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Factors contributing to delay in responding to the signs and symptoms of acute myocardial infarction
Factors Contributing
to Delay in Responding
to the Signs and Symptoms of Acute Myocardial THOMAS P. HACKETT, M.D. Boston,
Infarction*
and N. H. CASSEM, M.D.
Massachusetts
The delay time between the onset of symptoms and arrival at a medical facility for examination was studied in 100 randomly selected patients who had been admitted to a coronary care unit with a diagnosis of suspected or proved acute myocardial infarction. 1. The delay time did not differ significantly between private and ward patients. In general, the patient with coronary symptoms was apt to respond sooner than later. These patients who delayed 5 or 6 hours could easily have delayed 48 hours or longer. The half-time for reaching medical aid was 3.9 hours. 2. There was no significant relation between delay and age, sex, history of previous myocardial infarctions, socioeconomic scores and presenting symptoms. 3. The time of delay tended to diminish as the subjective severity of the symptoms mounted. However, there was no relation between the severity of the disease, as measured by the Peel score, and the time of delay. 4. There was a significant relation between the source of the symptom and delay. Thus, patients who recognized their heart as causing the symptom sought help sooner than those who displaced the cause to other organ systems. Patients who interpreted the symptom solely in terms of excluding the heart as causal delayed the longest. 5. The role of a second person in initiating the decision to seek help was significant. For the largest. number of patients, a family member made the decision. Spouses appeared to be less successful in reducing delay than friends or associates. The most influential person in reducing delay in our series was an unrelated friend or stranger who was not associated with the patient’s work. 6. Physicians caused or contributed to patient delay in 12 per cent of our cases. They rationalized the delay along the same lines as the patient. Other organ systems were blamed or the pain was minimized by calling it angina. Since referral to the hospital was a simple matter, no adequate reason can be given for the procrastination of these doctors. 7. The defense of denial is commonly used by the patient with coronary disease to control anxiety. The finding that no significant relation could be established between denial and delay in our data is explained. Denial was found to be significantly related to symptom displacement and the influence of another person on delay. Those patients who denied minimally recognized the heart as the source of trouble and did not require outside help to seek the advice of a physician. Patients whose denial was major displaced the source of trouble from the heart to other organ systems and tended to put off consulting a physician until someone else urged them to do so. * From the Department of Psychiatry, Massachusetts General Hospital. This work was performed under contract PHS-43-67-1443 with the National Institutes of Health, Public Health Services, U. S. Department of Health, Education, and Welfare. Address for reprints: Thomas P. Hackett, M.D., Department of Psychiatry, Massachusetts General Hospital, Boston, Mass. 02115. VOLUME
24,
NOVEMBER
1969
651
Hackett
652
D
MEDICAL ADVICE to seek help immediately, most patients with acute myocardial infarction tarry after the onset of chest pain for longer than their physicians desire. Typical delay times between the onset of symptoms and hospital admission reported by various investigators show that it may be common for as many as one third of patients to delay longer than 12 hours (Table I). The emphasis on swift recourse to medical assistance is based upon the high incidence of death shortly after the onset of symptoms. In a personal series, Fry4 reported that 53 per cent of deaths occurred within the first hour. In a more extensive series, Bainton and Peterson5 reported 63 per cent of deaths due to coronary heart disease occurred within the first hour after the onset of symptoms. Thus, it seems reasonable to assume, in accord with Oliver,‘j that 50 to GO per cent of deaths due to myocardial infarction occur within the first four hours. Yet it appears that at least half of such patients who reach medical assistance are likely to have delayed longer than this time. Nevertheless, very little research has been done on the phenomenon of delay as it occurs in acute myocardial infarction. We define delay as the number of hours between the time the patient first experiences cardiac symptoms and when he presents himself at a medical facility for examination. Procrastination, since it implies that the patient rather than external forces is responsible for tardiness, might be a more accurate term except that it suggests a deliberate intent, which is not always the case. Earlier reports7’8 touching on the psychology of delay dealt with painless infarctions of the heart. This area has been recently reviewed by Master and Geller.g Although the majority of these reports seek anatomic reasons for the apparent lack of pain, one sagacious investigatorlO suggested that some patients may deny they have pain-and hence seek no medical help-because they are afraid to know the diagnosis.
Table
ESPITE
I. Summary of Findings on Patient Delay from Onset of Symptoms to Hospital Admission Per Cent of Patients Delaying
Investigator Sloman’ McDonald2 Lawrie et ai.*
and Cassem In an earlier paper ” that specifically discussed delay in coronary disease, it was noted that in 32 patients hospitalized with a diagnosis of myocardial infarction, delay was a common response to chest pain, despite its severity. Eleven of the 32 patients took five or more hours to see a physician, while the remaining 21 visited a physician within five hours. A history of previous attacks of angina or of previous myocardial infarction did not significantly shorten the period of delay. The present study considers some simple observations about the extent and frequency of delay in myocardial infarction and possible correlations between delay and other variables. Although the ultimate goal in ferreting out the facts about delay is to find ways of diminishing it, this presentation will be confined to a description rather than an interpretation of data. METHODS
AND MATERIALS
One hundred randomly selected patients who had been admitted to one of three coronary care units with a diagnosis of proved or suspected myocardial infarction were interviewed and followed up as part of another study.12 These patients could be separated into two groups on the basis of their hospital status; 50 were private patients (group I) and 50 were ward cases (group II). There was no difference in the seriousness of illness between groups since both had comparable Peel prognostic scores” Information on delay was obtained both by interviewing the patient and by examining the hospital chart. RESULTS Table Table
II.
II lists the p’eriod of delay in groups I Incidence
Delay (hr. )
of Delay in 100 Coronary Unit Patients
Care
Group
No.
Totals
1
I II
9 10
19
l-5
I II
18 16
34
I
5 6
11
II 12
I II
11 13
24
9-12
No. of Cases
54 hr.
4-6 hr.
6-12 hr.
>I2 hr.
