Pharmacologic and hemodynamic influences on the rate of isovolumic left ventricular relaxation in the normal conscious dog.

We studied the effects of acute pharmacologic and hemodynamic interventions on isovolumic left ventricular relaxation in 19 conscious dogs using micromanometer tip catheters. Isoproterenol (11 studies) augmented peak rate of rise of left ventricular pressure [(+) dP/dt] by 1,275+/-227 (SE) mm Hg/s (P < 0.001) and dP/dt at an isopressure point of 35 mm Hg during isovolumic relaxation [(-) dP/dt(35)] by 435+/-80 mm Hg/s (P < 0.001). Peak (-) dP/dt decreased by 467+/-89 mm Hg/s (P < 0.002). The time constant, T, derived from the logarithmic fall of pressure during isovolumic relaxation, shortened from 20+/-2.8 to 14.9+/-1.8 ms (P < 0.003). Calcium (11 studies) increased peak (+) dP/dt and (-) dP/dt(35) (both P < 0.0001); peak (-) dP/dt was unchanged. T shortened from 20.4+/-1.8 to 17.3+/-1.5 ms (P < 0.002). Volume (13 studies) did not affect either dP/dt or T. Phenylephrine (13 studies) augmented peak (-) dP/dt, but reduced (-) dP/dt(35) (both P < 0.01); T lengthened from 22.1+/-1.5 to 32.5+/-1.5 ms (P < 0.01). In 15 studies, rapid atrial pacing increased peak (+) dP/dt and (-) dP/dt(35) (both P < 0.01). In the first post-pacing beat, peak (-) dP/dt and (-) dP/dt(35) decreased (both P < 0.01), although peak (+) dP/dt increased further. T paralleled values of (-) dP/dt(35). In five dogs, beta adrenergic blockade had no significant effect on any variable after calcium, volume, or phenylephrine infusion or during or after atrial pacing when the pre-and post-propranolol states were compared. We conclude that positive inotropic interventions augment both left ventricular contraction and relaxation. The changes in isovolumic relaxation are independent of alterations in sympathetic tone produced by beta-adrenergic blockade. Peak (-) dP/dt may not be a valid measure of left ventricular relaxation rate during acute alterations in inotropic state or afterload.

Alterations of myocardial dynamic stiffness implicating abnormal crossbridge function in human mitral regurgitation heart failure.

Mitral regurgitation (MR) causes ventricular dilation, a blunted myocardial force-frequency relation, and increased crossbridge force-time integral (FTI). The mechanism of FTI increase was investigated using sinusoidal length perturbation analysis to compare crossbridge function in skinned left ventricular (LV) epicardial muscle strips from 5 MR and 5 nonfailing (NF) control hearts. Myocardial dynamic stiffness was modeled as 3 parallel viscoelastic processes. Two processes characterize intermediate crossbridge cycle transitions, B (work producing) and C (work absorbing) with Q(10)s of 4 to 5. No significant differences in moduli or kinetic constants of these processes were observed between MR and NF. The third process, A, characterizes a nonenzymatic (Q(10)=0.9) work-absorbing viscoelasticity, whose modulus increases sigmoidally with [Ca(2+)]. Effects of temperature, crossbridge inhibition, or variation in [MgATP] support associating the calcium-dependent portion of A with the structural "backbone" of the myosin crossbridge. Extension of the conventional sinusoidal length perturbation analysis allowed using the A modulus to index the lifetime of the prerigor, AMADP crossbridge. This index was 75% greater in MR than in NF (P=0.02), suggesting a mechanism for the previously observed increase in crossbridge FTI. Notably, the A-process modulus was inversely correlated (r(2)=0.84, P=0.03) with in vivo LV ejection fraction in MR patients. The longer prerigor dwell time in MR may be clinically relevant not only for its potential role as a compensatory mechanism (increased economy of tension maintenance and increased resistance to ventricular dilation) but also for a potentially deleterious effect (reduced elastance and ejection fraction).

