Showing papers on "Ventricle published in 1979"

Myocardial infarct size and ventricular function in rats.

Abstract: To define the relationship between infarct size and ventricular performance, we performed hemodynamic studies in rats 21 days after left coronary artery occlusion. Ventricular performance was assessed under ether anesthesia by measurements of baseline hemodynamics and stressed performance as determined by the peak cardiac output and stroke volume obtained during intravenous volume loading and by the peak left ventricular developed pressure obtained during occlusion of the ascending aorta. Infarct size was determined by planimetry of the endocardial circumference of each of four histological slices of the left ventricle. Rats with small (4-30%) myocardial infarctions had no discernible impairment in either baseline hemodynamics or peak indices of pumping and pressure-generating ability when compared to the sham-operated, noninfarcted rats. Rats with moderate (31-46%) infarctions had normal baseline hemodynamics but reduced peak flow indices and developed pressure. Rats with infarctions greater than 46% had congestive heart failure, with elevated filling pressures, reduced cardiac output, and a minimal capacity to respond to pre- and after load stresses. The entire spectrum of postinfarction ventricular function was observed, from no detectable impairment to congestive failure. In this model of histologically healed myocardial infarction, the impairment of left ventricular function was directly related to the loss of myocardium.

Cross-sectional echocardiography. I. Analysis of mathematic models for quantifying mass of the left ventricle in dogs.

Abstract: Cross-sectional echocardiography was used to quantify left ventricular mass noninvasively in 21 dogs. Short- and long-axis cross-sectional images of the left ventricle were reproducibly traced at endocardial and epicardial borders during stop-motion video-tape replay. We used area, length and diameter measurements to calculate left ventricular mass by seven mathematic models, including the standard formulas used with M-mode echocardiography and cineangiography. Calculated mass was compared with excised weight of the left ventricle by regression and percent error analyses. Formulas using short-axis areas and long-axis length resulted in higher correlation coefficients (0.94--0.95) and lower mean errors (6--7%) than for standard formulas. Since short-axis areas account for regional left ventricular irregularities, noninvasive quantification of left ventricular mass by cross-sectional echocardiography in dogs is most accurate with formulas using short-axis areas.

Atrial induction of ventricular tachycardia: Reentry versus triggered automaticity

Abstract: Atrial stimulation induced a sustained ventricular tachycardia in two patients with mitral valve prolapse and in one patient who had mild hypertension without cardiac abnormalities. Exercise-induced sinus tachycardia also started the ventricular tachycardia in one patient. Evidence is presented to suggest that the mechanism of ventricular tachycardia in one patient was reentrant excitation and in another patient triggered automaticity. It is likely that the origin of the ventricular tachycardia was confined to a relatively protected small area near the posteroinferior portion of the left ventricle and was not due to macroreentry.

Fetal and Neonatal Pulmonary Circulation

Abstract: During fetal life, gas exchange is carried out in the placenta. The lung does not have a physiological role, apart from possible metabolic functions which include secretion of hormones, enzymatic conversion of inactive substances to functional hormones, and degradation of active materials to inactive metabolites. Blood flow through the lungs is quite low during fetal life; most of the systemic and umbilical venous blood returning to the heart is shunted through the foramen ovale to the left atrium and left ventricle, or through the ductus arteriosus directly from the pulmonary trunk to the descending aorta. About 85-90% of the blood ejected by the right ventricle is diverted from the lungs through the ductus arteriosus (48). Because the right ventri­ cle ejects about 66% of the combined ventricular output of the fetal heart, about 60% of the total output of the heart passes through the ductus arteriosus and thus does not enter the lungs. Should this volume of blood pass through the pulmonary circulation and return to the left ventricle, there would be an unnecessary increase in the volume of work placed on the heart. The low fetal pulmonary blood flow has been explained on the basis of a high pulmonary vascular resistance. Mter birth, however, a marked in­ crease in pulmonary blood flow is necessary to permit adequate gas ex­ change. This review considers: (0) pulmonary arterial pressures and flows in utero and changes during gestation; (b) patterns of fetal pulmonary blood flow; (c) factors that influence fetal pulmonary vascular responses; and (d) mechanisms responsible for the postnatal decrease in pulmonary vascular resistance.

