Normal Left Ventricular Function Group Research Articles

Various Echocardiographic Patterns of Left Ventricular Systolic Dysfunction Induced by Carbon Monoxide Intoxication.

Carbon monoxide (CO) intoxication could cause significant cardiac injury. Although cardiac dysfunction after CO intoxication can be presented, the echocardiographic findings after CO intoxication are poorly defined. The purpose of this study was to evaluate the clinical patterns of left ventricular (LV) systolic dysfunction using echocardiography. A total of 132 CO-intoxicated patients were enrolled. Clinical, demographic and laboratory data and echocardiographic findings were analyzed. The LV dysfunction group (29 patients) showed higher lactate level (5.8±3.3 vs. 4.1±3.5mmol/L, p=0.024) and lower base excess (BE) (-8.2±6.0 vs. -4.8±4.7mEq/L, p=0.001) compared with normal LV function group. Among the LV dysfunction group, three different echocardiographic patterns were presented. Regional wall motion abnormality was presented in 14 patients. Apical ballooning, typical finding of stress-induced cardiomyopathy, was presented in eight patients. Global hypokinesia of LV was presented in seven patients. Laboratory findings indicating the severity of CO intoxication, such as lactate level, pH value, BE and aspartate aminotransferase, showed statistical significance according to the patterns of LV dysfunction (p=0.033, 0.022, 0.02 and 0.006, respectively). Our results demonstrate that CO intoxication could induce various patterns of LV dysfunction. The patterns of LV dysfunction might affect subsequent clinical outcomes.

Cardiac-specific sympathetic activation in men and women with and without heart failure

BackgroundClinical outcomes for cardiovascular syndromes such as heart failure differ between men and women.ObjectiveTo seek phenotypic evidence for sex-differences in cardiac-specific sympathetic nervous system activation, as abnormal sympathetic nervous system...

Clinical Significance of Atrioventricular Plane Displacement for Evaluating Left Ventricular Diastolic Dysfunction

Background and Objectives:Atrioventricular plane displacement (AVPD) has been used for evaluating systolic function. However, its relations with other echocardiographic variables reflecting diastolic function are not well documented. This study was designed to assess the relations between AVPD and those echocardiographic variables known to reflect diastolic function, especially using mitral annulus velocity. Subjects and Methods: Eighty-seven patients with normal left ventricular (LV) systolic function (normal echocardiography group (Group I, n=44), concentric left ventricular hypertrophy (LVH) group (Group II, n=43)) and 51 patients with LV dysfunction (Group III) were studied. To evaluate the correlation with echocardiographic variables reflecting LV systolic and diastolic function, we measured mitral inflow velocity and mitral annulus Doppler tissue velocity. Results:AVPD was correlated negatively with age, the ratio of early diastolic mitral inflow velocity and early diastolic mitral annulus velocity (E/E’), isovolumic relaxation time, and E/A ratio. AVPD was correlated positively with deceleration time, ejection fraction, and systolic mitral annulus velocity (S’). By multivariate analysis, AVPD was independently correlated with S’ (β=0.4, p<0.001) and E’ (β=0.5, p<0.001) in the normal LV function group, and with S’ (β=0.6, p<0.001) and E/E’(β=-0.3, p=0.005) in the LV dysfunction group. Conclusion:AVPD may be used as a diagnostic tool for evaluating LV diastolic function. (Korean Circulation J 2003;33 (12):1110-1117)

The effects of dobutamine on cardiac sympathetic activity in patients with congestive heart failure

