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Incomplete structural reverse remodeling from late-stage left ventricular hypertrophy impedes the recovery of diastolic but not systolic dysfunction in rats.
J Hypertens 2019; 37(6):1200-1212JH

Abstract

OBJECTIVE

Pressure overload-induced left ventricular myocardial hypertrophy (LVH) regresses after pressure unloading. However, distinct structural alterations become less reversible during the progression of LVH, which might influence the restoration of cardiac function. Here, we investigated how a reverse remodeling process from early versus late-stage LVH affects different aspects of left ventricular function.

METHODS

Pressure overload was induced in rats for 6, 12 and 18 weeks. Sham-operated animals were used as controls. Pressure unloading was evoked by removing the aortic constriction at week 6 (early-debanded) and week 12 (late-debanded). Echocardiography and histological analyses were carried out to detect structural alterations. Pressure-volume analysis was performed to assess left ventricular function. Molecular alterations were analyzed by quantitative real-time-PCR, and western blot.

RESULTS

Myocardial hypertrophy regressed to a similar degree in early and late-debanded groups. Accordingly, no differences were detected in the extent of regression regarding left ventricular mass, cardiomyocyte diameter, heart weight-to-tibial length ratio and beta-to-alpha myosin heavy chain expression. In contrast, resorption of interstitial and perivascular myocardial fibrosis was only detected in the early-debanded group, whereas it persisted in the late-debanded group. Removing the aortic constriction normalized ventriculo-arterial coupling and increased systolic performance in both debanded groups. However, the residual dysfunction in active relaxation and passive stiffness was more severe in the late-debanded compared to the early-debanded group.

CONCLUSION

Early debanding led to complete structural reverse remodeling (reduced hypertrophy and fibrosis) and full restoration of left ventricular function. In contrast, myocardial fibrosis persisted after late debanding, which impeded the normalization of diastolic but not systolic function.

Authors+Show Affiliations

Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany. Heart and Vascular Center, Semmelweis University, Budapest, Hungary.Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany.Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany.Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany.Heart and Vascular Center, Semmelweis University, Budapest, Hungary.Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany. Heart and Vascular Center, Semmelweis University, Budapest, Hungary.Heart and Vascular Center, Semmelweis University, Budapest, Hungary.Heart and Vascular Center, Semmelweis University, Budapest, Hungary.Heart and Vascular Center, Semmelweis University, Budapest, Hungary.Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany.Heart and Vascular Center, Semmelweis University, Budapest, Hungary.Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31026245

Citation

Ruppert, Mihály, et al. "Incomplete Structural Reverse Remodeling From Late-stage Left Ventricular Hypertrophy Impedes the Recovery of Diastolic but Not Systolic Dysfunction in Rats." Journal of Hypertension, vol. 37, no. 6, 2019, pp. 1200-1212.
Ruppert M, Korkmaz-Icöz S, Loganathan S, et al. Incomplete structural reverse remodeling from late-stage left ventricular hypertrophy impedes the recovery of diastolic but not systolic dysfunction in rats. J Hypertens. 2019;37(6):1200-1212.
Ruppert, M., Korkmaz-Icöz, S., Loganathan, S., Jiang, W., Oláh, A., Sayour, A. A., ... Szabó, G. (2019). Incomplete structural reverse remodeling from late-stage left ventricular hypertrophy impedes the recovery of diastolic but not systolic dysfunction in rats. Journal of Hypertension, 37(6), pp. 1200-1212. doi:10.1097/HJH.0000000000002042.
Ruppert M, et al. Incomplete Structural Reverse Remodeling From Late-stage Left Ventricular Hypertrophy Impedes the Recovery of Diastolic but Not Systolic Dysfunction in Rats. J Hypertens. 2019;37(6):1200-1212. PubMed PMID: 31026245.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Incomplete structural reverse remodeling from late-stage left ventricular hypertrophy impedes the recovery of diastolic but not systolic dysfunction in rats. AU - Ruppert,Mihály, AU - Korkmaz-Icöz,Sevil, AU - Loganathan,Sivakkanan, AU - Jiang,Weipeng, AU - Oláh,Attila, AU - Sayour,Alex Ali, AU - Barta,Bálint András, AU - Karime,Christian, AU - Merkely,Béla, AU - Karck,Matthias, AU - Radovits,Tamás, AU - Szabó,Gábor, PY - 2019/4/27/entrez PY - 2019/4/27/pubmed PY - 2019/4/27/medline SP - 1200 EP - 1212 JF - Journal of hypertension JO - J. Hypertens. VL - 37 IS - 6 N2 - OBJECTIVE: Pressure overload-induced left ventricular myocardial hypertrophy (LVH) regresses after pressure unloading. However, distinct structural alterations become less reversible during the progression of LVH, which might influence the restoration of cardiac function. Here, we investigated how a reverse remodeling process from early versus late-stage LVH affects different aspects of left ventricular function. METHODS: Pressure overload was induced in rats for 6, 12 and 18 weeks. Sham-operated animals were used as controls. Pressure unloading was evoked by removing the aortic constriction at week 6 (early-debanded) and week 12 (late-debanded). Echocardiography and histological analyses were carried out to detect structural alterations. Pressure-volume analysis was performed to assess left ventricular function. Molecular alterations were analyzed by quantitative real-time-PCR, and western blot. RESULTS: Myocardial hypertrophy regressed to a similar degree in early and late-debanded groups. Accordingly, no differences were detected in the extent of regression regarding left ventricular mass, cardiomyocyte diameter, heart weight-to-tibial length ratio and beta-to-alpha myosin heavy chain expression. In contrast, resorption of interstitial and perivascular myocardial fibrosis was only detected in the early-debanded group, whereas it persisted in the late-debanded group. Removing the aortic constriction normalized ventriculo-arterial coupling and increased systolic performance in both debanded groups. However, the residual dysfunction in active relaxation and passive stiffness was more severe in the late-debanded compared to the early-debanded group. CONCLUSION: Early debanding led to complete structural reverse remodeling (reduced hypertrophy and fibrosis) and full restoration of left ventricular function. In contrast, myocardial fibrosis persisted after late debanding, which impeded the normalization of diastolic but not systolic function. SN - 1473-5598 UR - https://www.unboundmedicine.com/medline/citation/31026245/Incomplete_structural_reverse_remodeling_from_late-stage_left_ventricular_hypertrophy_impedes_the_recovery_of_diastolic_but_not_systolic_dysfunction_in_rats L2 - http://Insights.ovid.com/pubmed?pmid=31026245 DB - PRIME DP - Unbound Medicine ER -