Instantaneous pressure-volume relationship of the canine right ventricle.

Abstract: SUMMARY The instantaneous isovolumic and ejecting pressure-volume relationship of the right ventricle was studied in 11 cross-circulated, isolated canine hearts to characterize the right ventricular contractile state. Accurate measurement of volume was achieved by the use of a water-filled, thin latex balloon in the right ventricle connected to a special volume loading and transducing chamber. Pressure was measured with a miniature pressure transducer mounted within the balloon. Wide variations in loading conditions were achieved by changing the volume of air above the volumetric chamber. The pressure and volume data were collected from multiple beats under a constant contractile state in the same mode of contraction while the left ventricle was vented to air. Linear regression analysis applied to each of the isochronal pressure-volume data sets at 20-msec intervals from the onset of contraction showed a highly linear correlation between the pressure and the volume. Both the slope and the volume intercept of the regression lines changed with time throughout the cardiac cycle. The maximal slope of the regression line (E,,,,) averaged 2.50 ± 0.49 mm Hg/ml (mean ± SD) for ejecting beats and 2.68 ± 0.55 mm Hg/ml for isovolumic beats. Epinephrine infusions of 12.5 fig/min and 25.0 /ig/min increased E^u by 31% and 82%, respectively (P < 0.005). We conclude that: (1) The instantaneous pressure-volume relationships of the right ventricle in the isovolumic and ejecting modes can be regarded as linear, at least within the physiological range; however, these two modes of contraction did not yield an identical relationship. (2) The slope of these pressure-volume relationship curves changes with a change in the contractile state. Ore Res 44: 309-315, 1979 IT IS WELL KNOWN that there are major anatomical and physiological differences between the right and left ventricles. Compared with the left ventricle, the right ventricle has a greater regional variation in wall thickness and a more complex geometric shape. The developed pressure in systole is much smaller, and intraventricular pressure falls considerably while ejection proceeds. Much recent research has been focussed on left ventricular function, yet there is little quantitative information concerning the right ventricle, particularly with respect to the question of how to characterize contractile state and pumping ability. Those indices of contractile state used in characterizing left ventricular function have not been quantified in and shown to be valid for the right ventricle. Since there are major differences between left and right ventricles, we investigated whether right ventricular contractile state could be described in a similar fashion as left ventricular contractile state. In this study we determined the time-varying ratio of instantaneous pressure to volume, which has been shown to be sensitive to changes in left ventricular contractile state and nearly independent of

Determination of right atrial and right ventricular size by two-dimensional echocardiography.

Abstract: No data are available on determining right atrial and right ventricular size by two-dimensional echocardiography. We performed two-dimensional echocardiograms on eight human right-heart casts obtained at autopsy and on 50 patients who underwent complete left- and right-heart catheterization. Measurement of individual dimensions of the long and short axes of the right atrium and ventricle from right heart casts closely correlated with the volume of these structures as determined by water displacement. Further, individual dimensions by cross-sectional echo correlated well with actual casts dimensions. Subsequently, echocardiographic measurements of right atrial and ventricular long and short axes were obtained in the apical four-chambered view in a group of normals and compared with a group of patients with right ventricular volume overload states. Mean values for right atrial short-axis and long-axis measurements were greater in right ventricular volume overload patients than in normals: 6.5 +/- 0.3 vs 3.6 +/- 0.1 cm, and 6.0 +/- 0.3 vs 4.2 +/- 0.1 cm, respectively (both p less than 0.001). In addition, measurements of both individual dimensions as well as planed area of the right ventricle were greater in right ventricular volume overload patients than in normals: maximal short axis 6.1 +/- 0.3 vs 3.5 +/- 0.2 cm, mid-short axis 6.1 %/- 0.4 vs 2.8 +/- 0.2 cm, and area 40 +/- 2.6 vs 18 +/- 1.2 cm2 (all p less than 0.001). There were no differences in right ventricular long-axis measurement. Two-dimensional echocardiography provided better separation of normals from right ventricular volume overload patients than did M-mode techniques. Thus, two-dimensional echocardiography, with the apical four-chambered view, enables accurate visualization of the right atrium and ventricle in almost all patients. Futher, measurements of right atrial and right ventricular size by two-dimensional echocardiography readily distinguish normal patients from those with right ventricular volume overload.

