Hypertrophic cardiomyopathy and left ventricular hypertrophy in hypertensive heart disease with mildly reduced or preserved ejection fraction: insight from altered mechanics and native T1 mapping

2017 ◽  
Vol 72 (10) ◽  
pp. 835-843 ◽  
Author(s):  
L.-M. Wu ◽  
D.-A.L. An ◽  
Q.-Y. Yao ◽  
Y.-R.Z. Ou ◽  
Q. Lu ◽  
...  
Keyword(s):  
Heart Disease ◽  
Hypertrophic Cardiomyopathy ◽  
Left Ventricular Hypertrophy ◽  
Ejection Fraction ◽  
Ventricular Hypertrophy ◽  
T1 Mapping ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Preserved Ejection Fraction ◽  
Native T1

scholarly journals Native T1 mapping for differential diagnosis of left ventricular hypertrophy

2021 ◽  
Vol 22 (Supplement_2) ◽  
Author(s):  
D Lavall ◽  
NH Vosshage ◽  
S Stoebe ◽  
T Denecke ◽  
A Hagendorff ◽  
...  
Keyword(s):  
Differential Diagnosis ◽  
Heart Disease ◽  
Hypertrophic Cardiomyopathy ◽  
Cardiac Amyloidosis ◽  
T1 Mapping ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Characteristic Analysis ◽  
Native T1 ◽  
Healthy Control

Abstract Funding Acknowledgements Type of funding sources: None. Purpose The aim of this study was to investigate native T1 mapping cardiac magnetic resonance (CMR) tomography for the differential diagnosis of left ventricular (LV) hypertrophy. Background Mapping techniques are useful to characterize myocardial tissue abnormalities, particularly cardiac amyloidosis. However, specific cut-off values to differentiate LV hypertrophic phenotypes on 3.0 tesla CMR scanners have not been established, yet. Methods We retrospectively identified patients in the CMR database of Leipzig university hospital with increased LV wall thickness (≥12mm diameter at end-diastole) who were referred for the evaluation of LV hypertrophy or ischemia between 2017 and 2020 on a 3T scanner (Philips Achieva). Patients with suspected or confirmed myocarditis were excluded. Diagnosis of cardiac amyloidosis was made by either biopsy or non-invasively by bone scintigraphy and screening for monoclonal gammopathy. T1 mapping was measured as global mean value from 3 short axis slices of the LV. Results 128 consecutive patients were included in the study. 31 subjects without evidence of structural heart disease served as healthy control. The final diagnosis was cardiac amyloidosis in 24 patients (5 patients with light-chain, 18 with transthyretin amyloidosis, 1 undetermined), hypertrophic cardiomyopathy in 24, and hypertensive heart disease in 80 patients. Mean age of patients was 65 ± 13years, 84% were male. LV mass was increased in patients with LV hypertrophy compared to healthy control (p < 0.001). Native T1 values of the LV myocardium were higher in patients with cardiac amyloidosis (1409 ± 59ms, p < 0.0001 vs. all other groups) compared to healthy control (1225 ± 21ms), patients with hypertrophic cardiomyopathy (HCM; 1263 ± 43ms) and hypertensive heart disease (HHD; 1257 ± 41ms) (Figure). Patients with hypertrophic cardiomyopathy and hypertensive heart disease did not differ in their native T1 values, but both groups were increased compared to healthy control (p < 0.01). Receiver operating characteristic analysis of native T1 values demonstrated an area under the curve for the detection of cardiac amyloidosis of 0.9954 (p < 0.0001) vs. hypertrophic cardiomyopathy, hypertensive heart disease and healthy control. The optimal cut-off value was 1341ms, with a sensitivity of 100% and a specificity of 97%. Conclusion Native T1 mapping has high diagnostic accuracy for the diagnosis of cardiac amyloidosis among patients with LV hypertrophy. These data need confirmation in a prospective clinical trial. Study ID DRKS00022048

scholarly journals Potential of valsartan+sacubitril therapy in hypertensive heart disease

