Myocardial Ischemia

NEWS & PERSPECTIVE › MULTISPECIALTY Diagnosis and Management of Myocardial Ischemia (Angina) in the Elderly Patient

Donald D. Tresch, MD, Haritha R. Alla, MD, Medical College of Wisconsin, Division of Cardiology and Geriatrics, Milwaukee, WI Disclosures Am J Geriatr Cardiol. 2001;10(6)

An acute MI may be the initial clinical manifestation of CAD in elderly persons, although many elderly persons experience myocardial ischemia for years prior to an acute MI.

Unfortunately, due to the absence of symptoms and the atypical presentation of myocardial ischemia in elderly persons, CAD will not be diagnosed in many of these patients until an acute MI occurs. Numerous studies[4-6] have shown that 20%-50% of patients 65 years or older demonstrate silent myocardial ischemia upon stress testing or ambulatory electrocardiographic (EKG) monitoring.

Moreover, silent myocardial ischemia is a marker for future coronary events in these patients. Nonfatal MI and death are two to three times more common in patients with silent myocardial ischemia than in those without silent ischemia. The event rate is even higher if, in addition to ischemia, abnormal LV function[4,5,7] or ventricular tachyarrhythmias[8,9] are present.

Therefore, detection of silent myocardial ischemia in elderly persons is important. Some authors have concluded that performing stress testing in persons at the time of their retirement would be more cost effective than the usual practice of stress testing the 50-year-old junior executive. Symptoms in elderly patients with myocardial ischemia may be so atypical, compared to younger patients, that the symptoms may be misdiagnosed as being caused by another disorder or as related merely to aging.

Exertional angina pectoris is commonly the first manifestation of CAD in middle-aged persons, and is usually easily recognized due to its typical features. For elderly persons, however, this may not be the case. Due to limited physical exertion, many elderly persons with CAD will not experience exertional angina. Instead of angina, myocardial ischemia in elderly patients is commonly manifested as dyspnea.

Not infrequently, the dyspnea occurs in combination with angina, although the angina is frequently mild and is of little concern to the patients. In other elderly patients, myocardial ischemia appears as shoulder or back pain and may be misdiagnosed as degenerative joint disease; if the pain is localized in the epigastric area, it may be ascribed to peptic ulcer disease.
Positional postprandial epigastric discomfort that is burning in quality is often attributed to hiatal hernia or esophageal reflux, rather than myocardial ischemia.

Moreover, the frequent presence of comorbid conditions in elderly patients adds to the confusion and may lead to a misdiagnosis of symptoms that are actually due to myocardial ischemia.

Myocardial ischemia may be manifested as acute LV failure in elderly patients, with some patients presenting with acute pulmonary edema.[10-13] Chest pain may not be present, although the myocardial ischemia is severe enough to produce diastolic and/or systolic LV dysfunction. Many of these elderly patients are unaware of having CAD until the onset of the acute heart failure.

A history of hypertension is common and the patient's EKG and echocardiogram will demonstrate LV hypertrophy. Three-vessel CAD is usually found, but ventricular systolic function is only mildly depressed. With revascularization, these patients do well.
Cardiac arrhythmias can be another clinical manifestation of myocardial ischemia in elderly patients. Patients with myocardial ischemia may experience chest palpitations caused by ventricular premature beats.

Unfortunately, in other elderly patients, the arrhythmias may be ventricular tachycardia or fibrillation leading to sudden cardiac death. Prior to sudden death, these patients may be asymptomatic, with no awareness of the presence of CAD.

The initial evaluation of an elderly patient with myocardial ischemia should begin with a thorough history and complete physical examination, and determination of the coronary risk factors and comorbid illnesses. In addition, early assessment of clinical stability, with stratification into a high- or low-risk group, is necessary.[14]

In addition to advanced age, mortality and morbidity in elderly patients with myocardial ischemia are directly related to LV function, the extent of CAD, and the presence of comorbidity. Stress testing is important in stratification of elderly patients with myocardial ischemia, especially in asymptomatic patients (Table I).

