Cardiovascular System

Cardiovascular IV: Cardiac OMM

Research
Dennis A. Burke, D.O.
 Objectives
1. Describe the strategies for approaching
clinical research.
2. Describe the models for clinical research.
3. Describe the impact of the osteopathic
research on the MI patient.
4. Describe Irvin Korr’s research on the
autonomics.
5. Describe Louisa Burns research on
cardiac tissue
6. Describe the impact of osteopathic
research and its implications to current
medical practice.
7. Describe osteopathic diagnosis and
treatment into the overall medical
management of the patient who presents
with myocardial infarction
 The research challenge

• Research is the engine that

drives modern clinical practice
• Osteopathic profession and the
research culture
• Need to develop the
infrastructure for research
• Osteopathic Research will
define the profession and how
we use OMT.
 Research Challenge
• 1960s California merger
• Profession rallied and won,
but missed out on research
funding opportunities
• NIH expanded in 1960s,
with increased funding for
biomedical research
facilities.
• New DO schools in 1970s-
first wave of biomedical
research expansion was
over.
• By 2000, research efforts by
the profession had greatly
improved.
• However, it lacked an
element (maturity) that
characterized many
research efforts sponsored
by the NIH.
• NIH sponsored centers of
excellence for directed
research efforts.
 Osteopathic Research
Centers of Excellence

• UNT-COM
• AT Still Research Institute
 Strategies for OMT
Research
• Gold Standard =
randomized, double-blind,
placebo-controlled study
• Works very well for
pharmaceuticals, but not so
well for OMT
• Osteopathic physician
cannot be blinded to
whether OMT given or not.
 Randomization
• Population Selection- if data
for OMT research is used
from DO’s practice, this will
not be randomized.
• Patients typically self-select
to get osteopathic treatment,
and are motivated.
• This bias must be taken into
account.
 Placebo Control Groups
• Designed to take the
psychological effects of the
patient’s knowledge of effects of
medication on disease out of
the picture.
• “Sham OMT” has therapeutic
value from act of touch
• Structural exam is sometimes
used as the “sham”
• Both groups get structural
exam, control group rests while
other group gets OMT
• Can blind patient, and all
other personnel besides DO
• Light touch (sham OMT) vs.
OMT not an adequate
placebo design.
• You need a no-touch group
• Clinical efficacy study- be
careful not to have too many
assumptions in the study
• Enthusiasm to “prove” OMT
works
• Observational study
design can lead to
identifying what might be
efficacious for a specific
condition
• Then move to well-
controlled clinical efficacy
study to optimize getting
meaningful data.
Models of OMT Research
• Effectiveness of technique
vs. manipulative treatment
– Effect on patient’s complaint
is measured
– Functional outcome can be
measured (ie. clinically
disease-free patients with
SD have outcome measured
from OMT, such as ADLs)
Early Osteopathic Research
• Louisa Burns, MS, DO
• Started out as school teacher,
but developed spinal
meningitis and couldn’t work.
• Family moved to CA. She was
treated regularly with OMT by
George Burton, DO with highly
successful results.
• Graduated from Pacific College
of Osteopathy in 1903.
• Active in research from 1914-
1957.
 Louisa Burns D.O.
• Dr. Burns studied the
pathological effects on viscera
of induced somatic
dysfunctions, mostly in rabbits.
• Also described the pathological
changes in paraspinal
musculature in region of
somatic dysfunction. Typically,
histological changes of
congestion and fibrosis found.
• She also studied the impact of
OMT in humans on heart rate
and blood pressure.
• Wrote a textbook in 1948
published by the AOA,
“Pathogenesis of Visceral
Disease Following Vertebral
Lesions”
 Louisa Burns D.O.
• 32 rabbits with induced somatic
dysfunctions of T3 and T4.
• All showed some functional
disturbances of the heart while still
alive (ie. rapid and irregular heart
beat).
• Some rabbits would receive OMT
with a normalization of heart rate
during treatment.
• On autopsy, in the non-OMT rabbits
with somatic dysfunction of T3-4, the
heart was atonic and easily torn.
• Microscopic examination of the
myocardium in this group revealed
congestion, edema, capillary
hemorrhages and fibrosis.
 Louisa Burns D.O.

