Progression of left ventricular dysfunction in patients with heart failure. SOLVD Investigators. The Studies of Left Ventricular Dysfunction.
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Enalapril↗
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Results for “Ventricular Dysfunction”
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Predominant right ventricular dysfunction after right ventricular destruction in the dog.
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Animals↗
Comparative electrophysiological effects of captopril or hydralazine combined with nitrate in patients with left ventricular dysfunction and inducible ventricular tachycardia.
OBJECTIVE: To assess the electrophysiological and antiarrhythmic effects of pharmacological load manipulation by an angiotensin converting enzyme (ACE) inhibitor (captopril) and a direct vasodilator (hydralazine plus isosorbide mononitrate) in patients with inducible ventricular tachycardia and impaired left ventricular function. DESIGN: Randomised open label cross-over comparison of three regimens. SETTING: Tertiary arrhythmia referral centre. SUBJECTS: Eight patients with reduced left ventricular function and sustained ventricular tachycardia inducible by programmed stimulation. INTERVENTIONS: Three treatment regimens each of 48 hours duration: captopril, hydralazine plus isosorbide mononitrate, and control (no vasodilator). MAIN OUTCOME MEASURES: Changes in central haemodynamics, electrophysiological parameters, and induction of ventricular tachycardia during treatment with captopril, or hydralazine combined with nitrate, compared with a control period. RESULTS: Both vasodilator treatments produced similar balanced reductions in peak systolic pressures and filling pressures compared with controls. Captopril had no effect on sinus cycle length, atrial refractoriness, or intraventricular conduction, but prolonged ventricular effective and functional refractory periods and QT interval during constant rate atrial pacing. Hydralazine combined with nitrate did not significantly alter any electrophysiological variable. Ventricular tachycardia was similarly inducible during all three periods. CONCLUSIONS: Load manipulation by captopril but not hydralazine combined with nitrate prolonged ventricular refractoriness and repolarisation, possibly reflecting a combination of mechano-electrical effect with the restraining influence of ACE inhibitors on reflex sympathetic stimulation.
Aged↗
Effect of right ventricular dysfunction on left ventricular function.
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Blood Pressure↗
[Evaluation of right ventricular function by intraoperative transesophageal echocardiography for patients with left ventricular dysfunction].
We evaluated right and left ventricular function by intraoperative transesophageal echocardiography for the patients with left ventricular dysfunction (left ventricular ejection fraction (LVEF) < or = 40) who underwent isolated coronary artery bypass grafting (CABG). We divided these patients into two groups; group 1 who had difficulty of weaning from cardiopulmonary bypass due to hypotension (n = 8) and group 2 who did not have any difficulty of it (n = 17). Basement characteristics (age, gender, history of myocardial infarction, congestive heart failure, LVEF, severity of the right coronary artery disease) of both groups were not different significantly. Intraoperative characteristics (the number of distal anastomoses, duration of aortic cross-clamp and cardiopulmonary bypass, and bypass to the right coronary artery) were also not different between two groups. However, mean duration of ICU stay and in-hospital mortality were significantly longer and higher in group 1 than group 2. On the other hand, right ventricular systolic function was severely impaired, particularly postoperatively, in group 1 compared with group 2. Right and left ventricular systolic function of group 2 was fairly improved postoperatively. These results may indicate that right ventricular dysfunction is a potent predictor of postoperative morbidity and mortality for the patients with left ventricular dysfunction who undergo isolated CABG.
Aged↗
Predictors of operative risk for coronary bypass operations in patients with left ventricular dysfunction.
OBJECTIVES: The prevalence of ventricular dysfunction in patients undergoing coronary operations, as well as the prevalence of other risk factors in these patients, has been increasing. We identified the predictors of mortality and morbidity in patients with ventricular dysfunction to permit more accurate evaluation of risk and to direct future strategies to improve outcomes. METHODS: Demographic, intraoperative, and outcome data were collected prospectively on 20,614 patients undergoing isolated coronary operations at our institution from 1982-1997. Multivariable regression analyses were used to identify the independent predictors of mortality and low-output syndrome. RESULTS: Moderate ventricular dysfunction (ejection fraction, 20%-40%) was noted in 4107 (19.9%) patients, and severe dysfunction (ejection fraction, <20%) was noted in 680 (3.3%) patients. Patients with worse ventricular function had an increasing prevalence of other risk factors with time. Mortality decreased between the 1982-1986 and 1987-1991 cohorts but did not decrease further. Low-output syndrome was less common in the 1992-1997 cohort than in previous years. The predictors of mortality were ventricular dysfunction, age, reoperation, year of operation, urgency, female sex, and left main stenosis. Low-output syndrome was predicted by ventricular dysfunction, reoperation, year of operation, female sex, urgency, extensive coronary disease, age, left main stenosis, and symptom class. CONCLUSIONS: Despite the increasing prevalence and risk profile of patients with ventricular dysfunction, mortality rates and incidence of low-output syndrome declined with time. Patients with severe dysfunction were at greatest risk when facing reoperation or urgent operation. Earlier intervention and more aggressive preoperative optimization may improve outcomes in these high-risk patients.
