ReviewClinical utility of natriuretic peptides and troponins in hypertrophic cardiomyopathy
Section snippets
Background
Hypertrophic cardiomyopathy (HCM), an inherited cardiomyopathy occurring in about 1 in 500 people, is characterized by left ventricular hypertrophy (LVH) in the absence of underlying pressure overload. Approximately one third of the cases are due to one of at least 11 identifiable sarcomere protein mutations, generally autosomal dominant, leading histologically to myocardial and myocyte hypertrophy, myofibril disarray, myocardial fibrosis and abnormal intramural coronary arteries [1]. The
Pathophysiologic mechanisms of natriuretic peptide and troponin release in HCM
The inactive pro-peptide proBNP is released predominantly from the ventricles in response to increased myocyte stretch from increased left ventricular (LV) wall stress and pressure. ProBNP is cleaved by the enzyme corin into the bioactive hormone BNP and the inactive molecule NT-proBNP [2]. Measured NT-proBNP levels are much higher than BNP levels due to slower clearance of the former [3]. The biologic effects of BNP counteract key mechanistic pathways in congestive heart failure: (i) a
Biomarker correlates of clinical parameters in HCM
The next sections summarize data associating natriuretic peptides and troponins with LV structure, hemodynamics, symptoms and outcomes. The heterogeneity of these data with respect to study design and patient characteristics is noteworthy and is summarized in Table S1. With a few exceptions, the studies cited included small numbers of patients with varying geographic backgrounds, age, gender balance, and disease status, but generally used comparable (though not identical) biomarker assays. In
Natriuretic peptides vs. troponin: is one better than the other?
Although both natriuretic peptides and troponin correlate with markers of HCM disease progression, BNP may be a more sensitive indicator of LVH than troponin. Kubo and colleagues showed that the wall thickness threshold was lower for BNP elevation than for cTnI elevation [8]. Natriuretic peptides are also stronger predictors of hemodynamic parameters and clinical symptoms than troponin. Although a correlation between elevated troponin and elevated BNP has been demonstrated [26], [34], it is not
Conclusions
Troponins and natriuretic peptides are closely tied to the cellular basis of disease and hemodynamic burden in HCM. These biomarkers correlate closely with disease progression and functional status, and are adjuncts to the assessment of disease status. Both serum troponins and plasma natriuretic peptides predict clinical risk in HCM independently of established risk factors. Measurement of these biomarkers therefore may be useful in the routine clinical evaluation of stable HCM patients.
Conflicts of interest
None.
Funding source
This was an internally funded study.
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Cited by (19)
Advances in hypertrophic cardiomyopathy: What the cardiologist needs to know
2022, Revista Portuguesa de CardiologiaB-type natriuretic peptide and outcome in patients with apical hypertrophic cardiomyopathy
2020, Journal of CardiologyCitation Excerpt :The clinical course of patients with hypertrophic cardiomyopathy (HCM) is highly variable, ranging from asymptomatic status with normal life expectancy to severely limiting dyspnea, systemic embolic events, and sudden cardiac death [1–6]. Several biomarkers, particularly B-type natriuretic peptide (BNP), have recently been shown to be useful in risk stratification in HCM patients [7–10]. Although elevated BNP level predicts mortality in patients with HCM, the association between BNP level and outcome in patients with apical HCM, a phenotypic variant of HCM, remains unclear [7].
Prognostic Implications of Point-of-Care and Serial B-type Natriuretic Peptide Levels in Patients With Hypertrophic Cardiomyopathy
2018, American Journal of CardiologyCitation Excerpt :Our findings of independent associations among BNP and gender, advanced diastolic dysfunction, maximal LV wall thickness, and increased LA size are consistent with previous literature. Hypotheses for elevated levels include worse myocardial disarray, small intramural coronary artery disease mediated ischemia, myocardial fibrosis, and higher LV end-diastolic pressure.7,23 A summary of previous studies assessing the prognostic value of BNP or NT-pro BNP in patients with HC is provided in the Supplement Table 1.
B-type natriuretic peptide and risk of sudden death in patients with hypertrophic cardiomyopathy
2018, Heart RhythmCitation Excerpt :The clinical course of HCM is highly variable, ranging from asymptomatic status with normal life expectancy to severely limiting dyspnea, systemic embolic events, and sudden cardiac death.1–3 Several biomarkers, particularly B-type natriuretic peptide (BNP), have recently been shown to be useful in stratifying risk in patients with HCM.4–7 BNP is a biologically active peptide mainly produced by cardiac myocytes in response to neurohormonal activation, myocardial stretch, and wall tension.8
Prediction of Extensive Myocardial Fibrosis in Nonhigh Risk Patients With Hypertrophic Cardiomyopathy
2018, American Journal of CardiologyCitation Excerpt :Notably, the majority of HC patients is at nonhigh SCD risk and only 1 of 10 would demonstrate extensive LGE on CMR imaging. In this context, it has recently been hypothesized that biomarkers, and hs-cTnT in particular, may be used as a “gateway” to perform LGE CMR imaging.7,8 A strategy based on easily obtainable characteristics that would alter the pretest likelihood of extensive LGE before CMR imaging would increase efficacious use of LGE CMR imaging for SCD risk stratification in HC.7,8