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The International Journal of Cardiovascular Imaging
 
Int J Cardiovasc Imaging. 2010 April; 26(4): 469–472.
Published online 2010 March 6. doi:  10.1007/s10554-010-9602-7
PMCID: PMC2852595

Left ventricular mass assessment by CMR; how to define the optimal index

Cardiac magnetic resonance imaging (CMR) is an accurate and reliable means of evaluating cardiac morphology, and therefore very well suited for identifying and characterizing patients with various manifestations of left ventricular hypertrophy (LVH) [1, 2]. For instance, CMR can resolve the question whether training-induced LVH in athletes is a physiological rather than a pathophysiological phenomenon [35]. A meta-analysis, involving 59 studies and 1451 athletes (both endurance-trained and strength-trained athletes), showed that the athlete’s heart demonstrated normal systolic and diastolic cardiac function, implying that training-induced LVH in athletes is predominantly a physiological phenomenon [610]. However, in pathophysiological LVH, such as in patients with hypertension and hypertrophic cardiomyopathy, the presence of LVH portends a poor prognosis whereby there is a negative relation between prognosis and the stage of LVH [1121]. On the other side of the spectrum, a significant decrease in LV mass, such as in patients following myocardial infarction, may also be associated with a poor prognosis as these patients are prone to the development of heart failure [2239].

Within the latest 10 years, research in LVH as cardiac target organ damage has uncovered its prognostic importance. Several studies have indicated that adequate pharmacological treatment, such as beta-blocking agents, ACE-inhibition, and angiotensin II receptor blockade, is very effective in reducing LVH [4047]. In addition, reduction of LV mass is associated with substantial and significant reduction of cardiovascular morbidity and mortality [46]. Hypertension is strongly associated with increased risk of subsequent heart failure, and meta-analysis data have suggested that reduction in blood pressure and LV mass is associated with very substantial reductions in incident heart failure [47, 48]. Consequently, LV mass should be accurately calculated as mass size may have important clinical implications [4953].

Generally, LV mass divided by body surface area (BSA) has been used clinically to account for body size, but its validity is not fully clear. Methods to index LV mass for body size have not been investigated using CMR. In the current issue of the International Journal of Cardiovascular Imaging, Brumback et al. [54] sought for new accurate indices of LV mass. The main purpose of the study was to develop allometric indices for LV mass measured by CMR and to compare estimates of the prevalence and predictive value of LVH defined new allometric indices. Two indices were derived from linear regression models fit to CMR data from the reference sample of the Multi-Ethnic Study of Atherosclerosis (MESA) participants. The indices are called allometric as they are proportional to LV mass divided by a body size variable raised to a scalar exponent. The authors evaluated 5,004 participants from the MESA trial with CMR measurements of LV mass without signs of clinical cardiovascular disease at baseline who were followed for a median of 4.1 years. The new indices and limits for hypertrophy (95th percentile) were finally derived from 822 normal-weight, normotensive, non-diabetic subjects. There were 107 events consisting of coronary heart disease or stroke. The estimated prevalence of LVH at baseline and hazard ratio for events associated with LVH were 8% and 2.4 with the new allometric height-weight index, 11% and 2.2 with LV mass/BSA, 23–24% and 2.0–2.1 with height indices, and 20% and 1.7 with un-indexed LV mass. A statistically significant difference was detected between the hazard ratios based on the new height-weight index and un-indexed LV mass. It was concluded that the prevalence of hypertrophy is higher for indices that do not account for weight. The predictive value of hypertrophy was significantly better with the new allometric height-weight index than with un-indexed LV mass and may be better than indices without weight.

The current study is clinically important since an evaluation of the most suitable indices for LV mass has not previously been performed using CMR. An indexed LV mass should be more predictive of a cardiovascular event than un-indexed LV mass. Therefore, the authors should be complimented for developing new allometric indices for CMR-derived LV mass with potential major implications in clinical practice.

Open Access

This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.

Footnotes

Editorial comment on the article of Brumback et al. (10.1007/s10554-010-9584-5).

