Significant Change In Ejection Fraction Research Articles

??1-Adrenergic receptor polymorphisms and left ventricular remodeling changes in response to ??-blocker therapy

Large variability exists in the improvement in left ventricular (LV) function from beta-blocker treatment. We hypothesized that polymorphisms at codon 389 (Arg389Gly) and 49 (Ser49Gly) in the beta1-adrenergic receptor (AR) gene were associated with LV reverse remodeling changes in response to beta-blocker therapy among heart failure patients. We prospectively enrolled 61 beta-blocker naive patients with systolic heart failure. Patients underwent baseline echocardiography followed by metoprolol CR/XL. The dose was doubled on a biweekly basis up to 200 mg/day or attainment of maximum tolerated dose. Echocardiography was repeated after the patient received the target or highest tolerated dose for 3 months. Among patients with the Arg389Arg genotype, ejection fraction (EF) increased from 23+/-5 to 29+/-10 (P=0.008). Gly389 carriers did not demonstrate any significant change in EF (22+/-9 to 23+/-11; P=0.45). There was a significant between-group difference in EF by genotype (P=0.04). The Arg389Arg genotype was also associated with significantly greater reductions in LV end-diastolic and end-systolic diameters compared to Gly389 carriers. Patients with the Gly49 variant also had a significantly greater reduction in LV end-diastolic diameter compared to Ser49 homozygotes. Multiple regression analysis modeling revealed that the codon 389 polymorphism was a significant predictor of an improvement in EF and both codon 49 and 389 polymorphisms were significant predictors of final LV end-diastolic diameter. Heart failure patients with the Arg389Arg genotype and Gly49 carriers had greater improvements in LV remodeling from beta-blocker treatment.

Evidence for left ventricular remodeling after percutaneous coronary intervention: Effect of percutaneous coronary intervention on left ventricular ejection fraction and volumes

Background: Post-stress ejection fraction (EF), end-diastolic (EDV) and end-systolic (ESV) volumes by gated myocardial perfusion SPECT (MPS) are well validated, reproducible and of prognostic significance. However, little is known about the impact of percutaneous coronary intervention (PCI) on left ventricular volumes and remodeling. Methods: Thirty-eight patients who underwent MPS before and 6 months after PCI were evaluated. MPS were interpreted deriving summed stress (SSS), rest (SRS) and difference (SDS=SSS-SRS; extent of ischemia) scores. EF, EDV and ESV were generated by QGS™. Pre-PCI MPS were compared to post-PCI MPS. Results: Single vessel disease was present in 63% of patients. PCI of one vessel was performed in 82% of patients. After 6 months, SSS (10.6±6.3 vs. 2.8±4.3, p<0.001) and SDS (8.2±5.6 vs. 1.4±2.3, p<0.001) had improved; however, EF did not change significantly (55±10 vs. 57±13, p=ns). Still, EDV (105±25 ml vs. 96±25 ml, p=0.006) and ESV (49±19 ml vs. 41±18 ml, p=0.001) were significantly reduced. Conclusion: Results of MPS documented the beneficial effect of PCI on symptoms and extent of ischemia. In addition, the findings showed a significant decrease in ESV and EDV after PCI as compared to pre-PCI findings which points to a positive effect on left ventricular remodeling even in the absence of significant changes in EF.

Administration of growth hormone to patients with advanced cardiac heart failure: effects upon left ventricular function, exercise capacity, and neurohormonal status

