Predominant right ventricular dysfunction after right ventricular destruction in the dog.
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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.
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Twenty-one of 64 patients (33%) with pulmonary embolisms with right ventricular (RV) dilation and 6 of 126 patients (5%) with pulmonary embolisms without RV dilation died during hospitalization (p <0.001). In the 64 patients with RV dilation, in-hospital mortality occurred in 2 of 18 hemodynamically unstable patients (11%) who underwent pulmonary embolectomy, in 2 of 6 hemodynamically stable patients (33%) treated with thrombolytic therapy plus intravenous heparin, and in 17 of 40 hemodynamically stable patients (43%) treated with intravenous heparin (p <0.025 comparing pulmonary embolectomy with no pulmonary embolectomy).
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.
BACKGROUND: Left ventricular dilatation and elevated plasma natriuretic peptide levels predict adverse prognosis and the development of congestive heart failure after myocardial infarction. Altered matrix metalloproteinase (MMP) activity has been implicated in the structural changes associated with development of heart failure after myocardial injury. The aims of this study were to investigate plasma MMP-2, MMP-9, and tissue inhibitor of metalloproteinase (TIMP)-1 concentrations following acute myocardial infarction and their relationships with measures of left ventricular function. METHODS AND RESULTS: Plasma MMP-2, MMP-9, TIMP-1, and N-terminal proBNP (N-BNP) were quantified on 5 consecutive days in 60 patients with acute myocardial infarction (39 anterior). N-BNP was measured on day 3. Echocardiographic assessment of left ventricular wall motion index and volumes was performed during admission and 6 weeks later. Plasma MMP-9 showed peaks on days 1 and 4. MMP-2 levels, similar on each day, were higher after inferior myocardial infarction. Plasma MMP-2 showed strong, inverse correlation with left ventricular volumes during and after admission. Plasma MMP-9 correlated directly with N-BNP (P=.022) and inversely with wall motion index during admission (P=.05). TIMP-1 levels were higher after anterior (1269, 870-1466 ng/mL) compared with inferior (1183, 856-1419 ng/mL, P=.05) acute myocardial infarction and fell from day 1 through 5 (P <.0005). CONCLUSION: Plasma MMP-9 concentration correlates with neurohormonal and echocardiographic measures of left ventricular dysfunction after myocardial infarction. Higher left ventricular volumes are associated with lower plasma MMP-2 concentrations. Circulating MMP concentrations may provide insights into left ventricular remodeling after acute myocardial infarction.
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.
BACKGROUND: Surgical ventricular remodeling (SVR) is an accepted therapy for post-infarction ventricular remodeling. Current literature on SVR outcomes has focused on heterogeneous populations with regard to left ventricular function and New York Heart Association (NYHA) class. We assessed outcomes after SVR in patients with advanced congestive heart failure (CHF) (NYHA Class III/IV) and a pre-operative ejection fraction (EF) < or =20%. METHODS: Data were analyzed for 51 consecutive SVR patients from January 2002 to June 2004. Cardiac catheterization, echocardiography and magnetic resonance imaging (MRI) identified 62.7% (32 of 51) of patients with an EF < or =20%, with the majority having an EF < or =15% (65.6%; 21 of 32). Cox regression analysis was performed to determine predictors of mortality in patients with an EF < or =20%. Follow-up was 100% (32 of 32) complete. RESULTS: Mean age was 61.9 +/- 10.3 (range 40 to 80) years with a male:female ratio of 27:5. Operative mortality was 6.3% (2 of 32). Twenty-two percent (7 of 32) had concomitant mitral valve procedures. Follow-up demonstrated a statistically significant improvement in left ventricular volumes and EF in survivors. Cox regression analysis identified the following to be significant predictors of mortality: pre-operative left ventricular end-systolic volume index >130 ml/m2; pre-operative diabetes; and intra-aortic balloon pump usage. Pre-operatively, all patients (32 of 32) were categorized as NYHA Class III/IV, with 69% (22 of 32) improving to NYHA Class I/II at follow-up (p < 0.01). Survival did not differ statistically between patients with an EF < or =20% and an EF >20% (n = 19). CONCLUSIONS: Our results indicate that SVR improves left ventricular function and functional status for patients with advanced CHF and a pre-operative EF < or =20%. Therefore, SVR is a viable surgical alternative for patients with severe left ventricular dysfunction.
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.
