Wilhelm Rutishauser

Evaluation of Roentgen Cinedensitometry for Flow Measurement in Models and in the Intact Circulation

The flow of blood in vitro and in the carotid artery of the dog was calculated by a new cinedensitometric technique and compared with the flow as measured simultaneously by graduated cylinder and stopwatch. Cineangiographic films were projected onto a frosted screen and the light intensity was measured at two neighboring cross sections of the vessel in question. The passage of the contrast medium yielded a pair of indicator-dilution curves of which the difference in mean transit time was calculated. The distance between the cross sections and the diameter of the vessel was measured with the aid of x-ray-dense scales. The flow through the vessel was calculated as the product of cross-sectional area and mean velocity.The correlation coefficient between the volumetric flow and the flow as found by cinedensitometry was 0.976 in vitro and 0.946 in the intact dog with no systematic deviation from the line of identity. The method enables the blood flow in the intact circulation to be calculated in milliliters per second in any vessel that can be clearly visualized by cineangiocardiography.

High-fidelity left ventricular pressure measurements for the assessment of cardiac contractility in man

Abstract Left ventricular contractility was assessed in 110 patients by use of Vmax values derived from high-fidelity left ventricular pressure measurements. Instantaneous velocity of shortening of the contractile elements (V CE ) throughout the isovolumic phase of left ventricular systole was calculated by an analog computer using the formula: V CE in muscle lengths (ML)/ sec = ( dP / dt )/28 · P where P represents total left ventricular pressure and dP/dt its first derivative. Vmax was obtained by manual straight line extrapolation of the descending portion of the pressure-velocity curves. Group 1 (control subjects) consisted of 25 patients with no or minimal loading of the left ventricle. Vmax in Group 1 was 1.86 ML/sec. Group 2 consisted of 25 patients with atrial septal defect and Group 3 included 11 patients with slight left ventricular pressure load. In Groups 2 and 3, the Vmax value was not significantly different from that of Group 1. However, in Group 4, which consisted of 23 patients with moderate to severe left ventricular pressure load, Vmax was significantly reduced (1.53 ML/sec); in Group 5, which consisted of 14 patients with coronary artery disease and 6 patients with cardiomyopathy, Vmax was 1.21 ML/sec; and in Group 6, comprising 6 patients with mitral stenosis, Vmax was 1.26 ML/sec. In individual patients in Groups 3 to 5, assessment of contractility by comparison with resting Vmax values was not always satisfactory because of overlap with the range of the control subjects. Isometric exercise by handgrip carried out in 44 patients allowed further differentiation of individual contractile function. In Groups 1 and 2, the response to handgrip was characterized by a significant increase of Vmax with no alterations or changes not exceeding +4 mm Hg of left ventricular end-diastolic pressure. In Groups 3 to 5, we observed normal responses, as well as abnormal reaction to handgrip (increase of Vmax associated with an increase of left ventricular end-diastolic pressure that exceeded 4 mm Hg) and pathologic reaction to handgrip (decrease of Vmax accompanied by an increase of left ventricular end-diastolic pressure). Seven of 13 patients with a normal resting Vmax showed an abnormal or a pathologic reaction. A normal response to handgrip was observed in a few patients with depressed resting Vmax. It is concluded that identification of individual patients with impaired myocardial contractile function requires determination of Vmax both at rest and during an additional stress such as isometric exercise.

The contractile state of the hypertrophied left ventricular myocardium in aortic stenosis.

