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Extent of coronary artery disease as a predictor of outcomes in acute myocardial infarction complicated by heart failure, left ventricular dysfunction, or both.

BACKGROUND: Left ventricular systolic dysfunction (LVSD) and heart failure (HF) are powerful predictors of poor outcome after acute myocardial infarction (MI). It is not known, however, whether the extent of coronary artery disease (CAD) independently influences cardiovascular (CV) outcomes in these high-risk patients. METHODS: In the VALIANT, 14703 patients were randomly assigned to receive either captopril monotherapy, valsartan monotherapy, or a valsartan and captopril combination between 0.5 and 10 days after acute MI complicated by LVSD, HF, or both. Cox proportional hazards models were used to evaluate the relation between the extent of CAD (the number of diseased vessels as assessed by angiography) and a range of CV outcomes and all-cause mortality. RESULTS: Coronary angiography data were available on 5742 (40%) of the 14703 randomized patients. Single-vessel disease was reported in 1955 patients (34%), 2-vessel disease in 1598 (28%), and 3-vessel disease in 2189 (38%). For all CV outcomes, the risk increased with the severity of CAD (P for trend < .002). A comparison of single-, 2-, and 3-vessel disease showed that, after adjusting for all known covariates, including revascularization and ejection fraction, 2-vessel disease was associated with a 40% increased hazard (P = .008) and 3-vessel disease was associated with an 85% increased hazard (P < .001) for all-cause mortality. The fully adjusted hazard ratios for death and other CV outcomes increased significantly with increasing extent of CAD. CONCLUSIONS: Increasing extent of CAD, as detected by angiography, is a significant and independent risk factor for adverse CV outcomes after MI complicated by HF, LVSD, or both. The observed risk was apparent even after excluding patients who had undergone revascularization.

Aged↗

Determinants of pulmonary hypertension in left ventricular dysfunction.

OBJECTIVES: This study sought to analyze the determinants of pulmonary hypertension in patients with left ventricular dysfunction. BACKGROUND: Pulmonary hypertension in patients with left ventricular dysfunction is a predictor of poor outcome. The independent role of cardiac functional abnormalities in the genesis of pulmonary hypertension is unclear. METHODS: In 102 consecutive patients with primary left ventricular dysfunction (ejection fraction < 50%), systolic pulmonary artery pressure was prospectively measured by Doppler echocardiography (using tricuspid regurgitant velocity), and left ventricular systolic and diastolic function, functional mitral regurgitation, cardiac output and left atrial volume were quantified. RESULTS: Systolic pulmonary artery pressure was elevated in patients with left ventricular dysfunction (51 +/- 14 mm Hg [mean +/- SD]), but the range was wide (23 to 87 mm Hg). Of the numerous variables correlating significantly with systolic pulmonary artery pressure, the strongest were mitral deceleration time (r = -0.61, p = 0.0001; odds ratio of pulmonary pressure > or = 50 mm Hg [95% confidence interval] if < 150 ms, 48.8 [14.8 to 161]) and mitral effective regurgitant orifice (r = 0.50, p = 0.0001; odds ratio [95% confidence interval] if > or = 20 mm2, 5.9 [2.3 to 15.5]). In multivariate analysis, these two variables were the strongest predictors of systolic pulmonary artery pressure in association with age (p = 0.005). Ejection fraction or end-systolic volume was not an independent predictor of pulmonary artery pressure. CONCLUSIONS: Pulmonary hypertension is frequent and highly variable in patients with left ventricular dysfunction. It is not independently related to the degree of left ventricular systolic dysfunction but is strongly associated with diastolic dysfunction (shorter mitral deceleration time) and the degree of functional mitral regurgitation (larger effective regurgitant orifice). These results emphasize the importance of assessing diastolic function and quantifying mitral regurgitation in patients with left ventricular dysfunction.

Aged↗

Risk factors for sudden cardiac death in patients with chronic renal insufficiency and left ventricular dysfunction.

