1. Introduction

Angina pectoris (AP), which is one of the common clinical manifestations of coronary heart disease, is a clinical syndrome characterized by recurrent chest pain or discomfort caused by rapid and temporary ischemia and myocardial hypoxia [1, 2]. AP usually presents as a squeezing pain, stuffiness, or a pulling sensation in the chest. However, some patients may not exhibit chest symptoms but instead experience pain or discomfort in the lower jaw, scapula, shoulder, or fingers, while a few cases are mainly characterized by nonspecific symptoms such as fatigue or nausea. AP can be induced or aggravated by emotional excitement, strenuous exercise, cold exposure, and other stimuli, with rest or sublingual ingestion of nitroglycerin providing relief from this pain [3, 4]. AP severely affects left heart function and is considered a high-risk factor for acute myocardial infarction (AMI), heart failure, and sudden cardiac death. Moreover, AP prevalence in middle-aged people in Sweden was estimated to be 3.5% [5], whereas its prevalence was 4.69% and 7.02% in older men and women, respectively, in India [6].

Previous studies have demonstrated that AP prevalence is positively correlated with age, with nearly half of all cases occurring in the older population (> 65 years) [7, 8]. AP is also a precursor to coronary artery disease and commonly co-occurs with diabetes, hypertension, congestive heart failure, and peripheral vascular disease, which can result in further health problems [8]. Additionally, long-term pain in patients with AP can easily lead to anxiety and depression that worsen their mental health and substantially reduce their quality of life [9]. Some patients even succumb to AMI or heart failure. All these severe consequences exert a heavy economic burden on the families of the affected individuals and medical systems [10]. The current clinical treatment guidelines for AP primarily focus on drug control, with the preferred antianginal drugs consisting of short-acting nitrates, β-receptor antagonists, and calcium channel blockers [11]. However, these drugs have a limited analgesic effect and fail to meet the clinical analgesic needs, particularly in unstable angina pectoris (UAP) and variant angina. Therefore, studies exploring new and effective therapies for managing AP are urgently required.

The stellate ganglion (SG), also known as the cervicothoracic ganglion, is part of the cervical sympathetic chain and displays a high degree of variability in its morphology. The SG, which derives its name from its irregular star shape, presents as a fusion of the subcervical ganglion and the first thoracic ganglion anterior to the neck of the first rib in approximately 80% of individuals [12, 13]. In terms of its anatomical location, the SG is located within the vertebral artery triangle and bordered externally by the scalene muscle, internally by the longus colli, trachea, and esophagus, and posteriorly by the C7 transverse process and the prevertebral fascia, with the subclavian artery passing below [14]. Stellate ganglion block (SGB) is a treatment method involving the injection of a local anesthetic into the SG to selectively block the sympathetic nerves innervating the ipsilateral head, neck, chest, and upper limb regions [15]. In 2005, an international paper was published on the effectiveness of SGB in treating chronic refractory angina, leading to a rapid wave of research on this approach [16]. Subsequently, SGB has been gradually introduced into clinical practice. In recent years, evidence-based medicine has also demonstrated the benefits of drug injection therapy for circulatory disorders [17]. SGB is now widely used for managing cardiovascular diseases, immune disorders, endocrine diseases, and various pain syndromes [18, 19]. Prior researchers have shown that the cardiovascular effects mediated by SGB are strongly associated with the inhibition of sympathetic nerve activity, improvement of cardiac blood supply, and attenuation of the cardiac stress response [15, 20, 21]. Furthermore, SGB offers remarkable advantages such as high operability, strong pertinence, low levels of patient pain, and reliable curative efficacy. However, the efficacy and safety of SGB in AP treatment are still not corroborated by evidence-based medicine, and data supporting its standardized use are lacking. Therefore, this systematic review and meta-analysis comprehensively collated and analyzed the published randomized controlled trials (RCTs) on SGB treatment for AP. Our aim was to objectively assess the efficacy and safety of SGB in AP treatment to provide a data-driven basis for the clinical application of SGB in patients with AP.