ObjectivesThe goal of this work was to study the effects of short-term infusion of dobutamine on efferent cardiac sympathetic activity. BackgroundIncreased efferent cardiac sympathetic activity is associated with poor outcomes in the setting of congestive heart failure (CHF). Dobutamine is commonly used in the therapy of decompensated CHF. Dobutamine, through its effects on excitatory beta-receptors, may increase cardiac sympathetic activity. MethodsSeven patients with normal left ventricular (LV) function and 13 patients with CHF were studied. A radiotracer technique was used to measure cardiac norepinephrine spillover (CANESP) before and during an intravenous infusion of dobutamine titrated to increase the rate of rise in LV peak positive pressure (+dP/dt) by 40%. ResultsSystemic arterial pulse pressure increased significantly in response to dobutamine in the normal LV function group (74 ± 3 mm Hg to 85 ± 3 mm Hg, p = 0.005) but remained unchanged in the CHF group. Dobutamine caused a significant decrease in LV end-diastolic pressure in the CHF group (14 ± 2 mm Hg to 11 ± 2 mm Hg, p = 0.02), an effect not observed in the normal LV group. In the normal LV function group, CANESP did not change in response to dobutamine (75 ± 22 pmol/min vs. 72 ± 22 pmol/min, p = NS). In contrast, dobutamine infusion was associated with a significant reduction in CANESP in patients with CHF (199 ± 43 pmol/min to 128 ± 30 pmol/min, p < 0.0009). ConclusionsDobutamine infusion caused a significant sympatholytic response in patients with CHF. This sympathetic withdrawal response is probably related to reduction of LV filling pressures and/or activation of ventricular mechanoreceptors with dobutamine infusion.

Effect of Hyperoxia on Left Ventricular Function and Filling Pressures in Patients With and Without Congestive Heart Failure

To determine the effects of hyperoxia on left ventricular (LV) function in humans with and without congestive heart failure (CHF). An acute physiologic study of the effect of hyperoxia on right-heart hemodynamics, LV contractility (peak positive rate of rise of LV pressure [+dP/dt]), time constant of isovolumic left ventricular relaxation (tau), and LV filling pressures. Bayer Cardiovascular Clinical Research Laboratory at the Mount Sinai Hospital, Toronto, Ontario. Sixteen patients with stable CHF and 12 subjects with normal LV function received the hyperoxia intervention. Patients received 21% O(2) by a nonrebreather mask, followed by 100% O(2) for 20 min, and 21% O(2) for a 10-min recovery period. In response to hyperoxia, there was a 22 +/- 6% increase in LV end-diastolic pressure (LVEDP) in the CHF group and a similar 29 +/- 14% increase in LVEDP in the normal LV function group (p < 0.05 for both; mean +/- SEM). Hyperoxia was also associated with a prolongation in tau of 10 +/- 2% in the CHF group (p < 0.05) and 8 +/- 2% in the normal LV function group (p < 0.05). No changes in +dP/dt were observed in either group. Hyperoxia was associated with impairment of cardiac relaxation and increased LV filling pressures in patients with and without CHF. These observations indicate that caution should be used in the administration of high inspired O(2) fractions to normoxic patients, especially in the setting of CHF.

Reducing Cardiac Filling Pressure Lowers Norepinephrine Spillover in Patients With Chronic Heart Failure

We studied the cardiac sympathetic response to selective unloading of cardiopulmonary baroreceptors in subjects with normal left ventricular (LV) function and congestive heart failure (CHF). Eight patients with normal LV function (age 57+/-5 years, ejection fraction 58+/-2%) and 8 patients with CHF (age 60+/-2 years; ejection fraction 19+/-2%) were studied. Instrumentation consisted of an arterial line, a pulmonary artery catheter, and a coronary sinus thermodilution catheter. The radiotracer technique was used for measurement of cardiac norepinephrine spillover (CANESP) and total-body norepinephrine spillover. Lower-body negative pressure (LBNP) was applied at 2 levels: nonhypotensive and hypotensive LBNP. Nonhypotensive LBNP reduced filling pressures significantly in both groups. Arterial pressure did not change. This reduction in filling pressures caused a significant reduction in CANESP in the CHF group (from 167+/-53 to 125+/-37 pmol/min, P<0.05) but no change in the normal LV function group. Hypotensive LBNP caused a significant increase in CANESP in the normal group (73+/-13 vs 122+/-27 pmol/min, P<0.05) but no significant change in those with CHF. We conclude that selective reduction in filling pressures lowers cardiac norepinephrine spillover in patients with CHF. These findings suggest that a goal of CHF management should be to reduce cardiac filling pressures while avoiding systemic hypotension.