Experimental and clinical studies have shown that the administration of recombinant human growth hormone can improve deteriorated left ventricular function and hemodynamics in patients with heart failure. Herein, we compared the effects of growth hormone versus placebo upon resting left ventricular ejection fraction, exercise capacity and neurohormonal status in patients with advanced heart failure. Nineteen patients with advanced cardiac heart failure (ejection fraction <30%) were studied at baseline and after 8 weeks of treatment with growth hormone (0.03 U/kg per day) or placebo. Primary end points were resting left ventricular ejection fraction, peak oxygen consumption and neurohormonal status, including plasma norepinephrine levels and insulin like growth factor-1 and its binding protein-3. Results are presented as median and interquartile ranges. Patients receiving growth hormone had a significant increase in insulin growth factor-1 plasma levels (median difference growth hormone=83 ng/ml [57–170] versus placebo=−6 ng/ml [−23–6], P<0.05) and its binding protein-3. However, no significant increase in left ventricular ejection fraction after growth hormone treatment (ejection fraction pre=16% [13–18] and post=17% [14–27]) was noticed when compared to placebo (ejection fraction pre=20% [15–24] and post=20% [15–26]). Also, no significant effect of growth hormone treatment was seen on peak oxygen consumption or norepinephrine plasma levels. Although the administration of growth hormone to patients with advanced cardiac heart failure was associated with a significant increase in insulin growth factor-1, there were no significant changes in ejection fraction, exercise capacity and/or neurohormonal status.

Haemodynamics of the pressor effect of oral water in human sympathetic denervation due to autonomic failure

Oral water ingestion increases blood pressure in normal elderly subjects and in patients suffering from autonomic failure, but the time course of the haemodynamic changes is not known. We therefore studied 14 subjects with documented sympathetic denervation due to pure autonomic failure, with continuous haemodynamic recordings obtained before and after ingestion of 500 ml of distilled water at room temperature. The time course of changes in values of systolic and diastolic beat-by-beat finger blood pressure, heart rate, stroke volume, cardiac output, ejection fraction and total peripheral resistance were analysed. Systolic blood pressure rose from 115+/-8 mmHg (mean+/-S.E.M.) to 133+/-8 mmHg (P<0.001), and diastolic blood pressure from 64+/-4 to 73+/-4 mmHg (P<0.001), with the pressor response beginning a few minutes after water ingestion, plateauing between 10 and 35 min (peak at 14 min), and returning to baseline at 50 min. Heart rate fell from 71+/-2.5 to 67+/-2 beats/min (P<0.001), and total peripheral resistance increased from 1.31+/-0.19 to 1.61+/-0.24 m-units (P<0.001). There were no significant changes in ejection fraction, stroke volume or cardiac output. This study confirmed a pressor response to oral water in subjects with sympathetic denervation. The temporal profile of the response did not favour reflexly mediated sympathetic activation. As subjects with autonomic failure are prone to salt and water depletion, and since blood pressure is exquisitely sensitive to such changes, it may be that the observed response is due to repletion or restoration of intravascular and extravascular fluid volume.

Echocardiographic follow-up study of the Ross procedure in older versus younger patients

Objectives This study was designed to determine echocardiographic follow-up results of the Ross procedure in older adult patients with aortic valve disease. Background The excellent long-term results of the Ross procedure from several institutions have indicated that the pulmonary autograft may be the best available substitute for the diseased aortic valve in children and adolescents. The advantages of this operation include optimal hemodynamics and elimination of thromboembolic complications. These features may benefit older adult patients as well. Methods We reviewed data from 49 consecutive patients who had a Ross procedure between 1991 and 1996. Preoperative and postoperative Doppler echocardiographic studies were available for 44 patients (22 men, 22 women; mean [±SD] age 36 ± 14 years) who were grouped into <40 (n = 25) and ≥40 years old (n = 19). Measurements included left ventricular diastolic volume (LVDV), mass, and ejection fraction (EF); a peak pressure gradient across autograft in the aortic position and homograft in the pulmonary position; and valvular regurgitation. Results The mean length of echocardiographic follow-up was 36 ± 16 months. Postoperatively, there was a reduction in LVDV and left ventricular mass in both age groups: 153 ± 99 mL to 111 ± 72 mL (P =.015) and 210 ± 93 g to 152 ± 54 g (P =.002) for younger patients, 174 ± 115 mL to 126 ± 43 mL (P =.17) and 233 ± 71 g to 215 ± 65 g (P =.19) for older patients. No significant change in EF was noted in the younger age group. However, in the older age group a significant decrease to EF <25% was found in 2 patients 1 year after surgery. Moderate autograft regurgitation was also detected in 2 patients: 1 in each age group. Pressure gradients across the autograft remained within the normal range in both age groups. Two younger patients had severe homograft stenosis with peak gradients of 100 and 62 mm Hg. The older patients did not demonstrate homograft dysfunction. Conclusions The Ross procedure can be performed in selected older adults with aortic valve disease and provides durable valves in both aortic and pulmonic positions for at least 3 years after surgery but may result in less favorable left ventricular remodeling compared with that in the younger patients. Further follow-up will be necessary to determine the long-term outcome of the Ross procedure in this older adult patient population. (Am Heart J 2001;142:331-5.)

