Usefulness of left ventricular mass in predicting recovery of left ventricular systolic function in patients with symptomatic idiopathic dilated cardiomyopathy

Prognosis of idiopathic dilated cardiomyopathy (IDC) is variable. We determined the prognostic value of left ventricular (LV) mass and systolic and diastolic function in patients with IDC of <12 months duration. Clinical and echocardiographic assessment was performed at baseline and at 8+/-6 months follow-up in 25 patients (47+/-13 years) with IDC and an LV ejection fraction (LVEF1) of <40% (22+/-7%). Based on a follow-up LVEF (LVEF2) of < or >40%, patients were divided into unimproved (n = 13, LVEF2 = 21+/-9%) and improved groups (n = 12, LVEF2 = 51+/-11%). There was no difference in the LVEF1 (22+/-8% vs. 22+/-6%), LV end-systolic (5.7+/-0.8 vs. 5.8+/-0.9 cm) or end-diastolic (6.5+/-0.6 vs. 6.6+/-0.9 cm) dimension, wall stress (102+/-26 vs 99+/-28 g/cm2), end-systolic (1.7+/-0.3 vs. 1.8+/-0.2) or end-diastolic (1.7+/-0.3 vs. 1.6+/-0.1) sphericity, dp/dt (582+/-163 vs. 678+/-222 mm Hg/s), or right ventricular fractional shortening (20+/-9% vs. 27+/-7%, p = 0.06) in unimproved and improved groups. LV mass was lower (1.00+/-0.21 vs. 1.38+/-0.27 g/ml, p = 0007) and mitral inflow E-wave deceleration time shorter (97+/-42 vs. 164+/-58 ms, p = 0007) in the unimproved versus the improved group. On Pearson correlation analysis, LV mass (r = 0.62, p = 0.001), deceleration time (r = 0.68, p = 0.0002), wall motion score index (r = -0.47, p = 02), and dp/dt (r = 0.52, p = 03) were the significant predictors of LVEF2. There was correlation between LV mass (grams per milliliter) and deceleration time (r = 0.61, p = 0.001). During follow-up, death occurred in 1, and readmission for worsening heart failure in 4 patients in the unimproved group versus no hospitalization in the improved group. Thus, in patients with recent onset IDC, LV mass and diastolic function determine late outcome.     

Predictors of myocardial contractile reserve in patients with nonischemic dilated cardiomyopathy. An echo-stress dobutamine study

INTRODUCTION AND OBJECTIVES: Myocardial contractile reserve studies with low-dose dobutamine echocardiography have been shown to be useful to assess functional myocardial status. However, the variables associated with contractile reserve after inotropic stimulation are not well known. PATIENTS AND METHOD: We studied 50 patients (35 men, mean age 56.4 +/- 9.5 years) with nonischemic dilated cardiomyopathy (NIDC), LVEF 28.7% +/- 8.5% and wall motion score index (WMSI) 2.42 +/- 0.34 with low-dose dobutamine echocardiography. Left ventricular contractile reserve was assessed by a differential parameter defined as the difference between rest and stress WMSI (DeltaWMSI). RESULTS: After dobutamine infusion the WMSI was 1.95 +/- 0.58; from this value we calculated a DeltaWMSI of 0.45 +/- 0.39. None of the clinical variables showed a relationship with the presence of contractile reserve. In contrast, the following echocardiographic parameters correlated with DeltaWMSI: end-diastolic (p=0.05) and end-systolic (p=0.02) diameters, end-systolic volume index (p=0.01) and LVEF (p=0.002). In the multivariate analysis, only end-diastolic diameter was an independent predictor of contractile reserve (hazard ratio=0.852; 95% CI, 0.735-0.987; p=0.03). CONCLUSIONS: Ventricular diameters, end-systolic volume index and LVEF are related with improvements in myocardial contractility after dobutamine infusion, although only end-diastolic diameter was an independent predictor of contractile reserve. Thus, this parameter should receive particular attention in evaluations of the functional status of the myocardium in patients with NIDC.     

NT-proBNP response to dobutamine stress echocardiography predicts left ventricular contractile reserve in dilated cardiomyopathy

BACKGROUND: Brain natriuretic peptide (BNP) and left ventricular (LV) inotropic reserve are major prognostic indexes in heart failure (HF). AIMS: To investigate the relationship between N-terminal-proBNP (NT-proBNP) changes in response to dobutamine stress echocardiography (DSE) and the LV inotropic reserve, in HF patients with dilated cardiomyopathy (DC). METHODS: We studied 41 patients with DC, LVEF 31.6+/-7.7%, NYHA class II-III and 15 controls. Plasma NT-proBNP levels were measured before and 60 min after three 5-min stages of dobutamine (5 to 15 microg/kg/min). RESULTS: Based on NT-proBNP changes in response to dobutamine, patients were categorized into two groups: In Group A circulating NT-proBNP levels fell (-16.6+/-7.8%), and in Group B they increased (8.4+/-9.1%). Group A had a marked improvement in WMSI compared to Group B (32.1+/-9.7% vs. 18.8+/-15.9%, p<0.001). Multivariate analysis showed that NT-proBNP changes were an independent predictor of LV inotropic reserve (b= -0.55, p<0.001). A reduction of 21.3% in plasma NT-proBNP levels in response to dobutamine predicted an improvement in WMSI of >25% with a sensitivity of 100% and a specificity of 92.3%. CONCLUSIONS: NT-proBNP changes in response to dobutamine reflect improvement in LV contractility and constitute an independent predictor of LV inotropic reserve in patients with DC.     

