Clinical Investigations
Prognostic implications of an initial loss of cardiac metaiodobenzylguanidine uptake and diabetes mellitus in patients with left ventricular dysfunction*,**

https://doi.org/10.1054/jcaf.2003.14Get rights and content

Abstract

Background: Although altered cardiac sympathetic innervation is related to fatal outcome, the mechanisms and prognostic value of an initial cardiac metaiodobenzylguanidine (MIBG) defect are not known. Methods and Results: After quantitative cardiac MIBG imaging, 205 patients with left ventricular ejection fraction <50% were prospectively followed up with a primary end-point of cardiac death for 35 months. In regard to 38 cardiac deaths, consisting of 25 pump failure deaths, 11 sudden deaths, and 2 fatal acute myocardial infarctions, multivariate analysis identified diabetes mellitus as a significant independent predictor as well as reduced cardiac MIBG activity, use of nitrate, and New York Heart Association functional status. Independent of washout kinetics and cardiac function, patients with profound loss of initial MIBG uptake and those with late-phase MIBG activity of 1.74 or less had significantly greater mortality rates than did their counterparts. Initial cardiac MIBG activity closely correlated inversely with annual cardiac death rate. Conclusions: An initial cardiac MIBG defect and presence of diabetes mellitus indicate a low probability of long-term survival. The profound loss of initial MIBG activity is likely to be due to structural deficit of sympathetic neurons themselves, rather than accelerated sympathetic function, suggesting that denervation is one of mechanisms of cardiac sympathetic dysfunction leading to lethal clinical outcomes.

Section snippets

Patient selection

A total of 205 eligible patients who had been registered at 4 medical centers in Sapporo between 1996 and 1998 and who met the following inclusion criteria were enrolled in this study: (1) a left ventricular ejection fraction (LVEF) assessed by radionuclide ventriculography of less than 50%, (2) cardiac MIBG imaging having been performed within one week after cardiac function tests; (3) the final diagnosis of underlying cardiac dysfunction having been established by standard clinical

Clinical outcomes during follow-up

Thirty-eight (18.5%) of the patients had lethal cardiac events. The events were due to pump failure in 25 patients, to sudden cardiac death in 11 patients, and to fatal acute myocardial infarction in 2 patients. Eleven (5.3%) of the patients died from noncardiac causes; stroke in 2 patients, lung disease in 4 patients, malignancy in 2 patients, complication after noncardiac surgery in 2 patients, and rupture of aortic aneurysm in 1 patient. No patients underwent coronary intervention,

Discussion

The present results supported the hypothesis that a profound initial loss of cardiac MIBG uptake indicates a great probability of fatal outcomes; the annual mortality rate was 9.5% per year. Nevertheless, overall prognosis was most closely related to late cardiac MIBG activity (H/M ratio) independent of cardiac function, MIBG washout kinetics, and other variables. Therefore, although impaired cardiac MIBG activity at a late phase is most likely to reflect integrated abnormality of sympathetic

Conclusions

An initial deficit of cardiac MIBG uptake at an early postinjection stage indicates a high probability of cardiac death in patients with left ventricular dysfunction and diabetes mellitus. The profound loss of initial MIBG activity is likely to be due to a structural deficit of sympathetic neurons themselves, probably including diabetic cardiac neuropathy, rather than accelerated sympathetic function. Overall cardiac sympathetic nerve dysfunction can be an eventual independent predictor of poor

Acknowledgements

The authors thank all staff of the Cardiology Department and Division of Nuclear Medicine, Sapporo Medical University School of Medicine, Sapporo Jun-kanki Clinic, Hokkaido Cardiovascular Hospital, and Sapporo Social Insurance General Hospital, for their cooperation in clinical services.

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    *

    Reprint requests: Tomoaki Nakata, MD, PhD, Second Department of Internal Medicine (Cardiovascular Medicine), Sapporo Medical University School of Medicine, S-1, W-16, Chuo-ku, Sapporo 060-0061, Japan.

    **

    1071-9164/03/0902-0007$30.00/0

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