The goals of treatment in elderly patients with myocardial ischemia are 1) to relieve symptoms, if present, and to stabilize the acute pathophysiologic process; 2) to prevent recurrence or new onset of symptoms; and 3) to prevent progression and induce regression of the underlying pathophysiology to reduce future coronary events, including death.
The specific management of elderly patients with myocardial ischemia consists of 1) treatment of associated disorders that can precipitate or worsen ischemia; 2) reduction of coronary risk factors; and 3) use of pharmacologic agents. In high-risk elderly patients, coronary angiography is necessary, if there are no contraindications to revascularization.

Put me on the front porch...

with a cocktail & I'll tell you stories past sunset! That's how we do it in the south!  Call me crazy but, I come by it honest ~ I'm just willing to share a little more than others.

Which is unusual when there is supposed to be so much shame attached to our skeletons, that we keep them crammed in the back of the closet: well hidden!

It must be the tribal talking gene that came along in my DNA basket of goodies.

At this point, I guess I'm just hoping there's a comfy porch or rocking chair with my name on it somewhere with an interesting view, someone who wants to listen & hopefully I'm not a burden.

So I adopted the mantra...
IF YOU FIND YOUR WOUND `
YOU CAN BEGIN TO HEAL
and am willing to take the skeletons out of the closet & dance with them (how very UN-Southern, of me!) ...

I have -by necessity, due to physical ailments- had to start picking at proverbial scabs. I had been focusing on figuring out the signs & symptoms of my condition when it became apparent that all my world's were colliding ....
~ physical manifestations & emotional scaring ~
whoaa the motherload I have uncovered is a conspiracy theorists dream.... Man, this goes deep!

In fact, I still take pause over some of the things I have been enlightened with... Especially when I listen to things I am sharing & how they might be interpreted/heard by the listener of said tale (s).

So with much appreciation and copious amounts of humility I am ever so grateful and thankful to the scant few who took time to listen & show non-judgmental compassion/empathy.  Thanks to their support & understanding I have been able to work my way through some intensive therapies -mental, physical, genetic-!!

About our DNA .....

PREVALENCE
The prevalence of HLA-B27 varies between populations— from 50% in Haida Indians to 0/ nil in Australian Aborigines. In the UK general population it is about 8%. HLA-B27 is rare in the American black population whereas Eskimo populations carry it much more frequently than Western Europeans, with prevalence rates of 25% or more. This antigen is associated with ankylosing spondylitis in virtually all racial groups studied. 

PATHOGENESIS
HLA-B27 positive Caucasians have a 20-fold risk of developing any spondylarthropathy, particularly ankylosing spondylitis and undifferentiated spondarthritis.

Family and twin studies of ankylosing spondylitis have shown a polygenic pattern of genetic susceptibility with heritability in excess of 90%. The contribution of HLA-B27 to genetic susceptibility has been estimated to be 20–50% of the total.

Other HLA alleles, most notably HLA-B60 and HLA-DR1, may predispose to ankylosing spondylitis either independently of B27 or in conjunction with it.

MECHANISMS
The main natural function of HLA-B27 is to form a complex with β2microglobulin which can bind short antigenic peptides such as those derived from intracellular microorganisms. Following presentation at the cell surface, the complexes are specifically recognised by cytotoxic lymphocytes which then kill the infected cell.

Viral?/Organisms have been shown to trigger reactive arthritis, including Salmonella, Shigella, Yersinia, Campylobacter, Chlamydia, Mycobacteria and possibly Brucella, all of which habitually survive intracellularly. HLA-B27 appears to enhance the invasion of Salmonella into intestinal epithelial cells.

PREDICTIVE
{Insert genome suscept.
-first degree}
Generally, the value of testing for HLA-B27 depends upon the particular clinical situation. Beginning with a clinical estimate of the likelihood of ankylosing spondylitis or a related spondarthropathy.

Seronegative Spondarthritides

Ankylosing spondylitis
Reactive arthritis (Reiter’s syndrome)
Psoriatic arthropathy
Enteropathic arthropathy
Acute anterior uveitis
Juvenile spondarthritis
Undifferentiated spondarthritis
Isolated peripheral enthesitis

ASSOCIATIONS
HLA-B27 and ankylosing spondylitis remains the strongest known relationship between a major histocompatibility complex (MHC) antigen and a disease!

