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Angina pectoris with coexisting skeletal chest pain
Clinic&l communications
Angina pcturis wieh coexis+ing
skebal
&es+
pin
James B. McElroy, M.D.” Birmingham, Ala.
T
here are many excellent reports describing innocent causes of chest pain which may be confused with ischemic heart disease.‘-6 However, the frequent coexistence of angina pectoris with skeletal chest pain has not been sufficiently emphasized. In 1928, Eckerson and associates6 reported on 4 patients who, after a myocardial infarction, had persistent discomfort in the anterior chest not due to further myocardial ischemia. They attributed the pain to the presence of the myocardial scar. Musculoskeletal chest pain after myocardial infarction was found in 13 per cent of 60 patients studied by Edwards.7 In many of these patients the innocent disorder was confused with myocardial ischemia or necrosis. Others.8 have been impressed with the frequency of complaints of pain in the anterior chest wall after myocardial infarction, for a period of time up to 9 to 12 months. The present report indicates that a similar pain often exists in patients with angina pectoris who have no evidence of myocardial infarction. This study was undertaken to test the validity of our clinical impression that skeletal chest pain is more common in patients with angina pectoris than in individuals of the same age decade and sex who have no heart disease, and to suggest a diagnostic approach to these often difficult patients.
Plan
of study
The records of 2,213 referred medical patients were reviewed. Three hundred and three patients presented convincing evidence of angina pectoris. Three hundred and three control subjects were selected at random, except that the absence of any clinical evidence of heart disease was stipulated, and these were paired by age decade and sex with the patients of the angina pectoris group. The incidence of anterior chest pain of skeletal origin was determined for both groups. Angina pectoris group. A diagnosis of angina pectoris was made in 303 patients. Inclusion in this group was based on one or more of the following criteria, in addition to whether the history was typical or atypical : 1. POSITIVE
ELECTROCARDIOGRAPHIC
TEST.
From the Department of Medicine, Medical College of Alabama, Birmingham, Ala. Supported by The Pure Oil Foundation and The John Seward Johnson Charitable Trust. Received for publication May 11. 1962. *Instructor in Medicine. Medical College of Alabama, Address: 1316 South 19th St., Birmingham
296
EXER-
This is defined as a postexertional depression of the entire S-T segment below the base line (P-R segment) of at least 1 mm. in any lead, and having either a horizontal or sagging configuration. A depressed S-T junction which rose acutely into a T wave was not regarded as an indication of myocardial ischemia. Arrhythmias, conduction defects, and isolated T-wave changes alone after exercise were not considered to constitute a positive test. In patients who were taking digitalis, electrocardiographic changes after exercise CISE
5, Ala.
Vokme
Number
66 3
Angina
pectoris zwith coexisting skeletal chest pain
were not used as a criterion for the diagnosis of angina pectoris. 2. PROMPT AND COMPLETE RELIEF OFPAIN BY NITROGLYCERIN. Prompt is defined as within 10 minutes, and the word complete emphasizes that many patients with skeletal pain frequently state that they obtain some degree of relief, but not complete relief as is seen in most instances of angina pectoris. 3. CONSISTENT INCREASE IN THE AMOUNT OF EXERCISE DISCOMFORT PARED WITH
REQUIRED TO INDUCE CHEST AFTERNITROGLYCERIN AS COMA PLACEBO CONTROL. When
