Download ATYPICAL CHEST PAIN IN THE ELDERLY: PREVALENCE

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Remote ischemic conditioning wikipedia , lookup

Jatene procedure wikipedia , lookup

Quantium Medical Cardiac Output wikipedia , lookup

Coronary artery disease wikipedia , lookup

Management of acute coronary syndrome wikipedia , lookup

Transcript
■
REVIEW ARTICLE
ATYPICAL CHEST PAIN IN THE ELDERLY: PREVALENCE,
POSSIBLE MECHANISMS AND PROGNOSIS
Chung-Lieh Hung1,2, Charles Jia-Yin Hou1,2, Hung-I Yeh1,2, Wen-Han Chang2,3,4*
1
Cardiovascular Medicine and Medical Research, Mackay Memorial Hospital, 2Mackay Medicine, Nursing and
Management College and Taipei Medical University, 3Department of Emergency Medicine, Mackay Memorial Hospital,
and 4Graduate Institute of Injury Prevention and Control, Taipei Medical University, Taipei, Taiwan.
SUMMARY
Acute chest pain is a major complaint quite commonly presented at emergency departments. A differential
diagnosis of acute chest pain includes various disease entities, including some life-threatening disorders. Of
these, acute coronary syndrome garners much clinical attention and forms a specific disease that includes
a critical ST-segment elevation myocardial infarction and a less severe form of non-ST-segment elevation
myocardial infarction and unstable angina. As an urgent and life-threatening disease leading to a high morbidity and mortality, accurate diagnosis of acute coronary syndrome remains a clinical challenge. Efficient management of this syndrome may rely on a quick yet accurate diagnosis. A high misdiagnosis rate and
inappropriate discharge rate for acute coronary syndrome are still observed, especially in the elderly population, owing to a higher prevalence of atypical symptoms presented in this group. Moreover, the existence of
high comorbidities in the elderly population makes effective clinical approach complicated. A delay in the
identification and treatment may lead to worse outcomes in this patient population. The underlying pathophysiology and exact mechanisms are various. Patient evaluation strategies are currently being developed, as
are new diagnostic facilities aimed at preparing physicians for urgent intervention in a more cost-effective
manner. [International Journal of Gerontology 2010; 4(1): 1–8]
Key Words: acute chest pain, acute coronary syndrome, elderly population, myocardial infarction,
unstable angina
Introduction
Acute chest pain is one of the most common causes of
emergency department (ED) visits. In the United States,
more than 5 million people attend the ED with chest
pain each year, and more than 3 million of these
patients are hospitalized because of this condition at a
cost of more than 6 billion dollars1–3. Early recognition
of clinically life-threatening conditions, such as pulmonary embolism, aortic dissection and pneumothorax,
are crucial. Furthermore, early diagnosis and accurate
*Correspondence to: Dr Wen-Han Chang, Department of Emergency Medicine, Mackay Memorial
Hospital, 92, Section 2, Chung-Shan North Road,
Taipei, Taiwan.
E-mail: [email protected]
Accepted: May 12, 2009
International Journal of Gerontology | March 2010 | Vol 4 | No 1
© 2010 Taiwan Society of Geriatric Emergency & Critical Care Medicine.
diagnostic tools with subsequent appropriate treatment
strategies are important and can save lives, since failure to recognize such diseases at an early stage may
lead to a delay in treatment. Of all patients who present at the ED with acute chest pain, less than 25% have
acute coronary syndrome (ACS)4. A recent study revealed
that ACS actually comprised one-third of myocardial
infarction (MI) and two-thirds of unstable angina or
non-ST-segment elevation MI patients. It has been previously mentioned that approximately 4% of patients
with MI were inappropriately discharged from the ED in
a prospective multicenter trial involving 3,077 patients5.
Christenson et al.6 reported that up to 4.6% of patients
with acute MI and 6.4% of patients with unstable angina
were misdiagnosed in the ED in Canada in 2004, while
a lower rate was reported in the USA by Pope et al.7
In a prospective observational study with a focus on
the prevalence, clinical characteristics and outcomes of
1
■
chest pain, Canto et al.8 found that in 434,877 patients
diagnosed with MI, up to 33% did not present with typical chest pain. Therefore, early and accurate diagnosis of
ACS is fundamental for subsequent effective therapy. A
recent multinational, prospective, observational study
suggested that there is a higher rate of atypical presentation in the elderly population leading to a worse prognosis9. Patients with ACS discharged from the ED without
an accurate diagnosis had a mortality rate nearly twice
the mortality rate of those admitted to a hospital10. In
fact, dyspnea has been identified as the most frequent
symptom of myocardial ischemia in patients older than
85 years11. Age itself, together with sex and a family history of early coronary artery disease, is an important risk
factor for ACS12. In addition, both the prevalence and
severity of coronary artery disease increases with the
aging process, as well as morbidity and mortality13,14.