2. Material and Methods

This systematic review and meta-analysis followed the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement [22]. This systematic review was prospectively registered on PROSPERO (registration number: CRD42023485135).

3. Results

3.1. Literature Screening Process and Outcomes

According to the established search strategy, we retrieved 804 literature records, with no additional records. After deleting the duplicates, 516 articles were retained. Among them, 491 were excluded after reviewing the titles and abstracts, leaving 25 for further screening. The 491 articles that were excluded after applying our inclusion and exclusion criteria included six case reports, 22 animal experiments, 143 unrelated to AP, 277 unrelated to SGB, two conference abstracts, one scientific and technological achievement, one study protocol, one cell experiment, one news report, 32 reviews, and five meta-analyses. After further reading the full text of the remaining 25 articles, six non-RCT study designs, two articles with incomplete data, one article without full-text availability, six articles with inconsistent research purposes, three reviews, and one duplicate publication were excluded. Ultimately, six articles were included in the meta-analysis [20, 26–30]. The literature screening process is illustrated in Figure 1.

3.3. Methodological Quality in Included Studies

The Cochrane risk of bias assessment tool was utilized to assess the bias risk in the included studies. The six included studies were all clinical RCTs with no significant differences at baseline. All studies only mentioned randomization but did not specifically describe the method of random sequence generation and allocation concealment nor the implementation of blinding of the investigators, participants, and outcome evaluators. Nevertheless, all studies reported expected outcomes with complete outcome data and a low risk of other biases. The risk of bias assessment is detailed in Figures 2 and 3.

3.4. Meta-Analysis Results

3.4.1. Symptoms of AP

3.4.1.1. Frequency of AP

Two studies [26, 27] (n = 148 participants) reported AP frequency. No significant heterogeneity was found between the two studies (p = 0.96, I² = 0%); thus, the FEM was selected. The meta-analysis results showed that AP frequency in the experimental group was significantly lower than that in the control group (MD: −2.39, 95% CI: −2.77 to −2.02; Z = 12.44, p < 0.00001), as depicted in Figure 4. Therefore, SGB can substantially reduce AP frequency.

3.4.1.2. Duration of AP

Two studies [26, 27] (n = 148 participants) revealed AP duration. Similar to AP frequency, the FEM was chosen for assessing AP duration due to the nonsignificant heterogeneity (p = 0.85, I² = 0%). Subsequent analysis demonstrated that the experimental group had a significantly shorter AP duration than the control group (MD: −7.16, 95% CI: −7.68 to −6.65; Z = 27.33, p < 0.00001), as presented in Figure 5. Thus, SGB has a potential positive effect of shortening AP duration.

3.4.1.3. Pain Intensity of AP

Two studies [20, 29] (n = 68 participants) utilized visual analog scale (VAS) scores as a measure of pain intensity in patients with AP. Considering that the VAS scores were reported at multiple time points, we collated the data and conducted a subgroup analysis. Furthermore, the REM was selected owing to the significant heterogeneity between the two studies (p < 0.00001, I² = 93%). Additional analysis showed significant differences in the VAS scores between the experimental and control groups at 24, 72, 120, and 168 h after treatment (Table 3). These findings imply that SGB can effectively reduce VAS scores and alleviate the pain perception of patients with AP.

Table 3. Comparison of VAS scores between the experimental and control groups.