chest discomfort came on during exercise, the test was stopped immediately. The duration of exercise and the number of ascents required to precipitate pain were noted. The same rate of exercise was repeated after a placebo (saccharin tablet) and, finally, nitroglycerin; the patient rested 4.5 minutes between each exercise attempt. These tests were repeated several times on separate days under conditions which were similar as regards relationship to meals, emotional stress, and environmental temperature. To satisfy this criterion, the amount of exercise required to induce chest discomfort must be consistently increased approximately 50 per cent or more after nitroglycerin, with little or no increase after a placebo. Control group. Three hundred and three control subjects were selected at random, except that the absence of any clinical evidence of heart disease was stipulated. All had normal resting electrocardiograms, and the majority were exercised to their physical tolerance and exhibited a normal postexertional tracing. In all patients who had a history of chest pain, negative results were demonstrated by all of the objective criteria listed for the angina pectoris group Subjects from the control group who showed any of the following questionable changes in t.heir postexertional electrocardiograms were excluded : (1) depression of the entire S-T segment below the base line (P-R segment) of 0.5 minute or more, with a horizontal or sagging contour (S-T segment depressions of 0.5 mm. to less than 1 mm. were regarded as borderline) ; (2) arincluding ventricular, nodal, rhythmias, or atria1 premature contractions; (3) tran-
297
sient conduction defects; (4) T-wave inversions. Patients with benign arrhythmias or a history of palpitation were also omitted from this study. Patients were excluded from both groups when any one of the following conditions existed: (1) shoulder-hand syndrome; (2) valvular or congenital heart disease; (3) hiatal hernia, peptic ulcer, or gall-bladder disease; (4) history or clinical evidence of syphilis; (5) myocardial infarction without angina pectoris., Criteria for the presence of skeletal chest pain. The diagnosis of skeletal chest pain was made when a patient presented with a complaint of pain having the following characteristics: (1) Long duration, i.e., several weeks or more (as opposed to acute skeletal chest pain which sometimes follows some recent unusual effort or strain). (2) Described as a soreness, aching, tenderor sometimes as ness, sharp knifelike, tightness, (3) Intensity commonly minimal to moderate but occasionally severe. (4) Usually felt over the precordium, beneath the sternum, at the xiphoid, or at the chondrosternal or costochondral junctions. (5) At times well localized to a small area but usually diffuse. (6) Occasionally radiates into left arm. (7) Onset usually very gradual over many minutes, but at times practically instantaneous in that the maximal intensity is reached almost with the first sensation of discomfort. (8) Lasting seconds or hours (but not for a few minutes only). (9) Intensity usually waxes and wanes with specific body movements but may be constant. (10) Not usually precipitated by factors that increase cardiac work, such as exercise, emotional stress, and the postprandial state. (11) Not promptly and completely relieved by nitroglycerin. (12) Often associated with local tenderness. (13) Favorably affected by salicylates, warmth, local injections of procaine, and sometimes by steroidal hormones. Results Of the 303 patients with angina pectoris, 155 (51 per cent) had clinical evidence of anterior skeletal chest pain, whereas in the 303 control subjects, only 70 (23 per cent) exhibited this disorder (Table I). These
298
Am. Heart J. Sefitember, 1963
McElroy
Table I Number (angina1
in each group and control)
20-29 30-39 40-49 SO-59 60-69 IO-79 SO-90
:z 120 93 19 2
Totals
303
(number
1
data were analyzed by the chi square technique and were found to be highly significant (p < .OOl). The records of 1.50 of the 155 patients with both angina pectoris and anterior skeletal chest pain afforded reasonably certain evidence whether a prior myocardial infarction had occurred. Seventynine (53 per cent) of these 150 patients had no evidence of myocardial infarction. Discussion
