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Biomedical subjects

W H Gaasch

Publications and source records attributed to W H Gaasch.

At least 37 records · Page 2Linked to original sources
PubMed1996

The management of mitral valve disease.

Clinical investigators continue to make significant advancements in the diagnosis and treatment of patients with mitral valve disease. The salutary effects of mitral balloon valvotomy for mitral stenosis and the development of a reasonable approach to the asymptomatic patient with chronic mitral regurgitation are examples of relevant research that affects clinical outcomes. Recent developments in the management of patients with mitral valve disease are reviewed.

Catheterization↗
PubMed1995

Reduced left ventricular systolic pump performance and depressed myocardial contractile function in patients > 65 years of age with normal ejection fraction and a high relative wall thickness.

We studied the relation between relative wall thickness, left ventricular systolic pump performance, and myocardial contractile function in 77 older patients with normal ejection fraction who were free of valvular and myocardial ischemic disease. Group 1 comprised 49 patients with relative wall thickness > or = 0.45; group 2 (n = 28) had normal relative wall thickness. Pump performance was characterized by stroke volume index, cardiac index, and stroke work; myocardial function was characterized by midwall shortening and circumferential stress versus shortening relations. Group 1 patients had lower end-diastolic volume (83 +/- 3 vs 124 +/- 5 ml, p < 0.05), cardiac index (2.6 +/- 0.2 vs 3.5 +/- 0.1 L/min/m2, p < 0.05), and stroke work/100 g left ventricular mass (43 +/- 2 vs 53 +/- 3 g-m/100 g, p < 0.005). Although there was no significant difference with regard to ejection fraction or fractional shortening at the endocardium, fractional shortening at the midwall was significantly lower in group 1 than in group 2 (16 +/- 1% vs 19 +/- 1%, p < 0.005). This lower value for midwall shortening was observed despite lower values for endsystolic stress, implying decreased myocardial contractile function. Lower stroke volume index in group 1 patients, likely due to small chamber size, was not offset by increased heart rate, resulting in a low-normal cardiac index; in 33% of group 1 patients, cardiac index was < 2.2 L/min/m2, indicating reduced pump performance. Our data indicate an abnormality in pump performance and myocardial function in patients who have high relative wall thickness and normal ejection fraction.

Age Factors↗
PubMed1995

Geometric changes allow normal ejection fraction despite depressed myocardial shortening in hypertensive left ventricular hypertrophy.

OBJECTIVES: This study of hypertensive left ventricular hypertrophy 1) assessed myocardial shortening in both the circumferential and long-axis planes, and 2) investigated the relation between geometry and systolic function. BACKGROUND: In hypertensive left ventricular hypertrophy, whole-heart studies have suggested normal systolic function on the basis of ejection fraction-systolic stress relations. By contrast, isolated muscle data show that contractility is depressed. It occurred to use that this discrepancy could be related to geometric factors (relative wall thickness). METHODS: We studied 43 patients with hypertensive left ventricular hypertrophy and normal ejection fraction (mean +/- SD 69 +/- 13%) and 50 clinically normal subjects. By echocardiography, percent myocardial shortening was measured in two orthogonal planes; circumferential shortening was measured at the endocardium and at the midwall, and long-axis shortening was derived from mitral annular motion (apical four-chamber view). Circumferential shortening was related to end-systolic circumferential stress and long-axis shortening to meridional stress. RESULTS: Endocardial circumferential shortening was higher than normal (42 +/- 10% vs. 37 +/- 5%, p < 0.01) and midwall circumferential shortening lower than normal in the left ventricular hypertrophy group (18 +/- 3% vs. 21 +/- 3%, p < 0.01). Differences between endocardial and midwall circumferential shortening are directly related to differences in relative wall thickness. Long-axis shortening was also depressed in the left ventricular hypertrophy group (18 +/- 6% in the left ventricular hypertrophy group, 21 +/- 5% in control subjects, p < 0.05). Midwall circumferential shortening and end-systolic circumferential stress relations in the normal group showed the expected inverse relation; those for approximately 33% of the left ventricular hypertrophy group were > 2 SD of normal relations, indicating depressed myocardial function. There was no significant relation between long-axis shortening and meridional stress, indicating that factors other than afterload influence shortening in this plane. CONCLUSIONS: High relative wall thickness allows preserved ejection fraction and normal circumferential shortening at the endocardium despite depressed myocardial shortening in two orthogonal planes.

