CORRESPONDENCE: LETTERS TO THE EDITOR
Reply
Kristian Wachtell, MD, PhD*,
Mika Lehto, MD,
Eva Gerdts, MD, PhD,
Michael Hecht Olsen, MD, PhD,
Björn Hornestam, MD,
Björn Dahlöf, MD, PhD, FACC,
Hans Ibsen, MD,
Stevo Julius, MD, FACC,
Sverre E. Kjeldsen, MD, PhD, FACC,
Lars H. Lindholm, MD, FACC,
Markku S. Nieminen, MD, FACC and
Richard B. Devereux, MD, FACC
* Rigshospitalet, Department of Medicine B2142, 9 Blegdamsvej, DK-2100 Copenhagen, Denmark (Email: kristian{at}wachtell.net).
We would like to thank Dr. Ogimoto and colleagues for their interest in our study showing that losartan reduced the incidence of new-onset atrial fibrillation (AF) by 33% compared to atenolol (1). Dr. Ogimoto and colleagues note that the incidence of new-onset AF is numerically higher among black patients treated with losartan compared to those treated with atenolol. However, the data we presented do not provide statistical support for a difference in the incidence of new-onset strokes between blacks on losartan-based compared to atenolol-based treatment (n = 5 [1.9%] vs. 2 [0.8%], HR [hazard ratio] = 2.5 [95% confidence interval 0.48–12.8], p = 0.279). Furthermore, there was no association of black versus white ethnicity and new-onset AF (p = 0.11). Thus, the LIFE data do not document ethnic differences in either new-onset AF or treatment effects thereon.
The hypothesis that angiotensin-II receptor blockers might induce AF is not supported by existing data. The nonsignificant trend toward increased new-onset AF among patients treated with valsartan in the VALUE study may easily be attributed to the significantly higher blood pressure in the valsartan-treated patients compared to those treated with amlodipine, especially during the first part of the trial (2). Our model to predict new-onset AF (Table 5 in ref. 1) showed that systolic blood pressure is an independent predictor of new-onset AF (1). It is likely that the lower blood pressure among the amlodipine-treated patients is the direct cause of the trend toward lower new-onset AF. Because the LIFE study had similar blood pressure reduction in both treatment arms, our study is, contrary to previous studies (3–5), the first one able to determine that the lower incidence of new-onset AF it is due to blockade of the angiotensin-II receptor and not the antihypertensive properties of losartan (6).
The hypothesis that reduced activation of the renin-angiotensin system in patients with small left ventricular (LV) chamber sizes can cause AF is not validated from the LIFE data. In the LIFE echocardiography study, a representative sample of the LIFE study, including 10% of the overall population (7,8), increased (not reduced) LV chamber size was predictive of new-onset AF (Wachtell et al., unpublished data, May 2005). Furthermore, recently presented data show that patients who develop new-onset AF during systematic antihypertensive treatment have less reduction in left atrial size and less improvement in systolic LV function but similar LV mass and relative wall thickness reduction in response to blood pressure lowering (9).
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References
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- Wachtell K, Lehto M, Gerdts E, et al. Angiotensin II receptor blockade reduces new-onset atrial fibrillation and subsequent stroke compared to atenololthe Losartan Intervention For End point reduction in hypertension (LIFE) study. J Am Coll Cardiol 2005;45:712-719.[Abstract/Free Full Text]
- Julius S, Kjeldsen SE, Weber M, et al. Outcomes in hypertensive patients at high cardiovascular risk treated with regimens based on valsartan or amlodipinethe VALUE randomised trial. Lancet 2004;363:2022-2031.[CrossRef][ISI][Medline]
- Pedersen OD, Bagger H, Køber L, Torp-Pedersen C. Trandolapril reduces the incidence of atrial fibrillation after acute myocardial infarction in patients with left ventricular dysfunction Circulation 1999;100:376-380.[Abstract/Free Full Text]
- Madrid AH, Bueno MG, Rebollo JM, et al. Use of irbesartan to maintain sinus rhythm in patients with long-lasting persistent atrial fibrillationa prospective and randomized study. Circulation 2002;106:331-336.[Abstract/Free Full Text]
- Vermes E, Tardif JC, Bourassa MG, et al. Enalapril decreases the incidence of atrial fibrillation in patients with left ventricular dysfunctionInsight from the Studies Of Left Ventricular Dysfunction (SOLVD) trials. Circulation 2003;107:2926-2931.[Abstract/Free Full Text]
- Healey JS, Morillo CA, Connolly SJ. Role of the renin-angiotensin-aldosterone system in atrial fibrillation and cardiac remodeling Curr Opin Cardiol 2005;20:31-37.[ISI][Medline]
- Wachtell K, Bella JN, Liebson PR, et al. Impact of different partition values on prevalences of left ventricular hypertrophy and concentric geometry in a large hypertensive populationthe LIFE study. Hypertension 2000;35:6-12.[Abstract/Free Full Text]
- Devereux RB, Bella JN, Boman K, et al. Echocardiographic left ventricular geometry in hypertensive patients with electrocardiographic left ventricular hypertrophythe LIFE study. Blood Press 2001;10:74-82.[CrossRef][ISI][Medline]
- Wachtell K, Palmieri V, Gerdts E, et al. Left ventricular structural and functional response in hypertensive patients with new-onset atrial fibrillation and left ventricular hypertrophythe LIFE study. abstr J Am Coll Cardiol 2005;45:374A.
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