years, significant advances in the pharmacotherapy of HF have been achieved by the addition of angiotensin receptor/neprilysin inhibitors (ARNI), the If-channel blocker ivabradine, the SGLT2 inhibitors, and the sGC stimulator vericiguat (Figure 3) (7, 8, 9, 10). A 55-year-old HFrEF patient treated with ARNI, beta-blockers, a mineralocorticoid receptor agonist (MRA), and SGLT2 inhibitors will gain 8.3 years of life without cardiovascular death or hospital admission due to heart failure decompensation and an additional 6.3 years’ survival compared with the commonly employed combination of ACE inhibitors and beta-blockers (11). Older patients also benefit greatly. The introduction of cardiac resynchronization therapy (CRT), in which the actions of the two chambers of the heart are synchronized, in combination with an ICD has reduced the risk of death and cardiac arrest in HFrEF patients with a wide QRS complex (12, 13). The COAPT and RESHAPE-2 studies showed that in symptomatic HF patients with severe mitral valve failure who were already taking the maximally tolerated dosage of guideline-oriented HF pharmacotherapy, transcatheter mitral valve repair additionally decreased the rate of HF-related hospitalizations and deaths (14, 15). Further invasive procedures that can be considered are pulmonary vein isolation (PVI), a minimally invasive treatment of atrial fibrillation, and the implantation of a pulmonary artery (PA) pressure sensor or a ventricular assist device (VAD) in (pre)terminal HFrEF.

Figure 2

Cause of death

Figure 3

Treatment of patients with HFrEF

Current evidence on revascularization in HFrEF

We carried out a selective search of the literature for pertinent clinical studies and currently valid guidelines. The guidelines of the European Society of Cardiology (ESC) and the European Association for Cardiothoracic Surgery (EACTS) on myocardial revascularization recommend either coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) (16, 17). The goal is to protect myocardial tissue that is vital, or ischemically damaged yet still viable, from irreversible destruction by preserving coronary perfusion and the myocardial oxygen supply, thus achieving enhancement of contractile heart function and, ultimately, improvement of the overall prognosis (18). Invasive treatment by means of PCI or CABG has differing effects on the coronary system. CABG can be effective in preventing future myocardial infarctions, potentially influencing survival (5, 19).

The data on myocardial revascularization in HFrEF come predominantly from cardiosurgical studies that predate the crucial improvements in prognosis achieved by HF treatment in recent years. The evidence on the role of revascularization in HFrEF is based on a small number of randomized controlled trials, i.e., STICH, PARR-2, and HEART, all conducted before 2011, and REVIVED-BCIS2, which recruited patients between 2013 and 2020 (Table) (20, 21, 22, 23).

Table

Randomized controlled trials on revascularization in HFrEF patients with coronary heart disease

Revascularization versus optimal pharmacotherapy in HFrEF

The STICH study

In the STICH trial (Surgical Treatment for Ischemic Heart Failure), 1212 patients with HFrEF (EF ≤ 35%) and severe coronary heart disease were randomized to either optimal pharmacotherapy alone or pharmacotherapy with additional surgical revascularization (21). After a mean observation period of 56 months, the primary endpoint, death from any cause, did not differ significantly between the two arms of the study. However, the Kaplan–Meier curves crossed after about 2 years, owing to a lower event rate in the CABG arm. The long-term findings of STICH (mean observation time 9.8 years) showed 16% lower overall mortality in the CABG arm than in the group with drug treatment only (24). Interestingly, 18% (n = 220) of the patients in the STICH trial had moderate to severe mitral regurgitation (25). Within this small group of patients, those who received mitral valve treatment in addition to CABG profited (CABG with mitral valve treatment versus CABG alone: HR 0.41 [0.22; 0.77]), while this was not the case for persons who underwent CABG in isolation (HR versus optimized pharmacotherapy 1.20 [0.77; 1.87]) (25). It must be noted, however, that the effect of any mitral regurgitation that may have occurred was no longer demonstrable in the 10-year observation period which showed a survival benefit of CABG over pharmacotherapy (24).

Invasive treatment of patients with chronic CHD may have a prognostic component if an infarct-preventive action is present (whereby a surgical collateral [CABG0 is superior to PCI) (19, 26). Since, however, myocardial infarction is a minor cause of death in patients with HFrEF (and was not evaluated systematically in STICH), the effect of CABG in the STICH trial is currently difficult to explain.

The PARR-2 study

The participants in the PARR-2 trial (Positron Emission Tomography and Recovery Following Revascularization) were 430 patients with HFrEF (EF ≤ 35%) and coronary heart disease (22). Depending on their myocardial viability and the likelihood of left ventricular improvement, as determined by PET, the patients either underwent revascularization or received optimal pharmacotherapy. Persons with a moderate to high likelihood of improvement were assigned to revascularization, those with a low likelihood to drug treatment. The primary composite endpoint was defined as cardiac death, myocardial infarction, or renewed hospitalization for cardiac reasons. After 5 years’ follow-up, the patients randomized to PET-guided treatment had a cardiac event rate no lower than that in the standard treatment group (HR 0.82 [0.62; 1.07]; p = 0.15) (23). However, revascularization was not carried out in around 25% of the patients for whom it was indicated by the PET findings. Owing to the high number of crossover cases, the study results were crucially influenced by the treating physicians.

