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Salt sensitivity and left ventricular hypertrophy
1Department of Internal Medicine, Hospital Clinico, University of Barcelona, Spain.
Insights
Salt-sensitive hypertension is linked to increased left ventricular mass and poorer lipid profiles, raising cardiovascular disease risk. These findings highlight the importance of salt intake in hypertensive patients with cardiac hypertrophy.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Internal Medicine
Background:
- Essential hypertensive patients with left ventricular hypertrophy (LVH) face significantly higher cardiovascular disease mortality.
- LVH impairs myocardial oxygen supply-demand balance, reducing coronary reserve even without coronary artery stenosis, predisposing to ischemia and arrhythmias.
- Both hemodynamic and non-hemodynamic factors, including genetics, adrenergic system, renin-angiotensin-aldosterone system, and growth factors, contribute to LVH pathogenesis.
Purpose of the Study:
- To investigate the role of salt sensitivity in the development of left ventricular hypertrophy (LVH) and associated cardiovascular risk factors in essential hypertensive patients.
- To compare cardiovascular parameters, including left ventricular mass, albumin excretion rate, and lipid profile, between salt-sensitive and salt-resistant hypertensive individuals.
Main Methods:
- The study compared salt-sensitive and salt-resistant hypertensive patients.
- Evaluated left ventricular mass index (LVMI), albumin excretion rate, and lipid profiles.
- Assessed differences in myocardial structure and potential underlying mechanisms related to salt intake.
Main Results:
- Salt-sensitive hypertensive patients exhibited significantly increased left ventricular mass index (LVMI) compared to salt-resistant counterparts, primarily due to increased septal and posterior wall thickness.
- These patients also presented with a higher albumin excretion rate and a worse lipid profile, irrespective of blood pressure levels.
- The observed increase in LVMI in salt-sensitive patients appeared independent of volume overload, suggesting a different growth mechanism.
Conclusions:
- Salt-sensitive hypertensive patients demonstrate increased LVMI and adverse lipid profiles, even with similar blood pressure to salt-resistant patients.
- These factors contribute to a potentially higher risk of cardiovascular morbidity and mortality in salt-sensitive individuals.
- Understanding the mechanisms underlying salt-induced cardiac adaptation is crucial for managing cardiovascular risk in this population.
Abstract:
Essential hypertensive patients with left ventricular hypertrophy (LVH) increase their mortality rates due to all cardiovascular diseases from 3 to 10 times more than hypertensives without signs of cardiac hypertrophy. LVH modifies the equilibrium between the oxygen supply and demand by the myocardium. The coronary reserve is appreciably reduced in hypertensives with LVH even in the absence of any stenosis of coronary arteries. Thus, in patients with normal coronary angiogram, a predisposition toward myocardial ischemia already exists. This process has been associated with the increased incidence of ventricular arrhythmias in essential hypertensives with LVH, what could be linked to the increasing risk of sudden death in these patients. In addition to hemodynamic factors (pressure and volume overload) several non-hemodynamic factors have been involved in the pathogenesis of LVH in hypertension. LVH would develop in subjects with a particular genetic substrate by the overlap of high blood pressure values and several factors linked to the adrenergic system, the renin-angiotensin-aldosterone system, other vasoactive substances, and growth factors. It has been previously reported that NaCl ingestion is a powerful determinant of left ventricular hypertrophy in patients with essential hypertension. Furthermore, a relationship between left ventricular mass and abnormalities in intracellular Na+ or transmembrane Na+ transport has been observed in several studies. Salt-sensitive hypertensive subjects seem to exhibit an increased risk in terms of cardiovascular morbidity. We and others have observed a higher left ventricular mass, an increased albumin excretion rate and a worse lipid profile in salt-sensitive compared with salt-resistant patients. The increase in LVMI in salt-sensitive patients is mainly due to the increase in septal and posterior wall thickness, with normal diastolic diameter, suggesting that myocardial growth in these patients is not volume-dependent. The mechanism of this structural cardiac adaptation is not completely understood. Nevertheless, it is known that salt-sensitive and salt-resistant hypertensive patients differ in some adaptive responses to changes in dietary salt intake. Among them, the renin-aldosterone axis, the sympathetic nervous system and the intracellular ion composition could play a role in the development of myocardial growth. In conclusion, salt-sensitive hypertensive patients exhibited an increased LVMI and a worse lipid profile, compared with salt-resistant hypertensives, even at the same level of blood pressure. These characteristics may confer to salt-sensitive patients an increased risk in terms of cardiovascular morbidity and mortality.