The heart in rheumatoid arthritis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]
Overview
People with rheumatoid arthritis are more prone to atherosclerosis, and risk of myocardial infarction and stroke is markedly increased.[6] Other possible complications that may arise include: pericarditis, endocarditis, left ventricular failure, valvulitis and fibrosis.[1] Cardiac disease with rheumatoid arthritis can be related to granulomatous proliferation or vasculitis. Echocardiography has made diagnosing pericarditis and endocardial inflammation easier.
Various cardiac complications of rheumatoid arthritis are discussed below:
The cardiac complications in rheumatoid arthritis are due to involvement by rheumatoid nodulosis. There is increased risk of coronary atherosclerosis and thereby increasing the risk of heart failure and atrial fibrillation. Various cardiac complications include:
Coronary artery disease
There is increased risk of coronary artery disease in rheumatoid arthritis. It could be due to chronic inflammation caused by cytokines, lymphocytes, macrophages, and dendritic cells. Other factors responsible are coagulation abnormalities, immune complexes, and oxidative stress.[2][3][4]
Heart failure
The risk of heart failure is relatively more common in patient with coronary artery disease in rheumatoid arthritis. This is caused by left ventricular dysfunction, inflammatory mediators, and antirheumatic drugs.[5][2]
Atrial fibrillation
The risk of atrial fibrillation is common in patients with heart failure and coronary artery disease in rheumatoid arthritis.[6]
Aortic insuuficiency
RA rarely causes symptomatic AR, but can as a result of granulomatous nodules that may form on the aortic leaflets.[7]
Pericarditis
Pericarditis is common in active rheumatoid arthritis. Symptomatic patients have RA factor positive.[8]
Myocarditis
Myocarditis can take the form of either a granulomatous disease or interstitial myocarditis. Granulomatous involvement of the heart is localized and is specific for the rheumatoid involvement of the heart. Myocarditis, in contrast, involves not localized but diffuse infiltration of the myocardium by mononuclear cells, may involve the entire myocardium and yet have no clinical manifestations.[9]
Amyloidosis
Amyloidosis in RA has been reported in numerous case-series studies to be present in a high variation of frequency, probably due to patients’ selection. [10] Amyloidosis occurs preferentially in male patients with a longer disease duration. The relevance of cardiac involvement including cardiac amyloidosis is illustrated by the high frequency of cardiac failure as a cause of mortality in RA patients treated with hemodialysis [11]. Intensified immunosuppressive treatment should be considered if a RA patient is diagnosed with amyloidosis.
Endocardial Inflammation
Echocardiographic studies have reported evidence of previously unrecognized mitral valve disease diagnosed by a reduced E-F slope of the anterior leaflet of the mitral valve. Although aortic valve disease and arthritis are generally associated through ankylosing spondylitis, a number of patients with granulomatous nodules on the valve have been reported [12]
Management of conduction disturbances in rheumatic diseases
Pacemaker implantation is the method of choice for the treatment of complete heart block and other serious conduction abnormalities. Sophisticated pacing modalities and programmability as well as low-energy circuitry and new battery designs have increased device longevity and enabled wide clinical application. A simple VVI pacemaker (paces and senses the ventricle and is inhibited by a sensed ventricular event) may be adequate for transient or infrequent bradyarrhythmia. For frequent or persistent bradyarrhythmia, prolonged dependence on ventricular pacing may warrant use of a rate-responsive demand unit or, if no atrial or sinus node abnormalities are present, a dual-chamber system (DDD—both chambers are capable of being sensed and paced). New devices enable resynchronization therapy in patients with dilated cardiomyopathy and severely impaired contractility, with beneficial effect on haemodynamics and long-term survival.
References
- ↑ Wolfe F, Mitchell DM, Sibley JT; et al. (1994). "The mortality of rheumatoid arthritis". Arthritis Rheum. 37 (4): 481–94. PMID 8147925. Unknown parameter
|month=ignored (help) - ↑ 2.0 2.1 Van Doornum S, McColl G, Wicks IP (April 2002). "Accelerated atherosclerosis: an extraarticular feature of rheumatoid arthritis?". Arthritis Rheum. 46 (4): 862–73. PMID 11953961.
- ↑ Wållberg-Jonsson S, Cvetkovic JT, Sundqvist KG, Lefvert AK, Rantapää-Dahlqvist S (May 2002). "Activation of the immune system and inflammatory activity in relation to markers of atherothrombotic disease and atherosclerosis in rheumatoid arthritis". J. Rheumatol. 29 (5): 875–82. PMID 12022343.
- ↑ Wållberg-Jonsson S, Cederfelt M, Rantapää Dahlqvist S (January 2000). "Hemostatic factors and cardiovascular disease in active rheumatoid arthritis: an 8 year followup study". J. Rheumatol. 27 (1): 71–5. PMID 10648020.
- ↑ Schau T, Gottwald M, Arbach O, Seifert M, Schöpp M, Neuß M, Butter C, Zänker M (November 2015). "Increased Prevalence of Diastolic Heart Failure in Patients with Rheumatoid Arthritis Correlates with Active Disease, but Not with Treatment Type". J. Rheumatol. 42 (11): 2029–37. doi:10.3899/jrheum.141647. PMID 26373561.
- ↑ Lindhardsen J, Ahlehoff O, Gislason GH, Madsen OR, Olesen JB, Svendsen JH, Torp-Pedersen C, Hansen PR (March 2012). "Risk of atrial fibrillation and stroke in rheumatoid arthritis: Danish nationwide cohort study". BMJ. 344: e1257. PMC 3297675. PMID 22403267.
- ↑ Chand EM, Freant LJ, Rubin JW. Aortic valve rheumatoid nodules producing clinical aortic regurgitation and a review of the literature. Cardiovasc Pathol. Nov-Dec 1999;8(6):333-8.
- ↑ name="pmid11324775">Guedes C, Bianchi-Fior P, Cormier B, Barthelemy B, Rat AC, Boissier MC (April 2001). "Cardiac manifestations of rheumatoid arthritis: a case-control transesophageal echocardiography study in 30 patients". Arthritis Rheum. 45 (2): 129–35. doi:10.1002/1529-0131(200104)45:2<129::AID-ANR164>3.0.CO;2-K. PMID 11324775.
- ↑ Sigal LH, Friedman HD (March 1989). "Rheumatoid pancarditis in a patient with well-controlled rheumatoid arthritis". J. Rheumatol. 16 (3): 368–73. PMID 2724254.
- ↑ Wiland P, Wojtala R, Goodacre J, Szechinski J. The prevalence of subclinical amyloidosis in Polish patients with rheumatoid arthritis. Clin Rheumatol 2004;23:193–98.
- ↑ Kuroda T, Tanabe N, Harada T et al. Long-term mortality outcome in patients with reactive amyloidosis associated with rheumatoid arthritis. Clin Rheumatol 2005;3:1–8.
- ↑ Iveson JM, Thadani U, Ionescu M, et al: Aortic valve incompetence and replacement in rheumatoid arthritis. Ann Rheum Dis 1975; 34:312-320.