Right ventricular infarction. Clinical diagnosis and differentiation from cardiac tamponade and pericardial constriction.

Abstract: Twelve patients with a clinical diagnosis of right ventricular infarction are described. All had acute inferior wall myocardial infarction associated with the bedside findings of jugular venous distension, clear lungs on auscultation, and arterial hypotension. Hemodynamically, there was elevation of right-sided filling pressures not explained by normal or minimally elevated pulmonary wedge pressures. Four patients had an incorrect diagnosis of acute cardiac tamponade. However, a review of the data showed that the hemodynamic features of right ventricular infarction more closely resemble those of pericardial constriction, a point that may be helpful in distinguishing right ventricular infarction from cardiac tamponade. Invasive and noninvasive techniques that exclude the presence of pericardial fluid and suggest enlargement and abnormal contractility of the right ventricle were helpful in establishing the diagnosis of right ventricular infarction in several patients.

Cardiac function and morphology with aging in the spontaneously hypertensive rat

Abstract: To determine the effects of a chronic pressure load on cardiac function and morphology, spontaneously hypertensive rats (SHR) and two normotensive strains of Wistar rats (WKY and NWR) were studied under ether anesthesia at 13, 25, 52, and 90 wk of age. Although resting cardiac index of the SHR was comparable to that of WKY and NWR at all ages, the peak cardiac output and peak stroke volume per gram of left ventricle determined during a rapid intravenous infusion of Tyrode solution was markedly reduced in the SHR only at 90 wk of age. Autonomic inhibition did not alter the peak stroke volume attained, but reduced peak cardiac output at all ages in each of the strains. Absolute left ventricular dimensions in the SHR increased out of proportion to body growth, consistent with concentric hypertrophy. As peak pumping ability markedly declined from 52 to 90 wk of age in the SHR, the free wall of the left ventricle greatly thickened whereas the septum remained unchanged. At this time the right ventricle also hypertrophied. This disproportionate thickening of the walls of the left ventricle and the hypertrophy of the right ventricle were reflected in measurements of their fiber diameters. These alterations in ventricular architecture may contribute to the decrease in pumping ability observed in long-standing hypertension.

Acute displacement of the diastolic pressure-volume curve of the left ventricle: role of the pericardium and the right ventricle.

Abstract: IN CHRONIC CARDIAC DISEASE, the left ventricular diastolic pressure does not provide a reliable guide to the diastolic left ventricular volume,' and measurement of chamber volume, shape and wall thickness are necessary to identify changes in the myocardial stress-strain relation.' Under acute conditions, the stiffness of the left ventricular chamber progressively increases as passive diastolic filling occurs,3 but whether a single equation can describe this nonlinear pressure-volume curve in the human heart is not settled; this topic and the chronic adaptations that affect diastolic compliance have been examined in two recent reviews4'5 and will not be discussed here. Rather, certain factors that may be involved in acute displacements of the entire left ventricular pressurevolume curve will be considered, a phenomenon which is investigated in two clinical papers appearing in this issue of Circulation one concerned with pharmacologic interventions,6 the other with acute ischemia.7

A mathematical model of the dynamic geometry of the intact left ventricle and its application to clinical data.

