Cardiovascular diseases are common in systemic rheumatologic diseases. They can be presented at the time of diagnosis or after diagnosis. The cardiac involvements can be the first presentation of rheumatologic conditions. It means that a patient with rheumatologic disease may go to a cardiologist when attacked by this disease at first. These manifestations are very different and involve different structures of the heart, and they can cause mortality and morbidity of patients with rheumatologic diseases. Cardiac involvements in these patients vary from subclinical to severe manifestations. They may need aggressive immunosuppressive therapy. The diagnosis of these conditions is very important for choosing the best treatment. Premature atherosclerosis and ischemic heart disease are increased in rheumatoid arthritis and systemic lupus erythematosus, and may be causes of mortality among them. The aggressive control of systemic inflammation in these diseases can reduce the risk of cardiovascular disease especially ischemic heart disease. Although aggressive treatment of primary rheumatologic diseases can decrease mortality rate and improve them, at this time, there are no specific guidelines and recommendations, to include aggressive control and prevention of traditional risk factors, for them. 1. Introduction Systemic rheumatic diseases are autoimmune inflammatory conditions that involve several organs, frequently involving the blood vessels and the heart. Cardiac disease may occur in patients with a definite diagnosis of a rheumatologic disorder, or may be the initial manifestation in patients with no prior diagnosis. Cardiac involvements in rheumatic diseases can show themselves in different ways from asymptomatic or mild to severe or life-threatening and are significant causes of morbidity and mortality in patients with rheumatic disorders. Rheumatologic diseases can be considered as causes of myocardial, valvular, and pericardial and conduction system abnormalities. Because of these abnormalities, it is thought that rheumatologic disorders have been associated with premature atherosclerosis leading to ischemic heart disease at young ages. The increased risk of coronary disorders cannot be solely attributed to traditional cardiovascular (CV) risk factors, and may be a result of chronic systemic inflammation from the rheumatic disease. The prevalence and importance of cardiovascular disease in rheumatologic disorders have increased in the setting of therapeutic advances. One should consider chronic inflammation as a cause of cardiac diseases in people with
References
[1]
M. B. Owlia, “Acute rheumatic fever, an acute or a chronic joint disease?” Journal of Shahid Sadoughi University of Medical Sciences, vol. 19, pp. 561–567, 2011.
[2]
M. B. Owlia, “Clinical spectrum of connective tissue disorders,” Journal, Indian Academy of Clinical Medicine, vol. 7, no. 3, pp. 217–224, 2006.
[3]
M. J. Roman and J. E. Salmon, “Cardiovascular manifestations of rheumatologic diseases,” Circulation, vol. 116, no. 20, pp. 2346–2355, 2007.
[4]
G. Kitas, M. J. Banks, and P. A. Bacon, “Cardiac involvement in rheumatoid disease,” Clinical Medicine, vol. 1, no. 1, pp. 18–21, 2001.
[5]
C. Guedes, P. Bianchi-Fior, B. Cormier, B. Barthelemy, A. C. Rat, and M. C. Boissier, “Cardiac manifestations of rheumatoid arthritis: a case-control transesophageal echocardiography study in 30 patients,” Arthritis Care and Research, vol. 45, no. 2, pp. 129–135, 2001.
[6]
C. Turesson, A. Jarenros, and L. Jacobsson, “Increased incidence of cardiovascular disease in patients with rheumatoid arthritis: results from a community based study,” Annals of the Rheumatic Diseases, vol. 63, no. 8, pp. 952–955, 2004.
[7]
A. E. Voskuyl, “The heart and cardiovascular manifestations in rheumatoid arthritis,” Rheumatology, vol. 45, supplement 4, pp. iv4–iv7, 2006.
[8]
W. B. Lebowitz, “The heart in rheumatoid arthritis (Rheumatoid disease). A clinical and pathological study of sixty-two cases,” Annals of Internal Medicine, vol. 58, pp. 102–123, 1963.
[9]
S. W？llberg-Jonsson, M. L. Ohman, and S. R. Dahlqvist, “Cardiovascular morbidity and mortality in patients with seropositive rheumatoid arthritis in Northern Sweden,” Journal of Rheumatology, vol. 24, no. 3, pp. 445–451, 1997.
