Myocardial β-adrenoceptors in pacing-induced heart failure: regulation by enalapril?

1994 ◽  
Vol 72 (6) ◽  
pp. 667-672 ◽  
Author(s):  
Christine Forster ◽  
George O. A. Naik ◽  
Giulia Larosa
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Radioligand Binding ◽  
Left Ventricular ◽  
Converting Enzyme Inhibitors ◽  
Failure Group ◽  
End Stage Heart Failure ◽  
End Stage ◽  
The Impact ◽  
Enalapril Treatment

In heart failure, both the sympathetic nervous system and the renin angiotensin system play important pathophysiological roles, and the two systems may interact with each other, e.g., angiotensin II facilitating noradrenaline release. An abnormality in β-adrenoceptor density (i.e., a decrease) occurs in clinical and pacing-induced heart failure. This observation together with the therapeutic effectiveness of converting-enzyme inhibitors in the management of patients with heart failure led to the current investigation. The aim was to explore the impact of chronic enalapril treatment on the status of myocardial β-adrenoceptors in dogs paced (250 beats∙min−1) to end-stage heart failure. Placebo or enalapril treatment (5 mg b.i.d.) commenced 1 week after the onset of ventricular pacing and continued until end-stage heart failure was reached. Myocardial β-adrenoceptor density and affinity were assessed by radioligand binding with [125I]iodocyanopindolol. Left ventricular angiotensin II formation and noradrenaline concentration were measured. In addition, plasma renin activity and plasma noradrenaline levels were determined. The results showed that there was a significant increase in β-adrenoceptor density following enalapril treatment compared with placebo in the heart-failure group. Enalapril did not change the β-adrenoceptor density in the control animals. However, in both heart failure and control animals, enalapril caused an unexpected increase in Kd. Furthermore, in heart failure, enalapril caused a significant increase in myocardial angiotensin II formation. We conclude that enalapril prevents or reverses the myocardial β-adrenoceptor abnormality seen in heart failure and promotes angiotensin II formation.Key words: congestive heart failure, enalapril, cardiac β-adrenoceptors, angiotensin II formation.

scholarly journals Left ventricular systolic function decreases in lamin a/c cardiomyopathy wihout concomitant ventricular dilatation

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
ES Eystein Skjolsvik ◽  
OL Oyvind Haugen Lie ◽  
MC Monica Chivulescu ◽  
MR Margareth Ribe ◽  
AIC Anna Isotta Castrini ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricular ◽  
University Hospital ◽  
Lv Function ◽  
Lamin A ◽  
Age Related ◽  
End Stage Heart Failure ◽  
Lv Volumes ◽  
End Stage

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): This work was supported by the Norwegian Research Council [203489/030] onbehalf Department of Cardiology, Research group for genetic cardiac diseases and sudden cardiac death, Oslo University Hospital, Rikshospitalet, Oslo, Norwa Background Lamin A/C disease is an inheritable cardiomyopathy characterized by conduction abnormalities, ventricular arrhythmias and end stage heart failure with complete age-related penetrance. Purpose To assess left ventricular structural and functional progression in patients with lamin A/C cardiomyopathy. Methods We included and followed consecutive lamin A/C genotype positive patients with clinical examination and echocardiography at every visit. We evaluated progression of left- ventricular size and function by mixed model statistics. Results We included 101 consecutive lamin A/C genotype positive patients (age 44 [29-54] years, 39% probands, 51%female) with 576 echocardiographic exams during 4.9 (IQR 2.5-8.1) years of follow-up. LV ejection fraction (LVEF) declined from 50 ± 12% to 47 ± 13%, p < 0.001 (rate -0.5%/year). LV end diastolic volumes (LVEDV) remained stationary with no significant dilatation in the total population (136 ± 45ml to 138 ± 43ml, p = 0.60), (Figure). In the subgroup of patients >58 years, we observed a decline in LV volumes 148, SE 9 ml to 140, SE 9 ml p < 0.001 (rate -2.7 ml/year) towards end stage heart failure. Conclusions LVEF deteriorated, while LV size remained unchanged during 4.9 years of follow-up in patients with lamin A/C cardiomyopathy. In patients <58 years, we observed a reduction in LV volumes. These findings represent loss of LV function without the necessary compensatory dilation to preserve stroke volume indicating high risk of decompensated end stage heart failure in lamin A/C. Abstract Figure.

Angiotensin II Receptor Type 1 mRNA is Upregulated in Atria of Patients with End-stage Heart Failure

1997 ◽  
Vol 29 (8) ◽  
pp. 2299-2304 ◽  
Author(s):  
Raffi R Kaprielian ◽  
Emmanuel Dupont ◽  
Sassan Hafizi ◽  
Philip A Poole-Wilson ◽  
Asghar Khaghani ◽  
...  
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Receptor Type ◽  
Angiotensin Ii Receptor ◽  
End Stage Heart Failure ◽  
End Stage
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