These findings demonstrate that (at least in this series of patients) anterior skeletal chest pain is more common in patients with angina pectoris than in individuals of the same age decade and sex with healthy hearts. It was also found that skeletal chest pain often exists in patients with angina pectoris in the absence of evidence of myocardial infarction. It is likely that the incidence of chest wall pain found in the control subjects (23 per cent) is higher than in the comparable general population. All of these patients were referred by physicians, and in many instances the chest pain constituted the chief reason for such referral. This circumstance would tend to further increase the marked difference already noted in the incidence of skeletal chest pain in the two groups. The skeletal chest pain reported here seemsto be analogous to that of the shoulder-hand syndrome, although lessdramatic and without local swelling or involvement of the shoulders and hands. Presumably, a similar mechanism exists for both conditions. Skeletal chest pain may exist with the shoulder-hand syndrome, but patients
Angina1 group with skeletal
pain)
(number
Control group with skeletal
1 8 30 58 46 10 2 ~--
1 5 10 36 16 2 0 __-
1.55 (51%)
70 (23%)
pain)
who had involvement of the shoulders or hands were excluded from this study. Although the two conditions present entirely different clinical pictures, it is of interest that both have occasionally responded, at times dramatically, to oral cortisone therwy.g Certain conditions, such as distention of abdominal viscera, are known to cause reflex constriction of the coronary arteries; but this probably never induces angina1 pain in normal subjects.‘O In some patients with coronary atherosclerosis, however, skeletal chest pain can apparently precipitate angina1 attacks. We have observed several patients with typical angina pectoris whose pain and electrocardiographic changes could be produced by the skeletal chest pain acting as a trigger. The following case historyillustrates this phenomenon. Patient B. K. This .54-year-old white woman had had her first episode of chest pain 3 years prior to hospitalization. While planting flowers, she was seized with a severe, vise-like substernal constriction which radiated into both arms and hands and the anterior neck. A few minutes later she became un; conscious. A myocardial infarction was documented. In the subsequent ‘2 years, she sustained two other myocardial infarctions at approximately yearly intervals. For 2% years she had also had typical angina1 pain. Walking precipitated the discomfort only if undertaken within 2 to 255 hours after a meal, whereas excitement or anger readily induced pain. An identical discomfort would always follow the brushing of her teeth, bending forward, and certain specific movements of the arms, such as raising both arms above her head or reaching for an object on a high shelf. Nitroglycerin would consistently relieve the pain completely within 5 minutes. The patient was not aware of any other type of chest discomfort. Gall-bladder and gastrointestinal x-ray films were normal. Physical examination revealed a small pre-
Volune Number
66 3
Angina
pectoris with coexisting skeletal chest pain
cordial liftrr and a Grade 1, short, late systolic apical murmur. A resting electrocardiogram showed abnormal Q waves in Leads II, III, and aVF, with normal S-T segments and T waves in all 12 leads. When seen at the time of a ward visit on the following day, she exclaimed that she had just finished brushing her teeth and was having an episode of chest pain. Examination revealed a marked visible, as well as palpable, precordial lift, and during the pain the previously described Grade 1 murmur was of Grade 4 intensity. After nitroglycerin, the pain promptly subsided. The precordial lift was no longer visible and was barely palpable. The Grade 4 murmur returned to Grade 1 intensity. Several subsequent examinations revealed that the motion of her right arm, as used in brushing her teeth, would regularly induce angina1 pain and the above-described physical findings, together with marked depression and sagging of the S-T segments in the electrocardiogram. It was found that firm pressure upon the third left chondrosternal junction would regularly induce angina1 pain, with the attendant changes, whereas pain, to the point of weeping, by pressure on the Achilles tendon and fingernail, would cause none of the above-mentioned reactions. After procaine anesthetization of this tender area, neither the application of firm pressure nor any arm movement resulted in angina1 pain.
