HyperMED - Heart Disease
Heart disease and HBOT
Normobaric Oxygen Therapy (breathing 100% oxygen via a mask without a
hyperbaric chamber) has been used for many years in the management of ischemic
heart disease (Jain 1989). It is well known that cardiovascular diseases are
the leading cause of death in western countries and are reported to result in
more than 1 million deaths each year in the USA. Approximately half of all
cardiovascular deaths are due to coronary artery disease.
The risk factors for cardiovascular diseases include arteriosclerosis,
hypertension, hypercholesteremia, diabetes, old age and smoking.
The major factor in coronary artery disease and occlusion is atherosclerosis.
Kjeldsen (1969) accelerated arteriosclerosis of the aortic artery by inhalation
of low percentage oxygen in cholesterol fed rabbits. Decreased oxygen
accelerates hardening of major arteries. Kjeldsen (1969) furthered this theory,
when exposing rabbits to Hyperbaric Oxygen Therapy resulting in the reversal of
this atherosclerosis plaguing.
The American Heart Association endorses HBOT for Heart Attack : After being
exposed to the pioneering work of hyperbaricist George Hart, MD, at the
American Heart Association's (AHA) 65th Scientific Session held in New Orleans
on November 16, 1992, the AHA issued a press release praising the use of
hyperbaric oxygen to boost emergency treatment for heart attack. It advised
medical journalists that HBO as treatment 'enhances clot-dissolving drugs'
ability to minimise heart damage and save the lives of heart attack patients.
The addition of HBOT resulted in earlier relief of chest pain and
electrocardiogram (ECG) changes toward normal in patients treated with the
clot-dissolver, tissue plasminogen activator (TPA)'.
'HBOT also tended to preserve more of the heart's blood-pumping capacity,
compared to treatment with TPA alone', said Myrvin H. Ellestad, MD, director of
research at the Memorial Heart Institute at Long Beach Memorial Medical Center
in Long Beach, California. Laboratory studies have shown that hyperbaric oxygen
minimizes cell damage and death by reducing fluid accumulation in the injured
cells. 'We believe the same thing happens in patients,' said Dr. Ellestad. 'In
heart attacks, sort of the last straw that kills cells is increasing cell
water, which finally breaks the cell membrane. We believe hyperbaric oxygen's
primary effect in heart attack may be to reduce edema (fluid accumulation) in
heart cells.'
The Long Beach group studied forty-six heart attack patients, twenty-two who
received only TPA. The remaining twenty-four patients got TPA, followed by two
hours of treatment with HBOT. It provided a pure oxygen environment with twice
the normal atmospheric pressure (two atmospheres absolute). Patients treated
with HBO2 felt chest pain relief an average of 271 minutes after the onset of
heart attack symptoms, a statistically significant difference compared to the
671 minutes for patients who received only TPA. Dr. Ellestad said patients
'generally reported an easing of chest pain within ten minutes of entering the
hyperbaric chamber'.
HBOT reduced by 50 percent the time required for the heart to resume normal
electrical activity, as determined by electrocardiogram (ECG) finding called
'ST normalization'. (S and T waves are two specific points on an ECG tracing).
The time was 188 minutes for patients who went into the chamber compared with
374 minutes for those who did not. 'We've clearly shown that pain goes away
very quickly and ST elevation, which we think is a sign of the heart muscle
dying, returns to normal more rapidly,' said Dr. Ellestad. 'To me, the most
dramatic aspect of the study was watching as ST elevation returned to normal
after a patient went into the chamber. That tells me we're salvaging heart
muscle cells.' There's some evidence that HBO2 decreases activity by oxygen
free radicals. These are unstable molecules known to damage or destroy cells.
Patients who received HBOT also resulted with 'significantly lower blood levels
of the enzyme creatine phosphokinase, which is released during a heart attack
and indicates the extent of heart muscle damage'. These patients also had a
higher ejection fraction, a measurement that reflects how well the heart can
pump blood. Dr. Ellestad sees potential for even better results with HBO2 if
patients can begin oxygen therapy sooner.
