Variables Of Left Ventricular Function Research Articles

Continuous wave Doppler echocardiography for noninvasive assessment of left ventricular dP/dt and relaxation time constant from mitral regurgitant spectra in patients

Objectives. We previously demonstrated experimentally that the mitral regurgitant velocity spectrum can be used to estimate left ventricular pressure throughout systole and may provide a new noninvasive method for estimating maximal dP/dt and the relaxation time constant. This study was designed to test this method in patients.Background. The maximal first derivative of left ventricular pressure (dP/dt) and the time constant of left ventricular isovolumetric relaxation (τ) are important variables of left ventricular function, but the need for invasive measurement with high fidelity catheters has limited their use in clinical cardiology.Methods. Twelve patients with mitral regurgitation were studied. The Doppler mitral regurgitant velocity spectrum was recorded simultaneously with micromanometer left ventricular pressure tracings in all patients. The regurgitant velocity profiles were digitized and converted to ventriculoatrial (VA) pressure gradient curves using the simplified Bernoulli equation and differentiated into instantaneous dP/dt. The relaxation time constant (τ) was calculated assuming a zero pressure asymptote from catheter left ventricular pressure decay (τc) and forn the Dopplerderived VA gradient curve with corrections. Two methods were used to correct the Doppler gradient curve to better approximate the left ventricular pressure decay before calculating the relaxation time constant: 1) adding an arbitrary 10 mm Hg (τ10), and 2) adding the actual mean pulmonary capillary pressure (τla).Results. The Doppler-derived maximal positive dP/dt (1,394 ± 302 mm Hg/s [mean ± SD]) correlated well (r = 0.91) with the catheter-derived maximal dP/dt (1,449 ± 307 mm Hg/s). Although the Doppler-derived negative maximal dP/dt differed slightly from catheter measurement (1,014 ± 289 vs. 1,195 ± 354 mm Hg/s, p < 0.01), the correlation between Doppler and catheter measurements was similarly good (r = 0.89, p < 0.0001). The correlation between τ10and τcwas excellent (r = 0.93, p < 0.01), but the Doppler-derived τ10(50.0 ± 11.0 ms) slightly underestimated the catheter-derived τc(55.5 ± 12.8 ms, p < 0.01). This slight underestimation could be corrected by adding the actual pulmonary capillary wedge pressure to the Doppler gradient curve.Conclusions. Doppler echocardiography provides an accurate and reliable method for estimating left ventricular maximal positive dP/dt, maximal negative dP/dt and the relaxation time constant (τ) in patients with mitral regurgitation.

Long-term (3-month) effects of a new beta-blocker (nebivolol) on cardiac performance in dilated cardiomyopathy

Objectives. This study examined the long-term (3-month) effects of nebivolol, a new beta-adrenergic blocking agent, on cardiac performance in patients with dilated cardiomyopathy.Background. Several beta-blocking drugs have been reported to have a beneficial hemodynamic effect in patients with dilated cardiomyopathy, but few data obtained in a placebo-controlled randomized study have addressed the mechanisms of improvement.Methods. Twenty-four patients with dilated idiopathic (n = 22) or ischemic (n = 2) cardiomyopathy (ejection fraction 0.15 to 0.40) in stable New York Heart Association functional class II or III were entered into a double-blind randomized trial of nebivolol, a new, potent, selective beta1-antagonist. Exercise time, invasive hemodynamic data (12- and 24-h monitoring) and variables of left ventricular function were examined at baseline and after 3 months of orally administered nebivolol (1 to 5 mg/day, n = 11) or placebo (n = 13).Results. Heart rate decreased (group mean 85 to 71 beats/min vs. 87 to 87 beats/min with placebo) and stroke volume increased significantly (group mean 43 to 55 ml vs. 42 to 43 ml) with nebivolol; decreases in systemic resistance, systemic arterial pressure, wedge pressure and pulmonary artery pressure were not significantly different from those with placebo. Similar hemodynamic results were obtained in the catheterization laboratory. Analysis of high fidelity measurements of left ventricular pressure showed a decrease in left ventricular end-diastolic pressure in the nebivolol group (group mean 21 to 15 vs. 24 to 20 mm Hg with placebo) but no change in the maximal rate of pressure development or in two variables of left ventricular relaxation (maximal negative rate of change of left ventricular pressure [dP/dtmax]and the time constant tau). Left ventricular mass decreased (p = 0.04). Despite a decrease in heart rate with nebivolol, there was a slight decrease in left ventricular end-diastolic volume (p = NS). End-systolic volume tended to decrease (p = 0.07) despite no reduction in end-systolic stress. The net result was a significant increase in ejection fraction (group mean 0.23 to 0.33 vs. 0.21 to 0.23 with placebo), presumably as a result of an increase in contractile performance. This effect was corroborated by an increase in a relatively load-independent variable of myocardial performance.Conclusions. Nebivolol improved stroke volume, ejection fraction and left ventricular end-diastolic pressure, not through a measurable reduction in afterload or a lusitropic effect, but by improving systolic contractile performance.