References

1. Wall EE, Vliegen HW, Roos A, Bruschke AV. Magnetic resonance imaging in coronary artery disease. Circulation. 1995;92:2723–2739. [PubMed]
2. Germans T, Nijveldt R, Brouwer WP et al (2010) The role of cardiac magnetic resonance imaging in differentiating the underlying causes of left ventricular hypertrophy. Neth Heart J 18:135–143 [PMC free article] [PubMed]
3. Pluim BM, Lamb HJ, Kayser HW, Leujes F, et al. Functional and metabolic evaluation of the athlete’s heart by magnetic resonance imaging and dobutamine stress magnetic resonance spectroscopy. Circulation. 1998;97:666–672. [PubMed]
4. Pluim BM, Beyerbacht HP, Chin JC, et al. Comparison of echocardiography with magnetic resonance imaging in the assessment of the athlete’s heart. Eur Heart J. 1997;18:1505–1513. [PubMed]
5. Pluim BM, Chin JC, Roos A, et al. Cardiac anatomy, function and metabolism in elite cyclists assessed by magnetic resonance imaging and spectroscopy. Eur Heart J. 1996;17:1271–1278. [PubMed]
6. Hoogsteen J, Hoogeveen A, Schaffers H, Wijn PF, Wall EE. Left atrial and ventricular dimensions in highly trained cyclists. Int J Cardiovasc Imaging. 2003;19:211–217. doi: 10.1023/A:1023684430671. [PubMed] [Cross Ref]
7. Mihl C, Dassen WR, Kuipers H. Cardiac remodelling: concentric versus eccentric hypertrophy in strength and endurance athletes. Neth Heart J. 2008;16:129–133. [PMC free article] [PubMed]
8. Nassenstein K, Breuckmann F, Lehmann N, et al. Left ventricular volumes and mass in marathon runners and their association with cardiovascular risk factors. Int J Cardiovasc Imaging. 2009;25:71–79. doi: 10.1007/s10554-008-9337-x. [PubMed] [Cross Ref]
9. Bavelaar-Croon CD, Kayser HW, Wall EE, et al. Left ventricular function: correlation of quantitative gated SPECT and MR imaging over a wide range of values. Radiology. 2000;217:572–575. [PubMed]
10. Pluim BM, Zwinderman AH, Laarse A, Wall EE. The athlete’s heart: a meta-analysis of cardiac structure and function. Circulation. 2000;101:336–344. [PubMed]
11. Turakhia MP, Schiller NB, Whooley MA. Prognostic significance of increased left ventricular mass index to mortality and sudden death in patients with stable coronary heart disease (from the Heart and Soul Study) Am J Cardiol. 2008;102:1131–1135. doi: 10.1016/j.amjcard.2008.06.036. [PMC free article] [PubMed] [Cross Ref]
12. Meijs MF, Bots ML, Vonken EJ, et al. Rationale and design of the SMART Heart study: a prediction model for left ventricular hypertrophy in hypertension. Neth Heart J. 2007;15:295–298. [PMC free article] [PubMed]
13. Posma JL, Wall EE, Blanksma PK, Wall E, Lie KI. New diagnostic options in hypertrophic cardiomyopathy. Am Heart J. 1996;132:1031–1041. doi: 10.1016/S0002-8703(96)90018-6. [PubMed] [Cross Ref]
14. Vehmeijer JT, Christiaans I, Langen IM, et al. Risk stratification for sudden cardiac death in hypertrophic cardiomyopathy: Dutch cardiologists and the care of mutation carriers. Neth Heart J. 2009;17:464–469. [PMC free article] [PubMed]
15. Langerak SE, Vliegen HW, Roos A, et al. Detection of vein graft disease using high-resolution magnetic resonance angiography. Circulation. 2002;105:328–333. doi: 10.1161/hc0302.102598. [PubMed] [Cross Ref]