Instrumental validation of percutaneous transmyocardial revascularization: follow-up data at one year

Background. Despite the clinical efficacy of percutaneous transmyocardial revascularization (PTMR), up to date there are still no instrumental validations to demonstrate both the improved perfusion of treated areas and cardiac function. Methods. During the first year of follow-up after PTMR, 27 patients (group A) underwent 99mTc MIBI exercise-single photon emission tomography (SPET), while 30 patients (group B) underwent serial transthoracic echocardiography (TTE) evaluations with analysis of cardiac volumes and subendocardial layer thickness in systole. Results. All 57 patients had a significant angina Canadian Cardiovascular Society (CCS) class improvement. Group A patients (75%) had improved exercise-SPET perfusion in treated areas at 12 weeks after PTMR, and at the next follow-up. Group B patients had non-significant reduction in global volume and no significant change in ejection fraction. However, there was an improvement in thickness of the subendocardial-treated areas in systole that persisted during follow-up. Conclusions. The use of SPET and TTE validates the clinical efficacy of PTMR.

A LONGITUDINAL STUDY OF CARDIAC FUNCTION IN CHILDREN WITH CANCER OVER 40 MONTHS

A previous study demonstrated impaired systolic function in 29% of patients treated with an thracycline as part of their therapy for malignant disease. A follow-up echocardiographic study was performed to determine whether there had been further deterioration of cardiac function. At least 40 months after the first study, those patients in whom abnormal systolic function had been detected and who had not received further anthracycline were studied by echocardiography using the same protocol as the initial study (group A). A second group of pediatric oncology patients who had not been given anthracycline but who had previously had cardiac assessment was selected as a control group (group N). The age and sex distributions of the two groups were comparable. Group A comprised 29 patients assessed on 2 occasions at mean times of 46 months and 89 months from the last dose of anthracycline. The mean dose of anthracycline received was 233 mg/m2 (range 20-400). Nine of 16 patients and 4 of 5 patients who had abnormal ejection fraction (EF) and fractional shortening (FS) at first assessment had normal EF and FS at the second assessment. There were no significant changes in EF, FS, and left ventricular wall stress (LVWS) between the two examinations. In group N, 20 patients were assessed after a mean interval of 43 months. There were no significant changes in EF, FS, or LVWS between the two examinations. At the first but not the second examination there were significant differences in the left ventricular internal diameters, EF, FS, and LVWS between group A and group N. Mildly abnormal cardiac indices detected in children after cessation of treatment with anthracycline did not deteriorate in 3 to 4 years follow-up. A longer cardiac follow-up study is indicated to assess the late outcome.