Ingenuous interpretation of elevated blood levels of macromolecular markers of myocardial injury: a recipe for confusion.

Several assumptions about elevations of macromolecular markers of myocardial injury in blood require critical consideration. The dichotomy of modest, persistent elevations of troponins I and T as prognostic factors in patients with unstable angina and absent elevations of isoenzymes of creatine kinase is presently unexplained. Factors influencing the appearance of macromolecular markers of myocardial injury in blood are considered, including the need to estimate baseline values, to consider elevations as deviations from baseline rather than simply points within a distribution of baseline values in normal subjects, to recognize operative biochemical and physiologic determinants of marker release from injured myocytes and washout and to take into account the influence of apoptosis. Elucidation and consideration of mechanisms underlying the appearance of specific macromolecular markers in blood appear likely to improve diagnosis and explain the prognostic power of the troponins in patients with unstable angina. Detection of proteolytic breakdown products of troponins in blood is likely to explain the modest, persistent elevations seen in some patients with unstable angina and their prognostic implications.

Relation between left ventricular shape and exercise capacity in patients with left ventricular dysfunction.

OBJECTIVES: The aim of this study was to identify dynamic predictors of exercise duration in patients with systolic left ventricular dysfunction and to test the hypothesis that left ventricular shape is an independent determinant of exercise duration in these patients. BACKGROUND: Measurements of left ventricular volumes and ejection fraction at rest do not predict exercise capacity in patients with systolic left ventricular dysfunction. Left ventricular shape at rest has been reported to be an independent determinant of exercise duration in these patients. The significance of alterations in left ventricular shape that occur during dynamic exercise has not been investigated. METHODS: Twenty-one patients with a documented ejection fraction < 40% performed symptom-limited graded upright bicycle exercise with simultaneous quantitative two-dimensional echocardiography. End-diastolic volume, end-systolic volume, stroke volume, ejection fraction and sphericity index were measured at rest and peak exercise. RESULTS: Eleven patients exercised beyond stage II (6 min, 50 W), averaging 8.9 +/- 1.9 min; 10 patients were unable to complete stage II, averaging 4.9 +/- 0.9 min. No patient developed clinical evidence of ischemia during the exercise period. Of the echocardiographic variables considered, only end-systolic and end-diastolic sphericity indexes at peak exercise (r = 0.809 and 0.711, respectively) and the change in end-systolic sphericity index during exercise (r = 0.697) were strongly correlated with exercise duration. CONCLUSIONS: Conventional descriptors of left ventricular function are poor predictors of exercise capacity. Dynamic changes in heart shape correlate strongly with exercise duration and may be important determinants of exercise capacity in patients with systolic left ventricular dysfunction.

Effect of sodium nitroprusside on ventilation-perfusion mismatching in heart failure.

Sodium nitroprusside has been shown to lower arterial partial pressure of oxygen (PaO2) in patients with congestive heart failure and respiratory failure. The multiple inert gas elimination technique was used to evaluate the effect of sodium nitroprusside infusion on pulmonary gas exchange in five patients with congestive heart failure. During sodium nitroprusside infusion, mean values of cardiac output increased and mean values of arterial pressure, pulmonary artery pressure, pulmonary artery wedge pressure and pulmonary vascular resistance decreased. Cardiac output increased in each patient and PaO2 decreased in all but one patient (mean 75.6 +/- 15.1 to 68 +/- 17.5 mm Hg, p = 0.032). Distributions of ventilation and perfusion showed increased perfusion of lung units with low (less than or equal to 0.1) ventilation-perfusion ratios in all subjects during sodium nitroprusside infusion (mean 3.89 +/- 1.52 to 11.33 +/- 7.42% of cardiac output, p = 0.027, paired t test). The amount of shunt (fractional perfusion of lung units with ventilation-perfusion ratio = 0) increased in the two patients with some shunt present in the baseline measurements. The mean total low ventilation-perfusion perfusion (shunt plus ventilation-perfusion less than or equal to 0.1) was significantly increased from 4.38 +/- 1.54 to 14.7 +/- 9.37% (p = 0.023) during sodium nitroprusside infusion. Total low ventilation-perfusion perfusion was negatively correlated with mean pulmonary artery pressure and pulmonary artery wedge pressure (r = -0.949 and -0.946, respectively). Although sodium nitroprusside infusion increased cardiac output and overall oxygen transport in all patients, it worsened ventilation-perfusion mismatching. The mechanism is probably pulmonary vasodilation or increased cardiac output, or both.

