Severe Left Ventricular Dilatation Research Articles

Prevalence of QRS prolongation in a community hospital cohort of patients with heart failure and its relation to left ventricular systolic dysfunction

Adverse outcomes in heart failure occur more frequently with QRS prolongation. The results of our study have shown that 1/4 of community hospital patients with heart failure of sufficient severity leading to hospitalization have a QRS duration of ≥120 ms and that this degree of QRS prolongation is associated with substantially more severe left ventricular (LV) systolic dysfunction, LV dilation, and mitral regurgitation.

Transesophageal echocardiography of a new paravalvular echolucent area after aortic valve replacement

THIS CASE INVOLVES a 73-year-old man with severe aortic stenosis who was scheduled for aortic valve replacement. The patient had a 2-year history of exertional angina, occasional presyncopal episodes, shortness of breath on exertion, and orthopnea. He also had non-insulin-dependent diabetes mellitus and hyperlipidemia. His medications included atenolol, entrophen, and simvastatine. Preoperative transthoracic echocardiographic (TTE) assessment revealed severe aortic stenosis with an aortic valve area of 0.6 cm2 and a mean pressure gradient of 59 mmHg. Severe left ventricular dilatation with trivial mitral regurgitation and an ejection fraction of 35% were also noted. Coronary angiography was normal except for a 50% stenosis of the second diagonal artery.

Anatomic repair of anomalous left coronary artery from the pulmonary artery by aortic reimplantation: early survival, patterns of ventricular recovery and late outcome

Background To determine the early and late outcomes of patients presenting with anomalous left coronary artery from the pulmonary artery who had repair by aortic reimplantation. Methods From January 1952 to July 2000, 67 patients presented with anomalous coronary artery from the pulmonary artery. Forty-seven patients who had repairs performed by aortic reimplantation are the subject of this study. The median age at repair was 7.7 months. Before repair, 10 infants (21%) presented in extremis requiring ventilatory and inotropic support, and 38 infants (80%) presented in heart failure. Autologous pericardial hood coronary arterioplasty was used in 4 patients, and concomitant mitral valve repair was used in 1 patient. Results Hospital survival was 92%. Five children required postoperative extracorporeal membrane oxygenation for a median of 4 days (range, 2 to 8 days). Patients who had extracorporeal membrane oxygenation were significantly more likely to have presented in critical condition (40% vs 3% if no extracorporeal membrane oxygenation; p = 0.006) or with ventricular arrhythmias (67% vs 7%; p = 0.027), to have presented with significantly lower preoperative repair median ejection fraction (10%, n = 5 vs 40%, n = 38; p = 0.01) or to have presented with more severe left ventricular dilatation ( p = 0.03). Within a 15-year or less follow-up (mean, 4.7 years) there were no late deaths. Kaplan-Meier survival was 91% at 5 years, and freedom from reoperation was 93% at 10 years. At late follow-up, echocardiography demonstrated significant improvements in mean ejection fraction (64% ± 9% vs 33% ± 21% preoperatively, p < 0.0001); moderate mitral regurgitation (9% vs 38% preoperatively, p < 0.02); and wall motion abnormalities (15% vs 81% preoperatively, p < 0.002). The ratio of measured left ventricular end-diastolic dimension to the 95th percentile of normal declined from 1.4 ± 0.3 to 1.0 ± 0.1 ( p < 0.0006). Children who had extracorporeal membrane oxygenation had normal ejection fractions and ventricular dimensions at follow-up (n = 3). Repeated measures of mixed linear regression analysis demonstrated that normalization of ejection fraction and left ventricular function occurred within 1 year of repair. Improvements in mitral regurgitation lagged behind normalization of ejection fraction and left ventricular dilatation. Conclusions Anatomic repair of anomalous left coronary artery from the pulmonary artery by aortic reimplantation yields excellent early survival and late functional outcomes even in critically ill infants.