Special circumstances
I II
6 4
10
350 150 500
25 16 55
18 13 17
20 35 15
32 37 13
Unknown
I II
1 1
2 100
THE
Abl!ZRICANJOURNALOFCARDIOLOGY
Patient
Delay
in Acute
Myocardial
are 2 patients, 1 from each group, whose charts could not be found. Ten additional patients are listed under “special because they were admitted circumstances” after suddenly collapsing either on the street or at home or in the physician’s office; consequently, they could not be used to obtain information on delay. For these reasons, there was a total of 88 cases available for analysis of factors related to delay. There was no significant difference in the incidence of delay between the private and ward cases. Other than their socioeconomic background, neither group could be distinguished on the basis of the 10 variables used; consequently, in subsequent tables no distinction is made between private (group I) and ward (group II) patients. and
11. T,istecl as unknown
INCIDENCE
OF
20
1
DELAY
Further breakdown of delay data demonstrates that the median gives a more accurate representation of central tendency within the sample than does the mean. A few extended delay periods skew the data badly toward the long end, thereby distorting the spread. Mean = 10.6 hours (SD. Median = 4 hours Mode = 1 hour
= 15.8)
Plotting the number of patients per hour against the time of delay gives a rough estimate of rate change (Fig. 1). Examination of this chart reveals that the average victim of a coronary attack is likely to seek help sooner than later. The half-time expended by the group in reaching medical aid was 3.9 hours. As pointed out, four hours after the onset of symptoms is the point at which approximately half of those stricken with myocardial infarction will have died. Sixty-five per cent of our patients arrived for help by the end of six hours. After six hours, the rate abruptly falls. The rate at which patients seek medical care (Fig. 1) seems to be a negatively accelerated function rapidly approaching an asymptote of 1 or less after six hours. This could mean that the patient who waits 7 hours could as easily delay 48 hours. Since half of all coronary victims are believed to be dead within four hours of symptom onset, the factors that contribute to a prompt or a tardy response within this critical cluster of hours are essential to identify. FACTORS
ASSOCIATED
WITH
DELAY
Eleven variables were selected as possibly relevant to delay. These were age, sex, socioVOLUME
24,
6Ei3
Infarction
NOVEMBER
1969
0
2
4
6
8
10
30
HOURS
Figure 1.
Rate at which patients seek medical care for coronary symptoms as a function of time from onset of symptoms.
economic status, number of previous myocardial infarctions, type of presenting symptoms, severity of presenting symptoms, admission prognostic scores, displacement of symptoms, influence through advice of another person, physician delay, and the use of denial. Age: As the data indicate (Table III), several older patients did indeed delay longer. However, the age-delay regression was not statistically significant. Sex: Even though the median and mean delay of women was longer than that for men, this difference was not statistically significant (Table III).
Prior Myocardial Infarction: The population was divided into three groups: (1) those with no prior myocardial infarction; (2) those with one prior myocardial infarction; and (3) those with two or more. There is no evidence to support the notion that having experienced a myocardial infarction makes delay less likely on subsequent infarctions (Table III). Socioeconomic Status: A socioeconomic score based upon occupation, income and education was assigned to each patient. These were derived
654
Hackett Table
Factor
Age (yr.1
III.
and Cassem
Relation Between Twelve Factors and Duration of Delay
No.
Median (hr. 1
Mean & S.D. (hr. )
34 26 28 88
4.0 4.0 5.0
64 24 88
4.0 5.0
57 27 4 88
4.0 5.0 2.6
16 20 24 60
4.4 4.0 4.2
57
5.0
12.0
f
17.8
25 3 85
4.0 1.0
9.2 1.7
f f
12.0 0.8
Severity of symptoms Mild Moderate Moderate-severe Severe Total
3 10 11 61 85
24.0 24.0 5.0 4.0
Peel scores l-8 9-12 13-16 517 Total
35 23 22 8 88
4.8 3.0 5.0 4.8
Displacement of symptoms Heart Gastrointestinal Not heart Total
29 17 5 51
2.0 5.0 24.0
InfIuence of another No Yes Total
33 37 70
2.0 5.5
Sources of inlluence Nonfamily work Work Family Total
6 8 23 37
2.0 4.8 12.0
154 55-64 >65 Total Sex Male Female Total
Prior myocardial infarctions 0 1 2 Total 159 60-79 80-99 Total Presenting symptoms Chest pain alone Chest pain and dyspnea Dyspnea alone Total
10.7 8.5 12.7
10.4 11.9
11.0 11.0 3.8
15.1 9.7 9.8
26.8 22.4 8.1 8.1
Linear Regression r
P
f 18.2 f11.3 f 16.6 $0.087
N.S.
-0.047
N.S.
-0.056
N.S.
-0.057
N.S.
+o.
N.S.
f 16.2 f15.4
fl6.9 f 14.8 f 3.7
f25.18 f12.5 f 12.2
f f f f
133
19.9 17.6 8.5 14.9 -0.324
11.8 7.5 11.9 11.6
3.5 14.7 25.0
5.4 13.0
0.01
f 18.6 f 10.7 f 15.8 fl4.5 -0.064
N.S.