Observations suggesting a high incidence of exercise-induced severe mitral regurgitation in patients with mild rheumatic mitral valve disease at rest.

OBJECTIVES: The aim of this study was to determine the hemodynamic effects of upright bicycle ergometry in symptomatic patients with mild, mixed mitral stenosis and regurgitation. BACKGROUND: Patients with seemingly mild rheumatic mitral valve disease often complain of exertional dyspnea or fatigue. These symptoms are usually ascribed to flow-dependent increases in the gradient across the stenotic mitral valve. Although catheterization studies in these patients may demonstrate an increase in mitral valve gradient proportional to an increase in cardiac output, this approach does not specifically address the underlying mechanism of any observed increases in mitral gradient or left atrial (i.e., pulmonary capillary wedge) pressure. Exercise echocardiography is uniquely suited to the dynamic assessment of exercise-induced hemodynamic changes. METHODS: Fourteen symptomatic patients with exertional dyspnea and mild mitral stenosis and regurgitation at rest performed symptom-limited upright bicycle ergometry with quantitative two-dimensional, Doppler and color Doppler echocardiographic analysis. RESULTS: Average pulmonary artery systolic pressure in the 13 patients with adequate spectral signals of tricuspid regurgitation increased from 36 +/- 5 mm Hg (mean +/- SD) at rest to 63 +/- 14 mm Hg at peak exercise (p < 0.001). The mean transmitral pressure gradient in all patients increased from 4.5 +/- 1.4 mm Hg at rest to 12.7 +/- 2.7 mm Hg at peak exercise (p < 0.001). Five patients developed severe mitral regurgitation during exercise. CONCLUSIONS: Patients with exertional dyspnea and mild mitral stenosis and regurgitation at rest demonstrate a marked increase in pulmonary artery systolic pressure and mean transmitral pressure gradient during dynamic exercise. In a subset of these patients, marked worsening of mitral regurgitation appears to be the underlying mechanism of this hemodynamic deterioration. Because of the small sample size, this novel observation must be considered preliminary with respect to the true prevalence of exercise-related development of severe mitral regurgitation. If additional studies confirm the importance of this phenomenon, it has important implications for the management of patients with rheumatic mitral valve disease.

Absence of cardioversion-induced ventricular arrhythmias in patients with therapeutic digoxin levels.

To determine the incidence of cardioversion-induced ventricular arrhythmias in patients with therapeutic serum levels of digoxin, 19 patients (average age [+/- standard deviation] 61 +/- 12 years) undergoing elective direct current cardioversion for atrial fibrillation were studied. Only patients with therapeutic serum digoxin levels (range 0.5 to 1.9 ng/ml; mean 1.1 +/- 0.5) at the time of cardioversion were included. Patients with acute myocardial ischemia or unstable angina, serious electrolyte disturbance or those requiring class I antiarrhythmic agents for control of ventricular or supraventricular arrhythmias were excluded. Ambulatory electrocardiograms were recorded for 24 hours before and 6 hours after cardioversion. No patient developed malignant ventricular arrhythmias (ventricular triplets or tachycardia) in the immediate 3 hour period after cardioversion. Furthermore, there were no significant (p less than 0.05) differences in the frequency of ventricular premature beats or couplets before and after cardioversion. To determine whether the level of serum digoxin or the strength of the applied shock had a significant effect on the development of postcardioversion arrhythmias, the change in frequency of single premature ventricular beats after cardioversion was compared with the serum digoxin level (ng/ml) and the applied energy level (joules) by means of linear regression analysis. There was no significant (p less than 0.05) relation between these variables. These findings suggest that patients with therapeutic serum levels of digoxin may safely undergo cardioversion without the concomitant use of class I antiarrhythmic agents.

