ANP but not BNP Reflects Early Left Diastolic Dysfunction in Type 1 Diabetics with Myocardial Dysinnervation

M. Bayerle-Eder; M. Zangeneh; G. Kreiner; W. Raffesberg; P. Nowotny; H. Vierhapper; W. Waldhäusl; M. Wolzt; H. Pleiner; S. Gasic

doi:10.1055/s-2003-41306

Hormone and Metabolic Research, Table of Contents

Horm Metab Res 2003; 35(5): 301-307
DOI: 10.1055/s-2003-41306

Original Clinical

ANP but not BNP Reflects Early Left Diastolic Dysfunction in Type 1 Diabetics with Myocardial Dysinnervation

M. Bayerle-Eder ¹ , M. Zangeneh ² , G. Kreiner ² , W. Raffesberg ¹ , P. Nowotny ¹ , H. Vierhapper ¹ , W. Waldhäusl ¹ , M. Wolzt ³ , H. Pleiner ³ , S. Gasic ¹

¹ Department of Internal Medicine III, Division of Endocrinology and Metabolism
² Department of Internal Medicine II, Division of Cardiology
³ Department of Clinical Pharmacology, University Hospital Vienna, Austria

Abstract

Objective: We investigated whether plasma concentrations of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) reflect impaired diastolic relaxation or its improvement after ACE inhibition.

Methods: 7 long-term Type 1 diabetic patients with normal systolic but impaired diastolic function and with sympathetic myocardial dysinnervation and 10 controls were included. Exercise tolerance and maximal O₂ uptake were evaluated by bicycle exercise prior to the study. ANP, BNP and norepinephrine/epinephrine (NE/E) were determined at baseline and at 80 % V˙O₂max workload and after recovery, before and following 12 weeks of treatment with fosinopril (10 mg/d).

Results: Isovolumetric relaxation time (IVRT) and A/E wave ratio were increased by 26.7 ± 11.5 % and 54.4 ± 26.1 % in diabetic patients as compared to controls, respectively (p < 0.02). After 12 weeks of fosinopril treatment, no differences in IVRT or A/E wave ratio were detectable between groups. ANP was enhanced in Type 1 diabetes as compared to controls (baseline: 9.2 ± 3.0 vs. 4.5 ± 1.1; exercise: 22.4 ± 7.7 vs. 7.9 ± 1.2; recovery: 20.3. ± 4.6 vs. 9.5 ± 2.0 fmol/ml, p < 0.02). Fosinopril treatment abolished any differences between groups. BNP plasma levels did not differ between groups and no exercise dependent changes were observed. NE- and E-increase was greater at 80 % V˙O₂max work load in Type 1 diabetes than in controls (p < 0.05). Again, fosinopril abolished differences between groups.

Conclusion: In Type 1 diabetes, impaired diastolic function is associated with elevated ANP and catecholamine plasma levels that are normalized after ACE inhibition. Thus, ANP but not BNP appears to be a sensitive biochemical marker for early diastolic dysfunction in Type 1 diabetes.

