Biomedical subjects

W H Gaasch

Publications and source records attributed to W H Gaasch.

At least 19 recordsLinked to original sources

PubMed1991

Left ventricular function after surgical correction of chronic mitral regurgitation.

It is generally believed that mitral regurgitation (MR) creates a systolic 'unloading' effect by providing a low-resistance ejection into the left atrium; this is thought to increase the left ventricular ejection fraction (EF), and thus to mask a reduced contractile state. Similarly, mitral valve replacement (MVR), by removing the low-resistance regurgitant leak, has been thought to increase left ventricular afterload (systolic wall stress) and thereby cause the decrease in EF that is often seen postoperatively. These concepts have never been confirmed in patients with chronic MR. Accordingly, we evaluated systolic wall stress before and after MVR and assessed stress-shortening relations in two groups of patients with chronic MR (those with compensated and those with decompensated MR). Calculated values for circumferential and meridional wall stress were found to be normal or high in patients with chronic MR. This indicates that chronic MR is not associated with an unloading effect. In decompensated MR, systolic wall stress tends to increase after MVR; this can contribute to a postoperative decline in myocardial fibre shortening and a lower EF. By contrast, patients with compensated MR exhibit a decline in systolic wall stress after MVR; despite this postoperative decline in afterload, fibre shortening falls. This indicates that the fall in fibre shortening after MVR is not the result of increased systolic loading. In such patients, the valve replacement (with loss of integrity of papillary muscles and chordae, and a tethering of posterobasal wall motion by the prosthesis) is most likely responsible for the postoperative decline in fibre shortening and EF.

Chronic Disease↗

PubMed1991

Left ventricular function in rheumatic mitral stenosis.

Haemodynamic factors contributing to clinical disability in patients with rheumatic mitral stenosis have been under discussion and investigation for decades. Prior to the development of left heart catheterization, a low cardiac output in the presence of little or no pulmonary hypertension was taken as evidence for a myocardial 'insufficiency'. With the use of left heart catheterization, it was possible to exclude the presence of coronary artery disease and to assess directly the size and function of the left ventricle. Such studies indicate a tendency toward low-normal left ventricular end-diastolic volumes and low-normal ejection fractions. Modest reductions in the ejection fraction may be due to: (1) a restriction or tethering of posterobasal myocardium by the scarred mitral apparatus, or (2) abnormal interventricular septal motion related to right ventricular overload and unequal filling of the two ventricles. These and other factors, such as limited LV distensibility and variable diastolic suction, may affect ventricular function in rheumatic mitral stenosis. Thus, left ventricular dysfunction can generally be explained without implicating a rheumatic myocardial factor.

Cineangiography↗

PubMed1991

Load-dependent left ventricular relaxation in conscious dogs.

Load-dependent relaxation was studied in eight conscious dogs by inflating an intra-aortic balloon during late systole. Initially, the balloon was inflated at the aortic dicrotic notch and deflated before the next systole; subsequently, the inflation time was moved progressively earlier in 30-ms steps. This intervention produced an abrupt increment in left ventricular (LV) systolic pressure. The contraction duration was assessed by measuring the time required for LV pressure to fall by 50% of its maximum value (P50). The rate of LV pressure decline was assessed by measuring its peak negative first time derivative (-dP/dt) and the time constant of relaxation (tau). When the balloon was inflated during late systole (50 +/- 5 ms before aortic dicrotic notch), the time to peak -dP/dt fell, P50 fell, peak -dP/dt increased, and tau was unchanged. Thus the initial rate of LV pressure decline was accelerated, and the duration of the contraction was abbreviated. These data indicated that myocardial relaxation in the intact conscious dog is load dependent. Late systolic balloon inflations were performed after treatment with propranolol, verapamil, or caffeine. During propranolol and verapamil, the rate of LV relaxation (peak -dP/dt and tau) was slowed; however, the effects of balloon inflation on LV pressure transients were qualitatively similar to that seen in the baseline state. By contrast, caffeine prevented the abbreviation in the contraction duration caused by late-systolic balloon inflation. Thus LV relaxation remained load dependent when myocardial relaxation was slowed by propranolol or verapamil; load-dependent relaxation was attenuated by caffeine, presumably due to its influence on the sarcoplasmic reticulum.

