Left Ventricular Pressure Curve Research Articles

Unusual left ventricular wall motion and a loud added sound during the isovolumic relaxation period in a patient with hypertensive heart disease.

A 69 year old woman with hypertensive heart disease had a loud added sound which coincided with a sudden interruption of the early diastolic motion of the left ventricular posterior...

Idiopathic restrictive cardiomyopathy in childhood. A diastolic disorder characterized by delayed relaxation.

Six children with idiopathic restrictive cardiomyopathy were evaluated. Electrocardiographic evaluation disclosed left atrial dilatation and repolarization abnormalities. Echocardiographic examination showed gross left atrial enlargement (182 +/- 29% of predicted values, P < 0.001) in the presence of normal left ventricular cavity dimensions (99 +/- 6%, P: ns). Left ventricular wall thickness varied from normal to mild concentric hypertrophy (septum: 116 +/- 16%, P < 0.05). Global left ventricular systolic function was normal or slightly subnormal; however, the relaxation was significantly delayed throughout diastole. E/A ratio was 4.1 +/- 1.4 and deceleration time 94 +/- 7 ms. Marked ventricular filling occurred in mid-diastole as could be deduced from a prominent mid-diastolic mitral L wave on the Doppler flow tracing. Early filling contributed 56 +/- 6%, mid-diastolic filling 28 +/- 4% and atrial contraction 16 +/- 3% to total ventricular filling as estimated by determining E-area, L-area and A-area, respectively. The left ventricular pressure curve showed a steady decline during mid-diastolic filling. This implies that the driving force for mid-diastolic filling is not the increased left atrial pressure but suction by the ventricle. The restrictive haemodynamics are therefore not caused by increased intrinsic stiffness of the ventricular wall, but most likely result from serious dysfunction and delay of the active relaxation of the ventricle. Progression of the disease was observed in three out of six patients, resulting in death or extreme low cardiac output. The three other patients remained clinically stable during the follow-up period of 6-10 years.

Cardiovascular responses to beta-stimulation with isoproterenol in deep hypothermia.

The aim of this study was to investigate the effects of beta-stimulation in deep (25 degrees C) hypothermia. Cardiac catheterization was performed on seven anesthetized beagle dogs. They were cooled between ice bags down to 25 degrees C and received isoproterenol administered intravenously three times: at the normal body temperature (37 degrees C) before cooling, after cooling at 25 degrees C, and after rewarming at 37 degrees C. Circulatory function was measured for every 1 degree C of temperature change. Isoproterenol infusion at 37 degrees C induced cardiac acceleration, including the increases of heart rate, cardiac output, and peak first derivative of the left ventricular pressure curve. Systemic vascular and mean outflow resistances and mean aortic pressure decreased. During cooling, shivering thermogenesis continued, even down to 25 degrees C. At 25 degrees C, cardiac acceleration after isoproterenol infusion did not exist but relaxation rate increased slightly. Systemic vascular and mean outflow resistances decreased, but left ventricular end-diastolic and filling pressures increased. beta-Stimulation at normal body temperature increases shivering thermogenesis during cooling. The venous return to the left ventricle at 25 degrees C increased after isoproterenol infusion while systemic vascular resistance decreased, indicating systemic vasodilatation. This increase in preload is probably due to vasoconstriction in pulmonary vessels, which may be mediated by prejunctional beta-adrenoceptors. For cardiac inotrophy, the isoproterenol had no physiologically significant effects at 25 degrees C. After rewarming at 37 degrees C, the effects of isoproterenol were physiologically similar to the effects at the same temperature before cooling.