[10]
D. H. Solomon, E. W. Karlson, E. B. Rimm et al., “Cardiovascular morbidity and mortality in women diagnosed with rheumatoid arthritis,” Circulation, vol. 107, no. 9, pp. 1303–1307, 2003.
[11]
C. Gonzalez-Juanatey, J. Llorca, A. Testa, J. Revuelta, C. Garcia-Porrua, and M. A. Gonzalez-Gay, “Increased Prevalence of Severe Subclinical Atherosclerotic Findings in Long-Term Treated Rheumatoid Arthritis Patients Without Clinically Evident Atherosclerotic Disease,” Medicine, vol. 82, no. 6, pp. 407–413, 2003.
[12]
J. Sagristà-Sauleda, J. Angel, G. Permanyer-Miralda, and J. Soler-Soler, “Long-term follow-up of idiopathic chronic pericardial effusion,” New England Journal of Medicine, vol. 341, no. 27, pp. 2054–2059, 1999.
[13]
A. M. Nomeir, R. A. Turner, and L. E. Watts, “Cardiac involvement in rheumatoid arthritis. Followup study,” Arthritis and Rheumatism, vol. 22, no. 6, pp. 561–564, 1979.
[14]
F. Wolfe and K. Michaud, “Heart failure in rheumatoid arthritis: rates, predictors, and the effect of anti-tumor necrosis factor therapy,” American Journal of Medicine, vol. 116, no. 5, pp. 305–311, 2004.
[15]
P. J. Nicola, H. Maradit-Kremers, V. L. Roger et al., “The risk of congestive heart failure in rheumatoid arthritis: a population-based study over 46 years,” Arthritis and Rheumatism, vol. 52, no. 2, pp. 412–420, 2005.
[16]
C. S. Crowson, P. J. Nicola, H. M. Kremers et al., “How much of the increased incidence of heart failure in rheumatoid arthritis is attributable to traditional cardiovascular risk factors and ischemic heart disease?” Arthritis and Rheumatism, vol. 52, no. 10, pp. 3039–3044, 2005.
[17]
G. S. Bhatia, M. D. Sosin, J. V. Patel et al., “Left ventricular systolic dysfunction in rheumatoid disease: an unrecognized burden?” Journal of the American College of Cardiology, vol. 47, no. 6, pp. 1169–1174, 2006.
[18]
P. M. Seferovic, A. D. Ristic, R. Maksimovic et al., “Cardiac arrhythmias and conduction disturbances in autoimmune rheumatic diseases,” Rheumatology, vol. 45, supplement 4, pp. iv39–iv42, 2006.
[19]
C. A. Roldan, C. DeLong, C. R. Qualls, and M. H. Crawford, “Characterization of Valvular Heart Disease in Rheumatoid Arthritis by Transesophageal Echocardiography and Clinical Correlates,” American Journal of Cardiology, vol. 100, no. 3, pp. 496–502, 2007.
[20]
A. S. Villecco, E. De Liberali, B. Bianchi, and E. Pisi, “Antibodies to cardiac conducting tissue and abnormalities of cardiac conduction in rheumatoid arthritis,” Clinical and Experimental Immunology, vol. 53, no. 3, pp. 536–540, 1983.
[21]
M. Ahern, J. V. Lever, and J. Cosh, “Complete heart block in rheumatoid arthritis,” Annals of the Rheumatic Diseases, vol. 42, no. 4, pp. 389–397, 1983.
[22]
F. Wolfe, B. Freundlich, and W. L. Straus, “Increase in cardiovascular and cerebrovascular disease prevalence in rheumatoid arthritis,” Journal of Rheumatology, vol. 30, no. 1, pp. 36–40, 2003.
[23]
A. P. Beckhauser, L. Vallin, C. J. Burkievcz, S. Perreto, M. B. Silva, and T. L. Skare, “Valvular involvement in patients with rheumatoid arthritis,” Acta Reumatologica Portuguesa, vol. 34, no. 1, pp. 52–56, 2009.
[24]
N. J. Zvaifler and A. M. Weintraub , “Aortitis and aortic insufficiency in the chronic rheumatic disorders–a,” Arthritis and rheumatism, vol. 6, pp. 241–245, 1963.
[25]
J. Valaitis, C. G. Pilz, and M. M. Montgomery, “Aortitis with aortic valve insufficiency in rheumatoid arthritis,” AMA Arch Pathol, vol. 63, no. 3, pp. 207–212, 1957.
