Your Heart and HBOT

[Guest guest]

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 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.

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. 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.

W. , of Washington University School of Medicine, in St. Louis,

Missouri, speculates in a statement from the University.

Dr. 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. 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. says in a statement

from Washington University. According to the statement, Dr. 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