Left Ventricular Cavity Volume Research Articles

Valsalva maneuver to predict dynamic intraventricular obstruction during dobutamine stress echocardiography in patients with hypertension

We were to evaluate the effect of Valsalva maneuver with comparison to preload reduction by nitroglycerin (NTG) to predict intraventricular obstruction (IVO) during dobutamine stress echocardiography (DSE) in patients with hypertension. A total of 38 hypertensive patients (mean age 66.0±9.9 years; 32% male) were prospectively enrolled. The patients with positive exercise electrocardiography, transmural infarction, significant valvular heart disease, atrial fibrillation, beta-blocker therapy, and induced ischemia during DSE were excluded. The development of an IVO during DSE was defined as a late-peaking intraventricular pressure gradient (IVPG) >30 mmHg. The patients were divided into 2 groups, without IVO (n=11, non-IVO) and with IVO (n=27). IVO group had smaller left ventricular (LV) cavity and LV end-diastolic volume, and more increased interventricular septum thickness and higher basal septal thickness than non-IVO group. At rest, after Valsalva maneuver, during peak dose of dobutamine, and after NTG, IVPG was higher in IVO-group. To predict IVO during DSE, IVPG ≥5 mmHg after Valsalva maneuver had a sensitivity of 70.4% and specificity of 90.9%. and IVPG ≥4.5 mmHg after NTG had a sensitivity of 33.3% and specificity of 90.9%. Simple and safe Valsalva maneuver plays an effective role to predict dynamic IVO in patients with hypertension who might be good candidate for beta-blocker therapy and is even more sensitive than preload reduction by NTG.

Quantification of Left Ventricular Volumes and Ejection Fraction in Mice Using PET, Compared with MRI

PET has become an important noninvasive imaging technique in cardiovascular research for the characterization of mouse models in vivo. This modality offers unique insight into biochemical changes on a molecular level, with excellent sensitivity. However, morphologic and functional changes may be of equal importance for a thorough assessment of left ventricular (LV) pathophysiology. Although echocardiography and MRI are widely considered the imaging techniques of choice for the assessment of these parameters, their use with PET considerably increases study complexity and decreases cost- and time-efficiency. In this study, a novel method for the additional quantification of LV volumes and ejection fraction (EF) from PET was evaluated using cardiac MRI as the reference method. The radiolabeled glucose derivative 18F-FDG was injected into 33 mice (6 mice with previous permanent occlusion of the left anterior descending artery [LAD], 15 mice with a temporary 30-min occlusion of the LAD, and 12 mice without previous surgery). 18F-FDG uptake within the LV myocardium was measured using a dedicated small-animal PET scanner. After we reconstructed the images into 16 electrocardiogram (ECG)-gated frames, we determined the LV cavity volumes in end-diastole (EDV) and end-systole (ESV) and the EF using a semiautomatic segmentation algorithm based on elastic surfaces. A 6.3-T cardiac MRI examination was performed in the same animals using an ECG-triggered and respiratory-gated multislice cine sequence. The MR images were segmented with a semiautomatic algorithm using commercially available software. Overall, measurements from PET agreed well with those obtained by MRI. Mean EDV and ESV were slightly overestimated by PET (86+/-43 microL and 44+/-42 microL), compared with MRI (73+/-44 microL and 41+/-46 microL); mean (+/-SD) EF was similar (PET, 55+/-19 microL; MRI, 54+/-18 microL). Correlation between PET and MRI was excellent for EDV (0.97) and ESV (0.96) and good for EF (0.86). The slope of the regression line was nearly perfect for EDV (0.98) and EF (1.01) and slightly below 1 for ESV (0.90), indicating a good separation of abnormal and normal values with PET. The y-intercept was above zero for EDV (15 microL) and ESV (7 microL) and near to zero for EF (0.2%). The quantification of LV volumes and EF in mice with PET is both efficient and accurate. This method allows for combined molecular and functional imaging of the left ventricle within a single scan, obviating additional sophisticated MRI in many cases.

