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J Am Coll Cardiol, 2006; 48:1727, doi:10.1016/j.jacc.2006.07.028 (Published online 25 September 2006).
© 2006 by the American College of Cardiology Foundation
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CORRESPONDENCE: LETTER TO THE EDITOR

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Gurbir Bhatia, MRCP, Gregory Y.H. Lip, MD, FACC and Russell C. Davis, MRCP, MD*

* University Department of Medicine, City Hospital, Dudley Road, Birmingham B18 7QH West Midlands, United Kingdom (Email: Russell.Davis{at}swbh.nhs.uk).


We thank Dr. Roman for her interest in our study (1). Reported myocardial infarction (MI) was an independent predictor of left ventricular systolic dysfunction (LVSD) in both the rheumatoid and general populations, but the prevalence of LVSD was still higher in the rheumatoid population despite the prevalence of reported MI being not significantly different between the 2 populations (1). This may still relate to ischemic heart disease (IHD), which is more prevalent among rheumatoid patients (2). Indeed, IHD may be less clinically apparent among rheumatoid patients, partly because of their limited exercise tolerance due to arthritis and also misinterpretation of the cause of chest pain. For example, rheumatoid patients are more likely to experience unrecognized MI than nonrheumatoid control subjects (3). Furthermore, cardiac ischemia (identified by thallium scintigraphy) was more frequent (and more often clinically silent) in rheumatoid patients compared to counterparts with osteoarthritis (4). In our cohort (1), ischemic heart disease was the likely underlying cause of LVSD in subjects who had denied prior cardiac disease or cardiac symptoms.

Although diagnosed hypertension was more prevalent in the cohort with rheumatoid disease, this may partly reflect the fact that their blood pressures were probably measured more frequently than the general population cohort, and thus they were more likely to have been detected. Given that we found definite LVSD in only 2.0% of treated hypertensive subjects in another arm of the ECHOES (Echocardiographic Heart of England Screening) study (5), hypertension seems unlikely to explain most of the excess prevalence of LVSD in the rheumatoid population.

Finally, although the exact mechanism of the high prevalence of LVSD in subjects with rheumatoid disease is still uncertain, this does not detract from the main conclusion of our study (1), namely that clinicians should be aware of the association and consider echocardiographic screening for those at risk.


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 References
 

  1. Bhatia GS, Sosin, MD, Patel JV, et al. Left ventricular systolic dysfunction in rheumatoid disease: an unrecognized burden? J Am Coll Cardiol 2006;47:1169-1174.[Abstract/Free Full Text]
  2. Bhatia GS, Sosin, MD, Khattak FH, Lip GYH, Davis RC. Rheumatoid disease: a risk factor for ischaemic heart disease? Int J Cardiol 2005;105:1-10.[CrossRef][ISI][Medline]
  3. Maradit-Kramers H, Crowson CS, Nicola PJ, et al. Increased unrecognised coronary heart disease and sudden deaths in rheumatoid arthritis: a population-based cohort study Arthritis Rheum 2005;52:402-411.[CrossRef][ISI][Medline]
  4. Banks MJ, Flint EJ, Bacon PA, Kitas GD. Rheumatoid arthritis is an independent risk factor for ischaemic heart disease (abstr) Arthritis Rheum 2000;43:S385.
  5. Davis RC, Hobbs FDR, Kenkre JE, et al. Prevalence of left ventricular systolic dysfunction and heart failure in high-risk patients: community based epidemiological study BMJ 2002;325:1156-1158.[Abstract/Free Full Text]




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