Change In End-diastolic Volume Index Research Articles

Low Stroke Volume Index in Healthy Young Men Is Associated with the Incidence of Acute Mountain Sickness after an Ascent by Airplane: A Case-Control Study.

Background The aims of this study were to explore the characteristics of left ventricular (LV) functional changes in subjects with or without acute mountain sickness (AMS) and their associations with AMS incidence. Methods A total of 589 healthy men were enrolled and took a trip from Chengdu (500 m, above sea level (asl)) to Lhasa (3700 m, asl) by airplane. Basic characteristics, physiological data, and echocardiographic parameters were collected both at Chengdu and Lhasa, respectively. AMS was identified by the Lake Louise Questionnaire Score. Results The oxygen saturation (SpO2), end-systolic volume index, end-diastolic volume index (EDVi), stroke volume index (SVi), E-wave velocity, and E/A ratio were decreased, whereas the heart rate (HR), ejection fraction, cardiac index (CI), and A-wave velocity were increased at the third day after arrival, as evaluated by an oximeter and echocardiography. However, AMS patients showed higher HR and lower EDVi, SVi, CI, E-wave velocity, and E/A ratio than AMS-free subjects. Among them, SVi, which is mainly correlated with the changes of EDVi and altered LV filling pattern, was the most valuable factor associated with AMS incidence following receiver-operator characteristic curves and linear and Poisson regression. Compared with subjects in the highest SVi tertile, subjects in the middle SVi tertile showed higher multivariable Incidence Rate Ratios (IRR) for AMS with higher incidences of mild headache and gastrointestinal symptoms, whereas subjects in the lowest SVi tertile showed even higher multivariable IRR with higher incidences of all the symptoms. Conclusions This relatively large-scale case-control study revealed that the reduction of SVi correlated with the altered LV filling pattern was associated with the incidence and clinical severity of AMS.

Cardiac remodeling in aortic and mitral valve disease: a simulation study with clinical validation.

Remodeling is an important long-term determinant of cardiac function throughout the progression of heart disease. Numerous biomolecular pathways for mechanosensing and transduction are involved. However, we hypothesize that biomechanical factors alone can explain changes in myocardial volume and chamber size in valve disease. A validated model of the human vasculature and the four cardiac chambers was used to simulate aortic stenosis, mitral regurgitation, and aortic regurgitation. Remodeling was simulated with adaptive feedback preserving myocardial fiber stress and wall shear stress in all four cardiac chambers. Briefly, the model used myocardial fiber stress to determine wall thickness and cardiac chamber wall shear stress to determine chamber volume. Aortic stenosis resulted in the development of concentric left ventricular hypertrophy. Aortic and mitral regurgitation resulted in eccentric remodeling and eccentric hypertrophy, with more pronounced hypertrophy for aortic regurgitation. Comparisons with published clinical data showed the same direction and similar magnitudes of changes in end-diastolic volume index and left ventricular diameters. Changes in myocardial wall volume and wall thickness were within a realistic range in both stenotic and regurgitant valvular disease. Simulations of remodeling in left-sided valvular disease support, in both a qualitative and quantitative manner, that left ventricular chamber size and hypertrophy are primarily determined by preservation of wall shear stress and myocardial fiber stress. NEW & NOTEWORTHY Cardiovascular simulations with adaptive feedback that normalizes wall shear stress and fiber stress in the cardiac chambers could predict, in a quantitative and qualitative manner, remodeling patterns seen in patients with left-sided valvular disease. This highlights how mechanical stress remains a fundamental aspect of cardiac remodeling. This in silico study validated with clinical data paves the way for future patient-specific predictions of remodeling in valvular disease.

Diastolic Dyssynchrony in Acute ST Segment Elevation Myocardial Infarction and Relationship with Functional Recovery of Left Ventricle.

