Correspondence
Correction
Idiopathic Dilated Cardiomyopathy
N Engl J Med 1995; 332:1384-1386May 18, 1995
- Article
To the Editor:
Dec and Fuster (Dec. 8 issue)1 categorized the use of beta-blockers in patients with idiopathic dilated cardiomyopathy as investigational. There is now sufficient evidence to support their use as adjunctive therapy. Numerous clinical trials have evaluated the use of beta-blockers in conjunction with angiotensin-converting–enzyme inhibitors, nitrates, diuretics, and digoxin in patients with idiopathic dilated cardiomyopathy and have found improvements in ejection fraction, cardiac index, and New York Heart Association class and a decreased number of hospital admissions and cardiac transplantations.2-4 However, there have been trials5,6 that did not show such improvements. This is probably because patients were not started on low doses with a slow upward titration,5,6 the duration of the studies was short (e.g., one month),5,6 the study sample was small,5 the patient populations were not homogeneous (e.g., patients with ischemic dilated cardiomyopathy5 or alcoholic cardiomyopathy6 were included), and beta-blockers with intrinsic sympathomimetic activity were used (e.g., acebutolol).6
The authors reported that investigators in the Metoprolol in Dilated Cardiomyopathy trial4 were unable to show an improvement in survival. Although this is true, it may be misleading. Since cardiac transplantation is a well-recognized treatment for patients with this disease, this trial compared the need for transplantation in patients on placebo with that of those taking metoprolol. Nineteen patients taking placebo underwent heart transplantation, as compared with only two patients taking metoprolol. This difference was statistically significant. This trial also showed significantly fewer hospital admissions for patients taking metoprolol.
6 ReferencesCatherine E. Cooke, Pharm.D.
Philadelphia College of Pharmacy and Science, Philadelphia, PA 19104-44951
Dec GW ,Fuster V . Idiopathic dilated cardiomyopathy. N Engl J Med 1994;331:1564-1575
Full Text | Web of Science | Medline2
Wisenbaugh T ,Katz I ,Davis J , et al. Long-term (3-month) effects of a new beta-blocker (nebivolol) on cardiac performance in dilated cardiomyopathy. J Am Coll Cardiol 1993;21:1094-1100
CrossRef | Web of Science | Medline3
Woodley SL ,Gilbert EM ,Anderson JL , et al. β-Blockade with bucindolol in heart failure caused by ischemic versus idiopathic dilated cardiomyopathy. Circulation 1991;84:2426-2441
Web of Science | Medline4
Waagstein F , et al. MDC: β1-Blockade verhindert Herztransplantationen. Herz Kreislauf 1993;25:170-1705
Currie PJ ,Kelly MJ ,McKenzie A , et al. Oral beta-adrenergic blockade with metoprolol in chronic severe dilated cardiomyopathy. J Am Coll Cardiol 1984;3:203-209
CrossRef | Web of Science | Medline6
Ikram H ,Fitzpatrick D . Double-blind trial of chronic oral beta blockade in congestive cardiomyopathy. Lancet 1981;2:490-493
CrossRef | Web of Science | Medline
To the Editor:
Dec and Fuster provided a detailed discussion of both accepted and investigational therapies for idiopathic dilated cardiomyopathy. They failed, however, to address the important and expanding role of dynamic cardiomyoplasty in the treatment of this disease. Originally described by Carpentier and Chachques1 some 10 years ago, cardiomyoplasty involves the use of a skeletal-muscle flap, usually the left latissimus dorsi, which is wrapped around the heart and then electrically stimulated to help augment myocardial contractility. Carpentier's group2 followed 52 patients who had undergone cardiomyoplasty for severe heart failure, with idiopathic dilated cardiomyopathy being the primary cause in 13. There was improvement in functional status in the long-term survivors, with a reduction in the mean New York Heart Association class from 3.3 preoperatively to 1.6 postoperatively. Associated with this was an improved exercise capacity, a reduction in the number of annual hospitalizations from 2.4 to 0.4, and a reduction in the need for medications in 62 percent of the patients. A significant decrease in late mortality was also noted, with actuarial survival of 70 percent at seven years (excluding early postoperative mortality). Studies by other investigators have also consistently shown improved functional status, decreased mortality, and an improved quality of life, although whether there was long-term improvement in hemodynamic variables is less clear.3,4
