[Combined acute ascending aneurysm and chronic descending thoracic aneurysms].

A 66-year-old woman with a known chronic descending thoracic dissecting aneurysm was admitted following a chest X-ray which revealed a widening in the mediastinum and an increased cardiothoracic ratio. Echocardiography and chest CT showed a combined ascending thoracic dissecting aneurysm with a tripple lumen, pericardial effision, moderate aortic regurgitation, and the chronic descending thoracic dissection with incompletely thrombosed aneurysm. The chest CT also showed a normal aortic arch. The diagnosis was then made as combined acute ascending aortic dissection (DeBakey II) and chronic descending aortic dissection (DeBakey III). A 2-stage operation was planned, involving first a graft replacement of the ascending aorta, and then one month later a graft replacement of the descending aorta.

Contractile function of isolated feline cardiocytes in response to viscous loading.

The classical force-velocity relationship is a standard measure of the contractile function of isolated linear cardiac muscle, but no such simple index of contractile function exists for the isolated mammalian cardiocyte. Therefore, this study established an analogous viscosity-velocity relationship for the characterization of cardiocyte contractile function. For this purpose, force was imposed on unfettered adult feline cardiocytes as a series of defined viscous loads, which provided resistance to cardiocyte shape changes during contraction. This was done by increasing the viscosity of the Krebs superfusate (37 degrees C, pH 7.4) in graded, reproducible steps from 1 to 500 centipoise by the addition of methylcellulose. Sarcomere motion within each contracting cardiocyte was measured as movement of the diffraction pattern cast onto a photodiode array by a laser beam passing through the cell. Both the rate and extent of sarcomere shortening varied inversely with increasing viscosity, whereas neither resting sarcomere length nor osmolarity was altered. Further, increased inotropism effected by paired-pulse stimulation of cardiocytes caused an upward shift of the entire viscosity-velocity relationship. Thus the cardiocyte viscosity-velocity relationship is analogous in form to the force-velocity relationship of isolated linear cardiac muscle and provides a simple reproducible method for characterizing the contractile performance of relatively large numbers of cardiocytes isolated from a single specimen of myocardium.

Correlation of force-length area with oxygen consumption in ferret papillary muscle.

The ventricular systolic pressure-volume area correlates well with myocardial oxygen consumption. However, in isolated muscle preparations, there are experimental data based on both mechanical and energetic measurements that suggest that the pressure-volume area concept may not obtain. In the present study, force-length area, the analog of pressure-volume area for a linear muscle, was examined in the ferret papillary muscle preparation under a wide range of loading conditions. There were two major findings: first, force-length area is closely correlated with oxygen consumption (r = 0.94-0.98); this correlation is better than those for such other indexes as peak force and force-time integral. Furthermore, this relation of oxygen consumption with force-length area is independent of the mode of contraction (isometric or shortening), while the relations with the other indexes are not. Second, quick release imposed after end-systole during isometric contraction was found to curtail oxygen consumption. The first finding, the optimal correlation of force-length area with oxygen consumption, suggests both that the correlation of pressure-volume area with oxygen consumption on the ventricular level arises from a basic property of cardiac muscle and that force-length area may be the best mechanical index to use in calculating regional oxygen consumption for a ventricular segment. The second finding, however, suggests that the time-varying elastance model, on which the concepts of pressure-volume area and force-length area are based, may not provide a complete description of the mechanical basis of cardiac muscle energetics, especially during the isometric contraction.

Evaluation of right ventricular function in patients with idiopathic dilated and ischemic cardiomyopathy by equilibrium radionuclide ventriculography.

We performed equilibrium radionuclide ventriculography in 12 patients with idiopathic dilated cardiomyopathy, 11 patients with ischemic cardiomyopathy and 11 normal subjects to determine whether measurements of right ventricular function could be used to distinguish dilated cardiomyopathy from ischemic cardiomyopathy. The left ventricular ejection fraction in patients with dilated cardiomyopathy (26 +/- 8%, mean +/- SD) or ischemic cardiomyopathy (32 +/- 5%) was significantly lower than in normals (69 +/- 6%, p less than 0.001). The right ventricular ejection fraction (RVEF) in normals was 57 +/- 7%. RVEF was decreased in 11 of 12 patients with dilated cardiomyopathy and the mean value (32 +/- 10%) was significantly lower than that in patients with ischemic cardiomyopathy (56 +/- 7%, p less than 0.001), none of whom had decreased RVEF. Our data show that right ventricular dysfunction commonly exists in patients with dilated cardiomyopathy but not in patients with ischemic cardiomyopathy. This finding may be useful in the differentiation between dilated and ischemic cardiomyopathy.

