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Biomedical subjects

W H Gaasch

Publications and source records attributed to W H Gaasch.

At least 91 records · Page 5Linked to original sources
PubMed1981

Pericardial modulation of right and left ventricular diastolic interaction.

We studied the effects of the right ventricle (RV) and pericardium on left ventricular (LV) diastolic pressure-volume (P-V) relations in the normothermic isolated blood-perfused dog heart. Studies were performed at a constant heart rate (atrial pacing at 120 beats/min) with a coronary perfusion pressure of 100 mm Hg. LV volume was directly controlled by an intraventricular balloon, whereas RV filling pressure was increased stepwise from zero to 20 mm Hg. During progressive increases in RV filling pressure, with the pericardium intact, the LV diastolic P-V relations were shifted up and to the left; this leftward shift of the LV diastolic P-V relation was associated with an increase in the modulus of LV chamber stiffness. Closing the small pericardial incisions with sutures significantly increased this effect. In the absence of the pericardium, progressive filling of the RV resulted in minor changes in LV diastolic P-V relations. Only when the RV filling pressure was markedly elevated (20 mm Hg) was there a significant effect on LV diastolic pressure. The pericardium has a small but significant effect on LV diastolic P-V relations at physiological RV filling pressures, and this effect becomes considerable at high RV filling pressures. The RV influence on LV diastolic P-V relations is significantly modulated by the presence of tightness of the pericardium.

Animals↗
PubMed1981

Myocardial relaxation. III. Reoxygenation mechanics in the intact dog heart.

Reoxygenation of hypoxic isolated cardiac muscle results in prolonged duration of contraction-relaxation. To determine whether similar mechanical changes occur in the intact left ventricle (LV), and especially to assess the influence of prolonged relaxation on LV diastolic stiffness, we examined LV pressure transients (micromanometer) and changes in myocardial segment length (ultrasonic transit time) during reoxygenation in 22 anesthetized dogs following 15 minutes of hypoxia (PaO2 = 21 +/- 2 mm Hg). The time constant (T) of LV isovolumic exponential pressure decline was used as an index of myocardial relaxation; LV end-diastolic stiffness was assessed from stiffness constants derived from multiple coordinates of end-diastolic pressure and segment length (volume loading). During reoxygenation, after LV systolic pressure and segment length measurements had returned to control levels, relaxation was prolonged; T increased from a control of 32 +/- 2 to 44 +/- 3 msec at 5 minutes of reoxygenation (P less than 0.01). Prolonged relaxation resulted in a consistent increase in LV early-diastolic pressures. Furthermore, calculated values for LV end-diastolic stiffness increased during reoxygenation when the next beat began less than 3.5 T after maximum negative dP/dt; this condition was present more frequently at a heart rate of 150 beats/min than at 120 beats/min. Thus, rapid correction of acute hypoxia in the dog results in prolonged LV relaxation; prolonged relaxation can influence LV end-diastolic stiffness when relaxation is sufficiently slow and/or when diastole is sufficiently short.

Animals↗
PubMed1981

Left ventricular volume, mass, and function following surgical correction of chronic aortic regurgitation.

Following surgical correction of chronic aortic regurgitation, left ventricular (LV) volume falls to normal or near normal in most patients; this change generally occurs within the first week after surgery. During the ensuing six months, a significant regression of LV hypertrophy occurs, but most patients do not achieve a normal LV mass. The systolic ejection fraction may increase while the LV end-diastolic pressure almost uniformly falls to normal. Postoperative studies of LV volume mass and function should be aimed at identifying those patients which do not undergo these favorable changes so that medical therapy can be directed at this high risk group.

Aortic Valve Insufficiency↗
PubMed1980

Myocardial relaxation. II. Hemodynamic determinants of rate of left ventricular isovolumic pressure decline.

The hemodynamic determinants of the time constant of left ventricular (LV) isovolumic pressure (P) decline were studied in 32 anesthetized dogs. The time constant, tau (an index of LV relaxation), was determined from the best exponential fit of the equation P = Poe-t/r, to LVP measured at 5-ms intervals during isovolumic relaxation; Po = LVP at maximum negative dP/dt and t = time. At a constant heart rate of 120 beats/min, tau was determined during steady-state increases in preload (volume expansion), increases in afterload (methoxamine infusion), reductions in afterload (nitroprusside infusion), and in variably afterloaded beats at a constant preload (single-beat interventions). tau was directly related to LV systolic pressure and length during the alterations in LV loading conditions, but tau was not closely related to the extent of fiber shortening. During isoproterenol infusion, relaxation was more rapid (tau), and following the administration of propranolol, relaxation was prolonged (tau). While data from the variably afterloaded contractions indicate the presence of systolic load-dependent LV relaxation velocity, the steady-state studies do not exclude the possibility that altered contractility through reflex or other mechanisms contributes to the observed changes in tau.

Animals↗
PubMed1979

Left ventricular radius to wall thickness ratio.

