Related Experiment Videos
Diffuse reduction of myocardial beta-adrenoceptors in hypertrophic cardiomyopathy: a study with positron emission
D C Lefroy1, R de Silva, L Choudhury
1Medical Research Council (MRC) Cyclotron Unit, Royal Postgraduate Medical School, Hammersmith Hospital, London, England, United Kingdom.
Insights
Patients with hypertrophic cardiomyopathy have reduced myocardial beta-adrenoceptor density, indicating increased cardiac sympathetic drive. This finding suggests a potential marker for sympathetic function in this condition.
Area of Science:
- Cardiology
- Molecular Imaging
- Neuroscience
Background:
- Hypertrophic cardiomyopathy (HCM) can present without clear genetic or familial links.
- Increased sympathetic nervous system activity is suspected in HCM.
- Understanding sympathetic function in HCM is crucial for diagnosis and treatment.
Purpose of the Study:
- To assess myocardial beta-adrenoceptor density as a marker of sympathetic function in HCM patients.
- To compare beta-adrenoceptor density between HCM patients and healthy controls.
- To investigate the relationship between beta-adrenoceptor density and other physiological parameters in HCM.
Main Methods:
- Positron emission tomography (PET) was used to measure left ventricular beta-adrenoceptor density.
- Tracers [11C]CGP 12177 and [15O]water were employed for PET imaging.
- Plasma catecholamine levels were measured in all participants.
Main Results:
- Myocardial beta-adrenoceptor density was significantly lower in HCM patients compared to controls.
- Myocardial blood flow and catecholamine levels did not differ significantly between groups.
- Beta-adrenoceptor density was uniformly distributed in the left ventricle of both groups.
Conclusions:
- HCM patients exhibit a diffuse reduction in myocardial beta-adrenoceptor density.
- This reduction is likely due to beta-adrenoceptor downregulation from increased norepinephrine.
- Findings support the hypothesis of heightened cardiac sympathetic drive in hypertrophic cardiomyopathy.
Objectives:
This study was conducted to determine the myocardial beta-adrenoceptor density as a marker of sympathetic function in patients with hypertrophic cardiomyopathy and normal control subjects.
Background:
Although some cases of hypertrophic cardiomyopathy are familial with an autosomal dominant pattern of inheritance, there remains a substantial proportion of cases in which neither a family history nor genetic abnormalities can be demonstrated. Additional abnormalities, both genetic and acquired, may be important in the phenotypic expression of this condition. Clinical features of the disease and metabolic studies suggest an increased activity of the sympathetic nervous system.
Methods:
Eleven patients with hypertrophic cardiomyopathy, none of whom had previously received beta-blocking drugs, and eight normal control subjects underwent positron emission tomography to evaluate regional left ventricular beta-adrenoceptor density and myocardial blood flow using carbon-11-labeled CGP 12177 and oxygen-15-labeled water as tracers. Plasma catecholamines were also measured.
Results:
Mean (+/- SD) myocardial beta-adrenoceptor density was significantly less in the hypertrophic cardiomyopathy group than in the control group (7.70 +/- 1.86 vs. 11.50 +/- 2.18 pmol/g tissue, p < 0.001). Myocardial blood flow was similar in both groups (0.91 +/- 0.22 vs. 0.91 +/- 0.21 ml/min per g, p = NS). The distribution of beta-adrenoceptor density was uniform throughout the left ventricle in both groups. In the hypertrophic cardiomyopathy group, there was no correlation between regional wall thickness and myocardial beta-adrenoceptor density. There were no significant differences in either plasma norepinephrine or epinephrine concentrations between the two groups.
Conclusions:
There is a diffuse reduction in myocardial beta-adrenoceptor density in patients with hypertrophic cardiomyopathy in the absence of significantly elevated circulating catecholamine concentrations. This most likely reflects downregulation of myocardial beta-adrenoceptors secondary to increased myocardial concentrations of norepinephrine and is consistent with the hypothesis that cardiac sympathetic drive is increased in this condition.