[26]
M. Itoh, M. Yoshikai, H. Ohnishi, R. Noguchi, and K. Irie, “Aortic regurgitation associated with rheumatoid arthritis: a case report,” International Journal of Cardiology, vol. 127, no. 2, pp. e78–e79, 2008.
[27]
N. Minematsu, M. Yoshikai, K. Kamohara, and S. Tomimitsu, “Aortic valve regurgitation associated with rheumatoid arthritis; report of a case,” Kyobu Geka, vol. 57, no. 5, pp. 391–394, 2004.
[28]
M. Alpaslan, D. Evcik, and E. Onrat, “Aortic valve aneurysm: a novel cardiac manifestation of rheumatoid arthritis?” Journal of the American Society of Echocardiography, vol. 14, no. 11, pp. 1137–1138, 2001.
[29]
C. Didry, B. Combe, F. Flaisler, and J. Sany, “Aortic incompetence associated wth rheumatoid arthritis: prognosis is severe,” Revue du Rhumatisme et des Maladies Osteo-Articulaires, vol. 59, no. 9, pp. 571–576, 1992.
[30]
M. Hakala, T. Pettersson, M. Tarkka et al., “Rheumatoid arthritis as a cause of cardiac compression. Favourable long- term outcome of pericardiectomy,” Clinical Rheumatology, vol. 12, no. 2, pp. 199–203, 1993.
[31]
M. Yamakido, S. Ishioka, and M. Takeda, “Cardiac and pulmonary manifestations in rheumatoid arthritis,” Nippon Rinsho, vol. 50, no. 3, pp. 570–575, 1992.
[32]
L. Dutschmann, C. Ferreira, G. De Sousa et al., “Cardiac manifestations of connective tissue diseases,” Acta Medica Portuguesa, vol. 2, no. 2, pp. 103–110, 1989.
[33]
G. Lasek, H. H？ntzschel, H. G. Schulz, and T. Neumann, “Diagnosis of cardiac involvement in rheumatoid arthritis and some selected collagenoses,” Zeitschrift fur Die Gesamte Innere Medizin und ihre Grenzgebiete, vol. 41, no. 6, pp. 167–169, 1986.
[34]
D. Schorn, I. P. Hough, and I. F. Anderson, “The heart in rheumatoid arthritis: an echocardiographic study,” South African Medical Journal, vol. 50, no. 1, pp. 8–10, 1976.
[35]
J. Goldenberg, M. B. Ferraz, A. P. Pessoa et al., “Symptomatic cardiac involvement in juvenile rheumatoid arthritis,” International Journal of Cardiology, vol. 34, no. 1, pp. 57–62, 1992.
[36]
P. S. Lietman and E. G. Bywaters, “Pericarditis in juvenile rheumatoid arthritis,” Pediatrics, vol. 32, pp. 855–860, 1963.
[37]
R. C. Lawrence, C. G. Helmick, F. C. Arnett et al., “Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States,” Arthritis and Rheumatism, vol. 41, no. 5, pp. 778–799, 1998.
[38]
E. M. Tan, A. S. Cohen, and J. F. Fries, “The 1982 revised criteria for the classification of systemic lupus erythrematosus,” Arthritis and Rheumatism, vol. 25, no. 11, pp. 1271–1277, 1982.
[39]
K. G. Moder, T. D. Miller, and H. D. Tazelaar, “Cardiac involvement in systemic lupus erythematosus,” Mayo Clinic Proceedings, vol. 74, no. 3, pp. 275–284, 1999.
[40]
S. Manzi, E. N. Meilahn, J. E. Rairie et al., “Age-specific incidence rates of myocardial infarction and angina in women with systemic lupus erythematosus: comparison with the Framingham study,” American Journal of Epidemiology, vol. 145, no. 5, pp. 408–415, 1997.
[41]
K. de Leeuw, B. Freire, A. J. Smit, H. Bootsma, C. G. Kallenberg, and M. Bijl, “Traditional and non-traditional risk factors contribute to the development of accelerated atherosclerosis in patients with systemic lupus erythematosus,” Lupus, vol. 15, no. 10, pp. 675–682, 2006.