It remains very difficult to decide whether patients
should stay longer in the ED or if more extensive investigations are warranted, especially for the elderly with
multiple potential comorbidities. According to previous
studies, patients with ACS inappropriately discharged
from the ED generally have a worse prognosis owing to
a possible delay in the implementation of effective therapeutics and the risk of sudden death8,15,16.
In this article, we sought to review the prevalence
and prognosis of atypical chest pain in the elderly population. In addition, we discussed the possible underlying mechanisms and recent advances in diagnostic
tools and strategies that may help early identification
of the higher risk groups. These innovations should help
minimize the potential for misdiagnosis and inappropriate discharge of elderly patients with ACS who present with atypical symptoms.
Differential Diagnosis of Acute Chest Pain
in the ED
Common causes of chest pain include those stemming
from cardiac or noncardiac causes. Simple history taking, including gathering information about lifestyle,
smoking and past medical history, provides important
hints to discern possible acute coronary events during
the preliminary assessment. Disorders related to the
pulmonary, gastrointestinal and musculoskeletal systems and cardiac origins are all possible causes of chest
pain symptoms. A cost-effectiveness analysis revealed
that esophageal sources especially gastroesophageal
2
■
C.L. Hung et al
Table.
Clinical features that increase the likelihood of
acute myocardial infarction*
Clinical features
Pain in chest or left arm
Chest pain radiation
Left arm
Both left and right arms
History of myocardial infarction
Likelihood ratio
(95% confidence interval)
2.7†
2.8 (1.7–3.1)
7.1 (3.6–14.2)
1.5–3.0‡
Association with nausea
or vomiting
1.9 (1.7–2.3)
Association with diaphoresis
2.0 (1.9–2.2)
Hypotension (systolic blood
pressure < 80 mmHg)
3.1 (1.8–5.2)
*Adapted from reference 18; †data not available to calculate confidence interval; ‡in heterogeneous studies, the likelihood ranges are
reported as ranges.
reflux diseases were identified most frequently in patients presenting with acute chest pain in EDs17. Chest
pain suggestive of cardiac origin may refer to those
with a sensation of chest compression, squeezing, or a
penetrating sensation in the internal side or localized
behind the sternum. Panju et al.18 reported the likelihood ratios for ACS based on clinical features including
location, past medical history, associated symptoms,
and hemodynamic findings (Table). In addition, pain
radiating to the left shoulder, neck, jaws, teeth or arm
regions with aggravated intensity or accompanied with
sweating over a period of time may indicate an ischemic nature7,19. Swap and Nagurney20 reported that pain
that radiated to both arms/shoulders or exacerbated
by exertion or physical efforts may show a likelihood
ratio of ischemic coronary events of 2.3–4.7. Conversely, atypical chest pain may refer to a sharp, tingling, “burning” sensation or may be associated with
meals, localized to a small point or area or pain that
can be elicited by direct pressure, touch or postural
changes. Pain accompanied by fever or a history of past
chest pain not originating from a cardiac source may
help identify noncardiac causes. Recent guidelines from
the American College of Cardiology and American Heart
Association provide some useful information on identifying noncardiac origin ischemic episodes21.
Common causes of chest pain emanating from
cardiac causes other than coronary events include
pericardial or valvular heart diseases. Patients with pericarditis accompanying pleuritis may experience sharp
International Journal of Gerontology | March 2010 | Vol 4 | No 1
■
Atypical Chest Pain in the Elderly
pain during breathing and coughing. Valvular heart
diseases such as severe aortic valve stenosis or subaortic stenosis may also induce chest pain in the elderly,
whereas a young subject suffering atypical chest pain
with palpitations may have mitral valve prolapse disease22. Common noncardiac causes of chest pain include
pulmonary, vascular and gastrointestinal disorders. Of
all noncardiac causes presenting with acute chest pain,
pulmonary embolism, aortic dissection and pneumothorax are common life-threatening emergencies seen
in the ED. By differentiating the location of the pain, a
physician can identify the underlying disease easily.