The Efficacy of Amrinone or Adrenaline on Low Cardiac Output Following Cardiopulmonary Bypass in Patients with Coronary Artery Disease Undergoing Preoperative ß-Blockade

We examined 20 patients undergoing coronary bypass grafting for coronary artery disease with NYHA classifications of II and III who had been treated with beta-blocking agents. Patients were randomised for administration of either adrenaline (0.1 microgram/kg/min) or amrinone (bolus 1 mg/kg, continuous infusion of 5-10 micrograms/kg/min), if following cardiopulmonary bypass their cardiac index was < 2.4 L/min/m2 with normal peripheral resistance and normal or increased right- or left-ventricular filling pressures. Over a period of 1 hour, the hemodynamic parameters mean arterial pressure (MAP), cardiac index (CI), heart rate (HR), coronary perfusion pressure (CPP), total peripheral resistance (TPR), as well as the pressure-work index (PWI) were registered or calculated. By means of a coronary sinus catheter myocardial arterio-venous oxygen content difference (AVDO2cor), myocardial blood flow (MBF), using the thermodilution method, and myocardial oxygen consumption (MVO2) could be measured or calculated. Simultaneously, arterial and myocardial lactate concentrations and, using the arterio-venous lactate ratio, myocardial lactate extraction or production were quantified. Using a transseptal approach, the left-ventricular pressure curve was measured and used to differentiate for myocardial contractility (dp/dtmax). Following induction of anesthesia and after cardiopulmonary bypass, plasma levels of the used beta-blocking agent were determined. Both substances caused a significant increase in myocardial contractility, with adrenaline showing a more potent effect than amrinone. Both substances caused a significant increase in CI with a mild increase in HR. Amrinone caused a significant drop in TPR, while MAP remained practically constant.(ABSTRACT TRUNCATED AT 250 WORDS)

Logistic characterization of left ventricular isovolumic pressure-time curve.

Although some investigators have attempted to express the left ventricular pressure-time curve by mathematical functions such as exponential and sinusoidal functions, none of them reasonably fits the left ventricular pressure-time curve. In the present study, we hypothesized that a ventricular isovolumic pressure-time curve could be expressed as the difference between two S-shaped curves for pressure rising and falling, and proposed a new "hybrid logistic" function to express the left ventricular isovolumic pressure-time curve. We investigated how well this hybrid logistic function fits left ventricular isovolumic pressure curves experimentally observed under physiological preload and contractility in the excised cross-circulated left ventricles of 10 dogs. The new function precisely fitted the isovolumic pressure curves regardless of preload and contractility with correlation coefficients above 0.9996, much better than the previously proposed functions. The observed values characterizing the magnitude and time course of the isovolumic pressure curve such as peak +/- dP/dt also closely correlated with the corresponding theoretical values calculated by the present best-fit function. We conclude that our new hybrid logistic function reasonably characterizes the canine left ventricular isovolumic pressure-time curve within physiological ranges of preload and contractility. The present results indicate that this hybrid logistic function is useful to evaluate left ventricular contraction and relaxation comprehensively.

Noninvasive measurement of rate of left ventricular relaxation by Doppler echocardiography. Validation with simultaneous cardiac catheterization.

The instantaneous pressure gradient between the left ventricle and left atrium during systole can be calculated from the mitral regurgitation Doppler velocity curve. The purpose of our study was to determine the accuracy of measuring the time constant of relaxation (TAU) derived from the Doppler mitral regurgitation signal by comparing it with simultaneous high-fidelity left ventricular pressure measurements in humans. Twenty-five patients had continuous-wave Doppler mitral regurgitation recordings performed with simultaneous high-fidelity left ventricular pressure measurements. Fifteen of these patients had measurements of six to eight beats at various RR intervals. Doppler velocity curves were converted to left ventricular pressure curves by different methods through application of the modified Bernoulli equation at 3-msec intervals. The correlation between catheter-derived and Doppler-derived TAU was best when a zero asymptote and knowledge of the left ventricular end-diastolic pressure were used. A less optimal but acceptable method used the addition of 20 mm Hg to the Doppler-derived ventriculoatrial gradient. Use of a nonzero asymptote for calculation of TAU yielded poor correlation between catheter and Doppler measurements. The correlation of percentage change in Doppler-derived TAU plotted against percentage change in catheter-derived TAU was poor. The descending limb of the Doppler-derived mitral regurgitation velocity signal can be used as a semiquantitative estimate of the rate of ventricular relaxation. This method requires knowledge of left atrial pressure and may not be sufficiently accurate for detecting small changes in the rate of relaxation on a beat-to-beat basis.