BACKGROUND: Patients with ischemic left ventricular dysfunction have a high risk of sudden cardiac death (SCD). It is, however, unclear if the risk and risk factors of SCD in these patients is modulated by the coexistence of mild chronic renal insufficiency. METHODS: We performed a post-hoc analysis of the outcome associated with mild renal dysfunction, as defined by an estimated glomerular filtration rate (eGFR) of <75 ml/min/1.73 m2 in patients allocated to the conventional medical therapy arm of the Multicenter Automatic Defibrillator Implantation Trial-II. RESULTS: In multivariable analysis, renal dysfunction was independently associated with significant increased risks for all-cause mortality (hazard ratio [HR] = 1.86; 95% CI 1.13-3.05) and SCD (HR = 2.00; 95% CI 1.01-4.02), but not non-SCD, compared to patients without renal dysfunction. Independent predictors of SCD in patients with renal dysfunction were: increased resting heart rate (HR = 2.40; 95% CI 1.50-3.86); low diastolic blood pressure (HR = 3.23; 95% CI 1.52-6.66), and a prolonged QRS duration (HR = 1.63; 95% CI 1.02-2.61). Beta-blocker therapy was independently associated with a significant reduction in the risk of SCD in patients with an eGFR of <75 ml/min/1.73 m2 (HR = 0.61; 95% CI 0.38-0.99). CONCLUSION: These findings suggest that renal dysfunction significantly increases the risk for SCD in patients with left ventricular dysfunction, and that beta-blocker therapy reduces the risk of arrhythmic mortality in heart failure patients with coexisting renal insufficiency.

Adrenergic beta-Antagonists↗

Myocardial revascularization as a therapeutic strategy in the patient with advanced ventricular dysfunction.

The number of patients with severe ventricular dysfunction from coronary artery disease is constantly increasing. Although the medical management of these patients with angiotensin-converting enzyme inhibitors and beta-blockers has favorable impact on the morbidity and mortality the overall prognosis is still poor. Historically many of these patients have been referred for transplantation. In the past few years there has been an increasing amount of information about the utility of surgical revascularization in patients with low ejection fraction. Careful patient selection and optimal perioperative management is of critical importance for good outcome. Coronary artery bypass grafting (CABG) can be performed relatively safely despite the advanced level of left ventricular dysfunction. Quality of life is improved by CABG with elimination of angina and enhanced functional capacity. Improvement in the ejection fraction and increased survival after the operation has been objectively demonstrated. However patients with advanced right ventricular dysfunction, pulmonary hypertension, redo bypass and ungraftable coronaries should be considered for heart transplantation. In this review we describe our experience and focus on pertinent issues in patient selection, perioperative management and long term outcome after coronary artery bypass grafting.

Aged↗

Age and aneurysm position predict patterns of left ventricular dysfunction after subarachnoid hemorrhage.

Cardiac injury, including left ventricular dysfunction, frequently occurs in patients with subarachnoid hemorrhage. Patterns of left ventricular dysfunction often do not follow coronary artery distributions, and may correlate with myocardial sympathetic innervation. Left ventricular dysfunction of the anterior and anteroseptal walls that spares the apex is unusual for patients with myocardial infarction and may represent a neurally mediated pattern of injury. We performed serial echocardiography on 225 patients with subarachnoid hemorrhage and classified those with regional wall-motion abnormalities as following either an apex-sparing (AS) or apex-affected (AA) pattern. Wall-motion abnormalities were found in 61 of 225 patients studied (27%). The AS pattern was found in 49% of these patients. Younger age and anterior aneurysm position were independent predictors of this AS pattern. Both patterns of wall-motion abnormalities appear to be transient, reversible phenomena. The AS pattern may represent a unique form of neurally mediated cardiac injury.

Adult↗

Left ventricular dysfunction is associated with prolonged average ventricular fibrillation cycle length in patients with implantable cardioverter defibrillators.

OBJECTIVES: In cellular studies, ventricular refractoriness (ERP) is prolonged in heart failure (CHF), but clinical evidence is lacking. The average ventricular fibrillation cycle length (VFCL) has been shown to correlate with local ERP. We hypothesized that the VFCL increases with left ventricular (LV) dysfunction. Therefore, we evaluated intracardiac VFCL recorded by implantable defibrillators (ICD) in patients with and without LV dysfunction. METHODS: We analyzed intracardiac VFCL recorded by sensing leads of Ventak MINI (Guidant) ICD in 49 patients (35 men; age 54 +/- 13 years; 25 (51%) with coronary artery disease; mean LV ejection fraction (EF) 41 +/- 17%, range 76-10) from the European Ventak MINI Investigator Group. No patients were receiving antiarrhythmic drugs, including beta-blockers. Mean and median VFCL were obtained at predischarge testing during first charge time (4.5 +/- 2.7 s, range 1.4-11). RESULTS: Mean median VFCL was 186 +/- 21ms (range 150-230 ms). Patients with LVEF >/= 50% (n = 14) had shorter median VFCL than patients with LVEF < 50% (n = 35), (171 +/- 14 vs. 191 +/- 20 ms; p = 0.002). Median VFCL correlated with LVEF (r = -0.41; p = 0.003) and age (r = 0.28, p = 0.04), but was not significantly associated with charge time and defibrillation threshold at implant. Similar results occurred with mean VFCL. In multiple linear regression and correlation models, only LVEF% was a significant predictor (p < 0.05 for all models) of median VFCL. CONCLUSIONS: LV dysfunction prolongs averaged VFCL in patients at risk for malignant ventricular arrhythmias who have implantable cardioverter defibrillators. This phenomenon might be related to alterations in the ventricular refractory period.