The obvious conclusion drawn from these observations is that the skeletal tissues were capable of initiating reflex coronary constriction and angina1 attacks in this patient with advanced coronary artery disease. A similar patient has been reported on by Reeves and Harrison,‘O During an attack of angina1 pain, a precordial lift resulting from local ballooning of ischemic muscle may be identified occasionally in patients by special techniques, such as the kinetocardiogram, and by palpation in a somewhat lesser number.” We have, on rare occasions, detected for the first time a short, late, apical systolic murmur in patients during angina1 pain. Presumably, this finding is due to distortion of papillary muscles as the result of focal myocardial ischemia. Angina1 pain and characteristic electrocardiographic changes have occasionally been noted in our own patients with angina pectoris and a coexisting hiatal hernia, by distention of the stomach with air. Presumably, these phenomena are caused by reflex coronary constriction. In any patient with a complaint of chest pain, it is important to first exclude angina pectoris beyond any reasonable doubt before other causes of the discomfort are
299
sought. The presence of ischemic heart disease can usually be determined by a careful history when the complaints are typical. Skeletal chest pain which coexists with angina pectoris frequently modifies the symptoms of both disorders, so that an extremely puzzling situation results. In a considerable fraction of our own patients with both angina pectoris and skeletal chest pain, the more important ischemic pain was confused with or even masked by the coexistence of the innocent disorder. There is sound experimental evidence for the view that visceral pain and deep skeletal pain are mediated through a common deep sensory system.r2 It is not surprising that their characteristics should be similar, and that, on occasion, differentiation between the two may be extremely difficult. The importance of a careful and thorough history in evaluating any chest pain cannot be overemphasized. When the history is inconclusive, evaluation of the postexertional electrocardiogram and observation of the effect of nitroglycerin on the response to exercise discussed earlier will frequently be of crucial diagnostic value in determining whether angina pectoris exists. The reader is referred to the excellent papers of Wood,rS Scherf,14 and Lepeschkin15 for further details of the electrocardiographic exercise test. In the patient with atypical or puzzling chest pain, usually due to the coexistence of skeletal chest pain with angina pectoris, we believe that this approach offers a means whereby a reasonably certain answer can be obtained, and thus will frequently enable the physician to find the in the “haystack” of angina1 “needle” skeletal chest pain. The results reported here indicate that skeletal chest pain is more common in patients with angina pectoris than in individuals of the same age decade and sex with healthy hearts. Therefore, it is important to institute a meticulous search for angina pectoris in any patient presenting with obvious chronic skeletal chest pain. Summary
The records of 2,213 referred medical patients were reviewed. Three hundred and
300
Am. Heart .I. Sefitsmber, 1963
McElroy
three patients presented convincing clinical evidence of angina pectoris. An equal number of control subjects was randomly chosen on the basis of an absence of any cardiac disorder and were paired as to age decade and sex with the patients of the angina pectoris group. The incidence of anterior skeletal chest pain was determined for both groups. Clinical evidence of anterior chest pain of skeletal origin was present in 51 per cent of the patients with angina pectoris and 23 per cent of the control subjects. This represents a significant difference by chi square analysis (p < .OOl). In patients with angina pectoris, skeletal chest pain frequently occurs in the absence of a prior myocardial infarction. In some patients with angina pectoris and coexisting skeletal pain, the skeletal disorder may precipitate attacks of angina1 pain. A case history which demonstrates this phenomenon of “reflex angina” is presented. In a considerable fraction of the patients with angina pectoris the more important ischemic pain was confused with or even masked by the coexistence of the innocent disorder. Evidence is presented that skeletal chest pain is more common in patients with angina pectoris than in individuals of the same age decade and sex with healthy hearts. Therefore, it is important to institute a meticulous search for ischemic heart disease in any patient who presents with obvious skeletal chest pain.
REFERENCES 1. Miller,
A. J.,
and
Texidoe,
T.
A.:
The
“pre-
cordial catch,” a syndromeof anterior chest pain, Ann. Int. Med. 51:461,1959. 2. Wehrmacher, W. H.: The painful anterior chestwall syndromes,M. Clin. North America 42:111,19.58. 3. Engel, G. L.: Pseudoangina, AM. HEART J. 59:532, 4.
5. 6. 7. 8. 9.
10.
11. 12. 13.
14.
15.
1961.
