B-type natriuretic peptide predicting exercise tolerance in patients with coronary heart disease (original) (raw)
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Clinical Biochemistry, 2004
Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) are increased in conditions with cardiac ventricular volume and pressure overload. The general physiological and potential therapeutic roles of natriuretic peptides in respiratory disease, right ventricular (RV) dysfunction, and pulmonary arterial hypertension (PAH) are reviewed. BNP levels can be used to differentiate between dyspneic patients with a pure respiratory defect and those with RV dysfunction. BNP levels also correlate with mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance (PVR) in patients with PAH (atrial septal defect, chronic thromboembolic disease, and scleroderma). BNP is a predictor of mortality in patients with primary pulmonary hypertension (PPH). These are important clinical implications in that a noninvasive blood test may be used to identify high-risk patients for more invasive procedures such as cardiac catheterization. BNP or NT-proBNP measurements may also be used to guide therapy (e.g., pulmonary vasorelaxants) in PAH since upregulation of the natriuretic peptide pathway has been shown to reduce cardiac hypertrophy and PAH. Additionally, there may be therapeutic potential via recombinant BNP or neutral endopeptidase inhibitors in RV dysfunction and PAH.
Journal of Medical Biochemistry, 2009
Kratak sadr`aj: Natriuretski peptidi mogu imati klini~ki zna~aj u pra}enju terapijskih efekata kod pacijenata sa sr~anom insuficijencijom. Cilj ove randomizovane studije bio je da se ispita efikasnost razli~itih terapijskih protokola za sr~anu insuficijenciju kod pacijenata sa sr~anom insuficijenci jom na osnovu nivoa BNP-a u plazmi pre i posle terapije. [ezdeset dva pacijenta sa sr~anom insuficijencijom i povi-{enim nivoom BNP-a, dobi 55,82±9,09 god, sa II-III NYHA funkcionalnom klasom, ejekcionom frakcijom (EF) <45%, primali su 12 nedelja tradicionalnu farmakolo{ku terapiju za sr~anu insuficijenciju, i to: ACE inhibitore i b blokatore (1. grupa); ACE inhibitore i angiotenzin II receptor blokatore (ARBs) (2. grupa); ß blokatore i ARBs (3. grupa); ACE inhibitore, ß blokatore i ARBs (4. grupa). Ispitivali smo nivo BNPa u plazmi, hemodinamske parametre (pritisak u plu}nim kapilarima (PCWP), cardiac output (CO), EF i du`inu trajanja opte re}enja. Nivo BNP-a u plazmi se zna~ajno snizio u 4. grupi pacijenata, koji su bili na ACE inhibitorima, ß blokatorima i ARBs, u odnosu na ostale grupe. Tako|e je prime}en zna~ajan pozitivan uticaj na hemodinamske parametre i trajanje optere}enja u toj grupi pacijenata, u pore|enju sa ostalim ispitanicima. Mo`e se zaklju~iti da terapijski protokol koji uklju~uje ACE inhibitore, ß blokatore i ARBs kod pacijenata sa sr~a nom insuficijencijom i povi{enim BNP-om zna~ajno pobolj {a va kvalitet `ivota, funkciju leve komore, vrednosti hemodi namskih parametara i du`inu trajanja optere }enja. Sve te promene su udru`ene sa sni`enjem nivoa BNP-a u plazmi. Klju~ne re~i: B-tip natriuretskog peptida, sr~ana insu ficijencija, terapijski protokoli Summary: Natriuretic peptide BNP might be clinically useful for monitoring treatment effects in patients with heart failure (HF). In order to investigate the pharmacological effects of different therapy protocols for patients with HF based on the BNP level before and after therapy, we performed an open randomized comparative trial. Sixty-two HF patients with increased natriuretic peptide level, aged 55.82±9.09, II-III NYHA functional classes, ejection fraction (EF) <45%, received a 12-week treatment with either traditional pharmacotherapy for HF with ACE inhibitors and b-blockers (1 st group), or ACE inhibitors and angiotensin II receptor blo ckers (ARBs) (2 nd group), or b-blockers and ARBs (3 rd group), and ACE inhi bitors, b-blockers and ARBs (4 th group). We evaluated the BNP plasma level, hemodynamic state (pulmonary capillary wedge pressure (PCWP), cardiac output (CO), EF and exercise capacity. The BNP plasma level decreased significantly in the 4 th group of patients who received ACE inhibitors, b-blockers and ARBs, in comparison to other groups. A beneficial influ ence on hemodynamic and exercise capacity was significantly pronounced in this group, compared to the other therapy regimes. In conclusion, the therapeutic protocol: ACE inhibitors, b-blockers and ARBs in HF patients with increased natriuretic peptide level significantly improves the quality of life, left ventricular function, hemodynamic parameters and exercise capacity. All these changes were accompanied with a decreasing of the BNP plasma level.