Age Factors↗
Effect of amiodarone therapy on mortality in patients with left ventricular dysfunction and asymptomatic complex ventricular arrhythmias: Argentine Pilot Study of Sudden Death and Amiodarone (EPAMSA).
The efficiency of prophylactic antiarrhythmic treatment with amiodarone in reducing 1-year mortality in patients with reduced left ventricular ejection fraction ( < 35%) and asymptomatic ventricular arrhythmias (Lown classes 2 and 4) was investigated in a prospective, multicenter, randomized, controlled study. Among 127 patients who entered the study, 61 were assigned to no antiarrhythmic therapy (control group [CG] and 66 to amiodarone treatment (amiodarone group [AG]). Amiodarone was administered at a dosage of 800 mg/day for 2 weeks followed by 400 mg/day thereafter. A 12-month follow-up was completed for 106 patients (57 in the AG and 49 in the CG). Amiodarone reduced the overall mortality rate, which was 10.5% in the AG versus 28.6% in the CG (odds ratio [OR] 0.29; 95% confidence interval [CI] 0.10 to 0.84; log-rank test 0.02) and sudden death rate, which was 7.0% in the AG versus 20.4% in the CG (OR 0.29; 95% CI 0.08 to 1.00; log-rank test 0.04). Side effects were rare, and in only three patients did amiodarone treatment have to be discontinued.
Aged↗
Management of asymptomatic left ventricular dysfunction.
Asymptomatic left ventricular dysfunction should be treated as an early stage on the continuum that is chronic heart failure. The author presents the clinical trial data on which current management with angiotensin-converting enzyme inhibitors and beta-blockers is based. Issues surrounding screening are also discussed.
Adrenergic beta-Antagonists↗
Ventricular arrhythmias in hypertensive left ventricular hypertrophy. Relationship to coronary artery disease, left ventricular dysfunction, and myocardial fibrosis.
Ventricular arrhythmias occur with increased frequency in hypertensive patients with left ventricular hypertrophy (LVH). The relationships, however, between ventricular arrhythmias and coexistent coronary artery disease, left ventricular dysfunction and left ventricular fibrosis have not been examined in hypertensive LVH. We carried out coronary arteriography on fifteen hypertensive patients with LVH and nonsustained ventricular tachycardia (greater than or equal to 3 consecutive ventricular complexes) of whom nine (60%) were free of significant (greater than 50% stenosis) coronary disease. To identify other possible correlates of left ventricular arrhythmias, 28 patients with LVH, comprising 17 with ventricular tachycardia and 11 without ventricular arrhythmias, underwent quantitative assessment of left ventricular function (angiographic ejection fraction), left ventricular mass (echocardiography), and left ventricular fibrosis (endomyocardial biopsy). Ejection fraction was not significantly different between the two groups (53 +/- 8% v 62 +/- 2%, P = NS). However, left ventricular mass was significantly greater (442 +/- 28 g v 339 +/- 34 g, P less than .05) and percentage fibrosis significantly higher (19 +/- 4% v 3 +/- 1%, P less than .001) in those patients with ventricular tachycardia. Thus ventricular arrhythmias in hypertensive patients with LVH cannot be entirely attributed to coexistent coronary disease, nor to left ventricular dysfunction, but are related to the degree of cardiac hypertrophy and subendocardial fibrosis.
Biopsy↗
Cardiac tamponade in left ventricular dysfunction.
