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Increased Transforming Growth Factor-β Levels Associated With Cardiac Adverse Events in Hypertrophic Cardiomyopathy
Burak Ayça1, Irfan Sahin1, Suat Hayri Kucuk2
1Department of Cardiology, Bağcılar Education Research Hospital, Bağcılar, Istanbul, Turkey.
Insights
Elevated levels of transforming growth factor-beta (TGF-β) are found in hypertrophic cardiomyopathy (HCM) patients. Higher TGF-β indicates a poorer prognosis, with increased risk of adverse cardiovascular events.
Area of Science:
- Cardiology
- Genetics
- Biochemistry
Background:
- Hypertrophic cardiomyopathy (HCM) is a prevalent genetic heart condition.
- HCM involves ventricular hypertrophy, fibrosis, and relaxation issues, with unknown fibrosis mechanisms.
- Myocardial fibrosis in HCM pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the association between circulating transforming growth factor-beta (TGF-β) levels and prognosis in HCM patients.
- To determine if TGF-β levels can predict adverse clinical outcomes in individuals with HCM.
Main Methods:
- Compared TGF-β levels in 49 HCM patients versus 40 non-HCM controls.
- Followed HCM patients for 18 months, categorizing them by TGF-β levels (low vs. high).
- Assessed clinical outcomes including BNP, echocardiographic parameters, and adverse events.
Main Results:
- HCM patients exhibited significantly higher TGF-β levels than controls (P=0.005).
- High TGF-β group showed increased BNP, larger left atrium, thicker septum, higher NYHA class, and more hospitalizations/adverse events (P<0.001).
- TGF-β > 4877 pg/mL predicted adverse events with 72% sensitivity and 75% specificity (P=0.014).
Conclusions:
- Circulating TGF-β levels are elevated in HCM patients.
- Higher TGF-β levels correlate with a poorer prognosis and increased adverse events in HCM.
- TGF-β serves as a potential biomarker for predicting adverse outcomes in hypertrophic cardiomyopathy.
Background:
Hypertrophic cardiomyopathy (HCM) is a common genetic heart disease characterized by ventricular hypertrophy, myocardial fibrosis, and impaired ventricular relaxation. The exact mechanisms by which fibrosis is caused remain unknown.
Hypothesis:
Circulating TGF-β is related to poor prognosis in HCM.
Methods:
We compared TGF-β levels of 49 HCM patients with those of 40 non-HCM patients. We followed the patients with HCM for 18 months and divided them into 2 groups: low TGF-β (≤ 4877 pg/mL) and high TGF-β (> 4877 pg/mL). We compared the 2 groups in terms of brain natriuretic peptide (BNP), echocardiographic parameters, and clinical outcomes including myocardial infarction, arrhythmias, implantable cardioverter-defibrillator implantation, hospitalization, New York Heart Association (NYHA) class, acute heart failure, and mortality.
Results:
The HCM patients had higher TGF-β levels than those in the control group (P = 0.005). In the follow-up, those in the high TGF-β group had higher BNP levels, larger left-atrial size, thicker interventricular septum, NYHA class, more hospitalizations, and a greater number of clinical adverse events (P < 0.001, P = 0.01, P < 0.001, P = 0.002, P < 0.001 and P = 0.003, respectively). TGF-β level of > 4877 pg/mL can predict adverse events with a specificity of 75% and a sensitivity of 72% (P = 0.014). In multivariate regression analysis, TGF-β, BNP, and interventricular septum thickness were significantly associated with adverse events (P = 0.028, P = 0.030, and P = 0.034, respectively).
Conclusions:
The TGF-β level is higher in HCM patients and associated with a poor prognosis in HCM.
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