Chest Pain in Acute Myocardial Infarction: A Descriptive Study According to Subjective Assessment and Morphine Requirement

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1 Clin. Cardiol. 9, (1986) Chest Pain in Acute Myocardial Infarction: A Descriptive Study According to Subjective Assessment and Morphine Requirement J. HERLITZ. M.D.. A. RICHTEROVA, M.D., E. BONDESTAM. N.R., A HJALMARSON, M.D., s. HOLMBERG. M.D., c. HOVGREN. N.R Department of Medicine I, Sahlgrenska Hospital, Goteborg, Sweden Summary: In 722 patients with suspected acute myocardial infarction (MI) we have tried to describe the course of chest pain according to their own assessment and morphine requirement. Patients were asked to score pain from 0-10 every second hour after arrival in the coronary care unit (CCU) and also to score their maximal pain at home. A very high intensity of chest pain was observed at home (mean score 7.1). At arrival in the CCU the mean pain score already had declined to 1.8, although 51% still had chest pain. Pain score declined successively during the first 12 hours in the CCU. At 24 hours after arrival, 20% still had some chest discomfort. In one quarter of the series a score of more than 0 was observed later than 24 hours after arrival in CCU. Patients developing definite MI had, as expected, a longer duration of pain and a much higher requirement of morphine compared with those with no MI. The difference between MI and no MI patients regarding subjective assessment of the initial intensity of pain at home and in hospital was, however, surprisingly low. infarction (MI) the vast majority have chest pain, which is thought to reflect active cardiac ischemia. The intensity and duration of chest pain varies considerably (Herlitz et al., 1985) and is thought in part to reflect the extent of the ischemic damage (Herlitz et al., 1984; Ledwich, 1977; Ledwich and Mondragon, 1980). Quantification of chest pain is difficult and mostly made according to objective assessment by doctors and nurses. The purpose of this study was to try to describe the course of chest pain in suspected acute MI according to subjective assessment, and requirement of narcotic analgesics. Details regarding pain course in different types of infarction will be published subsequently. Patient Population All patients admitted to the CCU at Sahlgrenska Hospital between May 1, 1983 and May 31, 1984 with suspected acute MI were evaluated for inclusion. Key words: chest pain, suspected acute myocardial infarction Introduction Chest pain is one of the major symptoms in ischemic heart disease. Among patients admitted to a coronary care unit (CCU) with a suspicion of acute myocardial Address for reprints: J. Herlitz, M.D. Department of Medicine I Sahlgren's Hospital S Goteborg, Sweden Received: September 16, 1985 Accepted with revision: January 14, 1986 Methods Pain scoring. Pain was scored by the patient according to a visual scale from 0-10 where 0 meant no pain and 10 meant the most severe pain the patient could imagine. The figures between 0 and 10 corresponded to increasing severity of pain although there was no correlate in words. Pain was scored at the following times: Maximum pain at home (at the place where symptoms started; scored retrospectively at arrival in CCU), every second hour after arrival in CCU until there were 6 consecutive registrations (1 2 hours) with no pain. Thereafter, pain scoring stopped regardless of whether pain reappeared. Patient asleep was recorded as no pain. Administration of narcotic analgesics between the times at which pain was scored and also after the end of pain scoring was registered. Corrected pain score. In order to correct for previous treatment with narcotic analgesics, pain score was increased by 2.0 if the patient had received such treatment during the previous two hours.