BackgroundIncidence of diastolic dyssynchrony (DD) and its impact on functional recovery of left ventricle (LV) after ST segment elevation myocardial infarction (STEMI) is not known.MethodsConsecutive patients with STEMI who underwent successful revascularization were prospectively enrolled. Echocardiography with tissue Doppler imaging was performed within 48 hours of admission and at 6 months. LV end-diastolic volume index (EDVI), end-systolic volume index (ESVI), ejection fraction (EF), and left atrial volume index (LAVI) were calculated. Diastolic delay was calculated from onset of QRS complex to peak of E wave in tissue Doppler image and presented as maximal temporal difference between peak early diastolic velocity of 6 basal segments of LV (TeDiff). Study patients were compared with demographically matched control group.ResultsForty eight consecutive patients (55 ± 10 years, 88% male) and 24 controls (56 ± 6 years, 88% male) were included. TeDiff was higher in STEMI than in controls (35.9 ± 19.9 ms vs. 26.3 ± 6.8 ms, p = 0.025). Presence of DD was higher in STEMI than controls (58% vs. 33%, p = 0.046) according to calculated cut-off value (≥ 29 ms). There was no correlation between TeDiff and change in EDVI, ESVI, and LAVI at 6 months, however TeDiff and change in EF at 6 months was positively correlated (r = 0.328, p = 0.023). Patients with baseline DD experienced remodeling less frequently compared to patients without baseline DD (11% vs. 38%, p = 0.040) during follow-up.ConclusionSTEMI disrupts diastolic synchronicity of LV. However, DD during acute phase of STEMI is associated with better recovery of LV thereafter. This suggests that DD is associated with peri-infarct stunned myocardium that is salvaged with primary intervention as well as infarct size.

Stroke volume paradox in heart failure: mathematical validation

In some patients with ischemic cardiomyopathy, despite large increases in ventricular size with decreased cardiac output, the paradox of preserved stroke volume has been observed. Following surgical ventricular restoration, despite marked improvements clinically and in ventricular volumes and ejection fraction, a decrease in stroke volume was observed. 101 consecutive patients with postinfarction left ventricular aneurysms were studied by 2-dimensional echocardiography and contrast ventriculography at baseline, and 57 of these patients at 1.7 to 2.2 years (mean 1.95 ± 0.44 years) after surgical ventricular restoration. Surgical ventricular restoration resulted in a decrease in end-diastolic volume index of 40.2 mL (95% confidence interval: 33.6-46.7) and stroke volume index of 10.0 mL (95% confidence interval: 6.6-13.5), and an increase in ejection fraction of 6.7% (95% confidence interval: 5.5-7.9). The stroke volume index had a significant linear relationship with the end-diastolic volume index at rest in patients with end-diastolic volume index < 150 mL (r = 0.64, p < 0.001). In patients with end-diastolic volume index >150 mL, this linear relationship was not seen. The change in end-diastolic volume index and stroke volume index had a significant linear relationship (r = 0.72, p < 0.001) that persisted at 1.95 years after surgery. In ischemic cardiomyopathy, stroke volume increases linearly with increases in end-diastolic volume up to a certain magnitude of end-diastolic volume, beyond which it decreases. Hence, following surgical ventricular restoration, decreases in stroke volume are not a reflection of impaired cardiac function.

Relationship between circulating soluble Fas ligand and preexisting left ventricular hypertrophy in the setting of left ventricular remodeling after acute myocardial infarction

We aimed to investigate the effects of preexisting left ventricular hypertrophy (LVH) on the circulating concentration of soluble Fas ligand (sFasL) and also the relationship of sFasL to ventricular remodeling in patients with acute myocardial infarction (MI). Forty consecutive patients who presented with their first episode of acute MI were studied. These patients were then divided into two groups with regard to the presence of LVH. All the patients underwent complete transthoracic echocardiography with determination of end diastolic volume index and LV mass index within 24 h and at 6 months. sFasL levels were determined in serum on admission and at 24 h of admission. The serum sFasL concentration did not change significantly after acute MI at 24 h after admission in the study population (P=0.574), however, the serum level of sFasL concentration was significantly increased in the patients with preexisting LVH (P<0.001). There was a strong positive relationship between LV mass index and the serum level of sFasL concentration at 24 h after admission (r=0.611; P<0.001). Moreover, there was a stronger correlation between the change in end-diastolic volume index at 6 months and the serum level of sFasL in the LVH group compared with the group without LVH (r=0.499 and 0.181, respectively). In conclusion, we have shown that serum sFasL concentration at 24 h after admission was significantly higher in patients with LVH, and also, there is a close relationship between the serum level of sFasL and LV enlargement.