Indicators	Experimental group (x ± s, n)	Control group (x ± s, n)	MD (REM) (95% CI)	I2 (%)	p	Z	p
VAS score (24 h)
Guo et al. [29]	0.8 ± 0.8, 15	5.5 ± 1.5, 15
Yue et al. [20]	0.96 ± 1.24, 19	7.32 ± 1.76, 19
	n = 34	n = 34	−5.51 (−7.14, −3.89)	84	0.01	6.65	< 0.00001
VAS score (72 h)
Guo et al. [29]	0.7 ± 0.8, 15	5.2 ± 1.4, 15
Yue et al. [20]	0.78 ± 1.32, 19	7.38 ± 1.43, 19
	n = 34	n = 34	−5.54 (−7.60, −3.49)	92	0.0006	5.28	< 0.00001
VAS score (120 h)
Guo et al. [29]	0.7 ± 0.9, 15	4.2 ± 1.6, 15
Yue et al. [20]	0.81 ± 1.26, 19	7.24 ± 1.79, 19
	n = 34	n = 34	−4.96 (−7.83, −2.09)	94	< 0.0001	3.39	0.0007
VAS score (168 h)
Guo et al. [29]	0.8 ± 0.4, 15	3.4 ± 1.4, 15
Yue et al. [20]	0.91 ± 0.24, 19	7.45 ± 1.37, 19
	n = 34	n = 34	−4.58 (−8.44, −0.71)	98	< 0.00001	2.32	0.02
Total	n = 136	n = 136	−5.15 (−6.28, −4.02)	93	< 0.00001	8.93	< 0.00001

• Abbreviations: CI, confidence interval; MD, mean difference; REM, random-effects model; VAS, visual analog scale.

3.4.2. ECG Findings

3.4.2.1. HR

Two studies [20, 29] (n = 68 participants) provided HR data in patients with AP. Given that multiple time points were involved, data collation and subgroup analysis were performed. Additionally, the FEM was used for analysis because no significant heterogeneity was detected between the two studies (p = 0.89, I² = 0%). As observed in Table 4, the HR significantly differed between the experimental and control groups at 24, 72, 120, and 168 after treatment. Hence, SGB can adequately reduce the HR of patients with AP.

Table 4. Comparison of HR between the experimental and control groups.

Indicators	Experimental group (x ± s, n)	Control group (x ± s, n)	MD (FEM) (95% CI)	I2  (%)	p	Z	p
HR (beats/min, 24 h)
Guo et al. [29]	72 ± 12, 15	90 ± 12, 15
Yue et al. [20]	71.68 ± 12.45, 19	90.72 ± 10.48, 19
	n = 34	n = 34	−18.60 (−24.17, −13.03)	0	0.86	6.55	< 0.00001
HR (beats/min, 72 h)
Guo et al. [29]	70 ± 13, 15	92 ± 13, 15
Yue et al. [20]	70.46 ± 12.78, 19	93.89 ± 13.26, 19
	n = 34	n = 34	−22.80 (−28.98, −16.61)	0	0.82	7.22	< 0.00001
HR (beats/min, 120 h)
Guo et al. [29]	68 ± 12, 15	87 ± 15, 15
Yue et al. [20]	67.56 ± 11.48, 19	89.76 ± 14.38, 19
	n = 34	n = 34	−20.86 (−27.16, −14.56)	0	0.62	6.49	< 0.00001
HR (beats/min, 168 h)
Guo et al. [29]	73 ± 14, 15	88 ± 15, 15
Yue et al. [20]	72.52 ± 13.29, 19	88.56 ± 14.62, 19
	n = 34	n = 34	−15.60 (−22.35, −8.85)	0	0.88	4.53	< 0.00001
Total	n = 136	n = 136	−19.56 (−22.63, −16.48)	0	0.89	12.45	< 0.00001

• Abbreviations: CI, confidence interval; FEM, fixed-effects model; HR, heart rate; MD, mean difference.

3.4.2.2. Detection Rate of S-T Segment Elevation ≥ 0.1 mV After 24 h of Treatment

Two studies [20, 28] (n = 106 participants) reported the detection rate of S-T segment elevation ≥ 0.1 mV after 24 h of treatment. Moreover, considering that the heterogeneity between the studies was relatively small (p = 0.78, I² = 0%), the FEM was chosen for further analysis. The meta-analysis demonstrated that the detection rate of S-T segment elevation ≥ 0.1 mV after 24 h of treatment was significantly lower in the experimental group than in the control group (RR: 0.11, 95% CI: 0.03–0.44; Z = 3.10, p = 0.002), as illustrated in Figure 6. These findings suggest that SGB can significantly improve myocardial ischemic injury in patients with AP.

