Left ventricular hypertrophy regression during antihypertensive treatment

Eichstaedt, H.; Danne, O.; Schroeder, Rico; Kreuz, Deutsches Grünes

doi:10.1007/bf00207616

Cited by 4 publications

(3 citation statements)

References 33 publications

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“…ACE inhibitor therapy normalized PFF and PFR within 6 months. Previous animal studies indicate selective enhancement of active LV relaxation by ACE inhibitors, probably via an endogenous bradykinin/nitric oxide pathway (11, 12, 23). In our study, inhibition of the Reviv Angiotensin System (RAS) as a trigger of LV hypertrophy induced simultaneously a reduction of LV mass and an improvement of early diastolic filling.…”

Section: Discussionmentioning

confidence: 94%

The effects of ACE inhibitor therapy on left ventricular myocardial mass and diastolic filling in previously untreated hypertensive patients: A Cine MRI study

Hoffmann

Globits

Stefenelli

et al. 2001

Magnetic Resonance Imaging

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Cardiac remodeling in case of hypertension induces hypertrophy of myocytes and elevated collagen content and, subsequently, impaired diastolic filling of the left ventricle. The purpose of this prospective study was to evaluate changes of left ventricular (LV) myocardial mass, as well as diastolic filling properties, in hypertensive patients treated with the ACE inhibitor fosinopril. Sixteen hypertensive patients with echocardiographically documented LV hypertrophy and diastolic dysfunction received fosinopril (10 -20 mg daily). Measurements of LV myocardial mass and properties of diastolic filling (peak filling fraction (PFF); peak filling rate (PFR)) were performed prior to medication, as well as after 3 and 6 months of therapy using cine magnetic resonance imaging (MRI). LEFT VENTRICULAR (LV) HYPERTROPHY has been identified as an independent risk factor for cardiovascular mortality, accompanied by an increased incidence of ischemic events and sudden death or heart failure (1,2). The presence of LV hypertrophy in hypertensive patients can be initially regarded as an adaptive process that compensates for chronic pressure overload and preserves sufficient systolic wall stress and pump function (3). However, the remodeling process leads to functional changes like adaptive molecular modifications in myocardial myocytes, as well as morphologic alterations, including hypertrophy of myocytes and an elevated ventricular collagen content (myocardial fibrosis). These alterations are mainly triggered by angiotensin II (AT II) and are responsible for impairment of diastolic filling and increased myocardial stiffness of the LV (4,5).ACE inhibitors have been shown to effectively control blood pressure (BP) and reduce LV myocardial mass in numerous clinical and echocardiographic studies (6 -10). It is well-known that ACE inhibitors exert additional local actions, which are not related to only hemodynamic changes. Animal studies have proposed a selective enhancement of LV relaxation by ACE inhibitors via an endogenous bradykinin/nitric oxide pathway (11). In addition, ramipril has been demonstrated to have a direct effect on the mRNA expression for myocardial collagen I and II, unrelated to the effect of BP control (12).Although ACE inhibitors exert direct effects on the pathomechanism on cardiac alterations in the course of pressure overload, there is little information regarding the time course of BP lowering, reduction of LV mass, and subsequent normalization of diastolic filling. In the present study, we used serial clinical and cine MRI examinations to accurately analyze regression of LV hypertrophy, as well as its effects on parameters of LV diastolic filling during treatment with the ACE inhibitor fosinopril. METHODS PatientsSixteen previously untreated patients with essential hypertension (systolic BP ϭ 158 Ϯ 11 mm of Hg, dia-

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Section: Discussionmentioning

confidence: 94%

The effects of ACE inhibitor therapy on left ventricular myocardial mass and diastolic filling in previously untreated hypertensive patients: A Cine MRI study

Hoffmann

Globits

Stefenelli

et al. 2001

Magnetic Resonance Imaging

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“…Therefore, it is plausible that the α-blocking effect of carvedilol may provide superior benefit in terms of LVH regression, compared with traditional β-blockers. In fact, there are several preclinical and clinical studies available to suggest that carvedilol may be effective in the regression of LVH 73–75. In particular, the study by Verza et al examined the effect of 6 months of daily therapy with carvedilol 25 mg on LVH in elderly patients (mean age 69 years) with essential hypertension and LVH 74.…”

Section: Effect On Left-ventricular Hypertrophymentioning

confidence: 99%

“…In fact, there are several preclinical and clinical studies available to suggest that carvedilol may be effective in the regression of LVH. 73 – 75 In particular, the study by Verza et al examined the effect of 6 months of daily therapy with carvedilol 25 mg on LVH in elderly patients (mean age 69 years) with essential hypertension and LVH. 74 Carvedilol caused a significant reduction in systolic and diastolic BP ( Figure 6A ) and LVH, as measured by left ventricular mass in addition to left ventricular mass index ( Figure 6B ).…”

Section: Effect On Left-ventricular Hypertrophymentioning

confidence: 99%

Use of carvedilol in hypertension: an update

Leonetti¹,

Egan²

2012

VHRM

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β-blockers are effective antihypertensive agents and, together with diuretics, have been the cornerstone of pioneering studies showing their benefits on cardiovascular morbidity and mortality as a consequence of blood pressure reduction in patients with hypertension. However, evidence from recent meta-analyses have demonstrated no benefit afforded by atenolol compared with placebo in risk of mortality, myocardial infarction, or stroke, and a higher risk of mortality and stroke with atenolol/propranolol compared with other antihypertensive drug classes. Thus, the effect of these agents on cardiovascular morbidity and mortality in hypertensive patients, especially their use in uncomplicated hypertension, has remained largely controversial. However, it is recognized that the clinical studies used in these meta-analyses were mainly based on the older second-generation β-blockers, such as atenolol and metoprolol. Actually, considerable heterogeneity in, eg, pharmacokinetic, pharmacological, and physicochemical properties exists across the different classes of β-blockers, particularly between the second-generation and newer third-generation agents. Carvedilol is a vasodilating noncardioselective third-generation β-blocker, without the negative hemodynamic and metabolic effects of traditional β-blockers, which can be used as a cardioprotective agent. Compared with conventional β-blockers, carvedilol maintains cardiac output, has a reduced prolonged effect on heart rate, and reduces blood pressure by decreasing vascular resistance. Studies have also shown that carvedilol exhibits favorable effects on metabolic parameters, eg, glycemic control, insulin sensitivity, and lipid metabolism, suggesting that it could be considered in the treatment of patients with metabolic syndrome or diabetes. The present report provides an overview of the main clinical studies concerning carvedilol administered as either monotherapy or in combination with another antihypertensive or more frequently a diuretic agent, with particular focus on the additional benefits beyond blood pressure reduction.

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Optimizing the use of β-blockers in the effective treatment and management of heart failure: a case study approach

Eichhorn

Young

2001

The American Journal of Medicine

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Left ventricular hypertrophy regression during antihypertensive treatment

Cited by 4 publications

References 33 publications

The effects of ACE inhibitor therapy on left ventricular myocardial mass and diastolic filling in previously untreated hypertensive patients: A Cine MRI study

The effects of ACE inhibitor therapy on left ventricular myocardial mass and diastolic filling in previously untreated hypertensive patients: A Cine MRI study

Use of carvedilol in hypertension: an update

Optimizing the use of β-blockers in the effective treatment and management of heart failure: a case study approach

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