Measuring left ventricular function in the normal, infarcted and CORM-3-preconditioned mouse heart using complex admittance-derived pressure volume loops

Introduction Miniaturized conductance catheters have been successfully applied to measure left ventricular (LV) function in the mouse to assess cardiac or pharmacological interventions. Complex admittance, in contrast to existing methods using conductance catheters, produces an estimate of the parallel admittance of cardiac muscle that can be used to correct the measurement in real-time. The aim of this study was to validate the use of complex admittance to assess LV function in normal and infarcted hearts. Methods Using a single conductance catheter, we directly compared measures of LV function using a specially developed admittance system (ADVantage™ system) and a traditional conductance-derived pressure–volume (PV) system. We subjected mice to focal myocardial ischaemia-reperfusion injury while measuring cardiac function to determine the ability of the new system to distinguish between normal, and dysfunctional LV, contractile performance. Results LV pressure–volume loops from complex admittance is a reproducible and reliable method of determining LV function, producing data similar to that of the conductance catheter. Our data suggest that the ADVantage™ system records larger systolic LV cavity volumes when compared to the traditional conductance system in the same animal. In addition, we demonstrate marked LV dysfunction following coronary artery occlusion and reperfusion which is ameliorated using CORM-3, a cardioprotective agent that liberates carbon monoxide (CO). Conclusion The ADVantage™ system is both effective and reproducible in measuring LV function and dysfunction in the mouse, without the need for complicated interventions to calibrate the measurements. This may mark the way toward an accurate assessment of murine cardiac function.

Validation of a novel noninvasive cardiac index of left ventricular contractility in patients

Although there are several excellent indexes of myocardial contractility, they require accurate measurement of pressure via left ventricular (LV) catheterization. Here we validate a novel noninvasive contractility index that is dependent only on lumen and wall volume of the LV chamber in patients with normal and compromised LV ejection fraction (LVEF). By analysis of the myocardial chamber as a thick-walled sphere, LV contractility index can be expressed as maximum rate of change of pressure-normalized stress (d sigma*/dt(max), where sigma* = sigma/P and sigma and P are circumferential stress and pressure, respectively). To validate this parameter, d sigma*/dt(max) was determined from contrast cine-ventriculography-assessed LV cavity and myocardial volumes and compared with LVEF, dP/dt(max), maximum active elastance (E(a,max)), and single-beat end-systolic elastance [E(es(SB))] in 30 patients undergoing clinically indicated LV catheterization. Patients with different tertiles of LVEF exhibit statistically significant differences in d sigma*/dt(max). There was a significant correlation between d sigma*/dt(max) and dP/dt(max) (d sigma*/dt(max) = 0.0075 dP/dt(max) - 4.70, r=0.88, P<0.01), E(a,max) (d sigma*/dt(max) = 1.20E(a,max) + 1.40, r=0.89, P<0.01), and E(es(SB)) [d sigma*/dt(max)=1.60 E(es(SB)) + 1.20, r=0.88, P<0.01]. In 30 additional individuals, we determined sensitivity of the parameter to changes in preload (intravenous saline infusion, n = 10 subjects), afterload (sublingual glyceryl trinitrate, n = 10 subjects), and increased contractility (intravenous dobutamine, n=10 patients). We confirmed that the index is not dependent on load but is sensitive to changes in contractility. In conclusion, d sigma*/dt(max) is equivalent to dP/dt(max), E(a,max), and E(es(SB)) as an index of myocardial contractility and appears to be load independent. In contrast to other measures of contractility, d sigma*/dt(max) can be assessed with noninvasive cardiac imaging and, thereby, should have more routine clinical applicability.