Abstract Left ventricular dynamics and contractility were studied in 6 patients with assumed normal myocardial function (Group 1) and in 12 patients with aortic stenosis of a different degree separated into two groups, Group 2 with a mean systolic pressure gradient of below 50 mm. Hg and Group 3 with one of above 50 mm. Hg. None of the patients showed signs of left heart failure. Routine hemodynamic parameters (cardiac index, left ventricular pressure, rate of rise of left ventricular pressure, and aortic pressure) were evaluated in all three groups. End-diastolic volume ( EDVI ), left ventricular muscle mass ( LMMI ), and mean left ventricular wall thickness (h) were determined by angiocardiography. The following values were obtained: Group 1: EDVI , 98 ± 11 (S.E.) ml./M. 2 , LMMI , 115 ± 10 Gm./M. 2 , h, 0.91 ± 0.05 cm.; Group 2: EDVI , 120 ± 22 ml./M. 2 , LMMI , 157 ± 17 Gm./M. 2 , h, 1.15 ± 0.06 cm.; Group 3: EDVI , 105 ± 8 ml./M. 2 , LMMI , 234 ± 26 Gm./M. 2 , h, 1.45 ± 0.07 cm. The left ventricular contractile state was characterized by the instantaneous tension-velocity relationship throughout the isovolumic phase of the systole. It could be shown that the tension-velocity curve of patients with a pressure load is shifted downward and to the left compared with the curve of the controls. This shift was only significant, however, between Groups 1 and 3. By grouping the patients with aortic stenosis according to their age, two pressure-loaded groups with similar mean pressure gradients could be compared with the control group. Here again the tension-velocity curve was shifted to the left and downward with increasing age. This change was only significant if one compared the older age group with the control group. The present data suggest that the intrinsic contractile state of the myocardium of the left ventricle is impaired in patients with left ventricular hypertrophy from aortic stenosis but without heart failure. It would appear that the decrease in contractility is caused both by the severity of the pressure load and by the patients age.

Evaluation of Left Ventricular Function from Isovolumic Pressure Measurements During Isometric Exercise

Abstract In 24 patients left ventricular (tipmanometer) and aortic pressure measurements were carried out before and during a standardized handgrip. On the basis of findings at diagnostic cardiac catheterization, the patients were divided into 2 groups. Group 1 consisted of 13 patients without or with minimal loading of the left ventricle; group 2 comprised 11 patients with a primarily pressure-loaded left ventricle or coronary heart disease. During handgrip left ventricular systolic pressure, end-diastolic pressure and heart rate increased significantly in both groups. However, the extent of the increase of left ventricular end-diastolic pressure was considerably greater in group 2 (+8.2 mm Hg) than in group 1 (+2.0 mm Hg). Both left ventricular maximal dP/dt and the maximal quotient (dP/dt)/P, which represents a measure of the velocity of shortening of the contractile elements, increased significantly in group 1; in group 2 only maximal dP/dt increased significantly, and this increase was only about half of that observed in group 1. The time intervals from the onset of contraction to the points of maximal dP/dt and maximal (dP/dt)/P, respectively, shortened significantly during handgrip in group 1 and remained unchanged in group 2. We conclude that (1) left ventricular contractile function is impaired in patients in group 2 compared with that in group 1; (2) the primary response of the normal or near normal left ventricular myocardium to an acute load produced by handgrip is enhancement of the contractile state; and (3) the compromised left ventricular myocardium is most likely to utilize the Frank-Starling mechanism to generate increased pressure.

Atriogenic Diastolic Reflux in Patients with Atrioventricular Block

In five patients with total A-V block studied by thermodilution, infusion of 10 to 25 ml of cold saline into the right ventricle over a period of several seconds resulted in lowering right atrial temperature usually 0.25 to 0.7 second after P waves not followed in normal temporal sequence by QRS complexes. In three of these patients, in whom left heart catheterization was performed, the same phenomenon could be detected during and after infusion of cold saline into the left ventricle while temperature was measured by a thermistor introduced by transseptal route into the left atrium. Isolated atrial contractions, although capable of partially closing the A-V valves as indicated by the higher ventricular than atrial pressure, lead to atriogenic reflux from the ventricle. Ventricular contraction, however, whether normal or extrasystolic, produced efficient closure of the A-V valves.