Importance of left ventricular minimal pressure as a determinant of transmitral flow velocity pattern in the presence of left ventricular systolic dysfunction

Objectives. This study was designed to assess whether the transmitral flow velocity pattern provides an estimation of left atrial pressure irrespective of the presence of left ventricular systolic dysfunction and, if not, to clarify the mechanism.Background. The pulsed Doppler transmitral flow velocity pattern, particularly peak early diastolic filling velocity, has been shown to change in parallel with left atrial pressure. However, extremely elevated left atrial pressure in association with heart failure does not necessarily cause an increase in peak early diastolic filling velocity in patients.Methods. Left atrial pressure was elevated with intravenous saline infusion in 11 dogs (normal left ventricular function group) and hemodynamic, transesophageal Doppler echocardiographic and M-mode echocardiographic variables were recorded at three different loading levels. In another 12 dogs, left atrial pressure was elevated by production of left ventricular systolic dysfunction with the stepwise injection of microspheres into the left coronary artery (left ventricular dysfunction group) and the same set of recordings was obtained at three different levels of dysfunction.Results. Peak early diastolic filling velocity increased with left atrial pressure in the normal left ventricular function group and correlated with mean left atrial pressure (r = 0.61, p < 0.01) and early diastolic left atrial to left ventricular crossover pressure (r = 0.71, p < 0.01). In contrast, peak early diastolic filling velocity did not increase with left atrial pressure in the left ventricular dysfunction grtup and did not correlate with mean left atrial pressure (r = −0.05) or the crossover pressure (r = 0.06). Peak early diastolic filling velocity correlated well with the difference between the crossover pressure and left ventricular minimal pressure in the left ventricular dysfunction group (r = 0.64, p < 0.01). In contract to peak early diastolic filling velocity, deceleration time of the early diastolic filling wave correlated with mean left atrial pressure and the crossover pressure irrespective of the primary cause of preload alteration (r = −0.54, r = −0.59, p < 0.01 respectively, n = 69 for all data).Conclusions. Preload dependency of the Doppler transmitral flow velocity pattern is hampered if an increase in left atrial pressure is due to left ventricular systolic dysfunction. In this setting, the increase in left ventricular minimal pressure due to left ventricular systolic dysfunction cancels the effect of the increase in left atrial pressure on the flow velocity pattern.

Right ventricular function in an operating room model of mechanical left ventricular assistance and its effects in patients with depressed left ventricular function.

Approximately 20% of patients who receive left ventricular assist devices (LVADs) for refractory cardiac failure after open heart surgery have had complications of right ventricular failure. To evaluate this problem in the diseased heart we simulated an LVAD in the operating room by bypassing and unloading the left ventricle with the heart-lung machine before routine open heart surgery. Right ventricular function was assessed in 12 patients with preoperative left ventricular ejection fractions of less than 0.55 (poor left ventricular function) (mean +/- SEM 0.40 +/- 0.03) and 10 patients with ejection fractions greater than 0.55 (normal left ventricular function) (0.63 +/- 0.02). Measurements before and during left ventricular bypass in the normal left ventricular function group revealed no change in cardiac output (from 5.7 +/- 0.6 to 5.8 +/- 0.4 liters/min), with a decrease in right ventricular end-diastolic pressure (from 8 +/- 2 to 6 +/- 1 mm Hg). However, in the poor left ventricular function group, cardiac output was increased significantly during left ventricular bypass from 4.5 +/- 0.2 to 5.3 +/- 0.4 liters/min and right ventricular end-diastolic pressure was decreased significantly from 13 +/- 2 to 8 +/- 2 mm Hg. During bypass there were significant reductions in mean pulmonary arterial pressure from 17 +/- 3 to 10 +/- 2 mm Hg in the normal left ventricular function group and from 27 +/- 3 to 12 +/- 2 mm Hg in the poor left ventricular function group. These measurements reflect passive changes in pulmonary pressures due to reductions in left ventricular filling pressure during left ventricular bypass.(ABSTRACT TRUNCATED AT 250 WORDS)