Regional myocardial blood flow reserve impairment and metabolic changes suggesting myocardial ischemia in patients with idiopathic dilated cardiomyopathy

OBJECTIVES: We performed positron emission tomography (PET) to evaluate myocardial ischemia in patients with idiopathic dilated cardiomyopathy (IDC). BACKGROUND: Patients with IDC have anatomically normal coronary arteries, and it has been assumed that myocardial ischemia does not occur. METHODS: We studied 22 patients with IDC and 22 control subjects using PET with nitrogen-13 ammonia to measure myocardial blood flow (MBF) at rest and during dipyridamole-induced hyperemia. To investigate glucose metabolism, fluorine-18 deoxyglucose (18FDG) was used. For imaging of oxygen consumption, carbon-11 acetate clearance rate constants (k(mono)) were assessed at rest and during submaximal dobutamine infusion (20 microg/kg body weight per min). RESULTS: Global MBF reserve (dipyridamole-induced) was impaired in patients with IDC versus control subjects (1.7 +/- 0.21 vs. 2.7 +/- 0.10, p < 0.05). In patients with IDC, MBF reserve correlated with left ventricular (LV) systolic wall stress (r = -0.61, p = 0.01). Furthermore, in 16 of 22 patients with IDC (derived by dipyridamole perfusion) mismatch (decreased flow/increased 18FDG uptake) was observed in 17 +/- 8% of the myocardium. The extent of mismatch correlated with LV systolic wall stress (r = 0.64, p = 0.02). The MBF reserve was lower in the mismatch regions than in the normal regions (1.58 +/- 0.13 vs. 1.90 +/- 0.18, p < 0.05). During dobutamine infusion k(mono) was higher in the mismatch regions than in the normal regions (0.104 +/- 0.017 vs. 0.087 +/- 0.016 min(-1), p < 0.05). In the mismatch regions 18FDG uptake correlated negatively with rest k(mono) (r = -0.65, p < 0.05), suggesting a switch from aerobic to anaerobic metabolism. CONCLUSIONS: Patients with IDC have a decreased MBF reserve. In addition, low MBF reserve was paralleled by high LV systolic wall stress. These global observations were associated with substantial myocardial mismatch areas showing the lowest MBF reserves. In geographically identical regions an abnormal oxygen consumption pattern was seen together with a switch from aerobic to anaerobic metabolism. These data support the notion that regional myocardial ischemia plays a role in IDC.     

Amount of left ventricular hypertrophy determines the plasma N-terminal pro-brain natriuretic peptide level in patients with hypertrophic cardiomyopathy and normal left ventricular ejection fraction

BACKGROUND: N-terminal pro-brain natriuretic peptide (NT-proBNP) is increased in patients with hypertrophic cardiomyopathy (HCM); however, the determinants of NT-proBNP level have not been clarified in HCM. HYPOTHESIS: This study was performed to determine the relationship between NT-proBNP levels and various echocardiographic variables of patients with HCM and normal left ventricular ejection fraction (LVEF). METHODS: We assessed plasma NT-proBNP levels and echocardiographic variables of 36 patients (19 men, 58 +/- 14 years) with HCM and an LVEF of > or = 55%. Echocardiographic variables measured were LV wall thickness, end-diastolic LV internal dimension (LVIDd) and volume (LVEDV), LV mass, and LV mass index (LV mass/body surface area, LVMI). Left ventricular outflow tract pressure gradient, transmitral E and A velocities, deceleration time (DT) of the transmitral E wave, and septal annular E' velocity were measured by Doppler technique. The relationship between echocardiographic variables and plasma NT-proBNP level was analyzed. RESULTS: The plasma NT-proBNP level was 775.2 +/- 994.2 pg/ml (range 33.1-4729.0 pg/ml). It showed positive correlations with LV end-diastolic septal thickness (r = 0.39, p = 0.010) and LVMI (r = 0.27, p = 0.050), while it revealed negative correlations with LVIDd (r = -0.44, p = 0.004), LVEDV (r = -0.44, p = 0.004) and DT(r = -0.31,p = 0.034). The NT-proBNP level was higher in the patients with than in those without LV diastolic dysfunction (p = 0.033) and was independently related to LVIDd (p = 0.001), LVMI (p = 0.006) and DT (p = 0.031) by multivariate analysis. CONCLUSION: In patients with HCM and normal LVEF, the amount of LV hypertrophy and LV diastolic dysfunction may exert a significant role in determining plasma NT-proBNP level.     