+0.442
+0.253
<0.05
+0.317
<0.05
f 4.9 z!z 24.0 f22.5
* f
2.33 f 8.81 f 17.22 i
9.3 18.4
1.9 9.5 21.6
N.S. = not significant. THE
AMERICAN
JOURNAL
OF
CARDIOLOGY
Patient
Delay in Acute Myocardial
from prc-established census data from the U. S. Bureau of Census.4 There was no significant correlation between these scores and delay time (Table III). It appears that neither education nor income bracket insures a more prompt response to the signs and symptoms of myocardial infarction. Presenting Symptoms. Table III shows that more than half the patients presented with chest pain alone, but over a quarter had dyspnea as well. The category “other” included sweating, palpitations, numbness of fingers, and dizziness with weakness. Those patients with dyspnea alone had the shortest delay time. The small size of the group detracts, of course, from the significance of this finding. It is our impression that the appearance of dyspnea considerably shortens the tendency to prolong delay. Our data, measured from the onset of the first symptom, does not allow us to isolate this phenomenon. Shortness of breath may induce anxiety along the lines described in the James-Lange theory. This notion is appealing in its simplicity. On the other hand, the presence of dyspnea may signal the presence of genuine heart disease to the patient. One man, who delayed several hours despite severe chest pain, decided to consult his physician when his breathing became labored. He explained his delay by saying, “If it doesn’t affect your breathing, it can’t be your heart.” .Cuerity of Symptoms.. Although it is difficult to classify a symptom as subjective as pain or as individually variable as shortness of breath, we have attempted to do so. Since we seldom saw the patient at the time he was admitted to the emergency ward, our rating is based upon notes in the chart by the admitting physician along with the patient’s own retrospective estimation of discomfort. Table III presents the distribution. Contrary to our earlier work4 these data reveal what appears to be a positive relation between severity of symptom and length of delay (p 0.01). As the rated severity of symptoms increased, patients sought help more rapidly. More Objective Evaluation of Severity: Since there is some question about the reliability of rating the severity of symptoms and because our findings are contrary to previous work,l’ we have looked at these data from another standpoint. The Peel prognostic index, which offers an objective assessment of the patient’s over-all organic illness, was scored for each patient at the time of admission. The Peel scores were divided into four groups. The expected morVOLUME24, NOVEMBER1969
Infarction
655
tality for each group score was as follows: l-8 = 2.5 per cent, 9-12 = 12.5 per cent, 13-16 = 23.7 per cent, and above 17, 63.7 per cent. It was found that the aVerage patient, with a mean score of 10.2, fell into the category in which expected mortality is about 12.5 per cent. There was no significant relation between delay and the various prognostic groups (Table III). Thus, while it may be true that, as the symptoms become more severe, the patient is less apt to delay, the same does not hold for the severity of the disease itself. One cannot say that the worse the disease, the more swiftl>. the patient is apt to seek medical help. Displacement of Symptoms: Previous work” demonstrated that the patient may interpret the symptoms of cardiac difficulty as originating from sources other than the heart. The incidence of this displacement is presented in Table III. Sufficient information for inclusion in this section was available for only 56 of the 88 patients. Twenty-nine, half the sample, knew their symptoms stemmed from the cardiovascular system, a realization that was immediate in all but 3 patients. Those 3 realized that the source was the heart as pain increased. Four patients attributed the symptoms to their lungs and 1 to his “nerves.” Those people who referred symptoms to their gastrointestinal tract thought that they had “gas” or “indigestion.” A few blamed the gall bladder and 1 ascribed the symptoms to hiatus hernia. Those who indicted the lungs blamed “smoke-filled rooms,” or too man) cigarettes, and the like. The 5 remaining patients shared the disbelief that the heart was at fault. Patients who recognized the true source of their trouble came for help much sooner. This relation was significant at the 0.01 level. Of the patients who attributed symptoms to the gastrointestinal tract, none came to a physician within the first hour. The group who interpreted their symptoms simply as not coming from the heart delayed the longest, by far. Thus, we have something of a spectrum effect, with acknowledgment of the heart as the responsible agent at one end and denial of even the possibility that it is the offender at the other extreme. In between are patients who displace the source of trouble to organ systems of which acute involvement was less forbidding than the heart. It is not at all clear why patients chose the gastrointestinal tract or respiratory system rather than the heart. The most logical explanation.
Hackett and Cassem
656 Table IV. Incidence of Delay by Physicians
Physician Delay
No. of Patients
Physicians Outside Hospital
Yes
12
No
69
Swift referral to emergency ward
18
18
1 100
28
Unknown Total
10
which may be incorrect, is that trouble with these other organ systems is usually not as dangerous as cardiac disease. Moreover, most individuals have had “indigestion” and “lung congestion ” in the past and successfully survived them. Given a choice of alternative explanations for pain in the chest, it is not unreasonable to assume that the sufferer would choose a condition unlikely to threaten his life, preferably one that he had experienced and overcome in the past. The Influence of Another Person on Patient Delay: Earlier studies” have indicated that probably the most important factor in reducing patient delay has been the influence of another person upon the patient’s decision to seek medical help. The distribution of those who required this influence is presented in Table III. Who this other person was is also shown in Table III. One can see from this analysis that for the largest number of patients in the study, it was a family member who convinced the patient to seek medical aid. It is also clear that the patient who decides to seek medical assistance on his own comes faster than one who needs help with that decision. A bimodal response curve could be envisaged in which those who decide for themselves come early and those unable to decide come late. If one assumes that those who delay do so because they tend to deny the significance of their symptom-even in the face of severe pain and despite an awareness that the heart may be involved-then the only effective type of interruption of delay is from another person who correctly interprets the facts by stripping away denial. Spouses appear to be less influential in reducing delay than friends or associates. The median delay for those assisted by family members was 12 hours compared to 2 hours for those assisted by friends. In a number of instances, it
was an insistent employer who literally ordered the patient to the hospital. When the source of influence was put to statistical test, the unrelated person who was not work-associated (either friend or stranger) was most effective in producing prompt action by the patient with coronary symptoms. Physician Delay: Occasionally, before the patient reaches the hospital, he may have contact with a physician either by phone or in person. It sometimes happens that despite genuine coronary symptoms the patient’s arrival at the hospital may be delayed by the physician himself. The incidence of this phenomenon in our study is presented in Table IV. Twelve of 100 patients were delayed in being hospitalized by a physician. The physician employed the same maneuvers used by patients who delayed. He either blamed other organ systems or minimized the pain by calling it angina. In some cases, medication was given and the patient was instructed to wait. In other cases, an appointment was made for an office visit the next day. The 28 physicians involved had offices outside the hospital and could easily have taken the opportunity to refer the patient to a hospital for definitive diagnosis. Eighteen did so swiftly. The remaining 10, largely for reasons unknown, delayed the patient’s entrance. One of the delaying doctors later admitted that he thought his patient was simply exaggerating his pain. In fact, this same physician doubted that the patient had true coronary disease until it was amply demonstrated angiographically. The Defense of Denial: The defense mechanism of denial is defined as the conscious or unconscious repudiation of part or all of the total available meaning of an event to allay fear, anxiety, or other unpleasant affects.15 The term major denial is used to describe patients who stated unequivocally that they felt no fear at any time throughout their hospitalization. Partial denial describes those who initially denied fright but eventually admitted feeling at least some fear. “Minimal denial” is applied to patients who complained of anxiety or who readily admitted being frightened; they showed no consistent criteria for denial. One would expect that the tendency to deny would correlate significantly with the tendency to delay. Statistical analysis fails to show a significant relation between time of delay and extent of denial (Table v). This raises obvious questions that strike at the core of our concept of denial. THE
AMERICAN
JOURNAL
OF CARDIOLOGY
Patient Table
Denial
No. of Cases
Minimal Partial Ma.jor Total
16 62 20 98
Delay in Acute Myocardial
Relation Between Denial and Duration
V.