4 ReferencesMichael D. Greenberg, M.D.
Georgetown University Medical Center, Washington, DC 20007-21971
Carpentier A ,Chachques JC . Myocardial substitution with a stimulated skeletal muscle: first successful clinical case. Lancet 1985;1:1267-1267
CrossRef | Web of Science | Medline2
Carpentier A ,Chachques JC ,Acar C , et al. Dynamic cardiomyoplasty at seven years. J Thorac Cardiovasc Surg 1993;106:42-54
Web of Science | Medline3
Moreira LF ,Bocchi EA ,Stolf NA ,Pileggi F ,Jatene AD . Current expectations in dynamic cardiomyoplasty. Ann Thorac Surg 1993;55:299-303
CrossRef | Web of Science | Medline4
El Oakley RM ,Jarvis JC . Cardiomyoplasty: a critical review of experimental and clinical results. Circulation 1994;90:2085-2090
Web of Science | Medline
To the Editor:
Dec and Fuster correctly noted that blacks in the United States have a two- to threefold increase in the risk of idiopathic dilated cardiomyopathy after other factors are taken into account.1 Two additional epidemiologic studies, with a case–control and a cohort design, have confirmed the predominance of idiopathic dilated cardiomyopathy among blacks.2,3
It should also be noted, however, that black patients with idiopathic dilated cardiomyopathy may be substantially more likely to die in the first two years after diagnosis than white patients, even after other prognostic factors are taken into account.4 The apparently poorer survival among blacks may be explained by greater severity of disease at the time of diagnosis, decreased compliance with treatment regimens, or racial differences in cardiac care, coexisting conditions, or biologic factors affecting survival.
4 ReferencesSteven S. Coughlin, Ph.D.
Tulane University Medical Center, New Orleans, LA 70112-26991
Coughlin SS ,Szklo M ,Baughman K ,Pearson TA . The epidemiology of idiopathic dilated cardiomyopathy in a biracial community. Am J Epidemiol 1990;131:48-56
Web of Science | Medline2
Coughlin SS ,Labenberg JR ,Tefft MC . Black-white differences in idiopathic dilated cardiomyopathy: the Washington, DC, Dilated Cardiomyopathy Study. Epidemiology 1993;4:165-172
CrossRef | Web of Science | Medline3
Coughlin SS ,Neaton JD ,Sengupta A ,Kuller LH . Predictors of mortality from idiopathic dilated cardiomyopathy in 356,222 men screened for the Multiple Risk Factor Intervention Trial. Am J Epidemiol 1994;139:166-172
Web of Science | Medline4
Coughlin SS ,Gottdiener JS ,Baughman KL . Black-white differences in mortality in idiopathic dilated cardiomyopathy: the Washington, DC, Dilated Cardiomyopathy Study. J Natl Med Assoc 1994;86:583-591
Web of Science | Medline
To the Editor:
Dec and Fuster omitted reference to the important clinical entity of reversible left ventricular dysfunction due to chronic tachycardia.1
The first series of patients with tachycardia-induced left ventricular dysfunction was described by Phillips and Levine.2 They concluded that “auricular fibrillation per se may produce cardiac dilation and progressive congestive heart failure . . . a truly reversible type of heart failure.” Subsequent series have demonstrated convincingly that atrial fibrillation with a rapid ventricular response may be the primary cause rather than the consequence of dilated cardiomyopathy. Furthermore, the left ventricular dysfunction may be completely reversible with control of the heart rate.3 The mechanisms of tachycardia-induced cardiomyopathy are uncertain, but theories include the depletion of phosphate energy stores, activation of the renin–angiotensin and sympathetic nervous systems, and myocardial ischemia.3,4
The above opinion expressed in this letter represents that of the author and not the Department of the Air Force.
