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PubMed2000

Asymptomatic left ventricular dysfunction in the community.

The syndrome of chronic heart failure (CHF) is usually attributable to left ventricular dysfunction (LVD), which is most commonly systolic in nature. Many patients who go on to develop heart failure pass through a phase in which they have significant systolic dysfunction but lack clinical symptoms and signs: so-called asymptomatic LVD (ALVD). Treatment of this asymptomatic phase with angiotensin-converting enzyme inhibitors can delay the progression to CHF and ameliorate its substantial morbidity and mortality. This article reviews the epidemiology of ALVD. ALVD is at least as prevalent as CHF, is mainly caused by ischemic heart disease, significantly impairs effort capacity, reduces quality of life, and is associated with a substantial mortality rate. As such, it would appear to satisfy many of the criteria required to screen for a disease. The natriuretic peptide hormones (atrial natriuretic peptide and brain natriuretic peptide ) are elevated in subjects with ALVD. BNP, in particular, has acceptable accuracy to detect LVD in the general population. In particular, it has a high negative predictive value meaning a low concentration makes the presence of significant LVD highly unlikely. As such it has the potential to be a cost-effective means of filtering subjects suspected of having LVD and allowing more appropriate use of tertiary referrals for specialist assessment and detailed echocardiography.

Disease Progression↗

PubMed2001

Effect of revascularization on left ventricular remodeling in patients with heart failure from severe chronic ischemic left ventricular dysfunction.

Few data exist regarding the effect of revascularization on left ventricular (LV) geometry in patients with severe LV systolic dysfunction and viable myocardium. We hypothesized that patients with chronic ischemic LV dysfunction but viable myocardium will have improved LV geometry after revascularization, which in turn will improve long-term outcome. Accordingly, 70 patients with severe ischemic LV dysfunction (LV ejection fraction <0.35) were studied at rest. They then either underwent revascularization (n = 36) or were treated medically (n = 34). Fifty-four patients had viable myocardium, and 16 did not. They were evaluated for change in LV function and geometry (size and shape) a mean of 21 months later. Further follow-up was performed for a mean of 3.5 years to determine outcome. Patients with viable myocardium had improvement not only in regional and global function, but also in LV geometry (shape and size), which was independent of and incremental to the improvement in function. On long-term follow-up, change in LV end-systolic volume was the only multivariate discriminator between 15 patients who died and 55 who did not, irrespective of whether they had undergone revascularization. Thus, measurement of the effect of revascularization of viable myocardium in chronic ischemic heart disease should not only include improvement in resting regional and global LV function, but also LV geometry. Improvement in LV geometry contributes to better LV systolic function, which in turn is the best predictor of survival after revascularization.

Cohort Studies↗

PubMed2002

Depressed inotropic response to increased preload in rabbit hearts with left-ventricular dysfunction induced by chronic myocardial infarction.

Chronic (8 weeks) coronary artery ligation caused marked left-ventricular dysfunction (LVD) in rabbits. The positive inotropic effect observed in vivo with intraventricular injection of saline in sham-operated (control) animals was reversed in rabbits with LVD. In vitro, a step increase in filling pressure from 10 to 15 cm H(2)O caused an immediate increase, followed by a slow increase, in left-ventricular peak systolic pressure (LVP(max)) and cardiac output (CO) over 5-7 min in sham-operated hearts. No significant slow positive inotropic effect was observed in hearts with LVD in response to a standard increase in filling pressure. Progressive increases in filling pressure increased (LVP(max)) and CO to a maximum value at 20 cm H(2)O in control hearts. In the LVD group, progressive increases in filling pressure caused a negative inotropic response and reduced CO. Hearts from the LVD group were significantly dilated compared with control hearts but no significant changes in myocardial compliance were observed in beating or quiescent hearts. These studies reveal an impaired inotropic response to increased ventricular filling in LVD rabbit hearts; this defect included the depression of the slow inotropic response to an increased end-diastolic volume. These changes appear not to be accompanied by altered passive mechanical properties.