Effects of oral equiblocking doses of a cardioselective and noncardioselective beta-adrenergic blocking agent on left ventricular function in the normal conscious dog.

The effects of propranolol, a noncardioselective beta-adrenergic blocking agent, and practolol, a cardioselective agent, on left ventricular function were compared in an awake dog model at an equiblocking dose range. Both agents produced modest depression of inotropic state at rest, and during volume and phenylephrine loading. No significant differences between the two agents were detected.

Hysteresis of left ventricular end ejection pressure-dimension relations after acute pressure loading in the intact canine heart.

The left ventricular end systolic pressure-volume relation of the isolated canine heart is linear and independent of the loading conditions. The effects of acute pressure loading on the left ventricular end ejection pressure-length relations were studied in the intact canine heart. The lengths of two wall segments of the left ventricle parallel to the minor axis were measured with pairs of miniature piezoelectric crystals. At two levels of filling pressure, with and without control of heart rate, acute increases in left ventricular afterload were produced for six successive beats by occluding the thoracic aorta. After abrupt release of this occlusion, at left ventricular end diastolic pressure less than 10 mmHg, end ejection lengths were longer than before the occlusion for both segments despite the same or lower end ejection pressures. When heart rate was not controlled the mean(SD) difference in end ejection length was 0.46(0.21) mm (n = 100). When heart rate was controlled by atrial pacing after autonomic blockade the difference was 0.37(0.11) mm (n = 80). In contrast, at left ventricular end diastolic pressure greater than 10 mmHg there was no significant difference between end ejection lengths before and after release of the aortic occlusion. Gradual release of the aortic occlusion over 4-5 beats produced clockwise hysteresis of the left ventricular end ejection pressure-length relation when left ventricular end diastolic pressure was less than 10 mmHg. No hysteresis occurred when left ventricular end diastolic pressure was greater than 10 mmHg. Hysteresis of the end systolic pressure-dimension relation was also seen when major and minor axis dimensions of the left ventricular were measured.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of oral propranolol in normal subjects.

The effects of oral propranolol were evaluated in 10 normal volunteers. The resting heart rate decreased from the mean control value of 68 plus or minus 3.3 (SE) to 56 plus or minus 2.8 beats per minute (bpm) on propranolol (p smaller than 0.001, paired test). Mean systolic blood pressur also decreased from 125 plus or minus 5.0 to 114 plus or minus 4.2 mm Hg (p smaller than 0.03). Resting systolic time intervals were unaffected by propranolol. Mean maximal treadmill exercise tolerance time was not significantly altered by propranolol although the mean heart rate systolic blood pressure product a maximal exertion was markedly decreased (1.91 plus or minus 0.17 vs 2.62 plus or minus 0.17 times 10-4, p smaller than 0.004) . The nonsignificant effect of oral propranolol on resting systolic time intervals and maximum exercise tolerance despite significant changes in heart rate and blood pressure at rest and duringexercise stand in contrast to the reported effects of intravenous propranolol. Explantations for this difference between the effects of oral and intravenous propranolol in normal subjects are examined.

Role of parietal pericardium in acute, severe mitral regurgitation in dogs.

Mitral regurgitation (MR) resulting from acute disruption of the mitral valve apparatus leads to serious hemodynamic sequelae. The lesion produces major elevation of left atrial (LA) and pulmonary artery pressures and decreases forward cardiac output. Clinical studies have shown hemodynamic patterns in acute MR similar to those seen in constrictive pericardial disease, suggesting that the pericardium serves to importantly limit cardiac filling in this condition. This hypothesis has not been tested in an animal model in which the intrapericardial pressure can be directly measured. In the present study intrapericardial and intracardiac pressures were measured in 8 dogs before and after the production of acute MR. After production of MR, mean LA pressure increased from 8 +/- 3 to 20 +/- 7 mm Hg (p = 0.004) and the peak LA V wave averaged 31 +/- 13 mm Hg. Mean right atrial pressure increased slightly, from 4 +/- 2 to 5 +/- 1 mm Hg (p less than 0.008). Intrapericardial pressure increased in each dog, but the increment was invariably small (1 +/- 2 to 3 +/- 2 mm Hg, p = 0.001) and there was no tendency to equalization of pressure between right- and left-sided cardiac chambers. Thus, the role of the pericardium in the immediate hemodynamic response to acute, severe MR is minor.