For example, lateralizing pain may be associated with
a pulmonary embolism or pneumothorax. Precordial
chest pain location can be associated with ACS, ascending aortic dissection and interscapular back pain, which
is typical of aortic dissections of the descending aorta.
Gastrointestinal system disorders with a “burning
sensation” linked to meal behavior may indicate a lesion
arising from the esophagus or stomach, such as gastroesophageal reflux disease, ulcers or even MalloryWeiss tears. Furthermore, chest pain arising from
musculoskeletal causes, cervical disc diseases or even
skin lesions may be easily diagnosed by the pain characteristics and physical examination.
Prevalence, Risk Factors and Prognosis of
Atypical Chest Pain in the Elderly
Previously published studies on the prevalence, risk
factors and prognosis of atypical chest pain in the elderly showed a 20–60% rate of unrecognized MI reflecting
possible differences in race, population, study design
and the definition used for MI diagnosis23–27. Specific
subgroups, including the elderly, persons with diabetes,
women and the very young, have been found to have a
higher misdiagnosis rate28. In the first three subgroups,
atypical symptoms are common, whereas the final
group is not usually considered owing to a generalized
low prevalence. In a large, prospective, populationbased cohort study with 4- to 20-year follow-up focusing on males in the Reykjavik area in Iceland,
nearly 30% of MIs were unrecognized16. The prevalence
increased steeply with age by up to 47% in the group
aged 75–79 years. Although there were no significant
differences in the risk profiles in the Reykjavik study,
increasing age (odds ratios, OR, 1.08; 95% confidence
interval, CI, 1.05–1.10), serum cholesterol level (OR,
International Journal of Gerontology | March 2010 | Vol 4 | No 1
■
1.06; 95% CI, 1.01–1.10), heavy smoking behavior (OR,
5.2; 95% CI, 1.6–15.2), cardiomegaly (OR, 2.0; 95% CI,
1.1–3.8), baseline angina symptoms (OR, 4.7; 95% CI,
2.8–7.7) and diuretics usage (OR, 6.2; 95% CI, 2.6–14.9)
were associated with a higher probability of unrecognized MI incidence. For those with unrecognized
MI, nearly one quarter of patients experienced sudden
death in the subsequent clinical course. In the
Honolulu, Hawaii, Heart Program published in 1989,
patients with unrecognized MI were associated with a
history of hypertension, diabetes or impaired glucose
tolerance, and higher levels of smoking behavior26.
In that study, the 10-year prognosis in terms of allcause mortality and associated cardiovascular disease
tended to be worse in the unrecognized group. Of
all 9,509 healthy adults followed for 5 years in the
Israeli Heart Attack study, age, left axis deviation by
electrocardiography (ECG), left ventricular hypertrophy,
smoking behavior, blood pressure, and the existence of
peripheral vascular disease after multivariate analysis
remained independent risk factors for the development
of unrecognized MI with a subsequent higher mortality
during 7-year follow-up25. In the Framingham Heart
study, nearly 53% of patients with unrecognized MI had
had a silent infarction with 47% having some atypical
symptoms with a 10-year mortality rate of up to 58%29.
Although the authors in that study failed to identify
any major predisposing risk factors for the onset of
unrecognized MI compared with those with recognized MI, they did notice that a history of diabetes,
hypertension and abnormal electrocardiograms were
associated with an increased incidence of unrecognized
MI. In the National Registry of Myocardial Infarction 2,
which enrolled 1,674 USA hospitals, 33% of patients
who had suffered an MI did not have the typical presentation of chest pain30. Similarly, those without chest
pain tended to be older, and there was a higher proportion of women, diabetics and heart failure comorbidities. Furthermore, patients with atypical presentations
were less likely to be treated with coronary angiography and percutaneous coronary intervention and had
a lower chance of anticoagulants, aspirin and β-blocker
usage in the same study. In a prospective, 8-year study
focusing on the prevalence, incidence and prognosis
of recognized and unrecognized MI in the aging population, about 34.7% of MI patients were older than
75 years. Around 7.9% of subjects had a history of
MI without ECG changes (existence of Q wave), and
6.4% of subjects had ECG evidence without having a
3
■
C.L. Hung et al
clinical MI history. Authors in that study concluded
that there was a higher prevalence of unrecognized
Q-wave MI in the old-old population aged 75–94 years31.
