Treatment of Isolated Left Ventricular Diastolic Dysfunction in Hypertension
2009; Lippincott Williams & Wilkins; Volume: 55; Issue: 2 Linguagem: Inglês
10.1161/hypertensionaha.109.144717
ISSN1524-4563
AutoresVittorio Palmieri, C Allison Russo, Jonathan N. Bella,
Tópico(s)Cardiac electrophysiology and arrhythmias
ResumoHomeHypertensionVol. 55, No. 2Treatment of Isolated Left Ventricular Diastolic Dysfunction in Hypertension Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBTreatment of Isolated Left Ventricular Diastolic Dysfunction in HypertensionReaching Blood Pressure Target Matters Vittorio Palmieri, Cesare Russo and Jonathan N. Bella Vittorio PalmieriVittorio Palmieri From the Congestive Heart Failure Center (V.P.), Laboratory of Echocardiography, Cardiology Unit, "Ospedale dei Pellegrini," Naples, Italy; Department of Medicine (C.R.), Columbia University, New York, NY; Division of Cardiology (J.N.B.), Bronx-Lebanon Hospital Center and Albert Einstein College of Medicine, Bronx, NY. , Cesare RussoCesare Russo From the Congestive Heart Failure Center (V.P.), Laboratory of Echocardiography, Cardiology Unit, "Ospedale dei Pellegrini," Naples, Italy; Department of Medicine (C.R.), Columbia University, New York, NY; Division of Cardiology (J.N.B.), Bronx-Lebanon Hospital Center and Albert Einstein College of Medicine, Bronx, NY. and Jonathan N. BellaJonathan N. Bella From the Congestive Heart Failure Center (V.P.), Laboratory of Echocardiography, Cardiology Unit, "Ospedale dei Pellegrini," Naples, Italy; Department of Medicine (C.R.), Columbia University, New York, NY; Division of Cardiology (J.N.B.), Bronx-Lebanon Hospital Center and Albert Einstein College of Medicine, Bronx, NY. Originally published7 Dec 2009https://doi.org/10.1161/HYPERTENSIONAHA.109.144717Hypertension. 2010;55:224–225Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: December 7, 2009: Previous Version 1 Arterial hypertension is a major risk factor for congestive heart failure. Left ventricular (LV) hypertrophy is often associated with arterial hypertension and characterizes subjects with a particularly elevated risk of untoward cardiovascular events, including heart failure.1 LV hypertrophy is, in turn, associated with impaired LV myocardial contractility and LV diastolic dysfunction. LV hypertrophy, impaired LV myocardial contractility, and LV diastolic dysfunction predict heart failure in population-based studies.2,3Subjects with heart failure but with normal LV ejection fraction, that is, with diastolic heart failure, exhibit abnormal LV diastolic function.4 However, Doppler parameters of LV diastolic function may be abnormal in the absence of overt heart failure. Such a condition, called "isolated LV diastolic dysfunction," bears independent prognostic significance in population-based and clinical studies.2,3,5 Thus, regression of isolated LV diastolic dysfunction may be considered an important therapeutic target in hypertension.In the general adult population without congestive heart failure, ≈30% may show LV diastolic dysfunction of any degree.6 In high-risk subgroups (patients >65 years of age, those with hypertension, and those with LV hypertrophy), the prevalence of isolated LV diastolic dysfunction rises to 60–80%.7 On the other hand, LV diastolic dysfunction may be found in ≈26% of hypertensive subjects without LV hypertrophy and with normal myocardial contractility.8LV hypertrophy regression, proven to be protective in hypertension,9 is a major determinant of LV diastolic dysfunction regression in hypertensive subjects.7 However, it remains to be explored whether isolated LV diastolic dysfunction regression would impact independently on cardiovascular prevention in arterial hypertension.In the present issue of Hypertension, Solomon et al10 focused on isolated LV diastolic dysfunction regression in hypertension using a novel study design. The large majority of the participants in the study by Solomon et al10 had impaired LV relaxation, which was more prevalent than LV hypertrophy. The study tested the hypothesis that lower in-treatment blood pressure (BP) target could result in greater LV diastolic dysfunction regression. Accordingly, Doppler parameters of LV diastolic function were compared between a regimen defined "intensive," because of a predefined systolic BP (SBP) target of <130 mm Hg, and a second regimen defined "standard," because of a prespecified SBP target of <140 mm Hg. Combinations of valsartan, either 160 or 320 mg, plus amlodipine, either 5 or 10 mg, were used; additional antihypertensive medications were added if needed to reach the BP targets. The main finding of the study was that changes in Doppler parameters of LV diastolic function were comparable, on average, between the 2 treatment arms. Hence, on the matter of the impact of aggressive or standard antihypertensive treatment on LV diastolic dysfunction regression, there is apparently no good news.However, the study cannot be simply "dismissed" as a negative result. As may be seen in Table 4 and Figure 4 of the study,10 BP reduction by either treatment regimen was associated with