Detection of different blood flow patterns in the true and false lumina with aortic root dissection by pulsed Doppler echocardiography.

We report a 53-year-old man with aortic dissection, in whom pulsed Doppler echocardiography showed two different flow patterns within the dilated aorta. Although two-dimensional echocardiography has been successful in making the diagnosis of aortic root dissection, several conditions producing false positives have also been noted. Simultaneous recording of pulsed Doppler echocardiography may be useful to provide additional diagnostic clues in selected cases.

Right and left ventricular dysfunction in patients with dilated cardiomyopathy: a study with equilibrium radionuclide ventriculography.

Right and left ventricular function was evaluated in 28 patients with dilated cardiomyopathy to determine whether both ventricular functions were equally impaired in each patient. The ejection fractions of both ventricles were measured using equilibrium radionuclide ventriculography. In 13 patients the left ventricular ejection fraction (LVEF) was lower than the right ventricular ejection fraction (RVEF) by 6% or more, their mean values being 24 +/- 8% (mean +/- SD) and 37 +/- 7%, respectively (group 1). The difference between the LVEF and RVEF was less than 6% in nine patients; LVEF 29 +/- 8% and RVEF 30 +/- 7% (group 2). In six patients the RVEF was lower than the LVEF by 6% or more, and their mean values were 21 +/- 6% and 37 +/- 10%, respectively (group 3). The frequency of ventricular tachycardia, which was determined by the Holter ECG, was significantly higher in group 3 (100%, 6/6) than in the others (group 1 + 2; 41%, 9/22), p less than 0.05. The NYHA functional class correlated well with the LVEF, but not with the RVEF. It was concluded that the left and right ventricular functions are not necessarily equally impaired in patients with dilated cardiomyopathy, and that the difference may correlate with their clinical features.

Length dependent potentiation and inhibition of post-rest twitch tension development in adult cat and kitten papillary muscles.

If a rest interval is applied to a regularly stimulated cardiac muscle, the first contraction after this interval (post-rest contraction) has either a greater (post-rest potentiation) or a smaller (post-rest inhibition) developed tension than the regular contraction. Positive inotropic interventions will augment the post-rest potentiation and reduce the post-rest inhibition. We examined the effects of muscle stretching on the post-rest contraction in papillary muscles isolated from adult cats and from kittens and compared the effects with those of two typical inotropic interventions: high frequency stimulation and high calcium concentration. We found that muscle stretching augmented the post-rest potentiation and reduced the post-rest inhibition in a manner similar to the two inotropic interventions in the adult cat papillary muscle, and that these effects were consistently reversed in the kitten papillary muscle. The similarity of the effect of muscle stretching to those of the two typical inotropic interventions in either adult cat or kitten papillary muscle suggests that the effect of muscle stretching is due to an inotropic effect of muscle length change.

Normalization of end-systolic pressure-volume relation and Emax of different sized hearts.

A shift of the ventricular end-systolic pressure-volume (P-V) relation and a change in its slope Emax reasonably reflect a change in contractility in a given ventricle. However, comparison of Emax's of different sized hearts may be difficult without an appropriate normalization. We attempted to normalize Emax of different sized hearts to the force-length (F-L) relation of unit mass of myocardium in the ventricular wall. We formulated the end-systolic P-V relation as (end-systolic pressure) = Emax (end-systolic volume Vi - Vd), where Vd = volume axis intercept of the end-systolic P-V relation line. As a first step, both thick wall sphere and cylinder models of the ventricle with a wall volume of Vm were used. Circumferential F-L relation of unit myocardium in different ventricular wall layers were formulated as functions of Emax, Vd, and Vm. We found that as long as the product of Emax and Vd remains constant, the F-L relation in the midwall layer and the average F-L relation in the wall remain relatively unchanged regardless of wide changes in Vm and Vi. The elevation of the F-L relation curve, which represents myocardial contractility, was found to change in proportion to Emax Vd, largely independent of Vm and Vi, or the size of the ventricle.

