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Transcript
Dr Charles Panackel
Consultant Gastroenterologist
Medical Trust Kochi
Introduction
 25% of general population experience chest pain at
some point of life
 Of these only 11 -39% have cardiac pain
Definition
 Noncardiac Chest pain can be defined as recurrent
angina-like or substernal chest pain believed to be
unrelated to the heart after reasonable cardiac
evaluation.
 What is reasonable ???
 Unexplained Chest Pain (UCP)
Epidemiology
• The mean annual prevalence of NCCP in the general
population is approximately 23-33%
• NCCP accounts for approximately 2% to 5% of all
presentations to hospital emergency
• Both sexes equally affected
• Women seek medical attention more commonly
Epidemiology
 Prevalence of NCCP decrease with increasing age.
 Patients with NCCP are




Younger,
Consume greater amounts of alcohol,
Smoke more,
Suffer from anxiety than their counterparts with ischemic heart
disease.
Natural History
 The long-term mortality of NCCP is low with
reported rates of 1% at 10 yr
 Morbidity is high
• At one year after diagnosis, it is seen that 47% limited
their activities, 51% were unable to work and 44% still
believed they had CAD.
 NCCP patients have continued high rates
healthcare use
Differential Diagnosis
NCCP
Miscellaneous
16%
Musculoskeletal
36%
Pulmonary
pericardial
Panic disorder
7.5%
5%
Esophageal
19%
Gastric/Biliary
Pancreatic
Chest pain of Esophageal origin
 Osler in 1892 first suggested that esophagus may be
source for Unexplained chest pain
 23–80% of Patients with Unexplained chest pain have
esophageal abnormalities
Differential Diagnosis
Psychological
comorbidity
Esophageal
Esophageal dymotility
GERD
Functional chest pain
of esophageal origin
15-18%
50-60%
32 -35%
Pathophysiology
 Chest pain of esophageal origin could be caused by
• Noxious event in the esophagus,
• Acid reflux
• Nonacid reflux
• Esophageal distension
• Disturbed motility
• Abnormal mechanophysical properties of esophagus
• Sustained contractions of longitudinal muscles
• Visceral hypersensitivity


Decrease in the esophageal nociceptive sensory receptor threshold,
Disorder in the nociceptive pathway in the peripheral or central nervous system


Autonomic dysregulation
Altered central processing of pain stimuli

Somatoform disorders
GERD and NCCP
GERD and NCCP
 GERD is by far the most common cause for NCCP
Esophageal Dysmotility and NCCP
 28% of patients with Non
GERD related NCCP
 No correlation between
symptoms and abnormality
on Manometry
 Response to muscle
relaxants poor
Functional chest pain of presumed
esophageal origin
 Recurrent episodes of substernal chest pain of visceral
quality with no apparent explanation.
 GERD and esophageal dysmotility should be ruled out.
 Up to 80% of the patients with functional chest pain
exhibit other functional disorders
 Visceral and somatic hypersensitivity
Approach to Non Cardiac Chest
Pain
 Cardiac source reasonably ruled out.
 Other causes ruled out
Approach to Noncardiac Chest Pain
 A careful, thorough history looking for cardiac risk factors,
 12-lead ECG, chest radiograph,
 Serial measurements of cardiac enzymes,
 If the patient is stable and the etiology is still unclear,
echocardiography and TMT
 Coronary angiogram
What should be done next?
 Endoscopy
 Ambulatory pH monitoring
 Combined Impedance-pH testing
 Esophageal manometry
 Acid suppression therapy or PPI test.
Endoscopy
 Variable diagnostic yield (10-44%) in NCCP
patients
 Not likely to change management
 Reserved for patients with NCCP and alarm
symptoms (Anemia, Dysphagia, GI Bleed, Persistent Vomiting, Weight loss)
Ambulatory 24 hr pH TESTING
Ambulatory 24 hr pH TESTING
 Sensitivity has ranged from 79% to 96% and specificity
from 85% to 100%
 Can be done on or off PPIs.
 Diary allows correlation between symptoms and acid
reflux.
Ambulatory 24 hr pH TESTING
 Invasive- greater pt discomfort ( occ chest pain)
 Can miss up to 25% of cases of reflux-not due to “acid”
 Value in patients with NCCP in whom objective evidence is
required
 Patients who do not respond to PPI
Impedance-pH monitoring
 Has added sensor for
impedance.
 It detects any bolus that
enters the esophagusacid, bile or other.
 Increases the sensitivity
of the probe
 Same disadvantages as
pH probe
 The gold standard for diagnosis of GERD-related NCCP.
Impedance-pH monitoring
Impedance-pH monitoring
Esophageal Manometry
 A thin probe is inserted intranasally and
advanced into distal esophagus.
 Measurements are recorded
as the
pt is asked to swallow sips of
water.
 Goal is to rule out motility
disorders of the esophagus as
for chest pain.
cause
Esophageal Manometry
 Esophageal motility disorder is seen in approximately
one third of NCCP patients.
 However, the relationship between these motility
disorders and chest pain is unclear
 Considered in patients with a negative work-up for
GERD-related NCCP.
 Role of manometry in NCCP is limited to diagnosis of
achalasia cardia
Proton pump inhibitor test
 Empiric trial of double dose PPI therapy for 4 weeks.
 Readily available
 Cheap
 Noninvasive
 Well tolerated with few if any side effects.
 Both diagnostic and therapeutic advantages
Proton Pump Inhibitor test
 Two meta-analyses combining 14 studies have
validated the PPI test.
 Sensitivity and specificity of 75-80%.
 Positive predictive value of ~90%.
 One study, using a decision analysis model, found
the “treat first” approach to be better
 11% more diagnostic accuracy
 43% reduction in invasive procedures
 $454 saving per patient as compared to proceeding with endoscopy
and pH monitoring.
NCCP Esophageal Origin
Alarm
Symptoms
Yes
Endoscopy
No
Impedence
pH
Monitoring
Normal
Esophageal
Manometry
Achalasia
No Response
PPI Test
Response
Reflux
GERD
Normal
Other spastic
disorders
Functional
esophageal pain
Psychological
evaluation
Treatment of NCCP of esophageal
origin
GERD-related NCCP
 Life style modification
 Elevation of the head of the bed,
 Weight loss,
 Smoking cessation,
 Avoidance of alcohol, coffee, fresh citrus juice,
 Medications that can exacerbate reflux such as
narcotics, benzodiazepines, and calcium-channel
blockers.
GERD-related NCCP
 The efficacy of histamine-2 receptor antagonists (H2
RAs) in GERD related NCCP range from 42% to 52%
 The efficacy of PPI in controlling symptoms in patients
with GERD related NCCP range from 57.1% to 87%
GERD-related NCCP
 PPIs reduce the number of chest pain episodes,
emergency department visits, and hospitalizations
owing to chest pain
 Patients with GERD-related NCCP should be treated
with at least double the standard dose of PPI until
symptoms remit
 Long-term maintenance PPI treatment has been
shown to be highly effective.
GERD-related NCCP
 Lap Fundoplication
 In carefully selected patients lap fundoplication results
symptom improvement in 48 % to 90% of patients with
NCCP.
NON GERD related NCCP
 Visceral hyperalgesia is the primary mechanism of pain in
patients with non-GERD-related NCCP
 NCCP patients with spastic esophageal motor disorders
respond better to pain modulators than to muscle relaxants.
 Patients with spastic esophageal disorders should receive a
trial of PPI
 Patients with achalasia respond to muscle relaxants, balloon
dilatation, botox injection or heller’s myotomy
NON GERD related NCCP
 Pain Modulators
 Tricyclic antidepressants (TCAs)
 Selective serotonin reuptake inhibitors
 Theophylline
 Trazodone.
NON GERD related NCCP
 TCA