2 ~~ ~~~ 424 Clin. Cardiol. Vol. 9, September 1986 Treatment of pain. First line of treatment for severe chest pain was morphine intravenously (i.v.), whereas less severe pain interpreted as angina pectoris required nitroglycerine sublingually. Morphine was with few exceptions (intolerance) the only narcotic analgesic used. In these few exceptional cases the doses of the actual drug (fortalgesic or pehtidine) were converted to equipotent morphine doses. Definition of early MI (duy 0-3). At least two of the three following must be fulfilled. 1. Chest pain of at least 15 minutes duration. 2. At least two values of serum (S) aspartate aminotransferase (ASAT) above the reference limit (0.7 pkat/l) with lower values of S-alanine amino- 3. transferase (ALAT). Evolution of Q waves or appearance or disappearance of ST elevation followed by T-wave inversion in at least two leads in B 12-lead standard electrocardiogram (ECG). The same criteria were applied for late MI (onset of symptoms later than 3 days after arrival in CCU). Definition ofpossible MI. Chest pain plus one of the following must be fulfilled: 1. Appearance of T-wave inversions in standard ECG 2. Only one raised S-ASAT value with a lower or normal S-ALAT 3. Appearance of Q waves or appearance or disappearance of ST elevation followed by T-wave inversion in only one lead. Determination of S-ASAT and S-ALAT were made once daily during the first 3 days in hospital. A 12-lead standard ECG was recorded once daily during the first 3 days in hospital. Serum activity of ASAT and ALAT were determined according to the Scandinavian Committee on Enzymes (1974). Statistical methods. Fischer s permuation test was used. A two-tailed test was applied. Results are expressed as mean f standard error of the mean (SEM) if not otherwise stated. Results In all, 722 patients were evaluated for inclusion in the study of which all were admitted to CCU due to a strong suspicion of acute MI. In 69 patients (lo%), pain was not assessed due to unconsciousness, bad clinical condition or technical reasons. The age varied between 33 and 92 years (median 70 years). In 39% there was a history of previous MI and in 59% a history of angina pectoris (Table I). Clinical Observations in Hospital During days 0-3, a definite MI developed in 327 patients (45%) and a possible MI in 86 patients (1 1.9%). In patients not fulfilling criteria for definite TABLE I Clinical characteristics Sex Men Women Age 570 years >70 years Clinical history Previous infarction Angina pectoris H y per t ens ion Congestive heart failure Therapy before admission Fu rosemide Beta blockers Ca antagonists Q, Median QJ Age (yrs) Time from onset of pain to (h): arrival in hospital I 2 6 arrival in CCU or possible MI, chest pain was interpreted as caused by ischemia in 64%. Late infarction (onset of symptoms more than 3 days after arrival in CCU) occurred in 1.7% of all patients (in 3.1% among those with early MI). The overall in hospital mortality was 7.2% and the overall incidence of ventricular fibrillation (VF) was 2.6%. Among patients with definite MI, the mortality rate was 14.7% and the incidence of VF was 5.2%. About 50% of the patients were given beta blockade on days 0-3. Pain Evaluation Maximal Pain at Home Table I1 shows the mean maximum pain score at home in patients with definite MI, possible MI, and no MI according to given criteria. The last group has been divided into those who upon leaving hospital were judged as having ischemic or no ischemic chest pain. Fairly small differences were observed between the groups when comparing mean values. The mean maximum pain score at home in patients with definite MI was 7.5 f 0.2 as compared with 6.6 f 0.2 in all patients not fulfilling criteria for MI (p<o.ool). Pain in CCU In all, the mean maximum pain score at home of 7.0 had declined to 1.8 at arrival in CCU. Whereas 98% of

3 J. Herlitz et al.: Chest pain in acute MI 425 TABLE II Mean maximum pain score at home and mean pain score during first 6 hours after arrival in the CCU Mean pain score in relation to arrival in CCU Hours Mean max pain score at home Definite MI Possible MI No MI ischemia no ischemia all patients had chest pain at home, only 5 1% had pain at arrival in CCU. Table I1 shows the mean pain score during first 6 hours in CCU in patients with definite MI, possible MI, and no MI (chest pain interpreted as caused by ischemia and chest pain interpreted as not ischemic). Figure 1 shows the mean maximum pain score at home and the mean pain score every second hour during first 24 hours in CCU in patients with definite MI and no definite MI. The duration of pain defined as time between arrival in CCU and the last time the patient scored pain > 0 is illustrated in Figure 2 for patients with definite early MI and no definite early MI. The mean duration of pain was 18.7 f 1.2 hours in MI patients versus f 0.8 hours in no MI patients (p<o.ool). Corresponding values for the median duration was 12 versus 4 hours. Requirement of Analgesics The percentage of patients requiring morphine during 2-h intervals in the first 24 h among patients with definite MI and no definite MI is shown in Figure 3. Narcotic analgesics were given to 10% of all patients after the end of pain scoring. During days 0-3, 27.4% of all patients were given nitroglycerine sublingually. o k r 0 At home s FIG. 1. Mean maximum pain score at home and mean pain score every second hour during first 24 hours after arrival in CCU in patients with definite MI (0-0) and no definite MI (0-0). Median time between onset of pain and arrival in CCU = 4 hours. Hours

