Right ventricular volume characteristics in ventricular septal defect

Right and left ventricular volume characteristics were determined from biplane cineangiocardiography in 37 patients with isolated ventricular septal defects. Patients were divided into three categories as determined by the degree of left-to-right shunt: small shunt-less than 35% of pulmonary blood flow (N=9); moderate shunt-35-49% (N=8), and large shunt-greater than 50% (N=20). Right ventricular (RV) end-diastolic volume was increased above normal in 15 of 20 studies performed in patients with large left-to-right shunts and averaged 159 +/- 10% of normal (P less than 0.001). In contrast, only one of the patients in the small shunt group and only half of the patients in the moderate shunt group showed increases in RV end-diastolic volume. The increase in RV volume was proportional to the corresponding increase in left ventricular end-diastolic volume, with the right ventricle ranging from 48 to 116% of LV end-diastolic volume (average 83%). Right ventricular ejection fraction was normal in all patient groups. Right ventricular outpur was increased commensurate with the increases in the RV end-diastolic volume. These data indicate that substantial augmentation in RV end-diastolic volume does occur in patients with isolated ventricular septal defects and large left-to-right shunts. These data can be explained by the significant diastolic and "isovolumic" shunting from left ventricle to right ventricle which occurs in these patients.     

Echocardiography in the evaluation of ventricular function

The ultrasonic beam used for quantitative assessment of left ventricular (LV) function traverses the heart in a projection similar to the familiar angiographic left anterior oblique projection. It crosses the anterior wall of the right ventricle, the right ventricular cavity, the interventricular septum, the LV cavity and the posterior wall of the left ventricle. Whereas the cyclic changes of the right ventricular diameter are rarely clearly determined by echocardiography, the easily assessed cyclic changes of the LV endocardial transverse diameter are useful measure of LV FUNCTION. Of practical importance are the percentage of systolic shortening of the LV diameter (%Sh) and the mean velocity of circumferential fiber shortening (VCF). There are several factors, such as placing of the ultrasonic transducer, the shape and size of the LV cavity and rotational movements of the heart as a whole, that influence echocardiographic determination of the transverse LV diameter. In patients with asynergic contraction, %Sh and VCF cannot be used as measures of overall LV performance, but localized contraction disturbances of the septum and the posterior wall may be detected from the reduced extent of wall motion in a given LV segment during a full sweep from the base to the apex. The most important indications for echocardiographic assessment of LV function are valvar diseases with chronic LV pressure or volume overload, and congestive cardiomyopathy. Echocardiography has proved useful in serial evaluation of LV function in patients undergoing valvar heart surgery. Assessment of LV volume by standard echocardiography using the cubic formula is not satisfactory. More accurate determination of volumes is provided by formulas that include the actual ratio of the LV long axis to the minor axis.     

MRI-derived ventricular volume curves for the assessment of left ventricular function

To assess the utility of double oblique, ECG-gated 1H magnetic resonance (MR) derived volume curves for assessing LV function, cardiac short axis images were acquired with a fast field echo technique. We applied this methodology to assess left ventricular function in three groups: normals, patients with left ventricular hypertrophy, and dilated cardiomyopathy. Six slices with 16-20 phases per RR interval were analyzed, representing the initial 75-80% of the cardiac cycle. For each slice, the endocardial border of the left ventricular (LV) chamber was manually traced. Using Simpson's rule, the total LV volume at a given phase was determined considering the traced area, thickness and position in three-dimensional space of each of the six constituent slices. The calculated volumes were plotted against time and the stroke volume, ejection fraction and cardiac output were determined. The volume vs time plots for the systolic and diastolic portions of the curve were individually fit to third degree polynomials using a least squares approximation. From the fit curves, the following data were extracted: the mean slope (dV/dT) during filling and emptying, and the time to 1/4, 1/3 and 1/2 filling and emptying. These parameters are valuable indices of the functional status of the myocardium; thus, accurate and useful estimates of LV function can be obtained using MRI derived volume curves in normal and abnormal states.     