767-1 Determinants of Defibrillation Energy Requirements in Heart Failure

A recent study using a monophasic, epicardial defibrillation system in a canine model has raised concern that congestive heart failure may dramatically increase the energy requirements of defibrillation. In order to test the effect of heart failure on the defibrillation efficacy of a transvenous biphasic defibrillation system, 16 dogs were studied; 11 dogs were ventricular paced at 225 ppm for two weeks to induce heart failure, and 5 control dogs remained unpaced. All dogs were tested using an endocardial right ventricular defibrillation lead and a cutaneous patch. Shocks were biphasic with equal leading edge voltages and fixed 65% tilt for each phase. Dose-response defibrillation probability curves were generated for each animal at baseline, after two weeks (at which time pacing was discontinued in the paced group), and then one week later. The ED20, ED50, and ED80 (the 20%, 50%, and 80% effective defibrillation energies, respectively) were determined for each dog at each study. In the paced dogs, the ejection fraction (EF) fell from 55% to 25% after pacing (p &lt; 0.0001), and rose to 46% one week after its discontinuation (p = 0.0002). The effective refractory period (ERP) prolonged from 152 to 170 msec (p &lt; 0.005), then shortened to 164 (p = NS). There was no significant change in EF or ERP in the control dogs between the three studies. The ED20, ED50, and ED80 remained unchanged in both the control and paced groups for all three studies, even with adjustment for dog weight or echocardiographic left ventricular mass. In a multiple regression model, EF did not significantly predict the ED50. However, the ED50 increased with increasing left ventricular (LV) size and decreased with LV wall thinning. Rapid pacing led to LV cavity dilatation and wall thinning; these two morphologic changes had opposing effects on defibrillation energy, so that there was no net change in the ED50 in heart failure. The defibrillation efficacy of a biphasic waveform in a transvenous lead system is not changed by the development of heart failure in the rapid paced canine model. The energy required for defibrillation was predicted by the ventricular size and wall thickness but not EF.

Serial changes in left ventricular function after coronary artery bypass: Implications in viability assessment

Improvement in left ventricular (LV) performance after coronary artery bypass surgery remains the gold standard in myocardial viability assessment. The time-related changes, however, are not well known. This study examined the LV ejection fraction (EF) by gated blood pool imaging early (6 ± 4 days) and late (62 ± 24 days) after surgery in patients with normal preoperative EF (group 1, n = 12) and those with LV dysfunction (group 2, n = 15). There were no changes in the clinical status between the early and late studies, and all patients had normal sinus rhythm. Group 1 had no significant change in EF (preoperatively 62%, early postoperatively 64%, late postoperatively 63%; p = NS). In group 2, EF was 26% ± 8% preoperatively; 30% ± 10% early postoperatively; and 34% ± 8% late postoperatively ( p < 0.05). Postoperatively there was ≥5% improvement in EF in 4 patients early and 11 patients late ( p < 0.05). Patients who showed early improvement continued to do so in the late study but, additionally, 7 patients showed improvement only in the late study. Thus the timing of EF measurement after surgery is important in patients with LV dysfunction but not in patients with normal LV function. Early assessment may underestimate the prevalence and degree of recovery.

Does ventricular fibrillation cause myocardial stunning during defibrillator implantation?

Induction of ventricular fibrillation (VF) is an important part of the process of inserting implantable cardioverter defibrillators (ICDs), allowing the measurement of defibrillation thresholds. However, animal studies have revealed that repeated cycles of VF and defibrillation result in depressed left ventricular (LV) function and reduced cardiac output. Short intervals of VF do not affect myocardial contractility but longer periods produce heart failure. Induced VF was used in a canine model to study profound myocardial stunning leading to heart failure, as well as the therapeutic potential of the phosphodiesterase inhibitor, amrinone (combined with epinephrine and norepinephrine). Amrinone was found to significantly (p < 0.05) increase contractility when added to a stable preparation supported by epinephrine and norepinephrine infusion; amrinone or catecholamines alone had no effect. In the clinical setting, the following factors may affect LV contractility during ICD surgery: catecholamines released as a result of hypotension; negative VF; ischemia; antiarrhythmic drugs; anesthetics; and bradycardia after device testing. Patients (n = 125) have tolerated ICD insertion well. Early data reveals no significant changes in ejection fraction. Though rare, death due to myocardial stunning and LV power failure can occur during ICD insertion. It may be possible to use arterial pressure monitoring to predict this event in vulnerable patients.