BACKGROUND: This study was designed to determine the effects of pretreatment with an angiotensin receptor blocker on left ventricular (LV) function and remodeling during acute myocardial infarction (MI). METHODS AND RESULTS: Sprague-Dawley rats were pretreated with candesartan (10 mg x kg(-1) x d(-1)) for 2 weeks and studied at 1, 3, and 6 minutes after MI. Compared with untreated rats, pretreatment with candesartan lowered (P<0.05) LV systolic pressure and the first derivative of LV pressure with respect to time but did not change LV end-diastolic pressure or improve LV regional function. With candesartan pretreatment, LV fractional shortening and ejection fraction increased (P<0.05) by 37% and 28%, and LV chamber dilation was attenuated (P<0.05). At 6 minutes after MI, LV endothelial nitric oxide synthase decreased in the infarcted and noninfarcted wall 47% (P=0.04) and 70% (P=0.002), and constitutive microtubulin increased 260% (P=0.0005) and 111% (P=0.003). Candesartan had no effect on LV tissue endothelial nitric oxide synthase levels but attenuated the increase in constitutive microtubulin by 77% (P=0.004) and 37% (P<0.05). CONCLUSIONS: Pretreatment with candesartan before an acute MI improves global LV function, prevents LV dilation, and blunts the increase in constitutive microtubulin, with minimal effects on LV hemodynamics, regional function, or tissue endothelial nitric oxide synthase. Thus, candesartan given before an MI attenuates LV remodeling and alters the cytoskeleton matrix of the left ventricle.
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.
UNLABELLED: Left ventricular ejection fraction (LVEF) is accepted as an important prognostic marker in patients (pts) with implantable cardioverter-defibrillators (ICD). The impact of this therapeutic approach in the survival of pts with life-threatening arrhythmias and severe left ventricular dysfunction remains a matter of discussion. OBJECTIVE: To evaluate the long-term clinical implications of severe left ventricular dysfunction in pts with an ICD implanted for secondary prevention of sudden cardiac death (SD). METHODS: Out of 70 pts undergoing ICD implantation in our institution over four consecutive years, we studied 24 pts with LVEF <35% and a post-ICD follow-up of >12 months (87.5% male; age 62.79 years). The index arrhythmia was ventricular tachycardia in 19 cases and SD with ventricular fibrillation in 5 cases. The underlying disease was ischemic cardiomyopathy (n=19), dilated cardiomyopathy (n=4) and hypertensive heart disease (n=1). Mean LVEF at the time of implant was 25 +/- 7% (between 11% and 34%; NYHA class II/III in 83.3%). A du chamber system was implanted in 5 cases, and an ICD plus cardiac resynchronization pacing in 2 cases. There was no perioperative mortality. At the time of discharge, 71.2% of the pts were taking amiodarone and 66.7 % beta-blockers. During a 38 +/- 16-month follow-up (4 appointments/year), we analyzed the following parameters: rehospitalization for cardiovascular cause, appropriate ICD shocks, inappropriate detections/therapy, nonfatal major arrhythmic events (arrhythmic storm, therapeutic exhaustion, recurrent ventricular tachycardia), cardiac mortality, SD and total mortality. RESULTS: Forty-five readmissions (1.9 +/- 2.3/pt) occurred in 14 pts (58%), 24.4% due to congestive heart failure. Appropriate ICD shocks (without hospitalization) occurred in 62.5% of the pts, 16.6% had inappropriate therapy (50% because of increased heart rate due to atrial fibrillation) and 37.5% suffered nonfatal major arrhythmic events. Death due to SD was 4.2%, cardiac mortality 12.5% and total mortality 25%. CONCLUSIONS: Severe left ventricular dysfunction is common in ICD pts. During long-term follow-up, the majority of these pts receive appropriate ICD shocks, which emphasizes the importance of SD prevention in this population. The frequent documentation of supraventricular arrhythmias (causing inappropriate ICD therapy) and nonfatal major arrhythmic events also reflects the presence of a worse arrhythmic substrate in this subgroup. Despite the poor initial prognosis associated with ventricular tachyarrhythmias in pts with severe left ventricular dysfunction, ICD therapy may contribute to a better long-term clinical outcome.
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.
Left ventricular (LV) function is an important predictor of cardiac morbidity and mortality. The role of echocardiography in the assessment of LV function is well established and has been expanded over the last few years with the development of new methodologies. Echocardiography can assess LV global and regional function, as well as systolic and diastolic function. It has the ability to measure volumes, including cardiac output, pressures, LV mass, dP/dt. It can also assess regional dysfunction using the wall motion score. However quantitation by standard echo can be limited, due to poor endocardial definition, time-consuming, and reproducibility, lack of accuracy, particularly considering it takes a lot of geometric assumptions. Therefore, new methodologies have been recently developed to increase echo accuracy. These include the introduction of second harmonics, which is becoming a standard in most equipments; the use of contrast echo to improve LV opacification and endocardial border definition; color kinesis, which allows automated segmental motion analysis; tissue Doppler imaging, which can help in the assessment of regional and diastolic function; and more recently the ability to assess strain and strain rate. This last technology has the ability to quantify local myocardial deformation and it has shown to be a potential strong marker of ischemia, as well as a predictor of LV myocardial recovery postrevascularization. In conclusion, echocardiography is widely used to assess LV function. The recent developments of new ultrasound-related technologies have further increased the interest and importance of echocardiography in the assessment of LV function.