Central neuromodulatory effect
Peripheral visceral analgesic effects
Calcium channels blocker
 TCA are started in low dose and titrated to a maximum
based on symptom improvement and development of
side effects.
 Because of their anticholinergic side effects, TCAs are
commonly administered at nighttime.
NON GERD related NCCP
 Benzodiazepine
 Alprazolam and clonazepam ameliorate chest pain in
patients with NCCP and panic disorder
 Addiction
Psychological evaluation
 Between 17 and 43% of the patients with NCCP have
some type of psychological abnormality.
 Psychological co-morbidity can lead to Visceral
Hypersensitivity.
 Psychotherapy is useful in patients with NCCP and
hypochondriasis, anxiety, or panic disorder.
NCCP
Esophageal
Origin
Impedance
pH
Monitoring
No Response
Response
PPI for 2-4
months
PPI Test
GERD
No GERD
Response
Increase dose of
PPI
Esophageal
Manometry
Achalasia
Relaxants
Balloon dilatation
Hellers myotomy
Normal
Other spastic
disorders
Functional
esophageal pain
PPI
Pain Modulators
Psychotherapy
Maintenance
Summary
 NCCP is a very common problem with high cost to the
healthcare system and significant morbidity to the
patient.
 The most common cause of NCCP is GERD.
 An empiric trial of high dose PPI therapy is the single
most effective approach to dealing with NCCP.
Summary
 Endoscopy is reserved for patients with alarm signs
 Impedence pH monitoring and Esophageal
manometry, has a limited role in NCCP
TREATMENT
Summary
 GERD related NCCP is treated with double dose PPI
 Non GERD related NCCP – the main stay of treatment
is Pain Modulators
 Psychotherapy for patients with psychological
comorbidity.
 Typical angina (80-90% likelihood of obstructive CAD),
 Atypical angina (40-80% likelihood)
 Noncardiac (20%-70% likelihood).
 Typical angina is characterized by the following three
characteristics:
 Retrosternal chest discomfort experienced as pressure or
heaviness;
 Duration of 5-15 min
 Induced by stress or exertion, a large meal, or exposure to
cold and relieved by rest or nitroglycerin.
 Mechanical distention, acid exposure, temperature,
and osmolality-related stimuli can all induce
esophageal pain.
 Esophageal dysmotility may also induce symptoms of
heartburn and chest pain.
 Visceral hypersensitivity has been implicated in the
pathogenesis of esophageal pain.
 Psychiatric disease plays a role in heartburn and chest
pain.
 The entity of noncardiac chest pain (NCCP) was first
described during the American Civil War when a
Philadelphia physician, Jacob Mendez Da Costa,
NCCP
Esophageal
Origin
Alarm
symptoms
No
Yes
PPI Test
Endoscopy
Response
present
No response
Impedence
pH
Measurement
GERD
No GERD
Esophageal
Manometry
Motility
disorder
Normal
Psychological
Evaluation