4 426 Clin. Cardiol. Vol. 9, September C FIG. 2 I >36 Duration of pain (h) The duration of pain in CCU defined as time between arrival in CCU and last pain score > 0 in patients with definite MI ( B) and no definite MI (0). Corrected Pain Score Figure 4 shows a mean corrected pain score every second hour during first 24 hours after arrival in the CCU in patients with and without definite MI, which means that the score given by the patient was increased by 2 if narcotic analgesics had been given during the 2- h interval before pain scoring. Discussion Chest pain is one of the main symptoms indicating active cardiac ischemia. The mechanism behind chest pain in ischemia is not fully understood. It has been suggested that mediators such as prostaglandins or bradykinin might be released from cells damaged from ischemia and stimulate pain receptors in sympathetic afferent nerves. Mechanoreceptors and chemoreceptors are most likely involved in the genesis of ischemic chest pain (Longhurst, 1984). The pattern of chest pain in patients with suspected acute MI is complex and the variability appears to be large (Herlitz et al., 1985). One of the reasons for these observations could be difficulties in assessment of pain by nurses and doctors in the CCU. The aim of this study was to try to describe the pattern of chest pain in an unselected population of patients with suspected acute MI based on subjective assessment. We are still searching for methods which directly reflect development of the ischemic damage. Although the variability in chest pain probably sometimes reflects patient variability rather than pain variability it has been shown that the duration of chest pain correlates quite well with other indirect markers of infarct evolution, such as ECG changes (Inoue et al., 1977; Sederholm et al., 1985), whereas no such correlation has been shown with calculated enzyme release (Sederholm et al., 1985). 40 a 10 Hours FIG. 3 Percentage of patients given morphine during 2-hour intervals during first 24 hours after arrival in CCU in patients with definite MI (B) and nodefinite MI (0).

5 J. Herlitz er al.: Chest pain in acute MI FIG 4 Mean maximum pain score at home and mean corrected pain score every second hour during first 24 hours after arrival in CCU in patients with definite MI (0-0) and no definite MI (0---0). Corrected pain score = pain score at each check up was elevated with 2.0 if morphine had been given in the previous 2-hour interval. We think it is worthwhile trying to further improve assessment of chest pain as an indicator of ongoing cardiac ischemia. The aim of such a work is to develop an instrument suitable for evaluation of interventions given early in suspected acute MI in order to limit infarct development and symptoms of ischemia, such as chest pain. The evaluation of chest pain in this study was mainly based on subjective assessment. Since patients were intermittently given morphine for chest pain the scoring was sometimes influenced by this treatment and therefore, underestimated the severity of chest pain. In the final analyses we tried to arbitrarily correct for this influence by increasing pain score by 2 if narcotics had been given previously. This was a very rough correction since the dose of morphine varied and one could expect the response to morphine to vary. In a few patients chest pain might be caused by other factors than ischemia such as pericarditis. This was however a rare phenomenon in this study mainly explained by the fact that pain scoring took place very early after hospitalization. The severity of chest pain at home varied considerably. In patients with definite MI, 30% scored their pain at home to the highest possible degree. At arrival in the CCU it had decreased in the majority of patients, many of which had been given narcotic analgesics in the emergency ward. After arrival in the CCU the mean chest pain score successively declined during first 12 hours, most rapidly during first 4 hours. After 12 hours it reached a plateau. It must be emphasized that in contrast to assessment of chest pain in hospital, chest pain at home was scored retrospectively soon after arrival in hospital, which might have influenced the results. Although the initial chest pain rapidly decreased already before arrival in the CCU our results clearly indicate that a large proportion of patients have chest pain which continues for a longer period, which mostly means ongoing ischemia and sometimes infarct development. One of the messages from this study is that the intensity of pain in the initial phase of suspected acute MI, based on subjective assessment, does not seem to differ much regardless of whether the patient develops a definite, possible, or no infarction. These results are in agreement with the clinical impression although it has, as far as we know, not been systematically evaluated previously. On the other hand, morphine was given much more often to patients with definite MI (in agreement with previous reports; Baker, 1985), which could partly explain why we found such small differences in pain intensity between MI and no MI patients. One other explanation could be that only a visual scale was used and no verbal scale to measure chest pain. It is important to stress that all patients evaluated had a strong suspicion of acute MI and that distinction of

