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Apical hypertrophic cardiomyopathy in Japan and the United States in brothers but not identical twins
READERS’ COMMENTS Apical Hypertrophic Cardiomyopathy in Japan and the United States in Brothers But Not Identical Twins
I read with interest the article by Kitaoka et al1 comparing apical hypertrophic cardiomyopathy (aHC) in Japan and the United States. Over 20 years ago2 I pointed out certain additional differences between the “pure” Japanese form of aHC and the nonJapanese form described in American patients. The former is more prevalent in Japan, predominantly in men, and is often associated with giant negative T waves, a QRS axis between 0° and 90°, and a QRS loop oriented to the left and inferiorly with characteristic elongated T loops oriented to the right and posteriorly. Septal Q waves are often lacking. The spade-like angiographic appearance is often present in the pure Japanese form also when diagnosed outside Japan3–5 and is identical to morphologic, electrocardiographic, and other findings in their Japanese counterparts. In our long-term follow-up study of pure aHC4 we found, as did Koga et al6, that Rwave voltage and T-wave negativity may progressively decrease in magnitude, thus modifying the diagnostic electrocardiographic hallmarks of the disease. Regarding the authors’ conclusion that aHC has a “benign clinical course,” this was not our experience when follow-up was extended to ⬎10 years4, because ventricular tachycardia, atrial fibrillation, and apical aneurysm may develop later on. In keeping with our findings, a report from Japan has also raised concern that patients with pure aHC are prone to life-threatening arrhythmias.6 Thus, a complacent approach to all Letters (from the United States) concerning a particular article in The American Journal of Cardiology姞 must be received within 2 months of the article’s publication, and should be limited (with rare exceptions) to 2 doublespaced typewritten pages. Two copies must be submitted.
such patients is unsafe. It will be very important to compare the natural history of the disease in your Japanese and American patients at extended long-term follow-up beyond 10 years. Thus, aHC may not represent a single entity, and although the “brothers share the same family name, they are from being identical twins and genetic counseling is indicated.” Edward G. Abinader,
MD
Haifa, Israel 15 January 2004
1. Kitaoka H, Doi Y, Casey SA, Hitomi N, Furuno T, Maron BJ. Comparison of prevalence of apical hypertrophic cardiomyopathy in Japan and the United States. Am J Cardiol 2003;92:1183–1186. 2. Abinader EG. Apical hypertrophic cardiomyopathy. Am J Cardiol 1983;51:1570 –1571. 3. Abinader EG, Rauchfleisch S, Naschitz. Hypertrophic apical cardiomyopathy: a subtype of hypertrophic cardiomyopathy. Is J Med Sci 1982;18:1005– 1009. 4. Abinader EG, Sharif D, Shefer A, Naschitz J. Novel insights into the natural history of apical hypertrophic cardiomyopathy during long-term followup. IMAJ. 2002;4:166 –169. 5. Kereiakes DJ, Anderson DJ, Crouse L, Chatterjee MB. Apical hypertrophic cardiomyopathy. Am Heart J 1983;105:855– 856. 6. Koga Y, Katoh A, Matsuyama K, Ikeda H, Hiyamuta K, Toshima H, Imaizumi T, Disappearance of giant negative T waves in patients with the Japanese form of apical hypertrophy. J Am Coll Cardiol 1995; 26:1972–1978.