Valvular pathology diagnosed with transesophageal echocardiography during aortic root replacement

A 22-year-old man was admitted with a known history of congenital aortic insufficiency (AI) after a 6-month history of worsening dyspnea on exertion, fatigue, and paroxysmal atrial fibrillation. His past medical history was significant for cocaine, marijuana, heroin, and tobacco abuse. He denied fevers, chills, rigors, or night sweats. A complete blood count revealed no abnormal leukocytosis. Medications included amlodipine, aspirin, and amiodarone. Echocardiogram revealed severe left ventricular (LV) dilatation (LV diastolic diameter 79 mm), severe AI, and a LV ejection fraction of 70% to 75%. Cardiac catheterization confirmed severe AI, LV ejection fraction of 55%, LV end-diastolic pressure of 30 mmHg, with right ventricular and pulmonary arterial pressures of 26/8 and 26/16, respectively.

Ultrafiltration and dry weight-what are the cardiovascular effects?

Long-term prognosis in dialysis is poor compared to that in healthy control persons. A worsening of the prognosis is noted especially for patients who at initiation of dialysis have congestive heart failure, ischemic heart disease, or left ventricular dysfunction or hypertrophy. This is the main reason that cardiovascular causes are the most common for morbidity in these patients. The weight obtained when normal urine output is present is the dry weight. With reduced ability to excrete the volume by the kidneys in end-stage renal disease (ESRD), the body will retain water and the patient will gain weight. This extra weight is due to volume overload. While volume overload may induce a rise in blood pressure, if the heart is in acceptable condition, a fast removal of fluid by ultrafiltration (UF) during dialysis may instead cause hypotension. Ultrafiltration failure in peritoneal dialysis (PD) patients may lead to successive water retention and overhydration with subsequent cardiac failure, while volume overload may occur over a few days in hemodialysis (HD) patients. Anemia or even too-high hematocrit may impair cardiac function further and worsen conditions caused by wrong dry weight. Thus, during long-term and sustained volume overload, left ventricular (LV) hypertrophy will occur in an eccentric manner. A sustained overload then may lead to cell death and LV dilatation and, eventually, systolic dysfunction. Once a severe left ventricular dilatation has developed, the blood pressure may decrease during volume overload. A worsened prognosis is seen if malnutrition and low albumin levels are present. Volume overload necessitates ultrafiltration to achieve dry weight. Thereby, volume contraction contributes to exaggerated stimulation of or response to activation of the RAS and alpha-adrenergic sympathetic systems. If ultrafiltration goes beyond these compensatory mechanisms, hypotension will occur and increase the risk for hypoperfusion of vital organs. Such episodes may cause cardiac morbidity, aspiration pneumonia, vascular access closure, or neurological complications (seizures, cerebral infarction), besides a more rapid lowering of residual renal function. Preventive measures are, first, finding the right dry weight; second, minimizing interdialytic weight gain; third, optimizing the target for hemoglobin (110-120 g/l); fourth, lowering dialysate calcium (1.25 mmol/l); and fifth, eventually using higher dialysate potassium if long dialyses are performed.

Case 1–2003 The use of intraoperative echocardiography during insertion of ventricular assist devices

Transesophageal echocardiography (TEE) assists in the intraoperative decision-making process during cardiac anesthesia and cardiac surgery. Mechanical ventricular support may be necessary to support the circulatory system temporarily or serve as a bridge to heart transplantation. A left ventricular assist device (LVAD) is most commonly used.1 Biventricular failure necessitates the use of an LVAD along with a right ventricular assist device (RVAD) to form a biventricular assist device (BIVAD) (Fig 1). TEE plays a vital role in evaluating effective mechanical assistance of the circulation.1-3 This case describes a BIVAD placement in a patient and shows the roles and limitations of TEE in this scenario.

Anaemia in chronic renal disease: lessons learned since Seville 1994.

