Left ventricular hypertrophy in mild essential hypertension. Its progression, prediction and treatment strategy.
Since the pathogenesis of left ventricular hypertrophy (LVH) in hypertension is thought to be multifactorial, the antihypertensive strategy also has to be multifaceted. Diagnosis of LVH is more reliable than ever with echocardiography either of the M-mode or 2D method. Diagnostic criteria have already been proposed by Ganau et al who classified LV morphology into 4 different sectors based on the standard values of left ventricular mass index (LVMI) and relative wall thickness in diastole (RWTd); normal, concentric remodeling, concentric hypertrophy and eccentric hypertrophy. The concentric hypertrophy pattern is the most risky with regard to prognosis. Therefore, its detection and prediction for further progression have to be conducted with relatively easy routine work-up procedures such as echocardiography and maximal exercise testing. The prediction of LVH progression has already been proposed based on several studies conducted in patients with borderline or mild hypertension. The following two predictors were defined as LVMI > 124 g/m2 and peak Ps at maximal exercise testing > 200 mmHg. Therefore, the patient who meets these criteria has to be treated with medications that are appropriately selected on an individualized basis. Both hyperinsulinemia and insulin resistance are thought to be involved in the initiation, promotion and potentiation of remodeling of the LV in hypertension. Physical fitness also seems to be decreased in a parallel manner. Selection of the most appropriate drug for a given patient has to be individually determined based on the risks that have to be corrected. Finally, arteriosclerosis, which is almost always initiated and progresses in concert with hypertension, must also be targeted with regard to such prognostic aspects as cardiovascular morbidity and mortality. Arteriosclerosis is pathogenetically independent from hypertension, but usually behaves in concert with it. Selection of medication must be focussed on an individualized basis not only for LVH, but also for improvement in arterial elasticity. Further clinical research is still needed to provide more reasonable approaches to patients with hypertension.
Third Department of Internal Medicine, Teikyo University School of Medicine, Ichihara, Japan.
N
N
Doba
H
H
Tomiyama
H
H
Yoshida
Y
Y
Kihara
G
G
Watanabe
S
S
Hinohara
D000804:Angiotensin II / Q000502:physiology; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001161:Arteriosclerosis / Q000150:complications; D018450:Disease Progression; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000188:drug therapy; D017379:Hypertrophy, Left Ventricular / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D009638:Norepinephrine / Q000502:physiology
D000959:Antihypertensive Agents; D000804:Angiotensin II; D009638:Norepinephrine