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S A Glantz

Publications and source records attributed to S A Glantz.

18 recordsLinked to original sources
PubMed1979

Determination of frequency response from step response: application to fluid-filled catheters.

The performance of a fluid-filled catheter can be described by reporting its undamped natural frequency and damping ratio. These parameters can be measured by subjecting the catheter to sinusoidally varying pressures at a wide variety of frequencies to obtain the frequency response. They can also be computed from the response to a step change in pressure, which is often easier to produce. This paper derives the required equations and includes a graph which permits one to look up the undamped natural frequency after measuring the period and decay rate of the oscillation following a step change in pressure.

Cardiac Catheterization↗
PubMed1979

Changes in the diastolic pressure-diameter relation after ventricular function curves.

Systolic performance depends on end-diastolic muscle fiber length, contractility, and afterload. Ventricular function curves are constructed using end-diastolic pressure instead of end-diastolic dimensions, on the assumption that end-diastolic pressure and end-diastolic dimensions (reflecting muscle fiber length) have a constant relation. That assumption has been rejected. Theorectically, ventricular function curves should change with changes in the diastolic pressure-dimension relation as well as with contractility or afterload. We measured pressures and dimensions in ventricles of six open-chest dogs before and after opening the pericardium to alter diastolic pressure-dimension relations with afterload constant. When an indicator of systolic performance (developed pressure times diameter change during systole) was plotted against end-diastolic pressure, data obtained with the pericardium closed and open resulted in two distinct curves, suggesting an increase in contractility with the pericardium open. However, when systolic performance was plotted against end-diastolic diameter, data obtained with the pericardiumclosed and open fell along one curve, indicating no change in contractility. Therefore, changes in the diastolic pressure-dimension relation to shift conventional ventricular function curves.

Animals↗
PubMed1978

Segment stroke work and metabolism depend on coronary blood flow in the pig.

We determined the mechanical and metabolic effects of graded myocardial ischemia in 23 open-chest, anesthetized pigs. By connecting the midportion of the left anterior descending artery (LAD) to the carotid artery via a constant volume, calibrated pump, we reduced the flow in the LAD to 0, 25, 50, and 75% of control rates for periods of 1 h. Flows of 100% and 150% were also examined. Using pairs of ultrasonic crystals to measure segment dimensions, we calculated segment shortening and thickening, and total and systolic stroke work in the ischemic and normally perfused segments. Blood gases, pH, and lactate and inosine balances were determined from the regional coronary venous blood. At coronary blood flows of 0, 25, 50, and 75% of normal resting flow, total segment work was 8 +/- 8, 25 +/- 4, 51 +/- 5, and 80 +/- 6% of control, respectively, while systolic segment work was -2 +/- 5, -10 +/- 5, 40 +/- 5, and 86 +/- 7% of control, respectively (means +/- SE). Thus, the decrease in total segment stroke work is proportional to the decrease in flow over the range 0-100%. However, no useful work (i.e., systolic work) is done until flow exceeds 25%. Segment shortening and thickening are significantly depressed with flows diminished by only 25%. Segmental inosine production correlates with lactate production and parallels decreased mechanical performance.

Animals↗
PubMed1978

A mechanism for shifts in the diastolic, left ventricular, pressure-volume curve: the role of the pericardium.

Attempts to explain acute shifts in the pressure-volume relationship by changes in myocardial stiffness have been unsupported by animal experimentation and discouraged by calculations showing that making half the ventricle rigid would hardly account for the clinically observed upward shifts in the curve. Data collected in open-chest anesthetized dogs during volume loading with the pericardium open and closed indicate that when the pericardium is closed, left ventricular enddiastolic pressure is better predicted by right ventricular pressure than by left ventricular dimensions. These data support the hypothesis that acute, upward shift in the pressure-volume curve may be caused by an increase in pericardial pressure, in turn caused by an increase in the volume of the intrapericardial contents. This follows from the fact that measured left ventricular diastolic pressure is equal to the sum of the pressure differences accross the myocardium and the pericardium. Thus, increases in pericardial pressure raise measured ventricular diastolic pressure without change in ventricular volume: hence, an upward shift in the pressure-volume curve.

Animals↗
PubMed1977

Cardiac dynamics.

