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Echocardiographic tamponade in severe left ventricular dysfunction: the impact of small pericardial effusion and the absence of pulsus paradoxicus.

Cardiac tamponade is a commonly encountered clinical entity. It is a clinical syndrome characterized by elevated filling pressures, pulsus paradoxicus, and eventually, hypotension. It occurs as intrapericardial pressure exceeds intracardiac pressures altering ventricular filling. Generally tamponade occurs with moderate or large accumulations of pericardial fluid that result in an increase in pericardial pressure. It is well known that rapid accumulation of relatively small volumes of fluid can cause tamponade pathophysiology. We report a less well-recognized phenomenon. In the setting of severe left ventricular dysfunction, small volumes of pericardial fluid can result in excessive intrapericardial pressure and echocardiographic tamponade in the absence of a significant pulsus paradoxicus.

Adult↗

Rationale and design of a randomized controlled trial to assess the safety and efficacy of cardiac resynchronization therapy in patients with asymptomatic left ventricular dysfunction with previous symptoms or mild heart failure--the REsynchronization reVErses Remodeling in Systolic left vEntricular dysfunction (REVERSE) study.

BACKGROUND: Cardiac resynchronization therapy (CRT) improves symptoms, reduces heart failure (HF)-related hospitalizations, and reverses left ventricular remodeling in some patients with moderate to severe HF and ventricular dyssynchrony defined by a prolonged QRS duration. The effects of CRT on HF outcomes in patients with asymptomatic left ventricular dysfunction (ALVD) or mild HF remain to be determined. METHODS: The REsynchronization reVErses Remodeling in Systolic left vEntricular dysfunction (REVERSE) study is a prospective, multicenter, randomized, double-blind, parallel, controlled clinical trial designed to establish whether CRT combined with optimal medical treatment can attenuate HF disease progression compared with optimal medical treatment alone in patients with ALVD +/- New York Heart Association class I American College of Cardiology/American Heart Association stage C or New York Heart Association class II HF, QRS duration > or =120 milliseconds, left ventricular ejection fraction < or =0.40, and left ventricular end-diastolic diameter > or =55 mm. The primary end point is the HF clinical composite response and left ventricular end-systolic volume index is the first-order secondary end point. Approximately 500 patients from 100 centers in the United States, Canada, and Europe will be randomized to CRT versus no CRT. The follow-up is 5 years in total with the primary and first secondary end points reported at 12 months. Enrollment began in September 2004 and is expected to be completed in 2006. CONCLUSION: REVERSE will assess the safety and efficacy of CRT in patients with ALVD or mild HF and electrocardiographic evidence of ventricular dyssynchrony.

Cardiac Output, Low↗

Left ventricular function during strength testing and resistance exercise in patients with left ventricular dysfunction.

PURPOSE: Deterioration in left ventricular function is a more sensitive marker of myocardial ischemia during exercise than ST segment depression. The current study was designed to evaluate left ventricular function during one-repetition-maximum (1-RM) strength testing and resistance exercise in cardiac patients with moderate left ventricular dysfunction. METHODS: Using echocardiographic methods, left ventricular function was evaluated in 15 patients with left ventricular dysfunction (age, 65 +/- 6.5 years; ejection fraction, 42.1 +/- 5.8). Measurements were performed during 1-RM testing and resistance exercise (20%, 40%, and 60% of 1-RM using 10 to 15 repetitions) on the one-arm biceps curl (BIC) and bilateral knee extension exercises and compared with measurements of left ventricular function during the symptom-limited graded exercise test (SL-GXT). RESULTS: During the knee extension exercise, there was a slight but significant reduction (P< or =.05) in ejection fraction values at the end of 60% 1-RM, as compared with rest and previous workloads. Significant increases in systolic blood pressure and left ventricular end-systolic volume ratio values (P< or =.05) from rest to exercise were observed across test modes and for all workloads. The prevalence of new wall motion abnormalities during knee extension and BIC 1-RM strength testing was comparable with that observed during SL-GXT. The greatest increase in new wall motion abnormalities was seen during 60% 1-RM of knee extension exercise, as compared with prior workloads, BIC exercises, and SL-GXT. CONCLUSIONS: Despite an increase in occurrence of ischemic changes during the highest resistance exercise workloads and with larger muscle mass, the findings are small in magnitude and do not suggest reduced cardiac performance.

