Search

Background: Bioprosthesis (BP) used for aortic valve replacement (AVR) in aortic valve disease are subject to structural valve deterioration (SVD) after 20 years or less which leads to reintervention. The diagnostic of SVD can be challenging in the presence of patient-prosthesis mismatch (PPM) which occurs when the effective orifice area (EOA) of the BP is too small for the metabolic needs of a patient. Both SVD and PPM are mainly diagnosed with echocardiography and are characterized by high transprosthetic mean and peak pressure gradients (MG and PG) and maximal velocity (Vmax) as well as reduced EOA. Easily accessible parameters are needed to distinguish SVD from PPM. Acceleration time (AT), ejection time (ET) and AT/ET have been proposed as accurate to identify SVD in presence of PPM. However, these parameters need to be validated. Objectives: The main goal of the present study is to determine the accuracy of AT and AT/ET and to validate new echocardiographic parameters that can distinguish SVD from PPM. New parameters proposed for this study are MG/EOA and PG over mean flow rate (PG/MFR). Methods: In a retrospective study, we analyzed echocardiographic data of 653 patients who underwent AVR. PPM was defined as a projected EOA to body surface area inferior to 0.85 cm 2 /m 2 . SVD was defined using a multiparametric integrative approach including morphological (fibrocalcific remodeling, thickening and stiffening of valve leaflets) criteria and hemodynamic changes according to American Society of Echocardiography/European Association for Cardiovascular Imaging recommendations. Results: EOA was lower and MG higher for patients with SVD compared to those with pure PPM. PG/Q and MG/EOA were significantly higher in patients with SVD compared to patients presenting pure PPM (PG/MFR: 0.22 mm Hg/ml/s ± 0.01 vs 0.15 mm Hg/ml/s ± 0.01; MG/EOA: 31 mm Hg/cm 2 ±2 vs 16 mm Hg/cm 2 ±2, p Conclusion: AT and AT/ET are not accurate parameters to identify SVD in presence of PPM. MG/EOA and PG/MFR represent interesting alternatives to conventional parameters.

Technical difficulties in recording phonocardiogram or indirect carotid pulse occasionally preclude determination of the systolic time intervals. Accordingly, an alternative method was tested in 52 patients, using high-speed strip chart recording of the aortic valve echocardiogram. Satisfactory records were obtained in 36. The interval from opening to closing of the aortic valve (ejection time) was subtracted from the interval between the Q wave of the electrocardiogram and the closing of the aortic valve (total electromechanical systole) to provide the pre-ejection period. When these intervals and the pre-ejection period/ejection time ratio were compared to corresponding values obtained by conventional methods from the simultaneously recorded phonocardiograms and indirect carotid pulses, a high degree of correlation (r greater than 0.97) was found. Differences between the two methods for each interval were insignificant, being greatest in the case of the ejection time but never exceeding 16 msec. These findings indicate that the echocardiogram of the aortic valve provides an alternative, noninvasive method for determination of the systolic time intervals whenever the usual methods fail.

The theoretical basis for the use of the systolic time intervals has been largely established. The method has been validated by direct measures from within the circulatory system. Standards for equipment and technique have been defined. Numerous clinical studies have demonstrated the value of this quantitative noninvasive technique for assessing left ventricular performance. At present there is need for further studies of the clinical usefulness of the systolic time intervals to improve both diagnosis and therapy of various cardiovascular disorders.

Systolic time intervals were measured in 253 normal children, with careful attention to precise recording and measuring techniques, to derive regression equations which could be used as reliable standards for clinical assessment of left ventricular performance in this age group. Using stepwise regression analysis, a highly significant correlation was found for electromechanical systole (QS2) and for left ventricular ejection time (LVET) with heart rate alone in both males and females, and age was not found to be a relevant variable. Similarly, for the preejection period (PEP) in males, heart rate was the only relevant variable. PEP in females showed a small but significant influence of age in addition to heart rate; in practice, this small influence can be neglected. Regression equations relating each of the systolic time intervals to heart rate alone were therefore derived for clinical use. The PEP/LVET ratio was found to be only weakly correlated with heart rate in males and with age in females, and in practice can be considered to be independent of these variables. The mean value of the PEP/LVET ratio and its standard deviation (0.30 +/- 0.04) can therefore be used for all children. We found that satisfactory recording of systolic time intervals can be obtained with little difficulty in almost all children using the techniques described. The method is therefore practical for clinical use in children, as it is in adults, and the normal standards derived in this study can serve as a reliable basis for its application.