Echocardiographic and hemodynamic data were measured in closed-chest dogs during graded cardiac tamponade (pericardial pressure 5, 10, and 15 mm Hg) before and after production of diffuse ischemic left ventricular dysfunction. Left ventricular dysfunction was produced by intracoronary injection of nonradioactive microspheres (54 +/- 3.9 mm diameter). Changes in left atrial pressure with cardiac tamponade were influenced by coexisting left ventricular dysfunction. Left atrial pressure increased with tamponade and was equal to pericardial pressure before left ventricular dysfunction was produced. However, after left ventricular dysfunction was produced, left atrial pressure was significantly higher than pericardial pressure before tamponade, but it fell toward pericardial pressure when tamponade was produced. Pulsus paradoxus (greater than 10 mm Hg) was present in all animals with cardiac tamponade before left ventricular dysfunction but in only one animal afterward. During each level of tamponade, the inspiratory fall of aortic systolic pressure was greater before than with left ventricular dysfunction. The slope of the linear regression between pericardial pressure and millimeters of mercury of inspiratory fall in aortic systolic pressure was significantly greater before than with left ventricular dysfunction (0.74 +/- 0.12 versus 0.32 +/- 0.12, p less than 0.05). Left ventricular dysfunction caused a leftward and upward shift of the pericardial pressure-volume relation. As a result, right atrial and ventricular collapse occurred with significantly smaller volumes of pericardial fluid after than before left ventricular dysfunction. We conclude that pulsus paradoxus may be absent in cardiac tamponade with coexisting left ventricular dysfunction and unequal filling pressures. Echocardiographic signs of cardiac tamponade may occur with small effusions in the presence of left ventricular dysfunction.
Animals↗
Left ventricular dysfunction: which role for calcium antagonists?
Left ventricular dysfunction is the most common cause of congestive heart failure. Thus, treating or preventing left ventricular dysfunction represents an important therapeutic goal. The use of calcium antagonists in the treatment of left ventricular dysfunction or congestive heart failure has been proposed for many years now, mainly because of their potent vasodilatory effect. However, despite the theoretical basis, the results of studies exploring the possible use of calcium antagonists in this setting have not been at all encouraging. It has been suggested that this is because calcium antagonists have important additional effects: they depress cardiac contractility and activate the neurohormonal system. The various calcium antagonists have different characteristics and can be potentially useful in a variety of clinical conditions. Amlodipine (a calcium antagonist with a minimal cardiodepressant effect, long half-life and minimal activity on the neurohormonal system) has been shown to be clinically useful in congestive heart failure of nonischaemic origin. Calcium antagonists capable of limiting heart rate increment are useful in limiting ischaemia-induced left ventricular dysfunction. Verapamil exerts a potent protective effect on both microvascular damage and mechanical recovery during prolonged ischaemia followed by reperfusion. Lastly, nisoldipine is capable of ameliorating left ventricular function in patients with left ventricular diastolic dysfunction and has, therefore, potential in the treatment of congestive heart failure of left ventricular diastolic dysfunction origin. Thus, calcium antagonists may have a role in the treatment of left ventricular dysfunction provided that patient characteristics, the underlying mechanisms of the left ventricular dysfunction and the various calcium antagonist characteristics are well understood and carefully considered.
Animals↗
Right and left ventricular dysfunction in patients with severe pulmonary disease.
OBJECTIVE: To determine the prevalence of right and left ventricular dysfunction in a prescreened population of patients with severe pulmonary disease, and to analyze the relationship between right and left ventricular function. DESIGN: Retrospective record review of 434 patients with severe pulmonary disease. PATIENTS: Patients with end-stage pulmonary disease, including alpha1-antitrypsin deficiency emphysema, COPD, cystic fibrosis (CF), idiopathic pulmonary fibrosis, and pulmonary hypertension (primary and Eisenmenger's syndrome), who were evaluated for lung transplantation between January 1993 and December 1995. MEASUREMENTS: Pulmonary function tests, arterial blood gases, radionuclide ventriculography, two-dimensional transthoracic echocardiography, pulmonary hemodynamics, coronary angiography. RESULTS: Right ventricular dysfunction (right ventricular ejection fraction [RVEF] <45%) was present in 267 patients (66%), but the prevalence was highest (94%) in patients with pulmonary vascular disease. Among the patients with airway or parenchymal lung disease, the prevalence ranged from 59% in COPD to 66% in CF. In contrast, left ventricular dysfunction (left ventricular ejection fraction [LVEF] <45%) was present in only 6.4%, but it, too, was most common in the group with pulmonary hypertension (19.6%). In the groups with parenchymal or airway disease, the prevalence was 3.6%, and there was no statistical difference among the four diagnoses (alpha1-antitrypsin deficiency emphysema; COPD; CF; idiopathic pulmonary fibrosis). LVEF showed a significant correlation with RVEF (r=0.44; p<0.05), and left ventricular dysfunction was associated with the presence of moderate-to-severe tricuspid regurgitation but not with coronary artery disease. In a subset of patients with both right and left ventricular dysfunction who subsequently underwent lung transplantation, RVEF and LVEF increased pari passu after transplantation. CONCLUSION: The prevalence of right ventricular dysfunction is high in patients with end-stage pulmonary disease, but the prevalence of left ventricular dysfunction is relatively low. Left ventricular dysfunction appears to be related to right ventricular dysfunction, perhaps through ventricular interdependence.