Median
Mean =t S.D.
5.2 4.0 5.0
12.0 f 18.2 8.9 f 11.9 15.8 f. 23.9
VI.
of Delay Linear Regression r
/r
N.S.
$0.130
If we turn to other variables for correlation with denial (Table VI), some interesting features appear. All those who demonstrated minimal denial knew the source of their symptoms. Denial was significantly related to symptom displacement (p < 0.05). With 2 exceptions, all those who showed major denial displaced their symptoms to other organ systems. The 2 exceptions are worth comment. One was the man, mentioned before, who had a special understanding with his cardiologist. The other patient turned out to have cholecystitis, not a coronary attack. If we correlate the influence of another person on delay with the type of denial, we find a trend for the degree of denial to be related to the source of decision making (0.10 < p < 0.20). This suggests that the person who denies minimally does not need much outside help to seek a physician for coronary symptoms. Those whose denial is major will delay seeking help unless someone else goads them into action. Those who partially deny occupy a mid-way position.
Why should some of those who demonstrated ma,jor denial reach a physician within one hour? The explanation is fairly simple. In all there were 5 such patients. In 2, symptoms developed while they were with someone who immediately sent thern to the hospital. Two others had symptoms that had been present but denied days before their actual entry into the hospital. The fifth was a man who maintained a special relation with his cardiologist. Their agreement was that if three nitroglycerine tablets did not relieve severe pain, he was to enter the emergency ward, which the patient did in a nonchalant, almost indifferent manner. Six who showed major denial were admitted within one to five hours. How can we explain this? One entered the hospital with a diagnosis of cholecystitis and fully expected his pain to be from the gall bladder. A second, brought in by relatives, had acute pulmonary edema, having been cared for at home through the previous week. The third, sent to the hospital by an industrial nurse, protested that all he wanted was an antacid for heartburn. No reason could be given by the fourth patient as to why she entered when she did and none was subsequently found. The last 2 patients appeared to both staff and investigators as terrified, although they denied fear. These reasons may explain why those who showed major denial behaved in what might be considered a paradoxical way. Table
657
Infarction
CONCLUSION If the population at large responds to the first symptom of myocardial infarction in a manner similar to the patients we have described, there is little doubt that delay contributes heavily to the national death rate. As this study demonstrates, we know almost nothing about the social, psychological, or genetic factors that facilitate
Factors Associated with Denial -
Denial
P
Minimal
Partial
Displacement of symptoms Heart Gastrointestinal
6 0
22 19
2 4
6.06749
2
0.02
Influence of another No Yes
4 1
24 27
5 10
3.30743
2
0.10
--
VOLUME
24, NOVEMBER
1969
Major
X2
df
658
Hackett
or inhibit the process of delay. Perhaps the most valuable lessen to draw from our findings is that traditional convictions are often wrong. A college education and familiarity with the symptoms of coronary disease do not guarantee a prompt and appropriate response. As yet we have no specific alternative method to propose for reducing delay, but that may come in time. This symposium has made the first advance by emphasizing the relevance of investigating delay. It is a beginning.
REFERENCES 1. SLOMAN, G. Coronary units: The Royal Melbourne Hospital. In: Acute Myocardial Infarction, pp. 8-12. Baltimore, 1968. Williams & Wilkins. 2. MCDONALD, E. L. The London Hospital. In Ref. 1, pp. 29-32. 3. LAWRIE, D. M., GREENWOOD, T. W., GODDARD, A coronary care unit in the routine M. et al. management of acute myocardial infarction. Lancct, 2:109, 1967. 4. FRY, J. Acute myocardial infarction in a British general practice. In Ref. 1, pp. 304-309. 5. BAINTON, C. R. and PETERSON, D. R. Deaths from coronary heart disease in persons 50 years of age and younger. New England J. Med., 268~569, 1963.
and Cassem 6. OLIVER, M. F. From data cited by BONDURAN.~, S. Symposium on the Pre-hospital Phase of Acute Myocardial Infarction, Rochester, N. Y. May 17-18, 1969. (This issue, pp. 612-616.) 7. ROSEMAN, M. D. Painless myocardial infarction: Review of literature and analysis of 220 cases. Ann. Int. Med., 41:1, 1954. 8. BRUENN, H. G., TURNER, K. B. and LEVY, R. L. Notes on cardiac pain and coronary disease: Correlations of observations made during life with structural changes found at autopsy in 476 cases. Am. Heart J., 11:34, 1921. 9. MASTER, A. M. and GELLER, A. J. The extent of asymptomatic coronary artery disease. Am. J. Card&., 231173, 1969. 0. BABEV, A. M. Painless acute infarction of the heart. New England J. Med., 220:410-412, 1939. 1. OLIN, H. S. and HACKETT, T. P. The denial of chest pain in 32 patients with acute myocardial infarction. J.A.M.A., 190:977, 1964. 2. MIRU: Task n; Psychiatric Studies; Contract No. PH 43-67-1443. 13. PEEL, A. A. F., SEMPLE, ‘r., WANG, I., LANCASTER, W. M. and DALL, J. L. G. .4 coronary prognostic index for grading the severity of infarction. Brit. Heart J., 24: 745, 1962. 14. U. S. Bureau of Census. Methodology and Score of Socioeconomic Status. Working Paper No. 15. \Vashington, D. C. 1963. 15. WEISMAN, A. D. and HACKETT, T. P. Predilection to death: Death and dying as psychiatric problems. Pqchosom. Med., 23:232, 1961.