Abstract: In this paper we examine the relations that may exist between the geometric variables most frequently used to describe left ventricular contraction. The left ventricle is represented by a thick-walled cylinder contracting both radially and longitudinally. For this model, wall thickening, mid-wall radius shortening and longitudinal axis shorteining can be shown to be uniquely related during contraction, whereas it can be demonstrated that internal radius shortening is not uniquely related to these variables, but is also determined by the specific geometry of the cylinder, expressed in terms of the mid-wall radius-to-wall thickness (R/h) ratio of the cylinder. Detailed analysis of the same variables in 44 normal subjects, 32 patients with aortic stenosis and 54 patients with valvular regurgitation (33 aortic and 21 mitral), strongly suggests that the same relations are also clinically applicable. For instance, ventricular longitudinal axis shortening can be estimated with some accuracy from the standard M-mode echocardiogram. Also, wall thickening can be viewed as the direct reflection of the shortening that occurs in the circumferential and longitudinal directions, whereas internal radius shortening is significantly influenced by the R/h ratio of the ventricle, a consideration which becomes important when analyzing results in patients with left ventricular hypertrophy.

Dynamic Aspects ofAcuteMitral Regurgitation: Effects ofVentricular Volume, Pressure andContractility ontheEffective Regurgitant Orifice Area

Abstract: SUMMARY Thedynamics ofacute mitral regurgitation werestudied insixopen-chest dogsinwhomaportion oftheanterior leaflet wasexcised. Phasic mitral andaortic flows weremeasured electromagnetically and left ventricular filling volume, regurgitant volume (RV)andforward stroke volume (SV) werecalculated. The systolic pressuregradient (SPG)between theleft ventricle (LV)andleft atrium (LA)wasobtained fromhighfidelity pressuretransducers. Theeffective mitral regurgitant orifice area(MRA)was calculated fromthe hydraulic equation ofGorlin. Volumeinfusion resulted insignificant increases inbothleft atrial andleft ventricular pressures;thus, the SPGwasunchanged andtheincrease inRV wasdueprimarily totheincrease inMRA.Angiotensin infused to raise arterial pressureresulted ingreater increments inleft ventricular thanleft atrial pressure, sothat SPG rosesignificantly. Theincrease inRVwasduetoincreases inbothMRA andSPG.Norepinephrine infusion increased systolic left ventricular pressureandSPG,while left ventricular end-diastolic pressureandleft atrial pressurediminished. Despite asignificant increase inSPG,RVdidnotincrease, duetoasubstantial decrease inMRA.Thus, angiotensin andvolume infusion induced asubstantial increase inregurgitation duetotheincreaseinMRA,while augmentation ofcontractility after norepinephrine infusion resulted ina decrease in regurgitation through reduction ofMRA.Thesefindings support theclinical viewthatmaintaining asmall LV withsustained myocardial contractility will reduce mitral regurgitation. Alternatively, left ventricular dilatation can enhance mitral regurgitation byincreasing theeffective regurgitant orifice independent ofSPG. NORMAL MITRALVALVEFUNCTIONdepends onthemechanical integrity ofthemitral annulus, valve leaflets, chordae tendineae, papillary muscles andthecontraction ofthefree left ventricular (LV) wall. Thefactors that determine theregurgitant flow inmitral insufficiency arethesystolic pressure gradient (SPG)between theleft ventricle andleft atrium, thesize oftheregurgitant orifice ortheareaof thedeficit inmitral closure, andtheduration ofthe regurgitation orthelength ofventricular systole.'s 2It hasbeentraditionally accepted that theregurgitant orifice isfixed under different circulatory states,' exceptintheclinical syndrome ofpapillary muscle dysfunction inwhich theproperties ofthesupporting structures maychange withtime.3 However, recent studies ofexperimental acute mitral insufficiency in thedoghavesuggested that thesize oftheregurgitant orifice isnotfixed.' Thepresent study wasdesigned to define theeffects ofalterations inventricular volume, pressure loading andmyocardial contractility onthe regurgitation ofexperimental acute mitral insufficiency,andtodetermine ifthesize oftheregurgitant orifice isaltered bythese interventions.

End-systolic pressure determines stroke volume from fixed end-diastolic volume in the isolated canine left ventricle under a constant contractile state.