3.4.2.3. Detection Rate of Abnormal T Waves After 24 h of Treatment

Only one study [20] (n = 38 participants) evaluated the detection rate of abnormal T waves after 24 h of treatment, demonstrating a significantly lower detection rate in the experimental group than in the control group (RR: 0.15, 95% CI: 0.04–0.59; Z = 2.73, p = 0.006). Thus, SGB has the potential to effectively reduce AP-induced myocardial damage.

3.4.2.4. S-T Segment Displacement After Treatment

One study [26] (n = 83 participants) assessed the S-T segment displacement after treatment, revealing a significant difference between the experimental and control groups (MD: −0.07, 95% CI: −0.10 to −0.04; Z = 5.26, p < 0.00001). These findings indicate that SGB is beneficial for recovering cardiac function in patients with AP.

3.4.3. Serum Myocardial Enzyme Level

Two studies [20, 29] (n = 68 participants) provided data on the level of the serum myocardial enzyme cTnI. In light of multiple time points in the data, we conducted collation and subgroup analysis. Furthermore, FEM analysis showed that the overall combined effect size (MD: −0.27, 95% CI: −0.28 to −0.27; Z = 190.49, p < 0.00001) was significantly different between the experimental and control groups. Given the significant heterogeneity between the two studies (p < 0.00001, I² = 100%), REM analysis was performed. This analysis demonstrated an overall combined effect size of MD = −0.30 (95% CI: −0.51 to −0.09; Z = 2.78, p = 0.005), as presented in Table 5. These results imply that SGB is a potential treatment strategy to reduce the levels of the serum myocardial enzyme cTnI in patients with AP.

Table 5. Comparison of meta-analysis results of cTnI levels using the FEM and REM in the experimental and control groups.

Indicators	Experimental group (x ± s, n)	Control group (x ± s, n)	FEM analysis results	REM analysis results
cTnI level (μg/L, 24 h)
Guo et al. [29]	0.046 ± 0.008, 15	0.052 ± 0.004, 15
Yue et al. [20]	0.039 ± 0.0078, 19	0.49 ± 0.0034, 19
	n = 34	n = 34	MD: −0.27, 95% CI: −0.27 to −0.26; Z = 178.13, p < 0.00001	MD: −0.23, 95% CI: −0.66 to 0.21; Z = 1.03, p = 0.30
cTnI level (μg/L, 72 h)
Guo et al. [29]	0.065 ± 0.001, 15	0.07 ± 0.078, 15
Yue et al. [20]	0.069 ± 0.0026, 19	0.67 ± 0.035, 19
	n = 34	n = 34	MD: −0.52, 95% CI: −0.53 to −0.50; Z = 69.40, p < 0.00001	MD: −0.30, 95% CI: −0.89 to 0.28; Z = 1.02, p = 0.31
cTnI level (μg/L, 120 h)
Guo et al. [29]	0.067 ± 0.004, 15	0.076 ± 0.048, 15
Yue et al. [20]	0.063 ± 0.0064, 19	0.7 ± 0.078, 19
	n = 34	n = 34	MD: −0.21, 95% CI: −0.23 to −0.19; Z = 20.80, p < 0.00001	MD: −0.32, 95% CI: −0.94 to 0.29; Z = 1.03, p = 0.30
cTnI level (μg/L, 168 h)
Guo et al. [29]	0.066 ± 0.006, 15	0.078 ± 0.062, 15
Yue et al. [20]	0.066 ± 0.0058, 19	0.75 ± 0.089, 19
	n = 34	n = 34	MD: −0.27, 95% CI: −0.29 to −0.24; Z = 21.24, p < 0.00001	MD: −0.35, 95% CI: −1.01 to 0.31; Z = 1.04, p = 0.30
Total (95%)	n = 136	n = 136	(p < 0.00001, I2 = 100%)	(p < 0.00001, I2 =  100%)
			MD: −0.27, 95% CI: −0.28 to −0.27; Z = 190.49, p < 0.00001	MD: −0.30, 95% CI: −0.51 to −0.09; Z = 2.78, p = 0.005

• Abbreviations: CI, confidence interval; cTnI, Cardiac Troponin I; FEM, fixed-effects model; MD, mean difference; REM, random-effects model.