During an average follow-up of 76.2 months, the total
mortality rate was borderline higher for subjects with
some evidence of MI at baseline than that of the control group (5.9/100 person-years vs. 3.9/100 personyears; p = 0.059). Of all 20,881 participants in the recent,
prospective Global Registry of Acute Coronary Events
study involving 14 countries, atypical presentations of
ACS (8.4% in the whole cohort) increased with age and
with a higher female sex proportion9. Similarly, a significantly higher prevalence of congestive heart failure and diabetes was observed in the atypical group in
which the patients were also undertreated. Among all
atypical presentations in that study, about 50% presented with dyspnea and approximately one-fourth
presented with diaphoresis or gastrointestinal symptoms. In that study, painless presentations of unstable
angina carried the highest incidence of developing
subsequent in-hospital morbidity and mortality (OR,
2.2; 95% CI, 1.4–3.5). All hospital outcomes including
congestive heart failure, pulmonary edema, major
arrhythmias, acute renal failure and mortality were
higher in the atypical group than the group with typical
symptoms (13% vs. 4.3%; p < 0.0001). In a populationbased cohort, named the Rotterdam study, men and
women aged 55 or older from 1990–1993 had an incidence rate of unrecognized MI of around 3.8 per 1,000
person years, compared with that of recognized MI at
about 5.0 per 1,000 person years32. In the Rotterdam
study, the proportion of unrecognized MI was lower in
men (33%) than in women (54%). However, age did not
play a major role in the incidence of unrecognized MI
in men compared with women.
Mechanisms of Atypical Chest Pain
The major underlying reasons why patients develop
ACS without chest pain are not clear or heterogeneous,
although several possible mechanisms may play a
role. Different theories of such atypical chest pain in
patients with ACS have been proposed; but to date, no
single mechanism satisfactorily explains the full spectrum in this clinical phenomenon. Chest pain may
arise from the stimulation of either visceral or somatic
pain fibers. Visceral fibers originate from the heart,
esophagus, blood vessels and visceral pleura, which
4
■
enter the spinal cord at multiple levels. Stimulation of
these fibers from any cause produces symptoms that
are poorly localized and often difficult for patients to
describe. In contrast, somatic pain fibers originate from
musculoskeletal structures, the dermis and parietal
pleura, which may produce pain following a dermatomal pattern that is well localized and easily described33.
It has been suggested that the lack of nerve innervations in a donor heart not linked to the host’s nerve
system may be the main reason for developing silent
ischemia34. The repeated silent ischemic episodes after
MI may be due to the deprivation of afferent innervations created by critically placed infarctions35. The
elderly appear to have a somewhat reduced pain perception and tend to have more comorbidities such as
diabetes36. Haro et al.37 reported that elderly patients
may actually present more frequently with complaints
of fatigue, worsening congestive heart failure or even
altered mental status, lightheadedness and syncope.
Diabetes itself, which is associated with autonomic
nerve dysfunction, has been proven to be a predisposing factor for asymptomatic myocardial ischemic
events4. Moreover, diabetic patients are also more
likely to present with exercise intolerance and severe
fatigue, which may be confused with heart failure
symptoms or lightheadedness38.
The higher incidence of atypical chest pain in the
female population is due to higher simultaneous symptoms such as neck and shoulder pain, nausea, fatigue,
and dyspnea. In addition, the female population tends
to have postmenopausal coronary artery disease, which
may lead to higher comorbidities like diabetes or hypertension39. The elderly may suffer from more comorbidities, and it is very likely that the aging process
results in a higher incidence of diabetes40,41. It has also
been mentioned that an altered threshold to pain perception or various noxious stimuli (such as electrical
shock, pressure or cold) known as the “defective warning system” has been shown by Droste et al.42,43 to be
related to silent infarcts. An increased incidence and
link between silent MI or sudden death with diabetes has
been suggested, although some epidemiologic studies
failed to demonstrate this point very well7,44. Psychologic factors have also been proposed as a possible
mechanism in silent infarcts associated with diabetes.
Furthermore, an excess of endogenous endorphins or
possibly a particular biochemical inflammatory system
activation pattern involving microenvironmental balance between proinflammatory and anti-inflammatory
International Journal of Gerontology | March 2010 | Vol 4 | No 1
■
Atypical Chest Pain in the Elderly
cytokines have also been reported to be possible causes
of silent myocardial ischemia45,46.