Cardiovascular disease is the major cause of death among patients with end-stage renal disease, accounting for almost half of all fatalities. In recent years much progress has been made in understanding the pathogenesis of cardiovascular disease in the uraemic population. Anaemia is a consistent finding in chronic renal disease, affecting up to 90% of patients, and the central role of anaemia in the development of cardiovascular dysfunction is now well established. A significant proportion of patients have established cardiovascular complications on initiation of dialysis, raising the possibility of early correction of anaemia as a strategy for preventing cardiovascular co-morbidities among renal patients. Randomized, controlled trials have shown that normalization of haemoglobin (Hb) with recombinant erythropoietin (rh-Epo) is of no cardiovascular benefit in haemodialysis patients with symptomatic heart failure, ischaemic heart disease, or severe left ventricular dilatation, although suggestive evidence exists for benefits at earlier stages of cardiac disease. Results from large-scale clinical trials are required to clarify the effects of early anaemia correction on mortality and cardiovascular function, as well as appropriate treatment targets in different patient populations. The potential exists for higher Hb levels to extend patient survival through cardioprotective effects.

Heterogeneity of left ventricular remodeling after acute myocardial infarction: Results of the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico-3 Echo Substudy

Background Left ventricular (LV) remodeling after acute myocardial infarction has still to be clarified in the thrombolytic era. Methods To evaluate timing and the magnitude and pattern of postinfarct LV remodeling, a subset of 614 patients enrolled in the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico-3 Echo Substudy underwent serial 2-dimensional echocardiograms at 24 to 48 hours from symptom onset (S1), at hospital discharge (S2), at 6 weeks (S3), and at 6 months (S4) after acute myocardial infarction. Results During the study period the end-diastolic volume index (EDVi) increased (P <.001) and wall motion abnormalities (%WMA) decreased (P <.001), whereas ejection fraction (EF) remained unchanged. Nineteen percent of patients showed a > 20% increase in EDVi at S2 compared with S1 (severe early dilation), and 16% of patients showed a > 20% dilation at S4 compared with S2 (severe late dilation). Independent predictors of severe in-hospital LV dilation were relatively small EDVi (odds ratio [OR] 0.961, 95% confidence interval [CI] 0.947-0.974, P =.0001) and relatively large %WMA (OR 1.030, 95% CI 1.013-1.048, P =.0005). Similarly, smaller predischarge EDVi (OR 0.975, 95% CI 0.963-0.987, P =.0001), greater %WMA (OR 1.026, 95% CI 1.008-1.045, P =.0042), and moderate to severe mitral regurgitation (OR 2.261, 95% CI 1.031-4.958, P = 0.0417) independently predicted severe late dilation. Importantly, 92% of the patients with severe early dilation did not have further dilation at S4, and 91% of patients with severe late dilation did not have in-hospital dilation. EF was unchanged over time in patients with early dilation, whereas it significantly decreased in those with late dilation. Conclusions Although in-hospital LV enlargement is not predictive of subsequent dilation and dysfunction, late remodeling is associated with progressive deterioration of global ventricular function over time: patients with extensive %WMA and not significantly enlarged ventricular volume before discharge are at higher risk for progressive dilation and dysfunction. (Am Heart J 2001;141:131-8.)

Relation of regional sympathetic denervation and myocardial perfusion disturbance to wall motion impairment in Chagas’ cardiomyopathy