Continuous on-line monitoring of left ventricular function with a new nonimaging detector: Validation and clinical use in the evaluation of patients post angioplasty

A new miniaturized nonimaging radionuclide detector (Cardioscint, Oxford, England) was evaluated for the continuous on-line assessment of left ventricular function. This cesium iodide probe can be placed on the patient's chest and can be interfaced to an IBM compatible personal computer conveniently placed at the patient's bedside. This system can provide a beat-to-beat or gated determination of left ventricular ejection fraction and ST segment analysis. In 28 patients this miniaturized probe was correlated against a high resolution gamma camera study. Over a wide range of ejection fraction (31% to 76%) in patients with and without regional wall motion abnormalities, the correlation between the Cardioscint detector and the gamma camera was excellent ( r = 0.94, SEE ± 2.1). This detector system has high temporal (10 msec) resolution, and comparison of peak filling rate (PFR) and time to peak filling (TPFR) also showed close agreement with the gamma camera (PFR, r = 0.94, SEE ± 0.17; TPFR, r = 0.92, SEE ± 6.8). In 18 patients on bed rest the long-term stability of this system for measuring, ejection fraction and ST segments was verified. During the monitoring period (108 ± 28 minutes) only minor changes in ejection fraction occurred (coefficient of variation 0.035 ± 0.016) and ST segment analysis showed no significant change from baseline. To determine whether continuous on-line measurement of ejection fraction would be useful after coronary angioplasty, 12 patients who had undergone a successful procedure were evaluated for 280 ± 35 minutes with the Cardioscint system. While the majority of patients showed no significant changes in ejection fraction or ST segments, four patients demonstrated substantial changes in ejection fraction. In two of these patients there was significant improvement in left ventricular function that occurred early after angioplasty and correlated with radionuclide angiograms at follow-up. One patient had two episodes of transient ischemia assessed by ejection fraction monitoring, one with and one without symptoms suggesting coronary spasm. The fourth patient demonstrated improvement in ejection fraction that over the course of the monitoring period returned to baseline with worsening ST segments. On follow-up angiogram the patient had an occlusion of the vessel that was dilated. The miniaturized detector system can be used to provide an accurate on-line continuous assessment of left ventricular ejection fraction. Particularly in the unstable cardiac patient, this system may be useful in monitoring therapy and in determining the effects of acute interventions.

Mechanisms for left ventricular systolic dysfunction in aortic regurgitation: Importance for predicting the functional response to aortic valve replacement

To test the hypothesis that the combined use of the time-varying distance concept and conventional circumferential stress-shortening relations would elucidate differential mechanisms for left ventricular systolic dysfunction in severe, chronic aortic regurgitation and therefore predict the functional responses to aortic valve replacement, 31 control patients and 37 patients with aortic regurgitation were studied. The studies included micromanometer left ventricular pressure determinations, biplane contrast cineangiograms under control conditions and radionuclide angiograms under control conditions and during methoxamine or nitroprusside infusions with right atrial pacing.The patients with aortic regurgitation were classified into three groups: Group I had normal Emaxand stress-shortening relations, Group II had abnormal Emaxbut normal stress-shortening relations and Group III had abnormal Emaxand stress-shortening relations. The left ventricular end-diastolic and end-systolic volumes showed a progressive increase and the ejection fraction showed a progressive decrease from Group I to III; these values differed from those in the control patients (p < 0.001). In Group I, then was a decrease in left ventricular volumes (p < 0.05) but no significant change in ejection fraction (61 ± 7% versus 63 ± 4%) after aortic valve replacement. In contrast, in Group II, reduction in left ventricular volumes (p < 0.01) was associated with an increase in ejection fraction from 50 ± 8% to 64 ± 11% (p < 0.01). Finally, in Group III, reduction in left ventricular volumes (p < 0.05) was associated with a further decrement in ejection fraction from 35 ± 13% to 30 ± 13%.Group I patients had compensated adequately for chronic volume overload. However, Group II had left ventricular dysfunction that was associated with an increase in the left ventricular volume/mass ratio compared with that in the control patients and Group I (p < 0.05 for both), suggesting inadequate hypertrophy and assumption of spherical geometry. Finally, irreversible myocardial dysfunction had supervened in Group III.In conclusion, a combined analysis of left ventricular chamber performance using the time-varying elastance concept and myocardial performance using conventional circumferential stress-shortening relations provides complementary information that elucidates differential mechanisms for left ventricular systolic dysfunction and therefore predicts the functional response to aortic valve replacement.

