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PubMed2006

Cardiac resynchronization therapy as an 'alternative' approach to a non-operable severe aortic stenosis with left ventricular dysfunction.

Severe symptomatic aortic stenosis (AS) is an indication for surgical replacement of the aortic valve in adults. Patients are often affected by comorbidities, and the surgical indication is sometimes problematic. Non-surgical techniques have been developed during the past few years, though their roles have not yet been established. Cardiac resynchronization therapy has been shown to be effective in selected patients, but no data yet exist on the role of this therapy in AS patients. The case is presented of a patient with non-operable severe symptomatic AS and cardiac dissynchrony who showed significant improvement following the implantation of a biventricular pacemaker.

Aged↗
PubMed1994

[Analysis of left ventricular function early after coronary artery bypass grating in patients with left ventricular dysfunction].

We analyzed left ventricular (LV) function early after coronary artery bypass grafting (CABG) in patients with LV dysfunction, whose LV ejection fraction (LVEF) was less than 0.4. 11 patients were divided into two groups: Group-A patients (G-A: n = 6) improved LVEF (post-op LVEF > 0.4) and Group-B patients (G-B: n + 5) did not improve LVEF (post-op LVEF < 0.4) one month after CABG. Preoperative status of coronary artery disease, cardiac function, operative procedure, and postoperative cardiac function were compared between two groups. All patient had old myocardial infarction. There were no differences in preoperative LVEF (0.30 +/- 0.06 in G-A and 0.31 +/- 0.06 in G-B), CI, and LVEDP between two groups. LVEDVI (85 +/- 19 in G-A and 159 +/- 50 ml/m2 in G-B) and LVESVI (60 +/- 14 in G-A and 113 +/- 49 ml/m2 in G-B) values were higher in G-B, respectively. Number of grafts was not different between two groups (2.3 in G-A and 2.4 in G-B). Postoperative LVEF value (0.53 +/- 0.07 in G-A and 0.34 +/- 0.04 in G-B) was lower in G-B. Thus, it might be difficult to obtain the recovery of LV function in patients with LV dilatation, early after CABG.

Adult↗
PubMed1995

Valve replacement for regurgitant lesions of the aortic or mitral valve in advanced left ventricular dysfunction.

Patients with aortic regurgitation and severe left ventricular dysfunction remain candidates for aortic valve replacement, as long as the risks of late left ventricular dysfunction and congestive heart failure have been fully discussed with the patient, the patient's family, and the referring physician. In contrast, patients with mitral regurgitation and severe systolic dysfunction are at considerable risk of more severe left ventricular dysfunction after operation, especially if mitral valve repair or chordal-sparing procedure cannot be performed. In patients who are candidates for such procedures that preserve the integrity of the subvalvular mitral apparatus, operation may be successful in selected patients despite moderate-to-severe depression of systolic function. Prognosis is guarded to poor in patients with regurgitant valvular lesions and advanced left ventricular dysfunction, and the emerging alternative treatments discussed in other articles in this Cardiology Clinics deserve consideration in these patients.

Aortic Valve↗
PubMed2000

Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction.

OBJECTIVE: Rapid ventricular pacing produces a reliable model of heart failure. Cessation after 4 weeks of rapid ventricular pacing results in rapid normalization of left ventricular function, but the left ventricle remains persistently dilated. We present novel data that show that prolonged rapid ventricular pacing (10 weeks) creates a model of chronic left ventricular dysfunction. METHODS: In 9 dogs undergoing 10 weeks of rapid ventricular pacing, left ventricular function and volumes were serially assessed by using 2-dimensional echocardiography and pressure-volume analysis for 12 weeks after cessation of pacing. RESULTS: Increased end-diastolic volume and decreased systolic and diastolic function were seen at the end of pacing. By 2 weeks of recovery from rapid ventricular pacing, end-diastolic volume and ejection fraction were partially recovered but did not improve further thereafter. Load-independent and load-sensitive indices of function obtained by pressure-volume analysis at 8 and 12 weeks of recovery confirmed a persistence of both systolic and diastolic dysfunction. In addition, left ventricular mass increased with pacing and remained elevated at 8 and 12 weeks of recovery. Four of these dogs studied at 6 months of recovery showed similar left ventricular abnormalities. CONCLUSION: Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction.

