Showing papers on "Ventricle published in 1999"

Effect of Pacing Chamber and Atrioventricular Delay on Acute Systolic Function of Paced Patients With Congestive Heart Failure

Abstract: Background—Previous studies of pacing therapy for dilated congestive heart failure (CHF) have not established the relative importance of pacing site, AV delay, and patient heterogeneity on outcome. These variables were compared by a novel technique that evaluated immediate changes in hemodynamic function during brief periods of atrial-synchronous ventricular pacing. Methods and Results—Twenty-seven CHF patients with severe left ventricular (LV) systolic dysfunction and LV conduction disorder were implanted with endocardial pacing leads in the right atrium and right ventricle (RV) and an epicardial lead on the LV and instrumented with micromanometer catheters in the LV, aorta, and RV. Patients in normal sinus rhythm were stimulated in the RV, LV, or both ventricles simultaneously (BV) at preselected AV delays in a repeating 5-paced/15-nonpaced beat sequence. Maximum LV pressure derivative (LV+dP/dt) and aortic pulse pressure (PP) changed immediately at pacing onset, increasing at a patient-specific optimal...

Left atrial appendage: structure, function, and role in thromboembolism

Abstract: The left atrial appendage (LAA) is derived from the left wall of the primary atrium, which forms during the fourth week of embryonic development. It has developmental, ultrastructural, and physiological characteristics distinct from the left atrium proper. The LAA lies within the confines of the pericardium in close relation to the free wall of the left ventricle and thus its emptying and filling may be significantly affected by left ventricular function. The physiological properties and anatomical relations of the LAA render it ideally suited to function as a decompression chamber during left ventricular systole and during other periods when left atrial pressure is high. These properties include the position of the LAA high in the body of the left atrium; the increased distensibility of the LAA compared with the left atrium proper; the high concentration of atrial natriuretic factor (ANF) granules contained within the LAA; and the neuronal configuration of the LAA. Thrombus has a predilection to form in the LAA in patients with atrial fibrillation, mitral valve disease, and other conditions. The pathogenesis has not been fully elucidated; however, relative stasis which occurs in the appendage owing to its shape and the trabeculations within it is thought to play a major role. Obliteration or amputation of the LAA may help to reduce the risk of thromboembolism, but this may result in undesirable physiological sequelae such as reduced atrial compliance and a reduced capacity for ANF secretion in response to pressure and volume overload.

Alterations in the Local Myocardial Motion Pattern in Patients Suffering From Pressure Overload Due to Aortic Stenosis

Abstract: Background—MR tissue tagging allows the noninvasive assessment of the locally and temporally resolved motion pattern of the left ventricle. Alterations in cardiac torsion and diastolic relaxation of the left ventricle were studied in patients with aortic stenosis and were compared with those of healthy control subjects and championship rowers with physiological volume-overload hypertrophy. Methods and Results—Twelve aortic stenosis patients, 11 healthy control subjects with normal left ventricular function, and 11 world-championship rowers were investigated for systolic and diastolic heart wall motion on a basal and an apical level of the myocardium. Systolic torsion and untwisting during diastole were examined by use of a novel tagging technique (CSPAMM) that provides access to systolic and diastolic motion data. In the healthy heart, the left ventricle performs a systolic wringing motion, with a counterclockwise rotation at the apex and a clockwise rotation at the base. Apical untwisting precedes diasto...

Matrix Metalloproteinase Inhibition During the Development of Congestive Heart Failure Effects on Left Ventricular Dimensions and Function

Abstract: —The development of congestive heart failure (CHF) is associated with left ventricle (LV) dilation and myocardial remodeling. The matrix metalloproteinases (MMPs) play a significant role in...

Ventricular Septal Defect.

Abstract: Ventricular septal defects (VSDs) are the most common congenital heart malformations seen in children. Because spontaneous closure occurs frequently, patients with small VSDs should be followed clinically with no limitations except endocarditis prophylaxis. Surgical closure is recommended for only small defects with significant associated lesions such as aortic regurgitation, aortic valve prolapse, right or left ventricular outflow obstruction, tricuspid regurgitation, left ventricle to right atrial shunt, or recurrent endocarditis. Enlarging left ventricular size or deteriorating left ventricular function would also be an indication for surgical repair. Moderate and large VSDs in infancy often require treatment of congestive heart failure with diuretics, digitalis, and afterload reduction. Surgical closure before 9 months of age is indicated for large VSDs and by 2 years of age for moderate shunts to prevent pulmonary vascular obstructive disease and the consequences of long-standing volume overload. Device closure of VSD is still in the investigational stage but holds promise for treatment of apical or multiple muscular VSDs.

