Effect of Spironolactone on Myocardial Fibrosis and Other Clinical Variables in Patients with Hypertrophic Cardiomyopathy

Maron, Martin S.; Chan, Raymond H.; Kapur, Navin K.; Jaffe, Iris Z.; McGraw, Adam P.; Kerur, Raj; Maron, Barry J.; Udelson, James E.

doi:10.1016/j.amjmed.2018.02.025

Cited by 59 publications

(32 citation statements)

References 15 publications

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“…Aldosterone signalling has also been implicated in fibrosis in HCM 52 ; however, spironolactone was demonstrated to be ineffective in a recent clinical trial (NCT00879060). 26 Similarly, N-acetyl cysteine showed promise with regard to fibrosis regression in pre-clinical studies, 53,54 but had no significant effect on imaging measures of hypertrophy or fibrosis in a small clinical trial (HALT-HCM, NCT01537926). 27 Finally, atorvastatin demonstrated effects on suppression of hypertrophy in pre-clinical models, 55 but had no effect and poor treatment adherence in a small early feasibility study in humans.…”

Section: Fibrosis and Adverse Remodelling -Angiotensin II Receptor Blmentioning

confidence: 99%

“…Recent evidence has also demonstrated important gender differences in HCM, with women being older and more symptomatic at presentation, and perhaps having lower survival when compared to men . Novel pharmacotherapies have attempted to address several important mechanisms in HCM ( Tables and ) …”

Section: Novel Pharmacotherapies For Hypertrophic Cardiomyopathymentioning

confidence: 99%

“…[14][15][16][17] Novel pharmacotherapies have attempted to address several important mechanisms in HCM ( Tables 1 and 2). [18][19][20][21][22][23][24][25][26][27][28]…”

Section: Introductionmentioning

confidence: 99%

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Hypertrophic cardiomyopathy: the future of treatment

Tuohy

Kaul

Song

et al. 2020

European J of Heart Fail

122

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Hypertrophic cardiomyopathy (HCM) is a heterogeneous genetic disorder most often caused by sarcomeric mutations resulting in left ventricular hypertrophy, fibrosis, hypercontractility, and reduced compliance. It is the most common inherited monogenic cardiac condition, affecting 0.2% of the population. Whereas currently available therapies for HCM have been effective in reducing morbidity, there remain important unmet needs in the treatment of both the obstructive and non‐obstructive phenotypes. Novel pharmacotherapies directly target the molecular underpinnings of HCM, while innovative procedural techniques may soon offer minimally‐invasive alternatives to current septal reduction therapy. With the advent of embryonic gene editing, there now exists the potential to correct underlying genetic mutations that may result in disease. This article details the recent developments in the treatment of HCM including pharmacotherapy, septal reduction procedures, mitral valve manipulation, and gene‐based therapies.

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Section: Fibrosis and Adverse Remodelling -Angiotensin II Receptor Blmentioning

confidence: 99%

Section: Novel Pharmacotherapies For Hypertrophic Cardiomyopathymentioning

confidence: 99%

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Hypertrophic cardiomyopathy: the future of treatment

Tuohy

Kaul

Song

et al. 2020

European J of Heart Fail

122

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“…В ряде исследований, включая полногеномный поиск ассоциаций (genome-wide association study -GWAS), показаны модифицирующие эффекты полиморфизмов, не редких вариантов, расположенных, как в самих генах саркомера и его окружения [26,27], так и генах, ассоциированных с развитием вторичной гипертрофии, в основном ренин-ангиотензин-альдостероновой системы (РААС) [28][29][30]. Последнее указывает на, возможно, общие пути патогенеза ГКМП и вторичной гипертрофии, однако применение препаратов из группы блокаторов РААС не продемонстрировало влияния ни на гипертрофию, ни на фиброз у больных с ГКМП [31,32]. В старшей возрастной группе, когда прогноз жизни оказывается более благоприятным, возможно, большее значение для пенетрантности относительно доброкачественных генетических вариантов имеют внешние факторы, возникающие с течением жизни, что может объяснять отсроченный дебют болезни.…”

Section: ïðè÷èíû ïîçäíåãî äåáþòà ãêìïunclassified

Hypertrophic cardiomyopathy in elderly: causes, diagnostic and treatment approaches

Чумакова

2020

Terapevticheskii arkhiv

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“…Elevated level of N-terminal pro B-type natriuretic peptide is associated with myocardial brosis in hypertrophic cardiomyopathy patients with preserved ejection fraction Background Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiomyopathy and its pathological features manifest as cardiac myocyte hypertrophy, disarray, and brosis [1,2]. Although, myocardial brosis is not so much a problem in itself, it is a feature of HCM with important clinical implications such as predisposition to sudden cardiac death (SCD) and progression to advanced disease [3,4]. Furthermore, myocardial brosis may be reversible and has been suggested as a powerful therapeutic target and prognosticator [5,6].…”

mentioning

confidence: 99%

Elevated level of N-terminal pro B-type natriuretic peptide is associated with myocardial fibrosis in hypertrophic cardiomyopathy patients with preserved ejection fraction

Shi

Liu

et al. 2020

Preprint

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Background: Myocardial fibrosis assessed by late gadolinium enhancement (LGE) on cardiovascular magnetic resonance (CMR) has been reported to be significantly correlated with cardiovascular outcomes in hypertrophic cardiomyopathy (HCM) patients. However, data regarding non-invasive markers for detecting myocardial fibrosis were inconsistent and, not systematically evaluated in HCM patients with preserved ejection fraction (EF).Methods: In this study, 86 HCM patients with preserved EF and 33 controls were enrolled. The left ventricular function, end-diastolic maximum wall thickness (MWT), global systolic strains and extent of LGE (% LGE) were assessed. The biochemical indices were also recorded before the CMR examination.Results: Serum high-sensitivity cardiac troponin I (hs-cTnI) and N-terminal pro b-type natriuretic peptide (Nt-proBNP) levels were elevated in LGE-positive patients compared with LGE-negative patients (p < 0.05 for all). The LGE-positive patients had lower global longitudinal (GLS) and circumferential (GCS) strains than the LGE-negative group and the healthy controls (p < 0.05 for all). The LGE% was independently associated with the Nt-proBNP levels (standardized β = 0.627, p < 0.001), beta-blocker treatment (standardized β = -0.372, p = 0.01), MWT (standardized β = 0.481, p = 0.001) and GCS (standardized β = 0.406, p = 0.013). In the receiver operating characteristic (ROC) curve analysis, the combined parameters of Nt-proBNP ≥ 108 pg/mL and MWT ≥ 17.3 mm had good diagnostic performance for LGE, with a specificity of 81.3% and sensitivity of 70.0%.Conclusions: This study suggests that Nt-proBNP may be a potential biomarker associated with LGE% and, combined with MWT, was useful in detecting myocardial fibrosis in HCM patients with preserved EF. Additionally, LV GCS may be a more sensitive indicator for reflecting the presence of myocardial fibrosis than GLS.

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Effect of Spironolactone on Myocardial Fibrosis and Other Clinical Variables in Patients with Hypertrophic Cardiomyopathy

Cited by 59 publications

References 15 publications

Hypertrophic cardiomyopathy: the future of treatment

Hypertrophic cardiomyopathy: the future of treatment

Hypertrophic cardiomyopathy in elderly: causes, diagnostic and treatment approaches

Elevated level of N-terminal pro B-type natriuretic peptide is associated with myocardial fibrosis in hypertrophic cardiomyopathy patients with preserved ejection fraction

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