Impairment of sinus node autonomic control and myocardial perfusion disturbances have been described in patients with chronic Chagas’ cardiomyopathy. However, it is not clear how these conditions contribute to myocardial damage. In this investigation, iodine-123 (I-123) meta-iodobenzylguanidine (MIBG) and thallium-201 myocardium segmental uptake were studied in correlation with the severity of left ventricular (LV) dysfunction detected in various phases of Chagas’ heart disease. Group I consisted of 12 subjects (43 ± 4 years, 7 men) with no symptoms and no cardiac involvement on electrocardiogram (ECG) or echocardiography; group II consisted of 13 patients (48 ± 3 years, 9 men) with abnormal resting ECG and/or echocardiographic segmental abnormalities, and LV ejection fraction of ≥0.5; group III was comprised of 12 patients (59 ± 3 years, 10 men) with more severe heart disease, LV dilation, and LV ejection fraction of <0.5. Eighteen control volunteers (38 ± 3 years, 9 men) were also included in the study. I-123 MIBG single-photon emission computed tomographic (SPECT) segmental uptake defects were observed in group I (33%), group II (77%), and group III (92%). Quantitative analysis showed mean areas of reduced LV I-123-MIBG uptake: group I was 3.7 ± 2.1%; group II was 8.3 ± 2.3%; and group III was 19.0 ± 3.3%. The differences between group I and both groups II and III were statistically significant (p <0.001, analysis of variance test). Myocardial perfusion defects (reversible, fixed, and paradox) were observed in group I (83%), group II (69%), and group III (83%). A marked topographic association between perfusion, innervation, and wall motion abnormalities (assessed by gated-SPECT perfusion studies) was observed in all the groups. Defects predominated in the inferior, posterior lateral, and apical LV regions. Thus, extensive impairment of cardiac sympathetic function at the ventricular level occured early in the course of Chagas’ cardiomyopathy and was related to regional myocardial perfusion disturbances, before wall motion abnormalities. Both conditions are associated with progression of ventricular dysfunction.

Diagnosis and indication for aortic valve replacement in asymptomatic and symptomatic patients with aortic regurgitation

Chronic volume overload is associated with dilatation and eccentric hypertrophy of the left ventricle (= ventricular remodeling). With the dilatation of the left ventricle and the shift of the pressure-volume-relationship to the right, the filling pressures can be kept normal despite severe regurgitation. Therefore, the patient with aortic regurgitation can remain asymptomatic over many years. Thus, the indication for aortic valve replacement in patients with severe aortic regurgitation is sometimes difficult and may lead to problems to choose the optimal time point for operation. As a general rule, symptomatic patients with severe aortic regurgitation should be operated as soon as possible. In asymptomatic patients with significant dilatation of the left ventricle and reduction of systolic pump function the therapy of choice is aortic valve replacement. Asymptomatic patients with normal left ventricular function have usually a good prognosis with a yearly mortality rate of approximately 0.04%. However, in the presence of significant dilatation of the left ventricle, i.e. enddiastolic chamber diameter more than 70 mm respectively endsystolic diameter more than 50 mm, patients have to be checked on a regular basis, i.e. in yearly intervals to detect left ventricular dysfunction in due time. According to the literature, asymptomatic patients with severe aortic regurgitation develop left ventricular dysfunction in a yearly rate of 4%. However, approximately 50% of all patients are even after 10 years asymptomatic. The indication for aortic valve replacement is given when the patient shows a deterioration of left ventricular function or becomes symptomatic. Valve replacement is also indicated in patients with an ejection fraction below 50% and/or endsytolic chamber diameter of more than 55 mm. Therapy of choice in symptomatic patients with severe aortic regurgitation is aortic valve replacement. In asymptomatic patients, operation depends on the degree of chamber dilatation respectively the severity of left ventricular dysfunction. In patients with severe aortic regurgitation but without clinical symptoms and moderate enlargement of the left ventricle regular check-ups in yearly intervals are indicated. In the presence of severe left ventricular dilatation check-ups should be performed on a half-year basis to prevent irreversible damage to the heart muscle.

Force-frequency relations in the failing rabbit heart and responses to adrenergic stimulation