Remodeling of chick embryonic ventricular myoarchitecture under experimentally changed loading conditions

Abstract: Adult myocardium adapts to changing functional demands by hyper- or hypotrophy while the developing heart reacts by hyper- or hypoplasia How embryonic myocardial architecture adjusts to experimentally altered loading is not known We subjected the chick embryonic hearts to mechanically altered loading to study its influence upon ventricular myoarchitecture Chick embryonic hearts were subjected to conotruncal banding (increased afterload model), or left atrial ligation or clipping, creating a combined model of increased preload in right ventricle and decreased preload in left ventricle Modifications of myocardial architecture were studied by scanning electron microscopy and histology with morphometry In the conotruncal banded group, there was a mild to moderate ventricular dilatation, thickening of the compact myocardium and trabeculae, and spiraling of trabecular course in the left ventricle Right atrioventricular valve morphology was altered from normal muscular flap towards a bicuspid structure Left atrial ligation or clipping resulted in hypoplasia of the left heart structures with compensatory overdevelopment on the right side Hypoplastic left ventricle had decreased myocardial volume and showed accelerated trabecular compaction Increased volume load in the right ventricle was compensated primarily by chamber dilatation with altered trabecular pattern, and by trabecular proliferation and thickening of the compact myocardium at the later stages A ventricular septal defect was noted in all conotruncal banded, and 25% of left atrial ligated hearts Increasing pressure load is a main stimulus for embryonic myocardial growth, while increased volume load is compensated primarily by dilatation Adequate loading is important for normal cardiac morphogenesis and the development of typical myocardial patterns Anat Rec 254:238–252, 1999 © 1999 Wiley-Liss, Inc

Long axis function in disease

Abstract: Although longitudinally directed fibres—situated mainly in the subepicardium and subendocardium regions of the left and right ventricular free walls and the papillary muscles—comprise only a small proportion of the total ventricular myocardial mass, they play a major role in the maintenance of normal ejection fraction and in determining atrioventricular interactions.1 Not surprisingly, therefore, loss of longitudinal fibre function leads to characteristic disturbances. Longitudinal function is always reduced when ventricular cavity size is increased, in addition ejection fraction is reduced and may be absent.2 3 This relation is consistent enough for long axis amplitude, or its equivalent, the amplitude of atrioventricular ring motion, to be used as an index of ejection fraction.4It applies not only to the left ventricle, where it can be shown to relate to prognosis but also to the right, where it provides a simple method of assessing right ventricular function.5 When overall long axis amplitude is low, peak shortening and lengthening rates are reduced. In restrictive left ventricular disease, long axis amplitude is low even when cavity size is normal at end diastole, although the effects of this reduction are apparent in a reduced amplitude of wall thickening and thus of shortening fraction.6 After mitral valve replacement, long axis amplitude is strikingly reduced; this does not occur with mitral valve repair or mild mitral stenosis,7 nor is it a consistent effect of cardiopulmonary bypass done for other reasons, and so is likely to be the result of loss of papillary muscle function. Although shortening fraction is frequently normal in such patients, normal wall thickening is associated with an exaggerated amplitude of epicardial motion, possibly to compensate for loss of the component owing to long axis shortening. Regional reduction in the extent and velocity of long axis shortening is common after …

Effect of Pacing Chamber and Atrioventricular Delay on Acute Systolic Function of Paced Patients With Congestive Heart Failure

Abstract: Background—Previous studies of pacing therapy for dilated congestive heart failure (CHF) have not established the relative importance of pacing site, AV delay, and patient heterogeneity on outcome. These variables were compared by a novel technique that evaluated immediate changes in hemodynamic function during brief periods of atrial-synchronous ventricular pacing. Methods and Results—Twenty-seven CHF patients with severe left ventricular (LV) systolic dysfunction and LV conduction disorder were implanted with endocardial pacing leads in the right atrium and right ventricle (RV) and an epicardial lead on the LV and instrumented with micromanometer catheters in the LV, aorta, and RV. Patients in normal sinus rhythm were stimulated in the RV, LV, or both ventricles simultaneously (BV) at preselected AV delays in a repeating 5-paced/15-nonpaced beat sequence. Maximum LV pressure derivative (LV+dP/dt) and aortic pulse pressure (PP) changed immediately at pacing onset, increasing at a patient-specific optimal...