Randomized, Double-Blind, Multicenter, Placebo-Controlled Study Evaluating the Effect of Aldosterone Antagonism With Eplerenone on Ventricular Remodeling in Patients With Mild-to-Moderate Heart Failure and Left Ventricular Systolic Dysfunction

Aldosterone antagonism has been studied in patients with advanced heart failure (HF) and also in patients with post-myocardial infarction and left ventricular (LV) dysfunction with HF symptoms. Few data are available on effects of aldosterone antagonism in patients with mild-to-moderate HF. In a multicenter, randomized, double-blind, placebo-controlled study in patients with mild-to-moderate HF and LV systolic dysfunction, patients with New York Heart Association class II/III HF and LV ejection fraction (EF) < or =35% were randomly assigned to receive eplerenone 50 mg/d versus placebo in addition to contemporary background therapy. Quantitative radionuclide ventriculograms to assess LV volumes and ejection fraction were performed at baseline and again after 9 months of double-blind treatment and were analyzed in a central core laboratory, blinded to treatment. The primary efficacy analysis was the between-group comparison of the change in LV end-diastolic volume index. Secondary analyses examined changes in LV end-systolic volume index and ejection fraction as well as markers of collagen turnover. Of the total 226 patients enrolled, 117 were randomly assigned to receive eplerenone and 109 to receive placebo. There was high use of contemporary background therapy at baseline, with > 90% use of angiotensin-converting enzyme inhibitors and/or angiotensin receptor blockers and > 90% use of beta-blockers. Over 36 weeks of treatment, there was no apparent between-group difference in the changes in end-diastolic volume index or end-systolic volume index. There was a reduction in the collagen turnover marker procollagen type I N-terminal propeptide and plasma B-type natriuretic peptide in the eplerenone group compared with placebo (P=0.01 and P=0.04, respectively). There was no change in symptom status or quality-of-life measures. In a clinically stable, well-treated population of patients with mild-to-moderate HF symptoms and LV dysfunction, 36 weeks of treatment of aldosterone antagonism with eplerenone at a dose of 50 mg daily had no detectable effect on parameters of LV remodeling.

Reverse remodeling and improved function by antihypertensive treatment in hypertensive patients with coronary artery disease

Although antihypertensive therapy reduces cardiovascular events, it is unclear whether there are differences in cardiac remodeling and function between treatments with nifedipine retard and angiotensin-converting enzyme inhibitors (ACE-Is). It is also not clear how antihypertensive therapy influences cardiac remodeling and function. Hypertensive patients with coronary artery disease were randomly assigned to the nifedipine retard (n = 108) or ACE inhibitors groups (n = 102) and treated for 3 years. The primary endpoints were changes in end-diastolic volume index (EDVI) and end-systolic volume index (ESVI) as indices of cardiac remodeling, whereas the secondary endpoints were changes in ejection fraction (EF), stroke volume index (SVI), cardiac index (CI) and regional wall motion as indices of cardiac function. Left ventriculography was performed at baseline and after 3 years of treatment. Fifty-eight and 61 patients, respectively, were subjected to the final analysis. Comparable changes in remodeling and function were obtained in the nifedipine retard group and the ACE-Is group. Both groups showed a significant reduction of EDVI and ESVI, and a significant increase in EF, SVI, and CI, whereas the decreased regional wall motion significantly improved. In both groups, weak but significant correlations were noted between treatment-induced changes of systolic blood pressure and those of primary and secondary endpoints. The above findings show that treatments with nifedipine retard or ACE-Is cause a comparable change in remodeling and cardiac function. Lowering of the blood pressure by either drug leads to reverse remodeling or improvement of cardiac function. In addition to alleviation of coronary artery damage by reducing blood pressure, there is a favorable effect on the left ventricular structure and function. Reducing the blood pressure is critically important for hypertensive patients with coronary artery disease.

The Effect of 7.2% Hypertonic Saline Solution with 6% Dextran 70 on Cardiac Contractility as Observed by an Echocardiography in Normovolemic and Anesthetized Dogs

We studied the effect of a small volume of 7.2% hypertonic saline solution (HSS) or HSS with 6% dextran 70 (HSD) on hemodynamic status, especially on cardiac contractility, in anesthetized dogs using the left ventricular end-systolic volume index (ESVI) and ejection fraction (EF), which can be obtained in noninvasive echocardiography. In the present study, the mean values of ESVI were unaffected by HSS and HSD infusion, whereas the left ventricular end-diastolic volume index (EDVI) was markedly and significant increased. As a result of the changes in EDVI but not in ESVI, EF increased transiently and significantly in the HSS and HSD group, whereas no such significant change was observed in the dogs that received isotonic saline solution. In addition, as a result of the increases in cardiac index but not arterial pressure, system vascular resistances (SVR) decreased transiently and significantly in the HSS and HSD groups, whereas no such significant change was observed in the ISS group. Therefore, the positive inotropic effects of HSS and HSD may be attributable to the increase in left ventricular preload and decreases in SVR rather than direct changes in myocardial contractility.

