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PubMed1992

Reversible left ventricular dysfunction induced by recurrent ventricular tachycardia.

Two cases of transient LV dysfunction associated with VT are described. Both patients had a history of palpitations of several years' duration without symptoms of congestive heart failure. The reason for presentation was an increase in frequency and duration of palpitation. Decreased LV wall motion, observed by 2DE, normalized shortly after treatment of the VT. Diffusely decreased LV wall motion is associated with frequent episodes of VT and may mimic DCM except that signs and symptoms of heart failure are absent.

Adult↗
PubMed1993

Changes in ventricular volume, wall thickness and wall stress during progression of left ventricular dysfunction. The SOLVD Investigators.

To assess the long-term changes in cardiac function in asymptomatic patients with severe left ventricular dysfunction, left ventricular (cineangiography) and right ventricular (radionuclide angiography) function were assessed at baseline in 49 patients enrolled in the prevention arm of the Studies of Left Ventricular Dysfunction. After an average follow-up period of 12.4 months, 30 patients (11 randomized to the placebo group and 19 to the enalapril group) could be restudied to assess the progression of ventricular dysfunction. After 1 year of follow-up, the changes in heart rate, left ventricular end-diastolic and systolic pressure and right ventricular volumes were comparable in both groups. However, there were modest but opposite changes in left ventricular end-diastolic volume (+9 ml/m2 with placebo vs. -10 ml/m2 with enalapril, p < 0.05) and end-systolic volume (+5 ml/m2 with placebo vs. -13 ml/m2 with enalapril, p < 0.05). Mean systolic wall stress increased insignificantly in both groups, whereas ejection fraction increased from 29% to 31% in the placebo group and from 28% to 32% with enalapril (p = NS, placebo vs. enalapril). Even in asymptomatic patients with severe left ventricular dysfunction, there was a slow progression of left ventricular dilation. Enalapril administration appeared to slow this progression, but wall stress was not normalized by the treatment at the doses used in the study, indicating that at least one of the stimuli for further remodeling remained present.

Adult↗
PubMed1993

Frequency and significance of right ventricular dysfunction during inferior wall left ventricular myocardial infarction treated with thrombolytic therapy (results from the thrombolysis in myocardial infarction [TIMI] II trial). The TIMI Research Group.

To determine the effect of thrombolytic therapy on the frequency of right ventricular (RV) dysfunction, and whether RV dysfunction is a risk factor for morbidity and mortality after discharge from the hospital, 1,110 patients in the Thrombolysis in Myocardial Infarction (TIMI) II trial with acute inferior wall left ventricular myocardial infarction were studied. RV dysfunction was defined as an RV wall motion abnormality on equilibrium radionuclide ventriculography performed a mean of 9 days after admission to the hospital. Fifty-eight patients (5%) had RV dysfunction. Baseline clinical characteristics among patients with and without RV dysfunction were similar. However, patients with RV dysfunction had a lower mean left ventricular ejection fraction (51.2 +/- 1.2% vs 55.5 +/- 0.3%; p < 0.001) and a greater frequency of in-hospital complications. Angiographic data from patients undergoing protocol catheterization 18 to 48 hours after hospital admission show that the infarct-related artery was more likely to be occluded in those with RV dysfunction (48% [15 of 31] vs 14% [68 of 495]; p < 0.001). There was no difference in the frequency of multivessel disease between the 2 groups. In patients with RV dysfunction in whom radionuclide ventriculography was repeated 6 weeks after hospital discharge, RV wall motion abnormalities persisted in only 18% (8 of 45). Mortality in the year after discharge was 3.5% (2 of 58) among patients with RV dysfunction compared with 1.7% (18 of 1,052; p = NS) among those without RV dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1993

Use of converting enzyme inhibitors in patients with asymptomatic left ventricular dysfunction.

The Studies of Left Ventricular Dysfunction (SOLVD) prevention trial evaluated 4,228 patients with a left ventricular ejection fraction < or = 35% who were not receiving drug therapy for heart failure. Patients were randomized to treatment with enalapril or placebo in a dose of 2.5 to 20 mg/day. Patients randomized to enalapril showed a 37% reduction in the development of heart failure and a 36% reduction in hospitalization for heart failure (p < or = 0.001). However, there was only an 8% reduction in total mortality and a 14% reduction in cardiovascular mortality (p = NS). On the basis of the SOLVD prevention trial, patients with asymptomatic left ventricular dysfunction due to either ischemic or nonischemic cardiomyopathy should be started on treatment with an angiotensin-converting enzyme inhibitor to prevent the development of and hospitalization for heart failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Assessing myocardial viability to help select patients for revascularization to improve left ventricular dysfunction due to coronary artery disease.