Noncompaction of the ventricular myocardium.

Abstract: Noncompaction of the ventricular myocardium is a rare congenital cardiomyopathy resulting from an arrest in normal endomyocardial embryogenesis. The characteristic echocardiographic findings consist of multiple, prominent myocardial trabeculations and deep intertrabecular recesses communicating with the left ventricular cavity. The disease uniformly affects the left ventricle, with or without concomitant right ventricular involvement, and results in systolic and diastolic ventricular dysfunction and clinical heart failure. Noncompaction was initially described in children. However, recent studies have characterized this disease in the adult population, in whom this process may be more prevalent than currently appreciated. We describe an illustrative case of isolated noncompaction of the ventricular myocardium in a 57-year-old woman with the typical clinical and echocardiographic features of the disease. The literature on the topic is reviewed.

Left ventricular pseudoaneurysm

Abstract: Received: February 22, 1999 Accepted with revision: April 13, 1999 diac ischemia. Two-dimensional echocardiography in the two-chamber view showed a pseudoaneurysm originating from the junctional area between the middle portion of the ventricular septum and the inferior left ventricular wall. Emergency coronary angiography showed multivessel disease with a total occlusion of the right coronary artery. Left ventricular angiography confirmed a well-demarcated pseudoaneurysm with an inferiorly located narrow neck (arrow) (Fig. 1, diastole). Figure 2 shows the left ventricle in systole with inferior akinesia and the pseudoaneurysm. Because of the high risk of rupture, immediate surgical repair was performed. which was successful.

Chronic myocardial infarction in the mouse: cardiac structural and functional changes.

Abstract: Objectives: We studied the effects of chronic left coronary artery ligation on cardiac structure and function in the mouse. Methods: Morphometric studies of the left ventricle were performed in coronary artery-ligated and sham-operated animals at one, two, three and five weeks after surgery. The fraction of DNA-synthesizing cells was determined as the fraction of cells incorporating 5′-bromo-2′-deoxyuridine, which was infused by osmotic minipumps one week before sacrifice. Collagen content of the septum was determined morphometrically. Left ventricular pressure and its derivatives were measured in separate groups of animals at one and three weeks after surgery. Results : Ligation of the main left coronary artery resulted in antero-apical infarction of the left ventricular wall, involving ∼40% of left ventricular circumference. Infarction resulted in thinning of the infarcted area and left ventricular dilatation. DNA synthesis increased, peaking between one and two weeks in the border-zone of the infarct (22-fold), septum (ten-fold) and right ventricle (five-fold). At five weeks, DNA synthesis was still increased in the border zone of the infarct. Septal collagen content increased ~eight-fold in infarcted mice at two weeks, and decreased thereafter; it was still significantly elevated at five weeks. Left ventricular systolic pressure, and maximal positive and negative d P /d t decreased following infarction; left ventricular end-diastolic pressure was elevated at three weeks, but this effect was not statistically significant. Conclusion: These data provide basic information on changes in cardiac structure and function in mice following chronic coronary artery ligation. They indicate the feasibility of induction of chronic myocardial infarction in this species. Furthermore, they show the similarity of cardiac structural and functional consequences of chronic myocardial infarction in mice to those previously described in rats.

Pressure Overload Induces Severe Hypertrophy in Mice Treated With Cyclosporine, an Inhibitor of Calcineurin

Abstract: Cardiac hypertrophy is the fundamental adaptation of the adult heart to mechanical load. Recent work has shown that inhibition of calcineurin activity with cyclosporine suppresses the development of hypertrophy in calcineurin transgenic mice and in in vitro systems of neonatal rat cardiocytes stimulated with peptide growth factors. To test the hypothesis that the calcineurin signaling pathway is critical for load-induced hypertrophy in vivo, we examined the effects of cyclosporine treatment on left ventricular hypertrophy induced by experimental ascending aortic stenosis for 4 weeks in mice. Left ventricular systolic pressure was elevated to a similar level in aortic stenosis mice that were treated with cyclosporine versus no drug. Left ventricular mass and myocyte size were similar in treated and untreated aortic stenosis animals and significantly greater than control animals, showing that cyclosporine treatment does not suppress hypertrophic growth. Both treated and untreated animals showed increased left ventricular expression of the load-sensitive gene atrial natriuretic factor. Calcineurin activity was measured in the left ventricle and the spleen from control mice and aortic stenosis mice treated with cyclosporine versus no drug. Levels of calcineurin activity were similar in the spleens of control and untreated aortic stenosis mice. However, calcineurin activity was severely depressed in left ventricular tissue of untreated aortic stenosis mice compared with control mice and was further reduced by cyclosporine treatment. Thus, pathological hypertrophy and cardiac-restricted gene expression induced by pressure overload in vivo are not suppressed by treatment with cyclosporine and do not appear to depend on the elevation of left ventricular calcineurin activity.