Slope of the end-systolic pressure-volume relation derived from single beat analysis is not always sensitive to positive inotropic stimuli in humans

Single beat estimation of the slope of the end-systolic pressure-volume relation assumes symmetric left ventricular pressure increase and decay and requires extrapolation of peak isovolumic developed pressure (Pmax) from the left ventricular pressure curve of an ejection contraction. To test the sensitivity of this slope to positive inotropic stimuli, biplane cineangiocardiography and simultaneous high-fidelity left ventricular pressure measurements were performed in 50 patients with heart disease. The end-systolic pressure-volume relations were assessed under baseline conditions and during norepinephrine infusion (n = 19) or after postextrasystolic potentiation (n = 24), or both (n = 7). Norepinephrine did not change left ventricular end-systolic volume despite significant elevations of end-systolic pressure. Postextrasystolic potentiation significantly decreased end-systolic volume in association with an unaltered left ventricular end-systolic pressure. The potentiation significantly decreased the pressure half-time of contraction, an index of the speed of the left ventricular pressure increase, while it increased the pressure half-time of relaxation, an index of the speed of the pressure decline, indicating asymmetric pressure increase and decay. The slope of the end-systolic pressure-volume relation increased from 3.3 to 4.4 mm Hg/ml/m 2 (p < 0.001) during norepinephrine infusion. In contrast, despite an augmented contractility, the slope decreased significantly from 3.2 to 2.4 mm Hg/ml/m 2 (p < 0.0001) after the potentiation. The slope showed a high correlation with Pmax (r = 0.86, p < 0.0001, n = 107). Thus, the slope of the end-systolic pressure-volume relation derived from single beat analysis is not always sensitive to inotropic interventions. Its sensitivity is highly dependent on the accuracy of extrapolation of Pmax, and this assessment of the contractile state is limited especially when isovolumic contraction and relaxation are dissociated.

Noninvasive Assessment of Myocardial Oxygen Supply/Demand

The ratio between the integrated pressure difference between aorta and left ventricle during diastole (diastolic pressure-time index; DPTI) and the area beneath the systolic portion of the left ventricular pressure curve (systolic pressure-time index; SPTI) is an invasive estimate of myocardial oxygen supply and demand. In order to provide a noninvasive method to assess myocardial oxygen supply/demand, 42 patients (group I) without transaortic valvular pressure gradient and 10 patients (group II) with 57.6±26.4 mm Hg pressure gradient were evaluated

Single-beat estimation of the slope of the end-systolic pressure-volume relation in the human left ventricle.

This study assessed a new method of estimating the slope (Ees) of the end-systolic pressure-volume relation (ESPVR) from a single beat of the human heart. Left ventricular pressure was recorded with a high-fidelity micromanometer in patients with heart disease during left ventriculography. Peak isovolumic pressure at the end-disastolic volume was estimated by a curve-fitting technique from an isovolumic left ventricular pressure curve. The ESPVR line was drawn from the estimated peak isovolumic pressure-volume point tangential to the left upper corner of the pressure-volume loop. The slope of this estimated ESPVR line from single-beat analysis was compared with the slope of the ESPVR line obtained from three pressure-volume loops in 16 patients given angiotensin II or nitroglycerin infusion. The estimated Ees was 5.0 +/- 2.2 mm Hg/ml/m2, and the conventional Ees was 4.9 +/- 2.7 mm Hg/ml/m2. The estimated Ees showed a positive correlation with the conventional Ees (r = 0.91, p less than 0.001, SEE = 1.2 mm Hg/ml/m2). In the other 13 patients, after dobutamine infusion (5 micrograms/kg/min i.v.) the estimated Ees increased significantly from 5.6 +/- 1.4 to 7.4 +/- 2.0 mm Hg/ml/m2 (p less than 0.01). Thus, the estimated Ees approximated the conventional Ees and was sensitive to a positive inotropic intervention. We conclude that this single-beat analysis method facilitates assessment of the beat-by-beat ESPVR of the human heart.