Left Ventricular Hypertrophy and Outflow Tract Obstruction in a Patient With Anorexia Nervosa

A 14-year-old girl was admitted to our hospital for hypoglycemia and cardiac tamponade. In the 14 months preceding this hospitalization, she became obsessed with food intake and exercise and developed amenorrhea, disturbed body image, and an intense fear of becoming fat. She subsequently lost 31 kg body weight (decreasing from 52 to 21 kg), meeting the diagnostic criteria for anorexia nervosa. Her rate of weight loss was almost constant for the first 11 months (1.6 kg/mo) but accelerated during the last 3 months before admission (4.7 kg/mo). Chest radiography after drainage of a pericardial effusion (Figure 1A) showed that the patient had an extremely small heart, with a cardiothoracic ratio of …

Effect of Endocardial Trabeculae on Left Ventricular Measurements and Measurement Reproducibility at Cardiovascular MR Imaging

To prospectively assess the effect of including or excluding endocardial trabeculae in left ventricular (LV) measurements and the reproducibility of these measurements at cine cardiovascular magnetic resonance (MR) imaging with true fast imaging with steady-state precession (FISP). The study was approved by the local ethics committee, and each subject gave informed consent before participating. Twenty healthy subjects and 20 consecutive patients underwent 1.5-T cardiovascular MR imaging. Seven to 12 short-axis views encompassing the entire LV were acquired by using true FISP. Endocardial and epicardial contours were traced manually. The data sets in each patient were analyzed twice: with inclusion of endocardial trabeculae in the LV cavity volume and with exclusion of endocardial trabeculae from the cavity volume. On the basis of these two contour sets, the end-diastolic (ED) and end-systolic (ES) LV volumes, ejection fraction (EF), and LV mass were calculated. Additionally, interobserver and interexamination reproducibility was assessed by using Bland-Altman analysis. Compared with exclusion of trabeculae, inclusion of trabeculae in the LV cavity volume resulted in significantly larger ED and ES LV volumes (mean differences, 21 mL +/- 11 [standard deviation] and 19 mL +/- 33, respectively; P < .001) and lower EFs (mean difference, -2% +/- 2; P < .001). The calculated LV mass was significantly smaller with inclusion than with exclusion of trabeculae (mean difference, -21 g +/- 12; P < .001). All interobserver and interexamination limits of agreement based on inclusion of trabeculae, except those for EF measurements, were superior to those based on exclusion of trabeculae. At measurement reproducibility comparisons, differences in interobserver ED LV volume and LV mass and interexamination LV mass were statistically significant, favoring the inclusion of trabeculae in the LV cavity volume. Trabeculae significantly affect quantifications of LV volume and mass. The superior reproducibility of LV measurements with the inclusion of endocardial trabeculae in the cavity volume favors this tracing algorithm for clinical use.

Aldosterone Receptor Blockade Prevents the Transition to Cardiac Pump Dysfunction Induced by β-Adrenoreceptor Activation

The transition from compensated to decompensated left ventricular hypertrophy (LVH) in hypertension involves excessive beta-adrenoreceptor (beta-AR) stimulation. To explore whether aldosterone receptor activation contributes toward beta-AR-induced left ventricular (LV) decompensation in hypertensive LVH, the effect of spironolactone (SPIRO; 80 mg x kg(-1) x day(-1)) on LV cavity dimensions, function, and chamber remodeling mechanisms was evaluated in spontaneously hypertensive rats (SHR) receiving a low dose of the beta-AR agonist isoproterenol (ISO) at 0.02 to 0.04 mg x kg(-1) . day for 4.5 months. ISO administered to SHR resulted in an increased 24-hour urinary aldosterone excretion and LV cavity dimensions, a right shift in LV diastolic pressure-volume relations, a decreased LV relative wall thickness, and increased total, noncross-linked, type I and type III myocardial collagen concentrations without further enhancing increased myocardial norepinephrine (NE) release. ISO reduced pump function without modifying intrinsic myocardial systolic function or inducing further myocyte necrosis or apoptosis. ISO only increased LV cavity volumes after prolonged periods of administration. SPIRO abolished ISO-induced chamber dilatation, wall thinning, and pump dysfunction and reduced total, noncross-linked, type I and type III myocardial collagen concentrations but failed to modify blood pressure, volume preloads, intrinsic myocardial systolic function, myocardial NE release, or the degree of necrosis or apoptosis. In conclusion, these results suggest that aldosterone receptor blockade, through load-independent effects, may be useful in preventing the transition from compensated LVH to dilatation and pump dysfunction mediated by chronic beta-AR activation.