Effect of Angiotensin Converting Enzyme Inhibitors and .BETA.-Blockers on Left Ventricular Remodeling After Coronary Artery Bypass Graft Surgery

Preventing left ventricular (LV) remodeling after coronary artery bypass graft surgery (CABG) is important to avoid long-term congestive heart failure. The present study evaluated the effects of angiotensin converting enzyme inhibitors (ACEIs) and beta-blockers on LV remodeling. Twenty-three patients with angina pectoris and 36 with old myocardial infarction underwent CABG. We assessed end diastolic volume index (EDVI), end systolic volume index (ESVI), and ejection fraction (EF) using left ventriculography before and after CABG. Changes in EDVI, ESVI, and EF were studied in the ACEI, beta-blocker, and control groups. Although EDVI was reduced in the ACEI group, ESVI and EF improved only slightly, whereas in the group given beta-blockers, ESVI was reduced, EF improved, and EDVI was minimally reduced. These results indicate that ACEIs and beta-blockers both protect against LV remodeling, although through different mechanisms.

Adjunctive effect of hyperbaric oxygen treatment after thrombolysis on left ventricular function in patients with acute myocardial infarction

Background The role of hyperbaric oxygen in patients with acute myocardial infarction is controversial, ranging from not beneficial to having a favorable effect. This randomized study was conducted to further assess the benefit of hyperbaric oxygen treatment after thrombolysis on left ventricular function and remodeling in patients with acute myocardial infarction. Methods Seventy-four consecutive patients with first acute myocardial infarction were randomly assigned to treatment with hyperbaric oxygen treatment combined with streptokinase (HBO+) or streptokinase alone (HBO−). Results There was a significant decrease of end-systolic volume index from the first day to the third week in HBO+ patients compared with HBO− patients (from 30.40 to 28.18 vs from 30.89 to 36.68 mL/m 2, P < .05) accompanied with no changes of end-diastolic volume index in HBO+ compared with increased values in HBO− (from 55.68 to 55.10 vs from 55.87 to 63.82 mL/m 2, P < .05). Ejection fraction significantly improved in the HBO+ group and decreased in the HBO− group of patients after 3 weeks of acute myocardial infarction (from 46.27% to 50.81% vs from 45.54% to 44.05 %, P < .05). Conclusions Adjunctive hyperbaric oxygen therapy after thrombolysis in acute myocardial infarction has a favorable effect on left ventricular systolic function and the remodeling process.

Early changes in left ventricular volume and function are predictors for long-term remodeling in patients with acute transmural myocardial infarction and preserved systolic function

Background We sought to describe the degree of long-term left ventricular (LV) remodeling after acute transmural myocardial infarction with preserved LV systolic function, and to evaluate whether Doppler echocardiographic parameters in the early phase could predict this process. Methods A total of 60 patients without heart failure and with LV ejection fraction ≥ 0.40 (mean 0.48 ± 0.054), were followed up with Doppler echocardiographic examinations at baseline, 3 months, and 1 and 2 years. Results There was a significant increase in LV end-diastolic volume index of 7% ( P = .006) and LV end-systolic volume index of 8% ( P = .03), and no change in ejection fraction. This remodeling was confined to 7 patients (12%) with a significant increase in LV end-diastolic volume index above 20 mL/m 2. There was also a significant increase in the deceleration time of both the early mitral filling wave (Δ early mitral filling wave = 58 milliseconds, P < .0005) and the diastolic forward component of pulmonary venous flow (Δ diastolic forward component of pulmonary venous flow = 61 milliseconds, P < .0005), and a shift in filling pattern with increasing prevalence of abnormal relaxation. Changes in end-diastolic volume index were predicted by baseline early mitral filling wave less than 100 milliseconds, but the most powerful predictors of 2-year remodeling were volume changes at 3 months. Conclusion Twelve percent of patients with Q-wave infarction and ejection fraction ≥ 0.40 experienced significant LV dilatation at 2 years, and this late remodeling was partly related to baseline filling characteristics.