16. Rebergen SA, Ottenkamp J, Doornbos J, Wall EE, Chin JG, Roos A. Postoperative pulmonary flow dynamics after Fontan surgery: assessment with nuclear magnetic resonance velocity mapping. J Am Coll Cardiol. 1993;21:123–131. [PubMed]
17. Germans T, Wilde AA, Echteld CJ, Kamp O, Pinto YM, Rossum AC. Structural abnormalities of the left ventricle in hypertrophic cardiomyopathy mutation carriers detectable before the development of hypertrophy. Neth Heart J. 2007;15:161–163. [PMC free article] [PubMed]
18. Rijsingen IAW, Hermans-van Ast JF, Arens YH, et al. Hypertrophic cardiomyopathy family with double-heterozygous mutations; does disease severity suggest double heterozygosity? Neth Heart J. 2009;17:458–463. [PMC free article] [PubMed]
19. Michels M, Hoedemaekers YM, Kofflard MJ, et al. Familial screening and genetic counselling in hypertrophic cardiomyopathy: the Rotterdam experience. Neth Heart J. 2007;15:184–190. [PMC free article] [PubMed]
20. Ten Cate FJ. Cardiomyopathies: a revolution in molecular medicine and cardiac imaging. Neth Heart J. 2009;17:456–457. [PMC free article] [PubMed]
21. Olimulder MA, Es J, Galjee MA. The importance of cardiac MRI as a diagnostic tool in viral myocarditis-induced cardiomyopathy. Neth Heart J. 2009;17:481–486. [PMC free article] [PubMed]
22. Dijkman PR, Wall EE, Roos A, et al. Acute, subacute, and chronic myocardial infarction: quantitative analysis of gadolinium-enhanced MR images. Radiology. 1991;180:147–151. [PubMed]
23. Roos A, Matheijssen NA, Doornbos J, Dijkman PR, Voorthuisen AE, Wall EE. Myocardial infarct size after reperfusion therapy: assessment with Gd-DTPA-enhanced MR imaging. Radiology. 1990;176:517–521. [PubMed]
24. Roos A, Matheijssen NA, Doornbos J, Dijkman PR, Rugge PR, Wall EE. Myocardial infarct sizing and assessment of reperfusion by magnetic resonance imaging: a review. Int J Card Imaging. 1991;7:133–138. doi: 10.1007/BF01798054. [PubMed] [Cross Ref]
25. Rugge FP, Wall EE, Dijkman PR, Louwerenburg HW, Roos A, Bruschke AV. Usefulness of ultrafast magnetic resonance imaging in healed myocardial infarction. Am J Cardiol. 1992;70:1233–1237. doi: 10.1016/0002-9149(92)90754-M. [PubMed] [Cross Ref]
26. Holman ER, Jonbergen HP, Dijkman PR, Laarse A, Roos A, Wall EE. Comparison of magnetic resonance imaging studies with enzymatic indexes of myocardial necrosis for quantification of myocardial infarct size. Am J Cardiol. 1993;71:1036–1040. doi: 10.1016/0002-9149(93)90569-X. [PubMed] [Cross Ref]
27. Wall EE, Bax JJ. Late contrast enhancement by CMR: more than scar? Int J Cardiovasc Imaging. 2008;24:609–611. doi: 10.1007/s10554-008-9312-6. [PMC free article] [PubMed] [Cross Ref]
28. Vliegen HW, Doornbos J, Roos A, Jukema JW, Bekedam MA, Wall EE. Value of fast gradient echo magnetic resonance angiography as an adjunct to coronary arteriography in detecting and confirming the course of clinically significant coronary artery anomalies. Am J Cardiol. 1997;79:773–776. doi: 10.1016/S0002-9149(96)00866-1. [PubMed] [Cross Ref]
29. Hoogendoorn LI, Pattynama PM, Buis B, Geest RJ, Wall EE, Roos A. Noninvasive evaluation of aortocoronary bypass grafts with magnetic resonance flow mapping. Am J Cardiol. 1995;75:845–848. doi: 10.1016/S0002-9149(99)80429-9. [PubMed] [Cross Ref]