Physiological early diastolic intraventricular pressure gradient is lost during acute myocardial ischemia.

A consistent pattern of intraventricular regional pressure gradients exists under physiological conditions during the rapid filling phase of diastole in the normal dog left ventricle. We hypothesized that this pressure gradient pattern is caused, in part, by early diastolic recoil of the left ventricular walls in conjunction with release of elastic potential energy stored during systole, generating suction and thus contributing to diastolic filling. If so, any condition that interferes with normal regional systolic function might be expected to modify the pattern of the normal early diastolic intraventricular pressure gradients. Accordingly, the present study was designed to determine whether acutely induced regional systolic left ventricular mechanical dysfunction is accompanied by changes in the pattern of the early diastolic intraventricular pressure gradients. Acute myocardial ischemia was induced by balloon occlusion of the left anterior descending coronary artery (LAD) in nine anesthetized closed-chest dogs. The maximum early diastolic intraventricular pressure gradient (MIVP) was measured between the mid-left ventricle and apex with a dual-sensor micromanometer (3-cm spacing between the sensors) before and 20 minutes after LAD occlusion. Ejection fraction (EF) and number of dyskinetic chords (DChords) were measured from left ventricular contrast ventriculograms. Twenty minutes after LAD occlusion, the nine dogs evidenced significant changes in EF (56 +/- 10% to 37 +/- 8%), DChords (0 +/- 0 to 17 +/- 16 chords), left ventricular minimum pressure (-1.7 +/- 0.5 to 0.0 +/- 1.5 mm Hg), left ventricular end-diastolic pressure (4.2 +/- 1.2 to 5.9 +/- 2.2 mm Hg), and heart rate (90 +/- 17 to 103 +/- 18 beats/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Improvement in symptoms and left ventricular performance after balloon aortic valvuloplasty in patients with aortic stenosis and depressed left ventricular ejection fraction.

The application of balloon aortic valvuloplasty to elderly patients with severe aortic stenosis and a low ventricular ejection fraction is undefined. Balloon aortic valvuloplasty was performed in a subset of 28 patients with low left ventricular ejection fraction (37 +/- 11%), severe aortic stenosis, and a mean age of 79 +/- 5 years. After valvuloplasty, significant increases were seen in aortic valve area (from 0.5 +/- 0.1 to 0.9 +/- 0.2 cm2), aortic systolic pressure (from 120 +/- 12 to 135 +/- 22 mm Hg), and cardiac output (from 4.2 +/- 1.1 to 4.8 +/- 1.6 l/min) (p less than 0.01), and significant decreases were seen in transaortic pressure gradient (from 69 +/- 25 to 35 +/- 15 mm Hg) and pulmonary capillary wedge pressure (from 24 +/- 9 to 20 +/- 7 mm Hg) (p less than 0.01). All patients had symptomatically improved at the time of discharge. Serial radionuclide ventriculography showed an increase in left ventricular ejection fraction from 37 +/- 11% before valvuloplasty to 44 +/- 14% within 48 hours after dilatation and to 49 +/- 13% at 3 months after dilatation. However, there was substantial heterogeneity of response. Thirteen patients (group A) showed progressive increases in left ventricular ejection fraction (from 34 +/- 11% to 49 +/- 15% to 58 +/- 11%, p less than 0.0001), whereas 15 patients (group B) showed no significant change in ejection fraction (from 41 +/- 10% to 40 +/- 13% to 41 +/- 10%, p = NS) over 3 months. There was no difference between these groups with respect to age, extent of coronary artery disease, history of myocardial infarction, and aortic valve area before and after valvuloplasty. However, peak systolic wall stress and left ventricular dimensions were higher in group B compared with group A. In conclusion, balloon aortic valvuloplasty may result in symptomatic improvement in patients with aortic stenosis and depressed left ventricular ejection fraction; some patients develop progressive increases in ejection fraction, whereas others fail to show improvement.

