Post from another cardiac web site concerning acid reflux

Below is a very long post from another cardiac web site. I thought it might be interesting to readers as the writer presents a very compelling story of acid reflux causing ectopic cardiac beats. The author even found a 1949 medical article (which he included) which describes the association between esophageal pathology and cardiac problems. I am presenting it as I feel that the acid reflux (GERD) connection with cardiac arrhythmias is a real connection, fairly easy to treat and not thought of by most patients or physicians.

(There are three more recent studies making the same point and I would be glad to send the abstracts to any one interested.)

Although this author did not have LAF, I do and have found a similar GERD treatment program to be very effective for me also.

Please find the post below:


Dear All



PVC?s ? Ectopic Beats ? etc



I AM NOT A DOCTOR, I have no medical qualifications whatsoever and I urge you to read the warning at the beginning of the Heart Forum about what to do if you think you are having a heart attack.



The information below is simply a history of how I treated myself, with great success, after a lifetime (from 20 years of age, I?m now 62) of various heart problems, including many years suffering the wretchedness of PVC?s.



The remedies I found may not work on you and should be discussed with your own doctor even though my prime medication can be bought over the counter.



I must try to keep this brief but, if I can, I?ll be happy to expand on any particular area upon request.



How I wish I had found the cause of my PVC?s years earlier and avoided all the wretched and alarming symptoms, and the occasional panic visits to emergency rooms when I was convinced my heart rhythm would not sustain me.



My history is essential as I have some genuine heart problems, but I?ll be as brief as possible (ages in brackets).



(20y) Rheumatic fever, chorea, tachycardia, the latter plaguing me for ten years with short episodes (hours to days) of pulse rates up to 200/minute. I must admit that Valium helped that condition because, being inexperienced, I really did panic with those attacks which made them worse of course.



(30-40y) Tachycardia no longer occurred, thank heavens but this is the period when I began to get very brief periods of PVC?s. Some were isolated and I now believe those are caused by ?wind around the heart? ? a conditioned mentioned in medical literature thoughout the ages, unpleasant, sometime scary.



(44y) My rheumatic fever had damaged my aortic valve and I got very sick but culminating in very successful valve replacement surgery with a pig?s valve which lasted 11 years. It was replaced with a human valve when I was 55 and it?s working beautifully.



However, about seven years ago I began to experience lots of PVC?s, one Holter Monitor picked up nearly 20,000(!) at the height of my suffering. (?They won?t kill you? was about the only comfort I had from my doctors.) I don?t have to elaborate to those of you who get PVC?s how bad I felt. Of course, my heart was my first suspicion having had two AVR?s but all the tests showed good results apart from the PVC?s (ectopic beats, extra-systoles).



I began to tie in these episodes with a feeling of ?indigestion? in all it?s forms. I noticed some foods made me worse, posture played a part too. I consulted a gastro-enterologist (GE) who, amazingly, thought my heart symptoms might be caused by acid reflux. I had a gastric endoscopy to reveal a hiatus hernia. He put me on LOSEC (Prilosec, Omeprazole) 40mg. They did ease my digestive discomforts quite markedly but did not affect my PVC?s to a noticeable extent at that time.



I was still pretty desperate and started to trawl the Internet for help. I felt I KNEW that my problem was related to my digestion problem even though LOSEC had not by them produced a miraculous cure. One day I found an article written in 1949(!) which seemed to give a clue that the esophagus could affect heart rhythm ? ?SOME CARDIOVASCULAR COMPLICATIONS OF ESOPAGEAL LESIONS? By A. WHITLEY BRANWOOD, M.D., F.R.C.P.(Edin) M.R.C.P. (Edinburgh Medical Journal 1949; 56;415-21]



This article gave me the confidence that I was on the right track. I recalled that my GE had said that Losec did not totally stop the acid and indeed I would often feel the reflux if I laid too flat in bed or if I bent forward. Also, with a hiatus hernia, all stomach contents including bile can run backwards into the esophagus and cause inflammation.