30. Wall EE, Dijkman PR, Roos A, et al. Diagnostic significance of gadolinium-DTPA (diethylenetriamine penta-acetic acid) enhanced magnetic resonance imaging in thrombolytic treatment for acute myocardial infarction: its potential in assessing reperfusion. Br Heart J. 1990;63:12–17. doi: 10.1136/hrt.63.1.12. [PMC free article] [PubMed] [Cross Ref]
31. Rugge FP, Boreel JJ, Wall EE, et al. Cardiac first-pass and myocardial perfusion in normal subjects assessed by sub-second Gd-DTPA enhanced MR imaging. J Comput Assist Tomogr. 1991;15:959–965. [PubMed]
32. Nijveldt R, Beek AM, Hirsch A, et al. ‘No-reflow’ after acute myocardial infarction: direct visualisation of microvascular obstruction by gadolinium-enhanced CMR. Neth Heart J. 2008;16:179–181. [PMC free article] [PubMed]
33. Wall EE, Heidendal GA, Hollander W, Westera G, Roos JP. I-123 labeled hexadecenoic acid in comparison with thallium-201 for myocardial imaging in coronary heart disease. A preliminary study. Eur J Nucl Med. 1980;5:401–405. doi: 10.1007/BF00261781. [PubMed] [Cross Ref]
34. Bavelaar-Croon CD, Pauwels EK, Wall EE. Gated single-photon emission computed tomographic myocardial imaging: a new tool in clinical cardiology. Am Heart J. 2001;141:383–390. doi: 10.1067/mhj.2001.112780. [PubMed] [Cross Ref]
35. Chamuleau SA, Eck-Smit BL, Meuwissen M, et al. Long-term prognostic value of CFVR and FFR versus perfusion scintigraphy in patients with multivessel disease. Neth Heart J. 2007;15:369–374. [PMC free article] [PubMed]
36. Tulevski II, Hirsch A, Sanson BJ, et al. Increased brain natriuretic peptide as a marker for right ventricular dysfunction in acute pulmonary embolism. Thromb Haemost. 2001;86:1193–1196. [PubMed]
37. Wall EE, Hollander W, Heidendal GA, Westera G, Majid PA, Roos JP. Dynamic myocardial scintigraphy with 123I-labeled free fatty acids in patients with myocardial infarction. Eur J Nucl Med. 1981;6:383–389. [PubMed]
38. Hoeven BL, Pires NM, Warda HM, et al. Drug-eluting stents: results, promises and problems. Int J Cardiol. 2005;99:9–17. doi: 10.1016/j.ijcard.2004.01.021. [PubMed] [Cross Ref]
39. Bax JJ, Lamb H, Dibbets P, et al. Comparison of gated single-photon emission computed tomography with magnetic resonance imaging for evaluation of left ventricular function in ischemic cardiomyopathy. Am J Cardiol. 2000;86:1299–1305. doi: 10.1016/S0002-9149(00)01231-5. [PubMed] [Cross Ref]
40. Braun S, Wall EE, Emanuelsson S, Kobrin I. Effects of a new calcium antagonist, mibefradil (Ro 40–5967), on silent ischemia in patients with stable chronic angina pectoris: a multicenter placebo-controlled study. The mibefradil international study group. J Am Coll Cardiol. 1996;27:317–322. doi: 10.1016/0735-1097(95)00472-6. [PubMed] [Cross Ref]
41. Portegies MC, Schmitt R, Kraaij CJ, et al. Lack of negative inotropic effects of the new calcium antagonist Ro 40–5967 in patients with stable angina pectoris. J Cardiovasc Pharmacol. 1991;18:746–751. doi: 10.1097/00005344-199111000-00013. [PubMed] [Cross Ref]
42. Nooijer R, Verkleij CJ, der Thüsen JH, et al. Lesional overexpression of matrix metalloproteinase-9 promotes intraplaque hemorrhage in advanced lesions but not at earlier stages of atherogenesis. Arterioscler Thromb Vasc Biol. 2006;26:340–346. doi: 10.1161/01.ATV.0000197795.56960.64. [PubMed] [Cross Ref]
