NYHA Class III (nyha + class_iii)

Distribution by Scientific Domains


Selected Abstracts


Is the Left Ventricular Lateral Wall the Best Lead Implantation Site for Cardiac Resynchronization Therapy?

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1p2 2003
MAURIZIO GASPARINI
GASPARINI, M., et al.: Is the Left Ventricular Lateral Wall the Best Lead Implantation Site for Cardiac Resynchronization Therapy?Short-term hemodynamic studies consistently report greater effects of cardiac resynchronization therapy (CRT) in patients stimulated from a LV lateral coronary sinus tributary (CST) compared to a septal site. The aim of the study was to compare the long-term efficacy of CRT when performed from different LV stimulation sites. From October 1999 to April 2002, 158 patients (mean age 65 years, mean LVEF 0.29, mean QRS width 174 ms) underwent successful CRT, from the anterior (A) CST in 21 patients, the anterolateral (AL) CST in 37 patients, the lateral (L) CST in 57 patients, the posterolateral (PL) CST in 40 patients, and the middle cardiac vein (MCV) CST in 3 patients. NYHA functional class, 6-minute walk test, and echocardiographic measurements were examined at baseline, and at 3, 6, and 12 months. Comparisons were made among all pacing sites or between lateral and septal sites by grouping AL + L + PL CST as lateral site (134 patients, 85%) and A + MC CST as septal site (24 patients, 15%). In patients stimulated from lateral sites, LVEF increased from 0.30 to 0.39(P < 0.0001), 6-minute walk test from 323 to 458 m(P < 0.0001), and the proportion of NYHA Class III,IV patients decreased from 82% to 10%(P < 0.0001). In patients stimulated from septal sites, LVEF increased from 0.28 to 0.41(P < 0.0001), 6-minute walk test from 314 to 494 m(P < 0.0001), and the proportion of NYHA Class III,IV patients decreased from 75% to 23%(P < 0.0001). A significant improvement in cardiac function and increase in exercise capacity were observed over time regardless of the LV stimulation sites, either considered singly or grouped as lateral versus septal sites. (PACE 2003; 26[Pt. II]:162,168) [source]


Addition of a Left Ventricular Lead to Conventional Pacing Systems in Patients with Congestive Heart Failure: Feasibility, Safety, and Early Results in 60 Consecutive Patients

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 8 2002
CINDY M. BAKER
BAKER, C.M., et al.: Addition of a Left Ventricular Lead to Conventional Pacing Systems in Patients with Congestive Heart Failure: Feasibility, Safety, and Early Results in 60 Consecutive Patients. Left bundle branch block worsens congestive heart failure (CHF) in patients with LV dysfunction. Asynchronous LV activation produced by RV apical pacing leads to paradoxical septal motion and inefficient ventricular contraction. Recent studies show improvement in LV function and patient symptoms with biventricular pacing in patients with CHF. The aim of this study was to determine the feasibility, safety, acute efficacy, and early effect on symptoms of the upgrade of a chronically implanted RV pacing system to a biventricular system. Sixty patients with NYHA Class III and IV underwent the upgrade procedure using commercially available leads and adapters. The procedure succeeded in 54 (90%) of 60 patients. Acute LV stimulation thresholds obtained from leads placed along the lateral LV wall via the coronary sinus compare favorably to those reported in current biventricular pacing trials. The complication rate was low (5/60, 8.3%): lead dislodgement (n = 1), pocket hematoma (n = 1), and wound infections (n = 3). During 18 months of follow-up (16.7%) of 60 patients died. Two patients that died failed the initial upgrade attempt. At 3-month follow-up, quality of life scores improved 31 28 points (n = 29), P < 0.0001). NYHA Class improved from 3.4 0.5 to 2.4 0.7 (P = < 0.0001) and ejection fraction increased from 0.23 0.8 to 0.29 0.11 (P = 0.0003). Modification of RV pacing to a biventricular system using commercially available leads and adapters can be performed effectively and safely. The early results of this study suggest patients may benefit from this procedure with improved functional status and quality of life. [source]


Levosimendan versus Dobutamine in Heart Failure Patients Treated Chronically with Carvedilol

