An eight-electrode conductance catheter previously developed by us and used to determine stroke volume in dogs was applied in human beings and dogs to measure absolute left ventricular volume quantitatively. For calibration we developed the formula V(t) = (1/alpha)(L2/sigma b)G(t) - Vc, where V(t) is time-varying left ventricular volume, alpha is a dimensionless constant, L is the electrode separation, sigma b is the conductivity of blood obtained by a sampling cuvette, and G(t) is the measured conductance within the left ventricular cavity. Vc is a correction term caused by the parallel conductance of structures surrounding the cavity and is measured in two ways. The first method, applicable in the anesthetized animal, consists of temporary reduction of volume to zero by suction. The second method uses a transient change in sigma b by injection of a small bolus of hypertonic saline (dogs) or 10 ml of cold glucose (humans) into the pulmonary artery. The validity of the formula was previously established for the isolated postmortem canine heart. The predicted linearity, slope constant alpha, and accuracy of Vc for the left ventricle in vivo were investigated by comparing the conductance volume data with results from independent methods: electromagnetic blood flow measurement for stroke volume and indicator dilution technique for ejection fraction (dogs), thermal dilution for cardiac output (12 patients), and single-plane cineventriculography for V(t) (five patients). In all comparisons, linear regression showed high correlation (from r = .82 [n = 46] to r = .988 [n = 20]) while alpha, with one exception, ranged from 0.75 to 1.07 and the error in Vc ranged from 0.5% to 16.5% (mean 7%). After positioning of the catheter, no arrhythmias were observed. It is concluded that the conductance catheter provides a reliable and simple method to measure left ventricular volume, giving an on-line, time-varying signal that is easily calibrated. Together with left ventricular pressure obtained through the catheter lumen, the instrument may be used for instantaneous display of pressure-volume loops to facilitate assessment of left ventricular pump performance.

To improve assessment of ventricular function during cardiac catheterisation there should be available a continuous registration of stroke volume and cardiac output in addition to ventricular pressure. To obtain the desired volumetric quantities a catheter has been developed which measures changes in intraventricular dimensions by electrical impedance. For this purpose, the catheter is equipped with eight electrodes spaced over a distance equal to the long axis of the left ventricle into which it is introduced. A constant current is imposed between the outermost electrodes while the inner six are used to measure resistance of volume segments of the blood contained within the ventricular cavity. The difference in resistance at the beginning and end of ejection is proportional to the contribution of each segment to stroke volume, which follows from addition of the segmental terms. Calibration is obtained by measuring electrical conductivity of a blood sample. The catheter was tested over a tenfold range of cardiac output, both in vitro, using an artificial heart model, while performance in vivo was evaluated in 12 dogs. In the animal study, stroke volume and cardiac output from the catheter were compared with flows obtained with an electromagnetic flowmeter. In both studies, linear regression analysis showed excellent correlation of cardiac output (r = 0.99, n = 10 in vitro, r = 0.95, n = 126 in vivo) while the regression equations were close to those of identity. Very good correlation (r = 0.98, n = 28) was also obtained for stroke volumes on a beat to beat basis during arrhythmia. It is concluded that the catheter, which has great potential for application in man, fulfills its primary aim of continuously recording stroke volume and cardiac output.

The effects of mechanical changes in loading conditions on the left ventricular end-systolic pressure-volume relation (ESPVR) were studied in nine open-chest dogs, including three dogs studied before and after beta-adrenergic blockade. Left ventricular pressure was measured with a micromanometer, and left ventricular volume was measured with a conductance catheter. ESPVRs were obtained by increasing left atrial inflow over wide volume ranges (as much as threefold) under three different conditions: control or high or low aortic impedance. High impedance was obtained by occlusion of the descending aorta, and low impedance was obtained by a shunt between the subclavian artery and the left atrium. In the unblocked animals in 21 of 28 runs, a second-order polynomial equation gave a better fit for the ESPVR than a linear relation. To quantify the effects of the changes in aortic impedance on the ESPVR, we calculated from the quadratic equation its volume intercept (V18) and its local slope (E18) at an end-systolic pressure (Pes) of 18 kPa. In the unblocked animals, a statistically significant difference was found in V18 between low impedance (21.50 +/- 6.27 ml) and high impedance (14.10 +/- 8.98 ml; p less than 0.005) and between control (19.14 +/- 9.58 ml) and high impedance (p less than 0.05). In most dogs, E18 was increased at high and decreased at low impedance, but not significantly. In the additional experiments with beta-blockade, the nonlinearity diminished somewhat, but the load dependency of the ESPVR remained present after beta-blockade because the same leftward shift of the ESPVR with high aortic impedance was found. Two other relations, namely, of dP/dtmax and of stroke work versus end-diastolic volume, were also investigated, which on the whole showed the same behavior as the ESPVR. These results indicate that the ESPVR and dP/dtmax-Ved and stroke work-end-diastolic volume relations, when studied over a wide volume range, are nonlinear and that changes in loading conditions influence indexes of contractility derived from these relations, especially the volume intercepts, in such a way that an increase in aortic impedance may be interpreted as an increase in contractility. Blocking the beta-adrenergic receptors did not influence the load dependency of the ESPVR but, in some cases, tended to decrease the nonlinearity in concordance with the relation between contractility and nonlinearity in isolated hearts.