At this time, I was still seeing cardiologists, one of whom was on the verge of convincing me to have a pacemaker!!! His theory was that if the heart were speeded up to 100+bpm from my normal 60-70, the ?ectopic? beats would not have time to come in before the next proper beat. Thank heavens I did note allow anything so drastic. [Side note ? I note that some people have mentioned breathlessness with PVC?s. That was also an occasional symptom with me, also yawning a lot. He explained why that happened, if the extra-systole occurred when certain valves were open, it can apparently cause a back flow to the lungs resulting in a feeling of breathlessness.]



Thinking about this for myself, I thought I might be better if my esophagus was protected (coated) with an antacid and started to take Gaviscon which claims it does that. I hated the taste of Gaviscon and tried Maalox (available worldwide). I took 10ccs after every meal and maybe another dose if I forgot and washed it away with (eg) a mid-meal drink). I also took 20ccs before going to bed. At this time also I started to be very careful to follow all the recommendations given to hiatus hernia patients, that is to sleep with the head and trunk raised, avoid tight clothing around the waist etc. Avoid caffeine and chocolate (difficult!) ? but see my list below.)



At the start of my new regime I was still having thousands of PVC?s a day but within a 3 or 4 days I noticed a huge reduction. Within two weeks they had practically disappeared! I reduced the Maalox to a smaller dose (5ccs) and 20ccs at night. A couple of weeks after that my PVC?s disappeared altogether!!!



It would be natural for you to think this was just a fluke and I was due for remission after a year or more of hell during which I thought my heart would fail, especially after two emergency room dashes when things got very bad.



However, read on. Some weeks after this I was off Maalox and gave up Losec on my GE?s advice (back then, it was recommended only for short-term use). Just days passed before my acid was out of control and PVC?s restarted! Back on Maalox and I contained them, a week later they were gone again. My GE said he would be happy for me to take Losec long-term and so I?ve been on 20mg/day for the last 5 years.



Occasionally, when I have not looked after myself (careless with my food, sleeping position etc) the PVC?s will flare up, just one or two a minute, not thousands. I revert to Maalox, and within 2-7 days I?m back to normal. It depends how long I take to realize they?re back before I start Maalox and that determines how long it takes to calm down my esophagus again. This pattern has gone on now for the last few years and I always know I can fix those wretched PVC?s.



Here are my personal tips on hiatus hernia (which, I understand, affects 50% of adults to some extent).



Avoid caffeine and chocolate (which has a caffeine-like chemical in it). These are important for two reasons. One, they stimulate the production of acid, and two, they both relax the sphincter around the esophagus where it enters the stomach which permits even more reflux (of acid, bile, stomach contents). I eat my chocolates during the day!



Dry (acidic) white wine, and red to a lesser extent, affect my esophagus badly. Wine will often start off an episode (the following day) that takes me days to correct.



Gassy drinks and food that produce gas push up stomach contents back through the sphincter, avoid them particularly in the evening.



Sleep with the head and trunk raised in bed or even when napping or watching TV on a settee in the daytime, avoid tight clothing around the waist, avoid bending forward too much.



I hope the above will help some of you see off or reduce the frequency and severity of those PVCs. You may have to be patient with the Maalox regime especially if you have long-term esophageal damage to heal. Read the warnings on Maalox or similar. You should obviously consult your doctor, you may have an ulcer, he may want to give you Losec or similar as a speed-up to this possible cure. Remember Gaviscon may be better, it?s more viscous, but doesn?t taste so good. Don?t wash away the Maalox by drinking, have a glass of water first.



Also remember that, in my experience, PVC?s can also be produced from bloating (gas) pushing up the stomach or diaphragm, straining on the toilet, being constipated to name but a few. By the way, I found that simethicone made my bloating symptoms much worse because I think it coalesces all the gas into one big bubble!