Role of Papillary Muscle in the Generation and Maintenance of Reentry During Ventricular Tachycardia and Fibrillation in Isolated Swine Right Ventricle

Abstract: Background—The role of papillary muscle (PM) in the generation and maintenance of reentry is unclear. Methods and Results—Computerized mapping (477 bipolar electrodes, 1.6-mm resolution) was performed in fibrillating right ventricles (RVs) of swine in vitro. During ventricular fibrillation (VF), reentrant wave fronts often transiently anchored to the PM. Tissue mass reduction was then performed in 10 RVs until VF converted to ventricular tachycardia (VT). In an additional 6 RVs, procainamide infusion converted VF to VT. Maps showed that 77% (34 of 44) of all VT episodes were associated with a single reentrant wave front anchored to the PM. Purkinje fiber potentials preceded the local myocardial activation, and these potentials were recorded mostly around the PM. When PM was trimmed to the level of endocardium (n=4), sustained VT was no longer inducible. Transmembrane potential recordings (n=5) at the PM revealed full action potential during pacing, without evidence of ischemia. Computer simulation studies...

A retinoic acid-inducible transgenic marker of sino-atrial development in the mouse heart.

Abstract: To study the specification of inflow structures in the heart we generated transgenic animals harboring the human alkaline phosphatase (HAP) gene driven by the proximal 840 bp of a quail SMyHC3 promoter. In transgenic mice, the SMyHC3-HAP reporter was expressed in posterior heart precursors at 8.25 dpc, in sinus venosa and in the atrium at 8.5 and 9.0 dpc, and in the atria from 10.5 dpc onwards. SMyHC3-HAP transgene expression overlapped synthesis and endogenous response to retinoic acid (RA) in the heart, as determined by antibodies directed against a key RA synthetic enzyme and by staining of RAREhsplacZ transgenic animals. A single pulse of all-trans RA administered to pregnant mice at 7.5, but not after 8.5, dpc induced cardiac dismorphology, ranging from complete absence of outflow tract and ventricles to hearts with reduced ventricles expressing both SMyHC3-HAP and ventricular markers. Blockade of RA synthesis with disulfiram inhibited RA-induced transcription and produced hearts lacking the atrial chamber. This study defines a novel marker for atrial-restricted transcription in the developing mouse heart. It also suggests that atrial-specific gene expression is controlled by localized synthesis of RA, and that exclusion of RA from ventricular precursors is essential for correct specification of the ventricles.

Endothelin System–Dependent Cardiac Remodeling in Renovascular Hypertension

Abstract: The aim of the present study was to analyze whether the cardiac endothelin system contributes to cardiac remodeling in rats with 2-kidney, 1 clip (2K1C) renovascular hypertension. The endothelin system seems to be a promising candidate for cardiac remodeling because endothelin (ET)-1 promotes growth of cardiomyocytes in vitro and induces cardiac collagen synthesis. The activity of the cardiac endothelin system was analyzed by measuring cardiac tissue big ET-1 and ET-1 concentrations as well as by estimating the cardiac expression of the ETA and ETB receptors 10 days, 4 weeks, and 12 weeks after the renal artery was clipped. The effects of long-term treatment with ETA, ETB, and combined ETA/ETB receptor antagonists on cardiac hypertrophy, media/lumen ratio of intracardiac arteries, and left ventricular fibrosis were also analyzed. This study demonstrated that the overall left ventricular cardiac endothelin system has a similar activity in the early, middle, and late stages of 2K1C renovascular hypertension compared with sham-operated controls. Fibrosis of the left ventricle and hypertrophy of intracardiac arteries, however, were markedly altered after long-term treatment with endothelin receptor antagonists in a blood pressure-independent manner. These 2 effects are mediated by different subtypes of endothelin receptors. ETA receptor blockade completely normalized the hypertrophy of intracardiac arteries (P<0. 01 compared with 2K1C without treatment) in renovascular hypertension, whereas the ETB antagonist reduced cardiac fibrosis of the left ventricle (P<0.001 compared with 2K1C without treatment) to baseline values. This study demonstrates that the cardiac endothelin system plays an important role in the development of cardiac fibrosis as well as in hypertrophy of intracardiac arteries in 2K1C renovascular hypertensive rats.