Evolution of and Advances in Diagnostic
Tools for ACS
Although much effort has been made to assist the early
detection of ACS, the misdiagnosis and inappropriate
discharge rates remain high (up to 10%) as shown in
previous studies5,6,20. It has been shown that elderly
patients with ACS are less likely to have typical ECG
findings than younger patients. Moreover, they are less
likely than younger patients to present with ST segment
elevations (31.4% vs. 50.1%; p < 0.05) and are more
likely to present with left bundle branch block (8.0%
vs. 0.6%; p < 0.05)47. Elderly patients are also more likely
to have pacing rhythms from a previous pacemaker
implant as well as a previous MI history, both of which
may lead to more frequent non-diagnostic ECGs of
acute myocardial injury. Comparison with previous ECGs
is thus necessary48. A flowchart based on a prospective
protocol as a predictive model implemented on ECG
and clinical variables further aids the decision strategy
in cardiac care unit admission with a similar sensitivity
compared with physicians and an even higher specificity49. Chest radiography is a cost-effective diagnostic
tool that may influence the management strategy in
up to 23% of patients presenting at the ED with chest
pain50. In patients with pneumothorax or pneumomediastinum, chest radiography may be conclusive and
diagnostic, and may also provide a hint for the diagnosis of aortic dissection. Cardiac biochemical markers such as creatine kinase and creatine kinase MB are
key in the establishment of MI, whereas a more sensitive marker, troponin I, provides a more sensitive and
prognostic tool for ACS51,52. The utility of the D-dimer
marker test in elderly patients with acute chest pain has
been shown to provide a high sensitivity and a negative predictive value in the diagnosis of pulmonary
embolism53. Systematic and well-designed diagnostic
strategies combining serial cardiac markers and ECG may
help identify patients suffering from ACS when compared with routine methods54. In the detection of wall
motion abnormalities related to a specific coronary artery
territory, cardiac echography is also a useful and reliable
tool in the diagnosis of acute myocardial ischemia55,56.
A triage algorithm, developed by Pelliccia et al.57, based
on a scoring system including serial cardiac enzymes
International Journal of Gerontology | March 2010 | Vol 4 | No 1
■
follow-up, ECG, resting echocardiography and clinical
features has further improved the accurate diagnostic
rate and treatment in the elderly population, resulting
in comparable outcomes with the younger age group.
Using resting sestamibi perfusion images based on initial ECG and cardiac enzymes for the effective identification of initially unsuspected, high-risk patients who
may require a prompt intervention from those who
are truly at low risk has also been proposed58. ECG is
efficient as a rapid and convenient bedside test for the
detection of wall motion abnormalities at rest or
under stress test in the diagnosis of ACS55,59. Recently,
it has been shown that cardiac biomarkers, such as
brain-type natriuretic peptide and N-terminal fragment
of the prohormone brain natriuretic peptide, released
from the ischemic myocardium as a clinical predictive
value after ACS may actually reflect the severity of
myocardial ischemia or be related to ventricular wall
stress and systolic dysfunction after infarct60. White
et al.61 reported that in a study of 69 patients who underwent 16-slice computed tomography, in the patients
with cardiac or non-cardiac chest pain presenting in
the ED compared with those diagnosed by traditional
methods, the sensitivity and specificity were high for
the establishment of cardiac cause (83% and 96%, respectively) of chest pain and all (including cardiac and
noncardiac) causes (87% and 96%, respectively). A recently developed “triple rule-out” strategy using a
64-slice computed tomography examination protocol
for evaluation of acute MI, pulmonary embolism and
aortic pathology on a single, 12-second study has also
been proposed with acceptable diagnostic accuracy62–64.
The widespread application of such imaging modalities implemented on traditional diagnostics, however,
poses its own disadvantages and shortcomings such as
radiologic exposure and contrast load. However, White
et al.61 have further expanded the current diagnostic
and treatment triage leading to potentially better outcomes in the elderly population.
Conclusion
The incidence of atypical symptoms in the elderly population with ACS presenting at the ED is high, and
accurate diagnosis and urgent therapeutic intervention remain a challenge. Comorbidities are common
in this population who has a higher risk of being misdiagnosed or inappropriately discharged, leading to
5
■
C.L. Hung et al
worse outcomes. Efficient triage and further integration
of clinical features, biomarkers and emerging diagnostic
cardiovascular imaging in the future may help improve the accuracy of the diagnostic rate with subsequent better outcomes in this patient population.
