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Biomedical subjects

W H Gaasch

Publications and source records attributed to W H Gaasch.

At least 73 records · Page 4Linked to original sources
PubMed1985

Measurement of peak systolic elastance in intact canine circulation with servo pump.

Peak systolic elastance (Emax) was measured in the intact canine circulation by means of a new experimental technique. In this technique the heart is isolated from the circulation during a single systole and subjected to controlled ventricular loads. An electropneumatic aortic occluder is used to isolate the ventricle, and a servo-controlled syringe pump is used to control the ventricular load. Because the experimental load is applied for a single heartbeat only, ventricular function can be measured without the interference of regulatory feedback mechanisms. In eight dogs, weighing 17-42 kg, the relationship between changes in endsystolic pressure and volume was determined from the single-beat application of purely compliant loads. The end-systolic relations were linear, and their slope, Emax, was inversely related to weight. The observed relation between Emax and body weight allows comparisons to be made between different preparations in which Emax has been determined. Values of Emax obtained from the single-beat preparation were found to be 27-74% above those reported in isolated heart preparations and nearly identical to those reported for in vivo or denervated in situ preparations.

Animals↗
PubMed1985

Left ventricular chamber filling and midwall fiber lengthening in patients with left ventricular hypertrophy: overestimation of fiber velocities by conventional midwall measurements.

Observations that the inner (subendocardial) half of the left ventricular wall contributes more to total left ventricular wall thickening than the outer (subepicardial) half may have important implications in the analysis of myocardial fiber length transients. Accordingly, we measured endocardial and midwall shortening and lengthening rates in normal and hypertrophic heart and compared the results obtained with conventional methods of measurement with those obtained with a modified model that does not depend on use of conventional assumptions about the midwall. This modified (two-shell) cylindrical model) method considers the substantial contribution of inner wall thickening and thus does not require the assumption of a theoretical midwall fiber that remains at the midwall throughout the cardiac cycle. Echocardiographic data from six normal subjects and six patients with concentric left ventricular hypertrophy (LVH) were examined; left ventricular wall thickness ranged from 8 to 10 mm in normal subjects and from 11 to 16 mm in the patients with LVH. By design, the standard measurements of left ventricular size (diastolic and systolic dimensions) and systolic function (fractional shortening and endocardial fiber shortening velocities) were equal in the two groups. Endocardial, conventional midwall, and modified midwall methods all indicate reduced fiber lengthening rates in patients with LVH; peak fiber lengthening rates for normal and LVH groups were 4.5 +/- 0.7 vs 3.1 +/- 0.8 sec-1 (p less than .02) at the endocardium, 2.3 +/- 0.4 vs 1.6 +/- 0.4 sec-1 (p less than .02) at the midwall (conventional method), and 2.1 +/- 0.3 vs 1.4 +/- 0.3 sec-1 (p less than .01) at the midwall (modified method).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly↗
PubMed1984

Chronic mitral regurgitation: predictive value of preoperative echocardiographic indexes of left ventricular function and wall stress.

The effect of mitral valve replacement on left ventricular volume, mass, function and clinical symptoms was examined in 20 patients with chronic mitral regurgitation. Pre- and postoperative echocardiograms demonstrated that two outcomes could be defined. Left ventricular dimension at end-diastole was reduced to normal postoperatively in the 16 Group I patients, but was unchanged in the 4 Group II patients. The Group I response was associated with a dramatic reduction in left ventricular mass and a decrease in clinical symptoms; all 16 patients reached New York Heart Association functional class I. No change in left ventricular mass was seen in the Group II patients and all four remained symptomatic despite continued medical therapy. Examination of the preoperative echocardiographic measurements indicates that these data have significant prognostic value in predicting surgical outcome. When ventricular dimension at end-systole exceeds 2.6 cm/m2 or fractional shortening is less than 31% or end-systolic wall stress index exceeds 195 mm Hg, all Group II patients are identified and there are no false positive results in Group I. It is concluded that echocardiographic measurements of left ventricular size, function and wall stress can provide important prognostic information in patients with chronic mitral regurgitation. Such data may allow improved patient selection and a better definition of an optimal time for mitral valve replacement.

Aged↗
PubMed1983

Assessment of the cardiac effects of hemodialysis with systolic time intervals and echocardiography.