Relation between left ventricular shape and Doppler filling parameters in patients with left ventricular dysfunction secondary to coronary artery disease.

Left ventricular (LV) shape is an independent predictor of exercise capacity in patients with systolic LV dysfunction. Recent studies suggest that end-systolic LV shape is related to the generation of restoring forces during contraction that facilitate filling at lower LV pressure during subsequent diastole. To test the hypothesis that preservation of a more elliptical LV shape would be associated with a distribution of diastolic inflow characterized by increased early relative-to-late filling, 32 outpatients with coronary artery disease and ejection fraction < 40% underwent quantitative 2-dimensional and Doppler echocardiography. LV volumes, ejection fraction, and eccentricity index were measured as were standard Doppler indexes of LV filling. Simple and multiple linear regression models were used to examine relations between LV shape and Doppler measurements. LV eccentricity at end-systole correlated strongly with the Doppler atrial filling fraction (r = -0.670; p < 0.001) and the ratio of early-to-late flow velocity integrals (r = 0.648; p < 0.001). No other 2-dimensional echocardiographic variable was significantly correlated with any other Doppler index of LV filling. Thus, LV shape at end-systole appears to be an important determinant of diastolic filling patterns. In patients with systolic LV dysfunction, preservation of a more elliptical chamber is associated with a diastolic inflow pattern characterized by increased early relative-to-late diastolic filling.

Effect of enalapril therapy on left ventricular mass and volumes in asymptomatic chronic, severe mitral regurgitation secondary to mitral valve prolapse.

Quantitative 2-dimensional and Doppler echocardiography was used to assess the longitudinal effects of angiotensin-converting enzyme inhibition in asymptomatic patients with chronic, severe mitral regurgitation due to mitral valve prolapse. Over a 6-month period, angiotensin-converting enzyme inhibition therapy resulted in significant reductions in left ventricular volumes and mass in association with a minor reduction in regurgitant fraction.

Efficacy and safety of nicardipine for chronic, stable angina pectoris: a multicenter randomized trial.

Nicardipine, a new calcium channel blocking drug of the dihydropyridine family, was administered to 63 patients at a dose of 30 or 40 mg 3 times daily in a multicenter, randomized, double-blind, placebo-controlled, crossover trial. Nicardipine midly increased heart rate (HR) at rest and midly decreased the blood pressure (BP) at rest. When generally similar responses to the 30- and 40-mg doses were averaged, nicardipine produced a 7% increase in peak exercise HR, which was balanced by a 6% decrease in peak exercise BP. Thus, no change occurred in the exercise HR-BP product. With nicardipine, treadmill exercise duration increased 9%, time to angina increased 15%, time to 1-mm ST-segment depression increased 16%, and oxygen consumption at peak exercise increased 13%. Mean anginal frequency declined, as did mean weekly sublingual nitroglycerin consumption, but not significantly. There were more cardiovascular side effects with nicardipine than with placebo, with at least 3 patients having increased angina judged by investigators as probably related to the drug. Vasodilatory side effects were also more frequent with nicardipine, but were generally mild and well tolerated; the drug had to be discontinued in only 1 patient, because of vasodilatory effects. Nicardipine is effective and generally well tolerated in patients with chronic stable angina.

Left ventricular systolic torsion and early diastolic filling by echocardiography in normal humans.