6 428 Clin. Cardiol. Vol. 9, September 1986 chest pain in no MI patients as caused by ischemia or not is often difficult. In the group of patients with no sign of acute MI, about two thirds were judged to have ischemic heart disease as cause of chest pain. This study most likely underestimates the severity of chest pain to some extent in suspected acute MI. First, pain was scored with two-hour intervals ignoring the interval in between and, second, pain scoring was completed after a 12-hour pain-free interval. For technical reasons we had no possibility of carefully evaluating the frequency of recurrent chest pain after a longer pain-free interval. The fact that 10% of the patients required morphine after pain scoring was completed indicates that recurrent chest pain is not uncommon. The occurrence of late infarction in this study was, however, surprisingly low, not in agreement with other reports (Buda et al., 1983; Fraker et al., 1979; Marmor et al., 198 l). Similar figures have, however, been reported from our group previously (Herlitz et al., 1985). One reason for these discrepancies could be variation in definition of late MI. In this definition we only included patients with reappearance of symptoms later than 3 days after arrival in CCU. The duration of chest pain obviously varies considerably. In the present study we found that about 25% of the patients have chest pain later than 24 hours after arrival in the CCU. This is in agreement with previous experiences (Herlitz et al., 1985). Information regarding chest pain, particularly chest pain at home, was missing in a fairly high group of patients due to poor patient condition or other technical reasons. The mortality rate was higher in patients in whom this information was missing compared with those in which it was not. This highlights one of the problems with subjective assessment of chest pain: a relatively large proportion of the most complicated infarctions might be missing due to difficulties in receiving adequate information. Conclusion This study describes the course of chest pain in suspected acute MI from onset of symptoms outside hospital up to the first 12-hour pain-free interval after arrival in the CCU. Pain at home was generally much worse than in the CCU. The intensity and duration of chest pain seemed to vary considerably, although the mean values indicated a rapid decline during the first 12 hours after arrival in the CCU after which a plateau phase occurred. A surprisingly low difference in subjective assessment of pain was observed when patients developing MI were compared with those who did not. Acknowledgments This investigation was supported by grants from the Swedish Medical Research Council (project no. B82-19X C), the Swedish National Association against Heart and Chest Diseases, the Goteborg Medical Society, and AB Hassle, subsidiary of Astra Pharmaceuticals, Sweden. Many thanks to the CCU staff for their skillful work. References Baker P: Suspected myocardial infarction: Early diagnostic value of analgesic requirements. Br Med J 290, 27 (1985) Buda AJ, Macdonald IL, Dubbin JD, Orr SA, Strauss HD: Myocardial infarct extension: Prevalence, clinical significance, and problems in diagnosis. Am Heart J 105, 744 (1983) Fraker, TD Jr, Wagner GS, Rosati RA: Extension of myocardial infarction: Incidence and prognosis. Circulation 60, ( 1979) Herlitz J, Hjalmarson ac, Holmberg S, Swedberg K, Waagstein F, Waldenstrom A, Waldenstrom J: Enzymatically and electrocardiographically estimated infarct size in relation to pain in acute myocardial infarction. Cardiology 7 1, 239 (1984) Herlitz J, Hjalmarson A, Holmberg S, RydCn L, Swedberg K, Waagstein F: Variability, prediction and prognostic significance of chest pain in acute myocardial infarction. Cardiology 73, 13 (1986) lnoue M, Hori M, Fukui S, Abe H, Minamino T, Kodama K, Ohgitani N: Evaluation of evolution of myocardial infarction by serial determinations of serum creatine kinase activity. Br Heart J 39, 485 ( 1 977) Ledwich JR: Chest pain in the early recognition of large infarcts. Can Med Asso J 1 16, 38 (1 977) Ledwich JR, Mondragon GA: Chest pain duration in myocardial infarction. JAMA 244, 2172 (1980) Longhurst JC: Cardiac receptors: Their function in health and disease. Prog Cardiouasc Dis 27, 201 (1 984) Marmor A, Sobel BE, Roberts R: Factors presaging early -recurrent myocardial infarction ( extension ). Am J Cardiol48, 603 ( ) Scandinavian Committee on Enzymes: Recommended methods for the determination of four enzymes in blood. Scand J Clin Lab Invest 33, 291 (1974) Sederholm M, Gr$ttum P, Kjekshus J, Erhardt L for the International Collaborative Study Group: Chest pain and its relation to CK release and ST/QRS vector changes in patients treated with intravenous timolol or placebo. Am Heart J 110, 521 (1985)