Aged↗

Ventricular remodeling in children with left ventricular dysfunction secondary to various cardiomyopathies.

The ventricular remodeling that occurs in adults with left ventricular (LV) dysfunction is characterized by a change in LV shape from an ellipse to more of a sphere and is associated with increased functional mitral regurgitation (MR), decreased exercise tolerance, and poor outcome. There are limited data on the occurrence and importance of LV remodeling in children with LV dysfunction. The purposes of this study were to evaluate in children with LV dysfunction (1) LV shape, (2) changes in LV shape as LV function improves, and (3) the relation between LV shape and functional MR. Children with LV dysfunction were identified and compared with controls. Patient demographics, treatment, and outcomes were noted. Echocardiograms were reviewed for LV function and shape (sphericity index). The echos of a subset of children whose LV ejection fractions (LVEFs) increased by >10% over a follow-up of >6 months were analyzed for changes in sphericity, mitral annulus size, and the degree of MR. Twenty-five children with LV dysfunction were compared with 37 age-matched controls. LV remodeling to a more spherical shape was inversely related to LVEF but was not associated with clinical outcome. In a subset of patients (n = 17) whose LVEFs improved, the reversal of remodeling (decrease in sphericity index) was associated with a decrease in MR and mitral annulus size. In conclusion, LV remodeling occurs in children with LV dysfunction. The reversal of this remodeling with a decrease in the degree of MR and the size of the mitral annulus occurs as systolic function improves.

Adolescent↗

Aortic valve surgery in patients with left ventricular dysfunction.

Patient with advanced left ventricular dysfunction and heart failure symptoms, either secondary to severe aortic stenosis and a low transvalvular gradient, or chronic aortic insufficiency are sometimes referred for cardiac transplantation. Now, with improvements in both myocardial protection and better valve prostheses, aortic valve surgery for patients with even the most advanced ventricular dysfunction can be performed with low risk.

Adult↗

Coronary revascularization in the treatment of moderate and severe postischemic left ventricular dysfunction.

Chronic postischemic left ventricular (LV) dysfunction can improve following coronary revascularization (hibernating myocardium). However, it is not clear whether the severity of LV dysfunction determines functional outcome after revascularization and the accuracy of tests to predict myocardial viability. We studied 47 patients with coronary artery disease and chronic LV dysfunction. Before coronary bypass, patients underwent (18F)2-fluoro-2-deoxy-D-glucose (FDG) positron emission tomography (PET) during euglycemic hyperinsulinemic clamp to assess viability. Global and regional LV function were assessed before and 4 to 6 months after surgery. Patients were arbitrarily divided into 2 groups with moderate and severe LV dysfunction. Group 1 (n = 26) had an ejection fraction (EF) of < or = 30% and group 2 (n = 21) > 30%. After bypass, the EF (22+/-6% vs 31+/-10%; p <0.0001) and global wall motion score (WMS) (2.05+/-0.39 vs 1.56+/-0.34; p <0.001) improved in group 1, whereas the EF (43+/-9% vs 43+/-12%; p = NS) was unchanged in group 2, although WMS tended to improve (1.42+/-0.38 vs 1.32+/-0.39; p = 0.09). The proportion of dysfunctional segments (72% vs 32%; p <0.0001) and FDG uptake in these segments (0.44+/-0.15 vs 0.34+/-0.15 micromol/g/min, p <0.0001) were greater in group 1 than in group 2. The baseline EF influenced the predictive accuracy of PET, with highest positive predictive accuracy in group 2 and highest negative predictive accuracy in group 1. Thus, coronary revascularization has the potential for greatest benefit in patients with the most severe dysfunction, but with evidence of viability, and the entity of LV dysfunction affects the predictive accuracy of viability studies.