Effects of ramipril on left ventricular mass and function in cardiovascular patients with controlled blood pressure and with preserved left ventricular ejection fraction: a substudy of the Heart Outcomes Prevention Evaluation (HOPE) Trial

OBJECTIVES: The purpose of this study was to assess the effects of ramipril on left ventricular mass (LVM) and function in vascular disease patients with controlled blood pressure (BP) and with preserved left ventricular ejection fraction (LVEF). BACKGROUND: Increased LVM and left ventricular (LV) volume and decreased LVEF predict clinical events. Angiotensin-converting enzyme inhibitors reduce LVM and LV volume and preserve LVEF in patients with hypertension and/or LV dysfunction, but have not been studied in patients with controlled BP and preserved LVEF. METHODS: We compared the effects of two doses of ramipril (10 mg/day and 2.5 mg/day) versus placebo in 506 patients with vascular disease on echocardiographic measures of LVM and LV function. RESULTS: Baseline BP and LVEF were similar, 131/76 mm Hg and 58%, in all treatment groups. After four years, LVM index increased by 3.98 +/- 2.08 g/m2 in the placebo and by 4.16 +/- 1.86 g/m2 in the ramipril 2.5 mg/day groups and decreased by 2.02 +/- 2.25 g/m2 in the ramipril 10 mg/day group (p = 0.02). The changes in LV end-diastolic and end-systolic volumes were 4.16 +/- 2.55 ml and 5.31 +/- 1.67 ml in the placebo, -0.43 +/- 2.75 ml and 2.90 +/- 1.45 ml in the ramipril 2.5 mg/day, and -5.90 +/- 2.93 ml and -1.90 +/- 1.55 ml in the ramipril 10 mg/day groups (p = 0.02 and p = 0.001). The changes in LVEF were -2.02 +/- 0.72%, -1.54 +/- 0.74%, and -0.17 +/- 0.72%, respectively (p = 0.01). CONCLUSIONS: Ramipril has beneficial effects on LV structure and function in vascular patients with controlled BP and with preserved LVEF.     

Hypertrophic cardiomyopathy with mild left ventricular remodeling: echocardiographic assessment using left ventricular wall motion score

OBJECTIVES: The present study sought to investigate the echocardiographic features of hypertrophic cardiomyopathy (HCM) with mild left ventricular (LV) remodeling, particularly in relation to wall motion abnormalities. METHODS: Among the 137 consecutive patients with HCM, 13 patients (mean age 52 +/- 13 years) who progressed to mild LV systolic dysfunction (LV ejection fraction (LVEF) of 35-50%) were studied. By reviewing the echocardiograms of these patients, wall motion score index (WMSI) was scored using 16 segments model. RESULTS: HCM patients with mild LV systolic dysfunction exhibited mild LV dilatation, mild left atrial dilatation, septal hypertrophy, and LV wall motion impairment localized in the septal and apical regions (septal WMSI 1.94 +/- 0.33 vs. total WMSI 1.51 +/- 0.25 and posterior WMSI 1.02 +/- 0.07; p < 0.001). During follow-up, further deterioration of LV systolic function (LVEF< 35%) was noted in five patients, who had less severe hypertrophy at the initial echocardiograms. These patients developed progressive LV cavity enlargement and more severe and extensive wall motion abnormalities, accompanied by septal akinesis and wall thinning, although posterolateral wall motion impairment was relatively mild (posterior WMSI 1.80 +/- 0.27 vs. septal WMSI 2.95 +/- 0.11; p < 0.001). CONCLUSIONS: Septal and apical wall motions are reduced in HCM with mild LV remodeling. As LV dysfunction progresses, septal akinesis and wall thinning develop and LV cavity enlargement becomes more prominent, though posterolateral wall motion impairment is relatively mild.     

Dobutamine as bridge to angiotensin-converting enzyme inhibitor-nitrate therapy in endstage heart failure