3.4.4. Clinical Efficacy

Three studies [26, 28, 30] (n = 240 participants) reported the clinical efficacy. As illustrated in Figure 7, FEM analysis (p = 0.48, I² = 0%) exhibited significant differences in the clinical efficacy between the experimental and control groups (RR: 1.27, 95% CI: 1.14–1.43; Z = 4.19, p < 0.0001). Thus, SGB is a promising treatment method for significantly improving clinical efficacy.

3.4.5. Measures of Vital Sign Parameters

3.4.5.1. MAP

Two studies [20, 29] (n = 68 participants) measured MAP levels. Considering that the data had multiple time points, we conducted data collation and subgroup analysis. Subsequent FEM analysis (p = 0.60, I² = 0%) showed that the MAP levels of the experimental group were significantly lower than those of the control group at 24, 72, 120, and 168 h after treatment, as shown in Table 6. Hence, SGB is a valuable approach for reducing MAP levels in patients with AP.

Table 6. Comparison of MAP levels in the experimental and control groups.

Indicators	Experimental group (x ± s, n)	Control group (x ± s, n)	MD (FEM) (95% CI)	I2 (%)	p	Z	p
MAP (mmHg, 24 h)
Guo et al. [29]	78 ± 11, 15	90 ± 10, 15
Yue et al. [20]	76.32 ± 14.11, 19	91.45 ± 12.33, 19
	n = 34	n = 34	−13.39 (−19.00, −7.78)	0	0.59	4.68	< 0.00001
MAP (mmHg, 72 h)
Guo et al. [29]	80 ± 11, 15	91 ± 13, 15
Yue et al. [20]	78.78 ± 14.46, 19	91.34 ± 14.29, 19
	n = 34	n = 34	−11.73 (−18.00, −5.46)	0	0.81	3.67	0.0002
MAP (mmHg, 120 h)
Guo et al. [29]	80 ± 10, 15	91 ± 11, 15
Yue et al. [20]	77.82 ± 13.54, 19	90.32 ± 12.18, 19
	n = 34	n = 34	−11.69 (−17.23, −6.15)	0	0.79	4.13	< 0.0001
MAP (mmHg, 168 h)
Guo et al. [29]	82 ± 9, 15	88 ± 10, 15
Yue et al. [20]	82.52 ± 11.59, 19	87.46 ± 12.34, 19
	n = 34	n = 34	−5.53 (−10.60, −0.45)	0	0.84	2.14	0.03
Total	n = 136	n = 136	−10.26 (−13.05, −7.47)	0	0.60	7.21	< 0.00001

• Abbreviations: CI, confidence interval; FEM, fixed-effects model; MAP, mean arterial pressure; MD, mean difference.

3.4.5.2. SpO₂

Two studies [20, 29] (n = 68 participants) investigated SpO₂ levels. In view of the multiple time points involved, we conducted data collation and subgroup analysis. The FEM analysis (p = 0.19, I² = 30%) demonstrated that the SpO₂ levels in the experimental group were significantly higher than those in the control group at 24, 72, 120, and 168 h after treatment (Table 7). These observations indicate that SGB can effectively enhance SpO₂ levels in patients with AP.

Table 7. Comparison of SpO₂ levels in the experimental and control groups.