The acute effects of hemodialysis on left ventricular (LV) function were studied with the use of externally recorded LV systolic time intervals and echocardiography; 10 patients with normal or near-normal predialysis LV function and no circulatory congestion were studied. Hemodialysis significantly decreased the LV ejection time (LVET) from 270 +/- 9 ms to 237 +/- 10 ms (p less than 0.001); no significant change was noted in the preejection period (PEP). The PEP/LVET ratio increased from 0.41 +/- 0.05 to 0.45 +/- 0.06 (p less than 0.05). The LV end-diastolic dimension decreased from 5.3 +/- 0.3 cm to 4.8 +/- 0.3 cm (p less than 0.001). Fractional shortening and ejection fraction did not change significantly, but hemodialysis slightly increased mean VCF from 1.2 +/- 0.1 s-1 to 1.4 +/- 0.1s-1 (p less than 0.005). Hemodialysis was associated with a 17% decrease (87 +/- 8 ml to 72 +/- 7 ml; p less than 0.001) in LV stroke volume as calculated from echocardiographic data. Small changes in heart rate and blood pressure were insignificant. We conclude that the postdialysis reduction in stroke volume was due primarily to an acute decrease in LV preload; dialysis also appears to be associated with a small increase in the LV contractile state.

Adult↗
PubMed1983

Chronic aortic regurgitation: prognostic value of left ventricular end-systolic dimension and end-diastolic radius/thickness ratio.

The prognostic value of preoperative echocardiographic data was assessed in 32 patients who underwent aortic valve replacement for chronic aortic regurgitation. All patients had preoperative studies and were followed up prospectively for 1 to 6 years after surgery. Postoperatively, 25 patients (Group A) achieved a normal left ventricular end-diastolic dimension and a significant regression of myocardial hypertrophy; 7 patients (Group B) had persistent left ventricular enlargement. During the follow-up period, the patients in Group A had fewer symptoms and used fewer medications than those in Group B. Moreover, survival at 4 years appeared to be better in Group A (96%) than in Group B (71%); two patients in Group B died with congestive heart failure; there were no such deaths in Group A. Preoperatively, a left ventricular dimension at end-diastole (DED) larger than 3.8 cm/m2 body surface area, a dimension at end-systole (DES) greater than 2.6 cm/m2 body surface area, an end-diastolic radius/wall thickness ratio (R/Th) greater than 3.8 or a product of R/Th and left ventricular systolic pressure (P X R/Th) exceeding 600 are predictive of a Group B result. If end-systolic dimension is greater than 2.6 and P X R/Th is greater than 600, all Group B patients can be identified; all but one patient in Group A had an end-systolic dimension less than 2.6 and P X R/Th less than 600. It is concluded that patients with chronic aortic regurgitation who are at risk of persistent postoperative left ventricular enlargement (with associated cardiac symptoms and reduced survival) can be identified by preoperative echocardiography.

Adolescent↗
PubMed1983

Systolic time intervals: assessment by isolated cardiac muscle studies.

To document the independent effects of acute changes in preload, afterload and inotropic state on the systolic time intervals, 10 isolated rat left ventricular muscle preparations were studied. Experiments were performed using physiologically sequenced contractions that simulate the loading conditions of the intact left ventricle. The preshortening period was measured from the time of the electrical stimulus to the onset of muscle shortening, and the isotonic contraction time was measured as the duration of shortening. These variables are analogous to the preejection period and the left ventricular ejection time in the intact heart. It was found that an isolated increase in preload shortened the preshortening period and prolonged the isotonic contraction time, whereas an increase in afterload prolonged the former and shortened the latter. Isoproterenol shortened both the preshortening period and the isotonic contraction time, while an increase in calcium shortened the preshortening period and lengthened the isotonic contraction time. All changes were significant (p less than 0.01) by analysis of variance. Thus, the similar dependence of preshortening period, isotonic contraction time and clinical systolic time intervals on changes in preload, afterload and inotropic state supports the derivation of systolic time intervals from fundamental principles of myocardial mechanics. These data provide an improved basis for the rational interpretation of systolic time intervals in patients with and without heart disease.

Animals↗
PubMed1983

Myocardial relaxation. VI. Effects of beta-adrenergic tone and asynchrony on LV relaxation rate.