Animals↗

PubMed2003

Beneficial hemodynamic and renal effects of intravenous enalaprilat following coronary artery bypass surgery complicated by left ventricular dysfunction.

OBJECTIVE: Angiotensin-converting enzyme inhibitors are an effective therapy for all stages of heart failure due to reduced systolic left ventricular function. Because sufficient data on intravenous angiotensin-converting enzyme inhibitors following coronary artery bypass surgery complicated by postoperative left ventricular dysfunction are unavailable, the efficacy and safety of intravenously administered enalaprilat were evaluated. DESIGN: A placebo-controlled, randomized, double-blind protocol. SETTING: Postoperative intensive care unit at the German Heart Institute Berlin. PATIENTS: Forty patients with a left ventricular ejection fraction <35% following coronary artery bypass surgery on the second postoperative day or after weaning from intra-aortic balloon counterpulsation. INTERVENTIONS: A loading dose of enalaprilat 0.625 mg infused over 1 hr was followed by 5 mg/24 hrs administered continuously for up to 72 hrs. MEASUREMENTS AND MAIN RESULTS: Systemic and pulmonary hemodynamic variables, blood gases, hormonal variables, renal function, and electrolytes were measured before and repeatedly during therapy. Acute effects were as follows: At 1 hr, enalaprilat increased the cardiac index (p <.001), stroke volume index (p <.001), and right ventricular stroke work index (p <.03) compared with placebo, whereas mean arterial pressure (p <.008) and both systemic (p <.001) and pulmonary (p <.02) vascular resistance decreased. Continuous effects were as follows: Over 72 hrs, enalaprilat decreased diastolic pulmonary artery pressure (p <.019), pulmonary artery occlusion pressure (p <.02), and central venous pressure (p <.02). The cardiac and stroke volume indexes were consistently higher in the enalaprilat group, whereas systemic and pulmonary vascular resistances were lower. The arterial blood-pressure lowering effect was blunted and heart rate remained unchanged. Mixed venous oxygenation (p <.02) was higher and arterial oxygenation was not modified. Finally, enalaprilat increased creatinine clearance (p <.002) and decreased creatinine (p <.02) and urea (p <.03). CONCLUSIONS: Intravenous enalaprilat safely and effectively improves cardiac and renal function following coronary artery bypass surgery complicated by postoperative left ventricular dysfunction.

Adult↗

PubMed1998

Prognostic value of myocardial viability in medically treated patients with global left ventricular dysfunction early after an acute uncomplicated myocardial infarction: a dobutamine stress echocardiographic study.

BACKGROUND: Residual viable myocardium identified by dobutamine stress after myocardial infarction may act as an unstable substrate for further events such as subsequent angina and reinfarction. However, in patients with severe global left ventricular dysfunction, viability might be protective rather than detrimental. The aim of this study was to assess the impact on survival of echocardiographically detected viability in medically treated patients with global left ventricular dysfunction evaluated after acute uncomplicated myocardial infarction. METHODS AND RESULTS: The data bank of the large-scale, prospective, multicenter, observational Echo Dobutamine International Cooperative (EDIC) study was interrogated to select 314 medically treated patients (271 men; age, 58+/-9 years) who underwent low-dose (</=10 microg x kg-1 x min-1) dobutamine for the detection of myocardial viability and high-dose dobutamine for the detection of myocardial ischemia (</=40 microg x kg-1 x min-1 with atropine </=1 mg) performed 12+/-6 days after an acute uncomplicated myocardial infarction and showing a moderate to severe resting left ventricular dysfunction (wall motion score index [WMSI] >1.6). Patients were followed up for 9+/-7 months. Low-dose dobutamine stress echocardiography identified myocardial viability in 130 patients (52%). Dobutamine-atropine stress echocardiography was positive for ischemia in 148 patients (47%) and negative in 166 patients (53%). During the follow-up, there were 12 cardiac deaths (3.8% of the total population). With the use of Cox proportional hazards model, delta low-dose WMSI (the variation between rest WMSI and low-dose WMSI) was shown to exert a protective effect by reducing cardiac death by 0.8 for each decrease in WMSI at low-dose dobutamine (coefficient, -0.2; hazard ratio, 0.8; P<0.03); WMSI at peak stress was the best predictor of cardiac death in this set of patients (hazard ratio, 14.9; P<0.0018). CONCLUSIONS: In medically treated patients with severe global left ventricular dysfunction early after acute uncomplicated myocardial infarction, the presence of myocardial viability identified as inotropic reserve after low-dose dobutamine is associated with a higher probability of survival. The higher the number of segments showing improvement of function, the better the impact is of myocardial viability on survival. The presence of inducible ischemia in this set of patients is the best predictor of cardiac death.

