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Diabetes Care 24:2019-2020, 2001
© 2001 by the American Diabetes Association, Inc.

Letters: Comments and Responses
Letter

Brain Natriuretic Peptide as a Potential Marker of Diastolic Dysfunction in Type 2 Diabetes

N. Norman Chan, MRCP, DCH and Steven J. Hurel, PHD, MRCP

Department of Diabetes, Endocrinology and Metabolism, University College London Hospitals, London, U.K.

In the January issue of Diabetes Care, Poirier et al. (1) reported on the prevalence of left ventricular diastolic dysfunction (LVDD), as determined by echocardiography in 46 middle-aged men with well-controlled type 2 diabetes. Remarkably, they found a prevalence of LVDD as high as 60%. Although this needs to be replicated with studies of much larger sample sizes, they nevertheless illustrated the importance of identifying pseudonormal patterns of ventricular filling, which have been underestimated by previous studies using Doppler assessment of transmitral flow velocity, to help diagnose early or subclinical LVDD (1). As elucidated by the excellent editorial of Gustafsson and Hildebrandt (2), the prognostic implication and possibility for intervention remain unknown and warrant further studies before early echographic screening in diabetic patients can be justified. We speculate that a potential marker of diastolic dysfunction in diabetic cardiomyopathy may help in the selection of high-risk diabetic patients for early cardiological assessment.

The natriuretic peptide family (including atrial, brain, and type C natriuertic peptide) plays a key role in the homeostasis of intravascular fluid balance and in the maintenance of cardiovascular hemodynamics (3). Originally isolated from porcine brain tissue (4), brain natriuretic peptide (BNP) is a vasodilator produced by cardiac myocytes in the ventricles and is degraded by neural endopeptidase. Along with atrial natriuretic peptide (ANP), BNP has effects on natriuresis, diuresis, and inhibition of the renin-angiotensin-aldosterone system, all of which contribute to the modulation and control of cardiovascular hemodynamics (5). There is growing evidence that BNP may be a marker of advanced heart failure (5,6). More importantly, it may also be a marker of early heart failure as manifested by isolated diastolic dysfunction (7) or diastolic dysfunction in association with hypertension (8). The underlying pathophysiology for elevated BNP levels in diastolic heart failure is not fully understood. However, it is likely that BNP production is increased as a compensatory response to diminish preload (vasodilatation) and postload (natriuresis and diuresis), thereby improving cardiac contractility. This is supported by the observation that infusion of BNP in patients with diastolic dysfunction improves hemodynamic response in isolated diastolic heart failure (9).

Although elevation of BNP in cardiac failure is not specific to disease states, BNP may be a useful tool in diabetic patients with microalbuminuria. This is supported by the study of Poirier et al. (1), in which there was a greater incidence of microalbuminuric patients in the group with abnormal ventricular relaxation pattern (15 of 28 [54%]) compared with the group with normal diastolic function (6 of 18 [33%]) (1). Furthermore, it has recently been shown by Yano et al. (10) that BNP is elevated in type 2 diabetic patients with microalbuminuria compared with those with normoalbuminuria. In their study, all microalbuminuric patients were normotensive, suggesting that any potential elevation of blood pressure commonly associated with microalbuminuria may have been compensated by the increased BNP level through its action on natriuresis and vasodilatation. Hence, it is at least physiologically plausible that increased circulating BNP concentrations in the presence of microalbuminuria may be a useful marker for early diastolic dysfunction in diabetic patients. Unlike ANP levels, which can be increased by acute hyperglycemia, circulating BNP concentrations have been shown to be unaffected by an elevated glucose level (11), making it more suitable for screening in diabetic patients. Further research will be required to determine the potential value of BNP in selecting microalbuminuric diabetic patients for further cardiological assessment.

Footnotes

Address correspondence to Dr. Steven J. Hurel, Department of Diabetes, Endocrinology and Metabolism, South House, The Middlesex Hospital, Mortimer St., London W1N 8AA, U.K. E-mail: steven.hurel{at}uclh.org.

References

  1. Poirier P, Bogaty P, Garneau C, Marois L, Dumesnil J-G: Diastolic dysfunction in normotensive men with well-controlled type 2 diabetes: importance of maneuvers in echocardiographic screening for preclinical diabetic cardiomyopathy. Diabetes Care 24:5–10, 2001[Abstract/Free Full Text]
  2. Gustafsson I, Hildebrandt P: Early failure of the diabetic heart (Editorial). Diabetes Care 24:3–4, 2001[Free Full Text]
  3. Levin ER, Gardner DG, Samaon WK: Natriuretic peptides. N Engl J Med 339:321–328, 1998[Free Full Text]
  4. Sudoh T, Kangawa K, Minamino N, Matsuo H: A new natriuretic peptide in the porcine brain. Nature 332:78–81, 1988[Medline]
  5. Cheung BMY, Kumana CR: Natriuretic peptides: relevance in cardiovascular disease. JAMA 280:1983–1984, 1998[Free Full Text]
  6. McDonagh TA, Robb SD, Murdoch DR, Morton JJ, Ford I, Morrison CE, Tunstall-Pedoe H, McMurray JJ, Dargie HJ: Biochemical detection of left-ventricular systolic dysfunction. Lancet 351:9–13, 1998[Medline]
  7. Lang CC, Prasad N, McAlpine HM, Macleod C, Lipworth BJ, MacDonald TM, Struthers AD: Increased plasma levels of brain natriuretic peptide in patients with isolated diastolic dysfunction. Am Heart J 127:1635–1636, 1994[Medline]
  8. Cheung BMY: Plasma concentration of brain natriuretic peptide is related to diastolic function in hypertension. Clin Exp Pharmacol Physiol 24:966–968, 1997[Medline]
  9. Marcus LS, Hart D, Packer M, Yushak M, Medina N, Danziger RS, Heitjan DF, Katz SD: Hemodynamic and renal excretory effects of human brain natriuretic peptide infusion in patients with congestive heart failure: a double-blind, placebo-controlled, randomized crossover trial. Circulation 94:3184–3189, 1996[Abstract/Free Full Text]
  10. Yano Y, Katsuki A, Gabazza EC, Ito K, Fujii M, Furuta M, Tuchihashi K, Goto H, Nakatani K, Hori Y, Sumida Y, Adachi Y: Plasma brain natriuretic peptide levels in normotensive noninsulin-dependent diabetic patients with microalbuminuria. J Clin Endocrinol Metab 84:2353–2356, 1999[Abstract/Free Full Text]
  11. McKenna K, Smith D, Tormey W, Thompson CJ: Acute hyperglycaemia causes elevation in plasma atrial natriuretic peptide concentrations in type 1 diabetes mellitus. Diabet Med 17:512–517, 2000 [Medline]

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