Connections Between Arthritis and Heart Disease
According to the American Rheumatism Association, arthritis is classified in one of two groups, either inflammatory or non-inflammatory (Huether & McCance, 2012, p. 996). With regard to the different types of arthropathies, the two main categories are osteoarthritis and rheumatoid arthritis. Osteoarthritis is considered non-inflammatory, however, according to new research and diagnostic techniques such as MMI (Muscoloskelatal Molecular Imaging) there is some new evidence that osteoarthritis does exhibit inflammatory properties (Huether & McCance, 2012).
There is no clear cut answer as to the root cause of arthritis, but it has been elucidated that there is a immuno component, as well as a genetic component. With certain types of arthritis, some patients develop cardiac abnormalities.
Rheumatic fever can cause debilitating symptoms affecting the heart muscle resulting in a deficiency in the patient’s quality of life. Cardiac monitor techs and nurses must be aware of some of the abnormal arrhythmias associated with arthritis. Inflammation is the main reason that patient’s with arthritis such as RA develop heart disease. Signs of inflammation of the heart muscle can be subtle or very pronounced. Myocarditis, endocarditis or pericarditis can cause ventricular arrhythmias such as junctional rhythms, ventricular tachycardia or ventricular fibrillation.
Signs of Osteoarthritis
Signs of OA usually occur with advancing age (Arthritis Foundation, n.d.). The pathophysiology of OA begins with destruction of the articular cartilage in joints such as the hand, hips and spine (Huether & McCance, 2012, p. 996). Destruction of this cartilage is mediated by pressure on affected joints that carry weight and have tensile strength. This is one of the reasons that individuals involved in sports or strenuous activities tend to be more susceptible to this type of arthritis. The cartilage becomes less viable due to pressure and longitudinal fissures occur thus eventually exposing the subchondral bone (Huether & McCance, 2012, p. 997). Cysts eventually develop and work their way into and through the synovial fluid and articular cartilage (Huether & McCance, 2012). Osteocytes resulting from the eroding cartilage have a tendency to remodel the bone.
Early signs of OA are pain and stiffness of the joints. The hallmark diagnostic marker of OA is the loss of proteoglycans, which is caused by matrix metalloproteinanses (Huether & McCance, 2012, p. 997). Stromelysin is another enzyme implicated in the digestion and disruption of proteoglycans.
These enzyme levels are extremely elevated in those suffering from OA. Proteoglycans are manufactured in the synovial membrane. Hyaluronic acid is a small subunit of the larger molecule glycosoaminoglycan. The macro-molcule proteoglycan aggregate helps prevent bacteria and other destructive organisms from damaging the synovial fluid due to it biological nature (McPhee & Hammer, 2010). Once the synovial fluid is depleted, infection can occur such as osteomyelitis. The mucopolysaccharides or GAG (glycosoaminoglycans) are broken down into fragments through the progression of OA (Longo et al., 2013). Cytokines are implicated in the breakdown of articular cartilage (Huether & McCance, 2012).
Diagnostic procedures that can be used to evaluate OA include MRI, CT scans or invasive techniques such as arthroscopy. Typically, pain and the description of where the pain occurs, when, how and how long the pain lasts is evidence of OA.
Ulnar drift is usually evident in advanced cases (McPhee & Hammer, 2010). Surgical procedures such as knee, joint or hip replacements are not unusual for more severe cases of OA. Non-surgical procedures include NSAID’s, resting the joint and assistive devices.
Arthritis and Depression
Arthritis is a debilitating disease, and the condition prevents the individual from completing tasks that were once done without a second thought. The deformation of the bones of the hand and other joints causes severe altered self image leading to depression (Arthritis Foundation, n.d.).
Depression is a maladaptive behavior that many individuals must deal with when suffering the ravages of arthritis.
Rheumatoid arthritis differs from OA in the sense that the synovial fluid is the first line of attack. RA causes swelling of the joint. The joint at the onset of an RA attack become warm to the touch and swollen. The skin is boggy and shiny over the joint areas. Inflammatory arthritis can be infectious or non-infectious, and has the ability to travel anywhere in the body. The symptoms of RA are malaise, fever, pain and stiffness of the affected joint.
There is a strong correlation between RA and genetics indicating strong familial tendencies. The human leukocyte antigen has been identified across all ethnicities as a precursor to RA (Huether & McCance, 2012, p. 999). Typical non-infectious RA can cause crystals of monosodium urate in and around the joint.
The pathophysiology of RA begins with the amino acid arginine being altered into the molecule citrulline. The synovial fluid via self – antigens comes under attack by interleukins and cytokines. Tumor necrosis factor TNF-α degrades the synovial fluid into a thick substance known as pannus (Huether & McCance, 2012). Self-antigens perpetuate the inflammation process due to the influx of auto-immune components of the body. There is purplish dusky hue that pervades the skin color over the affected joint. The pannus tissue hardens and remodels the bone to become lager, thus the joint loses its properties of movement. Cysts also form in the articulate cartilage and are able to migrate and drain through fistulae (Huether & McCance, 2012, p. 1001).
Diagnoses of RA include identifying the serum rheumatoid factor via blood work. Early blood work-up for anti-citrullinated protein antibody (ACPA) can be found many years prior to any outward signs of RA. This may be a pre-identification factor in early preventative measures.
Since RA is an auto-immune disease, the drugs associated with treatment include methotrexate, azathioprine, cyclosporine and TNF inhibitors (Huether & McCance, 2012, p. 1002). RA can cause many other health related issues due to the depression of the immune system.
Both RA and OA are debilitating diseases that affect the joints of the bone and the synovial fluid surrounding the joint and the heart. The body’s immune system is implicated in the emergence of arthritis. Preventative measures to stave off the beginnings of arthritis are now possible with biological markers that indicate a predisposition of developing the disease and thereby preventing future heart disease.
Maladaptive coping mechanisms occur with people affected by arthritis, and depression is one component. Early treatment and education in preventative measures is crucial for people to live a fully active life.
The arthritis foundation is a good resource for patients who have been diagnosed with arthritis. Coping with pain on a daily basis can put a strain on anyone. Understanding pain management and factors that can exacerbate arthritic flare ups is an important concept in patient teaching. The health care providers ability to recognize the ensuing ventricular arrhythmias associated with cardiac inflammation due to arthritis is important in order to improve the patient’s quality of life.
- Arthritis Foundation. (n.d.). http://www.arthritis.org/
- Huether, S., & McCance, K. (2012). Understanding pathophysiology (5th ed.). St. Louis, MO: Elsevier Mosby.
- Longo, D., Fauci, A. S., Kasper, D. L., Hauser, S. L., Jameson, J. L., & Loscalzo, J. (2013). Harrison’s manual of medicine (18 ed.). New York, NY: McGraw Hill Medical.
- McPhee, S. J., & Hammer, G. D. (2010). Pathophysiology of disease: An introduction to clinical medicine (6th ed.). New York, NY: McGraw-Hill Medical.