Aged↗

PubMed2005

Sudden death in patients with myocardial infarction and left ventricular dysfunction, heart failure, or both.

BACKGROUND: The risk of sudden death from cardiac causes is increased among survivors of acute myocardial infarction with reduced left ventricular systolic function. We assessed the risk and time course of sudden death in high-risk patients after myocardial infarction. METHODS: We studied 14,609 patients with left ventricular dysfunction, heart failure, or both after myocardial infarction to assess the incidence and timing of sudden unexpected death or cardiac arrest with resuscitation in relation to the left ventricular ejection fraction. RESULTS: Of 14,609 patients, 1067 (7 percent) had an event a median of 180 days after myocardial infarction: 903 died suddenly, and 164 were resuscitated after cardiac arrest. The risk was highest in the first 30 days after myocardial infarction--1.4 percent per month (95 percent confidence interval, 1.2 to 1.6 percent)--and decreased to 0.14 percent per month (95 percent confidence interval, 0.11 to 0.18 percent) after 2 years. Patients with a left ventricular ejection fraction of 30 percent or less were at highest risk in this early period (rate, 2.3 percent per month; 95 percent confidence interval, 1.8 to 2.8 percent). Nineteen percent of all sudden deaths or episodes of cardiac arrest with resuscitation occurred within the first 30 days after myocardial infarction, and 83 percent of all patients who died suddenly did so in the first 30 days after hospital discharge. Each decrease of 5 percentage points in the left ventricular ejection fraction was associated with a 21 percent adjusted increase in the risk of sudden death or cardiac arrest with resuscitation in the first 30 days. CONCLUSIONS: The risk of sudden death is highest in the first 30 days after myocardial infarction among patients with left ventricular dysfunction, heart failure, or both. Thus, earlier implementation of strategies for preventing sudden death may be warranted in selected patients.

Aged↗

PubMed1999

Non-cardioplegic coronary surgery in patients with severe left ventricular dysfunction.

OBJECTIVES: Although most surgeons use cardioplegia for myocardial protection during coronary artery bypass grafting (CABG), some still use non-cardioplegic methods with very good early and long-term outcome. However, the results in patients with severe left ventricular dysfunction remain unproved. This study evaluates the perioperative mortality and morbidity in patients with severe left ventricular dysfunction submitted to CABG using non-cardioplegic methods. METHODS: From April 1990 through December 1997, 3,180 patients were consecutively subjected to isolated CABG using non-cardioplegic methods, for construction of the distal anastomoses. This prospective study is based on the 107 (3.4%) patients with severe impairment of the left ventricular function (ejection fraction < 30%). The mean age at operation was 57.0 +/- 9.2 years and 95.3% of patients were male. Fifty three patients (49.5%) were in class CCS III/IV and 12 (11.2%) were subjected to urgent surgery. A history of previous myocardial infarction was recorded in 99 (92.5%) patients. Ninety seven (90.6%) patients had triple vessel and 17 (15.9%) left main stem disease, and 77 (71.9%) had a left ventricular end-diastolic pressure > 20 mmHg. Cardiopulmonary bypass time was 73.1 +/- 21.7 min. The mean number of grafts per patient was 3.2. At least one internal mammary artery was used in all cases and 16 patients (14.9%) had bilateral internal mammary artery grafts (1.2 arterial grafts/patient). Endarterectomies were performed in 23 (21.5%) patients. RESULTS: Perioperative mortality was 2.8% (respiratory-1; cardiac-2). Forty one (38.3%) patients required inotropes, but for longer than 24 h in only 12 (11.2%), and two (1.9%) needed intra-aortic counterpulsation. The incidence of myocardial infarction was 2.8%. Two (1.9%) patients had reintervention for haemorrhage and another five (4.6%) for sternal complications. The incidences of supraventricular arrhythmias, renal failure and cerebrovascular accident were 16.8%, 3.6% and 2.8%, respectively. The mean time of hospital stay was 9.3 +/- 6.4 days. CONCLUSION: These results appear to demonstrate that non-cardioplegic methods afford good myocardial protection and operating conditions with excellent applicability, even in patients with severe left ventricular dysfunction.