Left ventricular diastolic stiffness in dogs with congestive cardiomyopathy and volume overload

Mean functional diastolic stiffness, an estimate of the left ventricular resistance to filling during diastole, was measured in 10 normal dogs, 7 dogs with diseases causing volume overload (patent ductus arteriosus and primary mitral valve insufficiency), and 4 dogs with idiopathic congestive cardiomyopathy. It was measured as the increase in pressure during diastole (deltaP), divided by the corresponding increase in volume (deltaV). The pressure was measured at cardiac catheterization, and the volume was derived by a cineangiocardiographic method. There was no increase in diastolic stiffness of the hearts with volume overload compared with the normal hearts, but those with cardiomyopathy had a large increase, although the end-diastolic volumes in cardiomyopathy were generally less than in volume overload.     

Improvement of computerized biplane integration method for left ventricular volume determination by variation of long axis insertion (author's transl)

Biplane integration method for left ventricular volume determination is applicable to routine work since digital contour memories, calculation of the cross-section area and summation of all volume slices are computerized. The longest measured axis is recommended for volume calculation. A second calculation with interchanged axis and averaging of both results led to a correlation coefficient (r) of 0.997 (comparison of true volume and calculated volume). Comparison of stroke volume in patients with coronary heart disease determined by the Fick principle and the reported method showed a significantly better correlation for the biplane than for the monoplane method.     

Left ventricular diastolic pressure-volume relations in man

Diastolic function of the left ventricle was analysed in patients with different cardiac diseases: acute and chronic volume overload (in aortic and mitral incompetence), pressure overload and inappropriate ventricular hypertrophy (aortic stenosis and hypertrophic cardiomyopathy), congestive cardiomyopathy, and constrictive pericarditis. Most patients were receiving digitalis therapy at the time of study. A constant exponential relation between pressure and volume was assumed, and pressure-volume curves were constructed from two points: the instantaneous pressure-volume relation at beginning-diastole and at end-diastole. The determinants of left ventricular end-diastolic pressure were studied. Left ventricular end-diastolic pressure depended on the beginning-diastolic pressure and volume (O point), the slope of the pressure-volume curve (m), and the volume which distended the ventricle in diastole. In chronic volume loading and in congestive cardiomyopathy the curves were flatter than normal, so that left ventricular end-diastolic pressure was only slightly increased despite the large volume filling the ventricle. In pressure overload and in constrictive pericarditis the curves were steeper than normal. Acute changes in volume were accomplished by a shift up or down the pressure-volume curve but in these patients the slope was not altered: the ventricle had not had time to adapt and end-diastolic pressure was greatly increased.     

Contribution of long axis motion of left ventricular outflow to calculation of left ventricular stroke volume

Stroke volume can be calculated by using noninvasive Doppler techniques. The products of pulsed Doppler stroke distance of left ventricular outflow and left ventricular outflow area can often be used to calculate stroke volume. However, left ventricular outflow also moves longitudinally toward the apex of the ventricle during systole, so that zero velocity flow cannot be detected by the usual pulsed Doppler studies. We evaluated the contribution of these zero velocity flow to the noninvasive estimation of left ventricular stroke volume in 20 patients with left ventricular disease and in 20 age matched healthy controls. Left ventricular stroke distance was calculated by summing the Doppler stroke distance and the outflow long axis motion. The percentage of zero velocity flow for total stroke volume was calculated in each group. Cardiac output was also measured by thermo-dilution technique. The percentage of zero velocity flow for total noninvasive stroke volume in patients with left ventricular disease was 2.5 +/- 1.1 ml (4.0 +/- 1.5%), significantly lower than in normal subjects, 3.6 +/- 1.0 ml (5.5 +/- 1.5%) (p < 0.05). These long axis motions are significantly reduced, especially in left ventricular disease. Amplitudes of the left ventricular outflow long axis motion were correlated with Doppler stroke distance in all (r = 0.54, p < 0.01). In patients with myocardial infarction, stroke volume by thermo-dilution methods and calculated stroke volume showed good correlation both only by Doppler stroke distance (y = 1.044x + 0.547, r = 0.968) and by Doppler and long axis motion (y = 0.989x + 0.521, r = 0.974). Compared with stroke volume measured by thermodilution method, stroke volume calculated only by Doppler stroke distance was underestimated. We thus demonstrated the influence of zero velocity flow on left ventricular outflow both in patients with left ventricular disease and in normal subjects.     