PLEASE LET ME KNOW IF THE REGIME IS SUCCESSFUL FOR YOU, I MAY TRY TO GET THE CONDITION NAMED ?BREWER?S ESOPHAGUS?!



Hereunder is the article I referred to above.



All the very best.



Mike







SOME CARDIOVASCULAR COMPLICATIONS

OF ESOPAGEAL LESIONS



By A. WHITLEY BRANWOOD, M.D., F.R.C.P.(Edin) M.R.C.P.

(Edinburgh Medical Journal 1949; 56;415-21]



The esophagus is intimately related to the heart, aorta and great vessels and it is therefore not surprising that lesions of these structures may affect the esophagus (and thus vice-versa ?MJB!) Compression of this structure, perhaps producing dysphagia, is a well known complication of aortic aneurysm, right aortic arch, an anomalous right subclavian artery and, even, aneurysm of the innominate artery. A case of this latter condition has been described by Beristain and Balcells. The esophagus may also be pressed upon by a dilated pulmonary artery, by a pericardial effusion, by the enlarged left auricle of mitral stenosis, and Donovan et al have described displacement of the esophagus by an enlarged left auricle in cases of patent ductus arteriosus. Lesions of the esophagus, however, seldom affect the heart, although such cases have occasionally been described in the literature. The rarity of these conditions is nevertheless surprising, for not only is the esophagus closely related to the heart and aorta but both the esophagus and the heart are innervated by the vagus.



The vagus nerve is composed of parasympathetic efferent, somatic motor and sensory fibres. The motor fibres are distributed to the involuntary muscles of the bronchi, heart, esophagus, stomach and small intestine, while the sensory fibres are derived from the larynx, pharyinx, lungs, heart, esophagus, stomach and small intestine. Esophageal branches are given off from the vagus and form the esophageal plexus. From this plexus, filaments are distributed to the esophagus and to the back of the pericardium. Cardiac branches are also given off from the vagus and form the superficial and deep cardiac plexuses. It is feasible to suggest therefore that irritation of the vagal nerve endings, produced by lesions in the esophagus, may thus stimulate the cardiac branches.



Several patients with lesions of the esophagus have been observed, in whom there were associated abnormalities of the cardiovascular system.



ACUTE ESOPHAGITIS



Multiple extrasystoles were observed in five patients suffering from acute erosive esophagitis Two of the patients were women aged 26 and 35 years -- both had drunk lysol for suicidal purposes. The other patients were men aged 32, 36 and 40. One patient drank lysol, one ammonia and one sulphuric acid. The latter two patients did not recover. All developed extrasystoles. These were more marked during the periods of vomiting and retching. The pulse returned to normal in the three patients who recovered. Neither phenol, the active agent of lysol, nor the other corrosive sulphuric acid or ammonia are cardiac irritants. Phenol is a cardiac depressant, it causes marked fall in the blood pressure and a slowing of the heart rate. Ammonia and sulphuric acid produce liquefaction of the tissues and corrosion, respectively; neither has any direct action on the heart. It is suggested that the acute erosive esophagitis may have produced the extrasystoles by reflex action via the vagus.





ESOPHAGEAL DIVERTICULUM



Three patients were found to have esophageal diverticula. The first was a woman aged 48 who gave a history of having had pulmonary tuberculosis many years ago. Her present complaint was heartburn. A barium meal showed a traction diverticulum of the esophagus. Some months later she was seen again, when she was discovered to have paroxysmal auricular tachycardia. Her blood pressure was normal and no other evidence of cardiovascular disease could he found. The attacks could be induced by eating food rapidly or swallowing improperly masticated food. The paroxysms could he stopped by vagal stimulation or the administration of mecholin.



The second patient, a man aged 61, who had also suffered from pulmonary tuberculosis complained of palpitations whenever he drank hot liquids. He also had symptoms suggestive of a duodenal ulcer. An X-ray demonstrated an ulcer crater in the duodenum and also a traction diverticulum of the esophagus. An ECG showed multiple ventricular extrasystoles. A careful examination of the patient and an exhaustive inquiry into his habits revealed no precipitating factors to cause the extrasystoles. The third patient, a woman of 49, suffered from dysphagia. Radiological examination showed a traction diverticulum of the middle third of the esophagus. She also complained of palpitations after eating. An ECG showed ventricular extrasystoles and, like the previous case, no other cause could be found for these.