Gill, A. M., Jones,R. A., andPollack,L.: Tietze’s disease(nonsuppurativenonspecificswellings of rib cartilage),Brit. M. J. 2:1955,1942. Prinzmetal,M., and Massumi,R. A.: The anterior chestwall syndrome:chestpainresembling pain of cardiacorigin, J.A.M.A. 157:177,1955. Eckerson,L. B., Roberts,G. H., and Howard, T.: Thoracic pain persistingafter coronary thrombosis,J.A.M.A. 9:1780,1928. Edwards,W. L. J.: Musculoskeletal chestpain followingmyocardialinfarction, AM. HEART J. 49:713,1955. Jones,Logan: Personalcommunication. Russek,H. I., Russek,A. S., Doener,A. A., and Zohman,B. L.: Cortisonein the treatment of shoulder-handsyndrome following acute myocardial infarction, A.M.A. Arch. Int. Med. 91:487, 1953. Reeves, T. J., and Harrison, T. R.: Problems in the evaluation of pain in the chest, Mod. Concepts Cardiovas. Dis. 27:461, 1958. Harrison, T. R.: Palpation of the precordial impulses, Stanford M.-Bull. 13:385, 195.5. Lewis. T.: Pain. N. Y.. 1942. Macmillan. Wood; P., McGregor, M., Magi&on, O., and Whitaker, W.: The effort test in angina pectoris, Brit. Heart J. 12:363, 1950. Scherf, D., and Schaffer, A. I.: The electrocardiographic exercise test, AM. HEART J. 43:927, 1952. Lepeschkin, E., and Surawicz, B.: Characteristics of true-positive and false-positive results of electrocardiographic Master two-step exercise tests, New England J. Med. 258:511, 1958.
Angina pcturis wieh coexis+ing
skebal
&es+
pin
James B. McElroy, M.D.” Birmingham, Ala.
T
here are many excellent reports describing innocent causes of chest pain which may be confused with ischemic heart disease.‘-6 However, the frequent coexistence of angina pectoris with skeletal chest pain has not been sufficiently emphasized. In 1928, Eckerson and associates6 reported on 4 patients who, after a myocardial infarction, had persistent discomfort in the anterior chest not due to further myocardial ischemia. They attributed the pain to the presence of the myocardial scar. Musculoskeletal chest pain after myocardial infarction was found in 13 per cent of 60 patients studied by Edwards.7 In many of these patients the innocent disorder was confused with myocardial ischemia or necrosis. Others.8 have been impressed with the frequency of complaints of pain in the anterior chest wall after myocardial infarction, for a period of time up to 9 to 12 months. The present report indicates that a similar pain often exists in patients with angina pectoris who have no evidence of myocardial infarction. This study was undertaken to test the validity of our clinical impression that skeletal chest pain is more common in patients with angina pectoris than in individuals of the same age decade and sex who have no heart disease, and to suggest a diagnostic approach to these often difficult patients.
Plan
of study
The records of 2,213 referred medical patients were reviewed. Three hundred and three patients presented convincing evidence of angina pectoris. Three hundred and three control subjects were selected at random, except that the absence of any clinical evidence of heart disease was stipulated, and these were paired by age decade and sex with the patients of the angina pectoris group. The incidence of anterior chest pain of skeletal origin was determined for both groups. Angina pectoris group. A diagnosis of angina pectoris was made in 303 patients. Inclusion in this group was based on one or more of the following criteria, in addition to whether the history was typical or atypical : 1. POSITIVE
ELECTROCARDIOGRAPHIC
TEST.
From the Department of Medicine, Medical College of Alabama, Birmingham, Ala. Supported by The Pure Oil Foundation and The John Seward Johnson Charitable Trust. Received for publication May 11. 1962. *Instructor in Medicine. Medical College of Alabama, Address: 1316 South 19th St., Birmingham
296
EXER-
This is defined as a postexertional depression of the entire S-T segment below the base line (P-R segment) of at least 1 mm. in any lead, and having either a horizontal or sagging configuration. A depressed S-T junction which rose acutely into a T wave was not regarded as an indication of myocardial ischemia. Arrhythmias, conduction defects, and isolated T-wave changes alone after exercise were not considered to constitute a positive test. In patients who were taking digitalis, electrocardiographic changes after exercise CISE
5, Ala.
