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Coalition of Silicone Survivors
Ostermeijer/Patten       BP1002
COSSkids is onderdeel van Coalition of Silicone Survivors - Boulder Collorado USA
Oktober 2016
naar boven
Britta Ostermeyer Shoaib / Bernhard M. Patten
                        Atypical Chest Pain Syndrome in Patients With Breast Implants

                        Houston, Texas


                        Eleven patients, aged 36 to 55 years, with silicone breast implants had episodes of severe chest pain
                        similar to heart attacks 6 weeks to 7 years after breast implantation; one patient had a severe attack 1
                        month after explantation. The chest pain, which was not related to physical exertion, lasted from 15
                        minutes to 4 days, and descriptions of it varied from a "pressing" type of pain to "stabbing" pain with
                        radiation to the shoulders, left arm, and jaw. The associated symptoms were diaphoresis, nausea,
                        vomiting, dyspnea, and palpitations. All of the patients had a normal electrocardiogram (ECG) with the
                        exception of one, whose ECG showed nonspecific ST changes. Ten had cardiac evaluations, all of which
yielded normal results. All had implant removal, and five were found to have at least one ruptured
implant. Nine had an implant capsule biopsy; all had chronic inflammatory rinds, and five had free
silicone in tissue whether or not the implants were ruptured. All eight who had a pectoralis major
muscle biopsy had abnormal results: (neurogenic atrophy [six], fasciitis [three], myositis [one], chronic
inflammation [one], free silicone [one], and neuroma [one]). We concluded that silicone breast
implants may cause an atypical chest pain syndrome, probably due to local inflammatory reactions and
neuroma formation.
Reprinted from the Southern Medical Journal, Journal of the Southern Medical Association, Volume 87,
Number 10, October 1994, Pages 978-984, Copyright © 1994 by Southern Medical Association,
Birmingham, Alabama
AUGMENTATION MAMMAPLASTY was first practiced in Japan during World War II, when Japanese
women enlarged their breasts by direct injections of paraffin or silicone.1 In the United States, since the
silicone envelope-type prosthesis was introduced by Cronin and Gerow2 in 1962, breast implants have
been widely used. According to the Food and Drug Administration (FDA), approximately 1 million
women in the United States have received silicone breast implants.3 Silicone breast implants have been
associated with many complications, including fibrous capsule contracture,4,5 implant rupture,6,7 gel
bleed,8-10 silicone migration,8,11-13 human carcinogenicity,14-16 (degradation of polyurethane  into  2,4
diaminotoluene,  a  known  carcinogen), 17- 21 autoimmune  and  connective  tissue  diseases, 22-29 and
neurologic   problems.30-32 As a consequence of these reported complications and the failure of breast
implant manufacturers to provide the FDA with sufficient safety and efficacy data, the FDA ordered a
moratorium on January 6, 1992, on the further distribution of the silicone gel implants.3