Adult↗

Association of calcium channel blocker use with increased rate of acute myocardial infarction in patients with left ventricular dysfunction.

The Studies of Left Ventricular Dysfunction (SOLVD) assessed the effect of enalapril in patients with systolic left ventricular dysfunction (LVD). We performed retrospective analyses of the association between calcium channel blocker (CCB) use and fatal and nonfatal myocardial infarction (MI) in these patients. MI occurred in 11.5% of 845 patients receiving CCBs versus 7.5% of 2551 patients not receiving CCBs in the enalapril group and in 14.4% of 874 patients receiving CCBs versus 9.3% of 2527 patients not receiving CCBs in the placebo group. By multivariate Cox regression analysis, adjusting for comorbidity, cause and severity of LVD, heart failure, and concomitant drug use, CCB use was an independent predictor of MI (relative risk [RR] 1.37, confidence interval [CI] 1.14 to 1.63). The increase in MI risk was greater among patients with a higher heart rate (RR 1.46, CI 1.14 to 1.86) and lower blood pressure (RR 1.45, CI 1.14 to 1.86). The adjusted risk ratio for all-cause mortality associated with CCB use was 1.14 (CI 1.00 to 1.28; p = 0.0454). In this analysis of patients with LVD, CCB use was associated with significantly increased risk of fatal or nonfatal MI.

Angiotensin-Converting Enzyme Inhibitors↗

Severe left ventricular dysfunction secondary to primary pulmonary hypertension: bridging therapy with bosentan before lung transplantation.

When right ventricular failure develops secondary to primary pulmonary hypertension, right-left ventricular interaction may lead to severe impairment of left ventricular function. In such cases, many experts favor combined heart-lung transplantation by fear that the left ventricle may not recover after transplantation of the lungs alone. We report a case of primary pulmonary hypertension with severely diminished right and left ventricular function. The patient was rendered amenable to isolated pulmonary transplantation with the endothelin-receptor antagonist bosentan. The medication improved right and left ventricular function to the point that heart transplantation no longer appeared necessary. After double-lung transplantation the patient's cardiac function made a full recovery. This approach might be particularly welcome considering both the current donor organ shortage and the limited number of surgical teams with expertise in heart-lung transplantation.

Adult↗

Canine nonischemic left ventricular dysfunction: a model of chronic human cardiomyopathy.

BACKGROUND: The mechanisms of cardiac remodeling during chronic heart failure remain poorly defined. We sought to advance a chronic canine model of nonischemic cardiomyopathy. METHODS AND RESULTS: Male dogs (n = 6) received decremental right ventricular apical tachypacing (12 months) to achieve and maintain stable left ventricular (LV) dysfunction. After 10 months of tachypacing, 120 beats/min was sufficient to maintain stable LV dysfunction. Electrocardiography, echocardiography, and tissue Doppler imaging were done to evaluate electrophysiology, LV dimensions and function, and dyssynchrony during normal sinus rhythm. The 6-minute walk test was used to evaluate functional capacity. We observed increases in both QRS duration (P < .0001) and QRS amplitude (P < .0001). LV fractional shortening was reduced from a baseline of 38.0 +/- 1.4% to 11.2 +/- 1.4% (P < .0001). LV end-diastolic dimension increased from 3.8 +/- 0.1 cm at baseline to 5.3 +/- 0.3 cm (P < .0001); LV end-systolic dimension increased from 2.3 +/- 0.1 cm to 4.7 +/- 0.2 cm (P < .0001). LV mass increased from 85.9 +/- 3.5 g at baseline to 179 +/- 13.7 g (P < .0001). There was evidence of LV dyssynchrony (P < .04) during both normal sinus rhythm and right ventricular tachypacing, compared with control dogs. The distance a dog walked in 6 minutes was significantly less at 12 months compared with normal controls (540 +/- 32 m versus 277 +/- 64 m, P < .008). CONCLUSION: This nonischemic model of canine cardiomyopathy reproduces many aspects of chronic human heart failure including reduced fractional shortening, dilated ventricular dimensions, increased LV mass, decreased functional capacity, and dyssynchrony.