We studied the effect of left ventricular (LV) asynchrony and alterations in beta-adrenergic tone on the systolic load (pressure) dependency of LV isovolumic relaxation rate in anesthetized dogs. The time constant (T) of isovolumic exponential pressure decline was used as an index of relaxation rate. Variably afterloaded LV contractions resulted in a progressive increase in LV end-systolic pressure from 124 +/- 6 in the control beat to 176 +/- 11 mmHg in the third beat and a progressive lengthening of T from 19 +/- 2 to 30 +/- 4 ms. The direct relation between LV end-systolic pressure and T was nearly linear (r = 0.98), and the slope (k) of this relation was taken to reflect the systolic load dependency of T. Administration of isoproterenol (n = 6) produced a decrease in k from 0.11 +/- 0.02 to 0.08 +/- 0.02 (P less than 0.05); with propranolol (n = 6), k increased from 0.08 +/- 0.02 to 0.27 +/- 0.04 (P less than 0.01). Right ventricular epicardial pacing (n = 6) produced an asynchronous LV contraction and an increase in k from 0.09 +/- 0.02 (atrial pacing) to 0.25 +/- 0.04 (P less than 0.01). These studies confirm the dependency of LV relaxation rate on systolic loads and indicate that this form of load-dependent relaxation can be modified by alterations in beta-adrenergic tone and LV asynchrony. The observed alterations suggest the importance of temporal dispersion of the contraction-relaxation sequence as a mechanism responsible for disturbed relaxation.

Animals↗
PubMed1982

Amyloid cardiomyopathy: characterization by a distinctive voltage/mass relation.

Fourteen patients with biopsy-proved systemic amyloidosis underwent noninvasive cardiac testing to assess the presence and severity of cardiac amyloidosis. There was a clear tendency for electrocardiographic voltage to be low (sum of S wave in lead V1 plus R wave in lead V5 or V6 [SV1 + RV5 or V6] = 14.6 +/- 4.8 mm; normal range 15 to 35) and echocardiographic muscle cross-sectional area to be increased (11.4 +/- 2.7 cm2/m2; normal range 6 to 10). When the electrocardiographic or the echocardiographic data were examined individually, and especially when they were compared and contrasted with similar measurements from patients with pericardial disease (n = 8) or aortic valve disease (n = 24), it was apparent that the electrocardiogram and the echocardiogram had limited specificity in the diagnosis of amyloidosis. However, when the analysis combined these two techniques, a distinctive pattern emerged. There was an inverse correlation between voltage and muscle cross-sectional area (r = -0.79) in patients with amyloidosis; moreover, marked derangement of the voltage/cross-sectional area relation was associated with clinical symptoms and mortality. In addition, patients with amyloidosis and cardiac symptoms had abnormal left ventricular chamber radius to wall thickness ratios, consistent with infiltration of the myocardium as the primary abnormality in cardiac amyloidosis.

Adult↗
PubMed1982

Management of aortic valve disease.

The patient with severe aortic valve disease and significant symptoms is a clear-cut candidate for valve replacement surgery. Management of asymptomatic patients with aortic valve disease is less clear-cut. Because asymptomatic patients for the most part have a benign prognosis, careful individual evaluation for risk of progressive disease must be weighed against the risks of surgery.

Adult↗
PubMed1982

Regression of myocardial hypertrophy: electrocardiographic-echocardiographic correlations after aortic valve replacement in patients with chronic aortic regurgitation.

Serial electrocardiographic and echocardiographic left ventricular (LV) studies were performed in 21 patients before and after aortic valve replacement (AVR) for chronic aortic regurgitation. Changes in voltage (SV1 + RV5-6) after AVR were assessed and evaluated relative to changes in LV mass. Muscle cross-sectional area (CSA) derived from echocardiographic dimension and wall thickness data was used as an index of LV muscle mass (LV hypertrophy greater than 10 cm2/m2). In 15 patients, voltage was reduced after AVR: Seven had normal voltage (48 +/- 17 mm to 25 +/- 6 mm, p less than 0.005) and eight still had increased voltage (61 +/- 17 mm to 40 +/- 4 mm, p less than 0.01). Patients with normal voltage had complete regression of hypertrophy by echocardiography (CSA decreased from 13 +/- 3 cm2/m2 to 9 +/- 1 cm2/m2, p less than 0.025), while those who had persistently increased voltage had incomplete regression (15 +/- 2 cm2/m2, p less than 0.001). Reduction in voltage generally occurred in the first 6 months after AVR. Three patients with unchanged voltage had evidence of paraprosthetic regurgitation and minimal change in CSA. Three other patients with voltage had evidence of paraprosthetic regurgitation and minimal change in CSA. Three other patients with persistent LV enlargement without paraprosthetic regurgitation had a severe intraventricular conduction delay. Data from 59 electrocardiographic-echocardiographic studies before and after AVR revealed a strong correlation (r = 0.81) between voltage and muscle CSA. After surgical correction of chronic aortic regurgitation, regression of LV hypertrophy can be assessed by serial electrocardiographic studies. These ECG data identify patients with complete, incomplete or no regression of LV hypertrophy.