Vokme
Number
66 3
Angina
pectoris zwith coexisting skeletal chest pain
were not used as a criterion for the diagnosis of angina pectoris. 2. PROMPT AND COMPLETE RELIEF OFPAIN BY NITROGLYCERIN. Prompt is defined as within 10 minutes, and the word complete emphasizes that many patients with skeletal pain frequently state that they obtain some degree of relief, but not complete relief as is seen in most instances of angina pectoris. 3. CONSISTENT INCREASE IN THE AMOUNT OF EXERCISE DISCOMFORT PARED WITH
REQUIRED TO INDUCE CHEST AFTERNITROGLYCERIN AS COMA PLACEBO CONTROL. When
chest discomfort came on during exercise, the test was stopped immediately. The duration of exercise and the number of ascents required to precipitate pain were noted. The same rate of exercise was repeated after a placebo (saccharin tablet) and, finally, nitroglycerin; the patient rested 4.5 minutes between each exercise attempt. These tests were repeated several times on separate days under conditions which were similar as regards relationship to meals, emotional stress, and environmental temperature. To satisfy this criterion, the amount of exercise required to induce chest discomfort must be consistently increased approximately 50 per cent or more after nitroglycerin, with little or no increase after a placebo. Control group. Three hundred and three control subjects were selected at random, except that the absence of any clinical evidence of heart disease was stipulated. All had normal resting electrocardiograms, and the majority were exercised to their physical tolerance and exhibited a normal postexertional tracing. In all patients who had a history of chest pain, negative results were demonstrated by all of the objective criteria listed for the angina pectoris group Subjects from the control group who showed any of the following questionable changes in t.heir postexertional electrocardiograms were excluded : (1) depression of the entire S-T segment below the base line (P-R segment) of 0.5 minute or more, with a horizontal or sagging contour (S-T segment depressions of 0.5 mm. to less than 1 mm. were regarded as borderline) ; (2) arincluding ventricular, nodal, rhythmias, or atria1 premature contractions; (3) tran-
297
sient conduction defects; (4) T-wave inversions. Patients with benign arrhythmias or a history of palpitation were also omitted from this study. Patients were excluded from both groups when any one of the following conditions existed: (1) shoulder-hand syndrome; (2) valvular or congenital heart disease; (3) hiatal hernia, peptic ulcer, or gall-bladder disease; (4) history or clinical evidence of syphilis; (5) myocardial infarction without angina pectoris., Criteria for the presence of skeletal chest pain. The diagnosis of skeletal chest pain was made when a patient presented with a complaint of pain having the following characteristics: (1) Long duration, i.e., several weeks or more (as opposed to acute skeletal chest pain which sometimes follows some recent unusual effort or strain). (2) Described as a soreness, aching, tenderor sometimes as ness, sharp knifelike, tightness, (3) Intensity commonly minimal to moderate but occasionally severe. (4) Usually felt over the precordium, beneath the sternum, at the xiphoid, or at the chondrosternal or costochondral junctions. (5) At times well localized to a small area but usually diffuse. (6) Occasionally radiates into left arm. (7) Onset usually very gradual over many minutes, but at times practically instantaneous in that the maximal intensity is reached almost with the first sensation of discomfort. (8) Lasting seconds or hours (but not for a few minutes only). (9) Intensity usually waxes and wanes with specific body movements but may be constant. (10) Not usually precipitated by factors that increase cardiac work, such as exercise, emotional stress, and the postprandial state. (11) Not promptly and completely relieved by nitroglycerin. (12) Often associated with local tenderness. (13) Favorably affected by salicylates, warmth, local injections of procaine, and sometimes by steroidal hormones. Results Of the 303 patients with angina pectoris, 155 (51 per cent) had clinical evidence of anterior skeletal chest pain, whereas in the 303 control subjects, only 70 (23 per cent) exhibited this disorder (Table I). These
298
Am. Heart J. Sefitember, 1963
McElroy
Table I Number (angina1
in each group and control)
20-29 30-39 40-49 SO-59 60-69 IO-79 SO-90
:z 120 93 19 2
Totals
303
(number
1
data were analyzed by the chi square technique and were found to be highly significant (p < .OOl). The records of 1.50 of the 155 patients with both angina pectoris and anterior skeletal chest pain afforded reasonably certain evidence whether a prior myocardial infarction had occurred. Seventynine (53 per cent) of these 150 patients had no evidence of myocardial infarction. Discussion