• Microscopic examination of the

myocardium of rabbits who had
somatic dysfunctions treated
with OMT showed much less
pathological changes than
untreated, with control group
(ie. no somatic dysfunction)
showing no pathological
changes.
• Degree of pathological
changes corresponded to how
long the somatic dysfunctions
were present.
 A.T. Still, MD

• The significance of the

Autonomic nervous system was
recognized.
• “ Heart disease is never found
without an impingement of the
pneumogastric (vagus) nerve at
some point.”
-Research and Practice, pg. 99
 Wilbur V. Cole, D.O., M.A.
Neurologist and Researcher
• 1950’s: induced somatic
dysfunction of the atlas in rats
(steady pressure on transverse
process of C1 daily for 14
days, then twice weekly until
animal was sacrificed)
• Rats killed after 4 months
• Rats with somatic dysfunction
showed hemorrhages between
muscle fibers of myocardium.
• Rats in control group showed
normal myocardial tissue
 Irvin M. Korr, PhD
• PhD in physiology from Princeton
University
• Taught physiology at NYU school
of medicine.
• During WW II worked for the US
war department studying climate
physiology and aviation
medicine.
• Worked at KCOM and TCOM for,
publishing over 60 papers.
• Extensive research on role of the
ANS in health and disease.
• Advanced the concept of spinal
facilitation.
• Described the trophic function of
nerves.
 Irvin M. Korr, PhD
• Described how somatic
dysfunction could impact reflex
patterns between the MSK
system and ANS.
• Studied cutaneous sudomotor
and vasomotor changes
related to myofascial and
visceral distrubances. Changes
were due to afferent
bombardment triggering
increased SNS activity.
• Researched how a facilitated
sympathetic nervous system
could become a common
denominator in a wide variety
of disease entities.
SNS actually subservient to the “primary
machinery of life”, the MSK system.
 Irvin M. Korr, PhD

• Hyperactivity of the SNS has

been found to be
responsible for some of the
post-MI complications, such
as ventricular fibrillation and
other arrhymias.
• High SNS activity is
associated with cardiogenic
shock.
Nicholas AS, et al. A Somatic Component to
Myocardial Infarction. British Medical Journal.
1985 July 6; 291: 13-17.
• 3 groups with 62 patients total
• 25: acute MI
• 22: controls (no cardiac disease)
• 15: ancillary group (non-MI
cardiac disease)
Nicholas AS, et al. A Somatic Component
to Myocardial Infarction. British Medical
Journal. 1985 July 6; 291: 13-17.
• Control 29% had left-sided
thoracic dysfunctions but
were scattered throughout
T1-8
• MI patients 67% had left-
sided thoracic dysfunctions
clustered to T1-4 (p<0.001)
• Ancillary group: more
clustered to T1-4 than
controls but still more widely
distributed than MI patients
 Myron Beal, DO
“Somatic Dysfunction as a Predictor of
Coronary Artery Disease”, JAOA/Vol.85/No 5,
May 1985
• 99 patients scheduled for cardiac
catheterization.
• Examined with use of a compression
test by blinded D.O. the day prior to
cardiac cath.
• Varied cardiac diagnoses (CAD,
HTN, CHF, MI, angina, AS)
• Most common somatic dysfunction
found at T2 and T3 on the left.
• SD at C2 on the left was also found
in a higher proportion of pts. w/ CAD
 Myron Beal, DO
• In 70 pts, diagnosed SD correlated
with CAD on catheterization.
• 15 pts. were diagnosed with SD,
but the catheterization was
reported as normal or subclinical.
– 6 had subclinical CAD
– 1 had an enlarged heart
– 1 had R coronary artery spasm
– 2 had a H/O MI
– 1 had spontaneous cardiac arrest
with anoxic encephalopathy
– 1 had HTN
– 3 had symptoms of chest pain
 Palpatory Findings and the
Anatomical Locus of Acute MI
• JAOA Feb 1987, Hugo O.
Rosero, DO
• N=62
• 3 groups:
– 25 w/ acute MI
– 15 w/ heart disease other
than MI
– 22 w/ no CV disease
 Hugo O. Rosero, DO
1987

• Anterior wall MI- readily

palpable findings, described
as warmth and tense and
resistant musculature in the
upper thoracic spine.
• Inferior wall MI- palpable
findings in the thoracic spine
were more difficult to detect
and describe.
 Joseph Rogers, DO
JAOA, Sept 1976
• Referenced previous report of
improvement in EKG after
exercise before and after
exercise.
• Pts. w/ active substernal chest
pain had cardiac angiograms
that showed no blockage.
• Felt that vasospasm and
abnormal myocardial
metabolism were important
features of coronary
insufficiency, and that OMT
could play an important role in
care of these patients by
normalization of ANS tone.
 Fitzgerld M, Stiles E. Osteopathic
Hospitals’Solution to DRGs May Be
OMT. The DO. 1984 Nov; 97-101.
• 50 MI patients treated by
the same internist at a
hospital in Maine
• 19 received OMT, with first
treatment within 24 hours of
admission
13% decreased incidence of arrythmias, 14% decreased incidence
of shock, and 10% reduction in mortality in OMT group
 Anatomical & Physiological
Relationships