Background: Recent experiments have documented the importance of beta-adrenergic regulation of the force-frequency relation (FFR) in the normal and failing heart. As in isolated human cardiac muscle, a descending limb of the FFR occurs at high frequencies in the intact rabbit heart, and therefore a new model of atrial pacing-induced heart failure was developed in the rabbit. Responses of the FFR to beta-adrenergic stimulation were then assessed in the conscious state before and after the induction of heart failure. Methods and Results: Rapid atrial pacing for an average of 19.5 days in instrumented rabbits produced severe left ventricular dilation with reduced cardiac output (echocardiography) and depressed myocardial contractility and relaxation rate (left ventricular dP/dt, catheter-tip micromanometer), associated with reductions in beta-adrenergic receptor density and adenylyl cyclase activity. Before heart failure, heart rate was slowed in the conscious animal from 280 ± 30 (SD) to about 225 beats/min using a sinus node inhibitor (zatebradine), and heart rate was then increased in steps by atrial pacing from 250 to 450 beats/min; the heart rate-versus-left ventricular dP dt max (FFR) response showed an ascending response (increasing contractility), with a descending limb at rates greater than 375 beats/min, and dobutamine infusion amplified the ascending limb of the FFR (increased slope) and attenuated the descending limb. In heart failure the basal FFR was severely depressed with a descending limb over 350 beats/min; dobutamine shifted the FFR upward somewhat without change in the slope of the ascending limb, whereas dobutamine prevented the descending limb of the FFR. Similar responses were observed in the relations between heart rate and cardiac output. Conclusions: A new model of heart failure in the conscious rabbit was developed using rapid atrial pacing and applied to study force-frequency effects. In heart failure, normal beta-adrenergic amplification of the ascending limb of the FFR by dobutamine was absent, but a marked descending limb of the FFR at higher heart rates was prevented by dobutamine. Observed reductions in components of the beta-adrenergic receptor system likely were responsible for impaired beta-adrenergic FFR amplification, but the mechanism(s) for the descending limb and its correction by dobutamine are not yet established. These responses of the FFR may influence importantly the ability of the failing heart to respond to exercise and stress.

Myocardial involvement is very frequent among patients affected with subclinical Becker's muscular dystrophy.

Several cases of Becker's muscular dystrophy (BMD) have been reported, which showed mild or subclinical skeletal muscle involvement with an overt dilated cardiomyopathy. Here, for the first time, a group of 28 patients with BMD who had a subclinical or benign myopathy have been studied through a thorough cardiological assessment. Each patient underwent ECG and echocardiographic examinations. Molecular analyses of the dystrophin gene and protein were performed. An unexpectedly high incidence of myocardial involvement was observed among patients affected with subclinical (72%) or benign (60%) BMD. The cardiac involvement appears to develop early from the right ventricle. Both the increase in left ventricular end-diastolic volume and the reduction in the ejection fraction appeared to be age related. Severe left ventricular dilation with reduced ejection fraction, which could be complicated by life-threatening arrhythmias, may occur. Contrary to previous reports, which indicated the involvement of 5'-end mutations in cardiomyopathies as a result of dystrophin gene alterations, this study shows that despite the apparent concentration of deletions in two regions (5'-end and exons 47 through 49), no general conclusions can be drawn regarding the involvement of specific gene mutations in the development of cardiomyopathy. Cardiomyopathy is the main clinical feature and complication in patients affected by subclinical or mild BMD. The cardiac manifestation is characterized by early right ventricular involvement and is later associated with left ventricular impairment. In mild BMD, myocardial damage may develop because the patients, who are unaware of a possible cardiac involvement, are still able to perform strenuous muscle exercise and, through pressure or volume overload, may induce mechanical stress, which is harmful for dystrophin-deficient myocardial cells.

Idiopathic dilated cardiomyopathy in Dalmatians: Nine cases (1990–1995)

Objective To describe the historical, clinical, and echocardiographic findings in Dalmatians with dilated cardiomyopathy (DCM). Design Retrospective case series. Sample Population 9 Dalmatians with a diagnosis of DCM and congestive heart failure (CHF), 9 Doberman Pinschers with DCM and CHF, and 9 dogs of other breeds with DCM and CHF. Procedure Disease history; signalment; physical, radiographic, and echocardiographic examination findings; treatment; and outcome from medical records were analyzed. Results All Dalmatians were male, with a mean age of 6.8 years. Eight dogs had been fed a commercially available low-protein diet formulated for the prevention of urate uroliths. All dogs had clinical signs consistent with left-sided CHF and had marked left ventricular systolic dysfunction and severe left ventricular dilatation, although arrhythmias were not an important finding in this series of dogs. Median duration of survival was 10 months. Clinical Implications The DCM syndrome in Dalmatians has some qualities that are distinct from DCM in other breeds of dogs. (J Am Vet Med Assoc 1996;209:1592–1596)