THE
AMERICAN
JOURNAL
OF CARDIOLOGY
to Delay in Responding
to the Signs and Symptoms of Acute Myocardial THOMAS P. HACKETT, M.D. Boston,
Infarction*
and N. H. CASSEM, M.D.
Massachusetts
The delay time between the onset of symptoms and arrival at a medical facility for examination was studied in 100 randomly selected patients who had been admitted to a coronary care unit with a diagnosis of suspected or proved acute myocardial infarction. 1. The delay time did not differ significantly between private and ward patients. In general, the patient with coronary symptoms was apt to respond sooner than later. These patients who delayed 5 or 6 hours could easily have delayed 48 hours or longer. The half-time for reaching medical aid was 3.9 hours. 2. There was no significant relation between delay and age, sex, history of previous myocardial infarctions, socioeconomic scores and presenting symptoms. 3. The time of delay tended to diminish as the subjective severity of the symptoms mounted. However, there was no relation between the severity of the disease, as measured by the Peel score, and the time of delay. 4. There was a significant relation between the source of the symptom and delay. Thus, patients who recognized their heart as causing the symptom sought help sooner than those who displaced the cause to other organ systems. Patients who interpreted the symptom solely in terms of excluding the heart as causal delayed the longest. 5. The role of a second person in initiating the decision to seek help was significant. For the largest. number of patients, a family member made the decision. Spouses appeared to be less successful in reducing delay than friends or associates. The most influential person in reducing delay in our series was an unrelated friend or stranger who was not associated with the patient’s work. 6. Physicians caused or contributed to patient delay in 12 per cent of our cases. They rationalized the delay along the same lines as the patient. Other organ systems were blamed or the pain was minimized by calling it angina. Since referral to the hospital was a simple matter, no adequate reason can be given for the procrastination of these doctors. 7. The defense of denial is commonly used by the patient with coronary disease to control anxiety. The finding that no significant relation could be established between denial and delay in our data is explained. Denial was found to be significantly related to symptom displacement and the influence of another person on delay. Those patients who denied minimally recognized the heart as the source of trouble and did not require outside help to seek the advice of a physician. Patients whose denial was major displaced the source of trouble from the heart to other organ systems and tended to put off consulting a physician until someone else urged them to do so. * From the Department of Psychiatry, Massachusetts General Hospital. This work was performed under contract PHS-43-67-1443 with the National Institutes of Health, Public Health Services, U. S. Department of Health, Education, and Welfare. Address for reprints: Thomas P. Hackett, M.D., Department of Psychiatry, Massachusetts General Hospital, Boston, Mass. 02115. VOLUME
24,
NOVEMBER
1969
651
Hackett
652
D
MEDICAL ADVICE to seek help immediately, most patients with acute myocardial infarction tarry after the onset of chest pain for longer than their physicians desire. Typical delay times between the onset of symptoms and hospital admission reported by various investigators show that it may be common for as many as one third of patients to delay longer than 12 hours (Table I). The emphasis on swift recourse to medical assistance is based upon the high incidence of death shortly after the onset of symptoms. In a personal series, Fry4 reported that 53 per cent of deaths occurred within the first hour. In a more extensive series, Bainton and Peterson5 reported 63 per cent of deaths due to coronary heart disease occurred within the first hour after the onset of symptoms. Thus, it seems reasonable to assume, in accord with Oliver,‘j that 50 to GO per cent of deaths due to myocardial infarction occur within the first four hours. Yet it appears that at least half of such patients who reach medical assistance are likely to have delayed longer than this time. Nevertheless, very little research has been done on the phenomenon of delay as it occurs in acute myocardial infarction. We define delay as the number of hours between the time the patient first experiences cardiac symptoms and when he presents himself at a medical facility for examination. Procrastination, since it implies that the patient rather than external forces is responsible for tardiness, might be a more accurate term except that it suggests a deliberate intent, which is not always the case. Earlier reports7’8 touching on the psychology of delay dealt with painless infarctions of the heart. This area has been recently reviewed by Master and Geller.g Although the majority of these reports seek anatomic reasons for the apparent lack of pain, one sagacious investigatorlO suggested that some patients may deny they have pain-and hence seek no medical help-because they are afraid to know the diagnosis.
Table
ESPITE
I. Summary of Findings on Patient Delay from Onset of Symptoms to Hospital Admission Per Cent of Patients Delaying
Investigator Sloman’ McDonald2 Lawrie et ai.*
and Cassem In an earlier paper ” that specifically discussed delay in coronary disease, it was noted that in 32 patients hospitalized with a diagnosis of myocardial infarction, delay was a common response to chest pain, despite its severity. Eleven of the 32 patients took five or more hours to see a physician, while the remaining 21 visited a physician within five hours. A history of previous attacks of angina or of previous myocardial infarction did not significantly shorten the period of delay. The present study considers some simple observations about the extent and frequency of delay in myocardial infarction and possible correlations between delay and other variables. Although the ultimate goal in ferreting out the facts about delay is to find ways of diminishing it, this presentation will be confined to a description rather than an interpretation of data. METHODS
AND MATERIALS
One hundred randomly selected patients who had been admitted to one of three coronary care units with a diagnosis of proved or suspected myocardial infarction were interviewed and followed up as part of another study.12 These patients could be separated into two groups on the basis of their hospital status; 50 were private patients (group I) and 50 were ward cases (group II). There was no difference in the seriousness of illness between groups since both had comparable Peel prognostic scores” Information on delay was obtained both by interviewing the patient and by examining the hospital chart. RESULTS Table Table
II.
II lists the p’eriod of delay in groups I Incidence
Delay (hr. )
of Delay in 100 Coronary Unit Patients
Care
Group
No.
Totals
1
I II
9 10
19
l-5
I II
18 16
34
I
5 6
11
II 12
I II
11 13
24
9-12
No. of Cases
54 hr.
4-6 hr.
6-12 hr.
>I2 hr.