Enthesitis, defined as inflammation of the origin and insertion of ligaments, tendons, aponeuroses, annulus fibrosis and joint capsules, is a hallmark.

The concept of entheseal organ prone to pathological changes in spondyloarthritis is well recognized.

The relevant role of peripheral enthesitis is supported (heel pain or other well-defined enthesopathic pain), axial and peripheral spondyloarthritis.

Episodes of Achilles tendinitis, plantar fasciitis, posterior tibial tendinitis, & dactylitis. Also seen are lateral epicondyle, insertion of the patella tendon into the inferior pole of the patella, femoral quadriceps, and posterior tibial tendons. {continue}Hip disfunct:

Upper lobe fibrosis is the lung condition best known to correlate with HLA-B27.  The antigen may be positively, neutrally or negatively associated with asbestosis. Claims have also been made for an association with other pulmonary diseases, especially pleurisy, pleural abscess, bronchitis and pneumonia and pneumothorax, independently of the presence of ankylosing spondylitis.

Aortic regurgitation occurs in 2–10% of patients with ankylosing spondylitis, and cardiac conduction abnormalities including atrioventricular and intraventricular blocks have been found in one-third of patients with spondylitis.

HLA-B27 related cardiac lesions may be found in the absence of other rheumatological manifestations.
Indeed, an HLA-B27 associated cardiac syndrome comprising severe cardiac conduction system abnormalities and lone aortic regurgitation has been defined, whose link with B27 is almost as strong as that between B27 and ankylosing spondylitis.

Significant association has been reported between HLA-B27 and acute leukaemia, particularly acute myeloid leukaemia.HLA-B27 carriers may have an increased risk of acute leukaemia whilst those with concomitant ankylosing spondylitis may be predisposed to lymphoid malignancies.

While infection with HIV predisposes to spondyloarthropathy,HLA-B27 is the HLA class I molecule most closely associated with non-progression of HIV infection to AIDS.

HLA-B27 can be helpful in a patient complaining of low back pain of an inflammatory character in the absence of radiological signs of sacroiliitis or in patients with an asymmetrical oligoarthritis but without other features of spondarthritis. This has been acknowledged with the inclusion of HLA-B27 positivity as a criterion in the Amor classification criteria for spondyloarthropathy.

Likewise, testing for HLA-B27 can help to differentiate between alternative aetiologies in iritis and aortic regurgitation.

PROGNOSTIC VALUE

Whereas HLA-B27 does not seem to influence the severity of ankylosing spondylitis, in psoriatic spondylarthropathy it may determine not only susceptibility to the condition but also its clinical expression.

It correlates most strongly with isolated axial disease and it may confer some protection against peripheral joint erosions.

Patients with Reiter’s disease and Yersinia andSalmonella triggered reactive arthritis who are HLA-B27 positive have more severe acute disease, more extra-articular features and more frequent chronic back pain and sacro-iliitis.

In C. trachomatis reactive arthritis, more severe or chronic disease could be due to lower concentrations of interferon-γ in the synovial fluid of patients who are HLA-B27 positive than those who are HLA-B27 negative, with consequent impaired clearance of infective agents.

With regard to cardiac disease, the relative risk that a HLA-B27 positive man will need a permanent pacemaker has been calculated to be 6.7 compared with a man who has other B alleles. This association is not, however, present in female patients.

A poor outcome of back surgery has been found in patients possessing HLA-B27.

Atlanto-axial subluxation can occur.

HLA-B27 positive patients with rheumatoid arthritis have about twice the risk of developing subluxation of the cervical spine and an almost threefold risk of subaxial subluxation.

Thus, HLA-B27 may transpire to be a useful prognostic indicator for the later development of instability of the cervical spine and its complications in rheumatoid arthritis.

The discovery of the link between HLA-B27 and a large family of inflammatory rheumatic diseases was one of the seminal advances in rheumatology in the last century. Associations have subsequently been identified with other musculoskeletal and non-rheumatic diseases.