Indicators	Experimental group (x ± s, n)	Control group (x ± s, n)	MD (FEM) (95% CI)	I2 (%)	p	Z	p
SpO2 (%, 24 h)
Guo et al. [29]	92.4 ± 2.3, 15	91.4 ± 1.5, 15
Yue et al. [20]	92.38 ± 2.43, 19	91.35 ± 1.35, 19
	n = 34	n = 34	1.02 (0.09, 1.95)	0	0.97	2.14	0.03
SpO2 (%, 72 h)
Guo et al. [29]	94.9 ± 2.2, 15	92.4 ± 1.8, 15
Yue et al. [20]	94.48 ± 1.67, 19	92.24 ± 1.33, 19
	n = 34	n = 34	2.32 (1.52, 3.12)	0	0.77	5.69	< 0.00001
SpO2 (%, 120 h)
Guo et al. [29]	95 ± 2.6, 15	92.4 ± 1.6, 15
Yue et al. [20]	94.68 ± 2.38, 19	92.56 ± 1.82, 19
	n = 34	n = 34	2.33 (1.31, 3.34)	0	0.65	4.49	< 0.00001
SpO2 (%, 168 h)
Guo et al. [29]	95.5 ± 2, 15	92.4 ± 1.9, 15
Yue et al. [20]	95.37 ± 1.52, 19	92.35 ± 2.23, 19
	n = 34	n = 34	3.05 (2.14, 3.97)	0	0.93	6.54	< 0.00001
Total	n = 136	n = 136	2.19 (1.74, 2.64)	30	0.19	9.50	< 0.00001

• Abbreviations: CI, confidence interval; FEM, fixed-effects model; MD, mean difference; SpO₂, blood oxygen saturation.

3.4.6. Disease Improvement

The study by Wu et al. [26] (n = 83 participants) examined the transition rate from UAP to SAP to describe the level of disease improvement. The meta-analysis showed an effect size of RR = 1.69 (95% CI: 1.23–2.32; Z = 3.22, p = 0.001), indicating that SGB could effectively transform UAP into SAP and lead to significant disease improvement.

3.4.7. Postoperative Cardiovascular- and Cerebrovascular-Related Adverse Events

3.4.7.1. Incidence of AMI

Two studies [26, 27] (n = 148 participants) reported AMI incidence during follow-up. Given that no significant heterogeneity was observed between the two studies (p = 0.55, I² = 0%), FEM analysis was performed. The results revealed an overall combined effect size of RR = 0.28 (95% CI: 0.11–0.73; Z = 2.62, p = 0.009), as depicted in Figure 8. This finding indicates that SGB can significantly reduce AMI incidence in patients with AP.

3.4.7.2. Incidence of Interventional Therapy, Stroke, and Rehospitalization

Only one study [27] (n = 65 participants) assessed the incidence of interventional therapy, stroke, and rehospitalization during follow-up. The meta-analysis findings suggested that SGB could significantly reduce rehospitalization incidence; however, no such statistical significance was observed for interventional therapy and stroke incidence, as shown in Table 8.

Table 8. Comparison of interventional therapy, stroke, and rehospitalization incidence in the experimental and control groups.

Types of adverse events	Experimental group		Control group		RR, M-H test, FEM, 95% CI	Z	p
	Events	Total	Events	Total
Interventional therapy	3	35	7	30	0.37 (0.10, 1.30)	1.56	0.12
Stroke	2	35	3	30	0.57 (0.10, 3.20)	0.64	0.52
Rehospitalization	4	35	12	30	0.29 (0.10, 0.79)	2.40	0.02

• Abbreviations: CI, confidence interval; FEM, fixed-effects model; M-H test, Mantel–Haenszel test; RR, relative risk.

3.4.7.3. Incidence of Death

Two studies [26, 27] (n = 148 participants) investigated the incidence of death during follow-up. FEM analysis (p = 0.33, I² = 0%) showed no significant differences in the overall combined effect size between the experimental and control groups (RR: 0.28, 95% CI: 0.05–1.76; Z = 1.35, p = 0.18), as illustrated in Figure 9. Thus, SGB may not reduce death incidence in patients with AP.