Special circumstances
I II
6 4
10
350 150 500
25 16 55
18 13 17
20 35 15
32 37 13
Unknown
I II
1 1
2 100
THE
Abl!ZRICANJOURNALOFCARDIOLOGY
Patient
Delay
in Acute
Myocardial
are 2 patients, 1 from each group, whose charts could not be found. Ten additional patients are listed under “special because they were admitted circumstances” after suddenly collapsing either on the street or at home or in the physician’s office; consequently, they could not be used to obtain information on delay. For these reasons, there was a total of 88 cases available for analysis of factors related to delay. There was no significant difference in the incidence of delay between the private and ward cases. Other than their socioeconomic background, neither group could be distinguished on the basis of the 10 variables used; consequently, in subsequent tables no distinction is made between private (group I) and ward (group II) patients. and
11. T,istecl as unknown
INCIDENCE
OF
20
1
DELAY
Further breakdown of delay data demonstrates that the median gives a more accurate representation of central tendency within the sample than does the mean. A few extended delay periods skew the data badly toward the long end, thereby distorting the spread. Mean = 10.6 hours (SD. Median = 4 hours Mode = 1 hour
= 15.8)
Plotting the number of patients per hour against the time of delay gives a rough estimate of rate change (Fig. 1). Examination of this chart reveals that the average victim of a coronary attack is likely to seek help sooner than later. The half-time expended by the group in reaching medical aid was 3.9 hours. As pointed out, four hours after the onset of symptoms is the point at which approximately half of those stricken with myocardial infarction will have died. Sixty-five per cent of our patients arrived for help by the end of six hours. After six hours, the rate abruptly falls. The rate at which patients seek medical care (Fig. 1) seems to be a negatively accelerated function rapidly approaching an asymptote of 1 or less after six hours. This could mean that the patient who waits 7 hours could as easily delay 48 hours. Since half of all coronary victims are believed to be dead within four hours of symptom onset, the factors that contribute to a prompt or a tardy response within this critical cluster of hours are essential to identify. FACTORS
ASSOCIATED
WITH
DELAY
Eleven variables were selected as possibly relevant to delay. These were age, sex, socioVOLUME
24,
6Ei3
Infarction
NOVEMBER
1969
0
2
4
6
8
10
30
HOURS
Figure 1.
Rate at which patients seek medical care for coronary symptoms as a function of time from onset of symptoms.
economic status, number of previous myocardial infarctions, type of presenting symptoms, severity of presenting symptoms, admission prognostic scores, displacement of symptoms, influence through advice of another person, physician delay, and the use of denial. Age: As the data indicate (Table III), several older patients did indeed delay longer. However, the age-delay regression was not statistically significant. Sex: Even though the median and mean delay of women was longer than that for men, this difference was not statistically significant (Table III).
Prior Myocardial Infarction: The population was divided into three groups: (1) those with no prior myocardial infarction; (2) those with one prior myocardial infarction; and (3) those with two or more. There is no evidence to support the notion that having experienced a myocardial infarction makes delay less likely on subsequent infarctions (Table III). Socioeconomic Status: A socioeconomic score based upon occupation, income and education was assigned to each patient. These were derived
654
Hackett Table
Factor
Age (yr.1
III.
and Cassem
Relation Between Twelve Factors and Duration of Delay
No.
Median (hr. 1
Mean & S.D. (hr. )
34 26 28 88
4.0 4.0 5.0
64 24 88
4.0 5.0
57 27 4 88
4.0 5.0 2.6
16 20 24 60
4.4 4.0 4.2
57
5.0
12.0
f
17.8
25 3 85
4.0 1.0
9.2 1.7
f f
12.0 0.8
Severity of symptoms Mild Moderate Moderate-severe Severe Total
3 10 11 61 85
24.0 24.0 5.0 4.0
Peel scores l-8 9-12 13-16 517 Total
35 23 22 8 88
4.8 3.0 5.0 4.8
Displacement of symptoms Heart Gastrointestinal Not heart Total
29 17 5 51
2.0 5.0 24.0
InfIuence of another No Yes Total
33 37 70
2.0 5.5
Sources of inlluence Nonfamily work Work Family Total
6 8 23 37
2.0 4.8 12.0
154 55-64 >65 Total Sex Male Female Total
Prior myocardial infarctions 0 1 2 Total 159 60-79 80-99 Total Presenting symptoms Chest pain alone Chest pain and dyspnea Dyspnea alone Total
10.7 8.5 12.7
10.4 11.9
11.0 11.0 3.8
15.1 9.7 9.8
26.8 22.4 8.1 8.1
Linear Regression r
P
f 18.2 f11.3 f 16.6 $0.087
N.S.
-0.047
N.S.
-0.056
N.S.
-0.057
N.S.
+o.
N.S.
f 16.2 f15.4
fl6.9 f 14.8 f 3.7
f25.18 f12.5 f 12.2
f f f f
133
19.9 17.6 8.5 14.9 -0.324
11.8 7.5 11.9 11.6
3.5 14.7 25.0
5.4 13.0
0.01
f 18.6 f 10.7 f 15.8 fl4.5 -0.064
N.S.
