Significance of blood pressure levels achieved with felodipine anti-hypertensive treatment on cardiovascular structure and function changes

Vyssoulis, Gregory P.; Trikas, AG; Paleologos, A.A.; Toutouza, M.; Toutouzas, P.

doi:10.1038/sj.jhh.1000645

Cited by 3 publications

(1 citation statement)

References 33 publications

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“…In the present issue of Journal of Human Hypertension, there is a study by Vyssoulis et al 11 which addresses the topic of LVM reduction in relation to the level of BP reduction. In this prospective study, the effect of the calcium antagonist, felodipine, in reducing LVM was compared in four treatment groups which were based upon the DBP level which was finally achieved (Ͻ80 mm Hg, 80-84 mm Hg, 85-89 mm Hg and 90-94 mm Hg).…”

Section: And Cruickshank Et Almentioning

confidence: 99%

Regression of LVH or improved prognosis (or both): what is the question?

et al. 1998

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Left ventricular hypertrophy (LVH) can be regarded as an example of the evolution of cardiovascular disease en route to a bad outcome. Whilst LVH can also be regarded as an adaptive or compensatory response of the heart to increased blood pressure (BP) it is associated with many complications, such as sudden death, arrhythmias (including atrial fibrillation and ventricular arrhythmias), myocardial infarction, congestive heart failure and stroke. Of note, the frequency and severity of these complications are closer related to the degree of LVH than the level of the arterial pressure. Therefore, the effectiveness of anti-hypertensive treatment should not simply aim to reduce BP, but should also focus on the regression of hypertension-induced structural changes in the cardiovascular system, particularly LVH.Nevertheless, there is more to LVH than simply the elevation of BP. Other determinants of the development of LVH include hereditary and demographic factors such as age, gender, obesity, exogenous factors like dietary salt intake and alcohol, and neurohumoral factors such as the activity of the reninangiotensin-aldosterone system, the sympathetic system, insulin, parathyroid and other hormones. 1-2As hypertensive cardiovascular disease progresses, four pathophysiologic mechanisms are postulated to relate LVH with increased cardiovascular morbidity and mortality: 1 (i) impaired diastolic filling (reduction of early diastolic filling); (ii) myocardial ischaemia (impairment of coronary reserve); (iii) ventricular arrhythmias (which have been implicated in sudden death); and (iv) impaired myocardial contractility (resulting in dilatation of left ventricle and congestive heart failure).Given the large impact of LVH on hypertensive morbidity and mortality, it is not surprising that there have been more than 1000 clinical and experimental studies in both animals and humans in the literature on the issue of LVH regression. The main

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Section: And Cruickshank Et Almentioning

confidence: 99%

Regression of LVH or improved prognosis (or both): what is the question?

et al. 1998

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Mild left ventricular hypertrophy in essential hypertension: is it really arrhythmogenic?

Gatzoulis

Vyssoulis

Apostolopoulos

et al. 2000

American Journal of Hypertension

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Left ventricular hypertrophy (LVH) has been associated with an increased incidence of ventricular arrhythmias and sudden cardiac death in hypertensive patients. However, it is not known whether this relationship exists in early asymptomatic hypertensives with mild LVH. We prospectively examined 100 consecutive patients with essential hypertension, 35 without and 65 with mild LVH on echocardiography. All underwent a detailed noninvasive arrhythmia work-up and were subsequently followed-up for 3 +/- 1 years in an ambulatory hypertension clinic. None of the 12-lead electrocardiographic parameters examined differed between the two hypertensive groups. A similarly low incidence of simple forms of ventricular ectopy was present in both groups, whereas complex forms of ventricular ectopy were extremely rare in either group. The signal-averaged electrocardiographic parameters examined were also not significantly affected by the presence of mild LVH. Arrhythmia-related symptoms or malignant ventricular arrhythmia events were not observed in either group of patients during follow-up with antihypertensive treatment. The latter resulted in LVH regression in the 65 patients with mild LVH at baseline. It appears that mild LVH among ambulatory hypertensive patients does not carry an additive arrhythmogenic risk and can be successfully reversed with the appropriate antihypertensive therapy, with no need of additional antiarrhythmic management.

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