Aged↗

PubMed2003

Enalapril reduces the incidence of diabetes in patients with chronic heart failure: insight from the Studies Of Left Ventricular Dysfunction (SOLVD).

BACKGROUND: Diabetes mellitus is a predictor of morbidity and mortality in patients with heart failure. The effect of angiotensin-converting enzyme (ACE) inhibitors on the prevention of diabetes in patients with left ventricular dysfunction is unknown. The aim of this retrospective study was to assess the effect of the ACE inhibitor enalapril on the incidence of diabetes in the group of patients from the Montreal Heart Institute enrolled in the Studies of Left Ventricular Dysfunction (SOLVD). METHODS AND RESULTS: Clinical charts were evaluated for fasting plasma glucose (FPG) levels by blinded reviewers. A diagnosis of diabetes was made when a FPG > or =126 mg/dL (7 mmol/L) was found at 2 visits (follow-up, 2.9+/-1.0 years). Of the 391 patients enrolled at the Montreal Heart Institute, 291 were not diabetic (FPG <126 mg/dL without a history of diabetes), 153 of these were on enalapril and 138 were on placebo. Baseline characteristics were similar in the 2 groups. Forty patients developed diabetes during follow-up, 9 (5.9%) in the enalapril group and 31 (22.4%) in the placebo group (P<0.0001). By multivariate analysis, enalapril remained the most powerful predictor for risk reduction of developing diabetes (hazard ratio, 0.22; 95% confidence intervals, 0.10 to 0.46; P<0.0001). The effect of enalapril was striking in the subgroup of patients with impaired FPG (110 mg/dL [6.1 mmol/L] < or =FPG <126 mg/dL) at baseline: 1 patient (3.3%) in the enalapril group versus 12 (48.0%) in the placebo group developed diabetes (P<0.0001). CONCLUSIONS: Enalapril significantly reduces the incidence of diabetes in patients with left ventricular dysfunction, especially those with impaired FPG.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2003

[Reversible left ventricular dysfunction manifesting as hyperkinesis of the basal and the apical areas with akinesis of the mid portion: a case report].

A 60-year-old man underwent emergent cardiac catheterization because of anterior chest oppression. He had been treated with calcium antagonist and nitrate. Coronary angiography showed no organic stenosis. However, left ventriculography revealed that the basal and the apical areas were hyperkinetic and the mid portion was akinetic. Echocardiography showed that the bizarre-shaped left ventricular dysfunction had completely recovered after a week. Serial electrocardiography demonstrated initial ST-segment elevation in the precordial leads followed by T-wave inversion in II, III, a VF and V4-V6. Coronary artery spasm provocation tests were negative. Endomyocardial biopsy revealed focal myocardial depletion and mild fibrosis. The present case may be an atypical form of tako-tsubo-like left ventricular dysfunction in which the left ventricular contraction is symmetric with both hyperkinetic and akinetic areas.

3-Iodobenzylguanidine↗

PubMed2005

[Dobutamine hemodynamics for aortic stenosis with left ventricular dysfunction].