[42]
M. B. Urowitz, A. A. M. Bookman, and B. E. Koehler, “The bimodal mortality pattern of systemic lupus erythematosus,” American Journal of Medicine, vol. 60, no. 2, pp. 221–225, 1976.
[43]
E. Svenungsson, K. Jensen-Urstad, M. Heimbürger et al., “Risk factors for cardiovascular disease in systemic lupus erythematosus,” Circulation, vol. 104, no. 16, pp. 1887–1893, 2001.
[44]
S. Manzi, F. Selzer, K. Sutton-Tyrrell et al., “Prevalence and risk factors of carotid plaque in women with systemic lupus erythematosus,” Arthritis and Rheumatism, vol. 42, no. 1, pp. 51–60, 1999.
[45]
M. J. Roman, B. A. Shanker, A. Davis et al., “Prevalence and Correlates of Accelerated Atherosclerosis in Systemic Lupus Erythematosus,” New England Journal of Medicine, vol. 349, no. 25, pp. 2399–2406, 2003.
[46]
Y. Asanuma, A. Oeser, A. K. Shintani et al., “Premature Coronary-Artery Atherosclerosis in Systemic Lupus Erythematosus,” New England Journal of Medicine, vol. 349, no. 25, pp. 2407–2415, 2003.
[47]
A. Farzaneh-Far, M. J. Roman, M. D. Lockshin et al., “Relationship of antiphospholipid antibodies to cardiovascular manifestations of systemic lupus erythematosus,” Arthritis and Rheumatism, vol. 54, no. 12, pp. 3918–3925, 2006.
[48]
M. J. Roman, R. B. Devereux, J. E. Schwartz et al., “Arterial stiffness in chronic inflammatory diseases,” Hypertension, vol. 46, no. 1, pp. 194–199, 2005.
[49]
R. Omdal, P. Lunde, K. Rasmussen, S. I. Mellgren, and G. Husby, “Transesophageal and transthoracic echocardiography and Doppler-examinations in systemic lupus erythematosus,” Scandinavian Journal of Rheumatology, vol. 30, no. 5, pp. 275–281, 2001.
[50]
R. Cervera, J. Font, C. Pare et al., “Cardiac disease in systemic lupus erythematosus: prospective study of 70 patients,” Annals of the Rheumatic Diseases, vol. 51, no. 2, pp. 156–159, 1992.
[51]
J. Pieretti, M. J. Roman, R. B. Devereux et al., “Systemic lupus erythematosus predicts increased left ventricular mass,” Circulation, vol. 116, no. 4, pp. 419–426, 2007.
[52]
L. Klareskog, P. Stolt, K. Lundberg et al., “A new model for an etiology of rheumatoid arthritis: smoking may trigger HLA-DR (shared epitope)-restricted immune reactions to autoantigens modified by citrullination,” Arthritis and Rheumatism, vol. 54, no. 1, pp. 38–46, 2006.
[53]
W. G. Law, B. Y. Thong, T. Y. Lian, K. O. Kong, and H. H. Chng, “Acute lupus myocarditis: clinical features and outcome of an oriental case series,” Lupus, vol. 14, no. 10, pp. 827–831, 2005.
[54]
F. Perez-Villa, J. Font, M. Azqueta et al., “Severe valvular regurgitation and antiphospholipid antibodies in systemic lupus erythematosus: a prospective, long-term, followup study,” Arthritis Care and Research, vol. 53, no. 3, pp. 460–467, 2005.
[55]
P. Nihoyannopoulos, P. M. Gomez, J. Joshi, S. Loizou, M. J. Walport, and C. M. Oakley, “Cardiac abnormalities in systemic lupus erythematosus. Association with raised anticardiolipin antibodies,” Circulation, vol. 82, no. 2, pp. 369–375, 1990.
[56]
M. A. Khamashta, R. Cervera, R. A. Asherson et al., “Association of antibodies against phospholipids with heart valve disease in systemic lupus erythematosus,” The Lancet, vol. 335, no. 8705, pp. 1541–1544, 1990.
[57]
I. G. Crozier, E. Li, M. J. Milne, and M. G. Nicholls, “Cardiac involvement in systemic lupus erythematosus detected by echocardiography,” American Journal of Cardiology, vol. 65, no. 16, pp. 1145–1148, 1990.