Gene delivery to the myocardium by intrapericardial injection.

Abstract: Several studies have demonstrated the feasibility of gene transfer into the heart muscle. However, all the available data also indicate that the extent of transfection remains limited. As an alternative method to intravascular administration, we have developed a novel strategy which uses the pericardial sac. When a replication-deficient adenovirus containing the cDNA encoding a bacterial beta-galactosidase is injected into the pericardial sac of adult Wistar rats the staining is exclusively restricted to the pericardial cell layers. However, injecting a mixture of collagenase and hyaluronidase together with the virus, leads to a large diffusion of the transgene activity, reaching up to 40% of the myocardium. Transgene expression is predominant in the left ventricle and the interventricular septum but limited in the right ventricle. In vivo echocardiographic measurements of the left ventricular diameters at end diastolic and end systolic times show no difference between virus- and sham-injected animals, thus indicating a good clinical tolerance to this strategy of virus delivery. The same protocol has been used with the same efficiency in mice, which leads us to propose injection into the pericardial sac as an effective and harmless method for gene transfer into the heart muscle.

Pulmonary and circulatory blood flow support devices and methods for heart surgery procedures

Abstract: Pump and cannula systems inserted through the right side and/or left side of the heart provide protection against collapse of the heart chambers and veins and arteries and provide supplemental blood flow through same to enable beating heart bypass surgery on all vessels of the heart, including lateral and posterior vessels. The invention eliminates the use of cardiopulmonary bypass (CPB) machines. The invention further provides stents adapted for protecting from vein, artery, atrium and/or ventricle collapse during beating heart bypass surgery.

Regional contributions of Kv1.4, Kv4.2, and Kv4.3 to transient outward K+ current in rat ventricle.

Abstract: The aim of the present study was to assess differences in transient outward potassium current (I to) between the right ventricular free wall and the interventricular septum of the adult rat ventric...

Change in Ventricular Size and Effect of Ventricular Catheter Placement in Pediatric Patients with Shunted Hydrocephalus

Abstract: Objective The multicenter, randomized pediatric cerebrospinal fluid shunt valve design trial found no difference in the rate of shunt failure between a standard valve, a siphon-reducing valve (Delta; Medtronic PS Medical, Goleta, CA), and a flow-limiting valve (Orbis Sigma; Cordis, Miami, FL); however, the valves were expected to have different effects on ultimate ventricular size. Also, the catheter position or local environment of the ventricular catheter tip might have affected shunt failure. Therefore, we performed a post hoc analysis to understand what factors, other than valve design, affected shunt failure and to identify strategies that might be developed to reduce shunt failure. Methods Ventricular size was measured at as many as six different intervals, using a modified Evans' ratio (with incorporation of the frontal and occipital dimensions), in 344 patients. Ventricular catheter location was defined as being in the frontal horn, occipital horn, body of the lateral ventricle, third ventricle, embedded in brain, or unknown. The ventricular catheter tip was described as surrounded by cerebrospinal fluid, touching brain, or surrounded by brain parenchyma within the ventricle (slit ventricle). Repeated measures analysis of variance for unbalanced data was used to analyze ventricular size. A Cox model (with incorporation of time-dependent covariates) was used to evaluate the contribution of age, etiology, shunt design, ventricular size, ventricular catheter location, and environment among the cases. Results Ventricular volume decreased in an exponential fashion, forming a plateau at 14 months, and was similar for the three valves (P = 0.4). Frontal and occipital ventricular catheter tip locations were associated with a reduced risk of shunt failure (hazard ratios, 0.60 [P = 0.02] and 0.45 [P = 0.001], respectively). Ventricular catheter tips surrounded by cerebrospinal fluid or touching the brain were associated with a reduced risk of failure (hazard ratios, 0.21 and 0.33, respectively; P = 0.0001). Patients with myelomeningocele or large ventricles had increased risk of malfunction (hazard ratios, 1.78 [P = 0.006] and 2.33 [P = 0.03], respectively). Conclusion Decline of ventricular size over time is not affected by these different shunt valve designs. This suggests that the mechanical models of hydrocephalus on which the designs were based are inadequate. Ventricular catheter tip location and ventricular catheter environment are important. Techniques to accurately place ventricular catheters and new valve designs that effectively control ventricular size might reduce shunt malfunction.