Analysis of Variance↗

Aspartate and glutamate-enriched cardioplegia in left ventricular dysfunction.

BACKGROUND: The effects of exogenous L-aspartate and L-glutamate-enriched cardioplegia on postoperative left ventricular functions after coronary artery bypass surgery in patients with moderate left ventricular dysfunction (left ventricular ejection fraction [LVEF]= 30-40%) were studied. METHODS: In this prospective randomized study, 22 patients with moderate left ventricular dysfunction (mean LVEF = 37.27%+/- 3.43%), who underwent elective coronary artery bypass surgery, were examined. Isothermic substrate-enriched [L-aspartate and L-glutamate (13 mmol/L)] blood cardioplegia was used in 11 patients (Group AG), and cardioplegia including only potassium and sodium bicarbonate was used in 11 patients (Group C). All hemodynamic parameters for left and right heart were studied in both groups. Total perfusion time was 126.63 +/- 44.91 minutes versus 114.81 +/- 43.66 minutes (p = 0.54). The aortic cross-clamp time was 77.09 +/- 28.02 minutes versus 67.81 +/- 22.77 minutes (p = 0.4), respectively. The amount of cardioplegic solutions were 7218.2 +/- 3043.6 mL versus 5454.5 +/- 3048.1 mL (p = 0.167). Mean number of distal anastomosis were 3 +/- 0.89 versus 2.9 +/- 0.7 (p = 0.793). RESULTS: There was no difference between both groups in intra- and postoperative periods. In coronary sinus blood gas measures, myocardial acidosis caused by the aortic cross-clamp was found to be more severe in the Group C, but delta pH (0.12 +/- 0.14 vs. 0.092 +/- 0.058; p = 0.613) and delta lactate (1.39 +/- 1.03 vs. 1.62 +/- 0.85; p = 0.579) were similar in both groups. Free oxygen radical production caused by aortic cross-clamp was significant in the Group C. Not all myocardial enzymes, but Troponin-T levels were found higher in control group than the study group (0.6 +/- 0.36 vs. 0.36 +/- 0.25; p = 0.1). CONCLUSIONS: Although L-aspartate and L-glutamate favor myocardial metabolic functions, they do not have any affect on myocardial functional recovery in patients with moderate left ventricular dysfunction.

Aspartic Acid↗

Preoperative identification of patients likely to have left ventricular dysfunction after aortic valve replacement. Participants in the Veterans Administration Cooperative Study on Valvular Heart Disease.

The purpose of this study was to identify preoperative and intraoperative variables predictive of left ventricular dysfunction 6 months after aortic valve replacement. Patients were considered to have postoperative left ventricular dysfunction if the end-diastolic-volume index was greater than or equal to 101 ml/m2 or if the ejection fraction was less than or equal to 0.50. Data from 180 patients entered into the Veterans Administration Cooperative Study on Valvular Heart Disease who had technically satisfactory cardiac catheterizations 6 months postoperatively were analyzed by a series of univariate and multivariate analyses. For the 88 patients with preoperative aortic stenosis, the most powerful predictor of postoperative left ventricular dysfunction in the final multivariate model was preoperative left ventricular ejection fraction (p = 0.0001), followed by preoperative myocardial infarction (p = 0.012), aortic valve gradient (p = 0.020), and incomplete coronary revascularization (p = 0.059). Abnormal preoperative left ventricular ejection fraction had a sensitivity of 72% and a specificity of 82% in identifying patients with postoperative left ventricular dysfunction. Preoperative left ventricular systolic-volume index greater than or equal to 40 ml/m2 had a similar sensitivity and specificity (79% and 84%, respectively). For the 36 patients with aortic regurgitation, preoperative left ventricular ejection fraction was again the most powerful predictor of postoperative left ventricular dysfunction (p = 0.013), followed by left ventricular systolic pressure (p = 0.038) and arteriovenous oxygen difference (p = 0.054). For the 56 patients with mixed aortic stenosis and regurgitation, left ventricular systolic pressure (p = 0.007) and preoperative myocardial infarction (p = 0.022) were the variables predictive of postoperative left ventricular dysfunction. Although many patients with preoperative left ventricular dysfunction experience improved left ventricular performance after aortic valve replacement, performance does not always return to normal. For patients with either aortic stenosis or regurgitation, the strongest predictor of postoperative left ventricular dysfunction is preoperative dysfunction. These data support the concept that patients with moderate or severe aortic stenosis or regurgitation should be operated on before the onset of significant left ventricular dysfunction.