Key words

ACE-Inhibition - Biochemical Marker - Sympathetic

Full Text

References

1 Monteagudo P T, Moises V A, Kohlmann O Jr , Ribeiro A B, Lima V C, Zanella M T. Influence of autonomic neuropathy upon left ventricular dysfunction in insulin-dependent diabetic patients. Clin Cardiol. 2000; 23 371-375
2 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. 2001; 24 5-10
3 Schannwell C M, Schoebel F C, Heggen S, Marx R, Perings C, Leschke M, Strauer B E. Early decrease in diastolic function in young type I diabetic patients as an initial manifestation of diabetic cardiomyopathy. Z Kardiol. 1999; 88 338-346
4 Dietz R, Haass M, Kubler W. Atrial natriuretic factor. Its possible role in hypertension and congestive heart failure. Am J Hypertens. 1989; 2 29-33
5 Yano Y, Katsuki A, Gabazza E C, Ito K, Fuji 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. 1999; 84 2353-2356
6 Lang C C, Prasad N, McAlpine H M, Macleod C, Lipworth B J, MacDonald T M, Struthers A D. Increased plasma levels of brain natriuretic peptide in patients with isolated diastolic dysfunction. Am Heart J. 1994; 127 1635-1636
7 Nakao K. Natriuretic peptide family. Nippon Naibunpi Gakkai Zasshi. 1992; 68 134-142
8 Yamamoto K, Burnett J C Jr , Jougasaki M, Nishimura R A, Bailey K R, Saito Y, Nakao K, Redfield M M. Superiority of brain natriuretic peptide as a hormonal marker of ventricular systolic and diastolic dysfunction and ventricular hypertrophy. Hypertension. 1997; 30 305-306
9 La Villa G, Lazzeri C, Fronzaroli C, Franchi F, Gentilini P. Brain natriuretic peptide. Ann Ital Med Int. 1995; 10 233-241
10 Raev D C. Which left ventricular function is impaired earlier in the evolution of diabetic cardiomyopathy? An echocardiographic study of young type 1 diabetic patients. Diabetes Care. 1994; 17 633-639
11 Petersen J R, Drabaek H, Gleerup G, Mehlsen J, Petersen L J, Winther K. ACE inhibition with spirapril improves diastolic function at rest independent of vasodilation during treatment with spirapril in mild to moderate hypertension. Angiology. 1996; 47 233-240
12 Willenheimer R, Rydberg E, Oberg L, Juul-Moller S, Erhardt L. ACE inhibition with ramipril improves left ventricular function at rest and post exercise in patients with stable ischaemic heart disease and preserved left ventricular systolic function. Eur Heart J. 1999; 20 1647-1656
13 Kreiner G, Wolzt M, Fasching P, Leitha T, Edlmayer A, Korn A, Waldhäusl W, Dudczak R. Myocardial m-[123I]iodobenzylguanidine scintigraphy for the assessment of adrenergic cardiac innervation in patients with IDDM. Comparison with cardiovascular reflex tests and relationship to left ventricular function. Diabetes. 1995; 44 543-591
14 Kjeldsen S E, Erdine S, Farsang C, Sleight P, Mancia G. 1999 WHO/IHS Hypertension Guidelines - highlights and EHS update. J Hypertens. 2002; 20 153-155
15 Paillole C, Dahan M, Paycha F, Solal A C, Passa P, Gourgon R. Prevalence and significance of left ventricular filling abnormalities determined by Doppler echocardiography in young type I (insulin-dependent) diabetic patients. Am J Cardiol. 1989; 64 1010-1016
16 Vierhapper H, Nowotny P, Waldhäusl W. Effect of human atrial natriuretic peptide on 1-deamino-D-Arg-vasopressin-induced antidiuresis in man. Clin Endocrinol Metab. 1988; 66 124-127
17 Muders F, Kromer E P, Griese D P, Pfeifer M, Hense H W, Riegger G A, Eisner D. Evaluation of plasma natriuretic peptides as markers for left ventricular dysfunction. Am Heart J. 1997; 134 442-449
18 Musso N R, Vergassola C, Pende A. Reversed-phase HPLC separation of plasma norepinephrine, epinephrine and dopamine with three-electrode coulometric detection. Clin Chem. 1989; 35 1975-1977
19 Willenheimer R B, Erhardt L R, Nilsson H, Lilja B, Juul-Moller S, Sundkvist G. Parasympathetic neuropathy associated with left ventricular diastolic dysfunction in patients with insulin-dependent diabetes mellitus. Scand Cardiovasc J. 1998; 32 17-22
20 Sanchez-Barriga J J, Rangel A, Castaneda R, Flores D, Frati A C, Ramos M A, Amato D. Left ventricular diastolic dysfunction secondary to hyperglycemia in patients with type II diabetes. Arch Med Res. 2001; 32 44-47
21 Lerman A, Gibbons R J, Rodeheffer R J, Bailey K R, McKinley L J, Heublein D M, Burnett J C Jr . Circulating N-terminal atrial natriuretic peptide as a marker for symptomless left-ventricular dysfunction. Lancet. 1993; 341 1105-1109
22 Ferri C, Piccoli A, Laurenti O, Bellini C, de Mattia G, Santucci A, Balsano F. Atrial natriuretic factor in hypertensive and normotensive diabetic patients. Diabetes Care. 1994; 17 195-200