Systolic time intervals were measured in 27 normal newborn infants before and after administration of oral digoxin (30 µg/kg). Systolic intervals were also measured in 10 newborns and infants with congestive heart failure before and after this same 30 µg/kg dose of digoxin, but also after administration of a much larger "digitalizing dose" of 80 µg/kg. Preejection period (PEP) shortened significantly in the normal newborns following the smaller dose. Changes in ejection time (ET) were much less striking and appeared to be transient, lasting less than 8 hours. When small doses of digoxin were given to the babies with congestive failure, PEP again shortened significantly. In general, the larger doses of digoxin produced no further changes in PEP or ET, although there were individual exceptions. The demonstration that maximal inotropic effect, as measured by PEP changes, usually occurred with small doses of digoxin may have significant clinical implications in terms of present concepts of loading doses of digitalis in the pediatric age group.

A standard test was designed for measurement of the effect of epinephrine infusion on systolic time intervals in 14 normal subjects as a dose-response phenomenon. In order that we might examine the sensitivity of the test, it was applied in nine patients with idiopathic hypertrophic subaortic stenosis. Normal subjects had a characteristic response—a progressive shortening of the duration of electromechanical systole, left ventricular ejection time, and pre-ejection period. Their left ventricular ejection time, corrected for heart rate, did not change. Patients with idiopathic hypertrophic subaortic stenosis responded to epinephrine infusion with paradoxical lengthening of their left ventricular ejection time, corrected for heart rate. After beta blockade (with propranolol), reinfusion of epinephrine shortened the left ventricular ejection time, corrected for heart rate, to normal levels.

Using the apexcardiogram as a time reference for opening and closure of the aortic valve, systolic time intervals (STI) in infants were determined in 150 normal infants ranging in age from 1 day to 1 year. Thirty infants with congestive heart failure secondary to a variety of congenital and acquired heart diseases were studied in a similar manner for comparison. The data revealed that heart failure in the infant is not marked by any one pattern of STI. In specific disease entities associated with congestive heart failure, the STI appear to be consistent. In infants with congestive heart failure due to congenital heart disease, the STI do not correspond with values reported in the adult with hypertensive or arteriosclerotic disease. The differences are explained by viewing STI in infants primarily a function of hemodynamic alterations dictated by an underlying cardiovascular anomaly rather than a result of a primary myocardial derangement. The findings in the infant with chronic heart failure due to primary myocardial disease tend to parallel data previously reported in the adult with arteriosclerotic disease and chronic heart failure.

Coronary artery disease and angina pectoris are frequently associated with disordered myocardial function which may cause abnormalities in precordial motion, heart sounds, and/or systolic time intervals. The pathophysiologic basis for these abnormalities has been studied by correlating them with more direct measurements of myocardial function. Large a waves on the apexcardiogram and atrial gallops are related to accentuated left ventricular a waves which reflect diminished left ventricular compliance. Uncoordinated left ventricular contraction (asynergy) may cause abnormal systolic motion which can sometimes be recorded on the apexcardiogram. Ventricular (early diastolic) gallops in coronary artery disease are usually associated with extensive obstructive lesions, left ventricular asynergy, and a low cardiac output. Transient paradoxic splitting of the second sound in angina pectoris has been reported though rarely documented by phono-cardiography. Mitral insufficiency due to papillary muscle dysfunction implies significant damage to the papillary muscles and the surrounding ventricular wall, usually by severe coronary artery disease. Systolic time intervals are a sensitive technic which may reflect diminished contractility (prolonged preejection period) or low stroke volume (shortened left ventricular ejection time) in patients with coronary artery disease. However, systolic time intervals are also sensitive to many other pharmacologic and hemodynamic influences, including changes in left ventricular preload and afterload which may result in misleading values. Therefore, as a technic for evaluating individual patients with coronary artery disease and angina pectoris, the role of systolic time intervals remains limited.

Systolic time intervals were performed on 49 male subjects. Twenty-eight subjects were inactive with respect to a continuing exercise program and were classified as a sedentary group. Twenty-one subjects were physically active and were classified as an active group. The active group was composed of 12 members who were moderately active and nine members of a college track team. Using analysis of covariance no significant difference was found in the total duration of electromechanical systole (QS 2 ), left ventricular ejection time (LVET), or the preejection period (PEP) between the moderately active subgroup and the members of the track team. However, a highly significant difference was found between the sedentary and the active group in the QS 2 and PEP. The LVET was not significantly different. The results of this study appear to be consistent with the hypothesis that an increase in intrinsic myocardial performance is associated with physical conditioning. In addition, it is suggested that published equations for the QS 2 interval and the PEP may be applicable only to sedentary individuals.