This study describes a novel 2-dimensional echocardiographic technique to measure left ventricular (LV) systolic twist in humans and relates this measure to early ventricular filling. LV twist is the counterclockwise rotation of the left ventricle during systole when viewed from the apex. The effect of ventricular twist has been postulated to store potential energy, which ultimately aids in diastolic recoil, leading to ventricular suction. The generated negative early diastolic pressures may augment early ventricular filling. We measured ventricular twist in 40 patients with normal transthoracic echocardiograms. End-systolic twist was determined by measuring rotation of the anterolateral papillary muscle about the center of the ventricle. LV filling was assessed by analysis of transmitral Doppler flow velocities. The mean value obtained was 9 +/- 7 degrees of rotation. Twist measurements were highly reproducible with an intraobserver correlation coefficient of r = 0.881, p <0.001. The magnitude of ventricular twist was strongly correlated positively with acceleration of the mitral E-wave (r = 0.75; p <0.0001) and negatively with the mitral E-wave acceleration time (r = -0.83; p <0.0001).

Effects of exercise on left ventricular performance determined by echocardiography in chronic, severe mitral regurgitation secondary to mitral valve prolapse.

Data on the effects of exercise on left ventricular (LV) volumes and ejection performance in patients with severe mitral regurgitation (MR) are limited. With use of a matched-pairs design, 10 asymptomatic patients with chronic, severe MR and normal LV systolic function who were not receiving vasodilator therapy (group 1) and 10 matched normal control subjects with no structural heart disease (group 2) performed symptom-limited upright bicycle ergometry with quantitative echocardiographic analysis. An additional 8 patients with severe, chronic MR and normal LV systolic function who were receiving vasodilator therapy at the time of testing (group 3) were studied for comparison. The 3 cohorts exercised for similar periods of time. Group 1 and 3 patients had similar end-diastolic volumes at rest, both of which were significantly greater than those of normal controls. Although resting LV end-systolic volume was greater in groups 1 and 3 than in normal controls, the 3 groups had similar relative percent reductions in end-systolic volume during exercise (30 +/- 12%, 32 +/- 13%, and 30 +/- 24%; p = NS). A similar percent increase in LV ejection fraction was also observed in all 3 cohorts (18 +/- 9%, 15 +/- 9%, and 14 +/- 6%; p = NS). Forward stroke volume increased significantly in group 1 (59 +/- 21 and 71 +/- 18 ml; p <0.001) and in group 3 (59 +/- 17 and 68 +/- 13 ml; p < 0.05). Thus, in asymptomatic patients with chronic, severe MR and normal LV ejection fraction at rest, there is an improvement in LV ejection fraction and an increase in forward stroke volume during exercise. These effects are comparable to those observed in normal controls. Directional differences in the cohort receiving no activity therapy were indistinguishable from either patients receiving vasodilator therapy or normal control subjects.

Opacification phase effects of angiographic contrast medium on left ventricular size and function: influence of initial ventricular volume and the pericardium.

Prior studies of the opacification-phase effects of left ventricular (LV) injection of angiographic contrast medium (CM) on LV size and function have yielded discrepant results. A sensitive ultrasonic technique was used to measure LV dimension (Di) in 10 open-chest dogs with physiologic heart rates, and injection of saline (S) was compared with injection of CM. The influence of initial LV volume (LVVi) and that of the pericardium were analyzed. Changes in contractile state (CS) were assessed from the end-systolic (ES) pressure-Di relation. With both low and high LVVi, S and CM produced indistinguishable early (beat 5) increases in end-diastolic (ED) Di and ESDi. EDDi and ESDi subsequently returned to baseline after S but remained elevated through beat 12 after CM. The latter increase was progressive only with low LVVi. Depression of CS was evident by beat 7 after CM, while pericardiectomy did not alter the response to CM. Thus, CM produces opacification-phase depression of CS and increases in LV size which are in part dependent in LVVi.

Determinants of intrapericardial pressure in dogs.