      From 1985 to the present, almost 1,500 patients have been referred to us for the management of
neurologic symptoms occurring after insertion of silicone breast implants. While evaluating their cases,
we discovered that some of the patients had had episodes of severe chest pain with associated
symptoms of nausea, vomiting, diaphoresis, and dyspnea resembling the symptoms of heart attack and
requiring evaluation for possible myocardial infarction. Despite the initial workup for a possible infarct,
these women were eventually determined to have had noncardiac chest pain. In this article, we
describe the clinical symptoms and laboratory findings in the cases of 11 patients with an atypical chest
pain syndrome and silicone breast implants; all of the patients were referred to us for evaluation of
neurologic symptoms occurring after implantation of silicone breast implants.
The study subjects were 11 patients referred to us for evaluation of neurologic symptoms occurring after
implantation of silicone breast implants. Each gave a history and had a physical examination, completed
a questionnaire about implants and symptoms, and received laboratory testing, including a complete
blood count, urinalysis, SMA-15, and serum protein electrophoresis. The subjects were also tested for
quantitative immunoglobulins, complements C3 and C4, antinuclear antibodies (ANA), antimyelin
associated glycoprotein antibodies (anti-MAG), rheumatoid factor, antiganglioside GM1 antibodies (anti-
GM1) and antisulfatide antibodies. All patients had implant removal. At time of removal, 9 patients had
an implant capsule biopsy, and 8 had a pectoralis major muscle biopsy. Formalin sections obtained from
the implant capsule biopsy were stained with hematoxylin and eosin and read by a pathologist at the
Methodist Hospital. Frozen sections of muscle tissue were stained with nicotinamide adenine
dinucleotide (NADH)- tetrazolium reductase, myofibrillar adenosinetriphosphatase at a pH of 9.4, and
modified Gomori's trichrome.
In addition, we reviewed any available cardiac evaluation done by other physicians and medical records
of previous emergency department admissions. All patients were interviewed personally at the time of
presentation and again at a later date via telephone. They were all asked to describe the attack of chest
pain and were questioned regarding risk factors for coronary artery disease and possible noncardiac
causes of chest pain such as peptic ulcer, indigestion, esophageal reflux, hiatal hernia, esophageal
diseases, trauma to the chest and psychosomatic disorders.
Patient 1. A 44-year-old woman was referred to us by her family physician in Indiana for evaluation of
breast implant problems. In 1977 she had a saline breast implant on the left for Poland's syndrome.
Within the same year, she had a closed capsulotomy to release capsular contracture. In 1979 she had a
mastopexy on the right with insertion of a saline breast implant. In 1985 both of the saline implants
were replaced by polyurethane-coated silicone gel implants made by Surgitek (Racine, Wis).
Six months after the first implantation, muscle pain, burning and discomfort developed in the
shoulders, hips, and knees. Extreme fatigability also developed, to the point that she could not dress
herself, as well as joint pain, joint swelling and stiffness, dry eye syndrome, skin rash, Raynaud's
phenomenon, numbness of arms, hands, and fingers, and memory deficits. In 1991 Graves' disease
developed, and in 1992 she sought treatment for local chest problems, including tenderness, itching, a
burning sensation, and swelling in both breasts. She was admitted for evaluation of these symptoms.
The implants were removed but revealed no evidence of rupture. Biopsy specimens of the implant
capsules showed chronic inflammatory cells with numerous foamy histiocytes and refractile translucent
foreign material consistent with silicone. Pectoralis major muscle biopsy showed neurogenic atrophy.
On December 19, 1992, while sitting in her living room watching television, the patient experienced
acute onset of severe chest pain associated with diaphoresis, shortness of breath, nausea, and vomiting.
The pain was described as "pressurelike" and radiated bilaterally to the shoulders and to the left arm.
She thought she was having a heart attack but could not identify any relieving or aggravating factor.
After the chest pain persisted for 3 hours, she went to the Methodist Hospital emergency department.
According to the patient, she had often had chest pain since receiving the breast implants, but it had
never been as severe and intense as this episode. She had had heart catheterization to investigate the
chest pain, and the results were normal. She had no psychologic problems, hypertension, or diabetes.
Even though she had no previous history of gastrointestinal disease, she had an upper gastric
endoscopy, which yielded normal results. The family history was significant in that her father had died
of myocardial infarction at the age of 62. She did not smoke. She had been taking conjugated estrogens
(Premarin), 2.5 mg daily, since having a hysterectomy in 1978. On admission to the emergency
department, blood pressure was 130/80 mm Hg, and other vital signs were stable. The chest was clear on
auscultation. The heart rate and rhythm were regular, and S1 and S2 were normal, without any murmur
or gallop. Nitroglycerin was administered immediately but with no observable relief of symptoms.
Electrocardiogram (ECG) showed sinus tachycardia with no acute changes. Testing for total levels of
creatine kinase, creatine kinase MB, and lactate dehydrogenase was done serially over 3 days; all tests
yielded normal results. A normal two-dimensional echocardiogram was obtained with an ejection
fraction of 55%. The chest pain had resolved by itself within 24 hours after admission. Since the
December 1992 admission for chest pain, the patient has had no recurrence of any similar chest pain.
Patient 2. A 55-year-old woman came to our clinic in February 1992 for evaluation of symptoms related
to breast implants. The patient had had a right modified mastectomy in November 1987 and a left total
mastectomy in July 1988 for intraductal carcinoma of both breasts. Subsequently, in November 1988,
bilateral breast reconstruction was done using polyurethane-covered silicone gel breast implants made
by Surgitek. In January 1989 she had a left capsular contracture release by closed capsulotomy. In spring
1989 local problems, such as breast tenderness, pain, and tightness bilaterally, began to develop, and
she had an open capsulectomy for capsular release in the left breast in October 1989. In 1990 muscle
aches and pain, muscle weakness and fatigability, joint pain and stiffness, headache, dry eyes, dry
mouth and dry vagina (sicca complex), memory problems, and elevated temperatures developed.
In the same year, while working as a bank teller, she had an attack of severe chest pain. The pain lasted
3 days and was described as a "feeling of tightness" in the midchest that radiated to the left shoulder
and back. Accompanying symptoms included diaphoresis and a "smothering" feeling. She could not
identify any relieving or aggravating factor. She went directly to the emergency department. Her
cholesterol level was 234 mg/dL; otherwise, she had no risk factors for coronary artery disease. She did
not smoke and had no history of hypertension or diabetes. The family history was negative for coronary
artery disease. She had no history of gastrointestinal problems, psychologic problems, or trauma to the
chest. On admission to the emergency department, her systolic blood pressure was in the 200s; all other
vital signs were normal. On physical examination, lungs were clear to auscultation, heart rate and
rhythm were regular, and S1 and S2 were normal, without murmur or gallop. Nitroglycerin gave no relief
of pain. ECG was normal, and cardiac enzyme levels were all within normal ranges. Heart catheterization
yielded normal studies of coronary arteries, left ventricular function, and the thoracic aorta; there was
no evidence of inducible coronary vasospasm. She was discharged, and nifedipine was prescribed for
blood pressure control. Since discharge, she has had no recurrent severe chest pain but has continued to
have persistent local tenderness and pain in both breasts.
In 1991 the Surgitek implants were removed, and both implants were found to be ruptured. She
received replacement silicone gel implants made by Dow Corning (Midland, Mich) but continued to
have chest pain and systemic symptoms. She was then referred to us for further evaluation of her
problems. She had bilateral breast implant removal with left axillary lymph node excision. The implants
were found to be intact, and the lymph nodes showed varying degrees of sinus histiocytosis. Biopsy of
the implant capsule showed chronic inflammation. Biopsy of the pectoralis major muscle showed
neurogenic atrophy.

