Magnetic Resonance Imaging Left Ventricular Mass Reduction With Fixed-Dose Angiotensin-Converting Enzyme Inhibitor–Based Regimens in Patients With High-Risk Hypertension

Reichek, Nathaniel; Devereux, Richard B.; Rocha, Ricardo; Hilkert, Robert; Hall, D P; Purkayastha, Das; Pitt, Bertram

doi:10.1161/hypertensionaha.109.130641

Cited by 32 publications

(18 citation statements)

References 43 publications

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“…Particularly notable is the short duration of treatment required to detect such changes using a highly reproducible method such as CMR [42,43]. Echocardiographic studies of LVH regression have typically required longer treatment periods to demonstrate LVH regression as well as larger sample sizes.…”

Section: Implications For Clinical Trialsmentioning

confidence: 99%

Imaging in hypertensive heart disease

Janardhanan

Kramer

2011

Expert Review of Cardiovascular Therapy

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Hypertensive heart disease is the target organ response to arterial hypertension. Left ventricular hypertrophy represents an important predictor for cardiovascular events. Myocardial fibrosis, a common end point in hypertensive heart disease, has been linked to the development of left ventricular hypertrophy and diastolic dysfunction. Echocardiography is clinically useful in the detection of left ventricular hypertrophy and the assessment of diastolic function. Although echocardiography is more widely available, cardiac magnetic resonance has been demonstrated to be more reproducible for the estimation of left ventricular mass. Future developments in cardiac magnetic resonance techniques may facilitate the quantification of diffuse fibrosis that occurs in hypertensive heart disease. Thus, advances in cardiac imaging provide comprehensive, noninvasive tools for imaging left ventricular hypertrophy, diastolic dysfunction, myocardial fibrosis and ischemia observed in hypertensive heart disease. The objective of this article is to summarize the state-of-the-art and the future of multimodality imaging of hypertensive heart disease.

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Section: Implications For Clinical Trialsmentioning

confidence: 99%

Imaging in hypertensive heart disease

Janardhanan

Kramer

2011

Expert Review of Cardiovascular Therapy

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“…For instance, CMR has been used before to demonstrate a reduction in ventricular mass in a number of intervention studies in hypertensive patients. 25,26 There was no placebo CPAP used in this trial, and this is a potential limitation (discussed in main MOSAIC paper), but a placebo effect is unlikely to affect these objective measurements, particularly over an intervention period of six months.…”

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confidence: 99%

Effect of CPAP on Cardiac Function in Minimally Symptomatic Patients with OSA: Results from a Subset of the MOSAIC Randomized Trial

Craig

Kylintireas

Kohler³

et al. 2015

Journal of Clinical Sleep Medicine

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Study Objectives: Minimally symptomatic obstructive sleep apnea (OSA) is highly prevalent, and the effects of continuous positive airway pressure (CPAP) on myocardial function in these patients are unknown. The MOSAIC randomized, controlled trial of CPAP for minimally symptomatic OSA assessed the effect of CPAP on myocardial function in a subset of patients. Methods: Two centers taking part in the MOSAIC trial randomized 238 patients in parallel to 6 months of CPAP (120) or standard care (118). Of these, 168 patients had echocardiograms, and 68 patients had a cardiac magnetic resonance scan (CMR). A larger group (314) from 4 centers had brain natriuretic peptide (BNP) measured. Results: Mean (SD) baseline oxygen desaturation index (ODI) and Epworth sleepiness score (ESS) were 13.5 (13.2), and 8.4 (4.0), respectively. CPAP signifi cantly reduced ESS and ODI. Baseline LV ejection fraction (LVEF) was well preserved (60.4%). CPAP had no signifi cant effect on echo-derived left atrial (LA) area (−1.0 cm 2 , 95% CI −2.6 to +0.6, p = 0. O bstructive sleep apnea (OSA) has the potential to be signifi cantly detrimental to cardiac function.1 Extreme sub-atmospheric pressure swings during apneic events can transiently reduce left ventricular (LV) emptying, and lead to increased left atrial (LA) and LV volumes, as well diastolic dysfunction. Over time, the LA may irreversibly enlarge, and patients with OSA have been shown to be more likely to develop atrial fi brillation (AF) as a possible consequence.2 In addition, it has been suggested that OSA can affect the aortic root, leading to increased rates of dilatation in some populations. 3-5Patients with OSA also have associated medical conditions such as diabetes, hypertension, and upper body obesity, which are recognized risk factors for cardiac disease. Many of these patients will have impaired diastolic function as a precursor to systolic dysfunction, and identifying this is important to prevent further functional decline. This is quantifi ed by measuring mitral blood fl ow (E/A ratio and deceleration times) and LA size (diameter or area) by echocardiography. In addition, Effect of CPAP on Cardiac Function in Minimally Symptomatic S C I E N T I F I C I N V E S T I G AT I O N SLV mass (measured by echocardiogram) has been shown to be higher in these patients 6,7 ; it may not be independently associated with OSA and may be more directly related to obesity or hypertension. 8Although echocardiograms are considered the gold standard for detecting diastolic dysfunction, cardiac magnetic BRIEF SUMMARY Current Knowledge/Study Rationale: The effect of CPAP therapy on cardiac function in patients with minimally symptomatic OSA is unknown. We used three methods (echocardiography, cardiac MR and BNP measurements) to assess cardiac function at baseline and after six months in patients randomized to CPAP or standard care. Study Impact: There was no improvement in cardiac function in any of the three measurements although baseline cardiac dysfunction was mild. This would suggest that co...