BACKGROUND: Intravenous inotropic intervention in congestive heart failure is generally associated with a poor prognosis and is largely used as a "bridge" to mechanical support or heart transplantation. HYPOTHESIS: We hypothesized that the inotropic support afforded by dobutamine may serve as a bridge to the introduction and intensification of angiotensin-converting enzyme (ACE) inhibitor-nitrate therapy. METHODS: We studied the efficacy of transitioning inotrope-dependent patients in endstage heart failure from intravenous dobutamine to high-dose ACE inhibitor-nitrates, with 1-year follow-up. Forty-nine sequential dobutamine-dependent patients with left ventricular ejection fraction (LVEF) 17+/-17% were treated with increasing lisinopril (1.9+/-1.5 to 46+/-28 mg/day) and isosorbide dinitrate (7+/-6 to 229+/-161 mg/day). Outpatient dobutamine was continued or repeat infusions pursued, as indicated, and dobutamine was tapered when feasible. RESULTS: During the following year, 14 of 49 patients required repeat dobutamine, with home treatment with dobutamine for 6.3+/-3.7 months (n = 5). At 1 year, New York Heart Association (NYHA) classification improved from 3.6+/-0.5 to 1.9+/-1.0, p < 0.0001; yearly hospitalizations fell from 2.7+/-2.3 to 1.2+/-3.0, p = 0.02; and LVEF rose from 17+/-7% to 24+/-11%, p < 0.0001. At 1 year, 14 patients who remained dobutamine dependent had significantly more severe symptoms than dobutamine-independent patients (n = 35). Transplant or death occurred in 7 of 14 patients with follow-up dobutamine, and in 5 of 35 patients free of subsequent dobutamine, p = 0.03. Patients with poor outcome (transplant n = 10, death n = 12) continued to be more limited (NYHA 2.7+/-0.9 vs. 1.7+/-0.9, p = 0.0002), with more follow-up hospitalizations (3.6+/-5.4 vs. 0.6+/-0.8, p = 0.0004), and no improvement in LVEF (17+/-8vs. 28+/-11%, p = 0.003). CONCLUSIONS: Of the patients on dobutamine inotropic support, 70% were successfully transitioned to ACE inhibitor-nitrate therapy, with improved symptoms and LVEF, and with reduced hospitalizations and follow-up dobutamine or transplant. Thirty percent of patients with continued need for dobutamine had a significantly poorer 1-year clinical outcome.     

Surgical revascularization of the myocardium in patients with chronic coronary disease and depressed left ventricular function: 1-year observation

Many reports confirm the importance and benefit of the surgical revascularization (CABG) in patients with ischemic heart disease and severely depressed left ventricular (LV) systolic function. This mode of treatment is better than medical therapy in patients with very low LV ejection fraction (LVEF) and can prolong the life. However, the effect of CABG on LV hemodynamics is still unclear. The aim of the study was: 1) to assess the effect of CABG on LV hemodynamics in patients with low LVEF and 2) to examine the influence of two types of cardioplegia-crystalloid (CC) and blood (BC) cardioplegia--on LV function during 1 year follow-up. 122 patients with stable angina pectoris qualified for CABG were included in the study. Patients were divided into two groups: group I-47 pts with LVEF < or = 40% and group II--75 pts with LVEF > 40% and then patients were randomized for two types of antegrade-retrograde cardioplegia (CC--subgroups Ia, IIa and BC--subgroups Ib, IIb). Before operation and 4 times after CABG (after 2-6 weeks, 3 months, 6 months and 1 year) echocardiographic examination was performed. Diameters of left atrium and ventricle, LVEF and wall motion score index (WMSI) were calculated. During 1 year 8 patients died (5 of them during perioperative period and 3 patients during follow-up). Patients in group I before operation were in higher NYHA and CCS class and had more often myocardial infarction. During each of the five echocardiographic examination the values of LVEF and WMSI did not differ between subgroups Ia vs Ib and IIa vs IIb. In group I, especially in patients with very low LVEF < or = 30%, the values of LVEF and WMSI improved significantly (p < 0.001) during 1 year of follow-up. But in group II a transient deterioration of LVEF (p < 0.05) 2-6 weeks after CABG was noted. We conclude that surgical revascularization in patients with severe depressed hemodynamics improves LV systolic function during 1 year follow-up. The use of CC or BC did not seem to make any difference to the early and long-term hemodynamic effect of the revascularization.     

A new tool for estimating left ventricular ejection fraction derived from wall motion score index

BACKGROUND: Radionuclide angiography (RNA) and echocardiography (biplane Simpson method) are the most accepted techniques for left ventricular ejection fraction (LVEF) assessment. A new method to evaluate LVEF based on the regional wall motion assessment of the LV was attempted. OBJECTIVE: To develop a simple method for LVEF estimation using wall motion score index (WMSI) with transthoracic echocardiography (TTE). METHODS: Two hundred and forty-three patients with abnormal LV contractility had TTE and RNA performed less than three days apart. The WMSI was calculated in all patients using the 16-segment model as proposed by the American Society of Echocardiography. For the first 150 patients, a correlation between LV WMSI and RNA EF was established to create a regression equation. This regression equation (RNA LVEF=92.8-25.8xWMSI) was used on 93 consecutive patients to compare this equation with RNA EF. From the total cohort (243 patients), three subgroups were studied specifically: atrial fibrillation (AF) (n=50 patients), dyskinesia (DK) (n=40 patients) and aneurysm (AN) (n=42 patients). RESULTS: Correlation between RNA EF and WMSI in the first 150 patients was r=0.82. In the second group of 93 consecutive patients, WMSI EF derived from the estimated regression equation correlated well with RNA EF (r=0.86). Correlation remained high in the three subgroups: AF (r=0.87), DK (r=0.87) and AN (r=0.80). In the 111 patients without DK, AN or AF correlation between RNA and the studied method was even higher (r=0.91). In a random subgroup of 54 patients, RNA was compared with the biplane Simpson method (49 of 54 patients, r=0.82). In the same subgroup of 54 patients, the score was modified to allow for mild hypokinesia (score=1.5) and severe hypokinesia (score=2.5) (54 of 54 patients, r=0.83). CONCLUSION: LVEF assessment by this new simple mathematical model using the WMSI is feasible and easy to use during routine TTE. It has excellent correlation with other methods such as biplane Simpson and RNA.     