Aortic Valve↗

Non-ischemic left ventricular dysfunction after pediatric cardiac transplantation: treatment with plasmapheresis and OKT3.

BACKGROUND: Acquired left ventricular dysfunction after pediatric cardiac transplantation is associated with a high mortality rate. It often occurs without biopsy evidence of cellular rejection or severe transplant coronary arteriopathy. METHODS: We employed a protocol for treatment of acquired, non-ischemic left ventricular dysfunction utilizing plasmapheresis, monoclonal anti-T-cell antibody (OKT3), cyclophosphamide and steroids, regardless of the results of endomyocardial biopsy. Left ventricular dysfunction was defined as an echocardiographic shortening fraction of <29% and/or symptoms of congestive heart failure requiring inotropic support. Transplant coronary arteriopathy was excluded by coronary angiography in all cases. RESULTS: Ten pediatric heart transplant recipients were treated for 13 episodes of non-ischemic left ventricular dysfunction. Biopsy scores were low grade (ISHLT Grade 1A or 1B) in 8 episodes. Eight of 10 patients had a history of non-compliance in regularly taking immunosuppressant medications. Inotropic support was required in 9 of 13 cases, with a median duration of 5 days. Median left ventricular shortening fraction was 17% at time of presentation. Normalization of shortening fraction occurred a median of 40 days from the start of treatment. Survival to hospital discharge occurred in 11 of 13 (85%) patients. Long-term patient survival, however, was only 50% at 24 months after presentation with a first episode of acquired left ventricular dysfunction. CONCLUSIONS: Use of plasmapheresis, OKT3, cyclophosphamide and steroids resulted in successful short-term reversal of non-ischemic left ventricular dysfunction in pediatric heart transplant patients, but long-term survival remained poor.

Adolescent↗

[Tamponade in patients with systolic left ventricular dysfunction. An atypical presentation].

BACKGROUND: Left ventricular failure has been described following surgery due to localized compression of the left ventricle and in case of diastolic left ventricular dysfunction after pericardiotomy or pericardiocentesis. CASE REPORTS: Global heart failure was observed in 3 patients with dilated cardiopathy who developed tamponade. Systolic left ventricular dysfunction was caused by ischemic heart disease in one patient and secondary to anthracyclin chemotherapy in the two others. The effusion was successfully removed with pericardiocentesis in all three cases. No specific complications were observed. DISCUSSION: Although exceptional, tamponade may occur in patients with signs of left ventricular failure.

Adult↗

Prognostic significance of nonsustained ventricular tachycardia identified postoperatively after coronary artery bypass surgery in patients with left ventricular dysfunction.