Animals↗

PubMed1991

Left ventricular diastolic dysfunction limits use of maximum systolic elastance as an index of contractile function.

We tested the hypothesis that maximum systolic elastance (Emax) fails to detect a decline in left ventricular (LV) contractile function when diastolic dysfunction is present. Canine hearts were studied in an isolated blood-perfused heart apparatus (isovolumic LV); contractile dysfunction was produced by 60 or 90 minutes of global ischemia, followed by 90 minutes of reperfusion. Nine normal hearts underwent 60 minutes of ischemia, and five underwent 90 minutes of ischemia. After the ischemia-reperfusion sequence, developed pressure, pressure-volume area, and myocardial ATP level were significantly less than those at baseline in all 14 hearts. In the group undergoing 60 minutes of ischemia, LV diastolic pressure did not increase, whereas Emax decreased from 5.2 +/- 2.5 to 2.9 +/- 1.4 mm Hg/ml (p less than 0.05). In the group undergoing 90 minutes of ischemia, diastolic pressure increased (from 10 +/- 2 to 37 +/- 20 mm Hg, p less than 0.05), and Emax did not change significantly (from 5.1 +/- 4.3 to 4.3 +/- 2.5 mm Hg/ml). A second series of experiments was performed in 13 hearts with pressure-overload hypertrophy (aortic-band model with echocardiography and catheterization studies before the ischemia-reperfusion protocol). Five had evidence for pump failure, whereas eight remained compensated. After 60 minutes of ischemia and 90 minutes of reperfusion, developed pressure, pressure-volume area, and myocardial ATP level were significantly less than those at baseline in all 13 hearts. In the group with compensated LV hypertrophy, LV diastolic pressure did not change, whereas Emax decreased from 6.9 +/- 3.0 to 3.1 +/- 2.3 mm Hg/ml (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

PubMed1991

Left ventricular midwall mechanics in systemic arterial hypertension. Myocardial function is depressed in pressure-overload hypertrophy.

BACKGROUND: Left ventricular (LV) midwall geometry has been described conventionally as the sum of the chamber radius and half of the wall thickness; this convention is based on the assumption of uniform transmural thickening during systole. However, theoretical considerations and experimental data indicate that the inner half (inner shell) of the LV wall thickens more than the outer half (outer shell). Thus, an end-diastolic circumferential midwall fiber exhibits a relative migration toward the epicardium during systole. As a result, the conventional method provides an overestimate of the extent of the midwall fiber shortening. METHODS AND RESULTS: We developed an ellipsoidal model with a concentric two-shell geometry (nonuniform thickening) to assess midwall fiber length transients throughout the cardiac cycle. This modified midwall method was used in the analysis of LV cineangiograms from 15 patients with systemic arterial hypertension and 14 normal subjects. Study groups were classified according to LV mass index (LVMI): 14 normal subjects (group I), eight hypertensive patients with a normal LVMI (group II), and seven hypertensive patients with an increased LVMI (group III). There were no significant differences in LV end-diastolic pressure or volume among the three groups; the ejection fraction was slightly greater in group II (70 +/- 5%) than in groups I (65 +/- 8%) and III (66 +/- 4%), but this trend did not achieve statistical significance. Values for endocardial and conventional midwall fractional shortening (FS) were also similar in the three groups. By contrast, FS by the concentric two-shell geometry (modified midwall method) in group III (16 +/- 2%) was significantly less than that seen in groups I and II (21 +/- 4% and 21 +/- 5%, respectively; both p less than 0.05). This difference achieves greater importance when it is recognized that mean systolic circumferential stress was lower in group III (151 +/- 22 g/cm2) than in groups I and II (244 +/- 37 g/cm2 and 213 +/- 38 g/cm2, respectively; both p less than 0.01). The midwall stress-shortening coordinates in six of the seven group III patients were outside the 95% confidence limits for the normal (group I) subjects. Thus, despite a normal ejection fraction, systolic function is subnormal in hypertensive patients with LV hypertrophy. CONCLUSIONS: Chamber dynamics provide an overestimate of myocardial function, especially when LV wall thickness is increased. This is due to a relatively greater contribution of inner shell thickening in pressure-overload hypertrophy.