Heart rate variability in relation to severity of mitral regurgitation in Cavalier King Charles spaniels

Heart rate variability was measured in 81 Cavalier King Charles spaniels to investigate if it could be used to evaluate the severity of mitral regurgitation and to predict decompensation. Heart rate variability was assessed by the natural logarithm of the variance of the R-R intervals for 20 consecutive beats obtained from electrocardiographic recordings. Twenty-two of the dogs were clinically normal and 59 had mitral regurgitation caused by chronic valvular disease. The severity of mitral regurgitation was evaluated by echocardiography and thoracic radiography. Heart rate variability was found to be reduced (P < 0.001) among dogs with severe left atrial and ventricular dilatation and clinical signs of congestion. No significant differences in heart rate variability were found among normal dogs, dogs with only cardiac murmur, and dogs with echoradiographic evidence of slight to moderate left atrial and ventricular dilatation. Overall, an association was found between heart rate variability and left atrial to aortic root ration and left ventricular end diastolic diameters (r = 0.72 and 0.64, respectively, P < 0.001), as well as heart and respiratory rate (r = 0.80 and 0.69, respectively, P < 0.001). Multiregression analysis showed that, in order of importance, heart rate, left atrial diameter and respiratory rate had significant effects on heart rate variability. Among these parameters, heart rate variability and left atrial diameter were found to be most efficient in separating decompensated dogs from compensated. It is concluded that heart rate variability may provide the clinician with valuable information when assessing the severity of mitral regurgitation caused by chronic valvular disease.

Plasma concentration of atrial natriuretic peptide in relation to severity of mitral regurgitation in Cavalier King Charles Spaniels

Summary Plasma concentration of immunoreactive atrial natriuretic peptide (ir-anp) was investigated in 83 Cavalier King Charles Spaniels with variable severity of mitral regurgitation caused by chronic valvular disease (cvd). Severity of mitral incompetence was assessed by echocardiography. Significant differences in plasma concentrations of ir-anp were not found between clinically normal dogs (New York Heart Association functional class O), dogs with only cardiac murmur (class I), and dogs with echocardiographic evidence of slight to moderate left atrial and ventricular dilatation (class II). Dogs with severe left atrial and ventricular dilatation and clinical signs of congestion (classes III and IV) were found to have significantly (P &lt; 0.001) increased plasma concentration of ir-anp. Overall, moderate degree of association was found between plasma concentration of ir-anp and left atrial and left ventricular diameters (Pearson's r = 0.65, 0.60, respectively, P &lt; 0.001), as well as heart rate (r = 0.47, P &lt; 0.01). However, left atrial enlargement was found to have the predominant effect on plasma ir-anp concentration. It is concluded that the plasma concentration of ir-anp did not become markedly increased before decompensation of chronic mitral regurgitation associated with severe enlargement of the left atrium and ventricle in Cavalier King Charles Spaniels.

Effect of endurance training early or late after coronary artery occlusion on left ventricular remodeling, hemodynamics, and survival in rats with chronic transmural myocardial infarction.

