Cardiac repolarization and its relation to ventricular geometry and rate in reverse remodelling during antihypertensive therapy with irbesartan or atenolol: results from the SILVHIA study

Malmqvist, Karin; Kahan, Thomas; Edner, Magnus; Bergfeldt, Lennart

doi:10.1038/sj.jhh.1002250

Cited by 8 publications

(6 citation statements)

References 47 publications

(79 reference statements)

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“…These drugs reduce the QT interval. [30][31][32]69,70 Experimental studies have also demonstrated that ACEis reduce the QT interval. 1,3,48,74 The effects of either an ACEi or an ARB on the QT interval are exerted via mechanisms that regulate also the QT interval.…”

Section: Ace Inhibitors and Arbsmentioning

confidence: 95%

Modulation of the QT interval duration in hypertension with antihypertensive treatment

2015

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The duration of the QT interval as measured by 12-lead electrocardiography is a measure of myocardial repolarization and is widely used to describe cardiac abnormalities, to determine the presence of cardiac toxicity and to evaluate drug safety. In hypertension, the QT interval is a predictor of the risk of both coronary events and cardiovascular death, after adjusting for the effects of additional risk factors. The mechanism of QT interval prolongation is multifactorial and includes cardiomyocyte hypertrophy and increased left ventricular mass, with accompanying changes in left ventricular transmural dispersion of repolarization, as well as changes in the tone of the autonomic nervous system of some patients with hypertension and mechano-electrical feedback, although this mechanism is less likely. Antihypertensive drugs vary in their effect on QT interval duration. The mechanisms underlying their effect depend on changes in left ventricular mass and autonomic nervous system tone, as well as changes in the activity of cardiac ion channels. Although blood pressure reduction is the primary goal of antihypertensive drug therapy and although the choice of antihypertensive drug treatment regimens varies among different individuals, the data regarding the disparate effects of antihypertensive drugs on the duration of the QT interval warrant consideration when implementing long-term pharmacotherapy for hypertension.

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Section: Ace Inhibitors and Arbsmentioning

confidence: 95%

Modulation of the QT interval duration in hypertension with antihypertensive treatment

2015

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“…In hypertension associated with obesity, the duration of QTc interval is prolonged and tended to be decreased after blood pressure control and weight loss 6 . Antihypertensive drugs (angiotensin converting enzyme inhibitors and angiotensin receptor blockers) reduced the duration of QT interval due to their effects on the left ventricular mass which increases in hypertension 7, 8, 9. Beta-adrenoceptor blockers may also reduce the duration of the QT interval in a dose-dependent manner without having any effect on the blood pressure10, 11 while calcium channel blockers (dihydropyridine) do not exert a beneficial effect on QT interval 12 .…”

Section: Introductionmentioning

confidence: 99%

Subclinical ventricular repolarization abnormality in uncontrolled compared with controlled treated hypertension

Al-Nimer

Hussein

2017

Indian Heart Journal

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“…Consequently, its reduction is thought to be associated with regression of cardiac hypertrophy in terms of the reduction of left ventricular mass. Indeed, it was shown that antihypertensive drugs reduce QT duration as well as cardiac mass in hypertensive subjects which in turn reduces the incidence and severity of ventricular arrhythmias and the risk for cardiovascular events . Still, the relationship between QT reduction, antihypertensive and antihypertrophic action of antihypertensives is not understood.…”

mentioning

confidence: 99%

“…However, an inconsistency is seen in the clinic as a different influence of antihypertensives on QT duration was described after the reduction of BP and cardiac mass in the hypertensive population. Moreover, marked differences in reduction of QT abnormalities were published in spite of similar or even equivalent BP‐reducing action . From the entire group of antihypertensive drugs, dihydropyridine calcium channel blockers (CCBs) mediate their antihypertensive effects via vasodilatation but their efficacy could be significantly decreased by counter‐regulatory cardiac and the renal activation by the baroreflex that may influence cardiac repolarization .…”

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confidence: 99%

Discrepant Regulation of QT (QTc) Interval Duration by Calcium Channel Blockade and Angiotensin Converting Enzyme Inhibition in Experimental Hypertension

Klimas

Vaja

Vercinska

et al. 2012

Basic Clin Pharma Tox

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Antihypertensive treatment may reduce prolonged QT duration in hypertension. Generally, the reductions of blood pressure and/or of cardiac mass are believed to be the responsible factors. However, drugs are not equivalent in QT modulation despite similar antihypertensive and antihypertrophic action. We investigated the effect of a calcium channel blocker, lacidipine and an angiotensin-converting enzyme inhibitor, enalapril on QT duration in rats. Normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were treated with lacidipine (at the dose of 1.5 mg/kg per day for WKY and 3 mg/kg per day for SHR) or enalapril (5 mg/kg per day for WKY and 10 mg/kg per day for SHR) during 8 weeks. Tail-cuff systolic blood pressure (sBP), left ventricular weight (LVW), vascular function of isolated aorta and mesenteric artery and duration of QT (and QTc) interval on Frank electrocardiograms were evaluated. As expected, untreated SHR showed elevated sBP, impaired vascular reactivity, increased LVW and prolonged QT when compared with WKY (p < 0.05). After treatment, both agents markedly improved vascular reactivity and reduced sBP in SHR (p < 0.05). Additionally, enalapril reduced LVW in both hypertensive (by 17%; p < 0.05) and normotensive rats (by 13%; p < 0.05) and, consequently, corrected QT duration in SHR. Interestingly, lacidipine also reduced LVW in SHR (by 9%; p < 0.05), but without influence on prolonged QT. Moreover, lacidipine had no effect on LVW in WKYs but prolonged their QT interval (by 10%; p < 0.05). In conclusion, lacidipine did not reverse a progressive prolongation of QT in SHR, despite sBP lowering and LVW reduction. Thus, the lowering of blood pressure and/or reduction of LVW are not sufficient per se to normalize ventricular repolarization in hypertensive cardiac disease. More likely, modulation of QT prolongation by antihypertensive drugs is a function of their complex action on blood pressure, vascular function, cardiac mass and on reflex neurohumoral activation.The QT interval, a measure of cardiac repolarization, reflects several physiological conditions and is a non-specific marker of cardiotoxicity of drugs and cardiac pathology [1][2][3]. Prolonged QT interval (and its heart-rate correction; QTc) is independently associated with an increased risk of sudden cardiac death [4]. In addition, QT prolongation is a well known, but non-specific sign of the presence of left ventricular hypertrophy (LVH) in hypertension [5]. Consequently, its reduction is thought to be associated with regression of cardiac hypertrophy in terms of the reduction of left ventricular mass. Indeed, it was shown that antihypertensive drugs reduce QT duration as well as cardiac mass in hypertensive subjects which in turn reduces the incidence and severity of ventricular arrhythmias and the risk for cardiovascular events [6][7][8]. Still, the relationship between QT reduction, antihypertensive and antihypertrophic action of antihypertensives is not understood.Any agent that reduces blood pressure (BP) ...

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Cardiac repolarization and its relation to ventricular geometry and rate in reverse remodelling during antihypertensive therapy with irbesartan or atenolol: results from the SILVHIA study

Cited by 8 publications

References 47 publications

Modulation of the QT interval duration in hypertension with antihypertensive treatment

Modulation of the QT interval duration in hypertension with antihypertensive treatment

Subclinical ventricular repolarization abnormality in uncontrolled compared with controlled treated hypertension

Discrepant Regulation of QT (QTc) Interval Duration by Calcium Channel Blockade and Angiotensin Converting Enzyme Inhibition in Experimental Hypertension

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