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Biomedical subjects

William H Gaasch

Publications and source records attributed to William H Gaasch.

18 recordsLinked to original sources
PubMed2005

Left ventricular systolic performance, function, and contractility in patients with diastolic heart failure.

BACKGROUND: Patients with diastolic heart failure (DHF) have significant abnormalities in left ventricular (LV) diastolic function, including slow and delayed relaxation and increased chamber stiffness. Whether and to what extent these abnormalities in diastolic function occur in association with abnormalities in LV systolic performance, function, and contractility has not been investigated thoroughly. METHODS AND RESULTS: The systolic properties of the LV were examined in 75 patients with heart failure and a normal ejection fraction (ie, DHF) and 75 normal control subjects with no evidence of cardiovascular disease. LV systolic properties were assessed with echocardiographic and cardiac catheterization data. Stroke work (an index of LV systolic performance), preload recruitable stroke work and ejection fraction (indices of LV systolic function), systolic stress-shortening relationship, end-systolic pressure-volume relationship, and peak (+)dP/dt (indices of LV contractility) were examined. The systolic properties of the LV were normal in patients with DHF. Stroke work was 8.4+/-2.3 in DHF versus 8.8+/-2.5 kg . cm in controls (P=0.26). Preload recruitable stroke work was 99+/-22 in DHF versus 109+/-18 g/cm2 in controls (P=0.13). The relationship between stroke work and end-diastolic volume was similar in DHF and controls. Peak (+) dP/dt was 1596+/-362 in DHF versus 1664+/-305 mm Hg/s in controls (P=0.54). The end-systolic pressure-volume relationship was increased in DHF. The systolic stress versus endocardial fractional shortening relationship was similar in DHF and controls. CONCLUSIONS: Patients with DHF had normal LV systolic performance, function, and contractility. The pathophysiology of DHF does not appear to be related to significant abnormalities in these systolic properties of the LV.

Adult↗
PubMed2005

Exercise testing in aortic stenosis.

Physician-supervised exercise testing in asymptomatic patients with aortic stenosis allows an objective assessment of the hemodynamic response to exercise and it provides a measure of exercise capacity. Exercise testing cannot be used to determine the presence or absence of coronary artery disease, but limited data indicate that exercise testing can provide prognostic information. The results of such testing can be used to provide an exercise prescription and to reassure the patient who might otherwise excessively limit his or her activity.

Aortic Valve Stenosis↗
PubMed2004

Diastolic heart failure--abnormalities in active relaxation and passive stiffness of the left ventricle.

BACKGROUND: Patients with signs and symptoms of heart failure and a normal left ventricular ejection fraction are said to have diastolic heart failure. It has traditionally been thought that the pathophysiological cause of heart failure in these patients is an abnormality in the diastolic properties of the left ventricle; however, this hypothesis remains largely unproven. METHODS: We prospectively identified 47 patients who met the diagnostic criteria for definite diastolic heart failure; all the patients had signs and symptoms of heart failure, a normal ejection fraction, and an increased left ventricular end-diastolic pressure. Ten patients who had no evidence of cardiovascular disease served as controls. Left ventricular diastolic function was assessed by means of cardiac catheterization and echocardiography. RESULTS: The patients with diastolic heart failure had abnormal left ventricular relaxation and increased left ventricular chamber stiffness. The mean (+/-SD) time constant for the isovolumic-pressure decline (tau) was longer in the group with diastolic heart failure than in the control group (59+/-14 msec vs. 35+/-10 msec, P=0.01). The diastolic pressure-volume relation was shifted up and to the left in the patients with diastolic heart failure as compared with the controls. The corrected left ventricular passive-stiffness constant was significantly higher in the group with diastolic heart failure than in the control group (0.03+/-0.01 vs. 0.01+/-0.01, P<0.001). CONCLUSIONS: Patients with heart failure and a normal ejection fraction have significant abnormalities in active relaxation and passive stiffness. In these patients, the pathophysiological cause of elevated diastolic pressures and heart failure is abnormal diastolic function.

Case-Control Studies↗
PubMed2004

Lack of relationship between Doppler indices of diastolic function and left ventricular pressure transients in patients with definite diastolic heart failure.