Left bundle branch block induces ventricular remodelling and functional septal hypoperfusion

Left ventricular (LV) dilatation, hypertrophy, and septal perfusion defects are frequently observed in patients with left bundle branch block (LBBB). We investigated whether isolated LBBB causes these abnormalities. In eight dogs, LBBB was induced by radio frequency ablation. Two-dimensional echocardiography showed that 16 weeks of LBBB decreased LV ejection fraction (by 23+/-14%) and increased LV cavity volume (by 25+/-19%) and wall mass (by 17+/-16%). The LV septal-to-lateral wall mass ratio decreased by 6+/-9%, indicating asymmetric hypertrophy. After onset of LBBB, myocardial blood flow (MBF, fluorescent microspheres) and systolic circumferential shortening [CS(sys), magnetic resonance (MR) tagging] decreased in the septum to 83+/-16% and -11+/-20% of baseline, respectively, and increased in LV lateral wall to 118+/-12% and 180+/-90% of baseline, respectively. MBF and CS(sys) values did not change over 16 weeks of LBBB. Changes in external mechanical work paralleled those in CS(sys). Glycogen content was not significantly different between septum and LV lateral wall of LBBB hearts (16 weeks) and control samples, indicating absence of hibernation. The asynchronous ventricular activation during LBBB leads to redistribution of circumferential shortening and myocardial blood flow and, in the long run, LV remodelling. Septal hypoperfusion during LBBB appears to be primarily determined by reduced septal workload.

Efficacy of Erythropoietin on Dialysis in Patients with Beta Thalassemia Minor

Background: It is unknown whether chronic erythropoietin (EPO) treatment is able to normalize hemoglobin (Hb) levels and ameliorate cardiac remodeling avoiding blood transfusions in uremic blood transfusion-dependent patients with β-thalassemia minor (β-thal). Methods: In 12 hemodialysis (HD) patients with β-thal, requiring blood transfusions despite EPO therapy, we planned to increase Hb levels up to the target levels (11–12 g/dl) within a one-year period by administering progressively higher doses of EPO (correction phase). We also planned to maintain the Hb target for an additional year (maintenance phase). Results: In the year before the study, patients required 3.3 ± 0.9 units of packed red blood cells. At baseline, the Hb level obtained with an EPO dose of 212 ± 73 U/kg/week i.v. was 8.2 ± 0.8 g/dl. The EPO dose was gradually increased within the first year up to 458 ± 78 U/kg/week at month 12 (correction phase) and then significantly tapered down during the maintenance phase (390 ± 54 U/kg/week at month 24). During the correction phase, the Hb levels markedly increased (11.1 ± 0.3 g/dl at month 12) and did not change in the maintenance phase. No blood transfusion was required throughout the 2 years of follow-up. Left ventricular (LV) mass index progressively decreased from the basal value of 144 ± 12 to 124 ± 11 g/m² in the first year and normalized in all patients at month 24 (109 ± 12 g/m², p < 0.001); this occurred in the absence of any change of LV cavity volume index (<90 ml/m²). Conclusions: In HD transfusion-dependent patients with β-thal, the administration of high EPO dose for 2 years permits the attainment and the maintenance of Hb targets without blood transfusions. This therapeutic approach permits a complete remission of concentric LV hypertrophy without any adverse effects on the vascular system.