4 ReferencesKenneth Mishark, M.D., Maj., M.C., U.S.A.F.
David Grant U.S. Air Force Medical Center, Travis Air Force Base, CA 945351
Packer DL ,Bardy GH ,Worley SJ , et al. Tachycardia-induced cardiomyopathy: a reversible form of left ventricular dysfunction. Am J Cardiol 1986;57:563-570
CrossRef | Web of Science | Medline2
Phillips E ,Levine SA . Auricular fibrillation without other evidence of heart disease: a cause of reversible heart failure. Am J Med 1949;7:478-489
CrossRef | Web of Science | Medline3
Grogan M ,Smith HC ,Gersh BJ ,Wood DL . Left ventricular dysfunction due to atrial fibrillation in patients initially believed to have idiopathic dilated cardiomyopathy. Am J Cardiol 1992;69:1570-1573
CrossRef | Web of Science | Medline4
Armstrong PW ,Stopps TP ,Ford SE ,de Bold AJ . Rapid ventricular pacing in the dog: pathophysiologic studies of heart failure. Circulation 1986;74:1075-1084
CrossRef | Web of Science | Medline
To the Editor:
In their review of dilated cardiomyopathy, Dec and Fuster discussed familial (or genetic) cases. Among the modes of inheritance they mentioned was “mitochondrial inheritance” in patients with multiple deletions in the mitochondrial genome. We think the use of this term to refer to such patients is inappropriate.1 It is a substitute for the term “cytoplasmic or maternal inheritance,” which is generally used to describe transmission by means of the mitochondrial genome. Though point mutations in the mitochondrial gene are, in general, maternally transmitted,2 diseases associated with deletions and insertions of mitochondrial DNA, such as those found in chronic progressive external ophthalmoplegia, are either sporadic in nature or, in cases with multiple deletions, a result of autosomal dominant inheritance.3 Since all the mitochondrial-DNA replication enzymes are encoded by the nucleus, proteins encoded by nuclear DNA are suspected of causing these abnormalities.
3 ReferencesMasato Odawara, M.D.
Kamejiro Yamashita, M.D.
University of Tsukuba, Tsukuba, Ibaraki, 305 Japan1
Suomalainen A ,Paetau A ,Leinonen H ,Majander A ,Peltonen L ,Somer H . Inherited idiopathic dilated cardiomyopathy with multiple deletions of mitochondrial DNA. Lancet 1992;340:1319-1320
CrossRef | Web of Science | Medline2
Kadowaki T ,Kadowaki H ,Mori Y , et al. A subtype of diabetes mellitus associated with a mutation of mitochondrial DNA. N Engl J Med 1994;330:962-968
Full Text | Web of Science | Medline3
Zeviani M ,Servidei S ,Gellera C ,Bertini E ,DiMauro S ,DiDonato S . An autosomal dominant disorder with multiple deletions of mitochondrial DNA starting at the D-loop region. Nature 1989;339:309-311
CrossRef | Web of Science | Medline
To the Editor:
In Table 1 of their article on idiopathic dilated cardiomyopathy, Dec and Fuster list the known causes of dilated cardiomyopathy. The table lists doxorubicin and bleomycin as the chemotherapeutic agents known to cause dilated cardiomyopathy. Although doxorubicin is a well-known cause of cardiomyopathy, bleomycin is not known to cause any clinical cardiac toxicity. The only known organ toxicity of bleomycin is pulmonary toxicity, resulting in lung fibrosis. Mitoxantrone (Novantrone) is another chemotherapeutic agent (which should have been listed instead) known to cause cardiomyopathy, although it is clearly less cardiotoxic than doxorubicin and rarely produces dilated cardiomyopathy when used alone.
Sewa S. Legha, M.D.
University of Texas M.D. Anderson Cancer Center, Houston, TX 77030Author/Editor Response
The authors reply:
To the Editor: Dr. Mishark has correctly pointed out that chronic rapid atrial fibrillation may occasionally result in a dilated cardiomyopathy that is reversible with adequate rate control. Our experience, as well as a review of the published literature,1 suggests that this is an extremely uncommon event.
Dr. Legha has correctly pointed out that bleomycin was erroneously included in Table 1 of our article. Cyclophosphamide and mitoxantrone should have been included as cardiotoxic agents.
Dr. Coughlin has made important contributions to our understanding of the racial differences in the incidence of idiopathic dilated cardiomyopathy. We agree with his observation that black patients have not only a greater likelihood of idiopathic dilated cardiomyopathy, but also a poorer survival than whites. It is our suspicion that these apparent differences in survival are explainable on the basis of more advanced disease at the time of presentation rather than an underlying biologic difference in response to therapy or the rate of disease progression.