Animals↗

Brain natriuretic peptide and left ventricular dysfunction in Chagas' disease.

Left ventricular dysfunction in Chagas' disease is common but can be difficult to detect. We investigated whether measurement of plasma brain natriuretic peptide (BNP) could identify patients with left ventricular dysfunction who need further investigation or treatment. Among patients with an abnormal electrocardiogram or chest radiograph, a BNP concentration of 60.7 pmol/L or higher has a sensitivity and positive predictive value of 80%, and specificity and negative predictive value of 97%. Measurement of plasma BNP concentration could be a useful method to screen patients with Chagas' disease.

Adult↗

A functional role for endogenous atrial natriuretic peptide in a canine model of early left ventricular dysfunction.

Asymptomatic or early left ventricular dysfunction in humans is characterized by increases in circulating atrial natriuretic peptide (ANP) without activation of the renin-angiotensin-aldosterone system (RAAS). We previously reported a canine model of early left ventricular dysfunction (ELVD) produced by rapid ventricular pacing and characterized by an identical neurohumoral profile and maintenance of the natriuretic response to volume expansion (VE). To test the hypothesis that elevated endogenous ANP suppresses the RAAS and maintains sodium excretion in ELVD, we assessed the effects of antagonism of ANP on cardiorenal and neurohumoral function in ELVD. Chronic ANP suppression was produced by bilateral atrial appendectomies before the production of ELVD by rapid ventricular pacing (ELVD-APPX, n = 5). This group was compared with a separate group with ELVD and intact atrial appendages (ELVD-INTACT, n = 8). ELVD-APPX was characterized by lower circulating ANP (50 +/- 11 vs. 158 +/- 37 pg/ml, P < 0.05), activation of plasma renin activity (PRA) (9.4 +/- 2.4 vs. 0.6 +/- 0.4 ng/ml per h, P < 0.05) and aldosterone (36.4 +/- 12.5 vs. 2.5 +/- 0.0 ng/dl, P < 0.05) when compared to ELVD-INTACT. In comparison to the ELVD-INTACT group, sodium excretion was decreased before and during VE in the ELVD-APPX group. Acute ANP antagonism was produced by administration of the particulate guanylate cyclase coupled natriuretic peptide receptor antagonist, HS-142-1, to seven conscious dogs with ELVD and intact atrial appendages (ELVD-INTACT). HS-142-1 decreased plasma concentrations and renal generation of the ANP second messenger, cGMP, and was associated with activation of PRA and sodium retention with enhanced tubular sodium reabsorption. These data support a significant role for elevated endogenous ANP in the maintenance of sodium excretion and regulation of the RAAS in experimental ELVD.

Aldosterone↗

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↗

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↗

Coronary artery bypass surgery in patients with left ventricular dysfunction.

The effects of coronary artery bypass surgery in patients with left ventricular dysfunction (left ventricular ejection fraction of less than 45 percent) on survival, symptoms, left ventricular ejection fraction, and regional left ventricular function were prospectively assessed in 34 patients. Left ventricular function was serially assessed by nuclear angiocardiography. Operative mortality was 9 percent, and mortality during the follow-up period was 10 percent. Twenty of 21 patients with class III or IV anginal symptoms preoperatively improved by at least two functional classes. Seven of 10 patients with class III or IV symptoms of heart failure preoperatively improved by at least one functional class. Global left ventricular ejection fraction improved significantly with surgery (p less than 0.05). Regional left ventricular systolic function improved as well (p less than 0.005). These findings suggest that in selected patients with left ventricular dysfunction, coronary artery bypass surgery can be performed with acceptable mortality and may result in symptomatic and functional benefit.

Adult↗

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↗