OBJECTIVES: The purpose of this study was to compare invasive with noninvasive indices of diastolic function in a well-defined group of patients with diastolic dysfunction and a history of diastolic heart failure. BACKGROUND: Patients with heart failure and a normal left ventricular (LV) ejection fraction comprise a very large portion of the heart failure population and most are thought to have diastolic heart failure. While clinical and Doppler criteria for diastolic dysfunction and diastolic heart failure have been developed, there remains some controversy about the need for invasive cardiac catheterization and/or echo-Doppler evaluation of LV diastolic function. To date, there is no consensus as to the utility of these 2 methods in the diagnosis of diastolic heart failure. METHODS: Forty-seven patients (mean age 58 +/- 11 years) with a history of congestive heart failure and preserved ejection fraction (> or =50%) by echocardiography underwent a combined hemodynamic/echo-Doppler study. Patients with coronary disease were excluded. Invasive parameters of LV diastolic function (tau, LV diastolic pressures) and Doppler parameters (peak E, peak A, E/A ratio, isovolumic relaxation time, and E deceleration time) were measured using standard techniques. RESULTS: There was a close correlation between invasively-determined parameters (tau vs end diastolic pressure: r = 0.62, P <.001). The relationships between standard Doppler parameters and LV diastolic pressures were uniformly poor. However, the relationship between Doppler isovolumic relaxation time and tau improved considerably when patients were subgrouped by hemodynamic load. CONCLUSIONS: Standard echo-Doppler indices of diastolic function correlate poorly with LV diastolic pressure transients. The diagnosis of diastolic heart failure cannot be made on the basis of a single echo-Doppler parameter but, rather, all parameters must be examined in concert and used in combination with clinical observations.

Cardiac Catheterization↗
PubMed2004

Left ventricular diastolic dysfunction and diastolic heart failure.

Thirty to fifty percent of patients presenting with signs and symptoms of heart failure have a normal left ventricular (LV) systolic ejection fraction. The clinical examination cannot distinguish these patients (diastolic heart failure) from those with a depressed ejection fraction (systolic heart failure), but echocardiography can. The management of diastolic heart failure has two major objectives. The first is to reverse the consequences of diastolic dysfunction (e.g., venous congestion), and the second is to eliminate or reduce the factors responsible for diastolic dysfunction (e.g., myocardial hypertrophy, fibrosis, and ischemia).

Diastole↗
PubMed2003

Potentiation of atrial contractility by paired pacing augments ventricular preload and systolic performance.

BACKGROUND: Paired electrical stimulation and postextrasystolic potentiation (PESP) of contractility has been extensively studied in ventricular myocardium, but less is known about PESP of atrial contractility. Our aim was to determine whether PESP of atrial contractility could augment left ventricular (LV) preload and improve LV systolic performance. METHODS AND RESULTS: A paired electrical stimulus closely following the pacing stimulus was applied to isolated atrial and ventricular myocardium from 4 dog hearts, and the interval dependent force potentiation was examined. In isolated atrial myocardium, paired pacing increased the active tension from a baseline of 1.36 +/- 0.23 to 2.60 +/- 0.57 g/mm(2); in ventricular myocardium active tension increased from 2.58 +/- 0.42 to 3.81 +/- 0.27 g/mm(2) (both P <.01). Then, LV pressure (micromanometer) and segment length (ultrasonic crystals) were measured in the intact hearts of 7 anesthetized dogs in which premature stimuli were applied to the atrium. In intact hearts, paired pacing of the atrium (coupling interval 200 ms) increased LV end-diastolic pressure from 3.8 +/- 1.0 to 6.4 +/- 1.0 mm Hg; systolic pressure increased from 105 +/- 6 to 112 +/- 7 mm Hg (both P <.05). LV pressure-length loop area (regional stroke work) increased 10.5 +/- 0.2%. CONCLUSIONS: Isolated atrial myocardium exhibits substantial PESP of contractility, which is similar to ventricular myocardium. In the intact heart, atrial PESP augments LV systolic performance by effecting an increase in LV preload. This technique may provide a means of improving cardiac performance in patients with heart failure.

Animals↗
PubMed2002

Heart failure in pressure overload hypertrophy. The relative roles of ventricular remodeling and myocardial dysfunction.