Echocardiography was used to measure right ventricular systolic time intervals (RVSTI) in 85 normal children (group I) and in 229 patients undergoing cardiac catheterization (group II). Corrected right ventricular pre-ejection period (RPEPC) and right ventricular ejection time (RVETc) (based on regression analysis of group I) and RPEP/RVET were each correlated with pulmonary artery (PA) diastolic and mean pressures and pulmonary vascular resistance (PVR). The best correlation (0.83) was between a second degree polynomial of the RPEP/RVET and PA diastolic pressure. The RPEP/RVET allowed prediction of PA diastolic pressure within 10 mm Hg in 85% of the patients. The utility of RPEP/RVET was confirmed in sequential data of 22 patients, in whom alteration in RPEP/RVET accurately reflected the changing PA diastolic pressure. The RPEP/RVET could not be used to assess PA pressure in six patients with congestive cardiomyopathy nor in 18 patients with complete right bundle branch block (CRBBB).

One of the noninvasive methods of evaluating left ventricular performance is the measurement of left ventricular systolic time intervals (LVSTI). However, noninvasive measurement of right ventricular systole by this technique has been unreliable because of the inability to accurately time the onset of right ventricular ejection. Excellent correlation of LVSTI measured from the carotid pulse and those determined from the echocardiogram was demonstrated in 15 patients. STI of the right ventricle (RVSTI) were measured in a similar fashion from the pulmonary valve echo in 11 normal children. Right ventricular ejection time (RVET) was longer than left ventricular injection time (LVET). Right ventricular pre-ejection period and RPEP was shorter than left ventricular pre-ejection period (LPEP). In 15 children with transposition of the great arteries (TGA) the situation was reversed. RVET was shortened and RPEP was prolonged as the right ventricle contracted against systemic resistance; whereas, the LVET lengthened and LPEP shortened with ejection into a low pressure pulmonary circuit. Our studies in a total of 41 patients indicate the accurate, noninvasive measurement of right, as well as left, ventricular STI can be obtained with the use of echocardiography.

Systolic time interval measurements were made sequentially throughout pregnancy and during the postpartum period. Recordings were made in the supine and lateral positions. Although the greatest deviations from predicted values were present in the third trimester, changes were evident as early as the first trimester. During the first two trimesters the pre-ejection period (PEP) was significantly shortened. The left ventricular ejection time (LVET) remained normal while the PEP/LVET decreased. The third trimester was characterized by a markedly shortened LVET, a prolonged PEP, and an increased PEP/LVET, all more apparent in the supine than in the lateral position. These findings are consistent with impaired left ventricular performance and are probably due to decreased left ventricular preload resulting from diminished venous return secondary to inferior vena caval obstruction by the gravid uterus. In the postpartum period, the PEP/LVET remained elevated in both positions; the PEP was prolonged and the LVET shortened in the lateral posture. It is concluded that alterations in systolic time interval measurements occur normally during the course of uncomplicated pregnancy and persist into the postpartum period. Possible mechanisms are discussed.

Systolic time intervals (STI) were measured in matched patients with and without right ventricular failure (RVF). STI were calculated from brachial arterial pressure tracings obtained at cardiac catheterization in four groups of patients: 1) controls, without RVF; 2) acute pulmonary embolism with and without acute RVF; 3) mitral stenosis, with and without chronic RVF; 4) primary pulmonary hypertension, with chronic RVF. In patients with pulmonary embolism without acute RVF, STI were normal. However, patients with acute RVF due to pulmonary embolism had significantly shortened left ventricular ejection times (LVETc) and significantly increased pre-ejection periods (PEPc) and increased PEPc/LVETc ratios ( P < 0.05, P < 0.001, P < 0.001 respectively). Similar results were obtained in patients with chronic RVF. In patients with mitral stenosis without RVF, STI were normal. However, in patients with chronic RVF due to mitral stenosis or primary pulmonary hypertension, PEPc and PEPc/LVETc ratios were lengthened and LVETc was shortened ( P < 0.003, P < 0.005, and P < 0.001 respectively). PEPc/LVETc ratios increased as stroke index decreased ( r = –0.55). There was also an association between PEPc/LVETc and right atrial mean pressure ( r = 0.70). These data demonstrate that patients with acute and chronic right ventricular failure have abnormal systolic time intervals possibly secondary to left ventricular dysfunction.