Determination of global function and regional mechanics of dynamic cardiomyoplasty using magnetic resonance imaging

This study used tissue tagged magnetic resonance (MR) to assess regional strain and generate pressure-volume (PV) loops in a canine model of cardiomyoplasty (CMP). Three dogs with rapid ventricular pacing induced heart failure underwent dynamic CMP chronic cardiac assistance for 1 year. At the end of the study period, we performed a MR study with the myostimulator "on" and "off" and recording of left ventricular (LV) pressure. We determined the short axis displacement (D) and maximal and minimal principal strains (lambda1 and lambda2) by quantitative two-dimensional regional spatial modulation of magnetization visualization utility image analysis. LV PV loops were generated by combining the LV volume data from the MR images with the LV pressure recorded during imaging. Muscle stimulation produced a leftward shift of the LV PV loops in two of the three dogs, and an increase in LV peak pressure and dp/dt max. In contrast, short axis lambda1 and lambda2 did not change significantly (p = NS). D increased significantly in the anterolateral, posterolateral, and posteroseptal regions (p < 0.05) but did not change for the septal region (p = NS). Flap stimulation augments LV function in the absence of short axis strain change; this suggests that dynamic CMP exerts its main action along the long axis of the heart.     

Right ventricular mass estimation by angioechocardiography

A combined angiocardiographic-echocardiographic method for estimating right ventricular wall mass is described. Biplane cineangiocardiograms are analyzed for ventricular volume in end-diastole, and wall thickness is determined from echocardiograms obtained with a high frequency transducer and strip chart recorder, The intracavitary and the external surface volumes of the ventricle are derived, and the difference multiplied by 1.050, the specific gravity of myocardium. Excellent correlation was observed between right ventricular wall mass and body surface area in normal children (r = 0.93). The mean right ventricular mass was 44.5 g/M2 as compared to 78.1 g/M2 for the left ventricle, corresponding mass/EDV values were 0.48 g/cm3 and 1.26 g/cm3, respectively. In isolated right ventricular pressure overload, the increase in right ventricular mass is chiefly due to the increase in wall thickness; in volume overload, it is due mostly to the increase in chamber volume,     

Relationships between myocardial bioenergetic and left ventricular function in hearts with volume-overload hypertrophy

BACKGROUND: Left ventricular (LV) hypertrophy secondary to volume overload can result in alterations in myocardial bioenergetics and LV dysfunction. This study examined whether bioenergetic abnormalities contribute to the pump dysfunction. METHODS AND RESULTS: Severe mitral regurgitation (MR) was produced in 10 dogs by disruption of the chordal apparatus. Hemodynamics and ventricular function were examined 11.7 months later under baseline conditions and during treadmill exercise. Myocardial high-energy phosphates were measured by using magnetic resonance spectroscopy at rest, during coronary vasodilation with adenosine, and during oxidative stress induced by rapid pacing and dobutamine. Chronic MR caused a 30% increase in LV mass and a 65% increase in LV volume. In MR animals, the hemodynamic and LV function were normal at rest, but abnormalities developed during beta-blockade and exercise. Myocardial creatine phosphate-to-ATP ratios were significantly lower in each layer across the LV wall in MR hearts than normal hearts. Myocardial blood flow and coronary reserve were normal in MR hearts. Moreover, hyperperfusion did not correct the abnormal bioenergetics. Despite altered bioenergetics at rest, the MR hearts tolerated rapid pacing and dobutamine infusion well. CONCLUSIONS: In volume-overloaded LV hypertrophied hearts, alterations in myocardial high-energy phosphate levels do not induce abnormal mechanical performance at rest but may be related to a decreased contractile reserve during exercise.     