Patients with aortic stenosis (AS) and left ventricular (LV) systolic dysfunction have a poor short-term prognosis. In this setting, the decrease in transaortic gradients has an independent prognostic value for operative risk and long-term outcome. The 2 main issues for these patients are: (1) The real severity of AS; (2) How to stratify operative risk and evaluate long-term prognosis. Dobutamine Hemodynamics has the potential to address these issues. In case of relative AS, valve area is increased by dobutamine (final valve area > 1.2 cm2 with a mean pressure gradient <30 mmHg); on the basis of published data, medical treatment is justified in this case. Left ventricular contractile reserve is defined an increase in stroke volume, by 20% or more, under dobutamine. Operative risk is between 5 and 11% in case of LV contractile reserve and long-term outcome is improved by surgery in this case. In contrast, operative risk varies from 30 to 60% in case of exhausted reserve; this risk is also determined by other factors such as the presence of coronary artery disease and associated comorbidities. All these parameters are factored into risk-benefit analysis in order to determine the best therapeutic approach for each patient.

Aortic Valve Stenosis↗

PubMed1995

[Results of coronary surgery in mildly symptomatic patients with left ventricular dysfunction, multivessel disease and stenotic single residual patent vessel].

BACKGROUND: While efficacy of coronary artery bypass surgery in patients with depressed left ventricular function and myocardial ischemia is widely recognized, its results in patients in the absence of clinical evidence of myocardial ischemia remain uncertain. The purpose of this study was to evaluate the effects of coronary revascularization in comparison with conventional medical therapy in subjects with ischemic cardiomyopathy and myocardial ischemia presumed on the basis of angiographic anatomy but not demonstrated by functional testings. METHODS: We selected retrospectively patients who underwent coronary angiography from 1986 trough 1993 and met the following criteria: presence of three-vessel coronary artery disease, occlusion of two and significant luminal narrowing (> or = 50%) of the third major epicardial artery, left ventricular dysfunction (ejection fraction < or = 40%), no angina or presence of mild angina, absence of inducible ischemia on exercise test and, when performed, of redistribution in the vascular territory of the patent vessel. RESULTS: Thirty-one consecutive patients underwent isolated surgical revascularization treatment, while thirty medically treated patients with matched clinical characteristics were selected. Age (61 +/- 10 vs 62 +/- 9), gender (M/F 27/3 vs 24/7), NYHA class I-II (53 vs 62%) or NYHA III-IV (47 vs 38%), incidence of previous infarction (87 vs 94%), number of reversible defects in the vascular territory of the patient vessel on stress scintigraphy (0.6 vs 0.5), patent vessel (right coronary artery 7 vs 10; left circumflex 14 vs 12; left anterior descending 9 vs 9) and left ventricular ejection fraction (28 +/- 8 vs 31 +/- 7), were similar in the two groups (medical vs surgical). Surgically treated patients exhibited a lower proportion of overall cardiac deaths (7/31, 23% vs 19/30, 63%; p < 0.001), and more prolonged survival (67 +/- 9.3 vs 34 +/- 2.5 months; p = 0.04, Mantel and Cox test) than medically treated patients, respectively. The incidence of perioperative myocardial infarction was 10% (3/31). Causes of cardiac death were myocardial ischemia (9/19; 47%), sudden death (5/19; 26%) and heart failure (5/19; 26%) in medical patients, while were surgery (3 cases) and surgery related infection (1 case) (total 4/7; 57%), myocardial ischemia (1/7; 14%), sudden death (1/7; 14%) and heart failure (1/7; 14%) in surgical patients. Cox proportional hazard regression analysis with survival as the dependent variable, identified treatment, surgical or medical, as the best predictor of cardiac events (chi square improvement 9.36, p = 0.002). The next most powerful predictors were NYHA class and ACE-inhibitors treatment (chi square improvement 4.47 and 2.79, respectively). CONCLUSIONS: In patients with left ventricular dysfunction, multivessel coronary artery disease and single patent but stenotic residual vessel, coronary artery bypass grafting appear to offer a better survival than medical therapy, even in the absence of clinically evident myocardial ischemia.