Abnormal segmental contraction velocity in coronary artery disease produced by isometric exercise and atrial pacing

Since isometric exercise by sustained handgrip leads to a sizable increase in aortic pressure this maneuver was used in addition to atrial pacing to increase the imbalance between oxygen demand and supply in two groups of patients. Both groups were studied by left heart catheterization and cineangiography in the right anterior oblique projection, at rest, during atrial pacing and during combined pacing and handgrip exercise. Group 1, the control group, consisted of 10 patients without coronary artery disease having an ejection fraction of 0.61 to 0.82. Group 2 was composed of 10 patients with definite obstructive disease of one or more of the three main coronary arteries. At rest, ejection fraction was normal or nearly normal (range 0.54 to 0.78). Regional myocardial contraction performance was assessed by determining mean segmental shortening velocities at the basal (VSB), middle (VSM) and apical (VSA) short ventricular axes. Whereas at rest there was no significant difference between the two groups or any of the three velocities, during pacing, VSM and VSA were significantly smaller in Group 2 than in Group 1 (P smaller than 0.02). During pacing combined with handgrip exercise the difference between the two groups was clearly accentuated, all three velocities being highly significantly decreased in Group 2 (VSB, P smaller than 0.01; VSM and VSA, P smaller than 0.001). When evaluated individually the patients of Group 2 had in 9 segments during pacing values for VSB, VSM and VSA that were below the range of the normal subjects. During pacing combined with handgrip a newly abnormal shortening velocity was observed in 12 segments (VSB abnormal in 3 of 7, VSM in 4 of 7 and VSA in 5 of 7 instances). In conclusion, the combination of atrial pacing and handgrip exercise appears to be a useful stress maneuver to identify temporarily dysfunctioning segments in patients with coronary artery disease in whom atrial pacing alone is not sufficient to induce ischemic contraction disorders.

Use of apexcardiography to evaluate left ventricular diastolic compliance in human beings

The relation between various relative amplitude measurements of the left apexcardiogram and internally derived indexes of diastolic compliance of the left ventricle was studied in 29 patients. Simultaneous high fidelity recordings of the left apex tracing and left ventricular pressure were obtained in 11 patients without left ventricular disease (group I) and 18 patients with congestive cardiomyopathy (group II). In 204 normal subjects the ratio of the A wave amplitude to the total diastolic deflection (A/D ratio) of the left apexcardiogram was 31.4 +/- 11.4 (mean +/- standard deviation) percent, the ratio of the A wave amplitude to the total height (A/H ratio) 8.9 +/- 4.3 percent and the D/H ratio 30.4 +/- 14.7 percent. The A/D and A/H ratios were significantly (P less than 0.001 and P less than 0.005) increased in group II (69.2 +/- 12.2 percent and 16.8 +/- 8.2 percent, respectively); they were within normal limits in group I. In contrast, the D/H ratio was within normal limits in both groups of patients. The A/D ratio correlated significantly better with specific compliance (deltaV/deltaP.V) (r = -0.87) than did the A/H ratio (r = -0.53), whereas similar correlations were obtained with end-diastolic volume compliance (dV/dPV) (r = -0.61 and r = - 0.64, respectively). In contrast, the D/H ratio correlated significantly only with end-diastolic distensibility index (dV/dP) (r = -0.52). It is concluded that A wave amplitude/total diastolic deflection (A/D) ratio and, to a lesser degree, the A wave amplitude/total height (A/H) ratio of the left apexcardiogram correspond best to diastolic compliance and are useful noninvasive measurements of this property of the left ventricle.

