A. A. Charlier

Assessment of regional left ventricular relaxation in patients with coronary artery disease: importance of geometric factors and changes in wall thickness.

To assess local myocardial relaxation abnormalities in patients with coronary artery disease, local myocardial left ventricular wall stress was computed in nine normal subjects and in 22 patients with coronary artery disease. In normal left ventricles, the rate of decrease in isovolumic local stress was not significantly different from the rate of decrease in isovolumic pressure, and the residual wall stress at the end of isovolumic relaxation was uniformly low. In patients with coronary artery disease, the residual wall stress was increased both in infarcted areas and in non-infarcted areas perfused by stenosed arteries (43 +/- 31 and 30 +/- 19 kdyne/cm2, respectively, vs 9 +/- 5 kdyne/cm2 in normal areas; p less than .001). The rate of decrease in local stress in infarcted areas paralleled the rate of decrease in pressure (48 vs 49 msec; NS), but in ischemic areas the rate of decrease in stress was significantly slower than the rate of decrease in pressure (69 +/- 35 vs 48 +/- 15 msec; p less than .05). It is concluded that in patients with coronary artery disease, indexes based only on the analysis of decreases in isovolumic pressure underestimate the severity of local impairments in relaxation rate and cannot be used to predict the level of residual diastolic wall stress.

Long-term effects of xamoterol on left ventricular diastolic function and late remodeling: a study in patients with anterior myocardial infarction and single-vessel disease.

The purpose of the study was to examine whether the prolonged administration of the beta 1-adrenoceptor partial agonist xamoterol could improve left ventricular diastolic function and affect the global remodeling process of the left ventricle after anterior myocardial infarction. In 22 patients with anterior myocardial infarction and single-vessel disease, left ventricular angiography (+ Millar) was performed under basal conditions 1 to 2 months after the acute myocardial infarction. Eight patients were then treated for 3 months with placebo and 14 were treated with xamoterol (200 mg bid) and a second left ventricular angiographic study was performed. Angiograms were digitized frame by frame to derive the diastolic pressure-volume relationship and to compute wall stress. An index of elastic myocardial stiffness was computed at a constant stress of 30 kdynes/cm2 before and after treatment. To evaluate changes in left ventricular shape, segmental areas in anterior and inferior segments were computed and compared at end-diastole and end-systole. After xamoterol, left ventricular end-diastolic pressure and mean diastolic wall stress decreased (from 24 +/- 5 to 15 +/- 5 mm Hg and from 57 +/- 32 to 38 +/- 22 kdynes/cm2, respectively; both p less than .01 vs baseline and vs placebo). These changes were accompanied by a downward shift in the diastolic pressure-volume relationship and by a decrease in the index of myocardial stiffness from 526 +/- 270 to 371 +/- 194 kdynes/cm2 (p less than .02).(ABSTRACT TRUNCATED AT 250 WORDS)

Assessment of Left-ventricular Relaxation in Patients With Valvular Regurgitation

Impaired left ventricular (LV) relaxation has been demonstrated in patients with coronary heart disease and in patients with hypertrophic or congestive cardiomyopathy but not yet in those with aortic or mitral regurgitation. Indeed, in patients with valvular regurgitation the lack of isovolumic relaxation and variations in the filling rate invalidate most relaxation indexes. The aim of this study was to assess ventricular relaxation in patients with valvular insufficiency. The hemodynamic and angiographic data were analyzed during the phase of decreasing left ventricular elastance (that is, when pressure is decreasing while volume is increasing) in 57 patients (27 with valvular regurgitation, 17 normal subjects, and 13 patients with coronary heart disease). Starting from a fixed level of wall stress (40 kdyne/cm2), we determined the incremental LV elastance (ratio solΔAPΔV) and the changes in velocity of lengthening produced by a constant increase in LV volume (+ 20 ml/m2). In aortic and mitral regurgitation, both the incremental elastance (−0.52 versus —0.95 mm Hg/ml per m2 in normal subjects: p <0.001) and the changes in velocity of lengthening (+ 0.76 versus +1.17 circ/s; p <0.05) were abnormal. These indexes were also impaired in patients with coronary heart disease. Further, significant correlations were found in the whole group between incremental elastance and ejection fraction (r = 0.63), mean velocity of fiber shortening (r = 0.62), and end-systolic volume (r = 0.53), suggesting a relation between impaired incremental elastance and alterations in inotropic state or afterload, or both. This hypothesis was confirmed by the fact that patients who had a peak systolic wall stress of less than 400 kdyne/cm2 and a normal index of inotropic state also had normal incremental elastance: in contrast, all but 1 patient with the same afterload but abnormal contractility had abnormal incremental elastance. It is concluded that abnormalities in early diastolic filling are common in patients with valvular regurgitation and are likely to be related to impaired LV relaxation.