4. Discussion

AP is a prevalent progressive heart disease, which has been gradually increasing in incidence, particularly in the younger population. The pain in AP not only stems from the ischemic chest pain triggered by reduced coronary perfusion, but it is also closely associated with sympathetic overexcitation [20, 31]. Cardiac sensations are primarily conveyed by visceral sensory nerves. Myocardial ischemia and hypoxia can lead to the heightened excitation of the cardiac sympathetic nerves, which transmit the signals to the amygdala, hypothalamus, and insula to ultimately induce pain in the patients. Additionally, the excitation of the cardiac sympathetic nerves can cause cardiovascular contraction, further aggravating ischemia and hypoxia in the ischemic area of the heart and generating a vicious cycle of ischemia and pain [32, 33]. Ischemic stimulation can also induce the increased production of norepinephrine (NE), nerve growth factors (NGFs), and inflammatory factors, thereby triggering stress and inflammatory responses that further exacerbate myocardial injury and pain perception [18]. Therefore, a safe and efficient approach for blocking the transmission of pain signals and the production of pain-eliciting substances is crucial in AP treatment.

SGB can be performed unilaterally or bilaterally alternating, with a successful procedure reflected by Horner syndrome on the ipsilateral side. This treatment mainly regulates cardiovascular movement, pain transmission, and glandular secretion in the distribution area by inhibiting the function of the preganglionic and postganglionic fibers of the SG. SGB also modulates the functional activities of the autonomic nervous system, endocrine system, and immune system via the hypothalamic mechanism. In recent years, the application of ultrasound imaging technology has augmented the visualization, precision, and safety of SGB and notably reduced adverse events such as neurovascular damage caused by earlier blind exploration in the SGB procedure [34]. Consequently, ultrasound-guided SGB has become one of the most commonly used strategies for clinical pain treatment [35]. Prior studies have highlighted that SGB is primarily employed in AP treatment to inhibit the activity of the sympathetic nervous system and induce the following effects [15, 18, 20, 21, 36–39]: (1) effective alleviation of ischemic chest pain by dilating the coronary artery, increasing cardiac blood perfusion, improving myocardial blood and oxygen supply, and accelerating metabolite excretion; (2) protection of cardiac function by inhibiting overexcited cardiac sympathetic nerves to achieve reduced HR, myocardial contractility, and myocardial oxygen consumption; (3) blocking of the pain signal afference by cardiac sympathetic nerves; (4) regulating the stages of pain processing in the central nervous system and alleviating pain perception by affecting the amygdala, hypothalamus, and insula that have neuronal connections with the SG; and (5) effectively diminishing the cardiac inflammatory response and stress myocardial injury and relieving AP by decreasing the production of pain-inducing substances, such as NGFs, NE, neuropeptides, and inflammatory factors.

In this study, we conducted a systematic review and meta-analysis of six RCT studies (including 373 participants) to evaluate the efficacy and safety of SGB for AP treatment. For this purpose, we examined the differences in the outcome indicators, such as symptoms, ECG findings, serum myocardial enzyme levels, and clinical efficacy, between the experimental and control groups. Our results revealed that SGB significantly reduced VAS scores, AP frequency and duration, HR, the detection rate of S-T segment elevation ≥ 0.1 mV, the presence of abnormal T waves on ECG after 24 h of treatment, and the level of the serum myocardial enzyme cTnI, while it improved clinical efficacy. Moreover, the SpO₂ levels and the transition rates from UAP to SAP were significantly higher, and the MAP level and the incidence of AMI and rehospitalization were significantly lower in the experimental group than in the control group. Conversely, no significant differences were observed in the incidence of interventional therapy, stroke, and death between the two groups. Therefore, these findings indicate that SGB can effectively treat AP by significantly improving disease symptoms and ECG findings, alleviating myocardial injury, promoting cardiac function recovery, and lowering the occurrence rate of some cardiovascular- and cerebrovascular-related adverse events. However, SGB may not prevent death, stroke, and interventional therapy in patients with AP. The overall methodological quality was moderate based on the Cochrane Handbook items. According to the GRADE evidence rating system, the overall quality of the outcome indicators was low, with 12 (70.59%) indicators identified as low-quality evidence and five (29.41%) as very low-quality evidence. Additionally, given the limited number of included studies and small sample sizes, the obtained results require further validation. Although the absence of SGB-related adverse events in all included studies preliminarily suggests that SGB treatment for AP leads to fewer adverse reactions and increased safety, more high-quality evidence is required in the future to verify this conclusion.

