Chronic stable angina and point specificity

Stimulated by Zhao et al 2019.[1]

Photo by Dominik Lange on Unsplash.

This paper was published online earlier this week but appeared on my PubMed search this morning. I was planning to write about hemifacial spasm today, highlighting quite a big (n=539) neurosurgical review of MVD (microvascular decompression) from China,[2] but this paper on electroacupuncture (EA) in angina stole my interest, most notably by claiming point specificity – an extremely contentious issue in the acupuncture field.

404 patients with CSA (chronic stable angina) suffering a minimum of 2 angina episodes per week from 5 centres in China were randomised to one of four groups: DAM, NAM, SA and WL.

DAM stands for disease-affected meridian and the points stimulated were PC6 and HT5.

NAM stands for non-affected meridian and the points stimulated were LU9 and LU6.

SA stands for sham acupuncture and involved needle insertion at so called non-points. The difference was that there was no attempt to elicit typical needling sensation (de qi), but EA was applied in the same way as in DAM and NAM (see below). The sham points were on or close to the HT meridian half way along the forearm, but between HT3 and HT4, and on or close to the PC meridian at the anterior shoulder between deltoid and biceps, roughly 2-3cm above PC2, as far as I can tell.

WL stands for waiting list. This group had their acupuncture deferred for 16 weeks until after the study had concluded.

The acupuncture treatment was performed 3 times per week for 4 weeks, and there was follow-up after a further 3 months. In the three treatment groups EA was applied for 30 minutes at 2Hz and an intensity between 0.1 and 2.0mA “…until patients felt comfortable”. In order to apply EA a second finer needle (0.18x13mm) was placed superficially 2mm lateral to each point and at 2mm depth.

From a physiological perspective this is a mess

What can I say? From a physiological perspective this is a complete mess. We have a range of both manual and electrical stimulation within the same and adjacent myotomes. The EA could range from being subthreshold for A beta fibres in the skin (0.1–0.3mA) to being adequate stimulation for high threshold deep somatic afferents (1.5–2.0mA). The manual stimulation appears to be robust, with more stimulation in the DAM and NAM groups compared with the SA group, but the protocol refers to perpendicular needle insertion of 3–5cm at the sham points, so that is clearly going to be intramuscular insertion. The same protocol refers to perpendicular needle insertion of 2–4cm at PC6 (ie through the median nerve), HT5 (very close to the ulnar nerve and artery, and either exiting the skin on the dorsal aspect of the forearm or hitting ulna periosteum), LU9 (again at 2­­–4cm the needle would be coming out somewhere on the dorsal aspect of the wrist) and LU6 (deep in the muscles of the extensor compartment of the forearm).

The results demonstrate that the DAM group performed roughly twice as well as the NAM or SA groups in terms of the frequency of angina attacks, and the authors speculate that the difference is due to acupuncture point specificity, without giving any scientific rational for such.

There is no clear explanation for these results

I confess it is hard to come up with a clear physiological explanation for these results, if they are indeed genuine. It is conceivable that direct stimulation to the median nerve is the main difference between DAM and NAM groups, and Longhurst’s team clearly demonstrated effects on cardiovascular reflexes from this form of stimulation (in cats) and effects on blood pressure (in humans) compared with points directed at nerves to skin.[3] But Longhurst emphasised that the differences in the effects of different point combinations was related to stimulating deep somatic nerves compared with superficial nerves. It is hard to see how inserting needles 3–5cm in muscle will avoid stimulation of deep somatic nerves.

I remain perplexed by these data, and it is sad that John Longhurst is no longer with us to consult for an opinion on the hard physiology.[4]


1         Zhao L, Li D, Zheng H, et al. Acupuncture as Adjunctive Therapy for Chronic Stable Angina: A Randomized Clinical Trial. JAMA Intern Med Published Online First: 29 July 2019. doi:10.1001/jamainternmed.2019.2407

2         Zhang W-B, Min L-Z, Zhong W-X, et al. Surgical effect and electrophysiological study of patients with hemifacial spasm treated with botulinum toxin or acupuncture before microvascular decompression. Clin Neurol Neurosurg 2019;184:105417. doi:10.1016/j.clineuro.2019.105417

3         Longhurst JC. Acupuncture in cardiovascular medicine. In: Filshie J, White A, Cummings M, eds. Medical Acupuncture – A Western Scientific Approach. London: Elsevier 2016. 394–421.

4         Tjen-A-Looi SC, Longhurst CA. John C. Longhurst, MD, PhD (1947-2018): a pioneer in acupuncture hypertension research. Am J Physiol Heart Circ Physiol 2018;314:H1153–4. doi:10.1152/ajpheart.00169.2018

Declaration of interests MC