• Relevant Fascial Connections

– Superior
– Inferior
• Lymphatics
• ANS
• Thoracic and Cervical Spine
 Fascial Connections
Prevertebral fascia:
extends from the cranial base,
descending in front of the longus
colli muscle, extending laterally
to cover the anterior and middle
scalene muscles, and levator
scapulae muscle.
Inferiorly it goes into the
superior mediastinum, where it
blends with the anterior
longitudinal ligament at the level
of T3.
 Fascial Connection

Pretracheal Fascia: extends

from the hyoid, thyroid
cartilage, and arch of the
cricoid cartilage, lies deep to
the infrahyoid muscles, and
descends into the thorax to fuse
with the fibrous pericardium.
www.chestofbooks.com
Prevertebral fascia in blue
Pretracheal fascia in orange
 Pericardium
Fibrous pericardium- compact
collagenous fibrous tissue; attached to
sternum anteriorly (sterno-pericardial
ligament); posteriorly blends with
posterior mediastinal structures, which
are attached to vertebrae
Serosal pericardium- closed sac consisting
of a single layer of cells that is
contained within fibrous pericardium
Sterno-pericardial ligament
 Importance in
Considering Fascial
Connections
• Altered A-P and Lateral curves can
compromise cardiac function
• Thoracic, rib and diaphragm
somatic dysfunction can
significantly affect fibrous
pericardium
• Cranial base and cervical spine
dysfunctions can affect origin of
prevertebral and pretracheal fascia
Anatomy, Clemente, 4th ed.
LE or pelvic somatic dysfunction
can affect diaphragm, and
subsequently the pericardium.
 Lymphatics
• Lymphatics from the heart
primarily drain by the right
lymphatic duct.
• Impaired lymphatic drainage
has been linked to the
development of
atherosclerosis and HTN.
• Impaired lymphatic drainage
has also been implicated in
reduced collateral circulation
post-MI, and with increased
mortality and morbidity.
 A.J. Miller
Feinberg School of Medicine
Northwestern University
• “The possible role of the
cardiac lymphatic system in the
etiology and development of
various human conditions and
diseases has been almost
wholly ignored.”
• Dogs with surgically-impaired
cardiac lymphatics displayed
exaggerated and prolonged
inflammatory reactions post-MI.
 A.J. Miller
• “Impairment of lymph flow from
an organ is associated with
inflammation, fibrosis and
predisposition to infection.”
• “…the integrity of cardiac
lymph flow plays a role in the
development of coronary
epicardial atherosclerosis…”
– Medical Hypotheses 76 (2011)
604-606
 Jones and Min
Yale University School of Medicine
Journal of Cardiovascular Disease Research,
2011, Vol 2/No 3
• Acute myocardial lymph flow
impairment in dogs leads to
cardiac edema and
hemorrhage.
• Chronic myocardial lymph
flow impairment lead to
edema, hemorrhage,
deposition of fibrous and
elastin tissue, and reduced
cardiac function.
 Myocardial lymphatics in post-
mortem specimens are not grossly
visible, and require special staining
techniques.

www.hindawi.com
Lymphatic stomata
www.flylib.com
Mouse embryo- sympathetic nerve
fibers (green) follow the
development of cardiac vessels
www.nhlbi.nih.gov
 Sympathetic Nervous System
• Sympathetic cell bodies originate
in the first through sixth thoracic
cord segments
• Superior cervical ganglia lies
anterior to C2-3 TPS and gives off
a cardiac branch
• Middle cervical ganglia gives rise
to a cardiac branch, and is situated
anterior to C5-6 TPs.
• Inferior cervical (stellate) ganglia is
situated between C7 TP and neck
of 1st rib.
SNS Innervation of
the Heart
• Fibers of the right cardiac
plexus innervate the SA node,
with hypersympathetic activity
predisposing to SVTs.
• Fibers of the left cardiac plexus
innervate the AV node, with
hypersympathetic activity
predisposing to ectopic foci and
ventricular fibrillation.
• Asymmetry of SNS tone
between right and left cardiac
plexi has been implicated in the
development of arrythmias.
Sympathetic ganglia are enveloped in
the endothoracic fascia, and are
anterior to the rib angles.
 Parasympathetic
Innervation
• Vagus Nerve
• Courses through jugular
foramen, anterior to the
occipito-mastoid (OM) suture
• Inferior vagal ganglia are in
relation to C1-C2 vertebra
• Important areas of SD
reflecting vagal dysfunction
include the OM suture, OA, AA
and C2.
 Parasympathetic
Supply
• Right vagus primarily
innervates the SA node, with
right vagal hyperactivity
predisposing to sinus
bradyarrythmias.
• Left vagus primarily
innervates the AV node, with
left vagal hyperactivity
predisposing to AV blocks.
MYOCARDIAL INFARCTION
 INCREASED
SYMPATHETIC ACTIVITY
 CORONARY VASOSPASM
 EFFECT ON COLLATERAL
CIRCULATION
 EFFECTS ON MORBIDITY
AND MORTALITY
Coronary Collaterals
• Help protect the myocardium in
pts. w/ CAD
• Myocardial ischemia stimulates
collateral circulation functioning
and sprouting through
mechanisms involving altered
intraluminal shear stresses,
hypoxia, and chemical
mediators such as vascular
endothelial growth factors.
• Collaterals are prone to
vasospasm from increased
SNS tone, with diminished
development and sprouting in
hypersympathetic states.
SYMPATHETIC TONE AND
RATE OF MORTALITY
INCREASED SYMPATHETIC
TONE