Left ventricular dysfunction has become one of the most common causes of death, disability, and health care costs. Left ventricular dysfunction is usually due to coronary artery disease (CAD) and can be improved considerably by successful revascularization in many, but not all, patients. The key issue determining whether revascularization will relieve left ventricular dysfunction is whether the patient has enough viable myocardium to improve after revascularization. Viable myocardium is located anatomically in the subepicardial layers of the left ventricular wall, above the infarct in the subendocardial layers in the distribution of a stenotic coronary artery. Clinical history, physical examination, resting or exercise ECG, and imaging studies of left ventricular function often fail to distinguish patients with viable myocardium. Thallium-201 myocardial imaging at stress and rest is better if performed with reinjection of thallium-201 at rest, but this method still misses many patients with viable myocardium. Positron emission tomographic (PET) myocardial imaging to compare distributions of a perfusion tracer versus a metabolic tracer (fluorine-18-fluoro-deoxyglucose, 18FDG) has been cited as the "gold standard" method to identify viable myocardium by position papers from several professional organizations. PET imaging of rubidium-82, a potassium analogue ("washout" from "early" [first 1.5 minutes] to "late" [next 5 minutes] images) and gated magnetic resonance imaging (MRI) also show promise.

Cell Survival↗
PubMed1994

The ever expanding spectrum of ischemic left ventricular dysfunction.

Ischemic left ventricular (LV) dysfunction includes a number of discrete entities, such as acute LV failure in angina, acute myocardial infarction, and ischemic cardiomyopathy. Recently, new entities have arisen to expand the spectrum of ischemic LV function. These include postinfarct diastolic dysfunction, stunning, hibernation, and preconditioning. The tantalizing possibility exists that several of these states can coexist. There are widely differing underlying pathophysiologic states. Hence it is not easy to be dogmatic about whether a given group of therapeutic agents, such as the calcium antagonists, may be beneficial in ischemic LV dysfunction. Nonetheless, there is experimental evidence that calcium antagonists may benefit the specific entity of stunning and clinical evidence that they benefit postinfarct ischemic LV diastolic dysfunction. These agents, as a group, should be evaluated in reperfusion and postinfarct dysfunctional syndromes.

Acute Disease↗
PubMed1998

Coronary artery bypass grafting in patients with profound ventricular dysfunction.

Patients with severe ventricular dysfunction make up a special subset of patients who undergo coronary artery bypass procedures. For these patients, the risk associated with the bypass procedure is relatively high, but the opportunity-for-survival benefit is also greater. We studied 61 consecutive coronary artery bypass patients with preoperative ejection fractions < or = 25%, and further compared several subgroups: Group I (n = 30) ejection fractions ranged from 21% to 25%; Group II (n = 23) ejection fractions ranged from 16% to 20.9%; and Group III (n = 8) ejection fractions ranged from 10% to 15.9%. The overall mortality rate was 8% (5/61), with no deaths in Group III. The 41% (25/61) of patients who received left internal mammary artery conduits experienced a higher mortality rate, yet it did not differ significantly from that of patients who received only saphenous vein conduits. Intraaortic balloon pumps were placed in 48% (29/61) of the patients, with a progressively higher incidence in patients with poorer ventricular function (P < 0.05). Most intraaortic balloon pumps (59%) were placed intraoperatively. Two patients underwent placement of left ventricular assist devices, and 1 of these survived. Coronary artery bypass grafting in patients with poor ventricular function carries a substantial, but acceptable, mortality risk. Use of the left internal mammary artery did not improve perioperative mortality, and may have a negative impact in the early postoperative period. Intraaortic balloon pump use was most common in those patients with the worst ventricular function. Prophylactic intraaortic balloon pump use may be justified in candidates with ejection fractions < 20%.

Adult↗
PubMedDate not supplied

Assessment of synchronized direct mechanical ventricular actuation in a canine model of left ventricular dysfunction.

Direct mechanical ventricular actuation (DMVA) is an experimental procedure that provides biventricular cardiac assistance by intracorporeal pneumatic compression of the heart. The advantages this technique has over other assist devices are biventricular assistance, no direct blood contact, pulsatile blood flow, and rapid, less complicated application. Prior studies of nonsynchronized DMVA support have demonstrated that a subject can be maintained for up to 7 days. The purpose of this study was to determine the acute hemodynamic effects of cardiac synchronized, partial DMVA support in a canine model (RVP) of left ventricular (LV) dysfunction. The study consisted of rapidly pacing seven dogs for 4 weeks to create LV dysfunction. At the conclusion of the pacing period, the DMVA device was positioned around the heart by means of a median sternotomy. The animals were then imaged in a 1.5 T whole body high speed clinical MR system, with simultaneous LV pressure recording. Left ventricular pressure-volume (PV) loops of the nonassisted and DMVA assisted heart were generated and demonstrated that DMVA assist shifted the loops leftward. In addition, assist significantly improved pressure dependent LV systolic parameters (left ventricular peak pressure and dp/dt max, p < 0.05), with no diastolic impairment. This study demonstrates that DMVA can provide synchronized partial assist, resulting in a decrease in the workload of the native heart, thus having a potential application for heart failure patients.

Animals↗
PubMed1997

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↗
PubMed2001

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↗
PubMed2002

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↗
PubMed1989

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↗
PubMed1998

[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↗
PubMed2002

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↗
PubMed2002

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↗
PubMed1987

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↗
PubMed2000

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↗