Neurohumoral Profiles in Patients With Hypertrophic Cardiomyopathy-Differences to Hypertensive Left Ventricular Hypertrophy-

Abstract

ypertrophic cardiomyopathy (HCM) characteristically has severe myocardial hypertrophy, predominantly involving the interventricular septum of the nondilated left ventricle. Echocardiography is useful for the differential diagnosis of HCM, but it can be difficult to distinguish HCM from hypertensive heart disease (HHD) with left ventricular (LV) hypertrophy. Although concentric LV hypertrophy is observed in patients with HCM 1 and sometimes HCM patients present with hypertension as a complication, asymmetrical interventricular hypertrophy (ASH) is also observed in HHD. 2,3 Recently, ultrasonic myocardial tissue characterization by integrated backscatter has provided additional information about the pathological changes; however, it is still unable to completely differentiate HCM from HHD. 4 It has been reported that various neurohumoral systems are accelerated in patients with HHD or HCM. In HHD, the plasma concentrations of epinephrine and norepinephrine are increased, 5,6 and other trophic neurohumoral factors, such as angiotensin II 7 and endothelin-1, 8 are also increased. Moreover, it has been reported that atrial natriuretic peptide (ANP) is increased in patients with hypertension. 9 With regard to HCM patients, it has been reported that plasma concentrations of catecholamines 10 and endothelin-1 11 are increased, as well as those of ANP and brain natriuretic peptide (BNP). [12][13][14][15][16] However, there are no data on the differences in the neurohumoral profiles of HCM and HHD patients.Thus, in the present study we measured the plasma concentrations of catecholamines (epinephrine and norepinephrine), angiotensin II, endothelin-1 and natriuretic peptides (ANP and BNP) in patients with HCM and HHD without LV dysfunction to clarify the neurohumoral profile of HCM and its clinical implications. Methods SubjectsWe studied 40 patients with HCM, 35 with HHD and 15 healthy normal controls (Protocol 1). All patients were clinically evaluated and carefully diagnosed based on their family history, history of hypertension, echocardiography (UCG) and cardiac catheterization. 17,18 Patients with angina pectoris, low LV ejection fraction (LVEF: <50%), valvular heart disease, liver injury or renal dysfunction were excluded because all of these factors have effects on the Circ J 2004; 68: 444 -450 (Received November 28, 2003; revised manuscript received February 6, 2004; accepted February 13, 2004 Background Patients with hypertrophic cardiomyopathy (HCM) or hypertensive heart disease (HHD) have increased concentrations of various neurohumoral factors. Thus, the aim of the present study was to evaluate the differences in the neurohumoral profiles of HCM and HHD. Methods and Results Plasma concentrations of epinephrine, norepinephrine, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), angiotensin II and endothelin-1 were measured in 40 patients with HCM, 35 with HHD, and 15 controls. Additionally, the concentrations of these neurohumoral factors in the coronary sinus and aortic root were measured in...

Clinical Characteristics of Heart Disease Patients With a Good Prognosis in Spite of Markedly Increased Plasma Levels of Type-B Natriuretic Peptide (BNP)

“…It is known that natriuretic peptides are overexpressed in hypertrophied myocardium as a result of retranscription of embryonic cardiac-specific genes. 24 Although it is certain that the plasma BNP levels are increased in hypertensive patients with left ventricular hypertrophy leading to LV diastolic dysfunction, 25 the mean value of plasma BNP in such patients appears to be approximately 40 pg/ml, as reported in Japanese subjects. 26 This means that the mechanism of the markedly increased levels of plasma BNP in some cases with HCM might differ from that in hypertensive heart disease.…”

Prevalence of Isolated Atrial Amyloidosis in Young Patients Affected by Congestive Heart Failure

“…Indeed, ANP plasma levels closely parallel the instantaneous secretion rate, and therefore likely they greatly vary in response to different pathophysiological stimuli. The discovery that ANP amyloid associated with atrial myofibrils in most human hearts with dilated or hypertrophic cardiomyopathies [23, 24] suggests IAA as a potential major pathogenic process in CHF. In the light of this, we recently demonstrated the correlation between CHF and ANP amyloidosis [25].…”

“…At a cellular and molecular level, the focus of therapy for CHF must increasingly include the adverse changes in the ECM and cardiac amyloidosis [3]. During the past decades, medical management of heart failure has involved the blockade of the neurohormonal effects of angiotensin II, catecholamines, and aldosterone [23], but a poly pharmaceutical approach to the treatment of heart failure is emerging. However, as more antiamyloid therapies emerge, the uniform treatment of patients with multiple classes of medications is impractical and costly, so encouraging the prevention practices.…”

Selective Endothelin ETB Receptor Antagonist Improves Left Ventricular Function but Exaggerates Degeneration of Cardiomyocytes in J2N-k Hamsters

“…One possible explanation is that the ET-1/ETA system in cardiomyocytes augments cytokine-induced iNOS expression by stimulating a protein kinase C pathway and/or a cAMP pathway, thus contributing to enhanced iNOS mRNA concentrations. 19 Thus, the beneficial effects of ABT-627 might be related to decreased iNOS expression. Further investigations are required to elucidate the relationship between the ET-1/ETA system and iNOS protein expression in cardiomyopathy.…”

“…16,17 Several neurohumoral factors activated in chronic heart failure might augment cardiac iNOS expression and could cause cardiac dysfunction. 18,19 There might be some relation between ET-1 and iNOS in the failing heart, 20 but the precise mechanisms and the role of ET-1 and iNOS in CHF caused by IDC have not been clarified. The aim of this study was to compare the chronic effect of selective ETA and ETB receptor antagonist on cardiac function, ET-1 content, ultrastructure and histochemical changes of reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase …”