Decrease In Left Ventricular End-diastolic Volume Research Articles

Age-Related Changes in Heart Function by Serial Echocardiography in Women Aged 40–80 Years

To determine if a defined set of echocardiographic parameters at entry and exit of a longitudinal study over 5 years showed changes with aging. The cohort consisted of 484 randomly recruited women aged 40-80. They were examined by two echocardiography cardiologists, independent of the medical information for these women. Across the age decades (40-49, 50-59, 60-69, 70-79 years), body weight and body surface area (BSA) did not vary, and diastolic blood pressure (DBP) was stable; systolic blood pressure (SBP) progressively increased. There was gradual decline in left ventricular (LV) diastolic function, increase in LV muscle mass, and decrease in LV end-diastolic volume (LVEDV). The serial decrease in rate of change over 5 years in ejection fraction (ET) was small but significant across the four age decades. As expected, there were age-related changes in cardiac structure and function over time in women who showed no apparent cardiovascular disease (CVD) at entry to the study. The direction of these serial changes was toward the development of LV stiffness and likelihood of subsequent heart failure. The clinical significance of the decrease in rate of change in EF remains unclear.

Prognostic value of right ventricular mass, volume, and function in idiopathic pulmonary arterial hypertension

This study investigated the relationship between right ventricular (RV) structure and function and survival in idiopathic pulmonary arterial hypertension (IPAH). In 64 patients, cardiac magnetic resonance, right heart catheterization, and the six-minute walk test (6MWT) were performed at baseline and after 1-year follow-up. RV structure and function were analysed as predictors of mortality. During a mean follow-up of 32 months, 19 patients died. A low stroke volume (SV), RV dilatation, and impaired left ventricular (LV) filling independently predicted mortality. In addition, a further decrease in SV, progressive RV dilatation, and further decrease in LV end-diastolic volume (LVEDV) at 1-year follow-up were the strongest predictors of mortality. According to Kaplan-Meier survival curves, survival was lower in patients with an inframedian SV index <or= 25 mL/m(2), a supramedian RV end-diastolic volume index >or= 84 mL/m(2), and an inframedian LVEDV<or=40 mL/m(2). The RV contains prognostic information in IPAH. A large RV volume, low SV, and a reduced LV volume are strong independent predictors of mortality and treatment failure.

Diastolic ventricular interactions in endurance-trained athletes during orthostatic stress

Enhanced left-ventricular (LV) compliance is a common adaptation to endurance training. This adaptation may have differential effects under conditions of altered venous return. The purpose of this investigation was to assess the effect of cardiac (un)loading on right ventricular (RV) cavity dimensions and LV volumes in endurance-trained athletes and normally active males. Eight endurance-trained (Vo(2max), 65.4 +/- 5.7 ml.kg(-1).min(-1)) and eight normally active (Vo(2max), 45.1 +/- 6.0 ml.kg(-1).min(-1)) males underwent assessments of the following: 1) Vo(2max), 2) orthostatic tolerance, and 3) cardiac responses to lower-body positive (0-60 mmHg) and negative (0 to -80 mmHg) pressures with echocardiography. In response to negative pressures, echocardiographic analysis revealed a similar decrease in RV end-diastolic cavity area in both groups (e.g., at -80 mmHg: normals, 21.4%; athletes, 20.8%) but a greater decrease in LV end-diastolic volume in endurance-trained athletes (e.g., at -80 mmHg: normals, 32.3%; athletes, 44.4%; P < 0.05). Endurance-trained athletes also had significantly greater decreases in LV stroke volume during lower-body negative pressure. During positive pressures, endurance-trained athletes showed larger increases in LV end-diastolic volume (e.g., at +60 mmHg; normals, 14.1%; athletes, 26.8%) and LV stroke volume, despite similar responses in RV end-diastolic cavity area (e.g., at +60 mmHg: normals, 18.2%; athletes, 24.2%; P < 0.05). This investigation revealed that in response to cardiac (un)loading similar changes in RV cavity area occur in endurance-trained and normally active individuals despite a differential response in the left ventricle. These differences may be the result of alterations in RV influence on the left ventricle and/or intrinsic ventricular compliance.

Predictors of Remodeling in the CRT Era: Influence of Mitral Regurgitation, BNP, and Gender

Background We analyzed quantitative echocardiographic data from a large heart failure cohort receiving medical and cardiac resynchronization therapy (CRT) to determine baseline predictors of progressive left ventricular (LV) enlargement. Methods and Results Quantitative echocardiograms were obtained at baseline and after 6 months in 776 outpatients with chronic heart failure who participated in MIRACLE (Multicenter InSync Randomized Clinical Evaluation) and MIRACLE-ICD (Multicenter InSync ICD Randomized Clinical Evaluation). We used multivariable regression to determine clinical, therapeutic, and echocardiographic characteristics that predicted a subsequent change in left ventricular end-diastolic volume (LVEDV). Over 6 months, LVEDV increased in 308 (40%) and decreased in 468 (60%) patients. Baseline mitral regurgitation and levels of plasma brain natriuretic peptide (BNP) independently predicted LV enlargement, whereas CRT predicted a decrease in LVEDV (all P < .01). In all models tested, male gender was an independent risk factor for progressive LV enlargement ( P < .0001). Conclusion Men show more prominent LV dilation than women in chronic heart failure despite medical and device therapy. Rates of LV remodeling are influenced further by mitral regurgitation, plasma BNP, and CRT. Future studies should take these clinical factors into account when determining the influence of genetic factors and novel therapies on ventricular remodeling in chronic heart failure.

Effect of Thalidomide on Cardiac Remodeling in Chronic Heart Failure

Inflammation and matrix degradation may play a pathogenic role in chronic heart failure (CHF), and therefore, we examined whether thalidomide, a drug with potential immunomodulating and matrix-stabilizing properties, could improve left ventricular (LV) function in patients with CHF secondary to idiopathic dilated cardiomyopathy (IDCM) or coronary artery disease (CAD). Fifty-six patients with CHF and an LV ejection fraction (LVEF) <40% who were already on optimal conventional cardiovascular treatment were randomized to thalidomide (25 mg QD increasing to 200 mg QD) or placebo and followed up for 12 weeks. Our main findings were as follows: (1) During thalidomide treatment but not during placebo, there was a marked increase in LVEF (&7 EF units) along with a significant decrease in LV end-diastolic volume and heart rate. (2) This improvement in LVEF was accompanied by a decrease in matrix metalloproteinase-2 without any changes in its endogenous tissue inhibitor, suggesting a matrix-stabilizing net effect. (3) Thalidomide also induced a decrease in total neutrophil count and an increase in plasma levels of tumor necrosis factor-alpha, suggesting both proinflammatory and antiinflammatory effects. (4) The effect of thalidomide on LVEF was more marked in IDCM than in CAD, possibly partly reflecting that the former group was able to tolerate a higher thalidomide dosage. Although our results must be confirmed in larger studies that also examine the effects on morbidity and mortality, our findings suggest a role for thalidomide in the management of CHF in addition to traditional cardiovascular medications.

In Reply: Is the Decrease in LVEDV the Mechanism of Action of Continuous Positive Airway Pressure in Diastolic Heart Failure?

We read with great interest the comments by Drs. Agarwal and Gupta regarding our article (March 2005) 1 Bendjelid K Schutz N Suter PM et al. Does continuous positive airway pressure by face mask improve patients with acute cardiogenic pulmonary edema due to left ventricular diastolic dysfunction?. Chest. 2005; 127: 1053-1058 Abstract Full Text Full Text PDF PubMed Scopus (46) Google Scholar entitled “Does Continuous Positive Airway Pressure (CPAP) by Face Mask Improve Patients With Acute Cardiogenic Pulmonary Edema (ACPE) Due to Left Ventricular Diastolic Dysfunction?” The authors do not agree with the proposed mechanism of CPAP in patients presenting with ACPE that was illustrated by our study. Is the Decrease in LVEDV the Mechanism of Action of Continuous Positive Airway Pressure in Diastolic Heart Failure?CHESTVol. 128Issue 3PreviewWe read with interest the article by Bendjelid et al (March 2005),1 who present an interesting analysis that the benefit of continuous positive airway pressure (CPAP) in diastolic heart failure (DHF) is due to decrease in left ventricular end-diastolic volume (LVEDV) and mean arterial pressure. However, we do not agree with the authors on the proposed mechanism of CPAP in DHF. Full-Text PDF

Does Continuous Positive Airway Pressure by Face Mask Improve Patients With Acute Cardiogenic Pulmonary Edema Due to Left Ventricular Diastolic Dysfunction?

Continuous positive airway pressure (CPAP) by face mask is an effective method of treating severe cardiogenic pulmonary edema (CPE). However, to our knowledge, no study has provided a precise evaluation of the effects of CPAP on cardiac function in patients presenting with CPE and preserved left ventricular (LV) function. Prospective observational clinical study. A 14-bed, medical ICU at a university hospital. Nine consecutive patients presenting with hypoxemic acute CPE. All patients were selected for 30 min of CPAP with 10 cm H(2)O by mask with fraction of inspired oxygen adjusted for a cutaneous saturation > 90%. Doppler echocardiography was performed before CPAP application and during the last 10 min of breathing with CPAP. Two-tailed, paired t-tests were used to compare data recorded at baseline (oxygen alone) and after CPAP. Four patients presented CPE with preserved left ventricular (LV) function (a preserved LV ejection fraction [LVEF] > 45%, and/or aortic velocity time integral > 17 cm in the absence of aortic stenosis or hypertrophic cardiomyopathy). Oxygenation and ventilatory parameters were improved by CPAP in all patients. Hemodynamic monitoring and Doppler echocardiographic analysis demonstrated that in patients with preserved LV systolic function, mean arterial pressure and LV end-diastolic volume were decreased significantly by CPAP (p < 0.04). In patients with LV systolic dysfunction, CPAP improved LVEF (p < 0.05) and decreased LV end-diastolic volume (p = 0.001) significantly. CPAP improves oxygenation and ventilatory parameters in all kinds of CPE. In patients with preserved LV contractility, the hemodynamic benefit of CPAP results from a decrease in LV end-diastolic volume (preload).

Men and Women Remodel Differently in Chronic Systolic Heart Failure: Analyses from MIRACLE and MIRACLE-ICD

Background: Predictors of ventricular remodeling are well established in hypertensive heart disease and transmural infarction. Less is known about clinically relevant predictors of remodeling in chronic systolic heart failure. We tested the hypothesis that specific baseline characteristics would predict progressive left ventricular enlargement in a large cohort of patients with chronic systolic heart failure. Methods: MIRACLE (Multicenter InSync Randomized Clinical Evaluation) and MIRACLE-ICD were prospective, double-blind, randomized clinical trials designed to test the efficacy and safety of CRT and combined CRT/ICD therapy in outpatients with chronic systolic heart failure. We combined these studies into a single cohort since the inclusion criteria, mode of CRT, and timing of endpoint assessments were similar. Out of 1008 randomized participants, 776 underwent quantitative echocardiography at baseline and at six months. We used univariate and stepwise multivariable linear regression to determine which baseline characteristics predicted an increase or decrease in left ventricular end diastolic volume (LVEDV) over the subsequent six months. Results: LVEDV increased in 308 (40%) and decreased in 468 (60%) patients. In multivariable models, male gender, severity of mitral regurgitation, and plasma BNP levels were independent predictors of ventricular enlargement after adjustment for baseline LVEDV and randomization to CRT (all p<0.01; see Table for predicted changes in LVEDV). CRT was an independent predictor of a decrease in LVEDV, with greater reduction among patients with longer baseline QRS. In our final model, age and beta-blocker use did not independently predict change in LVEDV. Conclusion: Male gender, mitral regurgitation, and plasma BNP are independent predictors of left ventricular enlargement in chronic systolic heart failure. These findings emphasize the importance of volume load, caused by regurgitant valve lesions or manifested by increased BNP, in mediating ventricular remodeling. Moreover, they demonstrate that men and women may remodel differently, with men showing a higher likelihood of progressive LV enlargement. Further studies are indicated to determine genetic and gender-specific modifiers of ventricular remodeling. Tabled 1 Predicted Change in LVEDV (mL) at Six Months (CRT OFF) Gender MR index Plasma BNP (pg/mL) Male Female 0.1 0.3 100 500 1000 4.5 −19 −0.2 9.1 −6.3 1.1 4.2 Open table in a new tab

Acute effects of beating heart coronary surgery on left ventricular performance

Background The increasing use of off-pump bypass grafting (OPCABG), requires an evaluation of its effects on left ventricular (LV) performance. Methods In 8 patients with multivessel coronary disease who were undergoing to off-pump coronary artery bypass grafting, LV performance was analyzed from the pressure–volume (P-V) plane by the conductance catheter technique. Measurements were performed at base line, after the exposure of the vessels, after the application of the stabilization system, and at the end of the procedure. Results No significant changes in heart rate, LV end-systolic volume, LV end-diastolic pressure, mean pulmonary artery, and mean systemic blood pressure were observed in the various stages of the procedure. Cardiac index decreased during left anterior descending coronary artery grafting after application of the stabilizer with a concomitant decrease in LV end-diastolic volume, together with decreases in LV peak negative −dP/dt and increases in τ, indicating an impairment of LV relaxation but without a change in preload recruitable stroke work, indicating preserved LV contractile state. Exposure of posterior and lateral vessels induced a decrease in cardiac index and preload recruitable stroke work without a decrease in LV preload, indicating a decrease in LV contractile state together with a decrease in peak −dP/dt and increase in τ, indicating an impairment in LV relaxation Conclusions Off-pump coronary artery bypass grafting can be performed without decreasing LV performance. Major cardiac displacement like that used for posterior and lateral exposure induces acutely significant decrease in LV contractile state.

Acute Right Ventricular Dilatation in Response to Ischemia Significantly Impairs Left Ventricular Systolic Performance

Background—Right ventricular (RV) dilatation that occurs as a consequence of RV infarction is thought to produce hemodynamic instability by reducing left ventricular (LV) preload and compliance. We hypothesized that these geometric changes may also adversely affect LV systolic performance. Methods and Results—Twelve 40-kg pigs were studied. Integrated conductance catheters and micromanometers were placed in both the LV and RV to allow simultaneous recordings of pressure and volume and derivation of indices of contractile function. RV ischemia was induced by balloon occlusion of the proximal right coronary artery (RCA) under 3 conditions: 1) with the pericardium intact, 2) with the pericardium intact and inotropic support, and 3) with the pericardium wide open. With an intact pericardium, RCA occlusion produced a decrease in LV end-diastolic volume associated with a marked decline in the contractile function. With the pericardium open, the same ischemic insult resulted in both LV and RV dilatation, which p...

Acute right ventricular dilatation in response to ischemia significantly impairs left ventricular systolic performance.

Right ventricular (RV) dilatation that occurs as a consequence of RV infarction is thought to produce hemodynamic instability by reducing left ventricular (LV) preload and compliance. We hypothesized that these geometric changes may also adversely affect LV systolic performance. Twelve 40-kg pigs were studied. Integrated conductance catheters and micromanometers were placed in both the LV and RV to allow simultaneous recordings of pressure and volume and derivation of indices of contractile function. RV ischemia was induced by balloon occlusion of the proximal right coronary artery (RCA) under 3 conditions: 1) with the pericardium intact, 2) with the pericardium intact and inotropic support, and 3) with the pericardium wide open. With an intact pericardium, RCA occlusion produced a decrease in LV end-diastolic volume associated with a marked decline in the contractile function. With the pericardium open, the same ischemic insult resulted in both LV and RV dilatation, which produced a significantly smaller negative effect on cardiac output (P=0.03), LV systolic pressure (P=0.02), LV preload-recruitable stroke work (P<0. 01), and LV end-systolic pressure-volume relations (P<0.01). Similarly, administration of dobutamine during RCA occlusion decreased the ventricular volume changes and produced a relative improvement in LV contractile performance. The hemodynamic compromise seen in association with acute RV dilatation within an intact pericardium is partly attributable to impaired LV systolic performance and cannot be wholly ascribed to changes in LV preload or compliance.

Hemodynamic Response and Change in Organ Blood Volume During Spinal Anesthesia in Elderly Men with Cardiac Disease

Aging and disease may make the elderly patient with cardiac disease particularly susceptible to hypotension during spinal anesthesia.We studied 15 men, 59-80 y old, with histories of prior myocardial infarction (n = 9), congestive heart failure (n = 2), and/or stable myocardial ischemia (n = 11) given spinal anesthesia with 50 mg lidocaine in dextrose. Technetium-99m-labeled red blood cell imaging estimated left ventricular ejection fraction (EF) and changes in blood volume in the abdominal organs and legs. Arterial and pulmonary artery catheters provided hemodynamic measurements. Sensory block averaged T4 (range T1-10). Mean arterial pressure decreased 33% +/- 15% (SD) (P < 0.001), secondary to decreases in vascular resistance (SVR), -26% +/- 13% (P < 0.001) and cardiac output, -10% +/- 16% (P = 0.03). EF increased from 53% +/- 11% to 58% +/- 14% (P < 0.001) while left ventricular end-diastolic volume (LVEDV) decreased (-19% +/- 9%, P < 0.001). Blood volume increased in the legs (6% +/- 6%, P = 0.006), kidneys (10% +/- 9%, P < 0.001), and mesentery (7% +/- 5%, P 0.001) but not in the liver or spleen. Cardiac function was well maintained. We concluded that the primary mechanism of hypotension was a decrease in SVR, not cardiac output, despite the decrease in LVEDV. (Anesth Analg 1997;85:99-105)