15.
16.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
6
Barish RA, Doherty RJ, Browne BJ. Reengineering the
emergency evaluation of chest pain. J Health Qual 1997;
19: 6–12.
Roberts RR, Zalenski RJ, Mensah EK, et al. Costs of an
emergency department-based accelerated diagnostic
protocol vs. hospitalization in patients with chest pain:
a randomized controlled trial. JAMA 1997; 278: 1670–6.
Stussman BJ. National Hospital Ambulatory Medical
Care Survey: 1995 emergency department summary.
Adv Data 1997; 285: 1–19.
Lee TH, Goldman L. Evaluation of the patient with acute
chest pain. N Engl J Med 2000; 342: 1187–95.
Lee TH, Rouan GW, Weisberg MC, et al. Clinical characteristics and natural history of patients with acute
myocardial infarction sent home from the emergency
room. Am J Cardiol 1987; 60: 219–24.
Christenson J, Innes G, McKnight D, et al. Safety and efficiency of emergency department assessment of chest
discomfort. CMAJ 2004; 170: 1803–7.
Pope JH, Aufderheide TP, Ruthazer R, et al. Missed diagnoses of acute cardiac ischemia in the emergency
department. N Engl J Med 2000; 342: 1163–70.
Canto JG, Shlipak MG, Rogers WJ, et al. Prevalence, clinical characteristics, and mortality among patients with
myocardial infarction presenting without chest pain.
JAMA 2000; 283: 3223–9.
Brieger D, Eagle KA, Goodman SG, et al. Acute coronary
syndromes without chest pain, an underdiagnosed and
undertreated high-risk group: insights from the Global
Registry of Acute Coronary Events. Chest 2004; 126: 461–9.
Boie ET. Initial evaluation of chest pain. Emerg Med
Clin North Am 2005; 23: 937–57.
Jones ID, Slovis CM. Emergency department evaluation
of the chest pain patient. Emerg Med Clin North Am
2001; 19: 269–82.
Konotos MC. Evaluation of the emergency department
chest pain patient. Cardiol Rev 2001; 9: 266–75.
Lakatta EG, Levy D. Arterial and cardiac aging: major
shareholders in cardiovascular disease enterprises, part I:
aging arteries: a “set-up” for vascular disease. Circulation
2003; 107: 139–46.
Franklin SS, Larson MG, Khan SA, et al. Does the relation
of blood pressure to coronary heart disease risk change
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
■
with aging? The Framingham Heart Study. Circulation
2001; 103: 1245–9.
Calle P, Jordaens L, De Buyzere M, et al. Age-related differences in presentation, treatment and outcome of
acute myocardial infarction. Cardiology 1994; 85: 111–20.
Sigurdsson E, Thorgeirsson G, Sigvaldason H, et al.
Unrecognized myocardial infarction: epidemiology, clinical characteristics, and the prognostic role of angina
pectoris. The Reykjavik Study. Ann Intern Med 1995;
122: 96–102.
Borzecki AM, Pedrosa MC, Prashker MJ. Should noncardiac chest pain be treated empirically? A cost-effectiveness analysis. Arch Intern Med 2000; 160: 844–52.
Panju AA, Hemmelgarn BR, Guyatt GH, et al. Is this
patient having a myocardial infarction? JAMA 1998; 280:
1256–63.
Yen M, Wischmeyer JB, Kapadia SR. Chest pain assessment
at the hospital admission room. In: Griffin B, Topol D.
Cardiology textbook. Cleveland Clinic MediPage 2006;
506–14.
Swap CJ, Nagurney JT. Value and limitations of chest pain
history in the evaluation of patients with suspected
acute coronary syndromes. JAMA 2005; 294: 2623–9.
Braunwald E, Antman EM, Beasley JW, et al. ACC/AHA
2002 guideline update for the management of patients
with unstable angina and non-ST-segment elevation
myocardial infarction—2002: summary article: a report
of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines (Committee
on the Management of Patients With Unstable Angina).
Circulation 2002; 106: 1893–900.
Yen MH, Wischmeyer JB, Kapadia SR. Evaluation of
chest pain in the emergency department. In: Griffin BP,
Topol EJ, eds. Manual of Cardiovascular Medicine, 2nd
edition. Philadelphia: Lippincott Williams & Wilkins,
2004; 498–505.