Bisoprolol delays progression towards right heart failure in experimental pulmonary hypertension
2012
Background-In pulmonary arterial hypertension (PH), sympathetic adrenergic activity is highly elevated. Sympathetic overactivity is a compensatory mechanism at first, but might be detrimental for cardiac function in the long run. We therefore investigated whether chronic low-dose treatment with bisoprolol (a cardioselective -blocker) has beneficial effects on cardiac function in experimental PH. Methods and Results-PH was induced in rats by a single injection of monocrotaline (60 mg/kg). Pressure telemetry in PH rats revealed that 10 mg/kg bisoprolol was the lowest dose that blunted heart rate response during daily activity. Ten days after monocrotaline injection, echocardiography was performed and PH rats were randomized for bisoprolol treatment (oral gavage) or vehicle (nϭ7/group). At end of study (body mass loss Ͼ5%), echocardiography was repeated, with additional pressure-volume measurements and histomolecular analyses. Compared with control, right ventricular (RV) systolic pressure and arterial elastance (measure of vascular resistance) more than tripled in PH. Bisoprolol delayed time to right heart failure (PϽ0.05). RV afterload was unaffected, however, bisoprolol treatment increased RV contractility and filling (both PϽ0.01), and partially restored right ventriculo-arterial coupling and cardiac output (both PϽ0.05). Bisoprolol restored RV -adrenergic receptor signaling. Histology revealed significantly less RV fibrosis and myocardial inflammation in bisoprolol treated PH rats. Conclusions-In experimental PH, treatment with bisoprolol delays progression toward right heart failure, and partially preserves RV systolic and diastolic function. These promising results suggest a therapeutic role for -blockers in PH that warrants further clinical investigation. (Circ Heart Fail. 2012;5:97-105.) Key Words: pulmonary hypertension Ⅲ right ventricular dysfunction Ⅲ -adrenergic receptor blocker Ⅲ pressure-volume relationship Ⅲ Wistar rats P ulmonary arterial hypertension (PH) is a fatal disease, characterized by progressive vascular remodeling and increased right ventricular (RV) afterload, which eventually leads to manifest right heart failure (RHF) and premature death. Current available medical treatments aim to reduce RV afterload, thereby secondarily improving RV function. 1 No treatment is currently available that improves RV function directly, partially because it was not considered a therapeutic target in PH. 2 Clinical Perspective on p 105 Recently, several reports have shown that sympathetic activity is increased in patients with PH. 3-7 Similar to left heart failure (LHF), "ventricle-specific" down regulation of  1-adrenergic receptors was observed in RV samples of PH patients. 8 In addition, we recently demonstrated that exercise training was detrimental in experimental and progressive PH. 9 The deleterious effects could be related to bouts of exercise-induced sympathetic stimulation. Although increased adrenergic activity is a compensatory mechanism to maintain cardiac function by increasing contractility and heart rate, it became apparent that chronic adrenergic overactivity has, in the long run, detrimental effects on cardiac function. 10 This supports the use of -adrenergic blockade in LHF management, which has been demonstrated to significantly reduce mortality and left ventricular (LV) remodeling. 11 Nevertheless, and notwithstanding the substantial evidence of their beneficial effects in LHF, the use of -blockers currently is not recommended for patients with PH. 1 PH patients are unable to increase stroke volume during exercise,
Review on the Correlation between Natriuretic Peptide Levels and Heart Failure
Many studies have evaluated the diagnostic characteristics of BNP and NT-proBNP. Study populations have included patients with acute decompensated HF who present to the emergency room or patients with symptoms and signs of HF who are evaluated by primary care physicians. These studies have examined the performance of BNP and NT-proBNP in patients with various comorbidities and at different cut points. However, questions about issues such as optimal cut points still persist regarding the diagnostic capability of BNP and NT-proBNP. Consequently, a systematic review is needed to better understand the diagnostic capability of BNP and NT-proBNP.Clinically, HF is a syndrome with typical symptoms (e.g., breathlessness and fatigue) and signs (e.g., elevated jugular venous pressure and pulmonary crackles). Patients with HF may have either reduced or preserved left ventricular ejection fraction (LVEF). The diagnosis of HF can be difficult since the clinical features of the condition are not always sensitive or specific. No gold standard investigation exists to diagnose HF. The use of BNP or NT-proBNP in the diagnosis, prognosis, or treatment for HF requires knowledge of the variation in peptide levels over serial measurements. Currently, the evidence is uncertain concerning how much of a difference in BNP or NT-proBNP concentration is clinically important.The challenge of diagnosing HF emphasizes the importance of evaluating whether other investigations may help diagnose the condition. Furthermore, the characteristics of these other investigations should be examined for their prognostic utility and their usefulness in guiding HF therapy. The natriuretic peptides, i.e., B-type natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP), may be useful to help with diagnosis, prognosis, and management of HF. BNP and NTproBNP are secreted into the bloodstream by cardiac myocytes in response to increased ventricular wall stress, hypertrophy, and volume overload. BNP and NT-proBNP levels are increased in persons with HF, and low levels rule out HF. Thus, these peptides have emerged as promising markers for HF 1. Assessment of prognosis is important to promote better counseling of HF patients with regard to future therapies, including cardiac transplantation. Research suggests that BNP and NT-proBNP may provide incremental prognostic information beyond what is available from the clinical data such as New York Heart Association (NYHA) class, LVEF, and comorbidities 2. A systematic review is required to better understand whether BNP and NT-proB-NP provide prognostic information for patients with acute decompensated HF and chronic stable HF. The management of HF is essentially directed by an algorithm for medical therapy. Many times, patients are not fully optimized on therapy because clinicians believe, based on the clinical findings, that further optimization is unnecessary. This could result in under treatment for HF patients. Since BNP and NT-proBNP concentrations have been found to decrease with the escalation of therapy, sequential measurement of these markers may be a useful means of guiding HF treatment. To date, individual studies have not definitively demonstrated whether BNP or NT-proBNP test values can guide HF therapy. A systematic review of this issue would provide information to assess strategies to better optimize the management of HF patients. The use of BNP or NT-proBNP in the diagnosis, prognosis, or treatment for HF requires knowledge of the variation in peptide levels over serial measurements. Currently, the evidence is uncertain concerning how much of a difference in BNP or NT-proBNP concentration is clinically important. Given the many outstanding issues involved in using BNP and NT-proBNP for diagnosing, prognosticating, and treating HF, the following questions are to be addressed 3 : • Question 1: In patients presenting to the emergency department or urgent care facilities with signs or symptoms suggestive of heart failure (HF):