The Test
http://labtestsonline.org/understanding/analytes/hla-b27/tab/test/

The HLA-B27 test is primarily ordered to help strengthen or confirm a suspected diagnosis of ankylosing spondylitis (AS),reactive arthritis, juvenile rheumatoid arthritis (JRA), or sometimes anterioruveitis. The HLA-B27 test is not a definitive test that can be used to diagnose or rule out a disorder. It is one piece of evidence used along with the evaluation of signs,symptoms, and other laboratory tests to support or rule out the diagnosis of certain autoimmune disorders, such as ankylosing spondylitis and reactive arthritis.

Ankylosing spondylitis and reactive arthritis are both chronic, progressive conditions that occur more frequently in men than women. The first symptoms typically occur when a person is in their early 30's. Often, the initial symptoms of these autoimmune disorders are subtle and may take several years before characteristic degenerative changes to bones and joints are visible on X-rays.

Ankylosing spondylitis is characterized by pain, inflammation, and a gradual stiffening of the spine, neck and chest.Reactive arthritis is a group of symptoms that includes inflammation of the joints,urethra, and eyes as well as skin lesions.Juvenile rheumatoid arthritis is a form ofarthritis that occurs in children.Anterior uveitis is associated with recurring inflammation of the structures of one or both eyes.

The HLA-B27 test may be ordered as part of a group of tests used to diagnose and evaluate conditions causing arthritis-like chronic joint pain, stiffness, and inflammation. This group of tests may include an RF (rheumatoid factor) with either an ESR (erythrocyte sedimentation rate) or a CRP (C-reactive protein). HLA-B27 is sometimes ordered to help evaluate someone with recurrent uveitis that is not caused by a recognizable disease process.

When is it ordered?

An HLA-B27 test may be ordered when a person has acute or chronic pain andinflammation in the spine, neck, chest, eyes, and/or joints, and the doctor suspects the cause is an autoimmune disorder that is associated with the presence of HLA-B27. An HLA-B27 may also be ordered when someone has recurrent uveitis.

The HLA-B27 test is not diagnostic, but the results add information, increasing or decreasing the likelihood that the person being evaluated has the suspected autoimmune disorder.

Doctors frequently use the HLA-B27 test result when they suspect ankylosing spondylitis but the disease is in an early stage and the vertebrae in the spine have not yet undergone the characteristic changes that would be seen on X-ray.

What does the test result mean?

If a person is positive for HLA-B27 and has symptoms such as chronic pain,inflammation, and/ or degenerative changes to his bones (as seen on X-ray), then it supports a diagnosis of ankylosing spondylitis, reactive arthritis, or anotherautoimmune disorder that is associated with the presence of HLA-B27. This is especially true if the person is young, male, and if he experienced his first symptoms before the age of 40.

If HLA-B27 is negative, then the marker was not detected. This does not mean, however, that the person tested does not have the suspected condition since people who do not have the HLA-B27 antigen can also develop these autoimmune diseases. Likewise, someone who has the HLA-B27 antigen will not necessarily develop one of these conditions. Researchers are trying to determine what factors contribute to the higher likelihood of people with HLA-B27 developing these particular diseases and what actually triggers them.

Whether or not certain HLA antigens will be present is genetically determined. Their production is controlled by genes that are passed from parents to their children. If two members of the same family are HLA-B27 positive and one of them develops a disease associated with HLA-B27, then the other person is at an increased risk of developing a similar disease.

Is there anything else I should know?

Though the diseases associated with HLA-B27 occur more frequently in men, women can also be affected. However, the signs and symptoms related to the diseases can often be milder in women.

With new genetic testing methods, it is now possible to separate HLA-B27 into subtypes. So far, more than 70 different subtypes have been identified, such as HLA B27*05 and HLA B27*02. How the presence of these specific subtypes affects the likelihood of developing an autoimmune disease is not yet known

Important to speak to first degree relatives... !

It is important to inform first degree relatives regarding genetic predilection to associated conditions & syndromes in light of a positive HLA B27 result..

http://ghr.nlm.nih.gov/glossary=firstdegreerelative

Think about your troubles

As it would seem, everything comes together to work against me. Same issues are always the underlying factors.