Simulated left ventricular aneurysm and aneurysm repair in swine

Patch reconstruction of left ventricular aneurysm may be superior to linear closure, but this hypothesis has not been tested experimentally. Accordingly, six anesthetized domestic pigs were instrumented to measure regional left ventricular wall thickening, stroke volume, systolic left ventricular pressure, and myocardial oxygen consumption. With total bypass and cardioplegia, a 6 by 8 cm Dacron patch was inserted into the anteroapical left ventricle. Simulations were as follows: left ventricular aneurysm, patch open; patch reconstruction, 50% patch plication; standard repair, ventriculotomy edges approximated. Global function, from stroke work (stroke volume x integral of left ventricular pressure)-left ventricular end-diastolic pressure curves, was depressed in all three simulations compared with control. A tendency for stroke work to be greater for standard repair than for left ventricular aneurysm and patch reconstruction at higher preloads was not statistically significant. Mechanical efficiency, from stroke work/myocardial oxygen consumption (joules per milliliter oxygen per beat), was 2.43 +/- 0.52 (mean +/- standard error of the mean) (control), 2.22 +/- 0.94 (standard repair), 1.27 +/- 0.39 (patch reconstruction), and 1.09 +/- 0.37 (left ventricular aneurysm) (no significant differences). Regional work was calculated as regional left ventricular wall thickening x integral of left ventricular pressure. The slope of the regional work-end-diastolic wall thickness relation decreased in the posterior wall 14.0 +/- 2.9 (control) versus 8.4 +/- 2.0 (left ventricular aneurysm), 6.9 +/- 1.4 (patch reconstruction), and 7.4 +/- 1.4 (standard repair) (p less than 0.05). In the anterior wall, contractility did not change significantly (7.4 +/- 1.2, control; 7.8 +/- 2.7, left ventricular aneurysm; 5.0 +/- 0.4, patch reconstruction; and 5.3 +/- 0.4, standard repair). Decreased end-diastolic wall thinning anteriorly suggested tethering. These results in the normal left ventricle suggest that patch ventriculoplasty is of no greater benefit than linear repair. Either repair may impede function of adjacent myocardium through restriction of regional diastolic lengthening.

Transaortic Valve Gradient Determined by a Dual Lumen Pressure Monitoring Catheter

Simultaneous recordings of left ventricular (LV) and central aortic pressures (AO) provide the greatest accuracy for determination of the transaortic pressure difference. We describe a very simple technique for simultaneous measurement of LV and AO pressures using a new, dual lumen pressure monitoring catheter. Using this device, we compared simultaneous LV and AO as well as LV and femoral artery (FA) pressures before and after aortic valvuloplasty in seven consecutive patients. The difference between the mean aortic gradient or aortic valve area determined by the LV‐AO and LV‐FA measurement techniques was not statistically significant. Our initial experience with the double lumen pigtail catheter indicates that this device facilitates direct measurement of the LV‐AO pressure gradient and eliminates the need for two arterial punctures, a transseplal approach or alignment of LV and FA pressure curves.

Square root sign of left ventricular diastolic pressure curve in atrial septal defect.