Restrictive left ventricular filling in hypereosinophilic syndrome as a result of partial cavity obliteration by an apical mass: a strain/strain rate study

We present a case of hypereosinophilic syndrome with a large apical mass, which markedly reduced end-systolic left ventricular cavity volume. Standard blood pool Doppler findings showed a restrictive filling pattern. However, ultrasound-derived regional strain rate and strain parameters suggested that wall deformation was not compromised, inferring that the restrictive filling pattern in this case was solely as a result of the reduction in end-systolic cavity size.

Prevention of Left Ventricular Remodeling After Myocardial Infarction.

Postinfarction left ventricular remodeling begins early after acute myocardial infarction and may continue for months to years afterward. Early re-establishment of flow in the occluded artery is associated with smaller left ventricular cavity volumes and reduced remodeling. Acute percutaneous coronary intervention (PCI) or thrombolytic therapy (for patients more than 1 hour away from a catheterization facility) as early as possible after symptoms is critical. Late reperfusion (PCI more than 12 hours after infarction) may prove useful, and this will be determined by the results of ongoing clinical trials. Recurrent MI is reduced by antiplatelet agents (aspirin in most patients) and by 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors. Intravenous nitroglycerin may limit early (initial 24 hours) dilatation following infarction, but long-term use in asymptomatic patients is not efficacious. Beta- adrenergic receptor antagonists and angiotensin-converting enzyme (ACE) inhibitors have independent efficacy in attenuating the early and late phases of remodeling. The combined use of a beta-blocker and an ACE inhibitor has greater efficacy than either agent alone, provided they are tolerated hemodynamically. Although angiotensin II receptor antagonists have similar efficacy to ACE inhibitors and have fewer side effects, the angiotensin II receptor blockers should be reserved for patients intolerant to ACE inhibitors. In patients requiring diuretic therapy, spironolactone is preferred because of its salutary properties regarding extracellular matrix remodeling, specifically in reducing fibrosis. Surgical revascularization with or without associated mitral valve repair is useful in selected patients with severe ischemic mitral regurgitation or hibernating myocardium. New therapies directed at modulating the remodeling process may focus on manipulating the components of the extracellular matrix to reduce the deleterious impact of this process.

Heart-related indices in experimental diaphragmatic hernia

Background: Heart-related indices have been suggested as useful tools to evaluate left ventricular (LV) hypoplasia, which might predict the outcome of fetuses and infants with congenital diaphragmatic hernia (CDH). The current study analyzed the behavior of such indices in the nitrofen-induced CDH rat model. Methods: Dated pregnant Wistar rats received at day 9.5 of gestation either a dose of 100 mg of nitrofen or just the vehicle. Body, lung, and heart weights were measured in 12 newborn rats not exposed to nitrofen (Ctrl group) and 68 animals exposed to nitrofen: 30 without CDH (non-CDH group) and 38 with left CDH (CDH group). Each heart was fragmented in 7-μm thick sections. Only hearts with no evidence of cardiac morphologic defects (CMD) were studied further to estimate right and left ventricular cavity volumes, septal, right, and left ventricular free wall masses. These parameters allowed the calculation of the cardio-ventricular (CVindex) and LV mass indices. The aorta-to-pulmonary artery ratio also was calculated. Results: Excluding fetuses with CMD, the heart-to-body weight ratio was reduced significantly in animals exposed to nitrofen, whereas no significant differences were observed between non-CDH versus CDH groups. Although the left and right ventricular cavity volumes were both reduced significantly in nitrofen-treated rats, they were not changed significantly by the existence of CDH, and the calculated CVindex was similar in the 3 groups. Estimated septal and LV masses were reduced markedly in the nitrofen-treated animals and further reduced by the presence of CDH. However, when LV mass was normalized (LV mass index) the difference became restricted to the animals exposed to nitrofen but was not influenced by the presence of CDH. Finally, the aorta-to-pulmonary artery ratio was similar in all studied groups. Conclusions: The results of the current study suggest that, although nitrofen had been responsible by global heart hypoplasia, the presence of CDH was not associated with significant underdevelopment of the heart or of the LV in rat fetuses without CMD. Based on these results, we think that the evidence for prenatal counseling based on heart-related indices should be critically reconsidered. J Pediatr Surg 35:1449-1452. Copyright © 2000 by W.B. Saunders Company.