Transporting patients to a hyperbaric chamber facility and preparing them for
treatment requires about thirty minutes. He and his colleagues hope to reduce
that time at Long Beach Memorial by relocating the hyperbaric chamber to the
hospital's emergency room. This comment is obviously not applicable in
Australia given the fact that hyperbaric facilities are limited in number with
conditions treated restricted to only the 'approved list'.
Physician interest in Hyperbaric Medicine as a treatment for heart attack
patients goes back a number of years; however, the interest dwindled after the
emergence of TPA and other clot-dissolving agents. Then, an unusual event
prompted Dr. Ellestad and his colleagues to take another look at HBOT. George
Hart, MD, director of the Hyperbaric unit at the hospital and an investigator
in the study reported at the AHA 1992 New Orleans meeting, began having chest
pains and decided to treat himself in the oxygen chamber. The HBOT relieved his
heart pain in minutes. Being friends, Dr. Ellestad checked out what Dr. Hart
explained about his HBOT experience.
'Hyperbaric chambers are not standard equipment at either hospitals and or
medical centres. HBOT adds additional costs between US $200 and up to $750 per
day depending upon the facility and internal costs to the daily cost of
treating a heart attack patient,' Dr. Ellestad said. The Long Beach Memorial
Hospital's investigation is just one among many facilities now utilising the
benefits of HBOT in the treatment and management of patients with heart
disease.
Metabolic effects of Hyperbaric Medicine on the Heart
Mitochondrial respiratory rate is an essential component of myocardial
function. Reduction of oxygen tension results in suppression of mitochondrial
activity, which leads to abnormal physiological activity and response.
Reduction of oxygen tension results in the reduction of the physiological
capacity of cardiac energy metabolism.
Bondarenko (1981) studied the influence of HBOT on tissue metabolism in
patients with cardiac insufficiency. Metabolic effects of HBOT are not
secondary to changes of systemic circulation but in fact precede them, due to
the direct action of hypoxia on the metabolic processes in peripheral tissues.
HBOT was reported to have immediate positive metabolic effects on damaged
cardiac tissue.
Vesselinovitch (1974) reported regression of atherosclerosis in rabbits on a
combined regimen of low fat diet, hypolipidemic agents and Hyperbaric oxygen Therapy.
Further studies performed by Okamoto (1983) recorded that hyperoxia (40%
oxygen) reduces atherosclerosis, and hypoxia (5-10% oxygen) aggravates
atherosclerotic lesions by direct action on the vessel wall.
Hyperbaric Medicine and Myocardial Infarction
There is considerable evidence that Hyperbaric Oxygenation will favourably
influence the outcome in the acute myocardial infarction patient.
Koerner (1971) recommended oxygen concentrations at 50% for inhalation to
counteract hypoxia. Kones (1971) recommended 100% oxygen inhalation to overcome
hypoxia and to provide counter measures of metabolic influence.
Vin (1986) studied the effects of HBOT on myocardial infarction induced in
rabbits. ECG monitoring as well as post mortem examination of the heart was
done after three weeks of HBOT (2 ATA, performed for two hours daily). ECG
changes cleared up in the HBOT treated animals and post mortem examinations of
the heart revealed only minimal damage. ECG changes (ST segmental elevation)
persisted in the untreated control animals, and post mortem examinations showed
marked fatty degeneration in the heart muscle.
Cameron (1966) investigated the hemodynamic and metabolic effects of HBOT in 10
patients with acute myocardial infarction who breathed air, oxygen at
atmospheric pressure or oxygen at 2 ATA. Under HBOT conditions, the systemic
vascular resistance rose progressively accompanied by reduction of cardiac
output and stroke volume. Patients with raised lactic acid levels had these
reduced when they were exposed to HBOT.
The authors concluded that HBOT was beneficial with patients :
a.. hypoxia and hypotension (low blood pressure)
b.. suffering metabolic acidosis
c.. who have responded poorly to conventional therapy
Collective studies report that Hyperbaric Oxygenation will benefit the heart
that has suffered multiple small infarcts due to thrombosis or small vessel
embolus. Massive single infarct is recorded to be more difficult to treat.