INTRODUCTION: Nonsustained ventricular tachycardia (NSVT) occurs frequently in the postoperative period (< or = 30 days) after coronary artery bypass graft (CABG) surgery, a setting where many factors may play a role in its genesis. The prognosis of NSVT in this setting in patients with left ventricular (LV) dysfunction is unknown. This study was designed to assess its significance. METHODS AND RESULTS: We compared the outcome of untreated patients enrolled in the Multicenter Unsustained Tachycardia Trial with coronary artery disease (CAD), LV dysfunction, and NSVT identified postoperatively after CABG (n = 228; mean age 67 years, 84% males) versus nonpostoperative settings (n = 1,302; mean age 66 years, 85% males). Sustained monomorphic ventricular tachycardia was induced in 27% and 33% (P = 0.046) of patients with postoperative and nonpostoperative NSVT, respectively. The 2- and 5-year rates of arrhythmic events were 6% and 16%, respectively, in postoperative patients versus 15% and 29% in nonpostoperative patients (unadjusted P = 0.0020, adjusted P = 0.0082). The 2- and 5-year overall mortality rates were 15% and 36%, respectively, for postoperative patients versus 24% and 47% for nonpostoperative patients (unadjusted P = 0.0005, adjusted P = 0.027). Patients whose NSVT was identified early (<10 days) versus late (10-30 days) after CABG had significantly lower 2- (13% vs 23%) and 5-year (30% vs 52%) mortality rates (unadjusted P = 0.024, adjusted P = 0.018). CONCLUSION: In this population of patients with CAD and LV dysfunction, the occurrence of postoperative NSVT, especially within 10 days after CABG, portends a far better outcome than when it occurs in nonpostoperative settings. This suggests that in a such setting, NSVT represents a less specific risk factor for future events and should be considered when assigning risk and treatment of similar patients.

Adrenergic beta-Antagonists↗

Post-resuscitation right ventricular dysfunction: delineation and treatment with dobutamine.

BACKGROUND: Left ventricular dysfunction after resuscitation from cardiac arrest has been well described. Treatment with dobutamine improves post-resuscitation left ventricular function. Right ventricular function following resuscitation has not been investigated. The purposes of this study were to examine right ventricular function following resuscitation and determine whether dobutamine would improve post-resuscitation right ventricular function. METHODS AND RESULTS: Right ventricular function was measured in 28 swine (29+/-1 kg) before and after resuscitation from 15 min of untreated ventricular fibrillation. Twelve animals received dobutamine at 10 mcg/kg/min while 16 animals served as untreated controls. Among controls, right ventricular dysfunction post-resuscitation was demonstrated by a decrease in right ventricular ejection fraction and an increase in right ventricular end-diastolic pressure. Among animals treated with dobutamine, there was a significant improvement in right ventricular function post-resuscitation compared to untreated controls. CONCLUSIONS: This study establishes that right ventricular systolic and diastolic dysfunction does occur after prolonged cardiac arrest from ventricular fibrillation. Dobutamine can ameliorate post-resuscitation right ventricular dysfunction.

Animals↗

Predictors of postoperative ventricular dysfunction in infants who have undergone primary repair of a ventricular septal defect.

By means of postoperative radionuclide angiography we identified a subset of infants undergoing primary repair of their ventricular septal defects (VSD) who had postoperative morbidity and ventricular dysfunction. Twenty-three consecutive infants undergoing repair of an uncomplicated VSD were studied. Radionuclide-determined postoperative ventricular dysfunction (VD), as defined by a left ventricular ejection fraction less than 0.30 2 to 4 hours after surgery, was correlated with clinical signs of postoperative morbidity. Six patients developed postoperative VD. Clinical correlates of VD included the use of postoperative inotropic support, increased number of postoperative intensive care days, and a low growth rate 3 months postoperatively. Potential predictors of VD were evaluated. A preoperative pulmonary-to-systemic blood flow ratio (Qp/Qs) greater than 3.0 and a pulmonary-to-systemic vascular resistance ratio (Rp/Rs) less than 0.20, taken in combination, gave a positive predictive value for VD of 100%. It is concluded that the preoperative Qp/Qs and Rp/Rs can be used to predict those infants at risk for postoperative morbidity following repair of their VSD.

Cardiac Catheterization↗

Ventricular fibrillation threshold and local dispersion of refractoriness in isolated rabbit hearts with left ventricular dysfunction.

Patients with congestive heart failure or left ventricular dysfunction (LVD) have a high incidence of ventricular tachyarrhythmias and sudden cardiac death. In addition to structural, metabolic and neuroendocrine changes, mechanoelectrical feedback may play a role in arrhythmogenesis in heart failure. Three groups of rabbits (n = 10 for each) were studied: chronic coronary ligation with ejection fraction (EF) > or = 0.45 or < 0.45, and sham-operated controls. Ventricular fibrillation (VF) thresholds were measured at LV pressures of 0 and 40 mm Hg during modified Langendorff perfusion. Intervals between local activations during VF (VFI) were used as an index of refractoriness. Global dispersion was expressed as coefficient of variation of VFI; local dispersion by maximum difference in VFI between adjacent sites. Median VF threshold was lower at 0 mm Hg in the lower EF group compared to controls (30 vs. 67.5 mA, P<0.05). VF threshold in control hearts was lower at 40 mm Hg than at 0 mm Hg (P<0.01), but there was no further reduction in threshold in LVD hearts at 40 mm Hg. Global dispersion of VFI did not differ significantly between groups. Local dispersion of VFI in the lower EF group was greater than in controls at 0 mm Hg in the infarct border zone (P<0.05). At 40 mm Hg, local dispersion of VFI in zones bordering and remote from the infarct were greater in both LVD groups than in controls (P<0.05). Local inhomogeneity of refractoriness is more marked in the infarct border zone, but latent abnormalities are evident in normal myocardium of rabbits with left ventricular dysfunction and are revealed by left ventricular distension.