Abstract: We studied the effect of systolic pressure and volume changes on the end-systolic pressure at a fixed end-systolic volume in the left ventricle of excised, cross-circulated canine hearts. Instantaneous ventricular volume was controlled and both end-diastolic and end-systolic volumes were clamped, as preprogrammed by a volume servo pump system. Ventricular ejection was completed at the end of natural systole. When the onset and velocity of ejection were widely varied during contractions with a given set of end-diastolic and end-systolic volumes, the end-systolic pressure was little affected by the changes in the systolic pressure and volume under a stable contractile state. When the end-diastolic volume was increased from the isovolumic condition, the end-systolic pressure at the same end-systolic volume decreased (P < 0.05) from the peak isovolumic pressure by 5-14%, for an ejection fraction of 40-70%. When the end-systolic volume was decreased while the end-diastolic volume was fixed, the end-systolic pressure decreased in proportion to end-systolic volume. These results were interpreted to indicate that, when ejection ends at the end of systole, stroke volume of the ventricle with a given end-diastolic volume is determined predominantly by the end-systolic pressure rather than by the entire systolic courses of the pressure and volume, drc Res 44; 238-249, 1979

Dynamic aspects of acute mitral regurgitation: effects of ventricular volume, pressure and contractility on the effective regurgitant orifice area.

Abstract: The dynamics of acute mitral regurgitation were studied in six open-chest dogs in whom a portion of the anterior leaflet was excised. Phasic mitral and aortic flows were measured electromagnetically and left ventricular filling volume, regurgitant volume (RV) and forward stroke volume (SV) were calculated. The systolic pressure gradient (SPG) between the left ventricle (LV) and left atrium (LA) was obtained from high-fidelity pressure transducers. The effective mitral regurgitant orifice area (MRA) was calculated from the hydraulic equation of Gorlin. Volume infusion resulted in significant increases in both left atrial and left ventricular pressures; thus, the SPG was unchanged and the increase in RV was due primarily to the increase in MRA. Angiotensin infused to raise arterial pressure resulted in greater increments in left ventricular than left atrial pressure, so that SPG rose significantly. The increase in RV was due to increases in both MRA and SPG. Norepinephrine infusion increased systolic left ventricular pressure and SPG, while left ventricular end-diastolic pressure and left atrial pressure diminished. Despite a significant increase in SPG, RV did not increase, due to a substantial decrease in MRA. Thus, angiotensin and volume infusion induced a substantial increase in regurgitation due to the increase in MRA, while augmentation of contractility after norepinephrine infusion resulted in a decrease in regurgitation through reduction of MRA. These findings support the clinical view that maintaining a small LV with sustained myocardial contractility will reduce mitral regurgitation. Alternatively, left ventricular dilatation can enhance mitral regurgitation by increasing the effective regurgitant orifice independent of SPG.

Limited left ventricular response to volume overload in the neonatal period: a comparative study with the adult animal.

Abstract: Summary: The unique fragility of the neonatal circulation in response to disease states and various physiologic stimuli is apparent clinically, although underlying mechanisms have not been explored. Accordingly, this report examines and compares the influence on cardiac performance of changes in left ventricular (LV) filling pressure in six conscious, unscdated newborn lambs studied serially at 1 and 3 weeks of age and five adult sheep. All animals were instrumented chronically to assess LV internal dimensions and pressures and cardiac output. At constant heart rate, infusion of saline to comparably high LV end diastolic pressure was associated in the younger newborns with significantly elevated mean arterial pressures (MAP), reduced LV stroke volume, stroke work, and mean fiber shortening when compared to older newborns or adults. A separate analysis of the LV pressure-dimension relationships showed lowest LV compliance in the youngest animals with a progressive increase with age. Thus, these results suggest that the youngest newborns have limited preload reserve related to reduced LV compliance. With volume infusion, sacromeres are stretched fully; the rise in peripheral resistance creates a mismatch between aftcrload and the level of inotropic state. These findings provide a framework for viewing cardiocirculatory adaptation to left-to-right shunt lesions in the human newborn and support the contention that age-dependent, disadvantageous myocardial mechanical factors play a critical role in their clinical course. Speculation: The determinants of LV performance can best be described in terms of preload, afterload, and contractile state. The dynamic transition after birth from a single, parallel fetal circulation into separate, independent pulmonary and systemic circuits imposes marked loading alterations on the left ventricle of the newborn. Thus, preload increases dramatically in parallel with a 3-to 4-fold augmentation in pulmonary blood flow; systemic vascular resistance rises when clamping the umbilical cord removes the low resistance placental circulation, and when constriction of the ductus arteriosus occurs. Of course, the presence of a cardiac malformation may further accentuate either preload or aftcrload.