Aged↗

PubMed2004

Furosemide and the progression of left ventricular dysfunction in experimental heart failure.

OBJECTIVES: We tested the hypothesis that furosemide accelerates the progression of left ventricular systolic dysfunction in a tachycardia-induced porcine model of heart failure. BACKGROUND: Furosemide activates the renin-angiotensin-aldosterone system in patients with congestive heart failure (CHF). Such activation may contribute to CHF progression, but prospective data are lacking. METHODS: Thirty-two Yorkshire pigs were randomized to furosemide (1 mg/kg intramuscularly daily, mean 16.1 +/- 0.9 mg) or placebo. Thereafter, a pacing model of heart failure was utilized to produce systolic dysfunction in both sets of animals (fractional shortening <0.16 by echocardiogram). The goal was to determine if furosemide would accelerate the progression of left ventricular dysfunction in the "treated" group. After sacrifice, sodium-calcium exchanger currents and their responsiveness to isoproterenol were measured during voltage clamp. All investigators were blinded to treatment assignment. RESULTS: Furosemide shortened the time to left ventricular dysfunction (35.1 +/- 5.1 days in placebo versus 21.4 +/- 3.2 days for furosemide animals; p = 0.038, log-rank test). By day 14, aldosterone levels were significantly higher in furosemide animals (43.0 +/- 11.8 ng/dl vs. 17.6 +/- 4.5 ng/dl; p < 0.05). Serum sodium was reduced (133.0 +/- 0.9 mmol/l furosemide vs. 135.7 +/- 0.8 mmol/l placebo; p < 0.05), but no difference in norepinephrine, potassium, magnesium, creatinine, or urea nitrogen was present. Basal sodium-calcium exchanger currents were significantly increased and isoproterenol responsiveness depressed by furosemide. CONCLUSIONS: Tachycardic pigs given furosemide had significant acceleration of both contractile and metabolic features of CHF, including left ventricular systolic dysfunction, elevated serum aldosterone levels, and altered calcium handling in a controlled experimental model of heart failure.

Adrenergic beta-Agonists↗

PubMedDate not supplied

Plasma profiles of circulating granulocyte-macrophage colony-stimulating factor and soluble cellular adhesion molecules in acute myocardial infarction. Contribution to post-infarction left ventricular dysfunction.

No in vivo data exist about the relationship of circulating granulocyte-macrophage colony stimulating factor (GM-CSF) and soluble adhesion molecules ICAM-1 and VCAM-1 (sICAM-1 and sVCAM-1) to the severity of acute myocardial infarction (AMI) and the pathophysiological events of post-infarction left ventricular dysfunction. We investigated the kinetics of these inflammatory mediators in the plasma of patients with AMI, and correlated the findings with the clinical severity of the disease during the first week of hospitalization as well as the degree of left ventricular dysfunction one month after the AMI. Plasma levels of inflammatory markers were determined in 41 AMI patients (all received thrombolytic treatment) by ELISA assays, serially during the first week of hospitalization and one month after hospital admission. Patients (n = 20) with uncomplicated AMI (Killip class I) were classified as group A, patients (n = 21) with AMI complicated by heart failure manifestations (Killip classes II and III) were classified as group B, while 20 age- and sex-matched volunteers were used as healthy controls. A sustained increase in GM-CSF, sICAM-1 and sVCAM-1 plasma concentrations was observed only in group B during the first week of the study. Patients from group B exhibited significantly higher levels of GM-CSF (P < 0.01), sICAM-1 (P < 0.05) and sVCAM-1 (P < 0.01) than patients from group A and the healthy controls (P < 0.001). In group B patients, significant correlations were observed between the peak of GM-CSF levels and the peak of serum creatine kinase-MB (r = 0.42; P < 0.05), white blood cell counts (r = 0.67; P < 0.001) and LVEF (r =- 0.51; P < 0.01). At one month follow-up, patients (n = 17) with severe post-infarction left ventricular dysfunction (LVEF 35%). Significant correlations were observed between GM-CSF levels and left ventricular end-diastolic volume index (r = 0.55; P < 0.001) or left ventricular end-systolic volume index (r = 0.49; P = 0.001). We have found a significant elevation of plasma GM-CSF and soluble adhesion molecules during the course of AMI, with the highest values in patients with AMI complicated by heart failure manifestations and severe left ventricular dysfunction. These monocyte-related inflammatory mediators may actively contribute to the pathophysiology of the disease and post-infarction cardiac dysfunction.