[58]
G. Sturfelt, J. Eskilsson, O. Nived, L. Truedsson, and S. Valind, “Cardiovascular disease in systemic lupus erythematosus. A study of 75 patients from a defined population,” Medicine, vol. 71, no. 4, pp. 216–223, 1992.
[59]
A. Doria, L. Iaccarino, P. Sarzi-Puttini, F. Atzeni, M. Turriel, and M. Petri, “Cardiac involvement in systemic lupus erythematosus,” Lupus, vol. 14, no. 9, pp. 683–686, 2005.
[60]
Y. Finkelstein, Y. Adler, L. Harel, M. Nussinovitch, and P. Youinou, “Anti-Ro (SSA) and anti-La (SSB) antibodies and complete congenital heart block,” Annales de Medecine Interne, vol. 148, no. 3, pp. 205–208, 1997.
[61]
O. Vaarala, M. Manttari, V. Manninen et al., “Anti-cardiolipin antibodies and risk of myocardial infarction in a prospective cohort of middle-aged men,” Circulation, vol. 91, no. 1, pp. 23–27, 1995.
[62]
N. Ohara, T. Miyata, A. Kurata, H. Oshiro, O. Sato, and H. Shigematsu, “Ten years' experience of aortic aneurysm associated with systemic lupus erythematosus,” European Journal of Vascular and Endovascular Surgery, vol. 19, no. 3, pp. 288–293, 2000.
[63]
S. R. Johnson, D. D. Gladman, M. B. Urowitz, D. Iba？ez, and J. T. Granton, “Pulmonary hypertension in systemic lupus,” Lupus, vol. 13, no. 7, pp. 506–509, 2004.
[64]
F. Gabrielli, E. Alcini, M. A. Di Prima, G. Mazzacurati, and C. Masala, “Cardiac valve involvement in systemic lupus erythematosus and primary antiphospholipid syndrome: lack of correlation with antiphospholipid antibodies,” International Journal of Cardiology, vol. 51, no. 2, pp. 117–126, 1995.
[65]
Y. Molad, N. Levin-Iaina, M. Vaturi, J. Sulkes, and A. Sagie, “Heart valve calcification in young patients with systemic lupus erythematosus: a window to premature atherosclerotic vascular morbidity and a risk factor for all-cause mortality,” Atherosclerosis, vol. 185, no. 2, pp. 406–412, 2006.
[66]
M. E. Evangelopoulos, M. Alevizaki, S. Toumanidis et al., “Mitral valve prolapse in systemic lupus erythematosus patients: clinical and immunological aspects,” Lupus, vol. 12, no. 4, pp. 308–311, 2003.
[67]
A. Kahan, G. Coghlan, and V. McLaughlin, “Cardiac complications of systemic sclerosis.,” Rheumatology, vol. 48, supplement 3, pp. iii45–iii48, 2009.
[68]
A. Kahan, J. Y. Devaux, and B. Amor, “Nifedipine and thallium-201 myocardial perfusion in progressive systemic sclerosis,” New England Journal of Medicine, vol. 314, no. 22, pp. 1397–1401, 1986.
[69]
A. Vacca, P. Siotto, A. Cauli et al., “Absence of epicardial coronary stenosis in patients with systemic sclerosis with severe impairment or coronary flow reserve,” Annals of the Rheumatic Diseases, vol. 65, no. 2, pp. 274–275, 2006.
[70]
W. P. Follansbee, E. I. Curtiss, and T. A. Medsger Jr, “Physiologic abnormalities of cardiac function in progressive systemic sclerosis with diffuse scleroderma,” New England Journal of Medicine, vol. 310, no. 3, pp. 142–148, 1984.
[71]
K. S. Cheng, A. Tiwari, A. Boutin et al., “Carotid and femoral arterial wall mechanics in scleroderma,” Rheumatology, vol. 42, no. 11, pp. 1299–1305, 2003.
[72]
I. Moyssakis, E. Gialafos, V. Vassiliou et al., “Aortic stiffness in systemic sclerosis is increased independently of the extent of skin involvement,” Rheumatology, vol. 44, no. 2, pp. 251–254, 2005.
[73]
J. B. Kostis, J. R. Seibold, D. Turkevich et al., “Prognostic importance of cardiac arrhythmias in systemic sclerosis,” American Journal of Medicine, vol. 84, no. 6, pp. 1007–1015, 1988.