+0.442
+0.253
<0.05
+0.317
<0.05
f 4.9 z!z 24.0 f22.5
* f
2.33 f 8.81 f 17.22 i
9.3 18.4
1.9 9.5 21.6
N.S. = not significant. THE
AMERICAN
JOURNAL
OF
CARDIOLOGY
Patient
Delay in Acute Myocardial
from prc-established census data from the U. S. Bureau of Census.4 There was no significant correlation between these scores and delay time (Table III). It appears that neither education nor income bracket insures a more prompt response to the signs and symptoms of myocardial infarction. Presenting Symptoms. Table III shows that more than half the patients presented with chest pain alone, but over a quarter had dyspnea as well. The category “other” included sweating, palpitations, numbness of fingers, and dizziness with weakness. Those patients with dyspnea alone had the shortest delay time. The small size of the group detracts, of course, from the significance of this finding. It is our impression that the appearance of dyspnea considerably shortens the tendency to prolong delay. Our data, measured from the onset of the first symptom, does not allow us to isolate this phenomenon. Shortness of breath may induce anxiety along the lines described in the James-Lange theory. This notion is appealing in its simplicity. On the other hand, the presence of dyspnea may signal the presence of genuine heart disease to the patient. One man, who delayed several hours despite severe chest pain, decided to consult his physician when his breathing became labored. He explained his delay by saying, “If it doesn’t affect your breathing, it can’t be your heart.” .Cuerity of Symptoms.. Although it is difficult to classify a symptom as subjective as pain or as individually variable as shortness of breath, we have attempted to do so. Since we seldom saw the patient at the time he was admitted to the emergency ward, our rating is based upon notes in the chart by the admitting physician along with the patient’s own retrospective estimation of discomfort. Table III presents the distribution. Contrary to our earlier work4 these data reveal what appears to be a positive relation between severity of symptom and length of delay (p 0.01). As the rated severity of symptoms increased, patients sought help more rapidly. More Objective Evaluation of Severity: Since there is some question about the reliability of rating the severity of symptoms and because our findings are contrary to previous work,l’ we have looked at these data from another standpoint. The Peel prognostic index, which offers an objective assessment of the patient’s over-all organic illness, was scored for each patient at the time of admission. The Peel scores were divided into four groups. The expected morVOLUME24, NOVEMBER1969
Infarction
655
tality for each group score was as follows: l-8 = 2.5 per cent, 9-12 = 12.5 per cent, 13-16 = 23.7 per cent, and above 17, 63.7 per cent. It was found that the aVerage patient, with a mean score of 10.2, fell into the category in which expected mortality is about 12.5 per cent. There was no significant relation between delay and the various prognostic groups (Table III). Thus, while it may be true that, as the symptoms become more severe, the patient is less apt to delay, the same does not hold for the severity of the disease itself. One cannot say that the worse the disease, the more swiftl>. the patient is apt to seek medical help. Displacement of Symptoms: Previous work” demonstrated that the patient may interpret the symptoms of cardiac difficulty as originating from sources other than the heart. The incidence of this displacement is presented in Table III. Sufficient information for inclusion in this section was available for only 56 of the 88 patients. Twenty-nine, half the sample, knew their symptoms stemmed from the cardiovascular system, a realization that was immediate in all but 3 patients. Those 3 realized that the source was the heart as pain increased. Four patients attributed the symptoms to their lungs and 1 to his “nerves.” Those people who referred symptoms to their gastrointestinal tract thought that they had “gas” or “indigestion.” A few blamed the gall bladder and 1 ascribed the symptoms to hiatus hernia. Those who indicted the lungs blamed “smoke-filled rooms,” or too man) cigarettes, and the like. The 5 remaining patients shared the disbelief that the heart was at fault. Patients who recognized the true source of their trouble came for help much sooner. This relation was significant at the 0.01 level. Of the patients who attributed symptoms to the gastrointestinal tract, none came to a physician within the first hour. The group who interpreted their symptoms simply as not coming from the heart delayed the longest, by far. Thus, we have something of a spectrum effect, with acknowledgment of the heart as the responsible agent at one end and denial of even the possibility that it is the offender at the other extreme. In between are patients who displace the source of trouble to organ systems of which acute involvement was less forbidding than the heart. It is not at all clear why patients chose the gastrointestinal tract or respiratory system rather than the heart. The most logical explanation.
Hackett and Cassem
656 Table IV. Incidence of Delay by Physicians
Physician Delay
No. of Patients
Physicians Outside Hospital
Yes
12
No
69
Swift referral to emergency ward
18
18
1 100
28
Unknown Total
10
which may be incorrect, is that trouble with these other organ systems is usually not as dangerous as cardiac disease. Moreover, most individuals have had “indigestion” and “lung congestion ” in the past and successfully survived them. Given a choice of alternative explanations for pain in the chest, it is not unreasonable to assume that the sufferer would choose a condition unlikely to threaten his life, preferably one that he had experienced and overcome in the past. The Influence of Another Person on Patient Delay: Earlier studies” have indicated that probably the most important factor in reducing patient delay has been the influence of another person upon the patient’s decision to seek medical help. The distribution of those who required this influence is presented in Table III. Who this other person was is also shown in Table III. One can see from this analysis that for the largest number of patients in the study, it was a family member who convinced the patient to seek medical aid. It is also clear that the patient who decides to seek medical assistance on his own comes faster than one who needs help with that decision. A bimodal response curve could be envisaged in which those who decide for themselves come early and those unable to decide come late. If one assumes that those who delay do so because they tend to deny the significance of their symptom-even in the face of severe pain and despite an awareness that the heart may be involved-then the only effective type of interruption of delay is from another person who correctly interprets the facts by stripping away denial. Spouses appear to be less influential in reducing delay than friends or associates. The median delay for those assisted by family members was 12 hours compared to 2 hours for those assisted by friends. In a number of instances, it
was an insistent employer who literally ordered the patient to the hospital. When the source of influence was put to statistical test, the unrelated person who was not work-associated (either friend or stranger) was most effective in producing prompt action by the patient with coronary symptoms. Physician Delay: Occasionally, before the patient reaches the hospital, he may have contact with a physician either by phone or in person. It sometimes happens that despite genuine coronary symptoms the patient’s arrival at the hospital may be delayed by the physician himself. The incidence of this phenomenon in our study is presented in Table IV. Twelve of 100 patients were delayed in being hospitalized by a physician. The physician employed the same maneuvers used by patients who delayed. He either blamed other organ systems or minimized the pain by calling it angina. In some cases, medication was given and the patient was instructed to wait. In other cases, an appointment was made for an office visit the next day. The 28 physicians involved had offices outside the hospital and could easily have taken the opportunity to refer the patient to a hospital for definitive diagnosis. Eighteen did so swiftly. The remaining 10, largely for reasons unknown, delayed the patient’s entrance. One of the delaying doctors later admitted that he thought his patient was simply exaggerating his pain. In fact, this same physician doubted that the patient had true coronary disease until it was amply demonstrated angiographically. The Defense of Denial: The defense mechanism of denial is defined as the conscious or unconscious repudiation of part or all of the total available meaning of an event to allay fear, anxiety, or other unpleasant affects.15 The term major denial is used to describe patients who stated unequivocally that they felt no fear at any time throughout their hospitalization. Partial denial describes those who initially denied fright but eventually admitted feeling at least some fear. “Minimal denial” is applied to patients who complained of anxiety or who readily admitted being frightened; they showed no consistent criteria for denial. One would expect that the tendency to deny would correlate significantly with the tendency to delay. Statistical analysis fails to show a significant relation between time of delay and extent of denial (Table v). This raises obvious questions that strike at the core of our concept of denial. THE
AMERICAN
JOURNAL
OF CARDIOLOGY
Patient Table
Denial
No. of Cases
Minimal Partial Ma.jor Total
16 62 20 98
Delay in Acute Myocardial
Relation Between Denial and Duration
V.