Aged↗

PubMed1998

Predicting outcome after myocardial revascularization in patients with left ventricular dysfunction.

In order to identify the risk factors which could predict outcome after coronary artery bypass grafting in patients with left ventricular dysfunction, 80 consecutive patients with an ejection fraction < or = 30%, who underwent isolated coronary artery bypass grafting at the authors' centre between January 1994 and May 1996 were evaluated. Preoperatively, mean(s.d.) ejection fraction was 27.1(3.8)%, 56 patients (70%) had angina, and 56(70%) were in New York Heart Association (NYHA) functional class III or IV. There were five operative deaths, with a hospital mortality rate of 6.3%. Significant risk factors for hospital death were NYHA class IV, preoperative ventricular arrhythmias and left ventricular end-diastolic volume index > 110 ml/m2. At mean follow-up of 15(7) (range 6-30) months, there were six late deaths, five of which were from cardiac causes. Actuarial survival rate at 2 years was 82(5)% and freedom from cardiac death 84(5)%. Risk factors for overall mortality from cardiac causes were preoperative grade 2 mitral regurgitation, associated with left ventricular dilatation, and renal dysfunction (creatininaemia > or = 180 micromol/l). At follow-up, mean ejection fraction was 37.5(8.4)%, and the overall functional status had improved: 12 patients (18%) had angina and eight (12%) were in NYHA class III and IV. Myocardial revascularization in patients with left ventricular dysfunction can be performed with acceptably low operative risk, good survival rate at 2 years, and functional status improvement. Patients with extensive ventricular dilatation, associated with significant mitral regurgitation, have a lower life expectancy and less functional benefits from coronary artery bypass grafting. These patients are better treated by cardiac transplantation.

Aged↗

PubMed1998

Is heart rate variability a reliable method to assess autonomic modulation in left ventricular dysfunction and heart failure? Assessment of autonomic modulation with heart rate variability.

Autonomic dysfunction seems to be involved in the progression and prognosis of congestive heart failure. Measurement of heart rate variability (HRV) provides a noninvasive method to obtain reliable and reproducible information on autonomic modulation of heart rate, but there is a difficulty in using HRV as a quantitative estimate of autonomic dysfunction in heart failure. This study was aimed at testing the hypothesis that abnormal modulation of heart rate assessed by power spectrum analysis may be present also in asymptomatic patients with left ventricular dysfunction and progress in patients with overt symptoms of congestive heart failure. HRV was measured in three groups of subjects: Group 1: 30 patients with chronic heart failure; Group 2: 21 patients with asymptomatic left ventricular dysfunction; and Group 3: 25 healthy volunteers as control group. HRV was evaluated by autoregressive spectral analysis with 600-beat ECG samples, while subjects were quietly recumbent (BSI), in conditions of controlled breathing (15 acts/min) (RSC) and passive orthostatism after tilting (80 degrees) (TLT). Patients in group 1 showed a reduction in the standard deviation of the R-R intervals (SDRR) (p<0.0003) and in the low frequency component (LF) (p<0.0001) compared to normal subjects. Low frequency component was not detectable in 11 patients of group I (p<0.0008). On RSC and TLT, group 1 failed to show any modification in the low frequency and high frequency components (HF) under any stimulation. Group 2 showed no modification at baseline evaluation, no increase in the high frequency component on RSC and in LF during TLT compared to controls (p<0.01 and p<0.0001 respectively). At baseline, group 1 had a lower SDRR (p<0.03) and LF (p<0.0001) vs. group 2, whereas during stimulation the two groups exhibited the same behaviour. In conclusion, reduced heart rate variability is specific for both asymptomatic and symptomatic post-ischemic left ventricular dysfunction. Our results suggest that frequency domain analysis of heart rate variability during a stimulation test allows a more accurate definition of the degree of autonomic control of heart rate.