An early predictor of left ventricular remodeling after reperfused anterior acute myocardial infarction: ratio of peak E wave velocity/flow propagation velocity and mitral E wave deceleration time.

Several studies have demonstrated that the ratio of peak E wave velocity/flow propagation velocity (E/FPV) using color M-mode Doppler echocardiography and the mitral E wave deceleration time make it possible to estimate left ventricular filling pressure. Recent studies have indicated that deceleration time can predict left ventricular dilation after acute myocardial infarction. The purpose of this study was to determine whether the early assessment of deceleration time and E/FPV could predict left ventricular dilation after acute myocardial infarction. We studied 55 patients with first anterior acute myocardial infarction who underwent successful coronary angioplasty by two-dimensional (2-D) Doppler echocardiography within 12 hours and at 1 and 6 months after reperfusion. Patients were divided into three groups according to deceleration time and E/FPV immediately after reperfusion: (1). restrictive filling (deceleration time < 140 msec and E/FPV > or= 2.0), (2). elevated filling pressure (deceleration time >or= 140 msec and E/FPV >or= 2.0), (3). and normal filling pressure (deceleration time >or= 140 msec and E/FPV < 2.0). The end-diastolic volume index (EDVI) was similar in the three groups immediately after reperfusion. EDVI in the groups with restrictive filling and elevated filling pressure was significantly greater than that in the group with normal filling pressure at 6 months (93 +/- 11 and 89 +/- 16 vs 59 +/- 11 ml/m(2), respectively; P < 0.0001). E/FPV shows a better correlation with the change in EDVI at 6 months than deceleration time (r = 0.77; P < 0.0001 and r = - 0.46; P < 0.001, respectively). The early measurement of E/FPV provides a simple and accurate means for predicting left ventricular dilation after acute myocardial infarction.

The Doppler Echocardiographic Myocardial Performance Index Predicts Left-Ventricular Dilation and Cardiac Death after Myocardial Infarction

To investigate the value of the Doppler-derived myocardial performance index to predict early left-ventricular (LV) dilation and cardiac death after a first acute myocardial infarction (AMI), Doppler echocardiography was performed within 24 h of hospital admission, on day 5, 1 and 3 months after AMI in 125 consecutive patients. The index measured on day 1 correlated well with the change in end-diastolic volume index observed from day 1 to 3 months following AMI (r = 0.66, p < 0.0001). One-year survival in patients with Doppler index <0.63 was 89%, and 37% in patients with index ≧0.63, (p < 0.0001). Multivariate analysis identified myocardial performance index ≧0.63 (relative risk 5.6, p < 0.0001), E-wave deceleration time <140 ms (relative risk 2.7, p = 0.008) and Killip class ≧II (relative risk 4.0, p = 0.04) to be independent predictors of cardiac death. Therefore, we conclude that the Doppler echocardiographic myocardial performance index is a predictor of LV dilation and cardiac death after a first AMI.

Influence of treatment delay on long-term left ventricular function in patients with acute myocardial infarction successfully treated with primary angioplasty

Background Myocardial salvage has been shown to be dependent on the time elapsed from the onset of acute myocardial infarction (AMI) to reperfusion. The aim of this study was to evaluate the importance of time to reperfusion for left ventricular function recovery after primary angioplasty (percutaneous transluminal coronary angioplasty [PTCA]) for AMI. Methods Ninety-five patients undergoing long-term successful PTCA for AMI were studied. Echocardiography was performed before and 3, 7, 30, 90, and 180 days after PTCA. End-diastolic volume index (EDVI) and end-systolic volume index (ESVI), ejection fraction, and left ventricular wall motion score index (WMSI) were evaluated. Results Patients were divided into group A, 23 patients reperfused within 2 hours; group B, 32 patients reperfused between 2 and 4 hours; group C, 22 patients reperfused between 4 and 6 hours; and group D, 18 patients reperfused between 6 and 12 hours. Both EDVI and ESVI were reduced in groups A and B at 90 days. Groups C and D did not show any changes of EDVI and ESVI at any stage throughout the study. Ejection fraction improved only in groups A and B at 30, 90, and 180 days. At study entry, WMSI was similar in all groups. After 7 days, in group A and in group B, WMSI was improved, no changes were observed in group C, and a mild deterioration was observed in group D at 3 and 7 days. Subsequent evaluations showed progressive improvement of WMSI in all groups. Conclusions Myocardial salvage is achieved only in patients revascularized within 4 hours from AMI onset. However, revascularization after 6 hours may be worthwhile by preventing ventricular remodeling. (Am Heart J 2001;141:603-9.)

