Increased Brain Natriuretic Peptide Secretion is a Marker of Disease Progression in Nonobstructive Hypertrophic Cardiomyopathy

Pieroni, Maurizio; Bellocci, Fulvio; Sanna, Tommaso; Verardo, Romina; Ierardi, Carolina; Maseri, Attilio; Frustaci, Andrea; Crea, Filippo

doi:10.1016/j.cardfail.2007.01.011

« Previous Next »Journal of Cardiac Failure
Volume 13, Issue 5 , Pages 380-388, June 2007

Increased Brain Natriuretic Peptide Secretion is a Marker of Disease Progression in Nonobstructive Hypertrophic Cardiomyopathy

Maurizio Pieroni, MD, PhD
- From the Cardiology Department, Catholic University, Rome, Italy
- Reprint requests: Maurizio Pieroni Cardiology Department, Catholic University, Largo A. Gemelli 8, 00168 Rome, Italy.
Fulvio Bellocci, MD
- From the Cardiology Department, Catholic University, Rome, Italy
Tommaso Sanna, MD
- From the Cardiology Department, Catholic University, Rome, Italy
Romina Verardo, PhD
- From the Cardiology Department, Catholic University, Rome, Italy
Carolina Ierardi, MD
- From the Cardiology Department, Catholic University, Rome, Italy
Attilio Maseri, MD
- Cardio-Thoracic and Vascular Department, San Raffaele Hospital, Milan, Italy
Andrea Frustaci, MD
- Heart and Great Vessels Department “Attilio Reale,” La Sapienza University, Rome, Italy
Filippo Crea, MD
- From the Cardiology Department, Catholic University, Rome, Italy

Received 4 May 2006; received in revised form 29 January 2007; accepted 30 January 2007.

Rome, Italy; Milan, Italy

Abstract

Background

Hypertrophic cardiomyopathy (HCM) is associated with increased plasma brain natriuretic peptide (BNP), but sequential plasma and myocardial BNP assessment in stable and dilated HCM has never been performed.

Methods and Results

Forty consecutive HCM patients (42 ± 8 years, 25 males) underwent cardiac catheterization, angiography, and left ventricular (LV) endomyocardial biopsy. During follow-up (70.5 ± 6.7 months), 30 patients (Group 1) remained stable whereas 10 patients (Group 2) progressed to dilated phase. Group 2 patients underwent a second invasive study with LV biopsy. BNP plasma levels were measured at baseline and at follow-up in all patients. All biopsies were processed for histology and immunohistochemistry with anti-BNP antibodies. BNP plasma levels remained unchanged in Group 1, whereas it significantly increased in all Group 2 patients who exhibited an elevation of LV and right ventricular end-diastolic pressure. Immunohistochemistry showed an increase of BNP-positive myocytes in follow-up biopsies when compared with baseline (75.0 ± 15.0 % versus 29.8 ± 10.0 %; P = .005) with a significant correlation with LV end-diastolic pressure (r = 0.78, P < .001) and plasma BNP (r = 0.83, P < .001).

Conclusions

Progression to end-stage of HCM is characterized by further increase of myocardial and plasma BNP. Serial assessment of plasma BNP may provide noninvasive recognition of hemodynamic deterioration, allowing prompt institution of heart failure therapy.

Key Words: Brain natriuretic peptide, hypertrophic cardiomyopathy, heart failure, endomyocardial biopsy