[Left ventricular function before and after the surgery of mitral regurgitation. Relation between regurgitant fraction and left ventricular function].
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Adult↗
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Mitral valve replacement in children. Comparative study of pre- and postoperative haemodynamics and left ventricular function.
Haemodynamic variables and left ventricular function were studied before and after mitral valve replacement in 44 children age 3 to 17 years (mean 11.9 years). Thirty-nine Starr-Edwards prostheses and five Hancock prostheses were used; postoperative study took place two to six months (mean 3.9 months) after operation. Pulmonary hypertension was present preoperatively in most patients, with mean pulmonary artery pressures of 18 to 75 (mean 46.5 mmHg). Postoperatively there was a pronounced drop in pressure to a mean value of 25.6 mmHg, partially explained by a decrease in pulmonary capillary wedge pressure. Pulmonary arteriolar resistance, however, also decreased conspicuously from an average of 590 dynes s cm-5 m-2 preoperatively to 282 dynes s cm-5 m-2 postoperatively. A return to normal resistance was seen in every case when preoperative resistance did not exceed 650 dynes s cm-5 m-2; above this threshold some degree of pulmonary hypertension often persisted. The residual gradient across the prosthetic valve was slightly higher for the Hancock than for the Starr-Edwards prosthesis (mean 8.7 mmHg, vs mean 6.9 mmHg). The left ventricular end-diastolic volume was much increased before surgery, with a mean value of 190 ml/m2; it decreased conspicuously after operation to 103 ml/m2. The left ventricular ejection fraction ranged from 40% to 76% (mean 57%) before operation; there was no significant change after operation, with values ranging from 40% to 73%. This left ventricular dysfunction is probably the result of myocardial injury caused by a chronic volume overload and the sequelae of rheumatic carditis.
Adolescent↗
Serial assessment of left ventricular function after myocardial infarction.
Left ventricular (LV) function is an important predictor of morbidity and mortality after myocardial infarction (MI). Changes in LV function have been examined during the early and late phases after MI, but serial measurements of LV function during the subacute period have not been performed. To assess sequential changes in LV function during the subacute period after MI, we used quantitative two-dimensional echocardiography to examine 22 patients over a 1-year period. Twenty-one of the 22 patients had a Q-wave MI. Eleven had an anterior MI and 10 had an inferior MI; their peak creatine phosphokinase (CPK) was 1213 mIU/ml +/- 14. Three weeks after acute MI, LV ejection fraction (LVEF) had increased from 45% to 52%. Seven of 19 patients showed an LVEF < 43% at baseline. In five of these patients, LVEF improved, but in two patients, LVEF was still < 43% in week 3. There was a significant enlargement of LV end-diastolic volume (LVEDV) (94 ml to 112 ml, p < 0.05) across the four observations but no change in LV end-systolic volume (LVESV; 54 ml to 56 ml, p = n.s.). When two groups (G1 [depressed], LVEF < or = 43%; G2 [preserved], LVEF > 43%) were compared, the group with depressed LVEF demonstrated a higher probability of improvement in LVEF (34% to 47%, p < 0.001) and stroke volume (38 ml to 65 ml, p < 0.01).
Adult↗
Angiotensin converting enzyme inhibitors in bone marrow transplant recipients with depressed left ventricular function.
Pre-existing left ventricular dysfunction in patients undergoing induction therapy with cyclophosphamide prior to bone marrow transplantation (BMT) has resulted in overt heart failure in a large number of patients. This fact excludes the majority of such patients from consideration for BMT at many centers. We sought to determine if prophylactic treatment with the angiotensin converting enzyme inhibitor enalapril prevents this deterioration in pre-existing left ventricular dysfunction. We treated six consecutive patients with initial left ventricular ejection fractions (LVEF) by radionuclide gated blood pool imaging (RGBP) of < 50% (42 +/- 7%) with enalapril 5 mg orally twice per day started 48 h prior to induction therapy and continued throughout the follow-up period. Serial RGBP imaging demonstrated an increase in LVEF in all patients to 54 +/- 6% (P < 0.005). No patient experienced clinical deterioration during a follow-up period of 18 +/- 11 months. We conclude that prophylactic treatment with enalapril may prevent deterioration in pre-existing mild left ventricular dysfunction during BMT.