The influence of different types of loading intervention on the resulting end-systolic pressure-volume relation (ESPVR) of the left ventricle in situ was investigated in anesthetized open-chest dogs. Left ventricular volume was measured by conductance catheter and pressure was measured by tip-micromanometer. Two loading interventions were applied: a pressure intervention (INp) by gradually occluding the descending aorta and a volume intervention (INv) by rapidly infusing 180 ml blood into the vena cava. The pressure-volume loops during an intervention always showed a linear ESPVR, the slope of which, Ees, was calculated. Possible method-related artifacts were assessed and could be excluded. Results from 16 dogs show that Ees(INp) was always larger (1.37 +/- 0.45 kPa/ml) than Ees(INv) (0.73 +/- 0.32 kPa/ml) (p less than 0.001). This difference was enhanced by beta-blockade through metoprolol. The same phenomenon was found for the slope (SdPV) of the relation between dP/dtmax and end-diastolic volume: SdPV(INp) = 45.17 +/- 22.63 kPa/ml/sec and SdPV(INv) = 20.55 +/- 11.13 kPa/ml/sec. In seven dogs, a right heart bypass was performed to study the influence of stroke volume on the ESPVR by applying a pressure intervention under three conditions: with constant end-diastolic volume (decreasing stroke volume), Ees = 2.27 +/- 0.79 kPa/ml; with constant stroke volume, Ees = 1.59 +/- 0.51 kPa/ml; and with increasing stroke volume (and increasing end-diastolic volume), Ees = 1.36 +/- 0.49 kPa/ml. Analysis of variance revealed a statistically significant relation between Ees and stroke volume (p less than 0.01). From the right heart bypass experiments, we conclude that shortening-related deactivation plays a role in the observed behavior of the ESPVR. However, the results from the series with intact circulation indicate that aortic occlusion has an additional effect on the slope of the ESPVR, leading to increased myocardial inotropism, perhaps mediated through a peripheral stimulus in response to decreased perfusion.

Pharmaceutical treatment and implementation of cardiac rehabilitation programs have improved the prognosis of patients with acute myocardial infarction (AMI).¹ To achieve maximum benefit, compliance with medication intake and cardiac rehabilitation are essential for decreasing the risk of recurrent AMI, heart failure, and cardiovascular mortality. A recent study² showed that nonadherence to β-blockers, angiotensin-converting enzyme inhibitors, and statins was associated with an increase in cardiovascular-associated and all-cause mortality in patients with coronary artery disease. Other studies³ have shown that patients who are better informed are more adherent to therapy. Therefore, there is a need for an intervention that may help to improve the compliance of patients with guideline-based therapy.

A number of fundamental mechanical properties of cardiac muscle as well as of the total ventricle are discussed. These include: Starling's law, shortening deactivation, homeometric autoregulation, and so-called hyperactivation associated with a small amount of ejection. Whenever appropriate, muscle properties are related to those of the intact ventricle. The phenomenon of load-dependence of the end-systolic pressure-volume relationship (ESPVR) receives particular attention and is placed within the framework of shortening deactivation and homeometric autoregulation. However, this effect also leads to a more basic definition of myocardial contractility, based on the observed, rather parallel shift of the ESPVR with different afterload conditions. Using this definition, the conclusion is drawn that an increase in afterload is, in fact, met by the left ventricle increasing its inotropic state. Finally, within this approach, it is proposed that the value of end-systolic volume at a chosen constant end-systolic pressure (e.g. 13 kPa or 100 mmHg) be used to characterize changes in myocardial contractility in patients after an intervention. The way of obtaining this parameter is explained.