Effect of positive inotropic agents on the relation between oxygen consumption and systolic pressure volume area in canine left ventricle.

We analyzed the effect of positive inotropic agents on the relation between left ventricular oxygen consumption and the systolic pressure-volume area. Pressure-volume area is a measure of total mechanical energy for ventricular contraction, and is a specific area in the ventricular pressure-volume diagram circumscribed by the end-systolic and end-diastolic pressure-volume relation curves and the systolic segment of the pressure-volume trajectory. Either epinephrine (1 microgram/kg per min, iv) or calcium ion (0.03 mEq/kg per min, iv) was administered to canine excised cross-circulated hearts. These agents increased an index of ventricular contractility, Emax, or the slope of the end-systolic pressure-volume line, by 70%. The regression lines of ventricular oxygen consumption on pressure-volume area in control and in enhanced contractile states were of the same formula: ventricular oxygen consumption (ml O2/beat per 100 g) equals A times pressure-volume area (mm Hg ml/beat per 100 g) plus a constant B. Coefficient A remained unchanged at 1.8 X 10(-5) ml oxygen/(mm Hg ml), but constant B increased from 0.03 ml oxygen/beat per 100 g by more than 50% with either agent. The reciprocal of A reflects the energy conversion efficiency for the total mechanical energy, and this efficiency remained near 36%. The increase in B was equal to the directly measured increment in ventricular oxygen consumption for mechanically unloaded contraction. The basal metabolism remained unchanged. We conclude that the augmented oxygen consumption under the acutely enhanced contractile state with either epinephrine or calcium was caused primarily by an increased energy utilization associated with the excitation-contraction coupling.

Heart rate-independent energetics and systolic pressure-volume area in dog heart.

Left ventricular (LV) systolic pressure-volume area (PVA), a new measure of total mechanical energy for the contraction, linearly correlates with its oxygen consumption per beat (VO2) regardless of contraction mode in a canine heart with stable chronotropism and inotropism. PVA is the area in the pressure-volume (PV) diagram circumscribed by the end-systolic and end-diastolic PV relation curves and the systolic segment of the PV loop and has dimensions of energy. We investigated whether primary changes in heart rate would affect the VO2-PVA relation. In the excised cross-circulated canine heart with left ventricular load controlled with a servo pump, we changed heart rate by pacing to compare the VO2-PVA relations at low [124 +/- 17 (SD) min-1] and high (193 +/- 23) heart rates. In 15 left ventricles, VO2 (ml O2 X beat-1 X 100 g LV-1) was (1.75 +/- 0.57) X 10(-5) PVA (mmHg X ml X beat-1 X 100 g LV-1) + 0.031 +/- 0.011 (ml O2 X beat-1 X 100 g LV-1). The VO2-PVA relation was virtually independent of heart rate in individual hearts. We conclude that the load-independent VO2-PVA relationship is not affected by chronotropism in a given canine left ventricle.

Digital on-line computation of a predictor of cardiac oxygen consumption. Left ventricular systolic pressure volume area.

Left ventricular systolic pressure volume area (PVA) has been proposed as a reliable predictor of cardiac oxygen consumption per beat (VO2). PVA is the area in the pressure-volume (P-V) diagram that is circumscribed by the end-systolic and end-diastolic P-V relation curves and the systolic segment of the P-V loop trajectory. It represents the total mechanical energy required for the ventricle to contract, to change its wall's elastic state from end diastole to end systole, and to eject blood against afterload. PVA has so far been measured manually with a planimeter applied to the P-V diagram. To measure PVA more accurately and on line during experiments, we devised a new method of computing PVA with a digital computer. The method consists of integrating during systole the infinitesimally narrow triangular pressure volume area swept by the straight line segment connecting Vd (ventricular volume at which peak isovolumic pressure is zero) and the instantaneously counterclockwise moving P-V data point in the P-V plane, and adding a small area between the end-diastolic P-V relation curve and the line connecting Vd and the end-diastolic P-V point. This method has proved useful in our study of the relation between VO2 and PVA to evaluate the PVA's ability to predict VO2.