Traction diverticula of the esophagus are common. Kragh found the incidence to be 9,5 per cent. Tuberculosis of the bronchial lymph nodes is the most frequent cause. Penerman showed that 73 per cent. of traction diverticula were produced by tuberculosis. Feldman states that they are usually situated on the anterior or posterior aspect of the esophagus in its middle third and, although they occur at any age are most often seen over the age of 40. Extrasystoles and other arrhythmias may be produced by degenerative heart disease which is also more common after the age of 40. In the cases in this series, however, no abnormality was discovered on examination to suggest any disease of the cardiovascular system nor were any other etiological factors present to cause paroxysmal tachycardia or extrasystoles. The definite relationship of the onset of the arrhythmias to the intake of food or drink is very suggestive that the esophageal diverticulum may have been the precipitating factor in these cases whether the myocardium was healthy or diseased.



ESOPHAGEAL ULCER



A man aged 59 was admitted to hospital with a complaint of dysphagia and retrosternal pain following the intake of food. An X-ray showed an esophageal ulcer with superadded spasm at the lower end of the esophagus. It was noted that immediately after the intake of food and coincidental with the occurrence of pain, numerous extrasystoles were present and the patient complained of palpitations. The blood pressure was 135/80, the heart was not enlarged and there was no other clinical evidence of cardiac disease. An ECG taken when the patient's symptoms were acute showed ventricular extrasystoles, left axis deviation. with the QRS complexes deflected upwards in leads I and II and downwards in lead III. The T waves were flat in leads I and II and upright in leads III. The sternal lead showed a splintered Q wave and slight elevation of the ST segment while the T wave was inverted in the apical lead. Although there were no other features of coronary occlusion the ECG was suggestive of a healing anterior infarct. The patient remained in hospital a month. The ulcer was treated with rest, diet, alkalies and belladonna, At the end of this time the esophageal ulcer was still present and the ECG showed no change. The X-ray and ECG two months later were unchanged from the time of the original examination. The patient was seen again a year later. The esophageal ulcer could not now be demonstrated radiologically. An ECG showed normal sinus rhythm. There was no axis deviation, the T waves were upright in all the standard leads and apart from an occasional ventricular extrasystole the ECG was normal.



It is difficult to determine in this case whether the patient had a myocardial infarction or whether the ECG changes were related to the esophageal spasm, secondary to the ulcer. Apart from the ECG there were no other clinical features to suggest cardiovascular disease, least of all a coronary occlusion. The absence of the progressive ECG changes developing after an anterior myocardial infarction, together with the persistently abnormal ECG records, which were identical two months after his discharge from hospital, with the original examination, suggest a relationship between the esophageal ulcer and the abnormal ECG. Gilbert, Le Roy and Fenn have shown, in carefully performed experiments on dogs, that distension of the stomach excited a vago-vagal reflex which caused a decrease in the flow of blood through the circumflex branch of the left coronary artery. It is suggested that the ECG changes described in this case were a result of a similar reflex mechanism produced by spasm of the esophagus which was a feature of the ulcer.



CARDIOSPASM



A patient, aged 45, had complained of dysphagia and vomiting for eighteen months. For six months he had also suffered from nocturnal dyspnea. A barium swallow showed a constriction at the lower inch of the oesophagus. Through this a thin trickle of barium flowed into the stomach. Above this constriction, the esophagus was grossly dilated. The blood pressure was 115/70 and there were no clinical signs of cardiovascular disease. An ECG was normal. The nocturnal dyspnea was associated with engorgement of the neck veins, the expectoration of frothy sputum and with basal crepitations. It was relieved by the administration of oxygen and aminophylline or by venesection. These findings suggest that the attacks of nocturnal dyspnea were due presumably to the pressure of the grossly dilated esophagus upon the pulmonary veins producing an acute congestion and edema of the lungs.