Left ventricular relative wall thickness, expressed as the ratio of end-diastolic radius to wall thickness (R/Th ratio), has a constant relation with left ventricular systolic pressure in children and adults with a normal heart, subjects with physiologic forms of cardiac hypertrophy (athletes) and patients with compensated chronic left ventricular volume overload (chronic aortic regurgitation). Greatly increased values for the radius/thickness ratio, suggesting inadequate hypertrophy, indicate a poor prognosis in patients with chronic aortic regurgitation and in those with congestive cardiomyopathy; decreased values for this ratio are found in patients with hypertrophic cardiomyopathy (inappropriate hypertrophy) and in patients with compensated aortic stenosis (appropriate hypertrophy). In patients with compensated aortic stenosis, echocardiographic measurement of the left ventricular end-diastolic radius/wall thickness ratio has been used to estimate left ventricular systolic pressure. Measurement of left ventricular relative wall thickness appears to provide diagnostic and prognostic data in patients with a broad variety of cardiac disorders.

Aortic Valve Insufficiency↗
PubMed1979

Myocardial relaxation. I. Effect of nitroprusside on the tension prolongation phenomenon.

The effects of nitroprusside and cyanide on myocardial relaxation were studied during hypoxia and reoxygenation of isolated rat papillary muscle, and during segmental ischemia and reperfusion in the intact dog heart. Nitroprusside did not affect isolated muscle performance before or during hypoxia. During reoxygenation of hypoxic muscles, the tension prolongation phenomenon (which characterizes abnormal or prolonged relaxation) was only slightly attenuated by the addition of nitroprusside to the muscle bath; in contrast, cyanide (at concentrations that did not prevent the return of tension) abolished tension prolongation during reoxygenation. During reperfusion of ischemic segments in intact hearts, the prolongation of segment tension was not affected by systemic administration of nitroprusside, but was abolished by intracoronary cyanide. Attenuation of the tension prolongation phenomenon by nitroprusside in the isolated muscle may be due to the liberation of cyanide. Inasmuch as nitroprusside did not affect the tension prolongation phenomenon in the intact heart, it is unlikely that the influence of this drug on left ventricular diastolic compliance is mediated through an alteration in the tension prolongation phenomenon.

Animals↗
PubMed1978

Chronic aortic regurgitation: the effect of aortic valve replacement on left ventricular volume, mass and function.

Serial echocardiographic left ventricular (LV) studies were performed in 19 patients before (preop) and after (postop) aortic valve replacement (AVR) for chronic aortic regurgitation (AR); the effect of AVR on LV volume, mass and function was determined from the echocardiographic data. In the 12 patients who were considered to have successful surgical results, the average LV end-diastolic dimension fell from a preop value of 6.9 +/- 0.2 cm to 5.5 +/- 0.2 cm (P less than 0.01) at the time of the early postop study (seven to 10 days). Muscle cross-sectional area (CSA) derived from dimension and wall thickness data was used as an index of LV muscle mass (preop CSA = 26 +/- 1.3 cm2); CSA was unchanged at the early postop study, but subsequently fell to near normal within six months after AVR (20 +/- 1 cm2, P less than 0.01). There was a trend toward improvement in systolic performance by the late postop studies (12+ months). In two out of three patients with postop paravalvular AR, LV dimension increased after an initial fall. Four patients without paravalvular AR failed to show a significant reduction in LV dimension in the postop studies. In this group the preop studies showed a tendency toward a large end-diastolic dimension and decreased fractional shortening, but the single preop parameter which differentiated these four from the successfully treated group was an end-diastolic radius-to-wall thickness (R/Th) ratio greater than or equal to 4. Thus, successful AVR for chronic AR results in the normalization of LV volume and a decrease in LV muscle mass to near normal. The R/Th ratio has important prognostic value which appears to be independent of fractional shortening in some patients with chronic AR.

Adolescent↗
PubMed1978

The influence of acute alterations in coronary blood flow on left ventricular diastolic compliance and wall thickness.

The extent to which alterations in the coronary blood flow influence left ventricular (LV) diastolic compliance and wall thickness was studied in isolated, isovolumic (balloon in LV), blood perfused dog hearts. Studies were performed at a ventricular volume which was associated with an LV systolic pressure of 100 mm Hg and changes in LV diastolic pressure (at this constant volume) were taken as changes in LV diastolic complicance. When coronary perfusion pressure was reduced to zero (5 min of global ischemia), LV diastolic wall thickness fell from 9.9 +/- 0.9 mm to 9.2 +/- 0.7 mm (P less than 0.01) and LV diastolic pressure fell only 1.3 mm Hg (from 5.5 +/- 1.0 mm Hg to 4.2 +/- 1.1 mm Hg P less than 0.01). In contrast to these findings in 'near normal' ventricles, global ischemia in severely injured hearts (with unphysiologically high diastolic pressures) resulted in marked reductions in diastolic pressure. Thus, moment to moment changes in coronary blood flow can result in alterations in the diastolic properties of the LV. However, these are extreme interventions, and in the clinical setting, changes in coronary dynamics are unlikely to cause significant changes in LV diastolic pressure.

Animals↗
PubMed1977

Postextrasystolic compliance of the left ventricle.

