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  • Title: Salt sensitivity and left ventricular hypertrophy.
    Author: Coca A, De la Sierra A.
    Journal: Adv Exp Med Biol; 1997; 432():91-101. PubMed ID: 9433515.
    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.
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