The studies reported here were selected because of renewed interest in these areas, particularly as they relate to the evaluation and management of patients with coronary artery disease and heart failure. The first section emphasized a new conceptual approach to changes in the diastolic pressure-volume relation of the left ventricle. Although previous studies have concentrated on mathematical models which describe wall stress and stiffness as derived from the pressure-volume relationship, this review emphasizes that hemodynamic factors are very important in acutely altering the pressure-volume relationship of the left ventricle. This is partly due to alterations in right ventricular pressure, which subsequently influence the left ventricular pressure-volume relationship. In addition, recent studies have pointed out that compliance indices measured at low end-diastolic pressures differ from the indices measured at high end-diastolic pressures, so that limited information from one portion of the curve may not be generalized to describe the entire curve. The section on afterload emphasized the importance of this factor in influencing cardiac function, particularly in the presence of heart failure. In patients with both acute and chronic heart failure, vasodilator drugs which reduce ventricular afterload have produced substantial hemodynamic benefit by reducing the filling pressures of the right and left ventricles and increasing forward cardiac output. This hemodynamic improvement in response to afterload reduction is predictable from the different quantitative descriptions of ventricular afterload. Nevertheless, it is still unclear which method best describes afterload. Although wall stress, impedance, vascular resistance, and aortic pressure have all been utilized as a measure of afterload, each has some shortcomings which may limit its applicability. The final section reviewed approaches to the measurement of regionally ischemic myocardium. Since current studies have emphasized the importance of identifying and preserving ischemic, but viable, myocardium, this section has reviewed techniques for measuring local mechanical performance. Previous studies with the Walton-Brodie strain gauge and epicardial length gauge did not appear to be as satisfactory as more recent measurements with ultrasonic crystals, which can simultaneously measure wall thickness and segment length. These methods form the basis for ongoing experiments designed to evaluate approaches for preserving ischemic myocardium in the setting of experimental myocardial infarction.

Angina Pectoris↗
PubMed1976

Acute hemodynamic interventions shift the diastolic pressure-volume curve in man.

Frame-by-frame analysis of angiograms in 16 patients revealed that hemodynamic interventions are capable of producing substantial shifts in the diastolic pressure-volume curve. Angiotensin raises blood pressure and shifts the entire pressure-volume curve up, and nitroprusside lowers blood pressure and shifts the curve down. Indirect measurements of pleural pressure in seven patients (via esophageal pressure) showed that pleural pressure changes were too small to account for these shifts. Analyzing our results in terms of a theoretical pressure-volume equation previously validated in dog studies did not show the observed shifts to be the product of acute changes in the elasticity of the myocardium itself. This same analysis suggested that indirect changes in the external mechanical constraints acting on the left ventricle such as the right ventricular pressure, the pericardium, and perhaps viscoelastic effects related to changes in filling rate account for the pressure-volume curve shifts with intervention. The fact that one cannot in general relate a specific volume to a given pressure in the face of hemodynamic interventions calls into question the use of end-diastolic pressure interchangeably with end-diastolic fiber length when interpreting systolic events in terms of the Frank-Starling mechanism.

Adult↗
PubMed1976

Age-related changes in ouabain pharmacology. Ouabain exhibits a different volume of distribution in adult and young dogs.

To better understand why one must administer much higher doeses of digitalis glycosides to immature than to mature humans and animals, we studied ouabain pharmacokinetics in adult and young dogs. Consistent with reported observations that ouabain-binding, metabolism, and excretion do not change with age, we found no significant differences in the transfer coefficients in a linear two-compartment open model for ouabain pharmacokinetics following a bolus of 0.05 mg/kg. We did find, however, that young dogs had nearly twice the ouabain volumes of distribution per kilogram of body weight as adults (155.4 +/- 1.2 (SE) ml/kg vs. 80 +/- 0.6, P less than 0.0005) and that one could account for this difference with the fact that young dogs had nearly twice the plasma volume 108 +/- 9.8, vs. 68 +/- 7.3, P = 0.001) and interstitial fluid space (318 +/- 35 vs. 190 +/- 6.5, P = 0.006) as the adults. For the same dose per kilogram, left and right ventricular ouabain concentrations were inversely related to the volume of distribution, with the adults having significantly higher tissue levels and incidence of arrhythmias. One must give more ouabain to a young dog to get the same plasma concentration as in an adult because the mass of ouabain in rapid equilibrium with the plasma is diluted in a larger volume of distribution.

Aging↗
PubMed1976

Ventricular pressure-volume curve indices change with end-diastolic pressure.

Many indices have been proposed to describee the diastolic pressure-volume curve mathematically and permit quantification of the elastic properties of the myocardium itself in hopes that changes in the muscle caused by disease would b.e reflected in the diastolic pressure-volume curve. To date, none of the proposed indices has been shown convincingly to discriminate one group of patients from another. While this situation in part arises from the relatively large amount of noise introduced by the technical difficulties of measuring synchronous pressures and volumes during diastole in man, ther is a more fundamental difficulty. In practice, one can measure only a short segment of the entire pressure-volume curve, and the values of all diastolic pressure-volume curve parameters investigated change significantly when one uses different segments of the same pressure-volume curve to compute them. These results were derived from relatively noise-free pressure-volume curves obtained by filling nine excised dog left ventricles at a known rate and monitoring pressure-volume curve used to compute the parameter. Merely increasing measurement fidelity will not resolve this problem, because none of these parameters accurately characterizes the entire diastolic pressure-volume curbe from a segment like that which one can reasonably expect to obtain from humans.