This study investigates factors that influence the pressure measured in the intrapericardial (IP) space. Seven dogs were studied after they were anesthetized with pentobarbital sodium. With the chest closed, intravascular volume expansion by dextran infusion from a mean left atrial (LA) transmural pressure of 8.4 +/- 1.2 (SD) to 15.5 +/- 1.6 Torr caused an increase in mean IP of from 2.6 +/- 1.2 to 3.9 +/- 1.7 Torr (P less than 0.01). This reflected a predominant increase in the influence of the cardiac fossa (CF), which accounted for 56% of the IP pressure after volume expansion. In the open-chest state an increase in mean LA transmural pressure from 9.5 +/- 2.5 to 16.4 +/- 0.6 Torr caused IP pressure to increase from 1.1 +/- 0.9 to 3.0 +/- 1.6 (P less than 0.005), representing the influence of the elastic pericardium alone. The use of positive end-expiratory pressure (PEEP) significantly increased the influence of the CF. Of note, the relation of LA to right atrial (RA) pressure was significantly different with and without the influence of the CF; the RA-to-LA ratio was higher with the chest open under each set of volume conditions with and without PEEP. In four dogs, acute transection of the pericardiodiaphragmatic ligaments led to a small (1-2 Torr) but distinct drop in IP pressure. Thus, IP pressure is affected by the intracardiac volume, the elastic pericardium, the CF, and the pericardiodiaphragmatic attachments, all of which must be considered in an analysis of diastolic properties of the heart in situ.

Influence of the pericardium on right and left ventricular filling in the dog.

We compared the influence of the pericardium on left and right ventricular (LV, RV) filling by measuring LV and RV pressures and segment lengths (SL, LV free wall, and RV inflow and outflow tracts) in six open-chest, pentobarbital sodium-anesthetized dogs before and after pericardiectomy. End-diastolic pressure (EDP) was varied by partial caval occlusion and dextran infusion. At each site the ln EDP-SL relation was fitted by linear regression and characterized by its slope and 1-Torr EDP intercept. The slope and 1-Torr intercept of the LV ln EDP-SL relation changed variably after pericardiectomy, but in each dog a change occurred that shifted this relation downward. In contrast, the RV inflow tract slope invariably decreased significantly after pericardiectomy, whereas its intercept was unchanged in all but one dog. The RV outflow tract results were similar to the inflow tract but less consistent. By the use of the raw EDP-SL data points, we calculated that the absolute contribution of the pericardium to EDP (i.e., the effective pericardial surface pressure) was similar at the three sites. However, as EDP values increased the proportional contribution of the pericardium to right ventricular end-diastolic pressure (RVEDP) increased, whereas that to left ventricular end-diastolic pressure (LVEDP) remained relatively constant. As a result, at the higher EDP values tested, the pericardium was responsible for a larger proportion of RVEDP than LVEDP.(ABSTRACT TRUNCATED AT 250 WORDS)

Sonomicrometry: its application as a routine monitoring technique in cardiac surgery.

We utilized ultrasonic-dimension crystals in approximately 50 patients during a three-year period to evaluate clinical sonomicrometry as a routine monitoring tool in patients undergoing cardiac operations. Standard research piezoelectric pulse transit ultrasonic transducers were modified with a hooked attachment in a tethered configuration to facilitate accurate alignment and quick insertion for the measurement of myocardial segment length changes. These segment crystals were used both intraoperatively and postoperatively to evaluate the left ventricular pressure-geometry relationships and to serve as a continuous monitor of myocardial function. The left ventricular pressure-volume relationship was varied by temporarily reapproximating the pericardium (pericardial closure resulted in a 12% reduction in fractional shortening, a 5% decrease in end-diastolic segment length, and an 8% increase in pulmonary artery diastolic pressure). During both the intraoperative and postoperative periods, we found good correlation between thermodilution, stroke volume, and myocardial dimensions; no correlation was noted between pulmonary artery diastolic pressure and stroke volume. No bleeding or major complications resulted from the use of these sonomicrometry transducers. Our initial clinical experience with sonomicrometry seems to support its use as a potentially valuable monitoring tool.