Patient Demographics
The patients ranged in age from 36 to 55 years. The mean age at time of first implantation was 36 years
(range 29 to 52) (Table 1). The mean age at onset of the chest pain was 40 years (range 34 to 53). The
median latency period between implantation and development of the chest pain was 4 years. The types
of breast implants our patients had received and the reasons for implantation are summarized in Table
1. Five patients received more than one pair of implants due to local complications with the implants.
Local and Systemic Symptoms
All patients had local problems with their breasts, including capsular contracture, tenderness, soreness
or pain, heat and swelling, infections, and discharge or numbness of the nipples. They all had chest pain,
thought to be due to a possible myocardial infarction. Implant capsule biopsy specimens showed
chronic inflammation consisting of foamy histiocytes and plasma cells in all patients who had a biopsy
and foreign body giant cells and foreign material consistent with silicone in some (Table 1). Pectoralis
biopsy specimens were abnormal for all eight patients who had biopsies (Table 1).
In all cases, systemic symptoms developed, including myalgia, muscle weakness and fatigue, arthralgia,
joint swelling and stiffness, skin rash, headache, dry mouth, dry eyes, memory problems, hair loss,
sensitivity to sunlight, and numbness and a tingling sensation in the extremities. All patients were
admitted to the hospital for investigation of their systemic symptoms and were found to have
peripheral or central nervous system disease and circulating antibodies such as ANA, anti-GM1, anti-
MAG, or antisulfatide. Six patients had been admitted to the hospital previously for evaluation of chest