Our systematic review and meta-analysis study has a few limitations that should be considered. (1) The number and sample sizes of the included studies were small, and the outcome indicators were found to be low- or very low-quality evidence, all of which might have rendered the statistical analysis results unreliable. Therefore, future high-quality and large-sample clinical RCTs are essential and may prominently influence the existing evidence and alter the assessment results. (2) The included studies were published as early as 1996, with most conducted from 2006 to 2011. Hence, the included studies may not accurately reflect the current research status of SGB technology. Moreover, five of the included studies [20, 26–29] used blind exploration rather than ultrasound guidance for SGB, while another study [30] even used an earlier electrotherapy technology. These less advanced surgical methods may have led to the underestimation of the efficacy and safety of SGB for AP treatment. (3) The overall methodological quality of the included studies was moderate, with limitations such as suboptimal implementation of allocation concealment and blinding. Additionally, blinding of the investigators and participants may have been challenging because SGB is an invasive treatment, which could have further led to biased results. (4) Certain outcome indicators exhibited significant heterogeneity, possibly due to complex factors such as the methodological quality, sample size, and control interventions of the included studies, along with the type of AP and the age, comorbid condition, and physical health of the participants. Although all the control group interventions comprised conventional medical treatments, their specific regimens may have varied depending on the individual patients. Moreover, the surgical method and point of intervention (unilateral or bilateral) employed in the SGB procedure and the proficiency and accuracy of the operators may have contributed to the heterogeneity in the outcome indicators.

Finally, this study provided some prospects and suggestions for future research. First, multicenter, high-quality, and large-sample RCTs employing the latest surgical methods for SGB (such as ultrasound-guided SGB) for AP treatment are urgently required to verify our results and provide an accurate perspective on the therapeutic effect of SGB on AP at the current technological level. Second, safety should be considered a decisive factor in determining the clinical application value of an intervention. Therefore, future studies should equally focus on observing and accurately recording the safety-related indicators associated with SGB in AP treatment, with maximum possible follow-up to supplement the safety evaluation. Third, the prospective registration of clinical RCT studies is essential for effectively improving research transparency, reducing the risk of publication bias, and avoiding the duplication of effort and resource wastage. Lastly, RCTs should strictly adhere to standardized reporting guidelines, including the Consolidated Standards of Reporting Trials (CONSORT), to ensure research with high-quality methodologies.

5. Conclusion

Our systematic review and meta-analysis study suggests that SGB in patients with AP can safely and effectively improve disease symptoms and ECG findings, alleviate myocardial injury, promote cardiac function recovery, and reduce the incidence of AMI and rehospitalization. However, considering the limitations in this meta-analysis, more high-quality RCT studies are essential to validate these conclusions.

Conflicts of Interest

The authors declare no conflicts of interest.

Author Contributions

This study was codesigned by Y.W., J.X., W.Q., and F.L. F.L. and X.L. developed the search strategy. Y.Z. and J.H. participated in the data retrieval, collection, and extraction. Y.L. and L.Y. conducted data synthesis and analysis. J.Y. was responsible for resolving any differences that arose during the study. Y.S. supervised the review process. Y.W. drafted the manuscript. J.X. and W.Q. revised the manuscript. All authors have read and agreed to publish the final version of this manuscript.

Funding

This study received funding from the Regional Cooperation Program of the National Natural Science Foundation of China (Grant Nos. U21A20404, 82074556, and 82205286) and the Natural Science Foundation of Sichuan Province (Grant No. 2023NSFSC1819).