PubMed Health⌕ Search

Biomedical subjects

A S Blaustein

Publications and source records attributed to A S Blaustein.

30 records · Page 2Linked to original sources
PubMed1986

Myocardial relaxation: effects of preload on the time course of isovolumetric relaxation.

We studied the effect of an isolated increase in preload on isovolumetric relaxation in the intact dog heart and isometric relaxation in isolated cardiac muscle (dog and rat) preparations. In eight anesthetized dogs, 8 to 12 ml of blood was infused into the left ventricle during a single diastole. The exponential time constant (T) of isovolumetric relaxation was measured in single-beat experiments in which the left ventricular systolic pressure increased (112 +/- 2 to 128 +/- 3 mm Hg; p less than .05, n = 62). In a second series of experiments, left ventricular systolic pressure was held constant (109 +/- 2 to 107 +/- 2 mm Hg; p = NS, n = 23) by simultaneous ventricular infusion and aortic unloading. In the first protocol, T increased from 28.0 +/- 0.4 to 30.7 +/- 0.4 msec (p less than .05), whereas in the second protocol (constant systolic pressure) there was no change in T. The time course of isometric relaxation was also studied in six rat left ventricular papillary muscles and four dog right ventricular trabecular muscles. Preload was varied from 30% to 100% of the peak of the isometric length-tension curve in each muscle. Over this wide range of preload, the isometric force decline recordings were superimposable as long as the comparisons were made at equal levels of total load. Thus an isolated increase in preload does not influence the time course of isovolumetric relaxation.

Animals↗
PubMed1985

Asynchronous (segmental early) relaxation of the left ventricle.

Segmental early relaxation, a form of left ventricular asynchrony, refers to lengthening of a myocardial segment before mitral valve opening. This phenomenon may occur in normal and diseased hearts; when it is seen in a diseased ventricle it may occur in either the abnormally contracting segment or the normal segment. Experimental data indicate that altered loading conditions, especially nonuniform distribution of load or functional inhomogeneities (as may occur with regional ischemia), or both, may result in asynchronous relaxation of the left ventricle.

Acute Disease↗
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↗
PubMed1983

Adjunctive nifedipine therapy in high-risk, medically refractory, unstable angina pectoris.

Patients with unstable angina pectoris who remain symptomatic at rest after hospitalization are at increased risk of death or myocardial infarction. This report presents the results of adding the calcium influx blocking agent nifedipine to aggressive therapy with nitrates and beta-blocking drugs in 47 hospitalized patients. The patients were followed up for an average of 12 months. Twenty-two (47%) improved sufficiently to be discharged; despite this symptomatic improvement, 8 had cardiac events within 4 months. Eighteen patients had no symptomatic improvement and 7 of them had cardiac events in 4 months. In 7 others, relief was insufficient to permit discharge, and 1 of these patients had myocardial infarction. In all, 31 patients were treated with medical therapy only. Twenty-one of these patients had a favorable short-term response to nifedipine; 13 died or had an infarction in less than 4 months. Two of 16 patients who underwent coronary artery bypass surgery had cardiac events. The presence of electrocardiographic changes with pain did not identify either a group at higher risk or a group with a better outcome with nifedipine. We conclude that in a high-risk subset of patients with unstable angina pectoris, nifedipine does not reduce morbidity or mortality or the need for bypass surgery, but relieves symptoms in many patients. An early symptomatic response to nifedipine did not predict a reduced incidence of subsequent cardiac events.

Adrenergic beta-Antagonists↗
PubMed1983

Implications of increased myocardial isoenzyme level in the presence of normal serum creatine kinase activity.

Although increased serum creatine kinase (CK) activity in the presence of an increased level of myocardial-specific isoenzymes (CKMB) has been strongly associated with acute myocardial infarction, the significance of an increased serum CKMB level in the presence of a normal total CK level is uncertain. In 335 consecutive patients suspected of having an acute myocardial infarction and 71 control subjects, peak serum CKMB and CK levels were correlated with the presence of other clinical criteria for acute myocardial infarction: (1) typical chest pain, (2) increased myocardial lactate dehydrogenase (LDH1/LDH2), (3) acute electrocardiographic changes (new or ST-T wave changes with evolution), and (4) an elevated CKMB level on 2 or more determinations or a typical CK curve. No control subject had an increase in CK or CKMB or any of the 4 criteria for myocardial infarction. Of the 176 subjects with normal CK and normal CKMB (Group 1), only 11% had more than a single criterion, and none had more than 2 criteria consistent with myocardial injury. In contrast, of the 83 with elevated CK and CKMB levels (Group 2), 93% had 2 or more and 81% had 3 or more of the 4 criteria. Of the 63 patients with elevated CKMB but a persistently normal CK (Group 3), 65% had 2 or more criteria for acute myocardial infarction and 77% had subendocardial electrocardiographic changes; these patients resembled those with both elevated CK and MB. The phenomenon of elevated CKMB with normal CK occurred in 20% of the patients aged greater than or equal to 70 years but in only 10% of the younger group (p less than 0.01). These findings suggest that elevated CKMB with normal CK likely represents definite myocardial injury, is more likely represents definite myocardial injury, is more common in the elderly, and should be considered part of the spectrum of nontransmural myocardial infarction.

Aged↗
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↗
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↗
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↗
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↗