Global left ventricular shape is not altered as a consequence of physiologic remodeling in highly trained athletes

It is uncertain whether left ventricular (LV) shape is altered as a consequence of intensive athletic conditioning. We assessed LV dimensions and shape by Fourier analysis from digitized LV endocardial borders in 22 elite rowers and 14 untrained controls. Athletes had greatly increased LV cavity dimension, wall thickness, volume, and mass; however, LV shape was normal in athletes, and associated with normal ejection fraction and diastolic filling pattern.

Effect of hemoglobin levels in hemodialysis patients with asymptomatic cardiomyopathy

Hemoglobin levels below 10 g/dL lead to left ventricular (LV) hypertrophy, LV dilation, a lower quality of life, higher cardiac morbidity, and a higher mortality rate in end-stage renal disease. The benefits and risks of normalizing hemoglobin levels in hemodialysis patients without symptomatic cardiac disease are unknown. One hundred forty-six hemodialysis patients with either concentric LV hypertrophy or LV dilation were randomly assigned to receive doses of epoetin alpha designed to achieve hemoglobin levels of 10 or 13.5 g/dL. The study duration was 48 weeks. The primary outcomes were the change in LV mass index in those with concentric LV hypertrophy and the change in cavity volume index in those with LV dilation. In patients with concentric LV hypertrophy, the changes in LV mass index were similar in the normal and low target hemoglobin groups. The changes in cavity volume index were similar in both targets in the LV dilation group. Treatment-received analysis of the concentric LV hypertrophy group showed no correlation between the change in mass index and a correlation between the change in LV volume index and mean hemoglobin level achieved (8 mL/m2 per 1 g/dL hemoglobin decrement, P = 0.009). Mean hemoglobin levels and the changes in LV mass and cavity volume index were not correlated in patients with LV dilation. Normalization of hemoglobin led to improvements in fatigue (P = 0.009), depression (P = 0.02), and relationships (P = 0.004). Normalization of hemoglobin does not lead to regression of established concentric LV hypertrophy or LV dilation. It may, however, prevent the development of LV dilation, and it leads to improved quality of life.

Long-term changes in left ventricular hypertrophy after renal transplantation.

Concentric and eccentric left ventricular hypertrophy are common progressive disorders in dialysis patients and are associated with cardiac failure and death. Although partial regression of these abnormalities is known to occur during the first post-transplant year, their long-term evolution is unknown. A total of 143 of 433 dialysis patients participating in a long-term prospective cohort study received renal transplants. Laboratory parameters were assessed monthly. Echocardiography was performed annually. Left ventricular mass index (LVMI) and cavity volume index were calculated according to standard formulae. Multiple linear regression was used to model change in LVMI as a function of baseline clinical and laboratory variables. LVMI fell from 161 g/m2 at 1 year to 146 g/m2 (P=0.009) g/m2 after 2 years. No further regression was seen in years 3 and 4. Left ventricular volume index showed similar trends, with a decline from year 1 to year 2 (P=0.05) followed by stabilization in years 3 and 4. Older age, long duration of hypertension, need for more than one antihypertensive, high pulse pressure in normal-size hearts, and low pulse pressure in dilated hearts were significantly associated with failure of regression of LVMI between the first and second years (MLR, P<0.000001, r2=0.57). Regression of left ventricular hypertrophy continues beyond the first year after renal transplantation, reaching a nadir at 2 years and persisting into the third and fourth posttransplant years. Failure to regress was associated with older age, hypertension, high pulse pressure in normal-size hearts and low pulse pressure in dilated hearts.