[74]
B. Chang, L. Schachna, B. White, F. M. Wigley, and R. A. Wise, “Natural history of mild-moderate pulmonary hypertension and the risk factors for severe pulmonary hypertension in scleroderma,” Journal of Rheumatology, vol. 33, no. 2, pp. 269–274, 2006.
[75]
R. J. Byers, D. A. S. Marshall, and A. J. Freemont, “Pericardial involvement in systemic sclerosis,” Annals of the Rheumatic Diseases, vol. 56, no. 6, pp. 393–394, 1997.
[76]
D. Lautermann and J. Braun, “Ankylosing spondylitis—cardiac manifestations,” Clinical and Experimental Rheumatology, vol. 20, no. 6, pp. S-11–S-15, 2002.
[77]
A. Yildirir, S. Aksoyek, M. Calguneri, A. Oto, and S. Kes, “Echocardiographic evidence of cardiac involvement in ankylosing spondylitis,” Clinical Rheumatology, vol. 21, no. 2, pp. 129–134, 2002.
[78]
F. Brunner, A. Kunz, U. Weber, and R. Kissling, “Ankylosing spondylitis and heart abnormalities: do cardiac conduction disorders, valve regurgitation and diastolic dysfunction occur more often in male patients with diagnosed ankylosing spondylitis for over 15 years than in the normal population?” Clinical Rheumatology, vol. 25, no. 1, pp. 24–29, 2006.
[79]
C. Han, D. W. Robinson Jr, M. V. Hackett, L. C. Paramore, K. H. Fraeman, and M. V. Bala, “Cardiovascular disease and risk factors in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis,” Journal of Rheumatology, vol. 33, no. 11, pp. 2167–2172, 2006.
[80]
S. D. Kaplan, E. K. Chartash, R. A. Pizzarello, and R. A. Furie, “Cardiac manifestations of the antiphospholipid syndrome,” American Heart Journal, vol. 124, no. 5, pp. 1331–1338, 1992.
[81]
M. C. Amigo, “The heart and APS,” Clinical Reviews in Allergy and Immunology, vol. 32, no. 2, pp. 178–183, 2007.
[82]
P. Soltész, Z. Szekanecz, E. Kiss, and Y. Shoenfeld, “Cardiac manifestations in antiphospholipid syndrome,” Autoimmunity Reviews, vol. 6, no. 6, pp. 379–386, 2007.
[83]
F. Tenedios, D. Erkan, and M. D. Lockshin, “Cardiac Manifestations in the Antiphospholipid Syndrome,” Rheumatic Disease Clinics of North America, vol. 32, no. 3, pp. 491–507, 2006.
[84]
R. T. Urbanus, B. Siegerink, M. Roest, F. R. Rosendaal, P. G. de Groot, and A. Algra, “Antiphospholipid antibodies and risk of myocardial infarction and ischaemic stroke in young women in the RATIO study: a case-control study,” The Lancet Neurology, vol. 8, no. 11, pp. 998–1005, 2009.
[85]
F. J. Munoz-Rodriguez, J. C. Reventer Calatayud, J. Font Franco, G. Espinosa Garriga, D. Tàssies Penella, and M. Ingelmo Morin, “Valvular heart disease in patients with anti-phospholipid syndrome,” Revista Clinica Espanola, vol. 202, no. 10, pp. 529–533, 2002.
[86]
M. Shbeeb, K. M. Uramoto, L. E. Gibson, W. M. O'Fallon, and S. E. Gabriel, “The epidemiology of psoriatic arthritis in Olmsted County, Minnesota, USA, 1982-1991,” Journal of Rheumatology, vol. 27, no. 5, pp. 1247–1250, 2000.
[87]
J. M. Gelfand, D. D. Gladman, P. J. Mease et al., “Epidemiology of psoriatic arthritis in the population of the United States,” Journal of the American Academy of Dermatology, vol. 53, no. 4, pp. 573–577, 2005.
[88]
T. M. Madland, E. M. Apalset, A. E. Johannessen, B. Rosseb？, and J. G. Brun, “Prevalence, disease manifestations, and treatment of psoriatic arthritis in Western Norway,” Journal of Rheumatology, vol. 32, no. 10, pp. 1918–1922, 2005.