Relationship between duration of systolic upstroke of apexcardiogram and internal indexes of myocardial function in man

In 11 patients with nonobstructive cardiomyopathy and coronary heart disease and decreased myocardial function of the left ventricle, as well as in nine patients without left heart valvular or myocardial disease, left apexcardiograms were recorded during diagnostic heart catheterization, wherein micromanometers were used; ACGs were registered additionally in 54 healthy volunteers in order to establish the normal range of apexcardiographic parameters. In all cases the apex tracings were recorded by means of a pulse transducer with infinite time constant. The most important finding of this study was the close correlation between the duration of the systolic upstroke (SUT) of the apex tracing and some accepted isovolumic indexes of left heart function (isovolumic contraction time, time interval from the onset to peak of the first derivative of left ventricular pressure, maximal value of the first derivative of left ventricular pressure, and the peak measured velocity of shortening of the contractile elements). Further, the mean value of SUT in patients with impaired left myocardial function was significantly prolonged, compared to the control subjects; an overlap was apparent due to the fact that some of these patients showed a normal left myocardial performance at rest, having an abnormal response only to exercise tests. The apexcardiographic SUT can practically always be measured when the first derivative of apex tracing is simultaneously recorded. It showed itself to be only slightly influenced by the resting heart rate. The mentioned relationship of the systolic upstroke time of the ACG to internal isovolumic indexes of myocardial function makes this noninvasive measurable parameter an additional excellent tool for the evaluation of the left myocardial state, thus supporting a new aspect of the value of quantitative apexcardiography.

Cinéangiokardiographische Bestimmung des enddiastolischen Volumens und der Muskelmasse des linken Ventrikels

Vor Jahresfrist wurde an dieser Stelle uber Untersuchungen an 9 normal-und 15 volumenbelasteten linken Ventrikeln (LV) berichtet (8). In der Zwischenzeit wurde das Kollektiv auf 100 Falle erweitert unter Einbezug von Fallen mit druckbelastetem LV und einer Gruppe von Patienten mit Koronarsklerose oder Myokardiopathie. Mit derselben Methodik sollten folgende Fragen abgeklart werden: n n1. n nWie gros ist die Myokardhypertrophie bei den verschiedenen Belastungsarten und n n n n n2. n nWie verhalt sich der enddiastolische Wandstress, d. h. die Kraft pro cm2 Wandquerschnittsflache, dem als Mas fur die enddiastolische Faserdehnung und damit fur den Frank-Starling-Mechanismus entscheidende Bedeutung zukommt.

Diastolic amplitude time index: A new apexcardiographic index of left ventricular diastolic function in human beings

Left ventricular apexcardiography was performed in 260 normal subjects and 37 patients undergoing diagnostic cardiac catheterization: 13 without left heart disease (group 1), 18 with congestive cardiomyopathy (group 2) and 6 with idiopathic hypertrophic subaortic stenosis (group 3). In the patients undergoing catheterization the apexcardiogram was recorded simultaneously with left ventricular pressure (tipmanometer) and its first derivative (dP/dt). The following variables were measured in the apex tracing: (1) the time from the onset of the aortic component of the second heart sound (A2) in the phonocardiogram to the nadir of the apexcardiogram, termed total apexcardiographic relaxation time (TART), (2) the time from A2 to the onset of the systolic upstroke (C point) of the apexcardiogram (A2-C), and (3) the ratio of the A wave (A) to the total diastolic amplitude (D) of the apexcardiogram (A/D). The diastolic amplitude time index (DATI) was calculated according to the following formula DATI = (square root A2-C/TART)/(A/D). In the normal subjects the diastolic amplitude time index was 0.82 +/- 0.26 (mean +/- standard deviation). In group 1 this index was within normal limits; in groups 2 and 3 it was decreased (0.23 +/- 0.07 and 0.18 +/- 0.05, respectively). This index showed excellent correlation with specific compliance of the left ventricle (r = +0.90) and close correlations with the maximal rate of decrease of left ventricular pressure (minimal dP/dt) (r = +0.79) as well as the velocity of lengthening of the contractile elements at minimal dP/dt (r = +0.77); less close correlation was obtained with the end-diastolic volume compliance (r = +0.67). These results demonstrate that the diastolic amplitude time index reflects interpatient differences in both relaxation ability and diastolic distensibility of the human left ventricle. Thus, this measurement provides an important new method for noninvasive evaluation of the overall function of the left ventricle during diastole.