Prognostic significance of the dobutamine echocardiography test in idiopathic dilated cardiomyopathy

Dobutamine stress echo provides potentially useful information on idiopathic dilated cardiomyopathy (IDC). From February 1, 1997, to October 1, 1999, 186 patients (131 men and 55 women, mean age 56 ± 12 years) with IDC, ejection fraction <35%, and angiographically normal coronary arteries were studied by high-dose (up to 40 μ/kg/min) dobutamine echo in 6 centers, all quality controlled for stress echo reading. In all patients, wall motion score index (WMSI) (from 1 = normal to 4 = dyskinetic in a 16- segment model of the left ventricle) was evaluated by echo at baseline and peak dobutamine. One hundred eighty-four patients were followed up (mean 15 ± 13 months) and only cardiac death was considered as an end point. There were 29 cardiac deaths. Significant parameters for survival prediction at univariate analysis are: ΔWMSI (chi-square 20.1; p <0.0000), New York Heart Association (NYHA) class (chi-square 17.57; p <0.0000), rest ejection fraction (chi-square 10.41; P = 0.0013), angiotensin-converting enzyme inhibitors (chi-square 8.23; P = 0.0041), and hypertension (chi-square 8.08, P = 0.0045). In the multivariate stepwise analysis only ΔWMSI and NYHA were independent predictors of outcome (ΔWMSI = hazard ratio 0.02, p <0.0000; NYHA CLASS = hazard ratio 3.83, p <0.0000). Kaplan-Meier survival estimates showed a better outcome for patients with a large inotropic response (ΔWMSI ≥0.44, a cutoff identified by receiver-operating characteristic curves analysis) than for those with a small or no myocardial inotropic response to dobutamine (93.6% vs 69.4%, P = 0.00033). Thus, in patients with IDC, an extensive contractile reserve identified by high-dose dobutamine stress echocardiography is associated with a better survival.     

Myocardial viability detected by dobutamine echocardiography in patients with chronic coronary artery disease, and long-term outcome after coronary angioplasty

Viable but dysfunctional myocardium detected by dobutamine echocardiography (DE) predicts early improvement in regional left ventricular (LV) function after percutaneous transluminal coronary angioplasty (PTCA). Whether DE can predict the long-term (>2 years) outcome after PTCA is still unclear. Thus, 50 patients (age 60.4+/-9.5 years) with chronic coronary artery disease and regional LV dysfunction who underwent DE 1 week before PTCA to assess myocardial viability were followed for 4.0+/-0.8 years. Regional LV function and LV ejection fraction (LVEF) were evaluated by 2-dimensional echocardiography in patients who remained event-free (cardiac death or myocardial infarction or unstable angina pectoris) after PTCA. At late follow-up (>2 years after PTCA), 29 patients showed regional LV function improvement, 15 showed no improvement, 3 showed worsening and 3 patients had cardiac events (1 nonfatal myocardial infarction and 2 unstable angina pectoris). LVEF improved (0.53+/-0.09 to 0.60+/-0.09, p<0.001) in patients with improved regional LV function, but deteriorated (0.38+/-0.03 to 0.30+/-0.03) in the 3 patients with worsened regional LV function. Of the 29 patients with improvement, 27 (93%) had viable myocardium, whereas only 3 (20%) of the 15 with no improvement had viable myocardium and all 6 of those with poor outcomes (3 with cardiac events and 3 with worsening) had viable myocardium (chi2 = 28.9, p<0.001). Patients with viable myocardium and a poor outcome had a lower mean LVEF before PTCA, and at 1 week and 3 months after PTCA (p = 0.004, <0.001, and =0.001, respectively), and a higher restenosis rate (p = 0.007) than patients with viable myocardium and without a poor outcome. It is concluded that viable myocardium detected by DE may predict long-term improvement in regional and global LV function after PTCA. However, patients with viable myocardium and persistent low LVEF are at risk for cardiac events or worsening of LV function.     