Preoperative Left Ventricular Dysfunction and Operative Risks in Coronary Bypass Surgery

Preoperative left ventricular function variables were evaluated as potential risk factors for peroperative and postoperative complications in 183 consecutive patients undergoing coronary bypass surgery. Fifty-six patients had no abnormal criteria and 127 had at least one criterion (AN). The incidence of history of infarction was significantly greater in the AN (71.6 percent) than in the N (39.6 percent) group (p less than 0.04). During the early postoperative course, N and AN differentiated significantly in (1) the need for inotropic therapy (II vs 30 percent, p less than 0.05); (2) intra-aortic balloon pump (0 vs 13 percent); (3) arrhythmias (20 and 40 percent, p less than 0.002); and (4) stay in the Intensive Care Unit (2.3 +/- 0.8 and 3.9 +/- 2 days, p less than 0.01). Perioperative necrosis and mortality were not different. During a follow-up period of two years, N and AN did not show any difference in mortality and recurrence of angina.

A new electrocardiographic classification for post-myocardial infarction clinical trials

A new electrocardiographic code was developed for clinical trials involving patients with acute myocardial infarction (AMI). In the Multicenter Post-Infarction Program (MPIP), the electrocardiogram, classified by the Minnesota code, was not useful as a clinical predictor and played almost no role in subsequent analysis. To test its value the new code was applied to the electrocardiograms of 653 of the 866 patients in the MPIP data base who had sustained a first AMI. The MPIP code identifies AMI by region and severity. The 4 regions are anterior, lateral, inferior and posterior, defined by traditional criteria. Severity codes include Q-wave and non-Q-wave AMI, ST depression and no ischemic changes. The interpretation for each of 4 regions results in a 4-digit location severity code that is amenable to sorting and analysis. Fourteen separate and mutually exclusive groups were identified. Mortality gradients were found within the inferior AMI groups, but not within the anterior AMI groups. Mean ejection fraction was 50% for patients with isolated anterior infarction and decreased progressively (p < 0.0003) as the extent of lateral wall involvement increased. For isolated inferior AMI, mean ejection fraction was 53%; lateral or posterior involvement did not significantly change this. The MPIP code is easy to apply, correlates acceptably well with clinically relevant variables of left ventricular function and permits the electrocardiogram to be used as a clinical predictor in large clinical trials.

Diurnal variation in left ventricular function: a study of patients with myocardial ischaemia, syndrome X, and of normal controls.

Angina can occur in the early morning. The mechanism of this is unclear and both haemodynamic changes and coronary artery spasm may be important. The purpose of this study was to investigate the diurnal variation in pulmonary artery diastolic pressure (an indirect measure of left ventricular filling pressure) in six normal subjects, 18 patients with coronary artery disease, five with variant angina, and six with syndrome X. A transducer tipped catheter and a simple recording system were used to record ambulatory pulmonary artery diastolic pressure for 24 hours. Variation in pulmonary artery diastolic pressure was related to the timing of episodes of ST segment depression and elevation by simultaneously recording a frequency modulated electrocardiogram. Episodes of ST segment change occurred predominantly in the early morning (midnight to 6 am) in variant angina (eight out of 14 episodes) whereas in syndrome X all episodes were recorded during the day. In coronary artery disease both painful and painless episodes were distributed throughout the day, with 10 out of 67 episodes occurring between midnight and 6 am. A similar diurnal variation in pulmonary artery diastolic pressure was seen in the groups--that is, values were low during the day and higher at night, with the maximum values between midnight and 6 am. The 24 hour median pulmonary artery diastolic pressure was higher in patients with coronary artery disease than in the control group and those with syndrome X. The finding that pulmonary artery diastolic pressure, and therefore left ventricular end diastolic pressure, is greatest in the early morning may represent the background haemodynamic state in which other factors lead to myocardial ischaemia during these hours.