Systolic time intervals (STI) were determined from simultaneous records of the electrocardiogram, carotid pulse and phonocardiogram in 17 consecutive patients with thyrotoxicosis and sinus rhythm. None of the patients had clinical evidence of congestive heart failure. Intervals measured included electromechanical systole (Q-S 2 ), heart sound interval (S 1 -S 2 ) and left ventricular ejection time (LVET). From these, the pre-ejection period (PEP), isovolumetric contraction time (ICT) and Q-S 1 intervals were derived. Deviations (ΔSTI) of observed values from expected values (Weissler equations) for the same heart rate were obtained by subtraction. The mean deviation of the thyrotoxic patients ± sem from the normal population were ΔQ- S 2 * = –37.8 ± 4.2; ΔLVET = –4.0 ± 4.1; ΔPEP * = –33.8 ± 1.8. The shortening of PEP was due largely to a shortened ICT (ΔICT * = –27.2 ± 1.1). In eight patients studied serially during treatment the short PEP returned to the normal range concurrently with serum T 4 measurements. This study indicates that the PEP is a unique noninvasive measurement of biological end organ responsiveness with thyroid dysfunction; a short PEP is characteristic of uncomplicated thyrotoxicosis and serial changes in PEP may be a useful index of therapeutic response. * P < .001.

Systolic time intervals (STI) and serum digoxin concentrations (SDC) were measured in eight patients with compensated atherosclerotic and/or hypertensive heart disease who received oral digoxin 0.25 mg/day or 0.5 mg/day for alternate two-week periods without a loading dose. Control data were obtained both before and after the four weeks of treatment. After 13 days treatment with digoxin, 0.5 mg/day, there was a significant decrease in total electromechanical systole corrected for heart rate (QS 2 i), pre-ejection period (PEP), pre-ejection period corrected for heart rate (PEP 1 ) and PEP/left ventricular ejection time (LVET). After the thirteenth dose of 0.25 mg/day there was significant shortening of PEP 1 and PEP/LVET. Shortening of QS 2 i correlated significantly with SDC 24 hours after the thirteenth dose of 0.5 mg. These data suggest that after 13 days of treatment with 0.25 and 0.5 mg/day of digoxin, a positive inotropic effect occurs as reflected by STI shortening. A greater effect was recorded with the 0.5 mg dose.

This investigation was performed to determine the presence of unilateral or bilateral pulsus alternans in the systemic and pulmonary circulations in heart failure and to estimate the prevalence of pulsus alternans in congestive cardiomyopathy. The subjects were 36 adult patients in heart failure due to a variety of cardiopulmonary diseases. We measured left- and right-sided systolic time intervals from simultaneous dual echocardiograms of both semilunar valves. The alternans was left-sided in seven patients, right-sided in one patient and bilateral in six patients. Pulsus alternans was induced by ventricular premature complexes (VPCs), except in one patient with bilateral and persistent alternans. For a VPC to precipitate alternans, the early beat itself must be associated with an abbreviated ejection time. Echophonocardiographic records of 100 patients with congestive cardiomyopathy were reviewed for evidence of pulsus alternans. We found persistent alternans in 10 patients and VPC-induced alternans in seven patients. We could not measure any difference in severity of disease in patients with pulsus alternans compared with those without.

The effects of graded increments of passive head-up tilt on the duration of the systolic time intervals corrected for heart rate were investigated in 15 normal subjects. Head-up tilt caused a prolongation of the pre-ejection period and a shortening of the left ventricular ejection time, while total electromechanical systole diminished minimally. The lengthening of the pre-ejection period and abbreviation of the left ventricular ejection time increased progressively with stepwise increments of head-up tilt. The application of venous occlusive tourniquets produced changes in the systolic intervals directionally similar to those observed with head-up tilt. In contrast to the normal subjects, three patients with congestive heart failure demonstrated no change in the systolic time intervals during head-up tilt. After diuresis in two of the patients with heart failure, the responses of their systolic time intervals to head-up tilt returned toward normal.

The effects of 0.6 mg sublingual nitroglycerin on responses of the left ventricular (LV) systolic time intervals to a 4-min exercise step test were determined in 10 patients with angina and 10 normal controls. In normal subjects, the exercise test shortened total electromechanical systole corrected for heart rate (Q2 c 22 msec but left the LV ejection time corrected for heart rate (LVET c ) unchanged. By contrast, in the angina group, exercise failed to shorten the Q2 c but prolonged the LVET c 25 msec. In both groups, nitroglycerin shortened the LVET c and Q2 c after exercise. By decreasing LV afterload, preload, and hypoxia, and by improving LV function, nitroglycerin abolished the abnormal marked prolongation of LVET c after exercise in angina patients and converted the failure of their Q2 c to shorten after exercise into a normal shortening of Q2 c . Nitroglycerin also had marked effects at rest, which contributed importantly to its effects on the systolic temporal responses to exercise. Suppression by nitroglycerin of LVET c prolongation after exercise diminishes myocardial oxygen consumption and is antianginal. Most important, assessment of this action provides an objective, though noninvasive, means to evaluate the efficacy of nitrates in improving LV performance with exercise in angina patients.