Plasma brain natriuretic peptide as a novel therapeutic indicator in idiopathic dilated cardiomyopathy during beta-blocker therapy: a potential of hormone-guided treatment

BACKGROUND: Plasma brain natriuretic peptide (BNP) is a sensitive and specific marker of left ventricular (LV) function. In the treatment of heart failure, especially in idiopathic dilated cardiomyopathy (IDC), beta-blocker (BB) therapy has been established as a powerful strategy. The purpose of this study was to analyze relationships between changes in BNP level and LV function during BB therapy in patients with IDC. METHODS: In 30 patients with IDC who had already received conventional therapy, measurement for plasma BNP and norepinephrine levels and echocardiographic indices were evaluated before and 2 and 6 months after carvedilol in 21 patients and at baseline and after 6 months in 9 patients who did not receive carvedilol. RESULTS: After 6 months carvedilol treatment significantly improved LV end-diastolic dimension (LVEDD) (65 +/- 8 to 61 +/- 8 mm) and LV ejection fraction (LVEF) (34% +/- 13% to 43% +/- 12%) with intergroup differences; it significantly decreased BNP (127 +/- 113 to 69 +/- 92 pg/mL) with no intergroup difference; however, it did not decrease norepinephrine. BNP correlated strongly with LVEDD, LVEF, and LV mass index in carvedilol-treated patients. The degree of change in BNP correlated with that in LVEDD or LVEF 6 months after carvedilol. All 14 patients with decreased or unchanged BNP levels showed an increase in LVEF, and 4 of 7 with a rise in BNP had decreased or unchanged LVEF. According to receiver operating characteristic analysis, the optimal BNP levels for detecting LVEF <35% before and after carvedilol were 75.5 and 69 pg/mL, respectively. CONCLUSION: Plasma BNP levels may accurately reflect alteration in LV function and structure and can be used as a therapeutic indicator for risk stratification in patients with IDC during BB therapy.     

Relation between left ventricular regional radial function and radial wall motion abnormalities using two-dimensional speckle tracking in children with idiopathic dilated cardiomyopathy

Left ventricular (LV) regional radial function and its relation to radial wall motion abnormalities have not been investigated in children with idiopathic dilated cardiomyopathy (IDC). Radial strain was measured using 2-dimensional speckle tracking to evaluate regional radial function and wall motion in 6 LV segments in 24 children (0 to 18 years old) with IDC and 16 healthy controls. Patients and controls were similar in age. Patients with IDC had higher heart rates (97 +/- 28 vs 77 +/- 19, p <0.05) and decreased ejection fraction (34 +/- 12% vs 66 +/- 7%, p <0.0001) compared with controls. Radial strain in all segments was significantly lower in patients with IDC. In IDC, average radial strain correlated well with ejection fraction (r = 0.8, p <0.0001). The SD of time to peak radial strain among 6 LV segments was significantly higher in patients with IDC than in controls (56 +/- 38 vs 15 +/- 12 ms, p <0.0001). Segmental peak radial strain correlated closely to time to peak radial strain in controls (r = 0.98, p = 0.0008), but less in patients with IDC (r = 0.76, p = 0.07). In conclusion, LV regional radial function is impaired in pediatric IDC, in association with increased radial dyssynchrony, revealing a possible important mechanism for LV dysfunction in these children.     

The presence of contractile reserve has no predictive value for the evolution of left ventricular function following atrio-ventricular node ablation in patients with permanent atrial fibrillation.

AIMS: Transcatheter ablation of the atrio-ventricular (AV) node followed by ventricular pacing has been shown to improve symptoms and quality of life (QOL) of patients with permanent atrial fibrillation (AF). In a considerable number of patients, cardiac function deteriorates after AV node ablation. We aimed to determine whether the absence of contractile reserve assessed by low dose dobutamine stress echocardiography (LDDSE) could identify those patients whose left ventricular (LV) function deteriorates after AV node ablation. METHODS: All 25 patients studied had permanent AF for at least 12 months. LVEF was determined 6 days and 3 months after AV node ablation by radionuclide ventriculography (RNV), at a paced rate of 80 beats/min. Deterioration in cardiac function was defined as a decrease in LVEF>5%. LDSE was performed in all patients before and after ablation. The presence of contractile reserve was defined as an improvement in regional function of >or=1 grade at low dose dobutamine in at least 4 segments. QOL measurements were taken using Minnesota, NHBP and MPWB questionnaires. RESULTS: LVEF showed no improvement in the overall group (52.8+/-11.1% vs. 51.8+/-9.8%, p=NS). QOL showed significant improvement in all questionnaires (Minnesota: 4.1+/-2.1 vs. 2.5+/-2, p=0.001; NHBP: 54.8+/-43.3 vs. 34.2+/-34.3, p=0.002; MPWB: 22.2+/-4.6 vs. 19.4+/-6.2, p=0.03). There was no significant difference in change of LVEF between patients with and without contractile reserve (-0.4+/-8.7 vs. 1.6+/-11.3, p=NS). However, patients with a preserved LVEF at baseline showed more frequently a reduced LVEF after AV node ablation (62.2+/-10.4% vs. 47.5+/-7.6%, p=0.001). CONCLUSIONS: (1) The absence of contractile reserve does not predict deterioration of cardiac function after AV node ablation. (2) AV node ablation results in a significant improvement in QOL, which is not necessarily associated with improvement of LVEF. (3) Higher baseline LVEF predicts deterioration of cardiac function. These data suggest that although AV node ablation is an excellent way of controlling symptoms, it should be avoided in patients with normal LV function.     