Rosenman RH, Friedman M, Straus R, et al. Coronary
heart disease in the Western Collaborative Group Study:
a follow-up experience of 4 and one-half years. J
Chronic Dis 1970; 23: 173–90.
Kannel WB. Prevalence and clinical aspects of unrecognized myocardial infarction and sudden unexpected
death. Circulation 1987; 75: II4–5.
Medalie JH, Goldbourt U. Unrecognized myocardial
infarction: five-year incidence, mortality, and risk factors. Ann Intern Med 1976; 84: 526–31.
Yano K, MacLean CJ. The incidence and prognosis of
unrecognized myocardial infarction in the Honolulu,
Hawaii, Heart Program. Arch Intern Med 1989; 149:
1528–32.
Roseman MD. Painless myocardial infarction: a review
of the literature and analysis of 220 cases. Ann Intern
Med 1954; 41: 1–8.
International Journal of Gerontology | March 2010 | Vol 4 | No 1
■
Atypical Chest Pain in the Elderly
28. Croskerry P. Achilles’ heels of the ED: delayed or missed
diagnoses. ED Legal Lett 2003; 14: 109–20.
29. Margolis JR, Kannel WB, Feinleib M, et al. Clinical features of unrecognized myocardial infarction—silent
and symptomatic. Eighteen year follow-up: the Framingham Study. Am J Cardiol 1973; 32: 1–7.
30. Vaccarino V, Parsons L, Every NR, et al. Sex-based differences in early mortality after myocardial infarction.
National Registry of Myocardial Infarction 2 Participants.
N Engl J Med 1999; 341: 217–25.
31. Nadelmann J, Frishman WH, Ooi WL, et al. Prevalence,
incidence and prognosis of recognized and unrecognized
myocardial infarction in persons aged 75 years or older:
the Bronx Aging Study. Am J Cardiol 1990; 66: 533–7.
32. de Torbal A, Boersma E, Kors JA, et al. Incidence of recognized and unrecognized myocardial infarction in men
and women aged 55 and older: the Rotterdam Study.
Eur Heart J 2006; 27: 729–36.
33. Kelly BS. Evaluation of the elderly patient with acute
chest pain. Clin Geriatr Med 2007; 23: 327–49.
34. Gibson CM. Myocardial infarction. In: Rubin E, Gorstein F,
Schwarting R, et al, eds. Rubin’s Pathology: Clinicopathologic Foundations of Medicine. Maryland: Lippincott
Williams & Wilkins, 2001; 549.
35. Yeung AC, Barry J, Selwyn AP. Silent ischemia after
myocardial infarction. Prognosis, mechanism, and
intervention. Circulation 1990; 82(3 Suppl): II143–8.
36. Gregoratos G. Clinical manifestations of acute myocardial
infarction in older patients. Am J Geriatr Cardiol 2001;
10: 345–7.
37. Haro LH, Decker WW, Boie ET, et al. Initial approach to
the patient who has chest pain. Cardiol Clin 2006; 24:
1–17.
38. Cooper S, Caldwell JH. Coronary artery disease in people with diabetes: diagnostic and risk factor evaluation.
Clin Diabetes 1999; 17: 58–72.
39. Douglas PS, Ginsburg GS. The evaluation of chest pain
in women. N Engl J Med 1996; 334: 1311–5.
40. Caughey GE, Vitry AI, Gilbert AL, et al. Prevalence of
comorbidity of chronic diseases in Australia. BMC Public
Health 2008; 8: 221.
41. Fillenbaum GG, Pieper CF, Cohen HJ, et al. Comorbidity
of five chronic health conditions in elderly community
residents: determinants and impact on mortality. J
Gerontol A Biol Sci Med Sci 2000; 55: 84–9.
42. Droste C, Kardos A, Brody S, et al. Baroreceptor
stimulation: pain perception and sensory thresholds.
Biol Psychol 1994; 37: 101–13.
43. Droste C, Roskman H. Experimental pain measurement
in patients with asymptomatic myocardial ischemia.
J Am Coll Cardiol 1983; 1: 940–5.
44. Davis TM, Fortun P, Mulder J, et al. Silent myocardial
infarction and its prognosis in a community-based cohort
International Journal of Gerontology | March 2010 | Vol 4 | No 1
45.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
■
of type 2 diabetic patients: the Fremantle Diabetes Study.
Diabetologia 2004; 47: 395–9.
