Hi Alia,

may be it is so difficult to distinguish esophageal spasm from angina especially if it is Prinzmetal's angina, in many studies many patient suspected to have esophageal spasm and truly they have angina, I attached link may it help you to distinguish between two, despite that you have to exclude coronary artery disease as cause of chest pain then you can proceed in your approach

http://www.ncbi.nlm.nih.gov/pubmed/7234895

https://www.hon.ch/OESO/books/Vol_4_Prim_Motility/Articles/ART373.HTML

Thank you Sajedah

None of tests, except coronary angiogram will exclude coronary artery disease conclusively but there are some features in the clinical history that are important, although not always conclusive, but decrease/increase the probability of one over the other. The precipitating factors, character of pain, associated symptoms - sympathetic symptoms and duration of symptoms. Now a days troponin is very sensitive test for cardiac injury and if a patient has prolonged chest pain, atypical in charatcer lasting for more than an hour without negative troponin reduces the probability of ischemic pain. Although pain with effort increases probability of ischemic pain but bending and lifting activities can worsen reflux and esophageal symptoms as well, rather than walking staright. Pre-test probability based on risk factors and history is the main differentiating factor.

I agree that only coronary angiogram may "photographs" the anatomy of coronary arteries. However, there are vasospasm angina, which often occurs with normal coronary arteries, and cases of myocardial infarction with minimal or no coronary alterations. My personal opinion is, clinically, a more frequent relationship with meals and, very important, regurgitation in the nose characterize esophageal reflux. Occasionally, the administration of nitroglycerin or, alternatively, antacids may help to clarify the question according to the response obtained.

The patient with angina usually presents with typical chest pain which can irradiate to the left arm and the occurrence of which is related to the physical activity. These patients usually have a previous medical history of coronary artery disease (CAD), if not they can at least have some risk factors for CAD, such as elevated cholesterol, elevated body weight, as well as mention nicotine and alcohol abuse. The diagnostic tests, such as TropThs (taken at least 6 hours after the onset of pain), coronary angiogram, ECG taken during the angina and Echo can help to reveal ischemia signs in the myocardium. The administration of i/v or per-oral nitroglycerin relieves the symptoms of pain which does not happen if the patient has gastrointestinal diseases.The esophageal spasms are usually related to the food intake and can disappear after the administration of spasmolytic and antacid drugs. The esophagogastroscopy is also performed to resolve this issue. 

The response to Nitroglycerine doesn't differentiate between esophageal and cardac pain. In fact in a small study 52% of patients with esophageal disease (non-cardiac pain) and 51% of patients with ischemic pain (Cardiac pain) responded to Nitro. Nitro relaxes smooth muscles and lower 1/4rd of esophagus is a smooth muscle as well. It also helps to retard premature labour as uterine muscle is a smooth muscle as well. It is a MYTH, that response to Nitro helps distingush between these causes.

The answers of my colleagues and professors are very interesting and educating, but i like to comment on some of the mentioned points:

Pain of both coronary artery disease (CAD) and esophageal spasm could be of similar location , character , relation of nitrates, associated manifestations and both can be relieved by nitroglycerin thus character of chest pain and its relief after nitroglycerin doesn't differentiate between the 2 diseases.

Presence of acid reflux on Ph manometry or reflux esophagitis on upper endoscopy in a patient with chest pain identifies GERD but does not exclude presence of CAD , since GERD is a common disease and coexistence of GERD and CAD in same patient is still a possibility.

Coronary angiography the gold standard invasive test might be the only method to exclude CAD in such patient.

I agree with the remark of Dr. Ragai Fouda. In an acute pain crisis caused by "spasm", the administration of an anti-acid can be very enlightening.

I think all colleagues have highlighted the question very abundantly. But, if Alia would ascertain the most reliable clinical approaches to differentiate these conditions, I think it is vitallly important to emphasize the main obstacle to exclude vasospastic angina. This intermittent coronary abnormality tends to be very similar to esophageal spasm by inducing causes, clinical picture, duration and the reaction to vasodilating drugs regardless to a class. Tpoponin (I, T) levels are not always associated with coronary spasm particularly in cases without significant myocardial ischaemiс injuriy. Possibly, we can obtain the valuable information concerning transient coronary blood flow alterations during Holter ECG monitoring with obligate complaints, behavior, eating recording by a patient. In uncertain cases the most validated methods of ischaemic heart disease imaging should be performed.