Recurrent sustained ventricular tachycardia. 4. Pleomorphism.

Abstract: Two or more morphologically distinct ventricular tachycardias were observed during electrophysiologic study in 14 patients with chronic sustained ventricular tachycardia. Nine of these patients had clinical ventricular tachycardia with multiple morphologies. During the study 13 patients manifested both right bundle branch block (RBBB) and left bundle branch block (LBBB) morphologies. The remaining patient had RBBB with both right and left axis deviation. Changing morphologies were observed spontaneously in four patients and could be produced in all 14 by ventricular stimulation. In 12 patients both RBBB and LBBB originated in the left ventricle, and in 11 of these patients, from within a left ventricular aneurysm. Diastolic fragmented activity representing reentry was unchanged during both morphologies in four patients and during one morphology in five patients. Epicardial mapping confirmed the aneurysm as the site of origin of multiform ventricular tachycardias in two patients. Our data suggest that 1) ventricular tachycardia is frequently pleomorphic; 2) multiple morphologies usually represent variable exit sites and/or ventricular activation during the same tachycardia; and 3) there is a frequent association of pleomorphic ventricular tachycardia with left ventricle aneurysm.

Mechanism of reduction of mitral regurgitation with vasodilator therapy

Abstract: Acute mitral regurgitation was produced in six open chest dogs by excising a portion of the anterior valve leaflet. Electromagnetic flow probes were placed in the left atrium around the mitral anulus and in the ascending aorta to determine phasic left ventricular filling volume, regurgitant volume and stroke volume. The systolic pressure gradient was calculated from simultaneously measured high fidelity left atrial and left ventricular pressures. The effective mitral regurgitant orifice area was calculated from Gorlin's hydraulic equation. Infusion of nitroprusside resulted in a significant reduction in mitral regurgitation. No significant change occurred in the systolic pressure gradient between the left ventricle and the left atrium because both peak left ventricular pressure and left atrial pressure were reduced. The reduction of mitral regurgitation was largely due to reduction in the size of the mitral regurgitant orifice. Reduction of ventricular volume rather than the traditional concept of reduction of impedance to left ventricular ejection may explain the effects of vasodilators in reducing mitral regurgitation.

Method of and apparatus for automatically detecting and treating ventricular fibrillation

Abstract: Method of and apparatus for automatic defibrillation of the cardiac ventricles of a heart wherein both the mechanical and electrical activities of the ventricles are sensed and used as operating inputs to the controls. Electrical activity is detected and measured with a pair of electrodes, and the waves of an electrocardiogram (ECG) are analyzed. When such electrical analysis indicates that ventricular fibrillation is present and persists, an electrical circuit is actuated for detecting mechanical pumping activity of the heart. Mechanical pumping activity is measured by the change in impedance between the pair of electrodes in one of the ventricles. The change of ventricular impedance is caused by the varying volume of blood contained within the ventricle and depends upon whether the ventricle is in a contracted or a relaxed state. The defibrillator is actuated only when both the mechanical and electrical activity of the ventricle indicates a need for defibrillation. Because some conditions may be encountered which closely resemble ventricular fibrillation, the defibrillator quantitatively preprograms and weighs the relative importance of the electrical and mechanical signals from the heart.