BACKGROUND: A normally contracting right ventricular apex associated to a severe hypokinesia of the mid-free wall ('McConnell sign') has been considered a distinct echocardiographic pattern of acute pulmonary embolism. OBJECTIVE: To evaluate the clinical utility of the 'McConnell sign' in the bedside diagnostic work-up of patients presenting to the Emergency Department with an acute right ventricular dysfunction due to pulmonary embolism or right ventricular infarction. DESIGN: Among 201 patients, consecutively selected from our clinical database and diagnosed as having massive or submassive pulmonary embolism or right ventricular infarction, 161 were suitable for an echocardiographic review of regional right ventricular contraction and were included in the study. There were 107 cases with pulmonary embolism (group 1) and 54 cases with right ventricular infarction (group 2). All echocardiographic studies were randomly examined by two experienced and independent echocardiographers, blinded to the patient diagnosis and without Doppler informations. RESULTS: The McConnell sign was detected in 75 of 107 patients in group 1 (70%) and in 36 of 54 patients in group 2 (67%); the finding was absent in 32 cases in group 1 and in 18 cases in group 2 (P=0.657). The sensitivity, specificity, positive and negative predictive values of the McConnell sign for the diagnosis of pulmonary embolism were respectively 70, 33, 67 and 36%. CONCLUSIONS: In a clinical setting of patients with acute right ventricular dysfunction the McConnell sign cannot be considered a specific marker of pulmonary embolism.
AIM: To assess the influence of sex on right ventricular dysfunction (RVD) in patients with severe left ventricular systolic dysfunction. METHODS AND RESULTS: We studied 385 consecutive patients with left ventricular ejection fraction (LVEF) <0.35. All patients underwent invasive measurement of right ventricular and pulmonary artery pressures and evaluation of RVD by standard transthoracic echocardiography. Female patients (n=84, 21.8%) were significantly older than male patients (62.0+/-11.4 vs. 58.2+/-10.7 years), p=0.005. The prevalence of RVD was lower in women (26.5%) than in men (38.9%), p=0.03; both in patients with and without coronary artery disease (19.4% vs. 34.5% and 31.9% vs. 44.4%, respectively). Haemodynamic parameters and LVEF were similar in men and women. Low LVEF, pulmonary systolic pressure, degree of mitral regurgitation, male sex, and absence of significant coronary artery disease were independently correlated with RVD. CONCLUSION: Women with severe left ventricular systolic dysfunction have less RVD than men, despite similar haemodynamic parameters and LVEF.
Chronic left ventricular systolic dysfunction is a well recognized problem with an increasingly significant impact on healthcare in the form of congestive heart failure (CHF). Advances in medicine have led to improved survival after myocardial infarction (MI) and as a result, an increased prevalence of left ventricular systolic dysfunction. An increased incidence of thromboembolism, especially stroke, in patients with left ventricular systolic dysfunction is also well recognized. Pharmacological strategies to prevent stroke have been proposed in numerous studies. For example, anticoagulation in patients with atrial fibrillation and heart failure has been shown to reduce mortality rates and the incidence of stroke; however, its role in patients with left ventricular dysfunction and normal sinus rhythm is unclear and utilization of anticoagulation in these patients varies widely. The role of aspirin to prevent thromboembolism in patients with CHF is controversial. The relatively new pharmacological agent ximelagatran, which has an advantage of unmonitored oral administration has the potential to change the anticoagulation strategy in patients with heart failure. Important trials to define optimal therapy for reducing the risk of thromboembolism and death in patients with left ventricular systolic dysfunction and sinus rhythm include the recently reported WATCH (Warfarin and Antiplatelet Therapy in Chronic Heart failure) trial and the WARCEF (Warfarin versus Aspirin in Reduced Cardiac Ejection Fraction) trial, which is currently underway. The WATCH trial failed to outline significant differences between aspirin (acetylsalicylic acid), warfarin, and clopidogrel in the primary composite endpoint of all-cause mortality, nonfatal MI, and nonfatal stroke. Combined data from WATCH and WARCEF may provide sufficient statistical power to clarify outcomes such as stroke and death in patients with reduced cardiac ejection fraction. The pooled data may also help define optimal preventative measures for thromboembolism in patients with left ventricular systolic dysfunction and sinus rhythm.
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.