The second case was a woman of 42 years who had suffered from cardiospasm for many years. This, however; had not greatly inconvenienced her. For several years she had complained of cough and the expectoration of large quantities of purulent sputum. Recently she had suffered from severe progressive dyspnea. On examination she was cyanosed and dyspnoeic and had a tachycardia. Examination of the chest revealed evidence of bilateral bronchiectasis. This was confirmed by X-ray examination which showed, in addition, gross widening of the mediastinum produced by the dilated esophagus. This dilated esophagus made examination of the heart rather difficult but the appearances were suggestive of a prominent pulmonary conus and right-sided enlargement. This woman would appear to be suffering from cor pulmonale, a result of her bronchiectasis. Similar cases of bronchiectasis, resulting from the repeated aspiration of regurgitated esophageal contents have been reported in cases of cardiospasm by Johnstone and Wooler and by Belcher.



ESOPHAGEAL HIATUS HERNIA



Three patients suffering from esophageal hiatus hernia complained of retrosternal pain which radiated into the neck, left shoulder or down the left arm. The pain was described as crushing in character and could be brought on by exertion or following a meal. No abnormalities were detected on clinical examination of the cardiovascular system and repeated ECG examinations were normal. Another patient, a woman aged 45, with a hiatus hernia suffered from paroxysmal tachycardia. Here again no evidence of cardiovascular disease or any factor predisposing to this arrhythmia could be found.



The referred pain in these cases is perhaps due to communications between the esophageal and cardiac plexuses. Lesions of the esophagus could therefore cause pain which is referred to the same regions as that of primarily cardiac origin. Another possible explanation of this distribution of the pain is that suggested by Gilbert et al where distension of the stomach or hernial pouch may produce a diminished blood flow in the circumflex coronary artery. The association of hiatus hernia with cardiac disturbances are well known. Harrington, in a review of 60 cases of esophageal hiatus hernia, had 7 which were misdiagnosed as suffering from cardiac disease. Gilbert stated that hiatus hernia may induce attacks of paroxysmal auricular fibrillation, the arrhythmia coinciding with the protrusion of the stomach into the esophageal hiatus and disappearing when the stomach slipped back into place. Stubenbord recorded a case of a hiatus hernia in a patient aged 44 in which paroxysmal auricular fibrillation was the main presenting feature.



ESOPHAGEAL CARCINOMA



A case was seen in which a squamous epithelioma of the esophagus produced sudden death in a patient, by eroding into the aorta.



ESOPHAGEAL VARICES



The effects of rupture of esophageal varices upon the cardiovascular system with the resulting blood loss and shock, are too well known to demand further description.



SCLERODERMA OF THE ESOPHAGUS



The only instance of this condition was seen in a female patient aged 43. She died of cardiac failure secondary to cor pulmonale, this latter condition was a result of involvement of the pulmonary tissue by the scleroderma. Scleroderma of the esophagus per se does not produce any cardiovascular complications. The heart disease in these cases is a result of involvement of the lungs.



DISCUSSION



Lesions of the esophagus may affect the cardiovascular system by (1) reflex action, (2) direct involvement of the related structures, (3) indirectly.