CARDIOVASCULAR THERAPEUTICS, Issue 3 2008
Hamza Duygu
Introduction: Although beta-blockers are highly effective in the treatment of heart failure (HF), many patients with HF receiving a beta-blocker continue to become decompensated and require hospitalization for worsening HF. Levosimendan and dobutamine are used to manage decompensated HF, but their comparative effects on left ventricular (LV) function in patients prescribed beta-blockers are unknown. Aims: The aim of this study was to compare the effects of dobutamine and levosimendan on LV systolic and diastolic functions in chronic HF patients treated chronically with carvedilol. Forty patients with chronic HF who had NYHA class III to IV symptoms, a LV ejection fraction (LVEF) <40%, and ongoing treatment with carvedilol were enrolled in this randomized (1:1), dobutamine controlled, open-label study. Before and 24 h after treatment, LVEF, mitral inflow peak E and A wave velocity, E/A ratio, the deceleration time of the E wave (DT), isovolumic relaxation time (IVRT), peak systolic (Sm) and early diastolic (Em) mitral annular velocity, and systolic pulmonary artery pressure (SPAP) were measured by echocardiography. Results: Levosimendan produced a statistically significant increase in LVEF (28 5% vs. 33 3%), Sm (6.5 1.2 cm/s vs. 7.4 0.9 cm/s), DT (120 10 ms vs. 140 15 ms), and Em (7.5 0.4 cm/s vs. 8.1 0.5 cm/s) and significant decrease in E/A ratio (2.1 0.3 vs. 1.7 0.4) and SPAP (55 5 mmHg vs. 40 7 mmHg). No significant change occurred in LV systolic and diastolic function parameters, or SPAP with dobutamine treatment. Levosimendan did not significantly alter the heart rate (72 4 bpm vs. 70 3 bpm), systolic (105 5 mmHg vs. 102 4 mmHg), or diastolic blood pressure (85 5 mmHg vs. 83 5 mmHg) whereas with dobutamine treatment, all these parameters significantly increased. Conclusions: Dobutamine and levosimendan have different effects on LV functions in patients treated chronically with carvedilol. These differences should be considered when selecting inotropic therapy for decompensated HF receiving long-term carvedilol. [source]


Thromboxane and prostacyclin biosynthesis in heart failure of ischemic origin: effects of disease severity and aspirin treatment

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 5 2010
F. SANTILLI
Summary.,Background: Thromboembolism is a relatively common complication of chronic heart failure (HF) and the place of antiplatelet therapy is uncertain. Objectives: We characterized the rate of thromboxane and prostacyclin biosynthesis in chronic HF of ischemic origin, with the aim of separating the influence of HF on platelet activation from that of the underlying ischemic heart disease (IHD). Patients and Methods: We compared urinary 11-dehydro-thromboxane (TX)B2, 2,3 dinor 6-keto-PGF1,, 8-iso-prostaglandin (PG)F2,, and plasma N-terminal pro-brain natriuretic peptide (NT-pro-BNP), asymmetric dimethylarginine (ADMA), and soluble CD40 ligand (sCD40L), in 84 patients with HF secondary to IHD, 61 patients with IHD without HF and 42 healthy subjects. Results: HF patients not on aspirin had significantly higher urinary 11-dehydro-TXB2 as compared with healthy subjects (P < 0.0001) and IHD patients not on aspirin (P = 0.028). They also showed significantly higher 8-iso-PGF2, (P =,0.018), NT-pro-BNP (P = 0.021) and ADMA (P < 0.0001) than IHD patients not on aspirin. HF patients on low-dose aspirin had significantly lower 11-dehydro-TXB2 (P < 0.0001), sCD40L (P = 0.007) and 2,3-dinor-6-keto-PGF1, (P = 0.005) than HF patients not treated with aspirin. HF patients in NYHA classes III and IV had significantly higher urinary 11-dehydro-TXB2 than patients in classes I and II, independently of aspirin treatment (P < 0.05). On multiple linear regression analysis, higher NT-pro-BNP levels, lack of aspirin therapy and sCD40L, predicted 11-dehydro-TXB2 excretion rate in HF patients (R2 = 0.771). Conclusions: Persistent platelet activation characterizes HF patients. This phenomenon is related to disease severity and is largely suppressable by low-dose aspirin. The homeostatic increase in prostacyclin biosynthesis is impaired, possibly contributing to enhanced thrombotic risk in this setting. [source]