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“…In routine clinical work, cardiac MRI is more expensive and access more limited compared with widely available echocardiography. So far only few studies on regression of LVH have been performed with MRI [22][23][24][25][26][27]. In the current issue of the Journal of Hypertension, the study by Burns et al [28] presents the results of their open-label, randomized clinical trial that examined the hypothesis that a drug combination specifically selected to interfere with neuroendocrine pathways achieves more pronouced regression of LVH than a drug combination without these effects.…”

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Role of neuroendocrine activation for left ventricular hypertrophy in hypertension

Schneider

Schmieder

2012

Journal of Hypertension

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See original paper on page 2039T he development of left ventricular hypertrophy (LVH) imparts an adverse prognosis in patients with arterial hypertension [1,2]. A major goal of antihypertensive therapy is, therefore, to achieve reversal of LVH, which has repeatedly been demonstrated to improve prognosis [3][4][5][6].The lowering of blood pressure (BP) is widely viewed as the dominant factor for achieving reduction of an elevated LV mass in hypertension. On the basis of currently available evidence, the European Society of Hypertension Practice Guidelines recommend a target BP value of less than 140/ 90 mmHg, regardless of whether LVH is present or not [7]. Interestingly, in an open-label randomized study in 1111 hypertensive patients, electrocardiographic evidence of LVH after 2 years was less frequent in patients with tight BP control (<130 mmHg compared with those with usual BP control of less than 140 mmHg systolic) [8]. In accordance, there is recent evidence that targeting such a lower BP value of less than 130/80 mmHg has beneficial effects on diastolic function in patients with arterial hypertension [9]. As diastolic dysfunction is associated with adverse outcomes independently of LVH [10], target BP may need to be revised in the future for hypertensive patients with hypertensive heart disease.In addition to the role of BP, a positive relationship between level of sodium intake and LV mass was demonstrated decades ago [11]. Although only few data are available, there is some evidence from older studies that sodium restriction causes regression of LVH after several weeks of sodium restriction [12]. More recently, sodium restriction has also been shown to reduce ECG criteria of LVH. However, the fact that this appears to occur very rapidly, within 7 days, is puzzling, and may have more to do with alterations in the conduction of electrical signals through the chest wall than with true changes of cardiac structure after such a short period of intervention [13].Benefits of specific targeting of neuroendocrine pathways are spare in humans [14]. Nevertheless, at least animal studies provide strong evidence that increased levels of angiotensin II (Ang II) and aldosterone, as the primary effector molecules of the renin-angiotensin-aldosterone system (RAAS), as well as activation of the sympathetic nervous system (SNS) [15] can directly cause LVH. In humans, except perhaps for the role of aldosterone in the special case of primary hyperaldosteronism [16], the involvement of these factors in the genesis of LVH in patients with arterial hypertension is more difficult to demonstrate and has relied on cross-sectional data. Using a radioactive tracer spillover-technique, Schlaich et al. [17] have shown that sympathetic activation to the heart is increased in patients with hypertension who have LVH as compared with hypertensives without LVH. Interestingly, using this methodology, local cardiac Ang II levels were not found to correlate with LVH [18]. Only when the activity of the RAAS was related to sodium excretion, an i...

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Magnetic Resonance Imaging Left Ventricular Mass Reduction With Fixed-Dose Angiotensin-Converting Enzyme Inhibitor–Based Regimens in Patients With High-Risk Hypertension

Cited by 32 publications

References 43 publications

Imaging in hypertensive heart disease

Imaging in hypertensive heart disease

Effect of CPAP on Cardiac Function in Minimally Symptomatic Patients with OSA: Results from a Subset of the MOSAIC Randomized Trial

Role of neuroendocrine activation for left ventricular hypertrophy in hypertension

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