Remodeling of infarcted and noninfarcted ventricular regions, infarct expansion, shape distortion, and global left ventricular (LV) dilation influence LV performance and survival. The effect of chronic exercise, initiated early or later after infarction, on remodeling, hemodynamics, and survival has not been studied. A total of 156 rats were randomized after coronary artery occlusion or sham operation to remain sedentary or to start with swim training 4 days or 21 days after coronary occlusion, which was continued over 8 weeks (6 days per week, 90 minutes per day). These intervals after coronary artery ligation were chosen because final size of infarction is well reached after 4 days; histological evolution of scar healing is still in progress, and after 21 days, histological scar healing is completed. At 8 weeks, hemodynamics were measured and LV dilation quantitated by passive pressure-volume curves. In groups with small (< or = 35%) and large (> 35%) infarcts, the area enclosed by endocardial circumference, infarct size, LV diameter, scar thickness, and septal thickness were measured in stained transverse serial LV sections to assess aneurysmal shape distortion and the response of infarcted and noninfarcted myocardia. Survival was not influenced by infarction or exercise alone. In rats with small infarcts, LV volume and shape and long-term survival were not altered by chronic exercise initiated early or late after coronary artery ligation. Mortality rose in animals with large infarction as a result of exercise (P < .0001) and was 47.6% with early exercise and 26.7% with late exercise (P < .05, early versus late). Infarct size in rats with early exercise (48 +/- 3%) was similar compared with infarct size of rats with late exercise (46 +/- 2%, P = NS compared with early exercise). Exercise did not affect LV dysfunction (assessed by systolic and end-diastolic pressures and dP/dtmax) in survivors of small and large infarctions. LV volumes increased (P < .05) in sedentary rats by large infarction (n = 13, 0.48 +/- 0.04 mL) compared with volumes after sham operation (n = 33, 0.33 +/- 0.03 mL) and with exercise (early, n = 11, 0.56 +/- 0.04 mL; late, n = 11, 0.65 +/- 0.04; P < .05 versus sedentary). In nonsurvivors from early exercise, the area enclosed by LV endocardial circumference (which corresponds to LV volume) was increased by 195%, LV diameter was increased by 60%, and scar thickness was reduced by 37% (P < .05 versus respective control). Septal thickness increased in survivors by exercise (+25%) but decreased (-28.6%) in nonsurvivors (P < .0001 versus respective control). Endurance training in rats after small infarction, whether started early or late after left coronary artery ligation, was well tolerated without changes in LV volume, shape, hemodynamics, and long-term survival. Endurance training in rats with large infarction decreased overall survival (P < .0001). In survivors from late exercise, training caused aggravation of global LV dilation without additional shape changes. Endurance training after large infarction caused aggravation of remodeling to a degree that was not compatible with life in 27% of the rats with late exercise and in 48% with early exercise after coronary artery ligation, despite similar exercise. This was explained by extensive remodeling that was most pronounced in nonsurvivors from early exercise. In these rats, severe global LV dilation, distortion of LV shape, scar thinning, and a paradoxic reduction of septal thickness, ie, mismatch of infarcted and noninfarcted myocardia, were observed.

Restrictive left ventricular filling pattern in dilated cardiomyopathy assessed by doppler echocardiography: Clinical, echocardiographic and hemodynamic correlations and prognostic implications

Objectives. This study was undertaken to evaluate the frequency of restrictive left ventricular filling pattern in dilated cardiomyopathy, as well as its clinical and hemodynamic correlations and prognostic implications.Background. In dilated cardiomyopathy, as in other heart disease different left ventricular filling patterns were observed on Doppler echocardiography. Some patients showed a “restrictive filling pattern,” similar to that associated with restrictive cardiomyopathy, characterized by predominant E waves and a shortened E deceleration time.Methods. Pulsed Doppler transmitral curves were analyzed in 79 consecutive patients with dilated cardiomyopathy assigned to two study groups according to E deceleration time group 1 (n = 36) had a restrictive left ventricular filling pattern (E deceleration time <115 ms); group 2 (n = 43) had an E deceleration time ≥115 ms.Result. Patients in group 1 were significantly younger, in a higher New York Heart Association functional class, more frequently had a third heart sound and had a higher left ventricular pressure at catheterization. In addition, they showed more severe left and right ventricular dysfunction and dilation, a larger left atrium and more severe mitral regurgitation. A restrictive filling pattern was associated at Doppter study with a higher E wave velocity, lower A wave velocity and higher E/A ratio. During a follow-up interval of 22 ± 14 months, all 14 patients who subsequently died or required heart transplntation showed a restrictive left ventricular filling pattern. At multivariate analysis, E deceleration time was the most powerful independent prognostic indicator of poor outcome or transplantation.Conclusions. Restrictive left ventricular filling pattern is frequent in dilated cardiomyopthy, is associated with more severe disease and is a powerful indicator of increased mortality risk and need for heart transplantation.