The square root (dip and plateau) sign was observed in 7 of 21 adult patients with atrial septal defect (ASD). This study evaluated left ventricular (LV) diastolic filling dynamics and hemodynamic findings in 7 patients (Group 1) with, and 14 patients (Group 2) without the square root sign; 10 normal subjects (Group 3) served as controls. No significant differences were observed in LV end-diastolic and end-systolic volumes, ejection fraction, or left to right shunt. In Group 1, 77% of LV filling was completed in the first half of diastole; this percentage was 49% and 53% in Groups 2 and 3, respectively (both p less than 0.01 versus Group 1). Early diastolic filling velocity (at 20% of diastole) in Group 1 was significantly greater, and late diastolic filling velocity (at 80% and 90% of diastole) was reduced in Group 1 compared to those in Groups 2 and 3 (all p less than 0.05). The average values for right and left ventricular end-diastolic pressures were significantly higher in Group 1 (11 +/- 2 and 10 +/- 4 mmHg, p less than 0.05) than Group 2 (7 +/- 2 and 7 +/- 2 mmHg, p less than 0.05). It is suggested that a constrictive pathophysiology due to 4 chambers interaction or right ventricular constraint may play a role in the genesis of the square root sign in ASD.

The effect of atrial dilatation on the genesis of atrial arrhythmias.

The effect of atrial stretching on the genesis of atrial arrhythmias was studied in 26 dogs. Left atrial dilatation was produced by inflation of a balloon catheter. Electrophysiological studies were performed by programmed electrical stimulation of the atrium and ventricle. The irritability of the atrium markedly increased when it was distended and atrial arrhythmias (sustained or non-sustained atrial tachyarrhythmias) could regularly be induced by administration of an early extrastimulus or--more rarely--by atrial burst pacing. In 10 cases spontaneous atrial tachycardia appeared during atrial balloon dilatation. The atrial effective refractory period shortened and the atrial conduction time lengthened on atrial stretching, while other electrical variables (cycle length, sinus node recovery time, atrioventricular conduction time, intraventricular conduction, ventricular refractory period, QT interval) remained unchanged. Atrial balloon dilatation was not accompanied by marked haemodynamic changes, and the left ventricular pressure curve, the contractility of the left ventricle and the central venous pressure did not change significantly on atrial stretching. The experimental data suggest that the atrial dilatation plays an important part in the pathogenesis of atrial arrhythmias.

Validation of continuous-wave Doppler measurements of mitral valve gradients during exercise--a simultaneous Doppler-catheter study.

In patients with mitral stenosis, continuous-wave Doppler measurements of the maximal transmitral inflow velocity can be converted into transvalvular pressure gradients using the modified Bernoulli equation. Because of close correlations between Doppler- and catheter-measured gradients this method has become a valuable tool in non-invasive evaluation of mitral stenosis at rest. However, in some patients, exercise studies are necessary to determine the haemodynamic significance of the valve stenosis. The accuracy of continuous-wave Doppler in this setting has not yet been validated. Thus, in 20 selected patients with pure or predominant mitral stenosis, continuous-wave Doppler echocardiography was performed during left- and right-heart catheterization. At rest and during submaximal bicycle exercise, Doppler and pressure measurements were simultaneously performed. The Doppler gradient was calculated according to the modified Bernoulli equation while the mean manometric gradient was determined from the simultaneous pulmonary wedge and left ventricular pressure curves. Exercise caused a significant increase of cardiac output (4.8 +/- 1.3 to 5.7 +/- 1.31 min-1) and heart rate (59.7 +/- 12.0 to 95.3 +/- 14.3 beats min-1). The mean Doppler gradient increased from 6.8 +/- 2.1 to 12.2 +/- 3.2 mmHg. The manometric gradient showed a comparable increase of 9.5 +/- 2.4 to 17.2 +/- 3.7 mmHg, respectively. Correlation between Doppler and manometric data was close (y = 0.79x-0.67,r = 0.90,SEE = 0.97 mmHg) at rest and still good during exercise (y = 0.71x-0.10,r = 0.82,SEE = 1.97 mmHg). Thus, in some patients with borderline resting gradients and valve areas, exercise Doppler might allow further identification of the haemodynamic severity of mitral stenosis.