I have self managed for as long as I can muster. I don't worry, I give it to God, and every time I am reassured by his grace & mercy.

I know my body even if the recent doctors and their level of care can't appreciate. So begins a cycle of self diagnosis & homeopathic care only reaching out when pain becomes so unbearable & seemingly unsurmountable.

At this time, I have become increasingly aware that I must seek out a medically licensed professional for intervention. But, as most others would simply make an appointment or drive to the emergency room... I am not afforded the same luxury.

I am mortified by the prospect because of the contraindicated care and almost degrading process, as encountered on these occassions since diagnosis.

An effort in futility; getting "them" to understand that I have a tissue disorder that coincides & interferes with all of my associated signs & symptoms!

I am a Zebra not a Horse! 
[Not disturbed/Not a drug seeker]

So today I struggle with how to pay the past due premium on the Obama~care brand of BCBS or any subsequent bills if I were to actually go to a doc or ER.

I have a Tissue Disorder!! Goes by a lot of names (ie> Adiposis Dolorosa, Dercum's Disease, ..) and is under appreciated or misdiagnosed as a lot of other things because of its rarity.

My pain ebbs & flows, its chronic so I've dealt with it & educated myself along the way. Really since 1985 when I injured my neck/back in a type of MVA. Although a number of findings such as mild scoliosis, cervical spondylitis, & arthritic changes where found during chiropractic care it wasn't until after 2000 that clinical diagnosis was made.  The struggle is real!!

I pursued answers & treatment with nuerologist & orthopedist in conjunction with gp until it seemed more harm than good was coming of it. Focusing on self managed spinal care & pain management since having to discontinue Neurontin and interspinal injections as well as other therapies with regard to: thoracic outlet, cervical stenosis, levo-scoliosis, (including ischemic attacks & a bout with gastroenteritis).

So today, I acknowledge my fears and with the prayer that my grandmother spoke from Timothy... To set out to find a doctor !
(And hopefully with the white papers available from Dr.Karen Herbst (AZ) I will find THE doctor!)

geographically: (hoping for)
Rock Hill SC / Charlotte NC

discipline: (???)
Rheumatology, Endocrinology, Neurology

3yrs ~synovial cyst of transverse process at T12/L1, chronic pain/fatigue, Barrett's Esophagus, & abdominal free fluid.

2yrs ~2 bouts flu, followed by a shingles appearance rash on back, subsequent sinusitis with perceived decrease in hearing.

1yr ~Costochrondritis /Tietze,
(hypertension & murmur cardiologist contradicted) 
discontinued all prescriptions

6mon ~Progression of right-sided inflammation (joints & tissues) neck to toes with upper & lower nerve issues.  

(Experienced a carbuncle; now healed)

Currently Experiencing
Exhaustive Fatigue
throat constriction with pain 
(not globlous? nor sore throat)
pain at base of tongue, 
neck swelling & discomfort, persistent cough of sticky mucus,
neck muscles tight with spasm,
Swollen tonsils & nodes
Serious discomfort & perception of lump at collarbone/brachial area
vision changes, 
hip and shoulder laxity with pain
Changes in coccyx - sacral 
new worsening areas of 
numbness, tingling, & shooting 
Lipomas
intermittent disturbances
Rashes, 
bladder, & bowel
Livedo Reticularis

Familial; 

Maternal Grandmother suffers from a number of related conditions with tissue disorder as underlying cause including; thyroid, angina, loefflers, fibromyalgia, etc...

Eldest child schuerrman's spine & migraine syndrome

Middle child born with Mesynchemal Hamartoma of liver 

Youngest child gallbladder & migraines

Mother contracted Polio as child

Pufas.. Polyunsaturated fat.. Hypothyroid ~hashimoto~ Fix!

http://www.hypothyroidismrevolution.com/

Barrett's Esophagus from About.com

Barrett's Esophagus
By Sharon Gillson

Barrett's esophagus is a disorder in which the lining of the esophagus is damaged. This damage occurs when parts of the esophageal lining are repeatedly exposed to stomach acid, and are replaced by tissue that is similar to what is found intestine. This process is called intestinal metaplasia. The cells in the lining of the esophagus and the stomach have different functions, and are different types of cells. Also, their appearance is very different, making it easy for a physician to tell them apart when examining the esophagus and stomach. At the end of the esophagus, there is an area that marks the border between the cells of the esophagus and the cells of the stomach. With Barrett's esophagus, abnormal intestinal-like cells develop above this border. Causes of Barrett's Esophagus Barrett's esophagus is uncommon. The most common risk factor for Barrett's esophagus is long-term gastroesophageal reflux disease (GERD), though only a small percentage of GERD patients will develop Barrett's esophagus.