Adult↗
PubMed1995

Gender differences in older patients with pressure-overload hypertrophy of the left ventricle.

Left ventricular hypertrophy is an adaptive response to increased intraventricular pressure, and is consistently encountered in patients with hypertension or aortic stenosis. While it has long been appreciated that the extent of hypertrophy correlates positively with the level of pressure, the age of the individual, and with indices of body size, recent evidence suggests that left ventricular structure and function also varies with gender. Elderly women with aortic stenosis, in several recent studies, have been shown to develop more marked concentric hypertrophy, lower levels of wall stress, and higher indices of systolic function. Similarly, in recent studies of extreme hypertensive hypertrophy, there is a strong female preponderance. The explanation for these findings is not clear at present, though it is possible that men with extensive hypertrophy have succumbed to complications of vascular disease at an earlier age. The syndrome of extreme hypertrophy complicating hypertension and aortic stenosis, more commonly seen in women, requires a carefully tailored clinical approach.

Age Factors↗
PubMed1994

Impact of chamber geometry and gender on left ventricular systolic function in patients > 60 years of age with aortic stenosis.

In aortic stenosis, gender and other differences in the adaptive remodeling of the left ventricle have been described, but the influence of left ventricular (LV) geometry on systolic function is not widely appreciated. This study tested the hypothesis that the increased ejection fraction seen in some elderly women with aortic stenosis is due to changes in LV geometry, not increased myocardial mass or enhanced myocardial function. We therefore investigated gender-related differences in LV and myocardial function by analysis of end-systolic circumferential stress versus shortening relations in 65 patients (29 men and 36 women) with aortic stenosis who underwent cardiac catheterization and echocardiography. Despite similar degrees of aortic stenosis, there were significant differences between men and women with regard to LV geometry and function. When compared with men, women had higher peak LV pressures (205 +/- 27 vs 188 +/- 27 mm Hg, p < 0.01), higher ejection fractions (66 +/- 14% vs 57 +/- 18%, p < 0.05), smaller LV end-diastolic dimensions (43 +/- 8 vs 51 +/- 6 mm, p < 0.01) and higher relative wall thickness (0.66 +/- 0.27 vs 0.50 +/- 0.10, p < 0.01). LV mass was similar in the 2 groups. Mean values for stress were lower in women and there was a predominance of women at extremely low levels of stress; this subgroup had very high values for relative wall thickness and endocardial shortening, but overall stress-shortening relations were normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Diagnosis and treatment of heart failure based on left ventricular systolic or diastolic dysfunction.

Data from large and small clinical trials reflect major differences in the pathophysiology, treatment, and prognosis of left ventricular (LV) systolic and diastolic dysfunction. These studies also indicate that medical therapy can benefit patients with LV dysfunction regardless of whether or not they are symptomatic. Because the descriptive term congestive heart failure does not provide for these important distinctions, a new classification of LV dysfunction has been developed in which patients with LV dysfunction are categorized on the basis of normal or abnormal systolic function. This classification is based on a simple assessment of LV function, it is applicable to patients without symptoms, and it reflects differences in treatment and prognosis. Those with clinically significant LV systolic dysfunction (ie, an LV ejection fraction < 40%) benefit from therapy whether or not they have symptoms of heart failure. Those with LV dysfunction and a normal LV ejection fraction (ie, diastolic dysfunction) also benefit from medical therapy. Annual mortality is higher in those with systolic dysfunction than in those with diastolic dysfunction, but within each of these categories mortality is higher in those with symptoms than in those without. This classification can be useful in the diagnosis and treatment of individual patients as well as in epidemiologic surveys designed to assess medical practice patterns.