doi:10.1016/j.amjcard.2004.01.077
High Iron Stores and Ischemic Heart Disease in Rheumatoid Arthritis and Systemic Lupus Erythematosus
Fisher et al1 reported an increased risk of developing a firsttime acute myocardial infarction in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), with a substantially increased risk for subjects with both hyperlipidemia and inflammatory diseases. A plausible explanation of this detrimental association, which was not considered in the report,1 may also be related to the increased iron stores, frequently observed in both RA and SLE.2 Serum ferritin, a good indicator of the level of iron stored in the body, has been shown to be
©2004 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 94 October 1, 2004
related to the development of atherosclerosis,3,4 and this relation does appear to be strengthened by a synergistic association between elevated iron stores and low-density lipoprotein cholesterol.3–5 Thus, serum ferritin should be considered as an adjunctive risk factor for the development of ischemic heart disease in patients with RA or SLE. Luca Mascitelli,
MD
Udine, Italy Francesca Pezzetta,
MD
Tolmezzo, Italy 24 March 2004
1. Fischer LM, Schlienger RG, Matter C, Jick H, Meier CR. Effect of rheumatoid arthritis or systemic lupus erythematosus on the risk of first-time acute myocardial infarction. Am J Cardiol 2004;93:198 –200. 2. Tefferi A. Anemia in adults: a contemporary approach to diagnosis. Mayo Clin Proc 2003;78:1274 – 1280. 3. Kiechl S, Willeit J, Egger G, Poewe W, Oberhollenzer F. Body iron stores and the risk of carotid atherosclerosis: prospective results from the Bruneck study. Circulation 1997;96:3300 –3307. 4. Wolff B, Völzke H, Lüdemann J, Robinson D, Vogelsang D, Staudt A, Kessler C, Dahm JB, John U, Felix SB. Association between high serum ferritin levels and carotid atherosclerosis in the study of health in Pomerania (SHIP). Stroke 2004;35:453– 457. 5. Mainous AG III, Wells BJ, Everett CJ, Gill JM, King DE. Association of ferritin and lipids with C-reactive protein. Am J Cardiol 2004;93:559 –562.
doi:10.1016/j.amjcard.2004.04.079
Wake Up and Smell the Caffeine
In their article “Cardiovascular Effects of Caffeine in Men and Women,” Hartley et al1 report gender differences in the hemodynamic response to caffeine in young, healthy persons. Although the authors characterize the subjects they studied as “habitual users of caffeine,” they should more correctly be considered “regular drinkers of coffee,” and I believe there is a difference that greatly limits the relevance of their findings. In this study, 3.3 mg/kg of caffeine was mixed with 6 oz of grapefruit juice, which the subjects drank within 5 minutes. I know of no person who drinks his or her coffee this way. The men in this study averaged 80 kg, so each drank a cup of juice with an aver0002-9149/04/$–see front matter
981
I read with interest the article by Kitaoka et al1 comparing apical hypertrophic cardiomyopathy (aHC) in Japan and the United States. Over 20 years ago2 I pointed out certain additional differences between the “pure” Japanese form of aHC and the nonJapanese form described in American patients. The former is more prevalent in Japan, predominantly in men, and is often associated with giant negative T waves, a QRS axis between 0° and 90°, and a QRS loop oriented to the left and inferiorly with characteristic elongated T loops oriented to the right and posteriorly. Septal Q waves are often lacking. The spade-like angiographic appearance is often present in the pure Japanese form also when diagnosed outside Japan3–5 and is identical to morphologic, electrocardiographic, and other findings in their Japanese counterparts. In our long-term follow-up study of pure aHC4 we found, as did Koga et al6, that Rwave voltage and T-wave negativity may progressively decrease in magnitude, thus modifying the diagnostic electrocardiographic hallmarks of the disease. Regarding the authors’ conclusion that aHC has a “benign clinical course,” this was not our experience when follow-up was extended to ⬎10 years4, because ventricular tachycardia, atrial fibrillation, and apical aneurysm may develop later on. In keeping with our findings, a report from Japan has also raised concern that patients with pure aHC are prone to life-threatening arrhythmias.6 Thus, a complacent approach to all Letters (from the United States) concerning a particular article in The American Journal of Cardiology姞 must be received within 2 months of the article’s publication, and should be limited (with rare exceptions) to 2 doublespaced typewritten pages. Two copies must be submitted.