Aortic Valve↗
PubMed1982

Independent protection provided by red blood cells during cardioplegia.

Isolated, blood-perfused dog hearts were subjected to 2 hours of arrest at 27 degrees C and perfused at 15-minute intervals with either a potassium crystalloid cardioplegic solution (KCC) or an identical solution to which washed red blood cells were added (KrbcC). After reperfusion, hearts protected with KCC were easily defibrillated and systolic pressure returned to 62% of prearrest values 90 minutes after reperfusion. In hearts protected with KrbcC, systolic pressures recovered to 103% of prearrest values 15 minutes after reperfusion. Metabolic variables recovered more quickly in hearts perfused with KrbcC. Adenosine triphosphate did not decline with arrest in either group. Creatine phosphate values decreased with KCC and increased with KrbcC. The pH of the myocardial effluent fell to 6.48 during arrest with KCC and to 7.19 with KrbcC (p less than 0.001). Carbon dioxide tension increased with KCC, but decreased with KrbcC (p less than 0.001). Thus, marked improvement in recovery after 2 hours of arrest is seen with KrbcC. Protection beyond that provided by KCC appears solely due to the washed red cells, and may be the result of the buffering action of the red cell improved oxygen delivery.

Adenosine Triphosphate↗
PubMed1982

Effects of perfusion pressure on myocardial performance, metabolism, wall thickness, and compliance: comparison of the beating and fibrillating heart.

The effects of brief periods of graded reductions in perfusion pressure on normally beating and fibrillating hearts were examined. Mechanical and metabolic parameters were studied in the isolated, isovolumic (balloon in left ventricle), blood-perfused dog heart preparation. Experiments were carried out at perfusion pressures of 100, 75, 50, and 25 mm Hg, and comparisons of performance were made at the same ventricular volumes in the beating and fibrillating heart. A fall in perfusion pressure significantly decreased systolic performance in the beating heart. Diastolic pressure-volume relations were not altered by changes in perfusion pressure in the beating heart, but the fibrillating heart became significantly more compliant as perfusion pressure declined. Coronary blood flow and myocardial oxygen consumption were consistently higher during fibrillation than during sinus rhythm, and both parameters declined significantly at decreasing perfusion pressures. The fibrillating heart produced lactate at a perfusion pressure below 65 mm Hg, while the beating heart produced lactate at a perfusion pressure below 35 mm Hg. These studies demonstrate that brief periods of relatively modest decreases in perfusion pressure during ventricular fibrillation alter myocardial energy demand-supply relationships to result in ischemia of the fibrillating heart.

Animals↗
PubMed1981

Myocardial relaxation. V. Postextrasystolic contraction-relaxation in the intact dog heart.

Postextrasystolic (PES) relaxation of the left ventricle was studied in 24 anesthetized dogs using the time constant (tau) of the left ventricular isovolumic pressure decline as an index of global relaxation velocity. Using programmed atrial stimulation and a control RR interval of 500 msec, the "coupling interval/compensatory pause" was varied from 400/600 msec to 250/750 msec, and left ventricular pressure-segment length data from control beats were compared with data from PES beats. Contractile state and fractional shortening increased in the PES beat, but the relaxation time constant remained unchanged (control, 35 +/- 3 msec; PES at 250/750 msec, 36 +/- 3 msec) (p = NS). Pretreatment with propranolol did not qualitatively influence these results. Isoproterenol and calcium were given in doses sufficient to increase the time derivative of isovolumic pressure (maximal positive dP/dt) by an amount equal to that obtained with PES potentiation (approximately 50%); isoproterenol produced a substantial decrease in the relaxation time constant (38 +/- 4 to 30 +/- 6 msec, p less than 0.01), whereas calcium administration produced only a small decrease in the time constant (30 +/- 5 to 27 +/- 5 msec, p less than 0.05). Thus, in the intact dog heart, some positive inotropic interventions augment contraction and speed relaxation, but PES potentiation of contraction is not associated with a change in relaxation velocity.

Animals↗