Animals↗
PubMed1976

Acute changes in the diastolic pressure-volume relationship of the left ventricle.

Acute changes in the diastolic pressure-volume relationship of the left ventricle. Europ. J. Cardiol., 4/Suppl., 105-120. The present study was designed to investigate acute changes in the passive length-tension relations of isolated heart muscle and acute alterations of the left ventricular diastolic pressure-volume relationship of patients. In isolated heart muscle a constant lengthening and shortening technique with computer curve fitting was used to characterize the entire passive length-tension relation. There was no change in passive elastivity following an increase in stimulation frequency or an increase in muscle stretching rate. During the transition from stimulated to nonstimulated contractions, there was a shift to the left in the passive length-tension relation, with a shorter muscle length at the same resting force. In 10 patients undergoing revascularization for preinfarction angina, 7 patients showed a significantly reduced left ventricular enddiastolic pressure at the same enddiastolic volume, together with an improvement in postoperative ejection fraction. In 6 patients who experienced a perioperative myocardial infarction, variable changes in the pressure volume relationship occurred. These presumably reflected the opposite effects of stiffening of infarcted muscle and cardiac dilatation secondary to heart failure. 26 patients with chronic coronary artery disease had ventriculograms before and after 0.4 mg sublingual nitroglycerin. 9 patients showed a significant shift downwards in their pressure-volume relation, with a decreased enddiastolic pressure at the same volume. 2 showed a shift upwards, while the remaining patients showed no measurable change. It is proposed that this latter shift in pressure-volume relationships is due to hemodynamic factors rather than to intrinsic changes in muscle stiffness. Theoretical calculations utilizing A SIMPLIFIED SPHERICAL MODEL of the ventricle suggest that the magnitude of the changes observed cannot be explained by stiffening of the muscle alone and is therefore probably due to hemodynamic factors.

Cardiac Output↗
PubMed1975

Pharmacologic therapy of ventricular arrhythmias.

To treat patients with ventricular arrhythmias properly, one must characterize the arrhythmia, define the underlying heart disease and look for and treat reversible causes. When arrhythmias are suitable for pharmacologic suppression, it is necessary to predefine therapeutic goals, then carefully document that the drug accomplishes these goals. Knowledge of a drug's metabolism, excretion, active metabolites and plasma protein binding is often required for full understanding of its clinical effect. Pharmacokinetic principles require that antiarrhythmic drugs be given on a rigid schedule and that plasma drug levels be frequently determined. Use of compartment models and the principle of superposition can enable one to achieve and maintain therapeutic drug concentrations while avoiding toxic side effects. The drugs commonly used to treat arrhythmias, lidocaine, propranolol, procainamide, diphenylhydantoin and quinidine, as well as some newer agents, have specific pharmacokinetics and toxic effects that must be understood.

Anti-Arrhythmia Agents↗
PubMed1975

A three-element model describes excised cat papillary muscle elasticity.

The three-element model for skeletal muscle has been widely applied to cardiac muscle. It consists of an active contractile element (CE) that represents the muscle's response to stimulation, in series with an elastic element (SE) and the CE and SE in parallel with another elastic element (PE). There have been problems in interpreting experimental data on muscle elasticity using this model. Data seem to indicate that SE force depends not only on instantaneous length, but also initial length; it is not only elastic. Recent experiments seem to indicate that the SE has time-varying properties; it is not passive. This paper formulates a three-element model in which phi(x) = alpha[e beta(x-x*)-1] governs the elastic elements, where phi = force, alpha, beta = spring constants, x = length, and x* = rest length, which avoids these problems. The SE and PE have the same properties. (Typical values: alpha approximately equals .045 g/mm2, beta approximately equals 5.9 mm-1 for cat papillary at 29 degrees C.). By accounting for the nonlinearity of the SE-PE interaction, this three-element model leads to predictions that agree with published data on excised papillary muscle's elastic properties.

Animals↗
PubMed1975

Muscle stiffness determined from canine left ventricular pressure-volume curves.

We measured pressure-volume curves in nine excised dog ventricles and stress-strain curves in two to five muscle specimens from each ventricle to verify a derived formula that relates muscle stiffness to the ventricular pressure-volume curve. The assumptions underlying this formula are: (1) the ventricle is a uniform spherical shell, (2) all muscle fibers carry average stress and deform as if they were at the midwall, (3) static equilibrium exists, (4) internal pressure induces the only load, and (5) the muscles exhibit an exponential stress-strain curve given by the equation sigma(epsilon) = alpha(ebeta epsilon - 1), where sigma = stress, epsilon = strain, and alpha and beta are constants. There was no significant difference between the stiffness constant, beta, inferred from the left ventricle pressure-volume curves (14+/-4.3[SD]) and that measured directly from the muscle stress-strain curves (16+/-2.8).

Animals↗