Diagnostic value of BNP in diastolic heart failure

Dijastoličko zatajivanje srca zahvaća otprilike 40-50% bolesnika koji imaju znakove i simptome zatajivanja srca. BNP (engl. brain natriureticpeptide, moždani natrijuretski peptid; B-tip natrijuretskog peptida) je srčani neurohormon koji izlučuju mišićne stanice klijetke kao odgovor na povećan tlak ili volumen na kraju dijastole. Sve brojniji dokazi pokazali su da su koncentracije BNP povećane u slučaju zatajivanja srca, te da su te koncentracije osobito važne kod diferencijalne dijagnoze dispneje. Koncentracije BNP su povećane kod dijastoličkog, no obično su niže nego kod sistoličkog zatajivanja srca. Koncentracije BNP su u uzajamnoj vezi sa stupnjem dijastoličke disfunkcije, te su blago povišene među bolesnicima sa simptomima poremećenog opuštanja srčanog mišića, a najviše su među onima s restriktivnim tipom punjenja. Kod asimptomatičnih bolesnika s blagim oblikom dijastoličke disfunkcije, koncentracije BNP mogu biti unutar granica referentnog raspona. U ovom preglednom članku raspravljamo o dijagnostičkoj vrijednosti BNP u dijagnostici dijastoličkog zatajivanja srca.Diastolic heart failure affects approximately 40%-50% of patients presenting with signs and symptoms of heart failure. Brain natriuretic peptide (BNP) is a cardiac neurohormone secreted from ventricular myocytes in response to increased end-diastolic pressure or volume. Accumulating evidence showed that BNP concentrations are increased in heart failure, and it is especially important in the differential diagnosis of dyspnea. BNP concentrations are increased in diastolic heart failure, but they are typically lower in diastolic than that in systolic heart failure. BNP concentrations are correlated with the stage of diastolic dysfunction, being mild-moderately elevated among patients with evidence of impaired relaxation and highest among those with a restrictive filling pattern. In asymptomatic patients with mild degree of diastolic dysfunction BNP concentrations may be within normal range. In this review we discuss the diagnostic value of BNP in diastolic heart failure

Diagnostic value of BNP in diastolic heart failure

Dijastoličko zatajivanje srca zahvaća otprilike 40-50% bolesnika koji imaju znakove i simptome zatajivanja srca. BNP (engl. brain natriureticpeptide, moždani natrijuretski peptid; B-tip natrijuretskog peptida) je srčani neurohormon koji izlučuju mišićne stanice klijetke kao odgovor na povećan tlak ili volumen na kraju dijastole. Sve brojniji dokazi pokazali su da su koncentracije BNP povećane u slučaju zatajivanja srca, te da su te koncentracije osobito važne kod diferencijalne dijagnoze dispneje. Koncentracije BNP su povećane kod dijastoličkog, no obično su niže nego kod sistoličkog zatajivanja srca. Koncentracije BNP su u uzajamnoj vezi sa stupnjem dijastoličke disfunkcije, te su blago povišene među bolesnicima sa simptomima poremećenog opuštanja srčanog mišića, a najviše su među onima s restriktivnim tipom punjenja. Kod asimptomatičnih bolesnika s blagim oblikom dijastoličke disfunkcije, koncentracije BNP mogu biti unutar granica referentnog raspona. U ovom preglednom članku raspravljamo o dijagnostičkoj vrijednosti BNP u dijagnostici dijastoličkog zatajivanja srca.Diastolic heart failure affects approximately 40%-50% of patients presenting with signs and symptoms of heart failure. Brain natriuretic peptide (BNP) is a cardiac neurohormone secreted from ventricular myocytes in response to increased end-diastolic pressure or volume. Accumulating evidence showed that BNP concentrations are increased in heart failure, and it is especially important in the differential diagnosis of dyspnea. BNP concentrations are increased in diastolic heart failure, but they are typically lower in diastolic than that in systolic heart failure. BNP concentrations are correlated with the stage of diastolic dysfunction, being mild-moderately elevated among patients with evidence of impaired relaxation and highest among those with a restrictive filling pattern. In asymptomatic patients with mild degree of diastolic dysfunction BNP concentrations may be within normal range. In this review we discuss the diagnostic value of BNP in diastolic heart failure