Animals↗

Relationship of current and past smoking to mortality and morbidity in patients with left ventricular dysfunction.

OBJECTIVES: The aim of this study was to evaluate the impact of smoking in patients with left ventricular dysfunction. BACKGROUND: The impact of smoking in patients with left ventricular dysfunction has not been well-studied. METHODS: We compared the incidence of death, hospitalization due to heart failure and myocardial infarction (MI) in current smokers to ex-smokers of < or =2 years and ex-smokers of >2 years duration to never-smokers among participants of the Study Of Left Ventricular Dysfunction (SOLVD) Prevention and Intervention trials. Participants all had left ventricular ejection fraction (LVEF) <35% and follow-up was over a mean of 41 months. RESULTS: Complete smoking status and outcome data were available in 6,704 subjects. There were 1,562 current smokers, 1,317 ex-smokers of < or =2 years, 2,354 ex-smokers of >2 years and 1,471 never-smokers. After adjusting for baseline differences of age, LVEF, race and etiology of heart failure, current smoking was associated with a significantly increased all-cause mortality (relative risk [RR]: 1.41, 95% confidence interval [CI]: 1.25 to 1.58, p < 0.001) compared with ex-smokers and never-smokers. The incidence of death or recurrent congestive heart failure requiring hospitalization or MI was significantly greater (RR: 1.39, 95% CI: 1.26 to 1.52, p < 0.001) in current smokers compared with ex-smokers and never-smokers. There were no significant differences in the number of deaths or hospitalizations due to heart failure between ex-smokers and never-smokers. This effect was consistent across both the SOLVD Prevention and Treatment trials. CONCLUSIONS: Current smoking is a powerful independent predictor of morbidity (recurrent heart failure and MI) and mortality in patients with left ventricular dysfunction. Quitting smoking appears to have a substantial and early effect (within two years) on decreasing morbidity and mortality in patients with left ventricular dysfunction, which is at least as large as proven drug treatments recommended in patients with left ventricular dysfunction.

Aged↗

Relation of ventricular size and function to heart failure status and ventricular dysrhythmia in patients with severe left ventricular dysfunction.

Patients with severe left ventricular (LV) dysfunction may or may not have overt heart failure and ventricular dysrhythmia. To study factors behind this variability, we examined a subset of 311 patients from the Studies of Left Ventricular Dysfunction-95 with a history of moderate heart failure (treatment trial) and 216 with no failure (prevention trial), all with ejection fractions <0.35. Echocardiographic variables were compared between trials and also correlated with dysrhythmia in 258 patients, and with neurohormones in 199 patients. Compared with prevention patients, treatment patients had larger LV end-diastolic diameter, end-systolic volume, sphericity index, and ratio of early to late diastolic filling velocity by Doppler (E/A ratio), lower LV ejection fraction and atrial contribution to ventricular filling, and similar LV mass, end-diastolic volume, and estimates of systolic wall stress. With prevention and treatment patients combined, the prevalence of abnormally elevated atrial natriuretic peptide was 92% in the highest tertile of E/A ratio compared with 55% in the lower tertiles (p=0.006). Across tertiles of LV end-diastolic volume, there was an increase in the prevalence of nonsustained ventricular tachycardia (24%, 45%, and 45%; p=0.007) and premature ventricular complexes >10/hour (48%, 62%, and 80%; p<0.001). Thus, in severe LV dysfunction, ventricular filling indexes suggestive of high filling pressures, along with larger and more spherical ventricles, are particularly common in patients with overt heart failure, thus suggesting that diastolic properties and the degree of ventricular remodeling affect clinical status. Once ejection fraction is significantly reduced, the prevalence of ventricular dysrhythmia correlates with LV size rather than systolic function. This observation lends support to previous experimental findings on the role of myocardial stretch and scar in the genesis of dysrhythmia.

