Related Experiment Videos
Left ventricular mass is linked to cardiac noradrenaline in normotensive and hypertensive patients
1Department of Medicine, Heinrich Heine University, Düsseldorf, Germany.
Insights
Left ventricular hypertrophy is linked to increased cardiac noradrenaline release, independent of blood pressure. This suggests cardiac sympathetic activity plays a key role in hypertrophy development.
Area of Science:
- Cardiology
- Physiology
- Pharmacology
Background:
- Left ventricular hypertrophy (LVH) is a significant risk factor for heart failure, sudden death, and ventricular dysrhythmia.
- Experimental evidence suggests noradrenaline, beyond increased cardiac workload, may trigger myocardial hypertrophy.
Purpose of the Study:
- To investigate the relationship between left ventricular mass and cardiac noradrenaline levels.
- To determine if this coupling is independent of arterial blood pressure.
Main Methods:
- Cardiac catheterization excluded coronary artery disease.
- Noradrenaline levels were measured in arterial and coronary venous plasma via high-performance liquid chromatography.
- Left ventricular mass was assessed using echocardiography.
Main Results:
- Coronary venous noradrenaline concentrations were elevated in hypertensive patients with and without LVH, and in hypertrophic cardiomyopathy patients compared to normotensives.
- A net release of noradrenaline across the coronary circulation was observed in hypertensive patients and hypertrophic cardiomyopathy patients, unlike the net uptake in normotensives.
- Left ventricular mass significantly correlated with net noradrenaline release, independent of arterial blood pressure.
Conclusions:
- Increased left ventricular mass in both normotensive and hypertensive individuals is closely associated with heightened cardiac sympathetic activity.
- Further research is warranted to explore the potential benefits of sympatholytic therapy in patients with LVH and elevated cardiac noradrenaline release.
Background:
Left ventricular hypertrophy constitutes a powerful independent risk factor for heart failure, sudden death and ventricular dysrhythmia. Experimental data suggest that, apart from increased cardiac work load, noradrenaline may be one of the factors triggering myocardial hypertrophy.
Objective:
To test the hypothesis that the extent of left ventricular hypertrophy is coupled to cardiac noradrenaline independently from the magnitude of arterial blood pressure.
Patients And Methods:
Following exclusion of coronary artery disease by cardiac catheterization, cardiac noradrenaline release was measured in relation to left ventricular mass in 25 patients with arterial hypertension (HT), of whom five had left ventricular hypertrophy (HT + LVH) and 20 had normal left ventricular mass (HT - LVH), seven normotensive patients with hypertrophic cardiomyopathy (HCM) and a normotensive control group (n = 7). Noradrenaline was measured in arterial and coronary venous plasma using high-performance liquid chromatography. Coronary blood flow was quantified using the gas chromatographic argon method. Indices of left ventricular mass were calculated from the end-diastolic thicknesses of the interventricular septum and the posterior wall determined by echocardiography.
Results:
The coronary venous plasma concentration of noradrenaline was significantly higher in HT - LVH, HT + LVH and HCM than it was in normotensives. Whereas in normotensives there was a net uptake of noradrenaline (17 +/- 10 pmol/min) across the coronary circulation, a net release of noradrenaline was observed in HT - LVH (69 +/- 26 pmol/min), in HT + LVH (121 +/- 55 pmol/min) and in HCM (341 +/- 96 pmol/min). In a multivariate linear regression analysis model, left ventricular mass correlated significantly with the net noradrenaline release rate (r = 0.64, P < 0.001), whereas arterial blood pressure as an additional independent variable did not correlate with left ventricular mass.
Conclusion:
The present data demonstrate that an increased left ventricular mass in normotensive and in hypertensive patients is closely coupled to an increased cardiac sympathetic activity, supporting the need for additional studies to determine whether adjunctive sympatholytic therapy is beneficial in patients with left ventricular hypertrophy and increased cardiac noradrenaline release.