43. Laarse A, Kerkhof PL, Vermeer F, et al. Relation between infarct size and left ventricular performance assessed in patients with first acute myocardial infarction randomized to intracoronary thrombolytic therapy or to conventional treatment. Am J Cardiol. 1988;61:1–7. doi: 10.1016/0002-9149(88)91294-5. [PubMed] [Cross Ref]
44. Bakx AL, Wall EE, Braun S, Emanuelsson H, Bruschke AV, Kobrin I. Effects of the new calcium antagonist mibefradil (Ro 40–5967) on exercise duration in patients with chronic stable angina pectoris: a multicenter, placebo-controlled study. Ro 40–5967 International Study Group. Am Heart J. 1995;130:748–757. doi: 10.1016/0002-8703(95)90073-X. [PubMed] [Cross Ref]
45. Smilde TD, Zuurman MW, Hillege HL, et al. Renal function dependent association of AGTR1 polymorphism (A1166C) and electrocardiographic left-ventricular hypertrophy. Am J Hypertens. 2007;20:1097–1103. doi: 10.1016/j.amjhyper.2007.04.023. [PubMed] [Cross Ref]
46. Cowan BR, Young AA. Left ventricular hypertrophy and renin-angiotensin system blockade. Curr Hypertens Rep. 2009;11:167–172. doi: 10.1007/s11906-009-0030-9. [PubMed] [Cross Ref]
47. Baur LH, Schipperheyn JJ, Wall EE, et al. Beneficial effect of enalapril on left ventricular remodelling in patients with a severe residual stenosis after acute anterior wall infarction. Eur Heart J. 1997;18:1313–1321. [PubMed]
48. Fagard RH, Celis H, Thijs L, Wouters S. Regression of left ventricular mass by antihypertensive treatment: a meta-analysis of randomized comparative studies. Hypertension. 2009;54:1084–1091. doi: 10.1161/HYPERTENSIONAHA.109.136655. [PubMed] [Cross Ref]
49. Westenberg JJ, Braun J, Veire NR, et al. Magnetic resonance imaging assessment of reverse left ventricular remodeling late after restrictive mitral annuloplasty in early stages of dilated cardiomyopathy. J Thorac Cardiovasc Surg. 2008;135:1247–1252. doi: 10.1016/j.jtcvs.2007.10.021. [PubMed] [Cross Ref]
50. Baur LH, Schipperheyn JJ, Velde EA, et al. Reproducibility of left ventricular size, shape and mass with echocardiography, magnetic resonance imaging and radionuclide angiography in patients with anterior wall infarction. A plea for core laboratories. Int J Card Imaging. 1996;12:233–240. doi: 10.1007/BF01797736. [PubMed] [Cross Ref]
51. Geest RJ, Roos A, Wall EE, Reiber JH. Quantitative analysis of cardiovascular MR images. Int J Card Imaging. 1997;13:247–258. doi: 10.1023/A:1005869509149. [PubMed] [Cross Ref]
52. Marcus JT, DeWaal LK, Götte MJ, Geest RJ, Heethaar RM, Rossum AC. MRI-derived left ventricular function parameters and mass in healthy young adults: relation with gender and body size. Int J Card Imaging. 1999;15:411–419. doi: 10.1023/A:1006268405585. [PubMed] [Cross Ref]
53. Holman ER, Buller VG, Roos A, et al. Detection and quantification of dysfunctional myocardium by magnetic resonance imaging. A new three-dimensional method for quantitative wall-thickening analysis. Circulation. 1997;95:924–931. [PubMed]
54. Brumback LC, Kronmal R, Heckbert SR et al (2010) Body size adjustments for left ventricular mass by cardiovascular magnetic resonance and their impact on left ventricular hypertrophic classification. Int J Cardiovasc Imaging. doi:10.1007/s10554-010-9584-5 [PMC free article] [PubMed]

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