However, once Barrett's esophagus is present, there is a greater risk of developing esophageal cancer. Statistics show, though, that while the risk is increased, the overall risk is less than 1% per year of Barrett's esophagus patients developing this cancer.
When stomach acid backs up into the esophagus, it can cause injury to the normal lining of the esophagus. Esophageal injury with inflammation is called esophagitis. If this injury to the esophagus continues over many years, the injured normal lining of the esophagus will not grow back. Instead, it is replaced by an abnormal lining called Barrett's esophagus.

Symptoms of Barrett's Esophagus

Barrett's esophagus itself does not produce any symptoms. The acid reflux that causes Barrett's esophagus can have the symptoms of heartburn. If Barrett's esophagus has progressed to cancer of the esophagus, the symptoms can include difficulty swallowing or weight loss. Barrett's esophagus itself, however, does not cause symptoms.
Diagnosing Barrett's Esophagus

Individuals who have experienced acid reflux symptoms for a number of years should undergo an upper endoscopy exam to determine if they have Barrett's esophagus. Tissue samples from abnormal looking areas of the esophagus are taken during this procedure and examined under a microscope for the presence of abnormal cells. Tissue, showing intestinal metaplasia with goblet cells, is necessary to make the diagnosis of Barrett’s esophagus.
Treating Barrett's Esophagus

The best treatment strategy for Barrett's esophagus is prevention. When people are diagnosed with GERD, their doctor will work with them on lifestyle and diet modifications, and possible medications (such as antacids, proton pump inhibitors, and H2 blockers) to control the acid reflux.
Currently, there are no medications that will reverse Barrett's esophagus. Treating the underlying GERD, however, may slow the progress of the disease and help prevent complications. This includes:

Eating smaller, more frequent meals
Limiting intake of acid-stimulating foods and beverages
Not laying down for about two hours after you eat
Elevating the head a few inches while you sleep
Maintaining a reasonable weight
Quit smoking
Avoiding drink alcohol
Not wearing belts or clothes that are tight fitting around the waist
Taking any doctor-prescribed medications for acid reflux symptoms
Prognosis

An increased risk of esophageal cancer is present. A follow-up endoscopy to look for dysplasia or cancer is important.

Other ref: http://www.sts.org/patient-information/esophageal-surgery/barretts-esophagus

I pray to be her patient, Dr.Herbst!

Here is an excerpt of some typical medically based information, found readily on the web, with just a quick search on where my struggle begins.

Pain & weakness from Dercum’s Disease (adiposis dolorosa) is often attributed to lipomas (fatty deposits) applying pressure to nerves. This explanation is included in many definitions of the disease [1,2,3]. This theory has not been confirmed histopathologically in patients with Dercum’s Disease[4]. However, nerve compression secondary to adjacent lipomas is a recognized medical condition[5,6,7]. Most lipomas are asymptomatic, but they can cause pain when they compress nerves[8]. In fact, neuropathic pain related to subcutaneous lipoma without direct nerve compression is possible[9]. Lipomas exhibit a different cytokine profile than normal adipose, which may contribute to neural inflammation or microvascular changes[9].

In the meanwhile... I will chronicle medically related incidents while in prayer that a Doctor will be wise and thoughtful enough to take heed when we meet & ultimately work with Dr. Karen Herbst's (AZ) protocol, that I might eventually have relief from these varying conditions that plague!

I would like to will my body to Dr. Karen Herbst for her exclusive use! In fact she doesn't even need to wait til I'm dead!! 

And my greatest prayer would be that these efforts all go toward forwarding my descendants futures!!