Mapping of regional myocardial strain and work during ventricular pacing: experimental study using magnetic resonance imaging tagging

OBJECTIVESThe purpose of this study was to determine the spatial distribution of myocardial function (myofiber shortening and work) within the left ventricular (LV) wall during ventricular pacing.BACKGROUNDAsynchronous electrical activation, as induced by ventricular pacing, causes various abnormalities in LV function, perfusion and structure. These derangements may be caused by abnormalities in regional contraction patterns. However, insight into these patterns during pacing is as yet limited.METHODSIn seven anesthetized dogs, high spatial and temporal resolution magnetic resonance–tagged images were acquired in three orthogonal planes. Three-dimensional deformation data and LV cavity pressure and volume were used to determine midwall circumferential strain and external and total mechanical work at 192 sites around the left ventricle.RESULTSDuring ventricular pacing, systolic fiber strain and external work were approximately zero in regions near the pacing site, and gradually increased to more than twice the normal value in the most remote regions. Total mechanical work, normalized to the value during right atrial pacing, was 38 ± 13% (right ventricular apex [RVapex] pacing) and 61 ± 23% (left ventricular base [LVbase] pacing) close to the pacing site, and 125 ± 48% and 171 ± 60% in remote regions, respectively (p < 0.05 between RVapex and LVbase pacing). The number of regions with reduced work was significantly larger during RVapex than during LVbase pacing. This was associated with a reduction of global LV pump function during RVapex pacing.CONCLUSIONSVentricular pacing causes a threefold difference in myofiber work within the LV wall. This difference appears large enough to regard local myocardial function as an important determinant for abnormalities in perfusion, metabolism, structure and pump function during asynchronous electrical activation. Pacing at sites that cause more synchronous activation may limit the occurrence of such derangements.

Chairman's workshop report. Normalization of haemoglobin: why not?

It has been suggested that normalization of haemoglobin with epoetin in anaemic chronic renal failure (CRF) patients might result in even greater benefits than those currently achieved with partial haemoglobin correction. Four prospective randomized trials recently examined this hypothesis. The Scandinavian Multicentre Trial, which was completed in February 1998, included 416 haemodialysis, continuous ambulatory peritoneal dialysis and pre-dialysis patients. Preliminary analysis of the data found no differences with respect to safety between patients treated to achieve subnormal haemoglobin (9.0-12.0 g/dl) and those in whom haemoglobin was normalized (13.5-16.0 g/dl). The Canadian Multicentre Trial included 159 haemodialysis patients with asymptomatic left ventricular (LV) dysfunction. In patients with a normal LV cavity volume at enrolment, the change in LV cavity volume at 48 weeks was significantly greater in the control group (target haemoglobin 9.5-10.5 g/dl) than in the intervention group (target haemoglobin 13.0-14.0 g/dl). The Normal Hematocrit Cardiac Trial in the US included 1233 haemodialysis patients with clinically evident ischaemic heart disease or congestive heart failure. The trial was stopped in 1996 after an interim analysis showed increased mortality in the intervention group (target haematocrit 42%) compared with the control group (target haematocrit 30%). The higher haematocrit values themselves, however, did not appear to be responsible for the differences in mortality, as the mortality rates within each group decreased with increasing haematocrit. Nonetheless, until evidence is available from other trials demonstrating a benefit of normalizing haemoglobin, it has been recommended that a target haematocrit value of 42% be avoided in haemodialysis patients with clinically evident ischaemic heart disease or congestive heart failure. Further studies are also required to determine whether increasing haemoglobin to normal may prove to be beneficial in other patient groups. The Spanish Quality of Life Study of 134 haemodialysis patients found a significant improvement in all quality-of-life parameters when haemoglobin was increased to a mean of 12.5 g/dl. The investigators suggested that in patients without severe co-morbidity, the target haemoglobin should be as close to normal as possible.