Effects of propranolol and timolol on left ventricular volumes during exercise in patients with coronary artery disease

The hemodynamic effects of beta-receptor blocking agents on the ejection fraction of patients with coronary artery disease during exercise have been studied previously using radionuclide techniques. Left ventricular volume measurements and the peak systolic pressure/end-systolic volume (PSP/ESV) index have been shown to be variables of left ventricular function that are less influenced by preload and afterload than is ejection fraction. Left ventricular volumes and PSP/ESV were therefore measured in 18 patients with proven coronary artery disease in the control state and after 2 weeks of daily maintenance therapy with either 240 mg propranolol or 60 mg timolol. Values at rest and during symptom-limited upright exercise were compared using the first pass technique and a multicrystal scintillation camera. Left ventricular volumes were measured by the area-length method. Because there was no difference between the propranolol and timolol groups, the results for both groups were combined. The ejection fraction at rest after beta-receptor blocker treatment was not significantly different from pretreatment measurements because of an increase in both end-diastolic and end-systolic volumes (p less than 0.01). However, the value for peak systolic pressure/end-systolic volume (PSP/ESV) index at rest was lower after treatment. The exercise ejection fraction was greater after treatment (p less than 0.01), owing to an increase in end-diastolic volume and unchanged end-systolic volume. In addition, there was a significant improvement in the directional change in the PSP/ESV ratio between rest and exercise from pretreatment to treatment (-1.1 +/- 2.5 to +0.2 +/- 1.2, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiographic features of impaired ventricular function in diabetes mellitus.

In order to study left ventricular diastolic function in diabetes mellitus, simultaneous echo- and phonocardiograms were recorded in 142 diabetics (free from heart disease), 20 normal subjects, and 16 patients with coronary artery disease. The resultant traces were digitised, and left ventricular relaxation and the rate and duration of cavity dimension increase and wall thinning were determined. Diastolic variables of left ventricular function were normal in 12 young diabetics with no complications. Significantly delayed mitral valve opening relative to minimum dimension and aortic valve closure was found in all other groups of diabetics. Forty-four diabetics with severe microvascular complications had significantly reduced peak rate and prolonged duration of wall thinning and dimension increase. The abnormalities were unlike those found in subjects with coronary artery disease. The extent of microvascular complications was significantly correlated to most variables of diastolic function. This relation was maintained in 31 diabetics with significant cavity dimension increase during isovolumic relaxation (incoordinate relaxation). In 42 juvenile onset patients there was good correlation between the duration of diabetes and most variables of diastolic function. These studies show that the primary cardiac abnormality in diabetic micro-angiography is a prolonged duration and reduced rate of posterior wall thinning with impaired left ventricular dimension increase, reflecting abnormal myocardial properties.

Left ventricular function in diabetes mellitus. II: Relation between clinical features and left ventricular function.

We have shown a close relation between clinical microvascular complications and abnormalities of left ventricular function in 185 established diabetics without clinical heart disease. In 50 insulin-dependent diabetics who presented at under 20 years of age there was a correlation between the duration of diabetes and the isovolumic relaxation time, minimal dimension to mitral valve opening, and ratio of pre-ejection period to left ventricular ejection time. Diabetics with mild microvascular complications were similar to diabetics with no complications except for minor prolongation of the diastolic time intervals. Those with severe complications were significantly different from diabetes with milder complications and normal controls in all variables of left ventricular function. A close relation between left ventricular function and the microvascular complications index (code 0 when no complications to code 7 when all present and severe) was found for the following variables: isovolumic relaxation time, the interval from minimal dimension to mitral valve opening, ratio of pre-ejection period to left ventricular ejection time, and pre-ejection period index. It is concluded that in diabetes abnormalities of left ventricular function are related to duration of disease and complications; and that a diabetic specific heart muscle disorder occurs frequently in patients with severe microvascular complications.