These findings demonstrate that (at least in this series of patients) anterior skeletal chest pain is more common in patients with angina pectoris than in individuals of the same age decade and sex with healthy hearts. It was also found that skeletal chest pain often exists in patients with angina pectoris in the absence of evidence of myocardial infarction. It is likely that the incidence of chest wall pain found in the control subjects (23 per cent) is higher than in the comparable general population. All of these patients were referred by physicians, and in many instances the chest pain constituted the chief reason for such referral. This circumstance would tend to further increase the marked difference already noted in the incidence of skeletal chest pain in the two groups. The skeletal chest pain reported here seemsto be analogous to that of the shoulder-hand syndrome, although lessdramatic and without local swelling or involvement of the shoulders and hands. Presumably, a similar mechanism exists for both conditions. Skeletal chest pain may exist with the shoulder-hand syndrome, but patients
Angina1 group with skeletal
pain)
(number
Control group with skeletal
1 8 30 58 46 10 2 ~--
1 5 10 36 16 2 0 __-
1.55 (51%)
70 (23%)
pain)
who had involvement of the shoulders or hands were excluded from this study. Although the two conditions present entirely different clinical pictures, it is of interest that both have occasionally responded, at times dramatically, to oral cortisone therwy.g Certain conditions, such as distention of abdominal viscera, are known to cause reflex constriction of the coronary arteries; but this probably never induces angina1 pain in normal subjects.‘O In some patients with coronary atherosclerosis, however, skeletal chest pain can apparently precipitate angina1 attacks. We have observed several patients with typical angina pectoris whose pain and electrocardiographic changes could be produced by the skeletal chest pain acting as a trigger. The following case historyillustrates this phenomenon. Patient B. K. This .54-year-old white woman had had her first episode of chest pain 3 years prior to hospitalization. While planting flowers, she was seized with a severe, vise-like substernal constriction which radiated into both arms and hands and the anterior neck. A few minutes later she became un; conscious. A myocardial infarction was documented. In the subsequent ‘2 years, she sustained two other myocardial infarctions at approximately yearly intervals. For 2% years she had also had typical angina1 pain. Walking precipitated the discomfort only if undertaken within 2 to 255 hours after a meal, whereas excitement or anger readily induced pain. An identical discomfort would always follow the brushing of her teeth, bending forward, and certain specific movements of the arms, such as raising both arms above her head or reaching for an object on a high shelf. Nitroglycerin would consistently relieve the pain completely within 5 minutes. The patient was not aware of any other type of chest discomfort. Gall-bladder and gastrointestinal x-ray films were normal. Physical examination revealed a small pre-
Volune Number
66 3
Angina
pectoris with coexisting skeletal chest pain
cordial liftrr and a Grade 1, short, late systolic apical murmur. A resting electrocardiogram showed abnormal Q waves in Leads II, III, and aVF, with normal S-T segments and T waves in all 12 leads. When seen at the time of a ward visit on the following day, she exclaimed that she had just finished brushing her teeth and was having an episode of chest pain. Examination revealed a marked visible, as well as palpable, precordial lift, and during the pain the previously described Grade 1 murmur was of Grade 4 intensity. After nitroglycerin, the pain promptly subsided. The precordial lift was no longer visible and was barely palpable. The Grade 4 murmur returned to Grade 1 intensity. Several subsequent examinations revealed that the motion of her right arm, as used in brushing her teeth, would regularly induce angina1 pain and the above-described physical findings, together with marked depression and sagging of the S-T segments in the electrocardiogram. It was found that firm pressure upon the third left chondrosternal junction would regularly induce angina1 pain, with the attendant changes, whereas pain, to the point of weeping, by pressure on the Achilles tendon and fingernail, would cause none of the above-mentioned reactions. After procaine anesthetization of this tender area, neither the application of firm pressure nor any arm movement resulted in angina1 pain.