Angiotensin-converting enzyme (ACE) inhibitors revert abnormal right ventricular filling in patients with restrictive left ventricular disease

OBJECTIVES: Our aim was to determine mechanisms underlying abnormalities of right ventricular (RV) diastolic function seen in heart failure. BACKGROUND: It is not clear whether these right-sided abnormalities are due to primary RV disease or are secondary to restrictive physiology on the left side of the heart. The latter regresses with angiotensin-converting enzyme inhibition (ACE-I). METHODS: Transthoracic echo-Doppler measurements of left- and right-ventricular function in 17 patients with systolic left ventricular (LV) disease and restrictive filling before and 3 weeks after the institution of ACE-I were compared with those in 21 controls. RESULTS: Before ACE-I, LV filling was restrictive, with isovolumic relaxation time short and transmitral E wave acceleration and deceleration rates increased (p < 0.001). Right ventricular long axis amplitude and rates of change were all reduced (p < 0.001), the onset of transtricuspid Doppler was delayed by 160 ms after the pulmonary second sound versus 40 ms in normals (p < 0.001) and overall RV filling time reduced to 59% of total diastole. Right ventricular relaxation was very incoordinate and peak E wave velocity was reduced. Peak RV to right atrial (RA) pressure drop, estimated from tricuspid regurgitation, was 45+/-6 mm Hg, and peak pulmonary stroke distance was 40% lower than normal (p < 0.001). With ACE-I, LV isovolumic relaxation time lengthened, E wave acceleration and deceleration rates decreased and RV to RA pressure drop fell to 30+/-5 mm Hg (p < 0.001) versus pre-ACE-I. Right ventricular long axis dynamics did not change, but tricuspid flow started 85 ms earlier to occupy 85% of total diastole; E wave amplitude increased but acceleration and deceleration rates were unaltered. Values of long axis systolic and diastolic measurements did not change. Peak pulmonary artery velocity increased (p < 0.01). CONCLUSIONS: Abnormalities of RV filling in patients with heart failure normalize with ACE-I as restrictive filling regresses on the left. This was not due to altered right ventricular relaxation or to a fall in pulmonary artery pressure or tricuspid pressure gradient, but appears to reflect direct ventricular interaction during early diastole.     

Studies of left-ventricular function in anemia due to beta-thalassemia

Left-ventricular (LV) function was studied in 23 patients with anemia due to beta-thalassemia, of whom seven had thalassemia intermedia and the remainder thalassemia major. Two-thirds of the patients wih thalassemia intermedia and almost all the patients with thalassemia major were in clinical congestive heart failure. Despite this, resting measurements of ventricular size and systolic ventricular function were normal, indicating high-output cardiac failure. However, effort testing showed a flat response or decrease in the LV shortening fraction in patients with thalassemia major, and serial studies showed a decrease in the shortening fraction over a 4-yr period in some patients. LV diastolic function was studied by calculating peak LV filling rate and the pattern of LV filling in early diastole. Three patient with thalassemia major showed a pattern indicating abnormal LV distension. Since LV end-diastolic dimension was increased, volume overload was present in all patients. The results indicate that the following factors contribute to the genesis of cardiac failure in beta-thalassemia: 1) diminished response of systolic ventricular performance to exercise and later at rest; 2) ventricular volume overload; and 3) abnormal ventricular distension in diastole. Although the ventricular filling suggests abnormal LV compliance, the effect of right-ventricular volume overload or a pericardial factor cannot be excluded.     