Cardiomegaly↗

PubMed1991

Myocardial oxygen consumption and the left ventricular pressure-volume area in normal and hypertrophic canine hearts.

BACKGROUND: To assess and compare the energy demands of normal and hypertrophic hearts, we defined the relation between myocardial oxygen consumption (MVO2, an index of the energy consumed by contraction) and the left ventricular pressure-volume area (PVA, an index of the total mechanical energy generated by contraction) in eight normal and eight hypertrophic (aortic band model) dog hearts; MVO2 was also measured in the nonworking (empty beating) and basal (potassium arrest) states. METHODS AND RESULTS: The hearts were studied in an isolated, blood-perfused heart apparatus. The slope of the MVO2-PVA relation (the inverse of which reflects myofibrillar efficiency) was similar in normal and hypertrophic hearts (3.89 +/- 1.91 and 4.19 +/- 1.25 ml O2/mm Hg.ml.10(5), p = NS). The MVO2 in empty beating (0.038 +/- 0.006 and 0.041 +/- 0.015 ml/beat/100 g, p = NS) and potassium-arrested (1.95 +/- 0.06 and 1.98 +/- 0.20 ml/min/100 g, p = NS) hearts was likewise similar in the two groups. CONCLUSIONS: Basal and nonworking energy demands and working efficiencies of hypertrophic hearts are equivalent to those of normal hearts.

Animals↗

PubMed1991

Congestive heart failure in patients with normal left ventricular systolic function: a manifestation of diastolic dysfunction.

Diastolic dysfunction is a relatively common problem that may be mild and asymptomatic or may present with congestive heart failure and severe disabling symptoms. It is frequently due to coronary artery disease or left ventricular hypertrophy and it is especially common in the older population. The pathophysiology is related to increased left ventricular passive stiffness and impaired or slowed myocardial relaxation. Patients with diastolic dysfunction are best treated with calcium channel blocking agents or beta-blocking agents (drugs that are generally avoided in patients with significant systolic dysfunction). Most treatment is based on symptomatic relief, and therefore periods of cautious trial and error are the rule. Congestive symptoms are treated with agents that reduce pulmonary venous pressure; in general positive inotropic agents and arterial vasodilators are not useful in heart failure that is due to diastolic dysfunction.

Adrenergic beta-Antagonists↗

PubMed1990

Preload does not affect relaxation rate in normal, hypoxic, or hypertrophic myocardium.

To determine whether isolated changes in preload (end-diastolic force) can influence myocardial relaxation rate in normal or abnormal (hypoxic or hypertrophic) hearts, isolated LV papillary muscles from normal Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats were studied using physiologically sequenced contractions. While total (systolic) load and late (lengthening) load were held constant, maximum isometric force decline (peak -dT/dt) and maximum isotonic lengthening rate (peak +dL/dt) were measured at seven levels of preload that varied from 115 to 55% of the resting tension at maximum length-tension curves (Lmax). Muscles from normal rats were studied in the oxygenated state (95% O2-5% CO2) and in the hypoxic state (95% N2-5% CO2). Preload did not effect peak -dT/dt or peak +dL/dt in either oxygenated or hypoxic muscles. During hypoxia, peak -dT/dt and peak +dL/dt were 9.5 +/- 1.0 g.mm-2.s-1 and 0.3 +/- 0.1 muscle length/s, respectively, at a preload of 115% compared with 9.0 +/- 1.2 g.mm-2.s-1 and 0.2 +/- 0.1 at a preload of 55%. In separate experiments, the effect of preload on relaxation rate was studied in WKY and SHR rats. In neither group did preload have an independent effect on relaxation rate. In the SHRs, peak -dT/dt and peak +dL/dt were 24.3 +/- 5.3 g.mm-2.s-1 and 0.7 +/- 0.1 muscle length/s, respectively, at a preload of 115% compared with 24.7 +/- 6.6 and 0.8 +/- 0.1 at a preload of 55%. Thus, in hypoxic and hypertrophic myocardium, as in normal muscle, an acute isolated change in preload did not influence the rate of force decline or muscle lengthening.

Animals↗

PubMed1990

Tolerance of the hypertrophic heart to ischemia. Studies in compensated and failing dog hearts with pressure overload hypertrophy.