Normal Coronary Artery Patient Presenting with Left Ventricular Aneurysm

Left ventricular aneurysm (LVA) is one of the most important complications of myocardial infarction LVA is strictly defined as a distinct area of abnormal left ventricular diastolic contour with systolic dyskinesia or paradoxical bulging. LVA usually results from myocardial infarction. Other rare aetiologies of LVA include hypertrophic cardiomyopathy, Chagas' disease, sarcoidosis, congenital LVA, and idiopathic However, LVA formation in patients with idiopathic dilated cardiomyopathy is rarely reported, and the incidence, clinical features, and pathogenesis of LVA formation in patients with idiopathic dilated cardiomyopathy is not well understood. Here, we present a 45 years old, idiopathic dilated cardiomyopathy patient with LVA and normal coronary arteries The pathogenesis of LVA formation in patients with idiopathic dilated cardiomyopathy is not clear. One acceptable hypothesis is that coronary artery emboli originate from mural thrombi, present in some patients with idiopathic dilated cardiomyopathy, which develop due to local wall infarction and fibrosis. The local myocardial perfusion differences could be seen in idiopathic dilated cardiomyopathy and predominantly found in the anteroposterior axis of the left ventricle. Local fibrosis occurs more frequently on the anterior wall or posterior wall, and less frequently on the lateral or septal wall. In our patient, LVA existed in the septal segments.We could not define the exact mechanism of the septal aneurysm in our patient but we decided to present this abnormal case, which is different from cases thus far reported in the literature

Effects of a single, 24-hour, low-dose intravenous dobutamine infusion on left ventricular myocardial performance index in congestive heart failure: A prospective, nonrandomized study

AbstractBackground:Dobutamine, a predominantly beta-adrenergic sympathomimeticagent, is used for improving left ventricular (LV) systolic performance with different dosing regimens in patients with congestive heart failure (CHF). Myocardial performance index (MPI) is an indicator of LV global function that is correlated with LV end-diastolic pressure, and it is increased in CHF.Objective:The purpose of this study was to examine the effects of a single, 24-hour, low-dose, IV dobutamine infusion on LV systolic and diastolic function and on MPI in CHF as an indicator of LV global function, as well as the adverse effects (AEs) of the infusion.Methods:This prospective, nonrandomized study was conducted at theDepartment of Cardiology, Baskent University Hospital, Ankara, Turkey. Adult patients with LV ejection fraction (EF) <35%, sinus rhythm, and symptomatic CHF were treated using a standard protocol for at least 4 weeks. At the end of this period, patients with symptomatic CHF and EF <35% underwent echocardiography that included measuring isovolumic relaxation and contraction times (IRT and ICT, respectively) and LV ejection time (ET), and calculating LV MPI using the formula MPI = (IRT + ICT)/ET Dobutamine 2.5 μg/kg · min was then infused intravenously for 24 hours. Echocardiography was repeated 24 hours later and values were compared with preinfusion data. Patients were observed and monitored for CHF symptoms and AEs for 24 hours.Results:Forty-three patients were enrolled in the study, and 31 (22 men,9 women; mean [SD] age, 67.55 [11.78] years) continued after the 4-week standard-treatment period. Mean (SD) heart rate (74.93 [20.15] vs 80.23 [13.74] bpm, respectively), systolic blood pressure (129.00 [19.23] vs 126.67 [23.79] mm Hg), and diastolic blood pressure (75.80 [11.26] vs 74.96 [8.30] mm Hg) were statistically similar before and after the infusion. The mean (SD) end-diastolic volume was statistically similar to the preinfusion value (215.87 [76.74] vs 211.08 [65.51] mL); however, the mean (SD) end-systolic volume was significantly reduced (163.80 [63.86] vs 146.74 [53.12] mL; P = 0.01). Mean (SD) EF (25.33% [7.77%] vs 30.45% [7.63%]; P = 0.001) and stroke volume (SV) (54.92 [22.30] vs 63.59 [23.91] mL; P = 0.04) increased significantly. The mean (SD) early:late diastolic flow velocity (E/A ratio) (1.58 [1.36] vs 1.65 [1.27]), IRT (107.03 [35.37] vs 100.42 [34.32] ms), ICT (96.61 [34.27] vs 86.35 [44.80] ms), ET (240.65 [33.28] vs 243.48 [33.54] ms), and MPI (0.81% [0.28%] vs 0.78% [0.31%]) did not change significantly after dobutamine infusion. No AEs were observed.Conclusions:In this study of adult patients with symptomatic CHF, a single, 24-hour, low-dose, IV dobutamine infusion (2.5 μg/kg · min) was associated with decreased LV end-systolic volume and increased SV and EF However, LV diastolic function parameters, isovolumic time intervals, ET, and MPI were statistically similar to preinfusion values. The infusion was well tolerated