Median
Mean =t S.D.
5.2 4.0 5.0
12.0 f 18.2 8.9 f 11.9 15.8 f. 23.9
VI.
of Delay Linear Regression r
/r
N.S.
$0.130
If we turn to other variables for correlation with denial (Table VI), some interesting features appear. All those who demonstrated minimal denial knew the source of their symptoms. Denial was significantly related to symptom displacement (p < 0.05). With 2 exceptions, all those who showed major denial displaced their symptoms to other organ systems. The 2 exceptions are worth comment. One was the man, mentioned before, who had a special understanding with his cardiologist. The other patient turned out to have cholecystitis, not a coronary attack. If we correlate the influence of another person on delay with the type of denial, we find a trend for the degree of denial to be related to the source of decision making (0.10 < p < 0.20). This suggests that the person who denies minimally does not need much outside help to seek a physician for coronary symptoms. Those whose denial is major will delay seeking help unless someone else goads them into action. Those who partially deny occupy a mid-way position.
Why should some of those who demonstrated ma,jor denial reach a physician within one hour? The explanation is fairly simple. In all there were 5 such patients. In 2, symptoms developed while they were with someone who immediately sent thern to the hospital. Two others had symptoms that had been present but denied days before their actual entry into the hospital. The fifth was a man who maintained a special relation with his cardiologist. Their agreement was that if three nitroglycerine tablets did not relieve severe pain, he was to enter the emergency ward, which the patient did in a nonchalant, almost indifferent manner. Six who showed major denial were admitted within one to five hours. How can we explain this? One entered the hospital with a diagnosis of cholecystitis and fully expected his pain to be from the gall bladder. A second, brought in by relatives, had acute pulmonary edema, having been cared for at home through the previous week. The third, sent to the hospital by an industrial nurse, protested that all he wanted was an antacid for heartburn. No reason could be given by the fourth patient as to why she entered when she did and none was subsequently found. The last 2 patients appeared to both staff and investigators as terrified, although they denied fear. These reasons may explain why those who showed major denial behaved in what might be considered a paradoxical way. Table
657
Infarction
CONCLUSION If the population at large responds to the first symptom of myocardial infarction in a manner similar to the patients we have described, there is little doubt that delay contributes heavily to the national death rate. As this study demonstrates, we know almost nothing about the social, psychological, or genetic factors that facilitate
Factors Associated with Denial -
Denial
P
Minimal
Partial
Displacement of symptoms Heart Gastrointestinal
6 0
22 19
2 4
6.06749
2
0.02
Influence of another No Yes
4 1
24 27
5 10
3.30743
2
0.10
--
VOLUME
24, NOVEMBER
1969
Major
X2
df
658
Hackett
or inhibit the process of delay. Perhaps the most valuable lessen to draw from our findings is that traditional convictions are often wrong. A college education and familiarity with the symptoms of coronary disease do not guarantee a prompt and appropriate response. As yet we have no specific alternative method to propose for reducing delay, but that may come in time. This symposium has made the first advance by emphasizing the relevance of investigating delay. It is a beginning.
REFERENCES 1. SLOMAN, G. Coronary units: The Royal Melbourne Hospital. In: Acute Myocardial Infarction, pp. 8-12. Baltimore, 1968. Williams & Wilkins. 2. MCDONALD, E. L. The London Hospital. In Ref. 1, pp. 29-32. 3. LAWRIE, D. M., GREENWOOD, T. W., GODDARD, A coronary care unit in the routine M. et al. management of acute myocardial infarction. Lancct, 2:109, 1967. 4. FRY, J. Acute myocardial infarction in a British general practice. In Ref. 1, pp. 304-309. 5. BAINTON, C. R. and PETERSON, D. R. Deaths from coronary heart disease in persons 50 years of age and younger. New England J. Med., 268~569, 1963.
and Cassem 6. OLIVER, M. F. From data cited by BONDURAN.~, S. Symposium on the Pre-hospital Phase of Acute Myocardial Infarction, Rochester, N. Y. May 17-18, 1969. (This issue, pp. 612-616.) 7. ROSEMAN, M. D. Painless myocardial infarction: Review of literature and analysis of 220 cases. Ann. Int. Med., 41:1, 1954. 8. BRUENN, H. G., TURNER, K. B. and LEVY, R. L. Notes on cardiac pain and coronary disease: Correlations of observations made during life with structural changes found at autopsy in 476 cases. Am. Heart J., 11:34, 1921. 9. MASTER, A. M. and GELLER, A. J. The extent of asymptomatic coronary artery disease. Am. J. Card&., 231173, 1969. 0. BABEV, A. M. Painless acute infarction of the heart. New England J. Med., 220:410-412, 1939. 1. OLIN, H. S. and HACKETT, T. P. The denial of chest pain in 32 patients with acute myocardial infarction. J.A.M.A., 190:977, 1964. 2. MIRU: Task n; Psychiatric Studies; Contract No. PH 43-67-1443. 13. PEEL, A. A. F., SEMPLE, ‘r., WANG, I., LANCASTER, W. M. and DALL, J. L. G. .4 coronary prognostic index for grading the severity of infarction. Brit. Heart J., 24: 745, 1962. 14. U. S. Bureau of Census. Methodology and Score of Socioeconomic Status. Working Paper No. 15. \Vashington, D. C. 1963. 15. WEISMAN, A. D. and HACKETT, T. P. Predilection to death: Death and dying as psychiatric problems. Pqchosom. Med., 23:232, 1961.
THE
AMERICAN
JOURNAL
OF CARDIOLOGY