INCREASED MORTALITY
HYPERPARASYMPATHETIC
STATE
EXCESS
PARASYMPATHETIC ACTIVITY

HYPOTENSION

REDUCED
BLOOD FLOW
TO ISCHEMIC
AREA
LYMPHATICS
RIB DYSFUNCTION
AND
HYPERSYMPATHETIC ACTIVITY

IMPAIRED LYMPHATIC FLOW

IMPAIRED LYMPHATIC
DRAINAGE

COMPROMISED
HOMEOSTASIS

REDUCED COLLATERAL
CIRCULATION

ISCHEMIA

INCREASED
MORTALITY
AND MORBIDITY
 Post-MI
• Arrhythmias are common
with myocardial ischemia.
• Sympathicotonia
encourages
tachyarrhythmias and
increased parasympathetic
tone encourages
bradyarrhythmias and heart
blocks.
• Bradyarrhythmias and heart
block-vagal nerve activity
dominates.
– Common with inferior wall MI.
– Proximity of vagal fibers
– Blood supply of AV node comes
from right coronary artery in most
people, so it gets interrupted in
inferior wall MI.
– Inferior wall MI also associated
commonly with GI symptoms
– Somatic dysfunction: OA, AA, C2
or OM suture

• Tachyarrhythmias are more

likely if hypersympathetic tone
dominates.
Somatic dysfunction in upper
thoracic segments/ribs
 Stellate Ganglia

Left stellate ganglia post-MI is a source

of ventricular arrythmias
 Goals of Osteopathic
Manipulative Treatment

• Decrease nociceptive input

(afferent load) from muscles,
fascia, ligaments, and joints.
• Normalize facilitated segments
• Balance ANS tone
• Reduce fascial strain
• Enhance lymphatic flow
• Improve thoracic cage
compliance
Treatment Considerations
• Treat acute viscero-somatic
reflex first
• Use indirect techniques for
acute v-s reflex
• Gentle rib treatment
(endothoracic fascia and rib
raising) JAOA June 2010
• Treat cervical spine and cranial
base with BLT/BMT to address
vagus and cervical sympathetic
ganglia, as well as diaphragm
innervation
 Treatment
Considerations
• Address lower cervical spine
and rib 1 dysfunctions that
can affect the stellate
ganglion (thoracic inlet)
• Thoracic inlet indirect
treatment will also help
reduce dysfunctions
secondary to chest
compressions
• Hyoid and sternal
myofascial release
 Treatment
Considerations
• Pectoral traction for
improving lymphatic
function.
• Diaphragm release; may
need to address pelvic or LE
dysfunction as well.
• CV4 will aid in fluid
homeostasis and decreasing
patient stress levels.
 Right Pectoralis Muscle
Trigger Point

• Right pectoralis major

muscle trigger point
between Ribs 5-6, causing
somato-visceral reflex (SVT)
• If this trigger point is etiology
of the arrhythmia, the
arrhythmia responds to
manual treatment.
Cautions Regarding OMT in MI

– Avoid forceful or direct method

treatments
– Do not overtreat and tire the
patient

– Do not use treatment positions

that restrict respiratory efforts.

– Keep treatments brief; you will

often need to treat pts. more
than once daily
 Summary
• Osteopathic structural
examination can give
valuable diagnostic
information in the cardiac
patient.
• OMT can play an important
role in managing the post-MI
patient by improving fascial,
lymphatic and autonomic
components that are
implicated in some important
post-MI complications.