I cannot agree more with several of the previously made comments but I want to overemphasize that the clinical history remains the most important diagnostic tool in patients with nonacute chest pain symptom in the office and even so in the emergency department. Pain description obtained by a careful and physician-oriented history has excellent sensitivity and negative predictive value for the diagnosis when you classify it as definitely angina or definitely not angina. This is mostly true in acute chest pain patients in the ED where sensitivity=94% and negative predictive value=97% for non-ST elevation acute coronary syndrome (Bassan R et al, Critical Pathways in Cardiology 2004;3:1-7 and Arq Bras Cardiol 2000;74:22-29). Obviously, in acute chest pain a complete diagnostic workup (serial ECGs and cTn, chest X-ray, Echo) should be made but if there is no ST-segment elevation in the first ECG their sensitivity/NPV are stil much worse than the clinical history.

Interestingly, based on my experience, esophageal spasms quickly responses to hot water bottle put on the patient´s chest and epigastrium.

Thank you for your helpful answers.

Handgrip test, Ecostress test etc could help. Even a single ECG recorded during the pain could help!

Obvuiously if you do not record ECG DURING the pain... but can be difficult. the only way to describe the leasions is Coronary angiography.

it  is difficult to differentiate the two conditions clinically, even from historyvit is still difficult. anginal pain may be related to meals especialy  heavy meals.

I think to differentiate you will need an imaging  modality.

A nice cold glass of milk relieves esophageal spasm, with cold water doing the same but not for as long a time, nor as completely.

 The associated   clinical autonomic symptoms  may very  in both conditions and a care ful history will help a lot in   differentiating both  although  still there  will be chances of errors 

Excellent observation 

A very good topic to discuss. And I have got some observations-

1. Angina is effort related in most of the cases. oesophageal spasm is related to food' either during taking food or immediately after food. Oesophageal spasm is more common when patient go to bed after taking food.

2. In case of severe coronary artery disease, angina may develop after taking food. But these patients will also have effort angina.

3. Difficult situation is when you have to differentiate it from Prinzmetal angina. Because imaging modalities like CT CAG or CAG will fail to differentiate it, not event stress test. ECG during pain will be of great help. Long time ECG monitoring is one of the best tools.

4. In acute emergency, esophageal spasm is short lived. ECG and cardiac biomarkers will help to differentiate. Some times the pain reappear during or immediately after taking food in ED.

5. Sublingual nitrate may relieve both the pains and may be some time add more confusion.

 I had many similar situations  in my long and rich practice, most of them due to an acute  oesophageal spasm or to existing sliding hernia. Sometimes, it was enough to change the position of the patient to the supine one. So, I think, good anamnesis about the condition during which  the pain emerge, good physical examination, one ECG in the acute situation, and an experienced doctor will be enough for the right diagnosis. 

I agree fully with Dr. Aleksandar Nedok .

It's necessary to know whether or not the event is an acute process or not. It's basic and imperative!

a good anmnesis is necessary. angina is usually associated with chest pain triggered by effort and patients with risks factors for CAD while EE is not.. ultimatelly a treadmill stress test may solve the doubt..

unfortunaly sensitivity of treadmill stress test il low, and where is possible, stress echo with drug is better .

I use the effect of drinking a glass of water. If pain increases befor wanishing after à transitory blockade of water, it's absolutely specific.  Frequently, these criteria are not all present.

The primary goal of office evaluation is to exclude acute coronary syndrome and other potentially life threatening conditions by history, examination, and certain ancillary studies, there after a search for other causes like esophageal spasm is warranted. 

Good, efficient and low-cost practice necessitates favoring positive diagnosis compared with exclusion diagnosis.

Absolutely. 

Yes Electrical stiulation of oesophagus

Guy