Epicardial activation of the intact human heart without conduction defect.

Abstract: To describe the epicardial ventricular activation sequence in the intact human heart, we obtained epicardial maps from 11 patients with normal QRS undergoing open heart surgery. Epicardial breakthrough (EBT), defined as the emergence of a radially propagating epicardial wavefront, occurred in three to five sites in each patient, and was earliest in the anterior right ventricle, 7--25 msec (mean 17 msec) after the onset of the QRS in all patients. Subsequent EBT occurred in the inferior right ventricle (10 sites in 10 patients), in the anterolateral left ventricle (13 sites in 10 patients), and the inferior left ventricle (eight sites in seven patients). Latest epicardial activation (LEA), defined as the latest site of recordable epicardial activity, occurred in the basal segments in all patients, anteriorly in the right ventricle in five patients, and inferiorly in six patients, four on the right and two on the left. LEA occurred 63--96 msec (mean 77 msec) after the onset of the QRS, and was recorded within 20 msec of the end of the QRS in all patients. Sequence of epicardial activation reflected a fusion process among the wavefronts. This descriptive and quantitative data should provide a suitable basis for comparison of abnormal ventricular activation sequences in patients undergoing surgery for preexcitation or ventricular tachycardia.

Morphological variations in pulmonary atresia with intact ventricular septum.

Abstract: The morphological features of a series of 37 specimens of pulmonary atresia with intact ventricular septum were reviewed with particular emphasis on features which might influence the results of pulmonary valvotomy. The degree of right heart hypoplasia was quantified by measuring right and left heart dimensions and comparing them with 20 normal infant hearts. Right ventricular cavity size was usually smaller than normal but constituted a spectrum ranging from tiny to a dilated ventricle larger than normal. There was a positive correlation between triscuspid annular size and right ventricular size but no correlation between the size of the pulmonary artery and the right ventricle. Successful pulmonary valvotomy with subsequent adequate right ventricular function would have been precluded by a tiny right ventricular cavity or infundibular atresia in 14 specimens and by severe tricuspid stenosis or regurgitation in an additional 4. Severe right or left ventricular endocardial fibroelastosis may have adversely affected ventricular function in several others. Ten specimens displayed convex bulging of the left ventricular septal surface. If these these anatomical findings are representative for the condition as a whole, they provide a good explanation for its disastrous prognosis.

Accurate volume determination in the isolated ejecting canine left ventricle by two-dimensional echocardiography.

Abstract: Two-dimensional echocardiography can provide serial cross-sectional images of the left ventricular cavity. We examined whether such serial images from steady-state ejecting hearts would allow three-dimensional reconstruction and accurate volume estimation without major geometric assumptions. Cross-circulated, paced dog hearts were suspended in a blood-filled tank. Serial cross-sectional images were taken at 3-mm intervals along the vertical axis. Left ventricular cavity and muscle areas of each image were planimetered with a light-pen system and summated for volume: total volume = sigma (areas x 3 mm). Direct left ventricular volume was measured through the cardiac cycle with a volumetric chamber connected to a balloon in the ejecting left ventricle. In six hearts, 67 separate direct volume measurements (range 9.5--54.7 ml) from various points in the cardiac cycle were compared with the simultaneous echo volume measurements. By least squares linear regression, echo volume = 1.01 (direct volume) - 0.44 ml; r = 0.972, SEE = 2.93 ml. Provided accurate cross-sectional localization is available, these studies suggest that extremely accurate steady-state left ventricular volume can be determined noninvasively in the ejecting heart from multiple cross-sectional images.

Reaction of the myocardium to cryosurgery: electrophysiology and arrhythmogenic potential.