Animals↗
PubMed2001

Molecular genetics of left ventricular dysfunction.

The left ventricle (LV) plays a central role in the maintenance of health of children and adults due to its role as the major pump of the heart. In cases of LV dysfunction, a significant percentage of affected individuals develop signs and symptoms of congestive heart failure (CHF), leading to the need for therapeutic intervention. Therapy for these patients include anticongestive medications and, in some, placement of devices such as aortic balloon pump or left ventricular assist device (LVAD), or cardiac transplantation. In the majority of patients the etiology is unknown, leading to the term idiopathic dilated cardiomyopathy (IDC). During the past decade, the basis of LV dysfunction has begun to unravel. In approximately 30-40% of cases, the disorder is inherited; autosomal dominant inheritance is most common (although X-linked, autosomal recessive and mitochondrial inheritance occurs). In the remaining patients, the disorder is presumed to be acquired, with inflammatory heart disease playing an important role. In the case of familial dilated cardiomyopathy (FDCM), the genetic basis is beginning to unfold. To date, two genes for X-linked FDCM (dystrophin, G4.5) have been identified and four genes for the autosomal dominant form (actin, desmin, lamin A/C, delta-sarcoglycan) have been described. In one form of inflammatory heart disease, coxsackievirus myocarditis, inflammatory mediators and dystrophin cleavage play a role in the development of LV dysfunction. In this review, we will describe the molecular genetics of LV dysfunction and provide evidence for a "final common pathway" responsible for the phenotype.

Cardiomyopathies↗
PubMed1994

Relation of neurohumoral activation to clinical variables and degree of ventricular dysfunction: a report from the Registry of Studies of Left Ventricular Dysfunction. SOLVD Investigators.

OBJECTIVES: This study examined the relation between neurohumoral activation and severity of left ventricular dysfunction and congestive heart failure in a broad group of patients with depressed left ventricular function who were not recruited on the basis of eligibility for a therapeutic trial. BACKGROUND: Previous studies have established the presence of neurohumoral activation in patients with severe congestive heart failure. It is not known whether the activation of these neurohumoral mechanisms is related to an impairment in left ventricular function. METHODS: From the 6,273 patients recruited into the Studies of Left Ventricular Dysfunction Registry (SOLVD), a subgroup of 859 patients were randomly selected, and their plasma norepinephrine, plasma renin activity, arginine vasopressin and atrial natriuretic peptide levels were correlated with clinical findings, New York Heart Association functional class, left ventricular ejection fraction and drug use. RESULTS: There was a weak but significant correlation between ejection fraction and an increase in plasma norepinephrine (rho = -0.18, p < 0.0001), plasma renin activity (rho = -0.24, p < 0.0001) and arginine vasopressin (rho = -0.12, p < 0.003). The only exception was atrial natriuretic peptide, which showed the best correlation to ejection fraction (rho = -0.37, p < 0.0001). Deterioration in functional class was associated more with increases in atrial natriuretic peptide (p = 0.0003) and plasma renin activity (p = 0.0003) and less with an increase in plasma norepinephrine. Of the clinical variables, elevated jugular venous pressure and third heart sound (S3) gallop were significantly associated with increased levels of plasma norepinephrine, plasma renin activity and atrial natriuretic peptide. We then compared the relation of neurohormones with clinical signs, functional status, ejection fraction and drug therapy and controlled for mutual interactive effects. After adjustment, a decrease in ejection fraction was still significantly related to an increase in plasma norepinephrine, plasma renin activity and atrial natriuretic peptide. In contrast, only a difference between functional classes I and III/IV was associated with an increase in plasma renin activity and atrial natriuretic peptide levels. CONCLUSIONS: Neurohumoral activation in patients with heart failure is related to severity of left ventricular functional depression, and this relation is independent of functional class or concomitant drug therapy.

Aged↗
PubMed1999

Coronary artery bypass graft surgery in patients with ischemic cardiomyopathy and severe left ventricular dysfunction: short and long-term results.