[89]
C. Gonzalez-Juanatey, E. Amigo-Diaz, J. A. Miranda-Filloy et al., “Lack of Echocardiographic and Doppler Abnormalities in Psoriatic Arthritis Patients Without Clinically Evident Cardiovascular Disease or Classic Atherosclerosis Risk Factors,” Seminars in Arthritis and Rheumatism, vol. 35, no. 5, pp. 333–339, 2006.
[90]
J. M. Gelfand, A. L. Neimann, D. B. Shin, X. Wang, D. J. Margolis, and A. B. Troxel, “Risk of myocardial infarction in patients with psoriasis,” Journal of the American Medical Association, vol. 296, no. 14, pp. 1735–1741, 2006.
[91]
I. E. Lundberg, “The heart in dermatomyositis and polymyositis,” Rheumatology, vol. 45, supplement 4, pp. iv18–iv21, 2006.
[92]
K. Dankó, A. Ponyi, T. Constantin, G. Borgulya, and G. Szegedi, “Long-term survival of patients with idiopathic inflammatory myopathies according to clinical features: a longitudinal study of 162 cases,” Medicine, vol. 83, no. 1, pp. 35–42, 2004.
[93]
S. M. Sultan, Y. Ioannou, K. Moss, and D. A. Isenberg, “Outcome in patients with idiopathic inflammatory myositis: morbidity and mortality,” Rheumatology, vol. 41, no. 1, pp. 22–26, 2002.
[94]
A. J. Taylor, D. C. Wortham, J. R. Burge, and K. M. Rogan, “The heart in polymyositis: a prospective evaluation of 26 patients,” Clinical Cardiology, vol. 16, no. 11, pp. 802–808, 1993.
[95]
R. Stern, J. H. Godbold, Q. Chess, and L. J. Kagen, “ECG abnormalities in polymyositis,” Archives of Internal Medicine, vol. 144, no. 11, pp. 2185–2189, 1984.
[96]
L. F. Tami and S. Bhasin, “Polymorphism of the cardiac manifestations in dermatomyositis,” Clinical Cardiology, vol. 16, no. 3, pp. 260–264, 1993.
[97]
K. de Leeuw, J. S. Sanders, C. Stegeman, A. Smit, C. G. Kallenberg, and M. Bijl, “Accelerated atherosclerosis in patients with Wegener's granulomatosis,” Annals of the Rheumatic Diseases, vol. 64, no. 5, pp. 753–759, 2005.
[98]
M. Faurschou, L. Mellemkjaer, I. J. Sorensen, B. S. Thomsen, L. Dreyer, and B. Baslund, “Increased morbidity from ischemic heart disease in patients with Wegener's granulomatosis,” Arthritis and Rheumatism, vol. 60, no. 4, pp. 1187–1192, 2009.
[99]
Y. Hashimoto, M. Tanaka, A. Hata, T. Kakuta, Y. Maruyama, and F. Numano, “Four years follow-up study in patients with Takayasu arteritis and severe aortic regurgitation; assessment by echocardiography.,” International Journal of Cardiology, vol. 54, pp. S173–176, 1996.
[100]
G. S. Kerr, C. W. Hallahan, J. Giordano et al., “Takayasu arteritis,” Annals of Internal Medicine, vol. 120, no. 11, pp. 919–929, 1994.
[101]
K. Maksimowicz-McKinnon, T. M. Clark, and G. S. Hoffman, “Limitations of therapy and a guarded prognosis in an American cohort of Takayasu arteritis patients,” Arthritis and Rheumatism, vol. 56, no. 3, pp. 1000–1009, 2007.
[102]
D. H. Pfizenmaier, F. O. Al Atawi, Y. Castillo, K. Chandrasekaran, and L. T. Cooper, “Predictors of left ventricular dysfunction in patients with Takayasu's or giant cell aortitis,” Clinical and Experimental Rheumatology, vol. 22, no. 6, pp. S-41–S-45, 2004.
[103]
A. Alcelik, S. Karacay, I. N. Hakyemez, B. Akin, S. Ozturk, and H. Savli, “Takayasu arteritis initially mimicking infective endocarditis,” Mediterranean Journal of Hematology and Infectious Diseases, vol. 3, no. 1, Article ID e2011040, 2011.