Impaired Regional Diastolic Distensibility in Coronary-artery Disease - Relations With Dynamic Left-ventricular Compliance

The regional left ventricular distensibility and its relations with the dynamic left ventricular chamber compliance were studied in 11 normal subjects and in 30 patients with coronary artery disease. The regional peak filling rates were calculated from angiographic data in eight ventricular segments and used as an index of regional distensibility. A depressed global peak filling rate was observed in only 30% of the patients with angina pectoris, but regional abnormalities in peak filling rate were detected in 75% of these patients. A relation between alterations in regional peak filling rate and left ventricular compliance was evident in these patients. Despite comparable end diastolic volume and pressure (10 +/- 2 mm Hg vs. 10 +/- 3 in normal subjects; not significant), the patients with angina pectoris, whose ventricle had at least three segments with a reduced peak filling rate, had indeed significant increases in mean left ventricular filling pressure (14 +/- 4 mm Hg vs. 8 +/- 3 in normal subjects; p less than 0.01) and upward shifts of their left ventricular pressure-volume relation during rapid filling. Conversely, an increase in regional peak filling rate produced by intravenous administration of the calcium antagonist nicardipine in a subgroup of patients with poor diastolic function was accompanied by a reduction in mean left ventricular filling pressure and by a downward shift of the early diastolic left ventricular pressure-volume relation. It is concluded that even in the absence of clinical signs of ischemia and of a previous myocardial infarction, large areas with impaired distensibility are frequently present in patients with angina pectoris.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of octreotide on cardiovascular hormones and haemodynamics in conscious dogs.

Octreotide inhibits the secretion of several hormones and exerts vasopressor effects. To clarify the mechanism of atrial natriuretic factor (ANF) secretion and to assess the cardiovascular effects of octreotide in relation to changes in vasoactive peptide secretion, four groups of conscious dogs were studied: group I (n=11) received saline infusion after placebo, group II (n=10), the same infusion after octreotide, group III (n= 10), placebo only and group IV (n =10) octreotide injection only. Saline (10% body wt) was infused over 40 min after subcutaneous injection of placebo or octreotide (1 γ/kg). Saline produced a rise (p<0.001) of plasma ANF from 32.4±4.1 to 59.0±8.5 pM after placebo and from 35.6±5.5 to 77.0±12.6 pM after octreotide. This rise, not significantly different between groups I and II paralleled a 4–5-fold increase (p<0.005) of right and left atrial pressures. With a higher dose of octreotide (4 μg/kg) injected in 4 dogs, plasma ANF increased by 27.5±5 pM. During hypervolemia, plasma endothelial remained unchanged but plasma angiotensin II and epinephrine decreased (p<0.05) approximately by 80% without being affected by octreotide. Octreotide did not influence the basal secretion of ANF, endothelin-1, angiotensin II and catecholamines. However, in basal conditions, octreotide injection resulted in a 9% increase (p<0.005) of left ventricular systolic pressure, unobserved after placebo. Plasma glucose decreased (p<0.005) in groups receiving octreotide. Thus, octreotide does not impair the stretch-mediated release of ANF which implies a release mechanism independent from somatostatin receptors and consequent changes in intracellular c-AMP. Octreotide has also a pressor effect, unrelated to changes in vasoactive peptide production.

Validation Of An Index Of Left Ventricular Contractility In Man By Means Of A Simple Model Of The Left Ventricle And Of The Vascular Bed

Previous studies in patients with heart disease have shown that the stress-volume relation was linear during late ejection and that the slope of this linear portion (SLSV) could easily be determine...