BACKGROUND: We evaluated the prognostic value of preoperative parameters, surgical risk, functional benefits and long-term survival after myocardial revascularization in patients with established ischemic cardiomyopathy. METHODS: Seventy-one patients with ischemic cardiomyopathy, severe left ventricular dysfunction (left ventricular ejection fraction < 30%), and myocardial perfusion evaluated by Thallium-201 scintigraphy, were studied before and after myocardial revascularization, during hospitalization and throughout 48 months (average) of late follow-up. RESULTS: The early postoperative mortality was 2.8% and the five-year survival rate was 62.8%. When the survival rate was studied, there was no correlation with 1) the presence of Q-waves on preoperative cardiogram, 2) the presence of ischemia on Tl-201 scintigraphy, 3) the degree of left ventricular ejection fraction, or 4) the presence of angina. There was a statistically significant difference for survivors and non-survivors in the following parameters: 1) functional class IV of CHF, and 2) the presence of left bundle-branch block (LBBB). CONCLUSIONS: Our surgical results confirm that myocardial revascularization is a safe procedure, and that it increases late survival and improves the quality of life in patients with ischemic cardiomyopathy and severe left ventricular dysfunction. We also observed that due to heterogeneous coronary and myocardial patterns of ischemic cardiomyopathy, preoperative prognostic parameters are difficult to establish. Preoperative functional class IV congestive heart failure, and LBBB were the main predictors of poor outcome following surgical revascularization for ischemic cardiomyopathy.

Aged↗
PubMed1981

Aortic regurgitation. Detection of left ventricular dysfunction by exercise echocardiography.

Left ventricular performance was assessed in 20 symptom free patients and 10 with symptoms, all with isolated aortic regurgitation, by measuring the echocardiographic peak velocity of circumferential fibre shortening (echo peak Vcf) at rest and during graded bicycle ergometer exercise in the supine position. The normal left ventricular response during such exercise was first determined in 20 healthy controls. On the basis of their resting and exercise echo peak Vcf, the 30 patients with aortic regurgitation could be separated into three groups: Group 1 comprised 11 symptom free patients with a normal resting echo peak Vcf which increased normally with exercise; group 2 comprised nine symptom free patients with a normal resting echo peak Vcf but with a subnormal response to exercise; group 3 consisted of 10 patients with symptoms with a depressed resting echo peak Vcf which remained subnormal with exercise. Subsequent cardiac catheterisation disclosed normal ejection fractions in patients in group 1, borderline ejection fractions in those in group 2, and reduced ejection fractions in those in group 3. Echocardiographic assessment of left ventricular performance during supine isotonic exercise may provide a simple noninvasive method for the early detection of left ventricular dysfunction in symptom free patients with aortic regurgitation.

Adolescent↗
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↗
PubMed1996

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↗
PubMed1989

Hemodynamic effects of dilevalol in patients with systemic hypertension and left ventricular dysfunction.

Hemodynamic and left ventricular function parameters were measured in patients with mild to moderate hypertension and compromised left ventricular function who were given dilevalol, an antihypertensive agent with selective beta 2-agonism and nonselective beta-antagonist activity. After a 2- to 3-week placebo washout period, 9 patients were given dilevalol titrated upward from 100 to 600 mg twice daily over a 7-week period to achieve a supine diastolic blood pressure of less than 90 mm Hg with a decrease of greater than or equal to 10 mm Hg from baseline. Multigated radionuclide ventriculography and systolic and diastolic time intervals were performed after the pretreatment placebo washout, at the end of 2 weeks' maintenance dosing, and after a 7- to 10-day post-treatment discontinuation and placebo washout period. At an average daily dose of dilevalol, 444 mg, heart rate at rest decreased significantly (p less than 0.01) during treatment and increased during post-treatment placebo. Systolic and diastolic blood pressures at rest decreased significantly (p less than 0.01) during treatment and increased during post-treatment placebo. At maximal exercise, changes in blood pressure and heart rate were significantly blunted (p less than 0.05) during treatment. Ejection fraction at rest increased significantly (p less than 0.01) during treatment, with no significant change occurring during exercise, and decreased during post-treatment placebo. Preejection period decreased significantly during treatment (p less than 0.005) and increased during post-treatment placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

[Pulmo cardialis: effect of inhaled bronchodilators on airway resistance of acute left ventricular dysfunction].