Chest Pain and Evaluation of Chest Pain
The time of onset of the chest pain varied from 6 weeks to 7 years after breast implantation; one patient
had a severe attack 1 month after explantation (Table 2). In all cases, the chest pain came on suddenly
when the patients were not physically exerting themselves. The type of pain varied from a "pressing"
type of pain to "stabbing" pain. The pain was located mostly in the midchest with radiation to the
shoulders, left arm, back, and jaw and lasted 15 minutes to 4 days. Associated symptoms included
diaphoresis, nausea, vomiting, dyspnea, and palpitations. Five of the six patients who were admitted to
the hospital for evaluation of possible myocardial infarction got no relief of chest pain from
nitroglycerin. Patient 11 reported mild improvement in the chest pain after using a nitroglycerin patch
and massaging her breasts. Her cardiologist told her that she did not need the patch. The other five
patients never received nitroglycerin.
All patients had cardiac evaluations, except for patient 4, who had only an EGG because her physician
believed that her chest pain was not of cardiac origin. In her case, physical evaluation just before breast
implantation showed that her heart was in excellent condition because she was able to participate in
water sports and exercise strenuously without any problems. As a 34-year-old woman with no family
history of cardiac disease and a low cholesterol level, she was in a low-risk group for cardiac disease. All
patients had normal ECGs during and after the attack of chest pain, except for patient 11; at one point
her EGG showed nonspecific ST changes, but two dobutamine thallium 201 perfusion scintigraphy tests
yielded normal results. Her cardiologist did not think the changes were of clinical significance and did
not indicate ischemic disease. Five patients had exercise treadmill tests; all five yielded normal results.
Six patients had two-dimensional echocardiograms with ejection fractions of 55% to 70% and no
abnormal findings, except for patient 8, who was found to have mild mitral valve prolapse. Four patients
had a dobutamine thallium 201 perfusion scintigraphy study with normal results. Patient 9 had 24-hour
Holter monitoring with negative results. Patient 5 had a multiple gate acquisition analysis (MUGA)
showing a left ventricular ejection fraction of 74% and normal wall motion. Three patients had heart
catheterization with normal results. The four patients who went to the emergency department had
normal levels of cardiac enzymes; the studies, done serially over 3 days, included creatine kinase,
creatine kinase MB, and lactate dehydrogenase. After tests for heart disease yielded negative results,
our patients' cardiologists classified their chest pain as "noncardiac."
After implant removal, the symptoms lessened considerably in nine patients and subsided in two (Table
3). Only patient 1 had another attack shortly after having explantation, but her symptoms subsequently
improved as well.
Evaluation of Risk Factors for Coronary Artery Disease and Possible Sources of Noncardiac Chest Pain
None of the patients had a history of angina pectoris, dyspnea on exertion, or myocardial infarction
before breast implantation. None had diabetes mellitus. Four patients were found to have elevated
cholesterol levels (Table 3). Three patients smoked cigarettes (5 to 12 pack-years). Four had a family
history of coronary artery disease. Six patients had a history of surgical menopause; however, all of
them had been receiving hormone replacement therapy. Of the five patients who had upper gastric
endoscopy, one had reflux and hiatal hernia, one had mild esophagitis, two had a hiatal hernia, and one
had normal results (Table 3). The remaining six patients had no history of gastrointestinal problems.
None of the patients had a history of chest trauma or psychosomatic disorders.

Typical angina pectoris is described as a squeezing or pressing type of pain that comes on during
exertion, usually lasts less than 5 minutes, and may radiate to the left shoulder, left arm, and neck. It is
usually relieved with nitroglycerin and rest.33 Atypical angina pectoris manifests unusually with regard
to location, duration of pain, and relationship with exertion or stress. A diagnosis of nonspecific chest
pain should be considered when the pain is primarily unrelated to stress or exertion, although the
location, quality, or radiation of the pain often bear some resemblance to typical angina pectoris.34
When patients seek treatment with chest pain, it is essential to exclude cardiac causes before
evaluating for possible noncardiac sources. The initial cardiac work-up should include a history and
physical examination followed by diagnostic tests that may vary from patient to patient, depending on
the clinical presentation and cardiac risk factors.  These tests include ECG, treadmill exercise test, two-
dimensional echocardiogram, MUGA, thallium perfusion scintigraphy, positron emission tomography,
Holter monitoring, and, finally, coronary angiography.33 Once cardiac causes are excluded, the pain can
be classified as "noncardiac" chest pain.35 However, the description "chest pain of undetermined origin"
is currently preferred because it encompasses both noncardiac causes, such as esophageal diseases and
psychologic disorders, and obscure cardiac causes, such as microvascular angina and syndrome X, that
may be present even though the patient has a normal coronary angiogram.35-38