Echocardiographic Features of Primary Pulmonary Hypertension

Abstract: Primary pulmonary hypertension (PPH) is essentially a diagnosis of exclusion and usually is made late because of the nonspecific nature of the early signs and symptoms. Echocardiography is a key screening test in the diagnostic algorithm of patients with suspected PPH. The purpose of this study was to define the echocardiographic Doppler features in patients with PPH at the time of diagnosis. From 1992 to 1997, 51 patients were diagnosed with PPH at our institution. All underwent a standardized transthoracic echocardiographic examination, including a contrast study and transthoracic echocardiographic examination if indicated. Pulmonary artery systolic pressure was calculated from the tricuspid regurgitation jet. The majority of patients had pulmonary artery systolic pressure greater than 60 mm Hg (96%) associated with systolic flattening of the interventricular septum (90%), enlarged right atrium (92%) and ventricle (98%), and reduced right ventricular systolic function (76%). There was an increase in the interventricular septal thickness (>1.2 cm) in 21 (43%) of 49 patients, accompanied by a septal/posterior wall ratio greater than 1.3 in 11 (22%) of 49. Although a reduction in both left ventricular systolic and diastolic volumes was noted, global left ventricular systolic function was preserved in all patients. Mitral E/A ratio was less than 0.7 in 7 (22%) patients studied. Color Doppler revealed moderate to severe tricuspid regurgitation and pulmonic insufficiency in 41 (80%) of 51 and 16 (31%) of 51 of cases, respectively. Pericardial effusion (7 small and 1 moderate) and patent foramen ovale (n = 12) were also frequently detected. At the time of initial diagnosis, PPH is associated with secondary cardiac abnormalities in the majority of patients. (J Am Soc Echocardiogr 1999;12:655-62.)

Strain Rate Imaging by Ultrasound in the Diagnosis of Regional Dysfunction of the Left Ventricle.

Abstract: Strain Rate Imaging by Ultrasound in the Diagnosis of Regional Dysfunction of the Left Ventricle

Implantable stimulation system for providing dual bipolar sensing using an electrode positioned in proximity to the tricuspid valve and programmable polarity

Abstract: A single-pass pacing and/or shocking lead system is capable of sensing cardiac signal in the atrium and the ventricle in a “bipolar fashion” using a three-electrode structure: a first electrode in the atruim, a second electrode in the ventricle just below the tricuspid valve, and a third in the ventricle.

Major organ function under mechanical support: comparative studies of pulsatile and nonpulsatile circulation.

Abstract: We examined a major organ function during 3 h biventricular assisted circulation after acute myocardial infarction model in the pig. In left ventricular circulation, the outflow cannula was placed in the ascending aorta and an inflow cannula through the mitral valve in the left ventricle. A pump (pulsatile group, Zeon Medical, Inc., Tokyo, Japan and nonpulsatile group, Nikkiso HPM-15, Nikkiso, Inc., Tokyo, Japan) was connected to each cannula. In right ventricular circulation, the outflow cannula was placed in the pulmonary artery and an inflow cannula in the right ventricle. The right ventricular circulation was supported by a nonpulsatile pump (Nikkiso HPM-15). The items measured were the regional blood flows of the cortex and medulla in the kidney, white matter and gray mater in brain, and liver; renal arterial flow; carotid arterial flow; portal vein flow; common hepatic arterial flow; arterial ketone body ratio (AKBR); and lactate/pyrubic acid (L/P). In the pulsatile group, the renal cortical blood flow increased, and the medulla blood flow decreased. On the other hand, in the nonpulsatile group, both regional blood flows decreased. That means that in the pulsatile assisted group intrarenal redistribution improved rather than in the nonpulsatile assisted group. In addition the liver regional blood flow, AKBR, and L/P showed significant differences between the pulsatile and nonpulsatile groups. On the other hand, the white matter and gray matter regional blood flows and carotid arterial flow did not show significant differences between the groups. The results of our study indicated that pulsatile circulation produced superior circulation in the kidney and liver, and microcirculation on the cell level was superior as well in early treatment of acute heart failure.