Revascularisation is limited to the margins of massive infarcts with residual
damage.
Thurston (1973) carried out the first recorded randomised controlled
investigation into the effects of Hyperbaric Oxygenation. Of 208 post
myocardial patients, 103 were treated with HBOT and 105 controls were treated by
conventional methods at a London based hospital coronary care. 17 (16.5%) of
the patients in the HBOT group died compared with 24 (22.9%) in the control
group. Detailed analysis revealed that using the benefits of HBOT halved the
mortality rate in the high-risk patients.
The only patients' in the study that survived cardiogenic shock were in fact
the HBOT group. The incidences of arrhythmias were lower in the HBOT group and
many of them were reported to have completely disappeared with the HBOT treatments.
The authors concluded that HBOT was effective in both the treatment and the
overall management of cardiac myocardial infarction.
Efuni (1983) used HBOT as a combined therapy (antioxidant therapy) in acute
myocardial infarction in 30 patients. HBOT was performed at 1.5-2.0 ATA for
60-90 minute intervals but the treatment course was limited to six sessions
only. All patients had acute myocardial infarction of the left ventricle with
damage to the anterior wall of the heart and the time since the affliction was
12-48 hours. After six HBOT sessions, cardiac output and stroke volume was
recorded to have increased. Decrease in lactate : pyruvate ratio with a fall in
metabolic acidosis was also observed.
Hyperbaric Medicine and chronic ischemic Heart Disease : (angina pectoris)
Smetnev (1979) treated 79 patients with chronic ischemic heart disease using
Hyperbaric Oxygenation. 52 of these patients suffered angina pectoris and 25
had multifocal postinfarction cardiosclerosis with insufficiency of both systemic
and pulmonary circulation. HBOT in combination with drug therapy alleviated or
arrested the symptoms of angina and corrected the central hemodynamics in the
other patients.
Kuleshova and Flora (1981) reported the effects of HBOT in the rehabilitation
of 233 patients with ischemic heart disease. All patents received physical
therapy, autogenic training, massage and walking exercises. Group 1 (179
patients) received HBOT whilst group 2 (54 patients) served as controls.
HBOT was commenced daily for 60 minutes with exposures at 1.5-2.0 ATA. There
was immediate improvement in angina pectoris symptoms of the HBOT group :
a.. 72% of the HBOT group reported a reduction and clearance in
arrhythmias
b.. HBOT group performed at higher exercise load and duration than the
non-HBOT group
c.. HBOT group also adapted better to physical challenges
It was concluded that inclusion of Hyperbaric Oxygenation significantly
enhanced the functional compensatory possibilities in cardiovascular disease.
Goliakov (1986) studied the effects of HBOT on thromboelastogram, platelet
aggregation and prothrombin index in 40 patients with angina pectoris. There
was a decrease of fibrinogen and fibrinogen degradation products and clinical
effectiveness in 84% of the patients. Eroshina (1986) showed that HBOT improved
myocardial contractility in patients with chronic ischemic heart disease.
Goliakov (1986) demonstrated the effects of HBOT in reducing platelet
aggregation and the serum fibrinogen content was shown to produce a favourable
effect in 84% of the 40 patients with angina pectoris.
Hyperbaric Medicine and Cardiac Arrhythmias
Sinus bradycardia is the common physiological response to HBOT. During the
treatment of acute myocardial infarction with HBOT numerous clinical
observations confirm the improvement of cardiac arrhythmias.
Allaria (1973) observed that patients who suffered electrocution had residual
ECG abnormalities, which were reversed with HBOT. Zhivoderov (1980) noted
disorders of rhythm and conductivity in 85% of 75 patients with myocardial
infarction after the 15th day following the onset of the disease. Hyperbaric
Oxygenation was used in 14 patients and it was observed that arrhythmias
disappeared after the initial 10-12 exposures to HBOT.