Shortening of the intraventricular conduction time in premature ventricular beats during ventricular extrastimulation: possible role of dimensional shortening of the conducting distance during ventricular systole

INTRODUCTION: Conduction time (CT) is given by the formula: conducting distance divided by conduction velocity. Based on this formula, we hypothesized that CT shortening (i.e., supernormal conduction) may result from dimensional shortening of the distance of impulse propagation, which naturally occurs during ventricular systole. METHODS AND RESULTS: To test the above, two separate groups of patients were studied, group A (14 patients) for electrophysiologic study and group B (12 patients) for echocardiographic study. In group A patients, CT from the stimulus artifact to the basal lateral wall of the left ventricle (LV) (S-LV interval) was measured using right ventricular (RV) apical extrastimulus testing. S-LV interval shortening in premature RV beats was demonstrated in all 14 patients. The maximum shortening was 20 +/- 9 msec (range 10 to 40), and the maximum % shortening was 16% +/- 6% (7% to 27%). In group B patients with implanted pacemakers, the major (long) and minor (short) axis dimensions of the LV were measured with echocardiography. The major axis dimension was used as an approximate measure of the linear length from the RV apex to the basal lateral wall of LV. The maximum % shortening of the major axis dimensions was 15% +/- 4%, 16% +/- 2%, and 11% +/- 4% during VVI pacing, respectively, at paced cycle lengths of 1,000 (11 patients), 800 (5 patients), and 600 msec (12 patients). The maximum % shortening of the S-LV intervals was comparable in magnitude with that of the major axis dimensions: 20% versus 15% +/- 4%, 15% +/- 7% versus 16% +/- 2% and 16% +/- 6% versus 11% +/- 4%, respectively, at paced cycle lengths of 1,000, 800, and 600 msec. There was also a good temporal correlation between the electrophysiologic (CT shortening) versus echocardiographic (dimensional shortening) parameters. Thus, the intraventricular CT and the major axis dimension of the LV were shortened in a similar magnitude and also at a similar timing in the cardiac cycle. CONCLUSION: These findings suggest the possibility that supernormal conduction may result, at least in part, from dimensional shortening of the pathway length of impulse propagation from the stimulating to recording electrodes, which naturally occurs during ventricular systole.     

Effects of cardiomyoplasty on right ventricular filling during volume loading

BACKGROUND: Although cardiomyoplasty (CMP) is thought to improve ventricular systolic function, its effects on ventricular diastolic function are not clear. Especially the effects on right ventricular diastolic filling have not been fully investigated. Because pericardial influences are more pronounced in the right ventricle than in the left ventricle, CMP with its external constraint may substantially impair right ventricular diastolic filling. METHODS: Fourteen purebred adult beagles were used in this study. Seven underwent left posterior CMP, and 7 underwent a sham operation with a pericardiotomy and served as controls. Four weeks later, the hemodynamic effects of CMP were evaluated by heart catheterization before and after volume loading (central venous infusion of 10 mg/kg of 4.5% albumin solution for 5 minutes). RESULTS: In the CMP group, mean right atrial pressure and right ventricular end-diastolic pressure increased significantly from 3.1 +/- 1.2 mm Hg to 6.1 +/- 2.0 mm Hg (p < 0.001) and from 4.0 +/- 1.8 mm Hg to 9.6 +/- 2.5 mm Hg (p < 0.001), respectively. Volume loading in the control group did not significantly increase either variable. Right ventricular end-diastolic volume and stroke volume did not change significantly (from 53 +/- 9.3 mL to 60 +/- 9.0 mL and from 20 +/- 2.3 mL to 21 +/- 3.2 mL, respectively) in the CMP group. In the control group, however, right ventricular end-diastolic volume and stroke volume increased significantly from 45 +/- 7.7 mL to 63 +/- 14 mL (p < 0.05) and from 18 +/- 4.3 mL to 22 +/- 4.2 mL (p < 0.05), respectively. CONCLUSIONS: These results suggest that CMP may reduce right ventricular compliance and restrict right ventricular diastolic filling in response to rapid volume loading because of its external constraint.     