Cardiovascular Problems in Peritoneal Dialysis Patients: A Short Overview

cardiogram on starting dialysis. Forty-one percent had concentric left ventricular (LV) hypertrophy, 28% had LV dilatation, and 16% had systolic dysfunction. These results imply that the causes ofLV dysfunction occur in the predialysis phase of chronic renal failure. Two hundred and seventy-five patients had a f ollow-up echo cardiogram 17 months after starting dialysis therapy (12). Now the proportion of those who had a normal echocardiogram was 13%, the proportion with concentric LV hypertrophy was 40%, the proportion with LV dilatation was 26%, and the proportion with systolic dysfunction was 20% (12). In peritoneal dialysis patients, one might expect that blood flow would not increase as much as in hemodialysis patients, because no vascular access is required, and fluctuations in salt and water status are less variable. In 70 patients treated exclusively with peritoneal dialysis, LV cavity volume decreased by 5 mL/m2 during 1 year's follow-up (9). When compared to readings from hemodialysis patients, the differences in the changes in LV volume approached statistical significance (p = 0.06). In 55 normotensive CAPD patients who were on treatment for a mean of 28.8 ± 24.9 months, a high prevalence of left atrial dilatation and left ventricular hypertrophy was found (13). The latter was mainly the result of s eptal thickening. The degree ofventricular hypertrophy in these patients was related to the amount ofhypercirculation and to the quality of blood purification. Abnormal diastolic left ventricular filling in CAPD patients has been found in patients both with and without left ventricular hypertrophy (14,15). In these patients, a disturbed ratio exists between the ventricular rapid filling in protodiastole and the filling owing to atrial contraction, with a greater-thannormal atrial contribution. After init iation ofCAPD therapy, regression as well as progression in left ventricular hypertrophy has been described. Prospective studies did not show a deterioration in left ventricular function up to 2 years after the start of CAPD (16). Others did not observe changes in left ventricular mass, ejection fraction, or left ventricular telediastolic dimension, despite a fall in blood pressure

Laser-mediated reversal of cardiac expansion after myocardial infarction.

A complication of transmural myocardial infarction is infarct expansion, which can lead to the development of heart failure. However, the necrotic muscle is replaced by collagen, a material known to shrink when heated. Thus, the hypothesis was that thermally-induced scar shrinkage could reverse infarct expansion. Four weeks after transmural infarcts were produced by coronary occlusion, rats were randomized to control or treatment with a neodymium:yttrium-aluminum-garnet laser. The epicardial scar surface was irradiated until shrinkage was observed. Thirty minutes later, hearts were excised and fixed at a distending pressure of 15 mm Hg, left ventricular cavity volume was measured, and histologic analysis was performed. Cavity volume was reduced by laser treatment (0.72 +/- 0.07 ml vs. 0.54 +/- 0.05 ml; P= 0.044). In addition, treatment resulted in thicker scars, a leftward shift of the heart's electrical axis, and straightening of collagen fibers. Laser treatment resulted in thermally-mediated scar shrinkage, which reversed infarct expansion and reduced cavity volume.

Load-Independent Indices of Left Ventricular Function Using Automated Border Detection.

Echocardiographic automated border detection is the ability to assess left ventricular (LV) cross-sectional cavity areas and volumes on line. This capability has enabled the use of LV pressure-volume relationships as a means to determine LV function in a manner relatively independent of loading conditions. This discussion reviews previous validation studies in animal models and humans using LV cross-sectional area as a surrogate for LV volume and the clinical applications of LV pressure-area relations. Applications of arterial pressure as a substitute for LV ejection pressure to assess pressure-area relations are also reviewed, along with the use of pressure-area relations to assess right ventricular performance. Last, preload-adjusted maximal power as an alternative load-insensitive means to determine LV performance is discussed.