OBJECTIVES: We sought to explore the relative contributions of ventricular remodeling and myocardial dysfunction to heart failure in pressure overload hypertrophy (POH). BACKGROUND: The mechanism that underlies heart failure in POH is adverse left ventricular (LV) chamber remodeling or decreased myocardial function, or a combination of these. METHODS: Twenty weeks after suprarenal aortic banding in rats, animals with POH were classified as those with heart failure (POH-HF) or those with no heart failure (POH-NHF). The LV chamber and myocardial systolic and diastolic functions were determined from in vivo and ex vivo experiments. RESULTS: The LV mass was similar in both POH groups. Chamber remodeling in the POH-HF group was characterized by marked LV enlargement with a normal relative wall thickness (eccentric remodeling), whereas remodeling in the POH-NHF group was characterized by a normal chamber size and increased relative wall thickness (concentric remodeling). The LV systolic function, as determined in vivo from the end-systolic pressure-diameter relationship and ex vivo from the pressure-volume relationship, was lower in the POH-HF group than in the POH-NHF and sham-operated control groups. In contrast, myocardial function was similar in both POH groups, as determined in vivo from the stress-midwall fractional shortening relationship and myocardial systolic stiffness, and ex vivo from the slope of the LV systolic stress-strain relationship. The diastolic chamber stiffness constant was lower in the POH-HF group than in the POH-NHF group, but the myocardial stiffness constant was similar in the two POH groups. CONCLUSIONS: The two POH groups differed primarily in their remodeling process, which led to a chronically compensated state in one group and to heart failure in the other. Hence, heart failure in POH is more closely related to deleterious LV remodeling than to depressed myocardial function.

Animals↗
PubMed2002

Comparison of contractile function of diaphragm and cardiac muscle in response to paired electrical stimulation.

Paired pacing has been shown to potentiate contractile function of cardiac muscle, and it has been suggested that this may enhance contractile function of diaphragmatic muscle. The primary goal of this study was to study the effect of paired pacing on potentiation of contractile function of diaphragmatic muscle compared to atrial and ventricular myocardium. Diaphragmatic muscle was isolated from mouse and rat, and atrial and ventricular myocardium from dogs. Potentiation was induced by isolated extrastimuli (equal in duration and intensity to the pacing stimulus) and by repetitive extrastimuli (i.e. paired pacing) at a paced rate of 12, 30 and 60 beats/min. Baseline studies were performed while preparations were isometrically contracting at L(max) in oxygenated Krebs-Henseleit solution at 28 degrees C. Maximal force generation in response to a premature stimulus was determined at each rate by scanning the coupling interval between paced beats. Under baseline conditions, diaphragmatic muscle contracted faster than atrial and ventricular muscle. In all tissues, maximum potentiation (increase in force above baseline) was approximately 100% of baseline force, and peak potentiation occurred at shorter coupling intervals with increasing rates of stimulation. Single and paired pacing of diaphragm potentiated the contraction during which the extrastimuli were introduced, while in cardiac muscle, extrastimuli potentiated the contraction following the extrastimulus. The maximum potentiated response occurred when the extrastimulus was introduced prior to the development of peak force in diaphragmatic muscle. In contrast, in atrial and ventricular muscle, a single or paired premature stimulus potentiated the subsequent beat when delivered late during relaxation. In cardiac muscle, maximal potentiation gradually occurred following several repetitive stimuli. Following cessation of single and paired pacing, the beat following the potentiated response immediately returned to baseline in diaphragmatic muscle, while a gradual decline was evident over several subsequent beats in cardiac muscle. Increasing the bath temperature from 28 to 37 degrees C resulted in a leftward shift in the peak potentiated force vs. coupling interval curve without a decline in the magnitude of potentiated force in diaphragmatic muscle. In diaphragm muscle, exposure to ryanodine markedly decreased baseline force and maximal potentiation. We conclude that closely timed extrastimuli applied to diaphragmatic muscle can potentiate developed force in a given contraction, while in cardiac tissue a delayed stimulus potentiates the subsequent beat. These differences in contractile responsiveness are not due to differences in loading conditions, but appear to reflect intrinsic differences in calcium handling.

Animals↗
PubMedDate not supplied

Diagnostic criteria for diastolic heart failure.

A diagnosis of diastolic heart failure can be made if the patient exhibits clinical evidence of heart failure and has a normal left ventricular ejection fraction. The diagnosis is confirmed if there is evidence of ventricular hyperthrophy and/or concentric remodeling, left atrial enlargement, or laboratory evidence of diastolic dysfunction.

Diastole↗