The effects of a single premature contraction (PC) on left ventricular diastolic distensibility was studied in man, in the conscious chronically instrumented dog, and in the isolated (isovolumic) blood perfused dog heart. In the isolated dog heart at a constant volume, there was no difference in end-diastolic pressure when control diastolic pressure was compared to that following a PC. In man and conscious dogs, there was no difference between the overall pressure-volume or pressure-length plots when control diastolic data were compared to data from the diastole immediately following a PC (no change in the modulus of chamber stiffness). In the intact circulation of man dog, increased filling during the post PC pause causes the ventricle to operate higher on the steep (stiffer) portion of its pressure-volume or pressure-length curve (decrease in preload-dependent compliance). Thus, although a PC does not alter the modulus of chamber stiffness, a preload-dependent change in compliance may occur during post PC diastole.

Animals↗
PubMed1977

The effect of acute changes in coronary blood flow on left ventricular end-diastolic wall thickness. An echocardiographic study.

The effect of acute alterations in coronary blood flow (CBF) on left ventricular (LV) end-diastolic wall thickness was measured by reflected ultrasound in twelve anesthetized dogs. During five minutes of coronary ligation, wall thickness decreased from a control of 9.0 +/- 0.3 mm to 8.1 +/- 0.3 mm (P less than 0.001); during reperfusion (reactive hyperemia), wall thickness was greater than control (10.2 +/- 0.2 mm at one minute, P less than 0.001). Increased CBF produced by intracoronary nitroglycerin or papaverine resulted in transient increases in wall thickness from 8.9 +/- 0.1 mm to 9.7 +/- 0.2 at one minute (P less than 0.001) and 10.0 +/- 0.6 mm to 11.2 +/- 0.7 mm at one minute (P less than 0.001), respectively. The observed direct relation between CBF and wall thickness suggests a dynamic role for CBF in calculations of LV mass, diastolic wall stress, and myocardial stiffness constants.

Animals↗
PubMed1976

Left ventricular compliance: mechanisms and clinical implications.

Left ventricular diastolic compliance is determined by the level of operating pressure and the diastolic pressure-volume relation. This relation is curvillinear and the slope of a tangent (operative chamber stiffness) to the pressure-volume curve increases as the chamber progressively fills. Such preload-dependent changes in compliance occur during any acute alteration in ventricular volume. At a given diastolic pressure, operative chamber stiffness (or its reciprocal, operative chamber compliance) is determined by the relative values for ventricular volume and muscle mass and by the stiffness of a unit of myocardium. Thus, there may be a leftward shift of the diastolic pressure-volume curve (increase in the modulus of chamber stiffness) as a consequence of ventricular hypertrophy or an increase in the stiffness of heart muscle itself (increase in modulus of muscle stiffness). To distinguish between hypertrophy and stiff muscle, it is useful to examine the modulus of chamber stiffness, derived from pressure-volume data, together with the volume/mass ratio of the ventricle. In this fashion, changes in the modulus of chamber stiffness that are inappropriate for a given volume/mass ratio may be attributed to changes in the material properties of the heart muscle. Examples of clinical and experimental pressure-volume studies are presented to illustrate the variety of mechanisms by which acute and chronic changes in ventricular chamber compliance evolve during the course of clinical heart disease. The pathophysiology of pulmonary congestion is best understood by considering the factors responsible for producing changes in chamber stiffness of the ventricle, whereas an examination of muscle stiffness is likely to provide more insight into the extent of irreversible functional and structural defects of the myocardium.

Angina Pectoris↗
PubMed1976

Aortic valve closure: echocardiographic, phonocardiographic, and hemodynamic assessment.

The temporal relationship between the closure of the aortic valve (AoV) and the onset of the aortic component of the second heart sound (A2) was defined by simultaneous recording of AoV echogram, phonocardiogram (PCG), and electrocardiogram in 25 subjects. Ten subjects had no heart disease (normal); 15 suffered from various cardiac conditions other than AoV disease (patients). The point of coaptation (C) of the AoV cusps to the onset of A2, the C-A2 interval, was measured to the nearest 5 msec. in 125 cycles. Fifty-eight cycles had a C-A2 of 10 msec., and 47 cycles had a C-A2 of 15 msec. The remainder were distributed at intervals below 10 or above 15 msec. The average C-A2 interval was 11.48 +/- 0.38 msec. (mean +/- 1 S.D.). A similar distribution pattern was observed when the total number of cycles was divided into "normal" and "patient" groups. In 3 subjects, simultaneous equisensitive (catheter-tip micromanometer) left ventricular and central aortic pressures, PCG, and AoV echograms were recorded. C-A2 ranged from 0 to 10 msec.; the interval between left ventricular and aortic pressure at the level of the incisura-hangout interval-ranged from 8 to 20 msec. Inhalation of amyl nitrite in one subject produced a significant fall in arterial pressure, accompanied by prolongation of the hangout interval from 10 to 20 msec. and of the C-A2 interval from 0 to 8 msec. Thus, the C-A2 interval is an integral part of the hangout time. Data suggest that A2 does not originate from the coaptation of the aortic valve cusps per se, but is related to events that occur at the time of or slightly after coaptation.

Adolescent↗