Hemodynamic response and change in organ blood volume during spinal anesthesia in elderly men with cardiac disease.

Aging and disease may make the elderly patient with cardiac disease particularly susceptible to hypotension during spinal anesthesia. We studied 15 men, 59-80 y old, with histories of prior myocardial infarction (n = 9), congestive heart failure (n = 2), and/or stable myocardial ischemia (n = 11) given spinal anesthesia with 50 mg lidocaine in dextrose. Technetium-99m-labeled red blood cell imaging estimated left ventricular ejection fraction (EF) and changes in blood volume in the abdominal organs and legs. Arterial and pulmonary artery catheters provided hemodynamic measurements. Sensory block averaged T4 (range T1-10). Mean arterial pressure decreased 33% +/- 15% (SD) (P < 0.001), secondary to decreases in vascular resistance (SVR), -26% +/- 13% (P < 0.001) and cardiac output, -10% +/- 16% (P = 0.03). EF increased from 53% +/- 11% to 58% +/- 14% (P < 0.001) while left ventricular end-diastolic volume (LVEDV) decreased (-19% +/- 9%, P < 0.001). Blood volume increased in the legs (6% +/- 6%, P = 0.006), kidneys (10% +/- 9%, P < 0.001), and mesentery (7% +/- 5%, P 0.001) but not in the liver or spleen. Cardiac function was well maintained. We concluded that the primary mechanism of hypotension was a decrease in SVR, not cardiac output, despite the decrease in LVEDV.

Mitral valve repair is superior to valve replacement for the early preservation of cardiac function: Relation of ventricular geometry to function

The immediate effect of mitral valve repair (MVP) or replacement (MVR) on cardiac function was compared in patients with mitral regurgitation in relation to the changes in left ventricular (LV) function and geometry by using intraoperative transesophageal echocardiography in 29 patients with MVP and 21 patients with MVR, before and immediately after cardiopulmonary bypass. The LV volumes, ejection fraction, and long-axis and short-axis lengths and eccentricity index (ratio of long axis to short axis) at end-systole and end-diastole were measured. After both MVP and MVR, there were significant decreases in LV end-diastolic volume ( p < 0.0001). However, the ejection fraction did not change after MVP, whereas it decreased after MVR ( p < 0.0001). After MVP, there was an increase in eccentricity index at end-systole ( p < 0.0001). After MVR, there was no decrease in end-systolic volume, and the eccentricity index was lower than that after MVP ( p < 0.0001). The change in LV ejection fraction correlated with the changes in eccentricity index at end-systole ( r = 0.55; p < 0.0001) and end-diastole ( r = 0.42; p < 0.003). Immediate intraoperative LV function is preserved after MVP but is depressed after MVR for mitral regurgitation. The changes in ejection fraction correlate with changes in ventricular geometry.

Accelerated myocardial relaxation in conscious dogs during acute cardiac tamponade.

Eight chronically instrumented conscious dogs were used to test the hypothesis that left ventricular (LV) relaxation is accelerated during cardiac tamponade. The time constant of LV transmural pressure fall was measured before and during intrapericardial (IP) saline infusion (baseline) with and without beta-adrenergic blockade (propranolol 1 mg/kg iv). Heart rate was controlled by atrial pacing. Increasing IP pressure caused a progressive linear decrease in stroke volume before and during beta-blockade in each animal. The time constant of LV transmural pressure fall also decreased continuously with an increase in IP pressure from 26 +/- 7 ms during baseline to 18 +/- 5 ms during severe cardiac tamponade (P < 0.01) before beta-blockade. However, after beta-blockade, the time constant of LV transmural pressure fall was constant over a wide range of IP pressures despite a continuous decrease in LV end-diastolic volume. The time constant of LV transmural pressure fall was not altered by vena caval occlusions that caused the same decrease in LV preload observed during cardiac tamponade. We concluded that despite decreased pump function, LV relaxation was accelerated progressively during graded cardiac tamponade, and this change was dependent not on changes in loading conditions but on an intact beta-adrenergic influence.