Left ventricular geometric patterns and QT dispersion in untreated essential hypertension

The spectrum of left ventricular adaptation to hypertension, different types of hypertrophy patterns, and QT dispersion in different types of hypertrophy was investigated in 107 patients with untreated essential hypertension and 30 age- and gender-matched normal adults studied by 12-derivation electrocardiogram (ECG), two-dimensional, and M-mode echocardiography. Left ventricular mass (LVM), body mass index, total peripheral resistance (TPR), relative wall thickness (RWT), and QT dispersion were found to be statistically significantly higher in the hypertension group (P < .001 for all). Among hypertensive patients, 41.1% had both normal LVM and RWT, here called normal left ventricle in hypertension; 10.3% had concentric hypertrophy with increased LVM and RWT; 14.95% had eccentric hypertrophy with increased LVM and normal RWT; and 32.7% had concentric remodeling with normal LVM and increased RWT. Echocardiographically derived cardiac index was higher in the concentric hypertrophy and eccentric hypertrophy patterns (P = .002 and P < .0001, respectively), whereas TPR was higher in the concentric hypertrophy and concentric remodeling patterns (P = .017 and .02, respectively). QT dispersion values were found to be increased in the hypertensive group (P = .001), whereas similar values were calculated for different types of hypertrophy patterns. We conclude that the more common types of ventricular adaptation to essential hypertension are eccentric hypertrophy and concentric remodeling. Concentric hypertrophy is found to be associated with both volume and pressure overload, whereas eccentric hypertrophy is associated with volume overload only and concentric remodeling is associated with pressure overload. But different left ventricular geometric patterns seem to have similar effects on QT dispersion.     

Chronic L-arginine treatment increases cardiac cyclic guanosine 5'-monophosphate in rats with aortic stenosis: effects on left ventricular mass and beta-adrenergic contractile reserve

OBJECTIVES: We tested the hypothesis that nitric oxide (NO) cyclic guanosine 5'-monophosphate (GMP) signaling is deficient in pressure overload hypertrophy due to ascending aortic stenosis, and that long-term L-arginine treatment will increase cardiac cyclic GMP production and modify left ventricular (LV) pressure overload hypertrophy and beta-adrenergic contractile response. BACKGROUND: Nitric oxide cyclic GMP signaling is postulated to depress vascular growth, but its effects on cardiac hypertrophic growth are controversial. METHODS: Forty control rats and 40 rats with aortic stenosis left ventricular hypertrophy ([LVH] group) were randomized to receive either L-arginine (0.40 g/kg/day) or no drug for 6 weeks. RESULTS: The dose of L-arginine did not alter systemic blood pressure. Animals with LVH had similar LV constitutive nitric oxide synthase (cNOS) mRNA and protein levels, and LV cyclic GMP levels as compared with age-matched controls. In rats with LVH L-arginine treatment led to a 35% increase in cNOS protein levels (p = 0.09 vs untreated animals with LVH) and a 1.7-fold increase in LV cyclic GMP levels (p < 0.05 vs untreated animals with LVH). However, L-arginine treatment did not suppress LVH in the animals with aortic stenosis. In contrast, in vivo LV systolic pressure was depressed in L-arginine treated versus untreated rats with LVH (163 +/- 16 vs 198 +/- 10 mm Hg, p < 0.05). In addition, the contractile response to isoproterenol was blunted in both isolated intact hearts and isolated myocytes from L-arginine treated rats with LVH compared with untreated rats with LVH. This effect was mediated by a blunted increase in peak systolic intracellular calcium in response to beta-adrenergic stimulation. CONCLUSIONS: Left ventricular hypertrophy due to chronic mechanical systolic pressure overload is not characterized by a deficiency of LV cNOS and cyclic GMP levels. In rats with aortic stenosis, L-arginine treatment increased cardiac levels of cyclic GMP, but it did not modify cardiac mass in rats with aortic stenosis. However, long-term stimulation of NO-cyclic GMP signaling depressed in vivo LV systolic function in LVH rats and markedly blunted the contractile response to beta-adrenergic stimulation.     