Tolerance of the canine heart to prolonged ischemic arrest was studied in 10 hearts from normal control dogs and 15 hearts from dogs with left ventricular hypertrophy (LVH); experiments were performed 1 year after banding the aorta in 8-week-old puppies. At 1 year, hemodynamic studies revealed decreased left ventricular (LV) fiber shortening and elevated end-diastolic pressure (EDP) in five dogs (group with LVH failure); 10 dogs exhibited normal shortening and normal EDP (group with LVH compensation). The left ventricle-to-body weight ratio (g/kg) was 4.4 +/- 0.8 in the control group of dogs, 7.7 +/- 1.0 in the group with LVH compensation, and 10 +/- 2.5 in the group with LVH failure. The tolerance to 60 minutes of global ischemia (37 degrees C) followed by 90 minutes of reperfusion was studied in an isolated blood-perfused heart apparatus (isovolumic left ventricle, coronary perfusion pressure of 100 mm Hg). In the baseline (preischemic) state, coronary blood flow, myocardial oxygen consumption, lactate extraction, and myocardial high-energy phosphate content were essentially equal in the three groups; with LV volume adjusted to produce a systolic pressure of 100 mm Hg, there were no significant differences in LVEDP among the three groups. During ischemia, the diastolic (asystolic) pressure increased from 11 +/- 3 to 28 +/- 16 mm Hg (p less than 0.05) in the group with LVH failure; however, it did not increase in the control or the LVH compensation groups. Myocardial ATP levels declined equally in all three groups. During early reperfusion, lactate washout was lowest in the group with LVH failure. By 90 minutes of reperfusion, there were no significant differences in coronary blood flow, myocardial oxygen consumption, lactate extraction, or high-energy phosphate levels. High diastolic pressure persisted at 90 minutes of reperfusion in the LVH failure group (EDP was 34 +/- 19 mm Hg); however, there was no significant change in EDP during reperfusion in the control or with LVH compensation groups. After 90 minutes of reperfusion, developed pressures in the control (54 +/- 9 mm Hg), the LVH compensation (49 +/- 18 mm Hg), and the LVH failure (67 +/- 17 mm Hg) groups were not significantly different. These data indicate that hearts with compensated LVH do not exhibit an impaired tolerance to ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗

PubMed1990

Diastolic dysfunction of the left ventricle: importance to the clinician.

Diastolic dysfunction is a relatively common problem that may be mild and asymptomatic or may present with severe disabling symptoms. It is frequently due to coronary artery disease and/or LV hypertrophy and it is especially common in the older population. Patients with diastolic dysfunction and normal systolic function are best treated with calcium channel blocking agents or beta-blocking agents (drugs that are generally avoided in patients with significant systolic dysfunction). These drugs are used in the same dosage as is used in patients with angina or hypertension. Most treatment is based on symptomatic relief, and therefore periods of cautious trial and error are the rule. When diastolic dysfunction is associated with systolic dysfunction, it may be necessary to treat both conditions, but in general, positive inotropic agents and arterial vasodilators are not useful in patients with diastolic dysfunction.

Cardiomegaly↗

PubMed1989

Stress-shortening relations and myocardial blood flow in compensated and failing canine hearts with pressure-overload hypertrophy.