Influence of age on left ventricular performance during exercise in normal Japanese subject: Assessment by radionuclide ventriculography

To assess the effects of age on left ventricular performance, multistage supine ergometer exercise radionuclide ventriculography (RNV) was performed in 92 normal subjects. The subjects ranged in age from 24 to 86 years and were free of cardiopulmonary disease and diabetes. Age-related changes in exercise duration, left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), cardiac output (CO) left ventricular ejection fraction (LVEF), left ventricular dv/dt, systolic and diastolic time indexes of dv/dt, and peak systolic pressure/left ventricular end-systolic volume (PSP/LVESV) were analyzed at rest and during the peak exercise stage. Age-related decrease in LVEDV and peak diastolic dv/dt were significant at rest. The time indexes of ECG R to peak systolic dv/dt and time of end-systole to peak diastolic dv/dt also were prolonged with age. Both maximum heart rate and exercise duration were shown to decline with age. No age-related difference was observed in LVESV, LVEF or PSP/LVESV either at rest or during exercise. However, the change of LVEF and LVESV during exercise was less in subjects aged 60 or more. These results indicate decreased left ventricular function during exercise in elderly subjects.

Differing responses in right and left ventricular filling, loading and volumes during positive end-expiratory pressure

Using a combined hemodynamic and radionuclide technique, 20 patients with varied ventricular function were evaluated during positive endexpiratory pressure (PEEP) application. Left ventricular (LV) and right ventricular (RV) ejection fractions and cardiac output were measured, and ventricular volumes were derived. Seven patients (group 1) who had an increase in LV end-diastolic volume with PEEP and 13 patients (group 2) who had the more typical response, a decrease in LV end-diastolic volume with PEEP, were identified. Compared with group 2, group 1 patients had a higher incidence of coronary artery disease (5 of 7 vs 1 of 13, p < 0.0005) and lower cardiac output (3.9 ±1.6 vs 9.1 ±3.2 liters/min, p < 0.005), LV ejection fraction (27 ±13 vs 51 ±21%, p < 0.05), RV ejection fraction (15 ±6 vs 32 ±8%, p < 0.005) and peak filling rate (1.32 ±0.43 vs 3.51 ±1.70 end-diastolic volumes/s, p < 0.005). LV and RV volumes increased and peak filling rate decreased with PEEP in group 1, whereas in group 2 LV volume decreased and RV volume and peak filling rate remained unchanged. Using stepwise regression analysis, the change in LV volume with PEEP was related directly to baseline systemic vascular resistance and inversely to baseline blood pressure. Similarly, the change in peak filling rate with PEEP was inversely related to the change in RV end-diastolic volume. Thus, the hemodynamic response to PEEP is heterogenous and may be related to LV ischemia. In patients with coronary artery disease and severely depressed biventricular function, LV volume may increase, LV ejection fraction may decrease and filling may worsen with PEEP.

Effects of volume loading during experimental acute pulmonary embolism.