improvement in the Doppler parameter of LV diastolic function. Given the SDs seen in Table 3, within-group variability of end-study systolic BP prevailed on between-group differences, generating a significant overlap in final BP levels in the 2 groups. In fact, ≈50% of the patients in the intensive treatment arm did not reach the systolic BP target of systolic BP <130 mm Hg, whereas ≈25% of the patients in the standard treatment arm actually had systolic BP <130 mm Hg at 6-month follow-up. Nevertheless, isovolumic relaxation time, which is a measure of active LV relaxation, was shorter with intensive treatment and was so even when normalized by heart rate, which is important, because β-blockade was allowed in the study and was used in more than half of the patients in the intensive treatment arm. Table 4 showed that reduction in isovolumic relaxation time was consistent and progressively greater with a greater percentage reduction in systolic BP in the study. Hence, the impact of the 2 treatment regimens on LV diastolic function may not be as similar as it appears.Whether changes reported by Solomon et al10 indicate "true" LV diastolic function improvement could be disputed. Doppler echocardiography can be a reproducible method for assessment of LV diastolic function.11 However, assessment of intrinsic LV diastolic properties, that is, LV relaxation and chamber compliance, cannot be derived immediately from traditional Doppler parameters and may require more sophisticated approaches.12 This is because traditional Doppler echocardiography, such as the popular isovolumic relaxation time, E deceleration time, and E/A, are "load dependent." In contrast, tissue Doppler imaging and color M-mode–derived parameters of LV diastolic function, such as E′ and E-wave propagation rate, are significantly less preload dependent,12 and their combination with traditional Doppler parameters allow for better representation of LV relaxation and LV chamber compliance.12 Solomon et al10 found that E′ increased and E/E′ decreased with BP lowering, suggestive of improved LV relaxation and increase in LV compliance. Therefore, increase in E and in E/A and shorter isovolumic relaxation time and E deceleration time reported at follow-up10 could be put in the right context of true improvement in LV diastolic relaxation (and LV suction capability) with BP lowering.On a separate issue, the study by Solomon et al10 showed that final brachial and central systolic BPs were slightly lower in patients in the intensive treatment arm compared with those in the standard treatment arm; in contrast, LV mass and left atrial volume index regressions, augmentation index reduction, and LV ejection fraction increase were similar in the 2 treatment regimens. A seducing hypothesis is that LV mass regression and arterial stiffness reduction in hypertension may be more relevant (or more reliable) than BP lowering as predictors of LV diastolic function improvement during treatment in arterial hypertension. Previously, LV hypertrophy regression was identified as a relevant marker of significant improvement in LV diastolic function.7 Nevertheless, to this extent, the literature lacks consistent data. For instance, a previous double-blind, randomized trial reported significant LV hypertrophy regression with antihypertensive treatment (enalapril or nifedipine gastrointestinal therapeutic system) but also reported little change in traditional Doppler diastolic parameters.13 Current literature suggests that different antihypertensive medications may have substantially different impacts on LV mass regression14 and on central BP reduction, which could result in different impacts of LV diastolic function during antihypertensive treatment. Moreover, great interest exists on whether changes in isolated LV diastolic dysfunction have prognostic relevance independent of LV mass and left atrial volume index regressions and changes in central BP.To date, most of our knowledge of the relationship between Doppler parameters of LV diastolic function and cardiovascular risk prediction has been on the basis of observational studies. However, a new paradigm is emerging in arterial hypertension, characterized by intervention studies, variability in BP lowering, LV hypertrophy regression, arterial stiffness reduction, and changes in systolic and diastolic myocardial performances. Information on relationships of regression of these markers of cardiovascular disease, often preclinical, to outcome will increase in the near future. This is a new exciting frontier that should lead to better understanding of the pathophysiology of heart failure prevention, also contributing to improvement of quality of life in arterial hypertension. For now, the fact that isolated LV diastolic dysfunction may regress by lowering BP in patients with uncontrolled arterial hypertension is in itself good news indeed.The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.DisclosuresNone.FootnotesCorrespondence to Vittorio Palmieri, via Napoli 816, San Felice a Cancello (CE), 81027 Naples, Italy. E-mail [email protected] References 1 Vakili BA, Okin PM, Devereux RB. Prognostic implications of left ventricular hypertrophy. Am Heart J. 2001; 141: 334–341.CrossrefMedlineGoogle Scholar2 Aurigemma GP, Gottdiener JS, Shemanski L, Gardin J, Kitzman D. Predictive value of systolic and diastolic function for incident congestive heart failure in the elderly: the Cardiovascular Health Study. J Am Coll Cardiol. 