Adult↗
Right ventricular dysfunction after endocardiectomy for right ventricular endomyocardial fibrosis.
Early right ventricular failure following a large endocardiectomy in right endomyocardial fibrosis (EMF) is reported. This diagnosis was confirmed upon echocardiography by the presence of a dilated right ventricle, and hemodynamically (upon postoperative control catheterization) by the presence of right ventricular diastolic dysfunction. The role of the endocardiectomy and of the pericardium in the genesis of this ventricular dysfunction are discussed in the light of this case which was documented by a hemodynamic study and surgically confirmed.
Adolescent↗
Essential thrombocytosis associated with left ventricular dysfunction and large left ventricular thrombi.
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Adult↗
Mechanisms of transplant right ventricular dysfunction.
OBJECTIVE: Right ventricular (RV) dysfunction remains the leading cause of early mortality after cardiac transplantation. The effect of brain death and subsequent hypothermic cardioplegic arrest and storage on subsequent post-transplant right ventricular function was examined. SUMMARY BACKGROUND DATA: Right ventricular dysfunction in the donor heart usually is attributed to failure of the donor right ventricle to adapt to the sudden increase in afterload (pulmonary vascular resistance) in the recipient. Strategies to improve ventricular mechanics in the postoperative period are aimed at reducing pulmonary vascular resistance with vasodilators or augmenting right ventricular contractility with inotropic agents. Events occurring in the donor heart (brain death, hypothermic cardioplegic arrest, and storage) also may be directly related to post-transplant RV dysfunction. METHODS: A canine model of brain death and orthotopic cardiac transplantation was used. A dynamic pressure-volume analysis of RV mechanics was performed using micromanometers and sonomicrometric dimension transducers. Systolic function was assessed by measurement of preload recruitable stroke work (PRSW). Brain death was induced in 17 dogs by inflation of an intracranial balloon. Right ventricular function then was assessed serially to 6 hours (PRSW). Right ventricular adrenergic beta receptor density and function was sampled at control and after 6 hours of brain death. The effect of cardioplegic arrest and hypothermic storage was assessed in a second group of 17 dogs, using the same instrumentation and method of RV analysis. RESULTS: A significant decrease in right ventricular PRSW occurred after brain death, with the average decrease being 37% +/- 10.4% from the control. The RV myocardial beta adrenergic receptor density did not significantly change (253 +/- 34 fmol/ng control vs. 336 +/- 54 fmol/ng after brain death). The adenylyl cyclase activity of the RV beta receptor was assessed and was not altered by brain death. Orthotopic transplantation after cardioplegic arrest and hypothermic storage significantly decreased RV PRSW from 23.6 +/- 2.0 x 10(3) erg to 13.5 +/- 1.4 x 10(3) erg. CONCLUSIONS: These data indicate that the donor right ventricle is exposed to factors significantly detrimental to its mechanical performance well before facing an increased afterload in the recipient. Strategies to reduce RV dysfunction associated with brain death and hypothermic storage could positively impact post-transplant survival.
Animals↗
Left ventricular sensitivity to beta-adrenoceptor-stimulating drugs in patients with ischemic heart disease and varying degrees of ventricular dysfunction.