Mechanism of higher oxygen consumption rate: pressure-loaded vs. volume-loaded heart.

The greater cardiac oxygen consumption (VO2) under pressure than under volume load has been accounted for by the greater ventricular wall force under pressure load. We cannot fully agree with this because the wall force has not always been uniquely correlated with VO2. We attempted to account for the greater VO2 under pressure load by the ventricular systolic pressure-volume area (PVA), which we previously showed uniquely correlated with VO2. In isolated supported canine hearts, we produced servo-controlled ejecting contractions the stroke work (SW) of which was doubled from control by doubling ejection pressure (P) with comparable stroke volume (SV) and by doubling Sv with comparable P. Despite comparable increments in SW from 370 to 680 mmHg.ml under two different loads, VO2 and PVA increased significantly more under pressure load (from 0.033 ml O2/beat and 800 mmHg.ml to 0.0560 and 1,800, respectively) than under volume load (increasing to 0.038 and 1,200, respectively; P less than 0.01). These results suggested to us a new mechanism underlying the greater VO2 under pressure load.

Equal oxygen consumption rates of isovolumic and ejecting contractions with equal systolic pressure-volume areas in canine left ventricle.

Left ventricle systolic pressure-volume area (PVA) has been found to be highly linearly correlated with cardiac oxygen consumption rate per beat (VO2) in a given canine heart with a stable inotropic background. PVA is a specific area in the pressure-volume (P-V) diagram that is bounded by the end-systolic and end-diastolic P-V relationship lines and the systolic segment of the P-V loop, consisting of the sum of external mechanical work and what is considered the end-systolic elastic potential energy in the ventricular wall. In this study, we compared VO2's of steady state entirely isovolumic and variously ejecting contractions that were made to have equal PVA's in the canine left ventricle. We found that VO2's of these isovolumic and ejecting contractions with equal PVA's (isovolumic vs. ejecting = 1008 +/- 64 (SE) vs. 1022 +/- 62 mm Hg ml/beat, n = 32 pairs in 10 hearts) were equal to each other (0.0375 +/- 0.0021 vs. 0.0368 +/- 0.0021 ml O2/beat) regardless of the marked differences in stroke volume (0 vs. 9.8 +/- 0.6 ml), end-diastolic volume (20.3 +/- 0.8 vs. 23.7 +/- 0.9 ml), end-systolic volume (20.3 +/- 0.8 vs. 13.9 +/- 0.7 ml), peak pressure (123 +/- 5 vs. 88 +/- 5 mm Hg), stroke work (0 vs. 636 +/- 36 mm Hg ml/beat), and calculated peak total wall force (1588 +/- 77 vs. 1077 +/- 72 g). Therefore, we conclude that PVA can serve as a reliable predictor of VO2 in a given canine left ventricle with a stable inotropic background whether the contraction mode is isovolumic or ejecting.

Regression of cardiac oxygen consumption on ventricular pressure-volume area in dog.

Left ventricular systolic pressure-volume area (PVA) has been reported to be a reliable predictor of cardiac oxygen consumption rate per beat (VO2) in a given heart with a stable inotropic background. PVA is the specific area in the pressure-volume (PV) diagram, consisting of the area (EW) within the PV loop and the area (PE) bound by the end-systolic and end-diastolic PV lines and the relaxation segment of the PV loop. EW and PE correspond to the external mechanical work and the end-systolic elastic potential energy in the ventricular wall, respectively. We determined the optimal combination of EW and PE for the best prediction of VO2, using the linear multiple regression analysis. From EW, PE, and VO2, data of many isovolumic and ejecting contractions, the optimal coefficients of EW and PE were 1.67 +/- 0.43 (SD; 7 hearts) and 1.74 +/- 0.49 (10(-5) ml O2/mmHg . ml), virtually identical to each other, corroborating that PVA, i.e., a simple sum of EW and PE, can reliably predict VO2 of a given heart in a stable contractile state.