The HEART study

The HEART study (Heart Failure Revascularization Trial) was conceived for 800 patients with HFrEF (EF ≤ 35%) due to ICM with residual myocardial vitality (27). The participants were randomized to receive either optimal pharmacotherapy or invasive treatment. The trial had to be discontinued prematurely because of slow recruitment; only 138 persons could be randomized. No significant difference was found between the two treatment strategies. However, the statistical power was inadequate owing to the small number of patients.

The REVIVED-BCIS2 study

The goal of the REVIVED-BCIS2 trial (Revascularization for Ischemic Ventricular Dysfunction) was to investigate whether revascularization by means of PCI in addition to optimized pharmacotherapy is superior to drug treatment alone in terms of mortality and hospitalization owing to heart failure (20, 28). To this end, 700 patients with HFrEF (EF ≤ 35%) due to ICM were randomized. Over a mean observation period of around 3.5 years, there was no significant difference in occurrence of the primary endpoints between the PCI group and the group with optimal pharmacotherapy (HR 0.99, 95% CI [0.78; 1.27]; p = 0.96) (20). The EF did not improve in the PCI group. It should be noted that PCI could be performed safely in persons with HFrEF, as there was no elevation in periprocedural mortality.

Longer follow-up is necessary for conclusive evaluation of the REVIVED-BCIS2 trial. Moreover, the study exhibits methodological deficits. The extent of coronary heart disease and the existing ischemic burden prior to revascularization received inadequate consideration. In about 50% of patients, patients suffered from coronary 2-vessel disease, so the CHD burden was smaller thatn in the STITCH trial. There are no data on, for example, the degree of stenosis or the functional hemodynamic significance of the coronary stenoses. The invasively measured coronary fractional flow reserve (FFR) is the current gold standard for functional assessment of the hemodynamic efficacy of moderate stenoses (typically 40–90% of all stenoses) without clear signs of ischemia in non-invasive tests or in persons with multivessel disease. The FAME trial (Fractional Flow Reserve versus Angiography for Multivessel Evaluation) showed that an FFR-guided PCI strategy (using an FFR cut-off ≤ 0.80) is superior to angiographically guided PCI in persons with coronary multivessel disease (29, 30, 31).

REVIVED-BCIS2 recruited principally patients in NYHA stages I and II with few or no symptoms of angina pectoris, while the patients in the STICH study were much more symptomatic. REVIVED-BCIS2 and STICH also differed in patient characteristics and pharmacotherapy.

For instance, the average age in the REVIVED-BCIS2 trial was 70 years in the PCI group and 69 years in the group with optimal pharmacotherapy, while in the STICH trial it was 60 years in the CABG group and 59 years in the optimal pharmacotherapy group (21). Finally, there are important time-related differences in the drug treatment for HF between STICH and REVIVED-BCIS.

The role of revascularization in HFrEF

Inconclusive evidence

The prognostic significance of revascularization in HFrEF has to be interpreted in the light of decreasing numbers of deaths from cardiovascular causes (2). In the STICH study of ICM patients with HFrEF, the benefit of CABG compared with (now outdated) heart failure treatment emerged only over a long period of time, and it may be that persons with additional mitral valve treatment were the ones to profit (24). PCI may be a reasonable alternative for selected patients who still have angina pectoris-related symptoms despite optimal pharmacotherapy and are rated unsuitable for CABG after careful consideration of the surgical risk (15, 32). No studies have shown conclusively whether the results of PCI-based revascularization are fundamentally equivalent to those of CABG. The international initiative STICH3 is integrating separate studies comparing CABG and PCI with similar inclusion criteria into a large international program in an effort to identify potential differences in mortality (33).

Assessment of myocardial viability and ischemic burden

On the basis of the data available, neither routinely determining myocardial viability nor ischemic burden preoperatively seem to be crucial for whether revascularization will be beneficial (34). Nevertheless, in patients with symptoms of heart failure or angina pectoris, preoperative assessment of viability or ischemic burden by means of (stress) echocardiography, myocardial scintigraphy, (stress) magnetic resonance imaging (MRI), single-photon-emission computed tomography (SPECT), or positron-emission tomography (PET) may, in individual cases, help to identify persons who will likely benefit from revascularization (35). In REVIVED-BCIS2, the amount of non-viable myocardium was associated with event-free survival and the likelihood of improvement in left ventricular function (36). Moreover, according to recently published recommendations revascularization is beneficial in the presence of significant inducible ischemia (≥ 10% of LV mass) (16, 17, 37).

Practical recommendations

Management algorithm

In view of the somewhat contradictory and problematic study findings, we suggest an algorithm for the treatment of HFrEF patients with coronary multivessel disease and vessels amenable to invasive therapy (Figure 4). The challenge consists in differentiating the symptoms of heart failure (contractile dysfunction) from those of angina pectoris (myocardial ischemia). Optimal pharmacotherapy for heart failure is recommended in all patients, possibly along with CRT.