[104]
S. Ouali, S. Kacem, F. B. Fradj et al., “Takayasu arteritis with coronary aneurysms: causing acute myocardial infarction in a young man,” Texas Heart Institute Journal, vol. 38, no. 2, pp. 183–186, 2011.
[105]
G. Y. Lee, S. Y. Jang, S. M. Ko et al., “Cardiovascular manifestations of Takayasu arteritis and their relationship to the disease activity: analysis of 204 Korean patients at a single center,” International Journal of Cardiology, 2011.
[106]
T. Weyn, S. Haine, F. Van Den Branden, and V. Conraads, “Cardiac manifestation in Takayasu arteritis,” Acta Cardiologica, vol. 64, no. 4, pp. 557–560, 2009.
[107]
A. Ravelli, E. Pedroni, S. Perrone, R. Tramarin, A. Martini, and G. R. Burgio, “Aortic valve regurgitation as the presenting sign of Takayasu arteritis,” European Journal of Pediatrics, vol. 158, no. 4, pp. 281–283, 1999.
[108]
D. M. Nuenninghoff, G. G. Hunder, T. J. H. Christianson, R. L. McClelland, and E. L. Matteson, “Mortality of large-artery complication (aortic aneurysm, aortic dissection, and/or large-artery stenosis) in patients with giant cell arteritis: a population-based study over 50 years,” Arthritis and Rheumatism, vol. 48, no. 12, pp. 3532–3537, 2003.
[109]
R. T. Eberhardt and M. Dhadly, “Giant cell arteritis: diagnosis, management, and cardiovascular implications,” Cardiology in Review, vol. 15, no. 2, pp. 55–61, 2007.
[110]
L. Niclauss, I. Letovanec, P. G. Chassot, P. A. Gersbach, and L. K. von Segesser, “Acute aortic valve insufficiency and cardiogenic shock due to an isolated giant cell inflammation of the aortic valve leaflets: case report and review of the literature.,” The Journal of Heart Valve Disease, vol. 17, no. 3, pp. 343–347, 2008.
[111]
J. T. Lie, “Aortic and extracranial large vessel giant cell arteritis: a review of 72 cases with histopathologic documentation,” Seminars in Arthritis and Rheumatism, vol. 24, no. 6, pp. 422–431, 1995.
[112]
J. C. Jennette, R. J. Falk, K. Andrassy et al., “Nomenclature of systemic vasculitides: proposal of an international consensus conference,” Arthritis and Rheumatism, vol. 37, no. 2, pp. 187–192, 1994.
[113]
T. Iino, K. Eguchi, M. Sakai, S. Nagataki, M. Ishijima, and K. Toriyama, “Polyarteritis nodosa with aortic dissection: necrotizing vasculitis of the vasa vasorum,” Journal of Rheumatology, vol. 19, no. 10, pp. 1632–1636, 1992.
[114]
P. Y. Courand, P. Croisille, P. Khouatra, V. Cottin, G. Kirkorian, and E. Bonnefoy, “Churg-Strauss syndrome presenting with acute myocarditis and cardiogenic shock,” Heart, Lung and Circulation, vol. 21, no. 3, pp. 178–181, 2012.
[115]
W. Szczeklik, T. Miszalski-Jamka, L. Mastalerz et al., “Multimodality assessment of cardiac involvement in Churg-Strauss syndrome patients in clinical remission,” Circulation Journal, vol. 75, no. 3, pp. 649–655, 2011.
[116]
M. J. Strube, “Small sample failure of random assignment: a further examination,” Journal of Consulting and Clinical Psychology, vol. 59, no. 2, pp. 346–350, 1991.
[117]
T. Neumann, B. Manger, M. Schmid et al., “Cardiac involvement in churg-strauss syndrome: impact of endomyocarditis,” Medicine, vol. 88, no. 4, pp. 236–243, 2009.
[118]
A. D. Wagner, G. P. Meyer, M. Rihl et al., “Acute coronary syndrome associated with Churg-Strauss syndrome,” Vascular Health and Risk Management, vol. 3, no. 5, pp. 775–779, 2007.
[119]
M. B. Owlia and G. Mehrpoor, “Behcet's disease: new concepts in cardiovascular involvements and future direction for treatment,” ISRN Pharmacol, vol. 2012, Article ID 760484, 2012.