Serial changes in left ventricular (LV) size and function during the adaptation to chronic pressure overload and the transition to pump failure were studied in 16 conscious dogs (aortic bands placed at 8 weeks of age). Echocardiographic data at baseline and at 3, 6, 9, and 12 months after banding revealed a progressive increase in LV mass in all dogs. In six dogs with LV pump failure, there was a progressive decline in circumferential fiber shortening (29 +/- 4% at 12 months); this was significantly less than that seen in five littermate controls (38 +/- 3%, p less than 0.05). The average LV to body weight ratio in this group was 9.8 +/- 2.7 g/kg. In 10 dogs without pump failure (compensated LVH group), shortening exceeded that seen in the controls (43 +/- 4%, p less than 0.05); the LV to body weight ratio was 7.7 +/- 1.0 g/kg. At 12 months (cardiac catheterization), the LV end-diastolic pressure was higher in the failure (25 +/- 15 mm Hg) than in the compensated group (8 +/- 5 mm Hg, p less than 0.05); mean systolic stress was also higher in the failure group (313 +/- 67 g/cm2) than in the compensated group (202 +/- 53 g/cm2, p less than 0.05). The transmural distribution of myocardial blood flow was measured (at 12 months) with the radioactive microsphere technique; flow data were then related to an index of demand (a stress-time index). There was preferential blood flow to the subendocardial layers in the control (endo/epi = 1.28) and compensated hearts (endo/epi = 1.10), but in the failure group there was a relative decrease in subendocardial flow (endo/epi = 0.92). However, the absolute values for subendocardial flow in the normal, compensated, and failure groups were 77 +/- 54, 125 +/- 48, and 113 +/- 64 ml/min/100 g; the stress-time indexes in the subendocardial shell were 38 +/- 11, 74 +/- 19, and 93 +/- 34 g sec.10(2)/cm2/min. Despite what appears to be a marginal balance between blood flow and the stress time index in the failure group, the myocardial high energy phosphates were not depleted and the inoptropic state was not depressed. In this model of LV hypertrophy, the observed differences in fiber shortening can be explained on the basis of the inverse afterload-shortening relation; pump failure was due to an inadequate LV hypertrophy with afterload excess.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗

PubMed1989

The effect of acute alterations in left ventricular afterload and beta-adrenergic tone on indices of early diastolic filling rate.

The effects of an acute increase in left ventricular systolic pressure and the effects of an intravenous isoproterenol infusion on myocardial (segment) lengthening rate and chamber (minor axis dimension) filling rate were examined in 12 anesthetized dogs. Measurements of left ventricular systolic pressure (by micromanometer) and of segment length and chamber dimension transients (by ultrasonic crystals) were made in variably afterloaded beats (three-beat descending aortic cross-clamp) before and during an isoproterenol infusion that raised (+)dP/dt by 40%. During the baseline state, we found an inverse relation between the peak rate of increase in minor axis dimension [(+)dD/dt] and systolic pressure over a wide range of systolic pressures (110-160 mm Hg) and end-systolic dimensions (25-40 mm); peak (+)dD/dt and end-systolic dimension were also inversely related. During isoproterenol infusion, end-systolic dimension fell from 29.7 +/- 3.1 to 28.0 +/- 3.1 mm and (+)dD/dt increased from 79.6 +/- 8.0 to 90.1 +/- 8.7 mm/sec; however, the slope and y intercept of the relation between (+)dD/dt and end-systolic dimension were unchanged. Peak (+)dD/dt at a common end-systolic dimension of 31 mm was nearly equal during baseline and isoproterenol states (64.2 +/- 6.3 vs. 65.1 +/- 6.6 mm/sec). Similar results were found using segment length transients. We interpret these data to indicate that (+)dD/dt is strongly influenced by changes in systolic pressure and dimension and that isoproterenol-induced changes in (+)dD/dt are mediated, at least in part, through changes in systolic pressure and dimension.

Animals↗

PubMed1987

Distribution of a neutral cardioplegic vehicle during the development of ischemic myocardial contracture.

During prolonged ischemic cardiac arrest successful myocardial protection depends upon uniform delivery of cardioplegic solutions to all regions of the heart. Accordingly, we studied the regional and transmural distribution of a neutral crystalloid (dextran-saline) solution during normothermic (37 degrees C) ischemia in 18 isolated blood-perfused dog hearts (isovolumic left ventricle). In the baseline state, coronary perfusion pressure was 100 mmHg. At the onset of ischemia and every 15 min throughout ischemia, we infused 100 ml of crystalloid solution (37 degrees C) at a perfusion pressure of 100 mmHg and the distribution of crystalloid solution was assessed (radioactive microsphere technique). The hearts were reperfused after 60 min (n = 9) or 90 mins (n = 9) of ischemia. In the baseline pre-arrest state the left ventricle (LV) received 67 +/- 1.0% of the total coronary blood flow; the LV subendocardial to subepicardial flow ratio was 1.33 +/- 0.18, the LV end diastolic pressure was 7.5 +/- 0.4 mmHg, and mean transmural myocardial adenosine triphosphate (ATP) was 16.4 +/- 1.1 microM/g DW. At the onset and throughout the first 45 mins of ischemia (n = 9), regional and transmural distribution of the crystalloid solution was similar to that of coronary blood flow during the baseline state; there was no change in LV end diastolic pressure, but there was a moderate fall in ATP content (7.26 +/- 1.6 micron/g DW). After 75 mins of ischemia (n = 9), despite the development of ischemic contracture (LV end diastolic pressure exceeded 20 mmHg in all 9 hearts) and marked ATP depletion (2.76 +/- 0.5 microM/g DW), there was an increase in crystalloid solution delivery to the LV as a whole and the subendocardium in particular (the LV received 82 +/- 2.0% and the subendocardial to subepicardial flow ratio was 1.75 +/- 0.1). Even in a subgroup with severe contracture during ischemic arrest (LV end diastolic pressure greater than 60 mmHg, n = 4) there was no reduction in crystalloid solution delivery. Thus, the presence of ischemic contracture does not preclude delivery of crystalloid solution to the LV subendocardium.