Effects of captopril on left ventricular structure and function in SHR with established hypertension.

While antihypertensive therapy is considered to be an important clinical intervention in hypertensive patients, its effects on cardiac structure and function have not been intensely evaluated. In this study we tested the hypotheses that lowering blood pressure (BP) with the angiotensin I-converting enzyme inhibitor captopril, would: 1) normalize left ventricular mass and increase the cardiocyte mitochondria/myofibrils volume (Vmito/Vmyo) ratio; and 2) not compromise peak ventricular performance. We treated 16-week-old SHR and WKY with captopril (40-80 mg/kg) and hydrochlorothiazide (500 mg/l) via their drinking water. After six weeks of treatment peak cardiac performance was measured during rapid volume overload. Tissue samples from the left ventricular wall were analyzed by electron microscopy and stereology. Captopril lowered BP in SHR and WKY but had no affect on the left ventricular/body weight ratio. The only intracellular change in treated SHR was an increase in sarcoplasmic volume density. Treated WKY exhibited decreased midmyocardial mitochondrial volume density. At peak cardiac output, acceleration of flow and cardiac index were not affected by treatment. Stroke work at peak cardiac output was decreased in the treated groups due to a decrease in mean arterial pressure. In addition, captopril treatment resulted in a shift of the cardiac output (CO)-left ventricular end diastolic pressure (LVEDP) curves, such that LVEDP at peak cardiac output was approximately 50% less in the treated groups compared to their respective control groups. Although captopril was efficacious in lowering BP, it is suggested that lowering BP with this agent does not, at least within six weeks, lead to a reversal of hypertrophy or to a significant alteration in the volume densities of myofibrils and mitochondria. However, an important effect of this antihypertensive drug which may be of clinical significance, is that it leads to a leftward shift of the CO-LVEDP curve in both hypertensive and normotensive rats.

Digitizing and signal averaging of left ventricular pressure signals using a dedicated radionuclide imaging system.

A method for obtaining left ventricular (LV) volume curves, synchronized with average LV pressure (LVP) curves for calculation of LV contractility, is described. Multiple gated blood pool imaging was performed to calculate average LV volume curves. Simultaneously with this acquisition, LVPs and aortic pressures were measured by indwelling catheters and recorded on an FM tape recorder. These signals were fed to the computer as image information and averaged and processed by the software developed for this purpose. Pressure resolution of the calibrated images was 4 mmHg/pixel when provision was made for a maximum pressure of 200 mmHg. A good correlation (r = 0.99) was obtained between the calculated peak LVPs and mean peak LVPs read from the chart recorder. The regression equation was: digitized peak LVP = 1.04 x chart recording--5.11 mmHg and the standard error of the estimate was 2.9 mmHg. Similar results were obtained with the aortic pressure (AP) measurements (digitized AP = 0.94 x chart recording + 6.37 mmHg, the standard error of the estimate was 3.8 mmHg). The digitized data also allowed the construction of pressure-volume loops for interpretation of ventricular contractility.

Anabolic steroids alter the haemodynamic responses of the canine left ventricle

The effect of an anabolic steroid on canine left ventricular function was studied by catheterization exposing control (n = 7) and methandienone-treated (n = 6) dogs to pacing, volume and isoproterenol tests at the beginning of the experiment and 6 weeks later. The physical performance of the animals was evaluated by submaximal exercise test (SMT), in which the steroid-treated dogs had lower heart rate than the sedentary controls (P less than 0.001). Heart weight was greater in the steroid than in the control group (P less than 0.05). Isoproterenol infusion increased the maximum value of the left ventricular pressure curve (dP/dtmax) less in the steroid-treated than in the control animals (P less than 0.05). Also heart rate was lower in the steroid than in the control group after inotropic load, while end-diastolic, end-systolic and stroke volumes decreased significantly more in the control group (P less than 0.05). Systemic vascular resistance decreased in the steroid treated animals, but remained unchanged in the control group (P less than 0.05 between the groups). During volume overload dP/dtmax increased in the control group but decreased slightly in the steroid group (P less than 0.05 between the groups). The pressure-volume diagram showed that the left ventricle of the steroid-treated animals worked on higher ventricular volumes than in the control group. In conclusion, long-term methandienone treatment results in cardiac hypertrophy in dogs, reduces its response to an inotropic loads and leads to working on larger ventricular volumes.