2021 ◽  
Vol 26 (7) ◽  
pp. 4568
Author(s):  
A. G. Ovchinnikov ◽  
A. D. Gvozdeva ◽  
A. V. Potekhina ◽  
M. V. Vitsenya ◽  
F. T. Ageev
Keyword(s):  
Heart Failure ◽  
Heart Disease ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Hypertensive Heart Disease ◽  
Hypotensive Effect ◽  
Left Ventricular ◽  
Preserved Ejection Fraction ◽  
Neprilysin Inhibitor ◽  
Is Development

The course of hypertension is often complicated by left ventricular hypertrophy (or hypertensive heart disease, HHD). The main “corridor” of natural HHD is development of heart failure with preserved ejection fraction (HFpEF). With HFpEF, the bioavailability of natriuretic peptides (NP) is significantly reduced, as a result of which the activity of cGMP-PKG signaling pathway, which plays a key role in maintaining normal diastolic function, weakens. It is possible to increase the activity of this pathway using the neprilysin inhibitor sacubitril. In case of HFpEF, the greatest efficacy from valsartan+sacubitril therapy should be expected in patients with severe concentric LVH, who have the most pronounced natriuretic peptide deficiency. Valsartan+sacubitril therapy has a clear hypotensive effect, causes a reversal of left ventricular hypertrophy and fibrosis. Since no effective treatment has yet been found for HFpEF, the main way for HHD treatment should be to prevent the diastolic dysfunction progression, which justifies valsartan+sacubitril therapy starting from the early/ asymptomatic stages.

scholarly journals Left ventricular fibrosis and hypertrophy are associated with mortality in heart failure with preserved ejection fraction

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Pankaj Garg ◽  
Hosamadin Assadi ◽  
Rachel Jones ◽  
Wei Bin Chan ◽  
Peter Metherall ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
T1 Mapping ◽  
Left Ventricular ◽  
Preserved Ejection Fraction ◽  
Native T1 ◽  
Lv Mass ◽  
All Cause Mortality ◽  
Ventricular Fibrosis

AbstractCardiac magnetic resonance (CMR) is emerging as an important tool in the assessment of heart failure with preserved ejection fraction (HFpEF). This study sought to investigate the prognostic value of multiparametric CMR, including left and right heart volumetric assessment, native T1-mapping and LGE in HFpEF. In this retrospective study, we identified patients with HFpEF who have undergone CMR. CMR protocol included: cines, native T1-mapping and late gadolinium enhancement (LGE). The mean follow-up period was 3.2 ± 2.4 years. We identified 86 patients with HFpEF who had CMR. Of the 86 patients (85% hypertensive; 61% males; 14% cardiac amyloidosis), 27 (31%) patients died during the follow up period. From all the CMR metrics, LV mass (area under curve [AUC] 0.66, SE 0.07, 95% CI 0.54–0.76, p = 0.02), LGE fibrosis (AUC 0.59, SE 0.15, 95% CI 0.41–0.75, p = 0.03) and native T1-values (AUC 0.76, SE 0.09, 95% CI 0.58–0.88, p < 0.01) were the strongest predictors of all-cause mortality. The optimum thresholds for these were: LV mass > 133.24 g (hazard ratio [HR] 1.58, 95% CI 1.1–2.2, p < 0.01); LGE-fibrosis > 34.86% (HR 1.77, 95% CI 1.1–2.8, p = 0.01) and native T1 > 1056.42 ms (HR 2.36, 95% CI 0.9–6.4, p = 0.07). In multivariate cox regression, CMR score model comprising these three variables independently predicted mortality in HFpEF when compared to NTproBNP (HR 4 vs HR 1.65). In non-amyloid HFpEF cases, only native T1 > 1056.42 ms demonstrated higher mortality (AUC 0.833, p < 0.01). In patients with HFpEF, multiparametric CMR aids prognostication. Our results show that left ventricular fibrosis and hypertrophy quantified by CMR are associated with all-cause mortality in patients with HFpEF.

Methods for detection of left ventricular hypertrophy: Application to hypertensive heart disease

1993 ◽  
Vol 14 (suppl D) ◽  
pp. 8-15 ◽  
Author(s):  
R. B. Devereux ◽  
M. J. Koren ◽  
G. de Simone ◽  
P. M. Okin ◽  
P. Kligfield
Keyword(s):  
Heart Disease ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Hypertensive Heart Disease ◽  
Left Ventricular
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