Disturbance of left ventricular function leads to an impairment of ventilation: airway resistance increases, while pulmonary compliance is reduced. We therefore studied the effect of inhalable bronchodilators (Fenoterol, Ipratropium bromide) on oscillatory airway resistance in 16 patients with an acute left heart failure. The results show that the resistance can be significantly reduced to normal values by the bronchodilators. Fenoterol has the greatest spasmolytic potency, but Ipratropium bromide is also effective. Recompensation of left heart function alone does not lead to comparable acute effects on airway resistance. The possibility of immediate improvement of ventilation through the use of inhalable bronchodilators should therefore be considered in the treatment of acute left heart failure.

Airway Resistance↗
PubMed1998

The hemodynamic impact of diffuse myocardial ischemic lesions: an animal experimental model based on intracoronary microembolization.

In ischemic heart disease, left ventricular function is affected by a diffuse and segmental loss of myocardium. The decline in the incidence of myocardial infarction and improved early revascularization in acute transmural ischemia predict a change in the natural history of ischemic heart disease. It is now believed that, minor ischemic episodes, which are known to induce multifocal myocardial degeneration, will predominate in the near future. The objective of the present study was to develop a clinically relevant experimental model for investigation of the pathophysiological significance of diffuse ischemic myocardial lesions. Cardiac performance was gradually depressed by selective intracoronary microembolization in 13 pigs. Left ventricular function was quantitated by ejection fraction (EF), pulmonary pressure, cardiac output, and derivatives of left ventricular pressure. Left ventricular volume was estimated by epicardial echocardiography, using a new, unbiased stereological volume estimator. A chronic substudy was performed in order to characterize the histological changes and to evaluate the feasibility of establishing a chronic preparation of the model. Embolization induced acute left ventricular dysfunction; left ventricular pressure change decreased from 966+/-274 to 637+/-146 mmHg/s, and early diastolic relaxation from 1403+/-515 to 824+/-344 mmHg/s, respectively. Ejection fraction decreased by 45%+/-5% and cardiac output by 29%+/-11%. End-diastolic volume increased significantly, from 66.1+/-13.2 to 77.0+/-19.4 cm3, and end-systolic volume increased from 35.9+/-13.9 to 52.3+/-7.6 cm3. No change in heart rate or left ventricular filling pressure was observed. Diffuse ischemic myocardial injury was identified after a mean follow-up of 40 days. Intracoronary microembolization induces acute left ventricular dysfunction due to microinfarcts. Increased left ventricular end-diastolic volume is the initial compensatory response to the acute impairment of cardiac performance in nontransmural myocardial ischemia. This model is suitable for the evaluation of the hemodynamic changes secondary to acute and chronic diffuse loss of functional myocardium.

Animals↗
PubMed2005

Exercise-induced changes in mitral regurgitation in patients with prior myocardial infarction and left ventricular dysfunction: relation to mitral deformation and left ventricular function and shape.

AIMS: The aim of this study was to assess the relationship between exercise-induced changes in mitral regurgitation (MR) and echocardiographic characteristics of mitral deformation, global left ventricular (LV) function and shape at rest and after exercise. METHODS AND RESULTS: Forty consecutive patients with ischaemic MR due to prior myocardial infarction (MI), ejection fraction <45% in sinus rhythm underwent exercise-echocardiographic testing. Exercise-induced changes in effective regurgitant orifice (ERO) were compared with baseline and exercise-induced changes in mitral deformation and global LV function and shape. There was significant correlation between exercise-induced changes in ERO and changes in coaptation distance (r=0.80, P<0.0001), tenting area (r=0.79, P<0.0001) and mitral annular diameter (r=0.65, P<0.0001), as well as in end-systolic sphericity index (r=-0.50, P=0.001, respectively), and wall motion score index (r=0.44, P=0.004). In contrast, exercise-induced changes in ERO were not related to the echocardiographic features at rest. By stepwise multiple regression model, the exercise-induced changes in mitral deformation were found to independently correlate with exercise-induced changes in ERO (generalized r(2)=0.80, P<0.0001). CONCLUSION: Exercise-induced changes in severity of ischaemic MR in patients with LV dysfunction due to prior MI were independently related to changes in mitral deformation.

Echocardiography, Stress↗