Modeling the isovolumic relaxation period

The isovolumic relaxation period of the left ventricular pressure curve in man has been assumed to be best represented by an exponential decay. To determine which model most closely approximates the empiric pressure data of isovolumic relaxation in man, several models were compared. They included linear, exponential with a zero mmHg pressure asymptote, exponential with a variable asymptote, and second-to fifth-order polynomials. In addition, four different methods of computing parameters of isovolumic relaxation by the exponential model with a variable asymptote were tested. It was found that the isovolumic relaxation period approximates an exponential, that the theoretic asymptote is variable, and that the Levenburg-Marquardt algorithm can be used efficiently to model this period.

Time constant of isovolumic pressure fall: new numerical approaches and significance.

The effects of left ventricular diastolic pressure changes on the values of the time constant (T) of isovolumic pressure fall are controversial. Normally, T is calculated either by linear regression of 1n left ventricular pressure (LVP) vs. time (TL) or by using an exponential model with asymptote (PB, extrapolated base-line pressure to which LVP would fall if decay continued indefinitely). This study, in intact dogs, has been designed to revise the effects that drugs that alter load (angiotensin and nitroprusside, without and with autonomic blockade) and inotropism (isoproterenol and propranolol) might have on the relaxation rate using different numerical methods. We found that 1) the upward or downward translation of the LVP curve had an important effect on the value of TL calculated by the semilogarithmic method; 2) when a model with asymptote was used, the simultaneous changes of T and PB, were not related to the dose of the drug; 3) the values of TL and the -dP/dt values extrapolated to 15 mmHg from a model with PB, were much more sensitive to beta-agonist or antagonist drugs than to others whose action was through load alteration. We feel that some of the earlier studies on relaxation rate determinants should be revised as possibly some of the conclusions have been based on artifacts introduced by the method chosen for the computation of the relaxation parameters.

Left ventricular pressure-volume diagrams and end-systolic pressure-volume relations in human beings

Assessment of left ventricular pressure-volume relations serially in response to altered loading conditions and heart rate has been difficult to achieve with contrast ventriculography. Accordingly, to study changing pressure-volume relations during altered loading and heart rate, left ventricular pressure and radionuclide absolute volume curves (obtained using a counts-based method with attenuation factor corrections) were recorded in 20 patients. Ventricular pressure and radionuclide volume curves were digitized and synchronized to end-diastole, and pressure-volume plots were subsequently constructed from 32 pressure-volume coordinates throughout the cardiac cycle. In all patients, the correlation between radionuclide absolute volumes and angiographic ventricular volumes was r = 0.92. In 10 patients in whom both radionuclide and angiographic pressure-volume diagrams were constructed, the agreement between the two methods was excellent. With this method, end-systolic pressure-volume relations were examined during altered left ventricular loading conditions, pacing-induced incremental increases in heart rate and pacing-induced ischemia. Using pharmacologically induced changes in left ventricular loading conditions, the slope and volume intercept of the end-systolic pressure-volume line could be calculated as a means of assessing basal contractility. During pacing-induced tachycardia, the slope and volume intercept of the end-systolic pressure-volume line could be calculated to quantify the Treppe effect and assess negative inotropic changes secondary to ischemia. This study supports the validity of using serial recordings of left ventricular pressure and radionuclide volumes to assess left ventricular pressure-volume relations, and indicates that this approach may be useful in the analysis of end-systolic pressure-volume relations in patients.