Isakov (1981) used HBOT in 31 patients suffering paroxysmal tachyarrhythmias in
ischemic heart disease and concluded that the frequency and duration of the
paroxysms was reduced and that long-term remission occurred with ongoing HBOT
treatments. HBOT was also reported to reduce the number of extrasystoles.
Zhivoderov (1982) applied HBOT to 29 patents with ischemic heart disease
(68.9%). In 17 patients there was reported a disappearance of the
extrasystoles, which allowed the physical activity of the patients to be
increased. There was no change in the acid-base balance resulting from HBOT
treatments. Among 28 patients where HBOT was used along with antiarrhythmic
drugs, improvement was observed in 21 cases (77.8%). Goliakov (1986) showed
improvement of ventricular extrasystoles in 67% of the coronary disease
patients treated with HBOT.
Hyperbaric Medicine as an adjunct to heart surgery
Boerema (1961) was the first to report the use of HBOT in performing cardiac
surgery. Meijne (1973) considered HBOT to be indicated in palliative cardiac
surgery for high-risk cases. Efuni (1977) applied HBOT in the treatment of
congestive circulatory insufficiency in patients with rheumatic mitral disease.
The surgery consisted of mitral replacement with artificial valve insertion.
The operative mortality with HBOT was 9.3% compared with 18-26% for similar
operations conducted without HBOT.
The Sixth International Congress of Hyperbaric Medicine in Aberdeen, Scotland,
reported the benefits of HBOT in cardiac surgery as follows :
a.. HBOT increases the safe time on induced cardiac arrest
b.. HBOT reduces hypoxic complication and metabolic disturbances
associated with heart surgery
c.. HBOT enables surgery to be performed without blood transfusion in
certain patients
d.. HBOT is the treatment of choice for air embolism associated with
heart surgery
e.. HBOT has been demonstrated to be effective for the treatment of low
cardiac output syndrome developing after heart surgery, and associated
pulmonary hypertension (Yacoub '65)
Hyperbaric Medicine and the prevention of coronary artery disease
Atherosclerosis can be reversed with hyperoxia (increased Oxygenation). Recent
publications from the USA indicate that Hyperbaric Medicine is available in
most sophisticated cardiac hospital and medical facilities. The benefits for
both patient and hospital are quicker recuperation and a significant reduction
in mortality and associated complications.
HBOT has been demonstrated to reduce mortality in all cardiac associated
complications. It reduces the size of infarcts and cardiac scarring, and
improves heart stroke volume and ECG findings. HBOT reduces or totally
eliminates cardiac arrhythmias without the use of drugs.
Hyperbaric Medicine provides adjunctive benefits to the cardiac patient (Jain
1995) :
a.. HBOT improves the capacity for exercise, thereby reducing
hypertensive complications
b.. HBOT prevents recurrence of ischemic episodes
c.. HBOT decreases blood pressure in hypertensives
d.. HBOT reduces atherosclerosis when used on an ongoing basis
Acupuncture reduces Myocardial Ischemia in Animal Model
Recent publication reported in Reuters Health (13-6-00):- 'Electroacupuncture
improves blood pressure response and reduces myocardial ischemia during
stimulation of abdominal organs in an animal model of coronary artery disease'.
'Rather than increasing blood flow, we found that electro-acupuncture reduces
myocardial oxygen demand via opiate mechanisms,' Dr. John C. Longhurst, of the
University of California at Irvine, reported during a presentation at the
Workshop on Complementary and Alternative Medicine in Cardiovascular, Lung and
Blood Research at the National Institutes of Health.
Dr. Longhurst and colleagues used an animal model with partial coronary artery
occlusion to study the influence of electroacupuncture on myocardial ischemia.
After applying bradykinin to the animals' gallbladders, the acupuncture point
called, Neiguan which is located over the median nerve on the wrist, was
stimulated with electro-acupuncture to improve the 'imbalance between Oxygen
supply and demand.'
Dr. Longhurst said, 'Stimulation of Neiguan directly affected fibres in the
median nerve which subsequently activated opioid receptors in the brain
(rostral ventrolateral medulla), inhibiting sympathetic outflow decreasing the
pressor response induced by application of bradykinin on the gallbladder.'