Aged↗

Post-systolic shortening during dobutamine stress echocardiography predicts cardiac survival in patients with severe left ventricular dysfunction.

BACKGROUND: Patients with severe left ventricular dysfunction and myocardial viability by dobutamine stress echocardiography (DSE) or F18-fluorodeoxyglucose-single-photon emission computed tomography (FDG-SPECT), experience improved survival after coronary revascularization. Pulsed wave-tissue Doppler imaging (PW-TDI)-derived ejection phase shortening (EPS) and post-systolic shortening (PSS) velocities may help to quantify DSE. We assessed these variables in a prospective long-term follow-up. METHODS: Eighty patients (58 men, mean age 63+/-9 years) with left ventricular dysfunction (radionuclide ventriculography mean ejection fraction, 34+/-11%) underwent both DSE and FDG-SPECT for myocardial viability. Viable myocardium was improvement from rest to low dose or worsening of wall motion at peak DSE and normal perfusion, mildly reduced perfusion with FDG uptake or severely reduced or absent perfusion with increased FDG uptake (mismatch) at FDG-SPECT. EPS, PSS velocities and EPS/PSS ratio during DSE were analysed using a six-segment model. Coronary revascularization bypass grafting was performed in 62 patients. All patients completed a long-term (9-year) follow-up for cardiac death. RESULTS: The segmental prevalence of severe dyssynergy was 77%. On a patient basis myocardial viability was detected by EPS/PSS ratio (31%), FDG-SPECT (34%) and DSE (26%). A significant improvement of Kaplan-Meier survival was predicted in viable compared with nonviable revascularized patients (P < 0.01). Both EPS/PSS ratio and FDG-SPECT, compared to DSE alone, tended to allocate more accurately univariate prediction of death-free outcome (odds ratio, 2.5 and 2.7 compared with 2.1). CONCLUSIONS: TDI adds objective variables to DSE, helping to recognize viable myocardium and optimize prediction of death-free outcome in long-term follow-up, with favorable comparison with nuclear techniques.

Cardiomyopathies↗

Detection of left ventricular dysfunction after acute myocardial infarction: comparison of clinical, echocardiographic, and neurohormonal methods.

OBJECTIVE: The SAVE study showed that captopril improves mortality in patients with left ventricular dysfunction after myocardial infarction and that this benefit occurred even in patients with no clinically overt heart failure. On the basis of this, it seems important to identify correctly which patients have left ventricular dysfunction after a myocardial infarction. The objective was to compare various methods of identifying patients with left ventricular dysfunction (left ventricular ejection fraction, LVEF, < or = 40%) after acute myocardial infarction. The methods compared were echocardiography (quantitative and qualitative visual assessment), clinical evaluation (subjective assessment and three clinical score methods), and measurement of plasma concentrations of cardiac natriuretic peptide hormones (atrial and brain natriuretic peptides, ANP and BNP). DESIGN: Cross sectional study of left ventricular function in patients two to eight days after acute myocardial infarction. SETTING: Coronary care unit of a teaching hospital. PATIENTS: 75 survivors of a recent myocardial infarction aged 40 to 88 with no history of cardiac failure and without cardiogenic shock at the time of entry to the study. MAIN OUTCOME MEASURES: Sensitivities and specificities of the various methods of detecting left ventricular dysfunction were calculated by comparing them with a cross sectional echocardiographic algorithm for LVEF. RESULTS: Clinical impression was poor at identifying LVEF < 40% (sensitivity 46%). Clinical scoring improved this figure somewhat (modified Peel index sensitivity 64%). Qualitative visual assessment echocardiography was a more sensitive method (sensitivity 82%) for detecting LVEF < 40%. Plasma BNP concentration was also a sensitive measure for detecting left ventricular dysfunction (sensitivity 84%) but plasma ANP concentration was much poorer (sensitivity 64%). CONCLUSION: Left ventricular dysfunction is easily and reliably detected by echocardiographic measurement of LVEF and also by a quick qualitative echocardiographic assessment but is likely to be missed by clinical assessment alone. High concentrations of plasma BNP maybe another useful indicator of left ventricular dysfunction, particularly in hospitals where not all patients can be screened by echocardiography or radionuclide ventriculography after myocardial infarction.

Adult↗