The obvious conclusion drawn from these observations is that the skeletal tissues were capable of initiating reflex coronary constriction and angina1 attacks in this patient with advanced coronary artery disease. A similar patient has been reported on by Reeves and Harrison,‘O During an attack of angina1 pain, a precordial lift resulting from local ballooning of ischemic muscle may be identified occasionally in patients by special techniques, such as the kinetocardiogram, and by palpation in a somewhat lesser number.” We have, on rare occasions, detected for the first time a short, late, apical systolic murmur in patients during angina1 pain. Presumably, this finding is due to distortion of papillary muscles as the result of focal myocardial ischemia. Angina1 pain and characteristic electrocardiographic changes have occasionally been noted in our own patients with angina pectoris and a coexisting hiatal hernia, by distention of the stomach with air. Presumably, these phenomena are caused by reflex coronary constriction. In any patient with a complaint of chest pain, it is important to first exclude angina pectoris beyond any reasonable doubt before other causes of the discomfort are
299
sought. The presence of ischemic heart disease can usually be determined by a careful history when the complaints are typical. Skeletal chest pain which coexists with angina pectoris frequently modifies the symptoms of both disorders, so that an extremely puzzling situation results. In a considerable fraction of our own patients with both angina pectoris and skeletal chest pain, the more important ischemic pain was confused with or even masked by the coexistence of the innocent disorder. There is sound experimental evidence for the view that visceral pain and deep skeletal pain are mediated through a common deep sensory system.r2 It is not surprising that their characteristics should be similar, and that, on occasion, differentiation between the two may be extremely difficult. The importance of a careful and thorough history in evaluating any chest pain cannot be overemphasized. When the history is inconclusive, evaluation of the postexertional electrocardiogram and observation of the effect of nitroglycerin on the response to exercise discussed earlier will frequently be of crucial diagnostic value in determining whether angina pectoris exists. The reader is referred to the excellent papers of Wood,rS Scherf,14 and Lepeschkin15 for further details of the electrocardiographic exercise test. In the patient with atypical or puzzling chest pain, usually due to the coexistence of skeletal chest pain with angina pectoris, we believe that this approach offers a means whereby a reasonably certain answer can be obtained, and thus will frequently enable the physician to find the in the “haystack” of angina1 “needle” skeletal chest pain. The results reported here indicate that skeletal chest pain is more common in patients with angina pectoris than in individuals of the same age decade and sex with healthy hearts. Therefore, it is important to institute a meticulous search for angina pectoris in any patient presenting with obvious chronic skeletal chest pain. Summary
The records of 2,213 referred medical patients were reviewed. Three hundred and
300
Am. Heart .I. Sefitsmber, 1963
McElroy
three patients presented convincing clinical evidence of angina pectoris. An equal number of control subjects was randomly chosen on the basis of an absence of any cardiac disorder and were paired as to age decade and sex with the patients of the angina pectoris group. The incidence of anterior skeletal chest pain was determined for both groups. Clinical evidence of anterior chest pain of skeletal origin was present in 51 per cent of the patients with angina pectoris and 23 per cent of the control subjects. This represents a significant difference by chi square analysis (p < .OOl). In patients with angina pectoris, skeletal chest pain frequently occurs in the absence of a prior myocardial infarction. In some patients with angina pectoris and coexisting skeletal pain, the skeletal disorder may precipitate attacks of angina1 pain. A case history which demonstrates this phenomenon of “reflex angina” is presented. In a considerable fraction of the patients with angina pectoris the more important ischemic pain was confused with or even masked by the coexistence of the innocent disorder. Evidence is presented that skeletal chest pain is more common in patients with angina pectoris than in individuals of the same age decade and sex with healthy hearts. Therefore, it is important to institute a meticulous search for ischemic heart disease in any patient who presents with obvious skeletal chest pain.
REFERENCES 1. Miller,
A. J.,
and
Texidoe,
T.
A.:
The
“pre-
cordial catch,” a syndromeof anterior chest pain, Ann. Int. Med. 51:461,1959. 2. Wehrmacher, W. H.: The painful anterior chestwall syndromes,M. Clin. North America 42:111,19.58. 3. Engel, G. L.: Pseudoangina, AM. HEART J. 59:532, 4.
5. 6. 7. 8. 9.
10.
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