Primary Dysautonomies – ABC CARDIOL

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Original Article

Sympathetic Dysautonomia in Heart Failure by 123I-MIBG: comparison between Chagasic, non-Chagasic and heart transplant patients

Viviane Santuari Parisotto Marino et al. Sandra Monetti Dumont Luciene das Graças Mota Daniela de Souza Braga … Stephanie Saliba de Freitas Maria da Consolação Vieira Moreira

Abstract

Background:

Heart failure (HF) is a severe public health problem because of its high morbidity and mortality and elevated costs, thus requiring better understanding of its course. In its complex and multifactorial pathogenesis, sympathetic hyperactivity plays a relevant role. Considering that sympathetic dysfunction is already present in the initial phases of chronic Chagas cardiomyopathy (CCC) and frequently associated with a worse prognosis, we assumed it could be more severe in CCC than in cardiomyopathies of other etiologies (non-CCC).

Objectives:

To assess the cardiac sympathetic dysfunction ¹²³I-MIBG) of HF, comparing individuals with CCC to those with non-CCC, using heart transplant (HT) patients as denervated heart parameters.

Methods:

We assessed 76 patients with functional class II-VI HF, being 25 CCC (17 men), 25 non-CCC (14 men) and 26 HT (20 men), by use of cardiac ¹²³I-metaiodobenzylguanidine ¹²³I-MIBG) scintigraphy, estimating the early and late heart-to-mediastinum ratio (HMR) of ¹²³I-MIBG uptake and cardiac washout (WO%). The 5% significance level was adopted in the statistical analysis.

Results:

The early and late HMR values were 1.73 ± 0.24 and 1.58 ± 0.27, respectively, in CCC, and 1.62 ± 0.21 and 1.44 ± 0.16 in non-CCC (p = NS), being, however, higher in HT patients (p < 0.001). The WO% values were 41.65 ± 21.4 (CCC), 47.37 ± 14.19% (non-CCC) and 43.29 ± 23.02 (HT), p = 0.057. The late HMR values showed a positive weak correlation with left ventricular ejection fraction (LVEF) in CCC and non-CCC (r = 0.42 and p = 0.045; and r = 0.49 and p = 0.015, respectively).

Conclusion:

Sympathetic hyperactivity ¹²³I-MIBG) was evidenced in patients with class II-IV HF, LVEF < 45%, independently of the HF etiology, as compared to HT patients.

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Editorial

Cardiac Sympathetic Activity and the Neuro-Humoral Theory on Heart Failure with Reduced Ejection Fraction: Have We Learned Enough?

Thiago Quinaglia A. C. Silva et al. Otávio R. Coelho-Filho

Since the 1970s,^, in observational trials, and more recently in placebo-controlled randomized trials,^, antagonizing beta-1 adrenergic receptors in the myocardium has been shown to mitigate the burden of heart failure with reduced ejection fraction (HFrEF). Mortality has been reduced by 34-65% according to these studies. However, inhibiting the action of the peripheral sympathetic nervous system (SNS) by blocking alpha1 or stimulating alpha-2 central receptors has shown negative results or even an increased mortality, despite reducing norepinephrine plasma levels.^– This indicates that SNS effects on myocardial receptors, more than in peripheral receptors, play a pivotal role in HFrEF pathophysiology.

Hyper-activation of the SNS and the renin-angiotensin-aldosterone axis, combined with an increase in load-dependent peptides and inflammatory cascades constitute the neuro-humoral theory on HFrEF progression. While the neuro-humoral response counteracts and compensates for an initial myocardial insult, in the long-term it contributes to the progression of the disease to the point that cardiovascular homeostasis eventually succumbs if not treated properly. Therapies targeting all these neuro-humoral responses have dramatically changed the natural history of HFrEF.

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