Autonomic Nervous System↗

PubMed2004

A protocol to evaluate myocardial viability in ischemic left ventricular dysfunction using magnetic resonance imaging and a gadolinium-based contrast agent.

OBJECTIVES: A protocol to evaluate myocardial viability in ischemic left ventricular dysfunction using magnetic resonance imaging and a gadolinium-based contrast agent. METHODS: Twenty-two patients were prospectively offered a cardiac MR exam between November 2003 and June 2004. Twelve had a history of anterior wall MI, eight had a history of inferior wall MI and two patients had MI of undetermined location. Eight patients had left ventricular dysfunction. RESULTS: No patient with transmural scarring extending through more than 75% of the wall recovered normal wall motion despite revascularization when evaluated fourteen months later. Of the other three with scarring extending to less than 75% there was recovery in two patients. CONCLUSION: Viability assessment by cardiac MR using gadolinium contrast is a robust technique. No segment with >75% transmural enhancement (TE) recovers despite revascularization, while all segments with <25% TE recover contractility. Between these two extremes, methods other than extent of TE may have to be used, particularly low-dose dobutamine stress testing or evaluation of percentage of hyperenhanced area compared to the normal area in each segment.

Clinical Protocols↗

PubMed1989

Programmed ventricular stimulation in patients with left ventricular dysfunction and ventricular tachycardia: effects of acute hemodynamic improvement due to nitroprusside.

To assess the electrophysiologic effects of acute hemodynamic improvement in patients with left ventricular systolic dysfunction, 12 patients with a left ventricular ejection fraction less than 0.40 and a history of sustained monomorphic ventricular tachycardia were studied. All patients had underlying coronary artery disease. Patients underwent programmed cardiac stimulation in random order during a baseline period and with nitroprusside infusion. Mean pulmonary capillary wedge pressure decreased from 20 +/- 8 mm Hg at baseline study to 8 +/- 3 mm Hg during nitroprusside infusion (p less than 0.0001). Pulmonary artery, right atrial and systemic arterial pressures also decreased with nitroprusside (p less than 0.01). Cardiac output did not change. Left ventricular dimensions, determined by two-dimensional echocardiography, decreased significantly during nitroprusside infusion. The right ventricular effective refractory period, measured during ventricular drive trains at cycle lengths of 400 and 600 ms, were similar during baseline and nitroprusside periods (271 +/- 30 versus 274 +/- 31 ms at 600 ms, and 249 +/- 25 versus 246 +/- 18 ms at 400 ms). In 2 patients no ventricular arrhythmias were induced during either study period; in the other 10, ventricular tachyarrhythmias were induced during both periods. The mean number of extrastimuli required to induce a ventricular tachyarrhythmia was similar during the baseline period (1.8 +/- 0.6) and during nitroprusside infusion (1.9 +/- 0.7). As well, the mean cycle length of ventricular tachycardia induced was similar during the baseline period (347 +/- 61 ms) and during nitroprusside infusion (342 +/- 70 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1999

Right-sided pulsus alternans in diastolic left ventricular dysfunction.

Pulsus alternans is usually found in patients with reduced systolic ventricular function. We describe a patient with shortness of breath, hypertension, and left ventricular hypertrophy, but with normal left and right systolic function. Pulsus alternans was demonstrated in the pulmonary wedge position, pulmonary artery, and right ventricle, but not in the aorta or left ventricle. Cathet. Cardiovasc. Intervent. 47:336-339, 1999.

Diastole↗