'Our results suggest that both endorphins and enkephalins are the main
neuromodulators, and that beta receptors are very important,' said Dr.
Longhurst, 'the biggest challenge for researchers will be to identify specific
acupuncture points that impact higher neurological and systemic influences.
We have seen from a number of studies that electro-acupuncture seems to be effective
in reducing hypertension, arrhythmias and angina, but further studies are
needed to pinpoint all of the acupuncture points.'
Inconjunction to HBOT directed for cardiac and related consulting patients;
electro-acupuncture is applied to enhance the mechanisms and benefits of
collective treatments.
Antibiotic may help prevent Abdominal Aortic Aneurysms
A recent report in Reuters Health - Doxycycline may become the first
pharmacologic therapy to prevent the expansion of aortic aneurysms, based on
results of studies in mice. 'We expect the development of pharmacological
treatments such as doxycycline will diminish the need for surgical repair,' Dr.
Robert W. Thompson, of Washington University School of Medicine, in St. Louis,
Missouri, speculates in a statement from the University.
Dr. Thompson and colleagues developed a mouse model of delayed abdominal aortic
aneurysm by perfusing the aortas of a series of mice with elastase. Since
matrix metalloproteinases (MMPs) have been implicated in the rupture of such
aneurysms in humans, they examined the effects of doxycycline, an antibiotic
that is a non-selective MMP inhibitor, in this model.
The degeneration of elastase-induced aortic aneurysms was suppressed by
treatment with doxycycline, reported scientists in the Journal of Clinical
Investigation. This effect appears to be largely due to the suppression of
MMP-9, since disruption of the gene encoding this enzyme also prevented the
progression and rupture of aneurysms. Genetic deficiency of another MMP
specifically implicated in aneurysm development, MMP-12, did not prevent
aneurysm development on its own, but enhanced the protective effect of MMP-9
deletion when both genes were disrupted.
The findings demonstrate that 'MMP-9 plays a critical role in an experimental
model of aortic aneurysm disease,' Dr. Thompson and colleagues say. Further
studies revealed that inflammatory cells, particularly mononuclear phagocytes,
are the primary source of MMP-9 at the site of elastase-induced aneurysms.
'This might turn out to be the first feasible pharmacological therapy for
preventing aneurysm expansion in patients,' Dr. Thompson says in a statement
from Washington University. According to the statement, Dr. Thompson and
colleagues have already demonstrated in pilot studies that 'doxycycline can
reduce the size of aortic aneurysms in patients before surgical aneurysm
repair'. The team has also confirmed that doxycycline is safe and well
tolerated in this patient population (J Clin Invest 2000;105:1641-1649).
Conclusion
The nature of heart disease is such that insufficient oxygen is getting to the
heart. This results in various discomforts, which affect the patient including
difficulty breathing, inability to exert self, pressure in the chest and a host
of other secondary systemic problems. Dr Steenblock advocates HBOT as an
'internal organ stabilizer' and identifies the following :
a.. HBOT applied to the heart during critical loss of oxygen exerts a
remarkable defibrillating effect so that tremulous, rapid, ineffectual
contractions are prevented (this offsets the collapse of the heart muscle which
can otherwise lead to untimely death)
b.. HBOT combined with specific drugs enhances the effectiveness of both
oxygen delivery and the drugs
c.. Combining HBOT with selective drugs completely arrests or
considerably reduces angina attacks in patients otherwise resistant to
prolonged drug treatments
d.. Patients with cardiac pain from ischemic heart disease experience
complete relief along with disappearance of dyspnea (difficulty breathing) with
HBOT
e.. HBOT lowers elevated blood cholesterol (Borukhov)
f.. HBOT normalizes electrocardiograms (ECGs) in Soviet study
g.. HBOT exerts long term normalizing effects promoting circulating
blood throughout the entire body in patient's with diminished muscular power of
the heart
h.. HBOT exerts anti-arrhythmic action on the damaged heart
i.. Increases patient's tolerance to hard work and taking on physical
loads