The left ventricular sensitivity to sympathomimetic amines was assessed in 47 patients with ischemic heart disease and varying degrees of left ventricular dysfunction. Patients were divided into 3 subgroups according to their basal ejection fraction (less than or equal to 35%, between 36 and 54%, and greater than or equal to 55%). After injection of a bolus of isoproterenol (2 micrograms), the isovolumic indexes of inotropic state increased significantly less in patients with an ejection fraction less than or equal to 35% than in other patients, but the heart rate changes and the acceleration in the rate of isovolumic pressure fall were comparable in all subgroups. The dose-response curves to cumulative doses of xamoterol, a beta 1-adrenoceptor partial agonist, confirmed that the magnitude of the inotropic response was reduced during beta 1-stimulation in patients with an ejection fraction less than or equal to 35% when compared with patients with a greater ejection fraction. However, the dose of xamoterol necessary to produce 50% of the maximal inotropic response was not increased in patients with an ejection fraction less than or equal to 35% (range, 1.5-5.2 micrograms/kg; median 2.5 vs. median values of 2.3 and 3.3 micrograms/kg in the other subgroups; NS), and there was no shift to the right of the dose-response curve. It is concluded that in moderate ischemic heart failure, the magnitude of the inotropic response to isoproterenol or xamoterol is reduced. The absence of shift to the right of the dose-response curve to a beta 1-partial agonist suggests that this alteration in myocardial performance is not primarily caused by a decrease in beta-adrenoceptor responsiveness.
Aged↗
Natriuretic peptides and cyclic guanosine 3',5'-monophosphate in asymptomatic and symptomatic left ventricular dysfunction.
BACKGROUND: Screening for patients with asymptomatic left ventricular dysfunction is of considerable importance because they may benefit from early treatment with angiotensin converting enzyme inhibitors. It has been suggested that atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and cyclic guanosine 3',5'-monophosphate (cGMP) might be useful markers for screening. OBJECTIVE: To compare directly the power of the three immunoreactive forms of ANP (CT-ANP, beta-ANP, NT-ANP) and BNP and cGMP to detect asymptomatic left ventricular dysfunction. METHODS AND RESULTS: Radionuclide ventriculography was used to study left ventricular ejection fraction in 37 patients with asymptomatic left ventricular dysfunction, 32 patients with mild to moderate congestive heart failure, and 38 controls. CT-ANP, NT-ANP, beta-ANP, BNP, and cGMP were measured at rest and 3 minutes after exercise. Plasma BNP was the most sensitive marker for patients with asymptomatic left ventricular dysfunction but it reached only a sensitivity of 58% and a specificity of 76% at rest and a sensitivity of 65% and a specificity of 84% after exercise. Combined measurements of all natriuretic peptides and cGMP did not improve the power to detect asymptomatic left ventricular function above that of a single BNP measurement. CONCLUSIONS: Although natriuretic peptides and cGMP measured at rest and three minutes after ergometry may be useful for monitoring left ventricular dysfunction they are unlikely to be suitable for more general routine screening for completely asymptomatic left ventricular dysfunction.
Adult↗
Disruption of the relationship between renin and atrial natriuretic peptide early in the course of ventricular dysfunction.
BACKGROUND: Plasma renin activity is normal in left ventricular dysfunction in the absence of diuretic therapy. In health there is a reciprocal relationship between renin and atrial natriuretic peptide (ANP) but a positive correlation in advanced heart failure. The relationship between renin and ANP in mild left ventricular dysfunction is unknown. METHODS AND RESULTS: Patients with left ventricular dysfunction (n = 35, 18 without diuretic therapy) were compared to 20 age-matched healthy subjects. Plasma concentrations of active renin (PARC), ANP and norepinephrine were measured after 20 min rest and 45 min after an infusion of normal saline (10 ml/kg body wt.). Basal plasma ANP was increased in patients with left ventricular dysfunction compared to healthy subjects, whether or not they were receiving diuretics. PARC was similar in healthy controls and patients untreated with diuretics but was increased in diuretic treated patients. After saline loading in healthy subjects PARC fell while ANP rose. Patients with left ventricular dysfunction had a smaller decline in PARC, that did not achieve statistical significance, but had a greater increase in plasma ANP compared to healthy subjects (P<0.05). The close reciprocal relationship between PARC and ANP observed in healthy subjects before and after saline loading (r = 0.8, P<0.001 and r = 0.6, P<0.01) was weakened in those not receiving diuretics (r = 0.4, P<0.05 and r = 0.24, ns) and lost in those receiving diuretics (r = 0.1 and r = 0.08). CONCLUSIONS: Patients with left ventricular dysfunction have a disturbance of the normal reciprocal relationship between PARC and ANP which antedates diuretic treatment. This should be taken into account when interpreting plasma neuroendocrine measurements in patients with ventricular dysfunction.
Atrial Natriuretic Factor↗