Impact of left ventricular cavity size on survival in advanced heart failure

Although left ventricular (LV) dilation has been assumed to be deleterious, the physiologic significance of severe LV dilation in advanced heart failure and its impact on survival have not been defined. LV end-diastolic dimension was measured by M-mode echocardiography in 382 patients with class III or IV heart failure symptoms (mean LV ejection fraction 20 ± 8%) referred for evaluation for cardiac transplantation. All patients underwent right-sided heart catheterization, and received vasodilator and diuretic therapy adjusted to hemodynamic goals. Although 183 patients with massive LV dilation by LV index >4 cm/m 2 (LV index = LV end-diastolic dimension/estimated body surface area) had a similar severity of hemodynamic impairment to that of 199 patients with only moderate dilation (LV index <4 cm/m 2), with baseline mean cardiac index of 2 liters/m/m 2 and mean pulmonary arterial wedge pressure of 26 mm Hg in both groups, their actuarial 2-year survival without transplantation was much tower (49 vs 75%; p = 0.004). In the Cox proportional-hazards model, LV index predicted total and sudden death, independent of etiology of heart failure, ejection fraction and other parameters of disease severity. Follow-up echocardiograms (mean 13 ± 6 months) in 80 heart failure survivors without transplantation showed an increase in mean LV ejection fraction (22 ± 8% to 26 ± 13%), but no change in mean LV index in either the massive or moderately dilated groups. Thus, massive LV dilation is an independent contributor to poor outcome in patients with advanced heart failure, and may be stabilized by aggressive vasodilator and diuretic therapy.

Abnormal intraventricular flow patterns in left ventricular dysfunction determined by color Doppler study

We examined the relation between left ventricular (LV) flow dynamics measured by color Doppler, and either global or regional LV function in 19 normal subjects (group 1), in 55 patients with old myocardial infarction (MI) (29 without [group 2] and 26 with LV aneurysm [group 3]), and in 16 with idiopathic dilated cardiomyopathy (group 4). We calculated by M-mode color Doppler a flow persistence index (FPI) (duration of flow directed in systole toward the apex/LV ejection time). Contrast echocardiography was performed as a control method in 14 patients of the four groups. In normal subjects, rapid systolic inversion of flow toward the aorta was evident (FPI: 0.11 ± 0.16). In all but one patient in group 2, a similar LV flow pattern was observed, but FPI was greater (0.32 ± 0.26). In groups 3 and 4, a paradoxical antegrade LV flow pattern was evident during the entire period of systole (FPI: 1.13 ± 0.42 and 1.28 ± 0.36, respectively). LV flow patterns were reproduced in echo-contrast studies. FPI was related to LV end-diastolic volume ( r = 0.77), end-systolic volume ( r = 0.82), and ejection fraction ( r = −0.84). However, when data were analyzed separately in the different groups, these correlations were significant only in groups 2 and 3. Paradoxical flow pattern is not peculiar to regional LV dysfunction; it also occurs in global LV dysfunction. This LV flow abnormality may develop after MI even in the absence of severe LV dyssynergy or dilation, and is quantitatively related to the degree of LV dysfunction.

Mechanical left ventricular support as a bridge to cardiac transplantation in childhood

The mechanical extrathoracic "Berlin Heart" cardiac assist device was used for left ventricular support in an 8-year-old child of 27 kg body weight. Terminal left ventricular failure and life-threatening ventricular tachyarrhythmias in this child were sequelae of coarctation of the aorta, aortic stenosis and resultant severe left ventricular dilatation, hypokinesia and fibrosis. With the assist device, cardiogenic shock could be reversed. The child was extubated and mobilized during an 8-day waiting period for orthotopic heart transplantation. This case illustrates that the use of ventricular assist devices can be successfully extended to children and may be advantageous compared to other techniques of mechanical circulatory support, such as balloon pumping or extracorporeal membrane oxygenation.