Figure 4

Proposed management algorithm for HFrEF patients with coronary multivessel disease

If HF symptoms predominate, one should determine whether transcatheter mitral valve repair or other invasive procedures (PVI, VAD, etc.) are indicated. Diagnostic tests for myocardial vitality and ischemic burden are recommended to exclude that shortness of breath, the cardinal symptom of heart failure, is an expression of ischemia and therefore should be rated as “angina-equivalent”.

In cases in which angina pectoris symptoms predominate despite optimal pharmacotherapy, the extent of myocardial ischemia and/or remaining vitality should be determined. In the presence of inducible ischemia (≥ 10% of LV mass) and significant stenosis of a major coronary vessel (> 90%), or of an abnormal fractional flow reserve (FFR ≤ 0.80 or instantaneous wave-free ratio [iFR] ≤ 0.89), revascularization by CABG, possibly including mitral valve repair, is recommended in addition to optimal pharmacotherapy (16, 17). PCI should be considered as an alternative to CABG in coronary lesions of low complexity but high surgical risk. Determination of vitality may be useful to estimate the extent of scarring burden or hibernating myocardium. The decision cut-off for the extent of hibernating myocardium should be set at around 7% of LV mass; above this threshold, revascularization is likely to be beneficial.

Revascularization can also be considered in the presence of persisting angina pectoris symptoms with a high burden of suffering despite optimized pharmacotherapy and little evidence of ischemia. Here too, the data speak in favor of CABG as primary revascularization strategy in the presence of complex multivessel disease, while ischemia-triggered PCI with FFR ≤ 0.80 or iFR ≤ 0.89 should be considered in patients with high surgical risk and/or low coronary complexity (16, 32). Therefore, routine additional assessment of the surgical risk and the coronary complexity is crucial before making a final decision.

Surgical risk and coronary complexity

The risk score of the Society of Thoracic Surgeons (STS) and the Euro-SCORE-II are suitable tools for prediction of 30-day perioperative mortality. Both scores take account of various patient characteristics (demography, laboratory test results, comorbidities) as well as previous operations and planned operations. Thirty-day mortality < 4% seems to be acceptable for a decision in favor of CABG. For patients whose CABG risk is higher (30-day mortality ≥ 4%), the SYNTAX score/SYNTAX score II is helpful in assessing coronary complexity. SYNTAX is a score calculated using, among other factors, the number of vessel segments affected and the number of disadvantageous coronary lesion characteristics (e.g., long lesions, calcification). The score correlates with adverse events on PCI. In the case of low complexity (SYNTAX score ≤ 22) and/or high surgical risk, PCI can and should be considered (16, 17).

Conclusion

The main cause of death of patients with HFrEF has changed over the past 20 years. Non-cardiovascular diseases (above all, cancer) are gaining importance.

Advances in the treatment of HF are increasingly casting doubt on the role of revascularization in HFrEF. Revascularization is largely limited to symptom control in patients who continue to experience symptoms of angina pectoris despite optimal pharmacotherapy and/or display a considerable ischemic burden and/or extensive areas of hibernating myocardium.

To date, CABG is the only invasive treatment demonstrated to have any prognostic value.

Optimized HF therapy is of decisive prognostic importance, and the best possible treatment for patients with HF must be ensured.

In each patient with HFrEF and ICM, the task of the heart team is to ensure optimized HF treatment and to choose the appropriate method of revascularization in view of the person’s symptoms, the perioperative risk, and the complexity of the coronary findings.

Conflict of interest statement
BH has received fees from Bristol Myers Squibb, Boehringer Ingelheim, Inari, and Pfizer for lectures on topics unrelated to the content of this article.

JB has received fees from Novartis, Vifor, Bayer, Pfizer, Boehringer Ingelheim, AstraZeneca, Cardior, CVRx, BMS, Amgen, Corvia, Norgine, Edwards, and Roche for lectures on topics unconnected with this article, as well as departmental research funding from Zoll, CVRx, Abiomed, Norgine, and Roche, also unconnected with this article.

NF has received fees from AstraZeneca, Bayer Vital, Boehringer Ingelheim, GlaxoSmithKline, Novartis, Pfizer, and Daiichi Sankyo Deutschland for lectures on topics unrelated to the content of this article.

MB has received lecture fees from Abbott, Amgen, Astra Zeneca, Bayer, Boehringer Ingelheim, Bristol Myers Squibb, Cytokinetics, Edwards, Medtronic, Novartis, ReCor, Servier, and Vifor. MB is a member of the advisory boards of Amgen, Bayer, Boehringer Ingelheim, Cytokinetics, Edwards, Medtronic, Novartis, Pfizer, ReCor, Servier, and Vifor. He has received research funding from the German Research Foundation: DFG, SFB-TTR 219, S-01.

The remaining authors declare that no conflict of interest exists.

Submitted on 25 July 2024, revised version accepted on 22 November 2024

Translated from the original German by David Roseveare

Corresponding author
Prof. Dr. med. Bernhard Haring, MPH

Innere Medizin III

Universitätsklinikum des Saarlandes

Kirrberger Str. 100

66421 Homburg, Germany

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