Doppler-Derived Mitral Deceleration Time

The relation between remodeling and left ventricular (LV) diastolic function has not yet been fully investigated. The aim of this study was to determine whether early assessment of Doppler-derived mitral deceleration time (DT), a measure of LV compliance and filling, may predict progressive LV dilation after acute myocardial infarction (AMI). Fifty-one patients (aged 61+/-11 years; 6 women) with anterior AMI successfully treated with direct coronary angioplasty underwent 2-dimensional and Doppler echocardiographic examinations within 24 hours of admission, at days 3, 7, and 30 and 6 months after the index infarction. Mitral flow velocities were obtained from the apical 4-chamber view with pulsed Doppler. End-diastolic volume index (EDVI) and end-systolic volume index (ESVI) were calculated with the Simpson's rule algorithm. Patients were divided according to the DT duration assessed at day 3 in 2 groups: group 1 (n=33) with DT >130 ms and group 2 (n=18) with DT </=130 ms. Patency and restenosis rate at 6 months were similar between the 2 groups (94% group 1 vs 89% group 2; P=0.52; 27% group 1 vs 33% group 2; P=0.64, respectively). LV volume indexes were similar in both groups at baseline (EDVI: 71+/-3 group 1 vs 70+/-3 mL/m2 group 2, P=0.42; ESVI: 43+/-3 group 1 vs 48+/-3 mL/m2 group 2, P=0.13, respectively). From day 3 on, LV volume indexes progressively increased in group 2 and were significantly larger than those of group 1 at 6 months (LVEDVI 61+/-3 group 1 vs 104+/-6 mL/m2 group 2, P=0.00001; LVESVI 31+/-3 group 1 vs 73+/-6 mL/m2 group 2, P=0.00001, respectively). A significant inverse correlation was found between DT and changes in EDVI at 6 months (r=-0.68; P<0.0000001). By stepwise multiple regression analysis among several clinical, demographic, angiographic, and echocardiographic variables, DT was the most powerful predictor of EDVI changes at 6 months (P=0.02). These data suggest that early estimation (day 3) of Doppler-derived mitral DT provides a simple and accurate mean to predict late LV dilation after reperfused AMI.

Plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive ventricular remodeling after acute myocardial infarction

To investigate the relation between plasma brain natriuretic peptide (BNP) and progressive ventricular remodeling, we measured plasma BNP and atrial natriuretic peptide (ANP) in 30 patients with acute myocardial infarction on days 2, 7, 14, and 30 after the onset. Left ventricular end-diastolic volume index (EDVI), end-systolic volume index (ESVI), and ejection fraction (EF) on admission and 1 month after the onset were assessed by left ventriculography. Changes in EDVI (ΔEDVI), ESVI (ΔESVI), and EF (ΔEF) were obtained by subtracting respective acute-phase values from corresponding chronic-phase values. Plasma ANP on days 2 and 7 showed only weak correlations with ΔEDVI ( r = 0.48 and 0.54; both p < 0.01), whereas plasma BNP on day 7 more closely correlated with ΔEDVI ( r = 0.77; p < 0.001). When study patients were divided into two groups according to plasma BNP on day 7, the group with BNP higher than 100 pg/ml showed greater increases in left ventricular volume and less improvement in EF compared with the other group with BNP lower than 100 pg/ml (ΔEDVI = 10.4 ± 8 vs –3.4 ± 9 ml/m 2, DESVI = 6.2 ± 7 vs –4.9 ± 5 ml/m 2, and DEF = 1.0% ± 4% vs 4.9% ± 5%; p < 0.05, respectively). Multiple regression analysis revealed that only plasma BNP on day 7, but not ANP, peak creatine phosphokinase level, left ventricular end-diastolic pressure, or acute-phase EF, correlated independently with ΔEDVI ( p < 0.01). These results suggest that plasma BNP may be a simple and useful biochemical marker for the prediction of progressive ventricular remodeling within the first 30 days of acute myocardial infarction. (Am Heart J 1998;135:21-8.)