Diastole↗
PubMed1993

Left ventricular hypertrophy and mortality after aortic valve replacement for aortic stenosis. A high risk subgroup identified by preoperative relative wall thickness.

OBJECTIVES: We investigated the relation between the extent and pattern of left ventricular hypertrophy and surgical outcome in 54 patients undergoing aortic valve replacement for severe aortic stenosis. BACKGROUND: Previous work from our laboratory has demonstrated that a subgroup of patients, mostly elderly women with Doppler evidence of abnormal intracavitary flow acceleration, had an unexpectedly high in-hospital mortality rate after aortic valve replacement for aortic stenosis. We hypothesized that marked concentric hypertrophy, rather than the Doppler signal itself, was related to the poor outcome. METHODS: A retrospective analysis of the clinical, hemodynamic and echocardiographic data in patients who survived aortic valve replacement versus those who died in the hospital was performed. RESULTS: There were no differences between the 42 survivors and 12 nonsurvivors with regard to the clinical or hemodynamic variables. Of the echocardiographic variables analyzed, diastolic relative wall thickness was found to be significantly different between the two groups. Patients who died had significantly greater relative wall thickness (mean +/- SD) than those who survived (0.72 +/- 0.38 vs. 0.56 +/- 0.15, p = 0.04). Analysis by gender demonstrated that the relation between ventricular geometry and mortality held true only for women. CONCLUSIONS: We conclude that excessive ventricular hypertrophy, manifested as a markedly increased relative wall thickness, is associated with a significantly increased risk of postoperative mortality after aortic valve replacement for aortic stenosis.

Aged↗
PubMed1993

Cardiac function and functional capacity: implications for the failing heart.

The exercise capacity of patients with congestive heart failure is determined by factors including the interaction of the right and left ventricles and their respective circulations, lung mechanics, skeletal muscle metabolism, and blood flow. Therapeutic efforts should be directed at all of the units in this complex process rather than the response of an individual system. Multiple therapeutic regimens such as nitrates and angiotensin converting enzyme inhibitors in combination with physical training and other therapies that improve pulmonary function produce optimal results. Using this holistic approach to therapy, the physician may have a beneficial impact on the exercise capacity of patients with congestive heart failure.

Blood Circulation↗
PubMed1993

Protective effects of diltiazem on the mechanical performance of the hypoxic myocardium.

1. To determine whether diltiazem protects the hypoxic myocardium by reducing contractile work, we have compared the effects of diltiazem and quiescence on left ventricular (LV) papillary muscle subjected to hypoxia. Papillary muscles were obtained from male Charles River CD rats weighing 150-250 g. 2. Four groups of muscles were studied: control (N = 6), non-stimulation (N = 10), diltiazem 10(-4) M (N = 6) and diltiazem 10(-4) M plus non-stimulation (N = 10). 3. Isolated rat LV papillary muscles were studied in Krebs-Henseleit solution with a calcium concentration of 2.52 mM at 28 degrees C while contracting isometrically at a stimulation rate of 0.2 Hz. Resting tension and active isometric tension were measured. 4. Both diltiazem and quiescence significantly attenuated contracture tension during hypoxia (0.91 +/- 0.10 vs 2.26 +/- 0.49 g/mm2 for diltiazem vs control, and 0.55 +/- 0.18 vs 2.26 +/- 0.49 g/mm2 for quiescence vs control). Recovery of active tension was improved in the diltiazem groups during reoxygenation (4.16 +/- 0.42 vs 3.75 +/- 0.51, 3.53 +/- 0.15 vs 2.90 +/- 0.13, 5.84 +/- 0.33 vs 6.48 +/- 0.29 and 5.98 +/- 0.90 vs 7.67 +/- 0.68 g/mm2 for diltiazem, diltiazem non-stimulation, non-stimulation and control groups). 5. The results suggest that the protective effect of diltiazem during hypoxia was due to the reduction in energy demand of the myocardium.

Animals↗
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↗