Does Gestational Hypertension Contribute to Myocardial Fibrosis and Diastolic Dysfunction in Adult Offspring?

2021 ◽  
Vol 78 (23) ◽  
pp. e297
Author(s):  
David W.J. Armstrong ◽  
M. Yat Tse ◽  
Stephen C. Pang
Keyword(s):  
Diastolic Dysfunction ◽  
Myocardial Fibrosis ◽  
Gestational Hypertension ◽  
Adult Offspring

scholarly journals The Link Between Parathyroid Hormone, Myocardial Fibrosis and Diastolic Dysfunction in Individuals with Mild Renal Impairment

2012 ◽  
Vol 21 ◽  
pp. S228-S229
Author(s):  
T. Stanton ◽  
R. Leano ◽  
W. Petchey ◽  
B. Halsuka ◽  
N. Isbel ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Renal Impairment ◽  
Diastolic Dysfunction ◽  
Myocardial Fibrosis ◽  
Mild Renal Impairment

scholarly journals Diffuse Myocardial Fibrosis Is a Common Feature of Sickle Cell Anemia That Is Associated with Diastolic Dysfunction and Restrictive Cardiac Physiology

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 8-8
Author(s):  
Omar Niss ◽  
Michael D. Taylor ◽  
Robert Fleck ◽  
Tarek Alsaied ◽  
Jeffrey Towbin ◽  
...  
Keyword(s):  
Ejection Fraction ◽  
Diastolic Dysfunction ◽  
Myocardial Fibrosis ◽  
Research Funding ◽  
Systolic Function ◽  
Diffuse Myocardial Fibrosis ◽  
Normal Systolic Function ◽  
Lv Ejection Fraction ◽  
Focal Fibrosis ◽  
Restrictive Physiology

Abstract Background: We have recently shown that the cardiomyopathy of sickle cell anemia (SCA) is characterized by restrictive physiology (diastolic dysfunction, left atrial [LA] enlargement and normal systolic function) superimposed on hyperdynamic features (left ventricular [LV] enlargement and eccentric hypertrophy) (JACC Cardiovasc Imaging 9:244-253;2016; PNAS 2016 in press). Similar to other restrictive cardiomyopathies, SCA-related cardiomyopathy may lead to mild, secondary pulmonary hypertension (PH) with elevated tricuspid regurgitant jet velocity (TRV), and can be complicated by arrhythmias and sudden death. Diastolic dysfunction is the principal pathology leading to restrictive physiology. Myocardial fibrosis is a common cause of non-SCA restrictive physiology, but the cause of the diastolic dysfunction that underlies SCA-related cardiomyopathy is undetermined. Focal fibrosis, as detected by late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging (CMR), is rare in SCA. However, diffuse myocardial fibrosis, which is not detected by LGE, has not been studied before in SCA. Therefore, we aimed to detect myocardial fibrosis in SCA using a novel CMR T1-mapping technique to quantify the myocardial extracellular volume (ECV) fraction, which correlates with histologic diffuse fibrosis. Methods: We conducted a prospective study of children and adults with SCA (NCT02410811) who underwent CMR, echocardiography, and laboratory testing (including N-terminal pro-brain type natriuretic peptide [NT-proBNP], a marker of ventricular stress). ECV was measured from pre- and post-gadolinium T1 maps using a modified Look-Locker inversion recovery (MOLLI) sequence. Chamber sizes and cardiac performance were evaluated using CMR, while TRV and diastolic parameters were measured by echocardiography. Results: Twenty-five patients with a median age of 19 years (range 6-61 years) were evaluated. ECV was increased in all SCA patients (mean 44 ± 8% vs. 25 ± 3% in normal subjects, P<0.001). One patient had focal fibrosis by LGE and one had systolic dysfunction. Among patients with normal systolic function, 17 patients (71%) had diastolic abnormalities and 7 (29%) had normal diastolic function. Seven out of 17 patients with diastolic abnormalities (29% of the total group) met the definition of diastolic dysfunction, and 10 had inconclusive classification. Patients with diastolic dysfunction had significantly higher ECV (49 ± 7% vs 37 ± 4%, P=0.01; Panel A), NT-proBNP (191 ± 261 vs. 33 ± 33 pg/mL, P=0.04; Panel B), and lower hemoglobin (8.4±0.3 vs.10.9±1.4 g/dL, P=0.004, Panel C) compared to patients with normal diastolic function. Systolic function was similar in both groups (LV ejection fraction 61 ± 4% vs. 62 ± 3.4%, P=0.86). In patients with higher ECV (³40%), LV diastolic abnormalities were more common (99% vs 33%, P=0.003) and LA volume index was significantly increased (57 ± 11 vs. 46 ± 12 mL/m2, P=0.04) compared to patients with ECV <40%. Increased ECV was associated with anemia (R=-0.46, P=0.03; Panel D) and elevated NT-proBNP (R=0.62, P=0.001; Panel E), but not with LV ejection fraction (P=0.66; Panel F), LV mass (P=0.92) or TRV (P=0.65). Conclusions: ECV is markedly elevated in SCA, indicating the presence of significant diffuse myocardial fibrosis in all patients studied. High ECV is associated with more severe anemia, diastolic dysfunction, and high NT-proBNP. Diffuse myocardial fibrosis is a novel process underlying diastolic dysfunction and SCA-related cardiomyopathy, the features of which may be mistaken for pulmonary arterial hypertension. Identifying and therapeutically targeting the root-cause of myocardial fibrosis, or interrupting the development of myocardial fibrosis, should be studied to mitigate cardiopulmonary disease and decrease early mortality in SCA. Figure. Figure. Disclosures Quinn: Silver Lake Research Corporation: Consultancy; Eli Lilly: Research Funding; Amgen: Research Funding.