Direct evidence that left ventricular myocardium is incompressible throughout systole and diastole.

Incompressibility of left ventricular myocardium was tested utilizing isolated canine working left ventricular preparations. This ventricle functioned at levels comparable to the intact heart. The ventricular muscle volume was calculated with the videometric border recognition technique, which is probably the most satisfactory among the presently available techniques to measure left ventricular volume. The calculated wall mass throughout the cardiac cycle varied ranging between about +/- 5%. The difference between the calculated and weighed myocardial mass was within +/- 7% of the true weight. These findings warrant the idea that myocardial muscle mass is incompressible throughout systole and diastole; the assumption used to calculate some variables of left ventricular function.

Inotropic effect of post-stimulation potentiation in man: An echocardiographic study

To determine the magnitude of enhancement of the inotropic state in the intact human left ventricle, echocardiographic studies were performed in 11 subjects during pacing-induced changes in heart rate. Incremental atrial or ventricular pacing (80 to 160 beats/min) was performed for 1 minute at each rate, and echocardiographic variables of left ventricular function and indexes of left ventricular thickening were assessed for the post-stimulation beats and compared with the values obtained during sinus rhythm before pacing. For the first post-stimulation beat at maximal paced rates (146 ± 3 beats/min, mean ± standard error of mean), the ejection fraction (+23 percent P < 0.001), percent fractional shortening (+45 percent, P < 0.001) and mean velocity of circumferential fiber shortening (+45 percent, P < 0.001) increased significantly, whereas the end-systolic dimension (−22.4 percent, P < 0.001) and volume (− 52 percent, P < 0.001) decreased significantly. The end-diastolic dimension (+1.42 percent) and volume (+4.8 percent) did not change significantly. Similarly, septal thickening (+21.89 percent, P < 0.005), posterior wall thickening (+23.4 percent, P < 0.001), left ventricular thickening (+21.91 percent, P < 0.001) and the mean rate of left ventricular thickening (+33 percent, P < 0.001) increased significantly. Similar significant changes, although of a lesser magnitude, occurred at lower paced rates; the magnitude of these changes was proportional to the pacing rate. Decay in potentiation occurred within four to five beats after pacing was stopped at any given rate. Thus, in the intact human heart (1) the positive inotropic effects of stimulation on the left ventricle are reflected as post-stimulation potentiation, (2) potentiation is related to the pacing rate, and (3) decay in potentiation occurs rapidly when pacing is stopped.

Pump dysfunction after myocardial infarction: Importance of location, extent and pattern of abnormal left ventricular segmental contraction

To delineate the relative effects on left ventricular function of the site, extent and nature of abnormal left ventricular segmental contraction (dyssynergy) and thereby determine the mechanism by which anterior myocardial infarction results in greater depression of left ventricular performance than does inferior infarction, 43 patients with remote myocardial infarction of similar extent (average 38 percent of left ventricular systolic perimeter) and associated hypokinesia or dyskinesia confined to either the anterior or inferior wall were compared; 10 additional patients were evaluated who exhibited generalized dyssynergy (72 percent of left ventricular perimeter). When the pattern of dyssynergy and extent of infarction were similar, the location alone of dyssynergy did not influence variables of left ventricular function. However, paradoxical outward systolic movement (dyskinesia) of the anterior or inferior wall resulted in greater depression ( P < 0.05) of measures of left ventricular performance than did diminished inward systolic motion (hypokinesia) associated with infarction of similar extent and location. All measures of left ventricular performance were considerably more depressed ( P < 0.05) in the 10 patients with generalized dyssynergy than in the 43 patients with localized dyssynergy. Thus, the location of infarction is not a unique determinant of left ventricular performance. Instead, the size of infarction is the principal characteristic of dyssynergy that impairs left ventricular function; the severity of the pattern of dyssynergy is significant but of lesser importance. It is therefore concluded that the greater reduction of left ventricular function in anterior than in inferior myocardial infarction is largely the result of the more extensive area of necrosis rather than of the location of the infarction.