Abstract: The acute and chronic electrophysiological effects of a cryolesion produced in the left ventricle were studied in six dogs. All dogs had frequent ventricular premature beats (VPB) and five of six dogs had ventricular tachycardia during the first 4 days after the cryolesion; only one of the six dogs continued to have VPBs after 1 week, and this dog had identical VPBs before the creation of the cryolesion. Neither control dog had VPBs. Two additional dogs underwent epicardial and transmural mapping studies immediately after production of a cryolesion. VPBs in these animals were shown to originate at the border of the cryolesion. Epicardial activation sequence during normal sinus rhythm was not altered by the chronic cryolesion. The border zone of the chronic cryolesion was sharply demarcated with normal potentials recorded outside of the lesion and "extrinsic" potentials recorded within.

Effects of spontaneous respiration on canine left ventricular function.

Abstract: The purpose of this study was to determine the mechanism of the decrease in left ventricular stroke volume during spontaneous inspiration. We determined the transmural pressures of the left heart by measuring left atrial and diastolic left ventricular pressures relative to esophageal pressure. We estimated the directional changes in end-systolic and end-diastolic volumes of the left ventricle by determining the transit time of sound transmission between two ultrasonic crystals facing each other across the minor axis of the left ventricle. Left ventricular stroke volume decreased with spontaneous inspiratory effort as pleural pressure fell, regardless of whether lung volume increased or remained constant. The stroke volume was decreased during the fall in pleural pressure because of an increase in end-systolic volume with an essentially unchanged diastolic volume. Thus, the decrease in stroke volume was due to a decrease in ejection, rather than a decrease in filling of the left ventricle. We believe that left ventricular ejection was impeded by the fall in pressure around the heart relative to the pressure in the aorta. In spite of the essentially constant diastolic volume, diastolic left ventricular transmural pressure rose, suggesting that spontaneous inspiration decreases the diastolic compliance of the left ventricle. The change in diastolic compliance contributed to the decrease in stroke volume but was not the primary cause.

Right and left ventricular function after the Mustard procedure in transposition of the great arteries.

Abstract: Right and left ventricular function was assessed at cardiac catheterization in 33 asymptomatic patients 0.5 to 11 years (mean 4.6) after the Mustard operation for complete transposition of the great arteries. Ages at operation had ranged from 0.5 to 16 years (mean 4.2 years). Right ventricular function was assessed using videodensitometric determination of ejection fraction and ventricular volume data. Ventricular volumes were obtained by computerized video analysis utilizing Simpson's rule. The right ventricular ejection fraction was 37 +/- 11 percent (standard deviation), as assessed with videodensitometry and 42 +/- 10 percent as assessed with ventricular volume--both values less than normal (P less than 0.001). Right ventricular end-diastolic volume was significantly greater than normal (P less than 0.001) and averaged 202 +/- 70 percent, but left ventricular end-diastolic volume averaged only 125 +/- 53 percent. These observations after the Mustard operation indicate that right ventricular function is seriously decreased with relatively preserved left ventricular function. They support efforts for surgical correction utilizing the left ventricle as the systemic ventricle.

Left ventricular systolic pressure-volume area correlates with oxygen consumption.

Abstract: In 13 excised, cross-circulated canine hearts, we studied the correlation between left ventricular oxygen consumption per beat (MVO2) and the magnitude of a specific pressure-volume (P-V) area circumscribed by the end-systolic and end-diastolic P-V relationship curves and the systolic segment of the P-V trajectory of a left ventricular contraction. The pressure and volume load of the ventricle were changed with a volume servo pump in order to alter the P-V area, and MVO2 was measured (after each change in the pressure and volume load). In the data collected from both isovolumic and ejecting contractions of each left ventricle contracting with a stable inotropic background, we found a linear correlation between MVO2 and the P-V area. The average correlation coefficient was 0.92 +/- 0.016 (SE). Linear regression analysis yielded the formula: MVO2 (ml/beat) = alpha[P-V area (mmHg.ml/beat)] + b, where alpha, the slope coefficient, was (1.53 +/- 0.14) x 10(-5) and b, which probably represents the basal O2 consumption, was 0.019 +/- 0.003 ml/beta. We propose that the P-V area as defined above may be a good index of ventricular oxygen consumption under a given inotropic background.