Drs. Odawara and Yamashita have correctly stated that multiple deletions in mitochondrial DNA have been seen in both familial and sporadic cases of idiopathic dilated cardiomyopathy.2 Disease-specific point mutations have been reported in fatal infantile cardiomyopathy and maternally inherited myopathy–cardiomyopathy.3 Both maternal and autosomal patterns of inheritance have been suggested. Whether these mitochondrial abnormalities produce a dilated cardiomyopathy directly or are simply associated with other yet-to-be-defined mutations in nuclear DNA is uncertain.
More effective treatments are certainly needed for patients with idiopathic dilated cardiomyopathy and symptoms of advanced heart failure. We disagree with Dr. Cooke that beta-adrenergic blockers should no longer be considered investigational therapy. Her analysis of the Metoprolol in Dilated Cardiomyopathy trial is erroneous. This carefully designed trial failed to detect a survival benefit of metoprolol. The suggestion that metoprolol may have decreased the need for cardiac transplantation fails to recognize that the timing of transplantation is dictated by the availability of donor hearts and a patient's position on the waiting list rather than on the severity of disease. Doughty et al. have provided a recent detailed review of both the benefits and risks of this form of adjunctive therapy.4 Although we agree with Dr. Greenberg's assessment that the role of dynamic cardioplasty is expanding, we believe that his representation of the experience of Dr. Carpentier and colleagues with this technique5 is overly optimistic. Their report of a 70 percent rate of actuarial survival at seven years is misleading, since it excluded 23 percent of the patients who died in the early perioperative period. Current recommendations limit its use to patients with New York Heart Association class 3 heart failure rather than those with more advanced symptoms. It is well recognized that medical therapy for this degree of heart failure may often ameliorate symptoms and produce long-term survival rates that equal or exceed those of cardiomyoplasty. Although cardiomyoplasty is now available in Europe, the Food and Drug Administration has mandated that a prospective, randomized study be undertaken to determine its safety and efficacy.
5 ReferencesG.W. Dec, M.D.
Valentin Fuster, M.D.
Massachusetts General Hospital, Boston, MA 02114-26981
Grogan M ,Smith HC ,Gersh BJ ,Wood DL . Left ventricular dysfunction due to atrial fibrillation in patients initially believed to have idiopathic dilated cardiomyopathy. Am J Cardiol 1992;69:1570-1573
CrossRef | Web of Science | Medline2
Suomalainen A ,Paetau A ,Leinonen H ,Majander A ,Peltonen L ,Somer H . Inherited idiopathic dilated cardiomyopathy with multiple deletions of mitochondrial DNA. Lancet 1992;340:1319-1320
CrossRef | Web of Science | Medline3
Waagstein F ,Bristow MR ,Swedberg K , et al. Beneficial effects of metoprolol in idiopathic dilated cardiomyopathy. Lancet 1993;342:1441-1446
CrossRef | Web of Science | Medline4
Doughty RN ,MacMahon S ,Sharpe N . Beta-blockers in heart failure: promising or proved? J Am Coll Cardiol 1994;23:814-821
CrossRef | Web of Science | Medline5
Carpentier A ,Chachques JC ,Acar C , et al. Dynamic cardioplasty at seven years. J Thorac Cardiovasc Surg 1993;106:42-54
Web of Science | Medline
- Citing Articles (2)
Citing Articles
1
Cheuk-Kwan Sun, Li-Teh Chang, Jiunn-Jye Sheu, Chiang-Hua Chiang, Fan-Yen Lee, Chiung-Jen Wu, Sarah Chua, Morgan Fu, Hon-Kan Yip. (2009) Bone marrow–derived mononuclear cell therapy alleviates left ventricular remodeling and improves heart function in rat-dilated cardiomyopathy*. Critical Care Medicine 37:4, 1197-1205
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Aki Honda, Tamie Arai, Maki Akiyama, Eriko Masuda, Mizuka Kobayashi, Sumio Hoka. (2006) Anesthetic management of a patient with a history of Batista procedure for dilated cardiomyopathy undergoing gastric surgery. Journal of Anesthesia 20:3, 227-230
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