Left ventricular response to submaximal and maximal exercise in asymptomatic aortic regurgitation

In patients with chronic aortic regurgitation the quantitative changes in loading conditions and left ventricular performance from rest to submaximal exercise have not been related to the magnitude of change observed from rest to maximal exercise. Changes in end-diastolic volume index, as a measure of preload, and measures of contractile performance (ejection fraction and the systolic blood pressure/end-systolic volume index ratio) were assessed at rest, submaximal and maximal supine bicycle exercise using radionuclide angiography in 74 patients with chronic moderate to severe aortic regurgitation. With exercise, end-diastolic volume index decreased in a stepwise manner from 166 ± 47 to 152 ± 41 to 143 ± 41 ml/m 2 at rest, submaximal and maximal exercise, respectively. For the entire group, these changes were not associated with a significant change in ejection fraction but were associated with stepwise increases in systolic blood pressure to end-systolic volume index ratio. However, when patients were divided into 3 subgroups based on an increase (group I), minimal change (group II) or a decrease (group III) in ejection fraction from rest to maximal exercise, stepwise increases in systolic blood pressure to endsystolic volume index were again observed in groups I and II but not in group III. These changes were significantly greater in group I than in group II at submaximal and maximal exercise levels. Differences in ejection fraction response and end-diastolic and end-systolic volumes with exercise in the 3 groups were evident at the submaximal exercise level. These data suggest that the stepwise changes in left ventricular volumes and performance that occur during submaximal exertion are smaller but directionally similar to changes at maximal exertion. Conversely, the findings at maximal exertion may be used to infer the response of the left ventricle at submaximal exertion during activities of daily living.

An analysis of regional left ventricular function utilizing pressure-length relationship in patients with coronary artery disease.

Mechanisms related to increased left ventricular filling pressure associated with myocardial ischemia were studied in 13 patients with coronary artery disease. Single-plane left ventriculograms were obtained using a high fidelity micromanometer-tipped catheter in the control and post-pacing periods. All patients developed typical anginal pain during pacing tachycardia. Seven patients (group I) demonstrated no significant changes in ejection fraction (EF) and peak systolic pressure-end-systolic volume ratio (P/Ves) after rapid pacing. End-diastolic pressure (EDP), however, increased significantly from 14.9 +/- 4.9 to 24.4 +/- 8.5 mmHg (p less than 0.01). Six patients (group II) exhibited significant decreases in EF and P/Ves. Here again, EDP increased significantly from 14.0 +/- 7.6 to 28.0 +/- 7.7 mmHg (p less than 0.01). The regional myocardial function was expressed by a radial coordinate system with its origin at the center of gravity of the end-diastolic contour. In the normal segment, the end-diastolic length (EDL) was augmented by 13.6%, associated with a 22.4% increase in stroke excursion with pacing stress. In the ischemic segment, EDL remained unchanged, but stroke excursion was significantly reduced. The diastolic pressure-volume curve shifted directly upward or more to the right, while the diastolic pressure-length curve moved up on the single curve in the normal segment and shifted directly upward in the ischemic segment, so that pressure was higher at any given segment length in the ischemic segment, indicating regional alteration of the diastolic properties. Thus, an ischemic response to pacing tachycardia involves both systolic and diastolic impairment, but the latter is more sensitive.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of cardiac medications on ventricular performance: Emphasis on evaluation with radionuclide angiography