Evaluation of left ventricular early diastolic performance by color tissue Doppler imaging of the mitral annulus

A noninvasive assessment of left ventricular (LV) diastolic performance by tissue Doppler imaging was performed in 56 patients (8 patients with atypical chest pain, 42 with coronary artery disease with a previous myocardial infarction, and 6 without a previous myocardial infarction) who underwent cardiac catheterization. Mitral annular velocity (MAV) during early ventricular diastole was obtained by M-mode color tissue Doppler imaging at the posterior corner of the mitral annulus. In each patient, the negative peak of the first derivative of LV pressure decay (peak -dP/dt) and a time constant of LV relaxation (tau) were calculated from the LV pressure waves obtained by a catheter-tip micromanometer. LV end-systolic volume index was measured from contrast left ventriculography. MAV during early diastole was significantly correlated with tau (r = -0.73, p <0.001), peak -dP/dt (r = 0.58, p <0.001), and LV end-systolic volume index (r = -0.63, p <0.001). On multivariate regression analysis with MAV during early diastole, tau and LV end-systolic volume index were selected as prime determinants (r = 0.80, p <0.001). These findings suggest that MAV during early diastole has a direct relation to LV elastic recoil as well as to LV relaxation. MAV during early diastole gives important information regarding LV behavior in late systole to early diastole where LV early diastolic performance is determined.     

Reduced left ventricular hypertrophy in type 1 diabetic patients with end-stage renal failure. A comparison between groups investigated 1977-80 and 1991-93

BACKGROUND: During the last decade, control of hypertension, oedema, anaemia, uraemia, and blood glucose has improved in patients with diabetic nephropathy. We have investigated whether this has influenced cardiac function at the time of end-stage renal failure. STUDY DESIGN: Echocardiographic investigations were performed in 26 type 1 diabetic patients evaluated for kidney transplantation and the results compared with those obtained in healthy controls and in a similar group of patients investigated in 1977-1980. RESULTS: Blood pressure was 153 +/- 21/85 +/- 12 mmHg versus 174 +/- 17/91 +/- 9 (recent group versus early group). The left ventricular (LV) diameter index, a measure of volaemia, was increased in systole and diastole in the early but not in the recent group. Both groups had LV hypertrophy, but this was much less pronounced in the recent group; posterior wall thickness was 1.1 +/- 0.16 cm versus 1.3 +/- 0.26 cm (P = 0.0001) and LV mass index 132 +/- 43 g/m2 versus 166 +/- 44 g/m2 (P = 0.009). Blood pressure correlated significantly with indices of LV hypertrophy in the recent group. Systolic function was normal in both groups but diastolic function was disturbed in both and to the same extent, atrial systole contributing by 27 +/- 14% to ventricular filling. CONCLUSION: Better treatment of hypertension, fluid overload, and uraemia has led to less pronounced LV hypertrophy. The remaining correlation with blood pressure suggests that more could be gained by intensified antihypertensive treatment.     