Volume loading is used to treat hemodynamically compromised patients with acute pulmonary embolism despite data to suggest that volume loading after embolism might cause a leftward shift of the ventricular septum with a subsequent decrease in left ventricular (LV) end-diastolic volume and stroke work. We studied 10 closed-chest, anesthetized, and ventilated dogs to assess the effects of volume loading after pulmonary embolism caused by autologous clot. LV, right ventricular, and right atrial pressures as well as LV anteroposterior, septum-to-right ventricular, and septum-to-LV free wall diameters (sonomicrometry) were measured. Pericardial pressure was measured with flat, liquid-containing balloons. The effects of volume loading were assessed before embolism, after one episode of embolization, and after repeated embolizations. The LV area index (as a reflection of LV volume) increased during volume loading before embolism (2,870 +/- 430 to 3,080 +/- 520 mm2; p less than 0.05), did not change significantly during infusion of fluid after one embolization (2,850 +/- 470 to 2,860 +/- 500 mm2; p = NS), and decreased significantly during volume expansion after repeated embolizations (2,760 +/- 440 to 2,660 +/- 420 mm2; p less than 0.01). An index of LV stroke work increased (188 +/- 85 to 260 +/- 101 mm Hg x mm2; p less than 0.05), did not change significantly (188 +/- 39 to 203 +/- 52 mm Hg x mm2; p = NS), and decreased markedly (133 +/- 64 to 45 +/- 27 mm Hg x mm2; p less than 0.001) before embolism, after one embolization, and after repeated embolizations, respectively. The decrease in LV area index during volume loading after repeated embolizations was associated with an increase in septum-to-right ventricular free wall diameter (31 +/- 8 to 34 +/- 8 mm; p = 0.001) and a decrease in the septum-to-LV free wall diameter (44 +/- 5 to 42 +/- 5 mm; p less than 0.001), whereas the LV anteroposterior diameter did not change (62 +/- 5 to 63 +/- 5 mm; p = NS). This is compatible with a leftward septal shift being partially responsible for the decrease in LV end-diastolic volume; such a shift would be expected with the observed decrease in transseptal end-diastolic pressure gradient (-3 +/- 2 to -5 +/- 2 mm Hg; p = 0.001). In addition, after repeated embolizations, LV transmural pressure decreased in response to the volume load reflecting a marked increase in pericardial pressure.(ABSTRACT TRUNCATED AT 400 WORDS)

Importance of the “atrial kick” in determining the effective mitral valve orifice area in mitral stenosis

Atrial fibrillation with a rapid ventricular response in patients with mitral stenosis (MS) is often accompanied by pulmonary congestion and reduced cardiac output owing to a diminished diastolic filling period and the loss of the end-diastolic left ventricular (LV) pressure increment. To test the hypothesis that loss of atrial contraction (atrial kick) also results in a decrease in effective mitral valve orifice area, 6 patients with pure, isolated MS were studied in sinus rhythm during atrial pacing and simultaneous atrioventricular pacing. Atrial pacing at 140 beats/min caused no significant change from baseline in cardiac output or mitral valve area, but there was a decrease in LV end-diastolic volume and ejection fraction as well as an increase in left atrial pressure and mean diastolic gradient. Simultaneous atrioventricular pacing (to eliminate atrial kick) induced a decrease in cardiac output (4.4 ± 0.9 vs 5.2 ± 0.8 liters/min at 110 beats/min, 4.2 ± 0.9 vs 5.1 ± 0.9 liters/min at 140 beats/min; p < 0.05) and LV end-diastolic volume (77 ± 27 vs 93 ± 29 ml at 110 beats/min, 54 ± 17 vs 65 ± 19 ml at 140 beats/min; p < 0.05), an increase in left atrial pressure (28 ± 3 vs 20 ± 5 mm Hg at 110 beats/min, 30 ± 4 vs 25 ± 5 mm Hg at 140 beats/min; p < 0.05), and a decrease in mitral valve area (1.2 ± 0.4 vs 1.4 ± 0.5 cm 2 at 110 beats/min, 1.2 ± 0.4 vs 1.4 ± 0.4 cm 2 at 140 beats/min; p < 0.05). Thus, loss of atrial kick may cause pulmonary congestion and reduced cardiac output in patients with MS, partly because of a decrease in effective mitral valve area.

Ventricular performance and myocardial water content during hemodilution in dogs.

In dogs anesthetized with chloralose-urethan on right heart bypass, left ventricular (LV) performance was assessed at constant LV stroke work before and for up to 2.5 h after crystalloid hemodilution was established. Lowering the hematocrit from 43.3 +/- 1.3% to 13.6 +/- 1.7% (SE) did not significantly change LV end-diastolic pressure (LVEDP) initially. After 80 min LVEDP increased slightly by 1.7 +/- 0.6 cmH2O (P less than 0.05) at a stroke work of 17.3 +/- 2.3 g.m. The value of dP/dt did not change significantly throughout. When LV function curves were generated by increasing cardiac output, the stroke work attained at an LVEDP of 10 cmH2O decreased with hemodilution from 23.9 +/- 3.5 to 20.8 +/- 3.9 g.m (NS). LV wall water content increased with hemodilution, from which it could be calculated that there was an 18.6% increase in LV mass. Thus, despite an increase in LV external girth demonstrated by LV circumferential gauges, it is possible that increased wall thickness due to the water gain resulted in little change or an actual decrease in LV end-diastolic volume. Thus, profound hemodilution can be attained with only slight depression of LV performance.