With the advent of radionuclide angiography (RNA) and quantitative two-dimensional echocardiography (2DE), a great deal of interest has been generated in the noninvasive evaluation of the effects of an increasing number of active cardiac medications on ventricular performance. In this review, the effects of acute and chronic administration of vasodilators and antianginal, antihypertensive, inotropic, and antiarrhythmic agents on left ventricular (LV) ejection fraction (EF), volume, and diastolic properties and, to a lesser extent, on right ventricular (RV) EF will be discussed. The effects of these pharmacologic agents on intracardiac pressures, systemic pressure, systemic and pulmonary artery resistance, and cardiac output have been extensively studied and will not be included in this review. Table I presents a summary of these studies. Several points should be emphasized; first, a statistically significant change in EF may not be clinically relevant, for example, a decrease in EF from 60 to 55 may be statistically significant but clinically irrelevant. Statistical analysis is used only to judge whether data from the study are consistent or inconsistent with a null hypothesis. Second, the change in EF is analyzed as the mean change before and after therapy. Such analysis does not reflect the reproducibility and variability in these measurements. In good laboratories, the interand intraindividual variability is less than 5 % , but each laboratory should establish its own reproducibility results. A more important point, however, is the reproducibility of results when measurements are separated by days or weeks. Sequential studies in normal

Comparison of Effects on Left Ventricular Ejection Fraction of Iopamidol and Renografin During Left Ventriculography and Coronary Arteriography

The immediate effect (within 1 minute) of a nonionic contrast agent (iopamidol) and an ionic contrast agent (Renografin) on left ventricular systolic ejection fraction was studied in 30 randomized patients (15 in each group) using a nuclear probe technique. Both agents caused a significant rise in ejection fraction following left ventriculography (a 9.1% increase with iopamidol and 14.3% increase with Renografin, P = 0.01). Neither agent caused a significant change in ejection fraction following coronary angiography. We conclude that (1) iopamidol and Renografin both cause a small rise in left ventricular ejection fraction following ventriculography; (2) neither agent significantly changes systolic ejection fraction following left coronary angiography; and (3) the changes seen during ventriculography most likely represent complex preload and afterload interactions.

Left ventricular performance after mitral reconstruction for mitral regurgitation

Depressed left ventricular performance is often observed after mitral valve replacement for mitral regurgitation and is generally attributed to increased impedance to left ventricular ejection. We analyzed preoperative and postoperative catheterization data in 10 of 18 patients who underwent mitral reconstruction with preservation of the native valves and found a significant (p less than 0.05) fall in left ventricular end-diastolic volume index (from 143 +/- 39 to 84 +/- 21 ml/m2) and end-systolic volume index (from 50 +/- 24 to 32 +/- 12 ml/m2), with no significant change in ejection fraction (0.66 +/- 0.1 versus 0.62 +/- 0.1). These findings contrast with studies reported by others in comparable patients who had mitral valve replacement with no improvement in volume indices and a decline in ejection fraction postoperatively. We suggest that some of the left ventricular dysfunction observed after mitral replacement may be due simply to excision of the native valve. Mitral repair retains the tethering effect of chordal attachments and may thus prevent postoperative left ventricular dilatation and moderate the increase in wall stress that results from increased impedance to left ventricular ejection.

A cause of right ventricular dysfunction after cardiac operations

We examined the impact of mediastinal healing on right ventricular performance in three groups of five piglets by performing gated blood pool scans in two planes to determine right ventricular ejection fraction. Animals in Group I then had sternotomy and excision of anterior pericardium. Group II animals had a similar operation plus insertion of a silicone rubber sheet as a pericardial substitute. Group III animals (controls) had no operation. Each group was followed up for 60 days, after which gated blood pool scans were repeated in a manner identical to the initial study. Experimental animals in Groups I and II were then put to death and autopsied. Adhesion formation between the right ventricle and sternum was graded on a 0 to 3 scale. Group I animals showed a significant average decline in right ventricular ejection fraction of 19.2% (p less than 0.02). Group II animals demonstrated an average decrease in ejection fraction, although not significant, of 12.2%. Groups I and II combined showed a significant average loss in ejection fraction of 15.7% (p less than 0.01). Severity of adhesions between the right ventricle and sternum correlated well with loss of right ventricular ejection fraction (p less than 0.01). Group III controls demonstrated no significant change in ejection fraction. Mediastinal healing and fibrous attachment of the right ventricle to the sternum may play a significant role in loss of right ventricular ejection fraction after cardiac operations. Variability in loss of right ventricular ejection fraction is related to intensity of the mediastinal healing process.