The chest pain described by our patients was atypical in terms of duration (lasting from minutes to
days), setting (not associated with physical exertion, no relief with rest), and lack of response to
nitroglycerin. All had normal cardiac studies; consequently, their pain was classified as "non-cardiac"
chest pain or "chest pain of undetermined origin." Four patients had minor esophageal findings. None
of the patients had chest trauma or psychosomatic/psychologic disorders.
In addition to the above causes of noncardiac chest pain, microvascular angina must also be considered
in the differential diagnosis. Microvascular angina is defined as chest pain associated with abnormal
vasoconstriction of coronary vessels too small to be visualized by coronary angiography.36 In 1983
Cannon et al36 proposed that the mechanism responsible for this phenomenon is inappropriate coronary
vasodilator reserve. However, microvascular angina is usually not considered until the patients meet all
of the following criteria: an associated heritable musculoskeletal or neuromuscular disease,
cardiomegaly, arrhythmias, and widespread T wave inversion on the electrocardiogram.34 None of our
patients satisfied the criteria. Our patients did not have syndrome X, a condition associated with typical
chest pain, a positive exercise test, an abnormal coronary arteriogram, or reduced arterial dilatory
capacity after dipyridamole stimulation in the absence of organic heart disease.38 Thus, we have
described the cases of 11 patients who had severe chest pain with the associated symptoms of heart
attack, none of which proved to be of cardiac or established non-cardiac cause. Therefore, we suggest
that chest pain in such cases be reclassified; rather than "chest pain of undetermined origin," it should
be designated "atypical chest pain associated with breast implants."
In all cases in our study, chest pain developed some time after the patient received breast implants,
except for one case in which the patient had a severe attack 1 month after explantation. All patients had
explantation and reported improvement or even resolution of the chest pain. Five patients were found
to have at least one set of ruptured implants. Surgical pathology reports of the implant capsules showed
chronic inflammatory changes in all capsules and foreign body giant cells and refractile translucent
foreign material consistent with silicone in some (Table 1). Pectoralis muscle biopsy specimens showed
neurogenic atrophy, inflammatory changes, or a neuroma. Based on these findings, we hypothesized
that the silicone breast implants were responsible for the atypical chest pain syndrome in these
patients. The proposed mechanism responsible for the chest pain in our patients is a chronic local
inflammatory process stimulated by the breast implants and free silicone (gel bleed, implant rupture) in

In 1987 Kossovsky et al39 studied the bioreactivity of silicone and showed that the physical presence of
the silicone product, associated with a disruption of the contiguity of tissue structure, evokes a chronic
inflammatory response, leading to wound healing by second intention. The microscopic sequelae
included fibrous tissue encapsulation and contraction, inflammatory cell infiltration, and granuloma
formation.39 In the latter part of the same year, the same authors did a study that showed that the
inflammatory reaction to silicone is immunologically mediated.40 A chronic inflammatory process
induced by silicone may account for the local chest pain and affect the same dermatome as the referred
pain from the heart in these patients. In addition, one of our patients had a neuroma found on a
pectoralis muscle biopsy specimen. The neuroma could also have been responsible for the chest pain
because spontaneous discharges from the terminating axons in a neuroma tend to occur in nociceptive
axons (A and C fibers), and it has been proposed that this activity may cause the pain associated with
neuroma.41 In patients with implants placed in the retropectoral position, the surgical dissection of the
pectoralis muscle itself can contribute to the formation of neuromas.

We suggest that there is an association between breast implants and the development of an atypical
chest pain syndrome. Therefore, breast implants should be added to the list of possible noncardiac
causes of chest pain. However, the cases of all patients with chest pain should be evaluated for both
cardiac and known noncardiac causes of chest pain. If those tests yield normal results, the possibility
that the breast implants are the cause of the chest pain should be considered.
Acknowledgment. This study was funded by Mr. George Lindler, a retired Houston builder. Neither Mr.
Lindler nor any of the authors have any financial interest in the cases for or against breast implants.

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Britta Ostermeyer, M.D.
Health Sciences Consult Grp.
3960 Broadway, 3rd Floor
New York, NY 10032
naar boven
Dr. Britta Ostermeyer Shoaib M D
(Engels talig)