Abstract 4890: Myocardial Fibrosis and Diastolic Dysfunction Following Calcium-Channel Blockers or Angiotensin II Receptor Blockers in Hypertensive Patients

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Chikako Yoshida ◽  
Takeshi Tsujino ◽  
Akiko Goda ◽  
Mika Matsumoto ◽  
Yoshiro Naito ◽  
...  
Keyword(s):  
Diastolic Dysfunction ◽  
Myocardial Fibrosis ◽  
Collagen Degradation ◽  
Channel Blockers ◽  
Angiotensin Ii Receptor ◽  
Hypertensive Patients ◽  
Collagen Production ◽  
Receptor Blockers ◽  
Lv Diastolic Dysfunction ◽  
Lv Diastolic Function

Objectives : Myocardial fibrosis develops in the hypertensive heart, and brings about LV diastolic dysfunction. Myocardial fibrosis is regulated by collagen production and degradation. Collagen degradation is regulated by matrix metalloproteinases (MMPs), a family of zinc-dependent interstitial enzymes, and their tissue inhibitors (TIMPs). We investigated how long-term administration of calcium-channel blockers (CCB) or Angiotensin II receptor blockers (ARB) affects collagen production/degradation and LV diastolic dysfunction. Methods : Study population consisted of 44 untreated hypertensive patients (31 females, 13 males, mean age:57±11 years). They were randomly assigned to one of the 2 groups: CCB group in which Amlodipine of 5–10mg was given daily (n=22) and ARB group in which Losartan of 50–100mg was given daily (n=22). LV mass index (LVMI) and tissue Doppler early diastolic mitral annular velocity (E′) were echocardiographically assessed before and 6 and 12 months after treatment. Procollagen type I C-terminal propeptide (PICP) was determined with enzyme immunoassay as a serum marker of collagen production, while MMP-2 and TIMP-1 were determined with ELISA as makers of collagen degradation. Results (table ): E′ increased in the ARB group but not in the CCB group while reductions in blood pressure (BP) and LVMI were comparable between the group. PICP did not change after treatment in either group, but MMP-2 increased only in the ARB group. TIMP-1 did not change in either group. Conclusions : In spite of similar reduction of SBP and LVMI, ARB provided larger benefits on LV diastolic function than CCB. Collagen production was constant in both groups, but ARB facilitated more collagen degradation than CCB, and the difference should have contributed to the impact on LV diastolic function.

scholarly journals Neuregulin-1 antagonizes myocardial fibrosis and diastolic dysfunction in angiotensin-II treated mice

2013 ◽  
Vol 34 (suppl 1) ◽  
pp. P2434-P2434 ◽  
Author(s):  
A.- S. Hervent ◽  
L. Vandekerckhove ◽  
G. W. De Keulenaer
Keyword(s):  
Angiotensin Ii ◽  
Diastolic Dysfunction ◽  
Myocardial Fibrosis ◽  
Neuregulin 1

Effect of Anti-oxidant Treatment on Hyperhomocysteinemia-induced Myocardial Fibrosis and Diastolic Dysfunction

2008 ◽  
Vol 27 (11) ◽  
pp. 1237-1241 ◽  
Author(s):  
Jacob Joseph ◽  
Lija Joseph ◽  
Sulochana Devi ◽  
Richard H. Kennedy
Keyword(s):  
Diastolic Dysfunction ◽  
Myocardial Fibrosis ◽  
Anti Oxidant

P-270 Effects of Valsartan on Myocardial Fibrosis and Diastolic Dysfunction in Hypertensives

2009 ◽  
Vol 4 ◽  
pp. S128-S129
Author(s):  
Hisashi Kai ◽  
Yoshihiko Mizuta ◽  
Tsutomu Imaizumi
Keyword(s):  
Diastolic Dysfunction ◽  
Myocardial Fibrosis

scholarly journals Maternal Diastolic Dysfunction and Left Ventricular Geometry in Gestational Hypertension

Hypertension ◽  
2001 ◽  
Vol 37 (5) ◽  
pp. 1209-1215 ◽  
Author(s):  
Herbert Valensise ◽  
Gian Paolo Novelli ◽  
Barbara Vasapollo ◽  
Giancarlo Di Ruzza ◽  
Maria Elisabetta Romanini ◽  
...  
Keyword(s):  
Diastolic Dysfunction ◽  
Gestational Hypertension ◽  
Left Ventricular ◽  
Left Ventricular Geometry ◽  
Ventricular Geometry

scholarly journals Hypertensive Myocardial Fibrosis and Diastolic Dysfunction

Hypertension ◽  
2004 ◽  
Vol 43 (4) ◽  
pp. 739-745 ◽  
Author(s):  
Fumitaka Kuwahara ◽  
Hisashi Kai ◽  
Keisuke Tokuda ◽  
Motohiro Takeya ◽  
Akira Takeshita ◽  
...  
Keyword(s):  
Diastolic Dysfunction ◽  
Myocardial Fibrosis
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