Redefining cardiovascular performance during resuscitation: ventricular stroke work, power, and the pressure-volume diagram

OBJECTIVES: (1) To compare left ventricular stroke work index (SW) and left ventricular power output (LVP), hemodynamic variables that encompass blood pressure as well as blood flow, with the purely flow-derived hemodynamic and oxygen transport variables as markers of perfusion and outcome in critically injured patients during resuscitation. (2) To use the ventricular pressure-volume diagram to define characteristic hemodynamic patterns in the determinants of SW and LVP that are associated with survival. METHODS: This was a cohort study at a university Level I trauma center during the course of 1 year. A consecutive series of patients was monitored with a volumetric pulmonary artery catheter during the initial 48 hours of resuscitation. Heart rate, SW, LVP, cardiac index, and oxygen delivery and consumption during resuscitation were compared using multivariate logistic regression analysis with regard to the ability to clear lactate in less than 24 hours and survival. Receiver operating characteristic curves were constructed to determine threshold values for SW and LVP. Ventricular pressure-volume diagrams were used to describe characteristic patterns in the determinants of SW and LVP in survivors and nonsurvivors. Preload was expressed as left ventricular end-diastolic volume index, afterload as aortic input impedance (Ea), and contractility as ventricular end-systolic elastance (Ees). The ratio of Ea/Ees (RATIO) was used as a measure of ventricular-arterial coupling, which describes the efficacy of energy transfer from the heart to the vascular system. RESULTS: One hundred eleven patients (87 survivors, 24 nonsurvivors) met study criteria. Survivors had a significantly higher SW (4,510 +/- 1,070 vs. 3,440 +/- 980 mm Hg x mL x m(-2); p < 0.0001) and LVP (370 +/- 94 vs. 270 +/- 81 mm Hg x L x min(-2) x m(-2); p < 0.0001) than nonsurvivors. Heart rate, SW, and LVP were the only studied variables that were significantly related to lactate clearance and survival by logistic regression. Threshold values determined by the receiver operating characteristic curves were 4,000 mm Hg x mL x m(-2) for SW and 320 mm Hg x L x min(-1) x m(-2) for LVP. Survivors had better ventricular-arterial coupling than nonsurvivors, indicated by a lower RATIO (0.32 +/- 0.22 vs. 0.54 +/- 0.38; p = 0.003). This lower RATIO was attributable to lower levels of Ea (2.7 +/- 0.7 vs. 3.4 +/- 0.8 mm Hg x mL(-1) x m(-2); p = 0.0003) and a trend toward higher levels of Ees (13 +/- 11 vs. 9.9 +/- 7.3 mm Hg x mL(-1) x m(-2); p = 0.12). CONCLUSION: Thermodynamic perfusion variables that encompass both pressure and flow, such as SW and LVP, are more closely related to perfusion and outcome than the purely flow-derived variables. The higher SW and LVP in survivors is related to better ventricular-arterial coupling, and therefore more efficient cardiac function. Cutoff values for LVP of 320 mm Hg x L x min(-1) x m(-2) and for SW of 4,000 mm Hg x mL x m(-2) may be useful thresholds for evaluating hemodynamic performance during resuscitation.     

Influence of heart rate on stroke volume variability in atrial fibrillation in patients with normal and impaired left ventricular function

Both resting tachycardia and irregular ventricular rhythm may contribute to impaired cardiac performance in atrial fibrillation (AF). This study assesses the relation between resting heart rate and beat-to-beat changes in left ventricular (LV) ejection and filling in patients with normal and impaired LV systolic function. Beat-to-beat variation in LV outflow and inflow velocity-time integral was measured using pulsed Doppler ultrasound in 39 patients with chronic AF and normal (n=22) or impaired (n=17) LV systolic function. Aortic velocity-time integral variability increased with mean heart rate (p=0.003) even though RR interval variability decreased (p <0.001). Aortic velocity-time integral was more sensitive to the duration of both the preceding (p <0.001) and prepreceding (p <0.001) RR intervals at higher heart rates. These relations were similar for patients with normal and impaired LV systolic function. The sensitivity of the filling velocity-time integral to RR interval variability also increased with heart rate (p <0.001). However, at higher heart rates the filling velocity-time integral (p=0.009) and filling time (p=0.005) were less sensitive to change in RR intervals in patients with impaired LV function. We conclude that beat-to-beat stroke volume variability in AF increases with heart rate. Stroke volume variability was not influenced by LV systolic function.