Relationship between peripheral monocytosis and nonrecovery of left ventricular function in patients with left ventricular dysfunction complicated with acute myocardial infarction.

BACKGROUND: Although ischemic heart failure is a major cause of mortality after acute myocardial infarction (AMI), the factors that may influence the nonrecovery of left ventricular function (LVF) after an AMI are still unclear. The aim of this study was to identify predictors of nonrecovery of LVF in patients with left ventricular (LV) dysfunction (defined as an echocardiographic ejection fraction (EF)<40%) complicated with AMI who undergo successful primary percutaneous coronary intervention (PCI). METHODS AND RESULTS: LVF recovery was defined as improvement of LVEF more than 10% compared with baseline LVEF at follow-up. One hundred and eight patients with LV dysfunction after AMI were divided into 2 groups according to the LVF recovery at follow-up: patients with LVF recovery (n=64) vs patients without LVF recovery (n=44). The follow-up LVEF was measured at 8+/-4 months after PCI. Patients without LVF recovery were older (76+/-13 years vs 59+/-14 years, p=0.023) and the baseline peak monocyte count, creatine kinase, and troponin I levels were significantly higher in patients without LVF recovery than in patients with LVF recovery. Delta LVEF (follow-up LVEF-baseline LVEF) correlated with baseline peak monocyte count (r=-0.417, p<0.001), baseline peak creatine kinase (r=-0.269, p=0.005), and baseline peak troponin I levels (r=-0.256, p=0.007). Multivariate analyses showed that baseline peak monocyte count and old age were the independent predictors of nonrecovery of LVF (hazard ratio; 3.38, 95% confidence interval (CI): 1.16-5.43, p=0.012, and hazard ratio; 2.38, 95% CI: 1.09-4.87, p=0.025, respectively). CONCLUSION: Peripheral monocytosis is associated with nonrecovery of LVF in patients with LV dysfunction complicating an AMI who underwent successful primary PCI. These results suggest an important role of monocytes in the expansion of the infarct and the development of chronic ischemic heart failure after reperfusion therapy.     

Left ventricular inotropic reserve and right ventricular function predict increase of left ventricular ejection fraction after beta-blocker therapy in nonischemic cardiomyopathy.

OBJECTIVES: The purpose of this study was to determine whether higher left ventricular inotropic reserve, defined as the increase in left ventricular ejection fraction (LVEF) in response to intravenous dobutamine infusion, or other ventriculographic variables predict the increase in LVEF after beta-blocker therapy in patients with nonischemic cardiomyopathy (NICM). BACKGROUND: Long-term beta-blocker therapy increases LVEF in some patients with NICM. Other than dose, there are no definite predictors of LVEF increase. METHODS: Thirty patients with LVEF < or = 0.35 and NICM underwent assessment of LVEF at rest and after a 10-min intravenous infusion of dobutamine at 10 microg/kg/min, using equilibrium radionuclide ventriculography. Age was 49 +/- 11 years, 33% women, functional class 2.6 +/- 0.5, duration of chronic heart failure 3.2 +/- 2.9 years, LVEF 0.21 +/- 0.07, left ventricular end-diastolic volume index 180 +/- 64 ml/m2. Right ventricular ejection fraction (RVEF) was abnormal in 37%. Mean dobutamine-induced augmentation of LVEF (DoALVEF) was 0.12 +/- 0.08. Patients were started on one of three beta-blockers (carvedilol, bucindolol or metoprolol) and the dose was advanced to the maximum tolerated. RESULTS: Left ventricular ejection fraction, reassessed 7.4 +/- 5.9 months after maximum beta-blocker dose was reached, increased to 0.34 +/- 0.13 (p = 0.0006). The following baseline variables correlated with improvement of LVEF: DoALVEF (p = 0.001), RVEF (p = 0.005), systolic blood pressure at end of dobutamine infusion (p = 0.02) and dose of beta-blocker (p = 0.07). In a multivariate analysis, only DoALVEF (p = 0.0003) and RVEF (p = 0.002) were predictive of the increase in LVEF. CONCLUSIONS: Patients with nonischemic cardiomyopathy who have higher left ventricular inotropic reserve and normal RVEF derive higher increase in LVEF from beta-blocker therapy.     