Reflex action. This is the mechanism that occurs most frequently. It would appear to be mediated through the vagus nerve. The vagus is composed of parasympathetic efferent, somatic motor, visceral efferent and sensory fibres. It arises in the medulla oblongata and passes through the neck and thorax to the abdomen. The right and the left branches join to form the esophageal plexus. From this plexus nerves are distributed to the anterior and posterior surfaces of the stomach. The vagus also gives two other branches. The superior and inferior cardiac nerves, the former arises In the neck and the latter is given off in the thorax. All the branches contain parasympathetic efferent and sensory fibres. During the act of retching and vomiting the esophageal or gastric branches of the vagus nerve may be stimulated and thus reflexly excite the cardiac nerves. Any irritant lesion in the esophagus may act in a similar manner. If a hiatus hernia should be present then the resulting increased pressure upon the lower end of the esophagus which occurs during vomiting may also perhaps stimulate the esophageal plexus with reflex excitation of the cardiac branches. This mechanism may explain the arrhythmias seen in acute esophagitis, esophageal diverticula, esophageal ulcer, cardiospasm and hiatus hernia. The changes in the ECG and the pericardial pain present in the cases of esophageal ulcer and hiatus hernia may also be explained by a reflex mechanism, for according to the work of Gilbert et al, the vago-vagal reflex, induced by esophageal lesions, produce impaired blood flow. through the circumflex branch of the left coronary artery with resulting myocardial ischemia.



Direct Involvement of the Related Structures. Esophageal carcinoma may, very rarely, erode the aorta or left auricle producing haemorrhage or arrhythmias.



Indirectly. The enlarged esophagus in cases of achalasia may produce pressure on the pulmonary veins and cause paroxysmal dyspnea. Repeated attacks of aspiration pneumonia in these patients may result In bronchiectasis and finally heart failure. In scleroderma the esophageal changes are a feature of the disease while the cardiac lesions are a result of the pulmonary involvement. Rupture of esophageal varices usually result in severe haemorrhage with secondary effects on the cardiovascular system

Acute esophagitis occurs very frequently. The condition is often seen in a wide variety of diseases at post-mortem. Histological examination shows that these are ante-mortem lesions. Lesions of the esophagus should therefore, always be suspected in any arrhythmia that cannot be explained by disease of the cardiovascular system or other known causes.

Very interesting Lee, great post.
"Mike's" story is the mirror image of my own experience. Like Mike, I too suffered from tachycardia starting from my early 20's before developing ectopics and then afib when 43yrs of age. It was only after I visited a gastro and had all the ghastly tests that I realised my arrythmia and reflux was connected. The test that really connected everything was the 24hr pH test. The 24hr pH graph exactly matched my arrythmia pattern. The stomach endoscopy revealed loose LES (birth defect?)
If you want to know more of my story its in "the list" section.

Lee, have you had a 24hr pH study test, esophageal motility study or a stomach endoscopy?

Dean

I have had a holter, upper endoscopy and upper GI. I am being scheduled for the PH and manometry testing. My main proof is that, if I sleep flat or soon after a big meal or skip the PPI's the hollow feeling in my chest returns and so do the PAcs.

The UGI showed small hiatal hernia, some evidence of reflux, and a small esophageal diverticulum in the cervical esophagus.

I very much like the marked improvement I have had with the meds, avoiding triggers and elevating the head of the bed, but I would s to stop the meds and not feel so paranoid about what I eat.

I am actively reviewing all the research I can find concerning healing methodologies for GERD ranging from anti-reflux surgery, to eating alkaline foods to the role of Probiotics.

Lee,
I don't know if your doctors will do it but when you have your 24hr pH test see if you can have a holter monitor at the same time over the same period. You should then have absolute proof your GERD triggers ectopics and LAF. The graph of the pH test will peak and match the arrythmia shown on the holter.

I found probiotics to be basically useless expensive rubbish (hope Jackie doesn't see this!). If you want the real rambo of probiotics go for the organic natto food (50mg no less than 5 times a week). It tastes like dog **** but boy does it work. Natto is the only food fermented with a bacteria - bacillus subtilis. This bacterium has a real pac man effect and will complement the PPI by stopping opportunistic infections caused by the low stomach acid.
Other things about bacillus subtilis in the natto:
-has a strong natural ACE inhibatory action the same as if taking ACE tablets
-reduces Ca in the soft tissues and sends it into the bones through increasing matrix gla protein. Jap women use it for oesteoporosis. This is important as it counter acts the loss of bone Ca caused by the PPI.

Dean