Omecamtiv mecarbil in chronic heart failure with reduced ejection fraction, GALACTIC‐HF: baseline characteristics and comparison with contemporary clinical trials

Aims: The safety and efficacy of the novel selective cardiac myosin activator, omecamtiv mecarbil, in patients with heart failure with reduced ejection fraction (HFrEF) is tested in the Global Approach to Lowering Adverse Cardiac outcomes Through Improving Contractility in Heart Failure (GALACTIC‐HF) trial. Here we describe the baseline characteristics of participants in GALACTIC‐HF and how these compare with other contemporary trials. Methods and Results: Adults with established HFrEF, New York Heart Association functional class (NYHA) ≥ II, EF ≤35%, elevated natriuretic peptides and either current hospitalization for HF or history of hospitalization/ emergency department visit for HF within a year were randomized to either placebo or omecamtiv mecarbil (pharmacokinetic‐guided dosing: 25, 37.5 or 50 mg bid). 8256 patients [male (79%), non‐white (22%), mean age 65 years] were enrolled with a mean EF 27%, ischemic etiology in 54%, NYHA II 53% and III/IV 47%, and median NT‐proBNP 1971 pg/mL. HF therapies at baseline were among the most effectively employed in contemporary HF trials. GALACTIC‐HF randomized patients representative of recent HF registries and trials with substantial numbers of patients also having characteristics understudied in previous trials including more from North America (n = 1386), enrolled as inpatients (n = 2084), systolic blood pressure &lt; 100 mmHg (n = 1127), estimated glomerular filtration rate &lt; 30 mL/min/1.73 m2 (n = 528), and treated with sacubitril‐valsartan at baseline (n = 1594). Conclusions: GALACTIC‐HF enrolled a well‐treated, high‐risk population from both inpatient and outpatient settings, which will provide a definitive evaluation of the efficacy and safety of this novel therapy, as well as informing its potential future implementation

Diabetes and cardiac autonomic neuropathy: Clinical manifestations, cardiovascular consequences, diagnosis and treatment

Cardiac autonomic neuropathy (CAN) is a frequent chronic complication of diabetes mellitus with potentially life-threatening outcomes. CAN is caused by the impairment of the autonomic nerve fibers regulating heart rate, cardiac output, myocardial contractility, cardiac electrophysiology and blood vessel constriction and dilatation. It causes a wide range of cardiac disorders, including resting tachycardia, arrhythmias, intraoperative cardiovascular instability, asymptomatic myocardial ischemia and infarction and increased rate of mortality after myocardial infarction. Etiological factors associated with autonomic neuropathy include insufficient glycemic control, a longer period since the onset of diabetes, increased age, female sex and greater body mass index. The most commonly used methods for the diagnosis of CAN are based upon the assessment of heart rate variability (the physiological variation in the time interval between heartbeats), as it is one of the first findings in both clinically asymptomatic and symptomatic patients. Clinical symptoms associated with CAN generally occur late in the disease process and include early fatigue and exhaustion during exercise, orthostatic hypotension, dizziness, presyncope and syncope. Treatment is based on early diagnosis, life style changes, optimization of glycemic control and management of cardiovascular risk factors. Medical therapies, including aldose reductase inhibitors, angiotensin-converting enzyme inhibitors, prostoglandin analogs and alpha-lipoic acid, have been found to be effective in randomized controlled trials. The following article includes the epidemiology, clinical findings and cardiovascular consequences, diagnosis, and approaches to prevention and treatment of CAN