Tabibiazar R, Edelman SV. Silent ischemia in people
with diabetes: a condition that must be heard. Clin
Diabetes 2003; 21: 5–9.
Li JJ. Silent myocardial ischemia may be related to
inflammatory response. Med Hypotheses 2004; 62:
252–6.
Boucher JM, Racine N, Thanh TH, et al. Age-related differences in in-hospital mortality and the use of thrombolytic therapy for acute myocardial infarction. CMAJ
2001; 164: 1285–90.
Rich MW. Epidemiology, clinical features, and prognosis
of acute myocardial infarction in the elderly. Am J
Geriatr Cardiol 2006; 15: 7–11.
Goldman L, Cook EF, Brand DA, et al. A computer protocol to predict myocardial infarction in emergency department patients with chest pain. N Engl J Med 1988; 318:
797–803.
Bean DB, Roshon M, Garvey JL. Chest pain: diagnostic
strategies to save lives, time, and money in the ED.
Emerg Med Pract 2003; 5: 1–32.
Puleo PR, Meyer D, Wathen C, et al. Use of a rapid assay
of subforms of creatine kinase MB to diagnose or rule out
acute myocardial infarction. N Engl J Med 1994; 331:
561–6.
Zimmerman J, Fromm R, Meyer D, et al. Diagnostic
marker cooperative study for the diagnosis of myocardial infarction. Circulation 1999; 99: 1671–7.
Kruip MJHA, Slob MJ, Schijen JHEM, et al. Use of a clinical decision rule in combination with D-dimer concentration in diagnostic workup of patients with suspected
pulmonary embolism: a prospective management
study. Arch Intern Med 2002; 162: 1631–5.
Gomez MA, Anderson JL, Karagounis LA, et al. An emergency department-based protocol for rapidly ruling out
myocardial ischemia reduces hospital time and
expense: results of a randomized study (ROMIO). J Am
Coll Cardiol 1996; 28: 25–33.
Sabia P, Abbott RD, Afrookteh A, et al. Importance of
two-dimensional echocardiographic assessment of left
ventricular systolic function in patients presenting to
the emergency room with cardiac-related symptoms.
Circulation 1991; 84: 1615–24.
Hung CL, Lo CI, Yen CH, et al. Pattern and impact of
altered regional myocardial excursion on global ventricular performance after first-time acute anterior wall
myocardial infarction by real-time three-dimensional
echocardiography. Int J Gerontol 2008; 2: 196–205.
Pelliccia F, Cartoni D, Verde M, et al. Comparison of presenting features, diagnostic tools, hospital outcomes,
and quality of care indicators in older (> 65 years) to
younger, men to women, and diabetics to nondiabetics
7
■
58.
59.
60.
61.
8
C.L. Hung et al
with acute chest pain triaged in the emergency department. Am J Cardiol 2004; 94: 216–9.
Tatum JL, Jesse RL, Kontos MC, et al. Comprehensive
strategy for the evaluation and triage of the chest pain
patient. Ann Emerg Med 1997; 29: 116–25.
Hauser AM. The emerging role of echocardiography in
the emergency department. Ann Emerg Med 1989; 18:
1298–303.
Sabatine MS, Morrow DA, de Lemos JA, et al.
Multimarker approach to risk stratification in non-ST
elevation acute coronary syndromes: simultaneous
assessment of troponin I, C-reactive protein, and B-type
natriuretic peptide. Circulation 2002; 105: 1760–3.
White CS, Kuo D, Kelemen M, et al. Chest pain evaluation in the emergency department: can MDCT provide a
■
comprehensive evaluation? AJR Am J Roentgenol 2005;
185: 533–40.
62. Takakuwa KM, Halpern EJ. Evaluation of a “triple rule-out”
coronary CT angiography protocol: use of 64-section CT in
low-to-moderate risk emergency department patients
suspected of having acute coronary syndrome. Radiology
2008; 248: 438–46.
63. Schussler JM, Smith ER. Sixty-four-slice computed tomographic coronary angiography: will the “triple rule out”
change chest pain evaluation in the ED? Am J Emerg
Med 2007; 25: 367–75.
64. Runza G, La Grutta L, Alaimo V, et al. Comprehensive
cardiovascular ECG-gated MDCT as a standard diagnostic tool in patients with acute chest pain. Eur J Radiol
2007; 64: 41–7.
International Journal of Gerontology | March 2010 | Vol 4 | No 1