such patients is unsafe. It will be very important to compare the natural history of the disease in your Japanese and American patients at extended long-term follow-up beyond 10 years. Thus, aHC may not represent a single entity, and although the “brothers share the same family name, they are from being identical twins and genetic counseling is indicated.” Edward G. Abinader,
MD
Haifa, Israel 15 January 2004
1. Kitaoka H, Doi Y, Casey SA, Hitomi N, Furuno T, Maron BJ. Comparison of prevalence of apical hypertrophic cardiomyopathy in Japan and the United States. Am J Cardiol 2003;92:1183–1186. 2. Abinader EG. Apical hypertrophic cardiomyopathy. Am J Cardiol 1983;51:1570 –1571. 3. Abinader EG, Rauchfleisch S, Naschitz. Hypertrophic apical cardiomyopathy: a subtype of hypertrophic cardiomyopathy. Is J Med Sci 1982;18:1005– 1009. 4. Abinader EG, Sharif D, Shefer A, Naschitz J. Novel insights into the natural history of apical hypertrophic cardiomyopathy during long-term followup. IMAJ. 2002;4:166 –169. 5. Kereiakes DJ, Anderson DJ, Crouse L, Chatterjee MB. Apical hypertrophic cardiomyopathy. Am Heart J 1983;105:855– 856. 6. Koga Y, Katoh A, Matsuyama K, Ikeda H, Hiyamuta K, Toshima H, Imaizumi T, Disappearance of giant negative T waves in patients with the Japanese form of apical hypertrophy. J Am Coll Cardiol 1995; 26:1972–1978.
doi:10.1016/j.amjcard.2004.01.077
High Iron Stores and Ischemic Heart Disease in Rheumatoid Arthritis and Systemic Lupus Erythematosus
Fisher et al1 reported an increased risk of developing a firsttime acute myocardial infarction in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), with a substantially increased risk for subjects with both hyperlipidemia and inflammatory diseases. A plausible explanation of this detrimental association, which was not considered in the report,1 may also be related to the increased iron stores, frequently observed in both RA and SLE.2 Serum ferritin, a good indicator of the level of iron stored in the body, has been shown to be
©2004 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 94 October 1, 2004
related to the development of atherosclerosis,3,4 and this relation does appear to be strengthened by a synergistic association between elevated iron stores and low-density lipoprotein cholesterol.3–5 Thus, serum ferritin should be considered as an adjunctive risk factor for the development of ischemic heart disease in patients with RA or SLE. Luca Mascitelli,
MD
Udine, Italy Francesca Pezzetta,
MD
Tolmezzo, Italy 24 March 2004
1. Fischer LM, Schlienger RG, Matter C, Jick H, Meier CR. Effect of rheumatoid arthritis or systemic lupus erythematosus on the risk of first-time acute myocardial infarction. Am J Cardiol 2004;93:198 –200. 2. Tefferi A. Anemia in adults: a contemporary approach to diagnosis. Mayo Clin Proc 2003;78:1274 – 1280. 3. Kiechl S, Willeit J, Egger G, Poewe W, Oberhollenzer F. Body iron stores and the risk of carotid atherosclerosis: prospective results from the Bruneck study. Circulation 1997;96:3300 –3307. 4. Wolff B, Völzke H, Lüdemann J, Robinson D, Vogelsang D, Staudt A, Kessler C, Dahm JB, John U, Felix SB. Association between high serum ferritin levels and carotid atherosclerosis in the study of health in Pomerania (SHIP). Stroke 2004;35:453– 457. 5. Mainous AG III, Wells BJ, Everett CJ, Gill JM, King DE. Association of ferritin and lipids with C-reactive protein. Am J Cardiol 2004;93:559 –562.
doi:10.1016/j.amjcard.2004.04.079
Wake Up and Smell the Caffeine
In their article “Cardiovascular Effects of Caffeine in Men and Women,” Hartley et al1 report gender differences in the hemodynamic response to caffeine in young, healthy persons. Although the authors characterize the subjects they studied as “habitual users of caffeine,” they should more correctly be considered “regular drinkers of coffee,” and I believe there is a difference that greatly limits the relevance of their findings. In this study, 3.3 mg/kg of caffeine was mixed with 6 oz of grapefruit juice, which the subjects drank within 5 minutes. I know of no person who drinks his or her coffee this way. The men in this study averaged 80 kg, so each drank a cup of juice with an aver0002-9149/04/$–see front matter
981