Low dose dobutamine stress echocardiography predicts the improvement of left ventricular systolic function in dilated cardiomyopathy

OBJECTIVE: To determine whether dobutamine stress echocardiography can predict the improvement of left ventricular systolic function in patients with dilated cardiomyopathy (DCM). METHODS: Myocardial contractile reserve, as assessed by dobutamine stress echocardiography, was determined in 18 patients with DCM (mean (SD) age 53 (13) years, left ventricular ejection fraction (LVEF) 28 (10)%) and compared with changes in LVEF during a follow up period of 15 (8) months. The LVEF and regional left ventricular wall motion score (0, normal to 4, dyskinesis) of 12 segments in short axis and four chamber views were analysed before and after dobutamine infusion (5-20 microg/kg/min). RESULTS: During a follow up period of 15 (8) months, a significant improvement in LVEF (> 20%) was found in seven patients but not in the remaining 11. Baseline haemodynamic findings were similar in both groups. Patients with an improvement in follow up LVEF showed a greater change in wall motion score from baseline during dobutamine infusion than patients with no improvement (at rest, 1.7 (0.4) v 1.9 (0.2), NS; dobutamine 10 microg/kg/min, 0.6 (0.4) v 1.2 (0.4), p < 0.05). The percentage change in LVEF during dobutamine infusion was also significantly greater in patients who showed improvement than in those who did not. The change in LVEF during the follow up period (follow up LVEF/baseline LVEF) correlated well with the change in LVEF during dobutamine stress (LVEF at rest/LVEF at dobutamine 10 microg/kg/min; r = 0.74, p < 0.001). CONCLUSIONS: Changes in left ventricular systolic performance during low dose dobutamine stress echocardiography are a useful marker to predict the outcome of left ventricular systolic function in patients with DCM.     

Relation of myocardial blood volume to left ventricular function and future cardiac events in patients with idiopathic dilated cardiomyopathy.

BACKGROUND: The hypothesis that myocardial blood volume is associated with left ventricular (LV) dysfunction and future cardiovascular events in patients with idiopathic dilated cardiomyopathy (IDC) was tested using intravenous myocardial contrast echocardiography (MCE). METHODS AND RESULTS: Thirty-five patients with IDC and 10 age-matched healthy control subjects were enrolled. Using MCE, background-subtracted and peak myocardial contrast intensity (calibrated PMCI) were calculated as measures of myocardial blood volume. LV ejection fraction (LVEF) was calculated using the modified Simpson method. Patients with IDC were stratified into 2 groups according to the median value of the calibrated PMCI [high value group (n=17): calibrated PMCI > or = -22.7 dB, low value group (n=18): calibrated PMCI < -22.7 dB]. The calibrated PMCI was markedly reduced in patients with IDC compared with the control subjects (p=0.0025) and closely related to LVEF (r=0.688, p<0.0001). In the multivariate model, calibrated PMCI was the independent variable that predicted cardiac events in patients with IDC. According to the Kaplan-Meier analysis, cardiac event-free rates were significantly lower in the low-value group than in the high-value group (p<0.01). CONCLUSIONS: Myocardial blood volume is closely related to LV dysfunction and future cardiac events in patients with IDC.     

Reverse left ventricular remodeling by intermittent dobutamine infusions and amiodarone in end-stage heart failure due to idiopathic dilated cardiomyopathy

BACKGROUND: The aim of this study was to evaluate the long-term effect of combined intermittent dobutamine infusions (IDI) and oral amiodarone on reverse left ventricular (LV) remodeling and hemodynamics of patients with idiopathic dilated cardiomyopathy (IDC) and end-stage congestive heart failure (CHF). METHODS: This non-randomized, prospective, clinical trial included sixteen consecutive patients suffering from dyspnea for a mean of 76+/-43 months, who presented with acute cardiac decompensation and were weaned from dobutamine therapy after an initial 72-h infusion. They were then placed on a regimen of oral amiodarone, 400 mg/day and weekly IDI, 10 microg/kg/min, for 8 h. The long-term clinical outcomes and the effects of treatment on reverse LV remodeling (echocardiographic parameters) and hemodynamics were evaluated at 3, 6, and 12 months of follow up. RESULTS: A significant degree of reverse LV remodeling, hemodynamic improvements, and survivals >1.5 years were observed in 9 of the 16 patients (56%). In addition, 5 patients (31% of entire cohort) were weaned from IDI after a mean of 61+/-41 weeks, and 4 remained clinically stable for 116+/-66 weeks thereafter. At 12 months of follow-up, LV end-diastolic and end-systolic volume indices had decreased from 231+/-91 to 206+/-80 ml/m2 (P=0.002) and from 137+/-65 to 110+/-50 ml/m2 (P=0.003), respectively, right atrial pressure from 16+/-6 to 5.6+/-4 mm Hg, (P=0.031), and pulmonary capillary wedge pressure from 29+/-4 to 16+/-5.4 mm Hg, P=0.000, while LV ejection fraction had increased from 22+/-6% to 27.3+/-8% (P=0.006). CONCLUSIONS: In end-stage CHF due to IDC, long-term treatment with IDI and oral amiodarone caused reverse LV remodeling, and allowed permanent and successful weaning from IDI in 1/4 of patients.