2001; 37: 1042–1048.CrossrefMedlineGoogle Scholar3 Bella JN, Palmieri V, Roman MJ, Liu JE, Welty TK, Lee ET, Fabsitz RR, Howard BV, Devereux RB. Mitral ratio of peak early to late diastolic filling velocity as a predictor of mortality in middle-aged and elderly adults: the Strong Heart Study. Circulation. 2002; 105: 1928–1933.LinkGoogle Scholar4 Zile MR, Baicu CF, Gaasch WH. Diastolic heart failure–abnormalities in active relaxation and passive stiffness of the left ventricle. N Engl J Med. 2004; 350: 1953–1959.CrossrefMedlineGoogle Scholar5 Abhayaratna WP, Marwick TH, Smith WT, Becker NG. Characteristics of left ventricular diastolic dysfunction in the community: an echocardiographic survey. Heart. 2006; 92: 1259–1264.CrossrefMedlineGoogle Scholar6 Kuznetsova T, Herbots L, Lopez B, Jin Y, Richart T, Thijs L, Gonzalez A, Herregods MC, Fagard RH, Diez J, Staessen JA. Prevalence of left ventricular diastolic dysfunction in a general population. Circ Heart Fail. 2009; 2: 105–112.LinkGoogle Scholar7 Wachtell K, Bella JN, Rokkedal J, Palmieri V, Papademetriou V, Dahlöf B, Aalto T, Gerdts E, Devereux RB. Change in diastolic left ventricular filling after one year of antihypertensive treatment: the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) Study. Circulation. 2002; 105: 1071–1076.CrossrefMedlineGoogle Scholar8 Palmieri V, Russo C, Palmieri EA, Arezzi E, Pezzullo S, Minichiello S, Martino S, Migliaresi P, Celentano A. Isolated left ventricular diastolic dysfunction: implications for exercise left ventricular performance in patients without congestive heart failure. J Am Soc Echocardiogr. 2006; 19: 491–498.CrossrefMedlineGoogle Scholar9 Devereux RB, Wachtell K, Gerdts E, Boman K, Nieminen MS, Papademetriou V, Rokkedal J, Harris K, Aurup P, Dahlöf B. Prognostic significance of left ventricular mass change during treatment of hypertension. JAMA. 2004; 292: 2350–2356.CrossrefMedlineGoogle Scholar10 Solomon SD, Verma A, Desai A, Hassanein A, Izzo J, Oparil S, Lacourciere Y, Lee J, Seifu Y, Hilkert RJ, Rocha R, Pitt B; for the Exforge Intensive Control of Hypertension to Evaluate Efficacy in Diastolic Dysfunction Investigators. Effect of intensive versus standard blood pressure lowering on diastolic function in patients with uncontrolled hypertension and diastolic dysfunction. Hypertension. 2010; 55: 241–248.LinkGoogle Scholar11 Palmieri V, Innocenti F, Pini R, Celentano A. Reproducibility of Doppler echocardiographic assessment of left ventricular diastolic function in multicenter setting. J Am Soc Echocardiogr. 2005; 18: 99–106.CrossrefMedlineGoogle Scholar12 Oh JK, Hatle L, Tajik AJ, Little WC. Diastolic heart failure can be diagnosed by comprehensive two-dimensional and Doppler echocardiography. J Am Coll Cardiol. 2006; 47: 500–506.CrossrefMedlineGoogle Scholar13 Devereux RB, Palmieri V, Sharpe N, De QV, Bella JN, de Simone G, Walker JF, Hahn RT, Dahlöf B. Effects of once-daily angiotensin-converting enzyme inhibition and calcium channel blockade-based antihypertensive treatment regimens on left ventricular hypertrophy and diastolic filling in hypertension: the Prospective Randomized Enalapril Study Evaluating Regression of Ventricular Enlargement (PRESERVE) Trial. Circulation. 2001; 104: 1248–1254.CrossrefMedlineGoogle Scholar14 Fagard RH, Celis H, Thijs L, Wouters S. Regression of left ventricular mass by antihypertensive treatment: a meta-analysis of randomized comparative studies. Hypertension. 2009; 54: 1084–1091.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Iida M and Ishiguro Y (2021) Association of prediabetes with impaired left atrial contractility in patients with never-treated hypertension, Journal of Diabetes and its Complications, 10.1016/j.jdiacomp.2020.107827, 35:3, (107827), Online publication date: 1-Mar-2021. Gao Q, Cui X, Dong F, Fan W, Li P, Liu J, Lu J, Meng Y, Qu W, Zhou K and Lin Q (2020) Efficacy and Safety of Bushenjiangya-Optimized Granule for Left Ventricular Diastolic Dysfunction in Hypertensive Patients: A Double-Blind, Randomized, Placebo-Controlled Trial, Evidence-Based Complementary and Alternative Medicine, 10.1155/2020/7190352, 2020, (1-6), Online publication date: 19-May-2020. 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Louridas G and Lourida K (2016) Heart Failure in Patients with Preserved Ejection Fraction: Questions Concerning Clinical Progression, Journal of Cardiovascular Development and Disease, 10.3390/jcdd3030027, 3:3, (27) February 2010Vol 55, Issue 2 Advertisement Article InformationMetrics https://doi.org/10.1161/HYPERTENSIONAHA.109.144717PMID: 19996064 Originally publishedDecember 7, 2009 PDF download Advertisement SubjectsClinical StudiesEchocardiographyHeart Failure
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