Transesophageal two-dimensional echocardiographic analysis of right ventricular systolic performance indices during coronary artery bypass grafting

Sixteen patients (aged 59 ± 14 years) undergoing coronary artery bypass surgery were evaluated to delineate the intra-operative course of transesophageal echocardiographic right ventricular (RV) systolic performance indices. Pre-induction data included thermodilution RV ejection fraction (RVEF TD), 0.43 ± 0.13, RV end-diastolic volume index (EDVI), 110 ± 33 mL/m 2, cardiac index (CI), 3.4 ± 1.0 L/min/m 2, RV enddiastolic pressure (EDP), 7.1 ± 4.2 mmHg, and mean pulmonary artery pressure ( PAP ), 21 ± 6 mmHg. Eleven patients had significant right coronary artery (RCA) disease (>70% occlusion). Five patients arrived with an ongoing nitroglycerin infusion (1 to 3 μg/kg/min), which was maintained intraoperatively. Echocardiographic measurements included longitudinal-axis (LA) and short-axis (SA) planimetered area excursion fractions (2D LA and 2D SA, respectively) and LA maximal major and minor axis shortening fractions (max major LA and max minor LA, respectively). Hemodynamic measurements included RVEF TD, EDVI, CI, EDP, and PAP . Measurements were determined following induction/ endotracheal intubation, following sternotomy/pericardiotomy, and after cardiopulmonary bypass (CPB) with the chest open. All patients were maintained on vasodilator therapy post-CPB (nitroglycerin, 1 to 3 μg/kg/min [N = 16] and nitroprusside, 0.5 to 4.5 pg/kg/min [N = 4]) post-CPB. Two patients received inotropic support (epinephrine, 0.2 to 0.3 μg/ kg/min). CPB was associated with significant decreases in max major axis LA and 2D LA ( P < 0.05) as compared to measurements determined prior to CPB. Maximum major axis LA values pre-CPB were 0.35 ± 0.06 and 0.33 ± 0.08 versus post-CPB values of 0.24 ± 0.08. 2D LA values were 0.50 ± 0.16 and 0.47 ± 0.10 versus post-CPB values of 0.37 ± 0.11. 2D SA was maintained (values 0.43 ± 0.17 and 0.44 ± 0.18 versus post-CPB 0.52 ± 0.18). The pre-CPB maximum major axis LA/ maximum minor axis LA relationship was significant (γ = 0.71). There was no correlation between these variables post-CPB. Maximum major axisLA changes were unrelated to CPB duration, aortic cross-clamp time, cardioplegia dose, antecedent RV function, and the presence/ absence of RCA disease. Significant changes were also unrelated to changes in heart rate. There was no significant change in EDVI, EDP, and PAP measurements. These findings may indicate regional inhomogeneity of RV function or a spectrum of differing sensitivities to changes in RV performance of the respective measurement indices.

Effect of infarct size measured from antimyosin single-photon emission computed tomographic scans on left ventricular remodeling

To evaluate the effect of infarct size on left ventricular volumes and geometric remodeling, 26 patients with a first acute Q wave myocardial infarction (anterior in 14, inferior in 12) had the infarct sized from single-photon emission computed tomographic (SPECT) imaging of indium-111 antimyosin. All patients underwent gated blood pool scintigraphy before hospital discharge for determination of ejection fraction and end-diastolic and endsystolic volume indexes. Infarct size was quantitated from indium-111 antimyosin uptake in coronal slices with use of a threshold technique for edge detection. Nineteen of 26 patients had additional simultaneous acquisitions of indium-111 and thallium-201 uptake and the infarct was expressed as a percent of the total left ventricle.Infarct size was larger (59 ± 16 vs. 33 ± 16 g), predischarge ejection fraction lower (35 ± 5% vs. 60 ± 9%) and end-systolic volume index higher (57 ± 13 vs. 36 ± 10 ml/m2) in the group with anterior infarction. Despite these differences, predischarge end-diastolic volume index was not significantly different between the group with anterior (88 ± 17 ml/m2) versus inferior (89 ± 14 ml/m2) infarction. There was a significant inverse correlation between percent infarct size and ejection fraction for patients with dual isotope imaging (r = −0.90) and a significant direct correlation between infarct size and end-systolic volume index (r = 0.79, p < 0.01).Fourteen patients without subsequent myocardial infarction or coronary artery bypass grafting had a repeat gated blood pool study late (26 ± 15 months) after infarction. Patients with an anterior infarction had a significant increase in end-diastolic volume index (+10 ± 11 ml/m2), which was also significantly different from the change in end-diastolic volume index in the group with inferior infarction (−5 ± 5.2 ml/m2).These data suggest that infarct size and location have a profound effect on left ventricular function and chamber size. Anterior infarcts, because they are larger, cause more severe left ventricular dysfunction and higher end-systolic volume early. The consequent increases in end-systolic wall stress may be the driving mechanism for late left ventricular chamber enlargement. This method for measuring infarct size has potential usefulness for selecting patients who will benefit from pharmacologic intervention to prevent late left ventricular dilation.