23 Yamada J, Tanaka S, Sato T, Suzuki R, Fujii S. The medical evaluation of patients with diabetes mellitus in exercise therapy. J Nutr Sci Vitaminol. 1991; 37 17-24
24 McKenna K, Smith D, Tormey W, Thompson C J. Acute hyperglycaemia causes elevation in plasma atrial natriuretic peptide concentrations in Type 1 diabetes mellitus. Diabet Med. 2000; 17 512-517
25 Opocher G, Mantero F, Rocco S, Trevisan R, Fioretto P, Semplicini A, Morocutti A, Zanette G, Donadon V, Perico N. Atrial natriuretic factor in hypertensive and normotensive insulin-dependent diabetics. J Hypertens. 1989; 7 (6) S 236-S 237
26 Isotani H, Fukumoto Y. Reversibility of autonomic nerve function in relation to rapid improvement of glycaemic control. Hormon Metab Res. 2000; 32 115-117
27 Onuoha G N, Nicholls D P, Patterson A, Beringer T. Neuropeptide secretion in exercise. Neuropeptides. 1998; 32 319-325
28 Ishikawa S, Miyauchi T, Ueno M, Sagawa K, Sakai S, Ushinohama H, Kado H, Sunagawa H, Goto K, Sugishita Y, Honda S. Abnormal neurohumoral responses to exercise in patients with heart disease: inhibition of an increase in endothelin-1 production during exercise. J Cardiovasc Pharmacol. 1998; 31 (1) S 406-S 411
29 Nicholson S, Richards M, Espiner E, Nicholls G, Yandle T. Atrial and brain natriuretic peptide response to exercise in patients with ischaemic heart disease. Clin Exp Pharmacol Physiol. 1993; 20 535-540
30 Wambach G, Koch J. BNP plasma levels during acute volume expansion and chronic sodium loading in normal men. Clin Exp Hypertens. 1995; 17 619-629
31 Waku S, Iida N, Ishihara T. Significance of brain natriuretic peptide measurement as a diagnostic indicator of cardiac function. Methods Inf Med. 2000; 39 249-253
32 Isotani H, Kameoka K, Sasaki I, Hida H, Kakutani S, Tasaki T. Plasma brain natriuretic peptide levels in normotensive type 2 diabetic patients without cardiac disease. Diabetes Care. 2000; 23 859-860
33 Kawai K, Hata K, Takaoka H, Kawai H, Yokoyama M. Plasma brain natriuretic peptide as a novel therapeutic indicator in idiopathic dilated cardiomyopathy during beta-blocker therapy: a potential of hormone-guided treatment. Am Heart J. 2001; 141 925-932
34 Inoue M, Kanda T, Arai M, Suga T, Suzuki T, Kobayashi I, Nagai R. Impaired expression of brain natriuretic peptide gene in diabetic rats with myocardial infarction. Exp Clin Endocrinol Diabetes. 1998; 106 484-488
35 Bates E R, Shenker Y, Grekin R J. The relationship between plasma levels of immunoreactive atrial natriuretic hormone and hemodynamic function in man. Circulation. 1986; 73 1155-1161
36 Raine A E, Erne P, Burgisser E, Muller F B, Bolli P, Burkart F, Buhler F R. Atrial natriuretic peptide and atrial pressure in patients with congestive heart failure. N Engl J Med. 1986; 28 533-537
37 Yoshimura M, Yasue H, Okumura K, Ogawa H, Jougasaki M, Mukoyama M, Nakao K, Imura H. Different secretion patterns of atrial natriuretic peptide and brain natriuretic peptide in patients with congestive heart failure. Circulation. 1993; 87 464-469
38 Taddei S, Virdis A, Mattel P, Favilla S, Salvetti A. Angiotensin II and sympathetic activity in sodium-restricted essential hypertension. Hypertension. 1995; 25 595-601
39 Seidelin P H, Coutie W J, Pai M S, Morton J J, Struthers A D. The interaction between noradrenaline and angiotensin II in man: evidence for a postsynaptic and against a presynaptic interaction. J Hypertens. 1987; 5 (5) S 121-S 124
40 Hoogenberg K, Navis G, Dullaart R P. Norepinephrine-induced blood pressure rise and renal vasoconstriction are not attenuated by enalapril treatment in microalbuminuric type 1 diabetes. Nephrol Dial Transplant. 1998; 13 640-645
41 Lee C C, Sidani M A, Hogikyan R V, Supiano M A. The effects of ramipril on sympathetic nervous system function in older patients with hypertension. Clin Pharmacol Ther. 1999; 65 420-427
42 Maruyama R, Hatta E, Yasuda K, Smith N C, Levi R. Angiotensin-converting enzyme-independent angiotensin formation in a human model of myocardial ischemia: modulation of norepinephrine release by angiotensin type 1 and angiotensin type 2 receptors. J Pharmacol Exp Ther. 2000; 294 248-254
43 Willenbrock R, Ozcelik C, Osterziel K J, Dietz R. Angiotensin-converting enzyme inhibition, autonomic activity, and hemodynamics in patients with heart failure who perform isometric exercise. Am Heart J. 1996; 131 999-1006

S. Gasic, M. D.

Division of Endocrinology and Metabolism · Department of Internal Medicine III ·

Währinger Gürtel 18-20 · 1090 Vienna · Austria

Phone: +43 (1) 40400-4310

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Email: Michaela.Bayerle-Eder@akh-wien.ac.at