Adenosine Triphosphate↗

PubMed1987

Phase-plane analysis of left ventricular chamber filling and midwall fiber lengthening in patients with left ventricular hypertrophy.

Echocardiographic measurements of the left ventricle were used to define rates of circumferential fiber lengthening at the endocardium and midwall in 12 normal subjects and six patients with concentric left ventricular hypertrophy (wall thickness 11 to 16 mm). There was no difference in chamber size and systolic shortening in the two groups, but peak normalized lengthening rate [endocardial (+) VCF] was less than normal in the group with hypertrophy (4.8 +/- 1.4 and 3.1 +/- 0.9 sec-1, respectively, p less than .05). These results were contrasted with midwall (+) VCF data derived from two models that take into account nonuniform thickening across the left ventricular wall. Both models assume a constant left ventricular mass. The first allows changes in long axis and muscle cross-sectional area; the second assumes a constant cross-sectional area. Peak midwall (+) VCF with the first model was 2.1 +/- 0.5 sec-1 in the normal group and 1.4 +/- 0.3 sec-1 in the group with hypertrophy (p less than .01); with the second model peak midwall VCF was 2.8 +/- 0.6 and 1.4 +/- 0.4 sec-1 (p less than .01) in the two groups. The time to peak VCF and the dimension at the instant of peak (+) VCF were similar in the two groups. Phase-plane plots of length and velocity (dimension vs dD/dt) allow visual inspection and quantification of the relationships between instantaneous dimension, rate of change of dimension, and time in normal and hypertrophic hearts. These plots indicate abnormal filling of the left ventricular chamber and lengthening of midwall fibers in left ventricular hypertrophy.

Cardiomegaly↗

PubMed1985

Left ventricular stress-dimension-shortening relations before and after correction of chronic aortic and mitral regurgitation.

Mechanical characteristics of the left ventricle in chronic aortic regurgitation (AR) differ from those in chronic mitral regurgitation (MR). The differences are thought to be responsible, in part, for the changes in left ventricular (LV) function observed after surgical correction of AR or MR. To test this hypothesis, LV stress-dimension-shortening relations were determined before and after valve replacement in patients with compensated and decompensated chronic AR and MR. Echocardiographic data from 32 patients with AR and 20 patients with MR were used; preoperatively, all 52 patients had LV enlargement. Based on postoperative data, 2 subgroups were defined for each lesion: Patients in group A achieved a normal end-diastolic dimension (less than 3.3 cm/m2) and patients in group B had persistent LV enlargement. Preoperatively, the patients in group A with AR had increased peak systolic stress, but end-systolic stress and fractional shortening were normal; the patients in group B with AR had increased peak systolic stress, increased end-systolic stress and depressed shortening. One year after aortic valve replacement the patients in group A had normal systolic wall stresses and normal shortening, whereas those in group B had persistently abnormal wall stresses and a decrease in shortening. Preoperatively, patients in group A with MR had only modest elevations of peak stress, while end-systolic stress and fractional shortening were normal; in patients in group B with MR the peak stress was similar to that seen in group A, but end-systolic stress was increased and shortening was depressed.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve Insufficiency↗

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↗

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↗