Relation of left ventricular volume and function over one year after acute myocardial infarction to infarct size determined by technetium-99m sestamibi

Twenty patients with a first acute myocardial infarction (AMI) (15 anterior, 5 inferior) who received successful reperfusion therapy underwent tomographic imaging with technetium-99m (Tc-99m) sestamibi and radionuclide ventriculography at discharge, 6 weeks, and 1 year after AMI. Patency of the infarct-related artery after reperfusion (thrombolysis, 8 patients; coronary angioplasty, 12 patients) was confirmed by angiography in all patients. Tc-99m sestamibi perfusion defect at discharge (a measure of infarct size) was quantitated using previous methods and expressed as a percentage of the left ventricle (28 ± 19%, range 0 to 59%). This perfusion defect size correlated closely with ejection fraction at discharge (r = −0.87), 6 weeks (r = −0.81) and at 1 year (r = −0.78, all p < 0.0001). Perfusion defect size at discharge also correlated closely with end-systolic volume index at discharge (r = 0.71, p < 0.0005), 6 weeks (r = 0.63, p < 0.005) and at 1 year (r = 0.76, p < 0.0001). Perfusion defect size at discharge did not correlate significantly with end-diastolic volume index at discharge or at 6 weeks, but did correlate at 1 year (r = 0.66, p < 0.005). There was no significant group change in end-systolic or end-diastolic volume indexes from discharge to 1 year later, although 7 patients had definite individual changes in end-diastolic volume index (3 increased and 4 decreased). There was no relation between defect size and late changes in end-systolic volume index, but there was a weak correlation between defect size and late changes in end-diastolic volume index (r = 0.42, p = 0.07). Tc-99m sestamibi perfusion defect at discharge correlates with ejection fraction, and end-diastolic and endsystolic volume indexes 1 year after AMI. In most patients with patent infarct-related arteries after AMI, there does not appear to be a significant overall increase in ventricular volume during the first year after infarction.

Exercise intolerance in patients with heart failure and preserved left ventricular systolic function: Failure of the Frank-Starling mechanism

Invasive cardiopulmonary exercise testing was performed in 7 patients who presented with congestive heart failure, normal left ventricular ejection fraction and no significant coronary or valvular heart disease and in 10 age-matched normal subjects. Compared with the normal subjects, patients demonstrated severe exercise intolerance with a 48% reduction in peak oxygen consumption (11.6 ± 4.0 versus 22.7 ± 6.1 ml/kg per min; p < 0.001), primarily due to a 41% reduction in peak cardiac index (4.2 ± 1.4 versus 7.1 ± 1.1 liters/mm per m2; p < 0.001).In patients compared with normal subjects, peak left ventricular stroke volume index (34 ±9 versus 46 ± 7 ml/min per m2; p < 0.01) and end-diastolic volume index (56 ± 14 versus 68 ± 12 ml/min per m2; p < 0.08) were reduced, whereas peak ejection fraction and end-systolic volume index were not different. In patients, the change in end-diastolic volume index during exercise correlated strongly with the change in stroke volume index (r = 0.97; p < 0.0001) and cardiac index (r = 0.80; p < 0.03). Pulmonary wedge pressure was markedly increased at peak exercise in patients compared with normal subjects (25.7 ± 9.1 versus 7.1 ± 4.4 mm Hg; p < 0.0001). Patients demonstrated a shift of the left ventricular end-diastolic pressure-volume relation upward and to the left at rest. Increases in left ventricular filling pressure during exercise were not accompanied by increases in end-diastolic volume, indicating a limitation to left ventricular filling.These data suggest that abnormalities in left ventricular diastolic function limited the patients' ability to augment stroke volume by means of the Frank-Starling mechanism, resulting in severe exercise intolerance. These findings provide a pathophysiologic rationale for symptoms of chronic fatigue and dyspnea on exertion, which are often present in patients with a history of congestive heart failure and preserved systolic function.