Adolescent↗
[Coronary artery bypass grafting in patients with poor left ventricular function using retrograde continuous cold blood cardioplegia].
Patients with poor left ventricular function or those requiring urgent surgery may have more extensive ischemic myocardial injury if myocardial preservation is incomplete. We have performed coronary artery bypass grafting (CABG) aimed at complete revascularization in such cases using RC-CBCP, which is considered more effective on myocardial preservation during aortic cross-clamping in particular to protect ischemic area distal to severe coronary artery stenosis or obstruction. In the present study, in 25 patients with poor left ventricular function (left ventricular ejection fraction; LVEF less than or equal to 0.3) including 10 patients who required urgent surgery, the operative results were evaluated. All the distal and proximal anastomoses of grafts (average 2.5 grafts) were completed during one aortic cross-clamping using RC-CBCP, therefore graft flow was obtained immediately after release of the aortic clamping. Though this method required 142 minutes of a mean aortic cross-clamping time, myocardial protection was considered to be preferable judging from postoperative isoenzymatic evaluation and improved ventricular function. Fifteen patients with elective CABG were all alive and restored to NYHA class I to II. Among 10 patients requiring urgent CABG, 4 patients with acute myocardial infarction died but others were restored to NYHA class I to II. We conclude that it is important to aim at complete coronary revascularization in patients with poor left ventricular function and RC-CBCP achieves more effective myocardial protection during CABG in the patients.
Adult↗
[Effect of infusion of hyperosmolar mannitol on left ventricular function in essential hypertension].
The left ventricular function of the heart was examined by means of the method of equilibrium-radionuclide ventriculography in 40 patients with essential hypertension (EH)--20 patients in stage I (H1), 20 patients in stage II (H2) according to WHO criteria--and in 18 normotensives (N). The examination was performed at rest and immediately after stress by intravenous infusion of hyperosmolar mannitol. At rest, the parameters of global systolic and diastolic functions of the left ventricle in normotensives do not differ significantly from the values in both groups of hypertensives. The global ejection fraction (GEF), peak ejection rate (PER) and peak filling rate (PFR) were in H2 significantly lower than in H1. Sectorial ejection fraction (SEF) in the apicoseptal area is in H2 significantly lower than H1 and N. After infusion of hyperosmolar mannitol the GEF and PFR increased in N and H1 only. When comparing all groups after infusion of mannitol the PFR in H2 is significantly lower also in comparison with N with the tendency (significant limit) to lower values of GEF and PER. PER and PFR were significantly lower and the end-diastolic volume (EDV) was significantly higher in H2 in comparison with H1. SEF was significantly lower in H2 in comparison with N in 3 out ot 9 sectors and in comparison with H1 in 8 out of 9 sectors. The infusion of hyperosmolar mannitol reveals subclinical disturbances of the diastolic and partially also of the systolic function of the left ventricle in stage II of EH which is very useful for diagnosis and treatment. (Tab. 4, Fig. 3, Ref. 22.).
Adult↗
Effect of early treatment with propranolol on left ventricular function four weeks after myocardial infarction.
Left ventricular function and exercise capacity were assessed in 79 patients randomised to receive intravenous and oral propranolol (n = 44) or conventional therapy (n = 35) within four hours of onset of their first myocardial infarction. Cineangiocardiography and exercise testing were performed four weeks after infarction to allow for maximum recovery of myocardial function. Left ventriculography showed no improvement in ejection fraction or preservation of regional contractile function in patients treated with propranolol compared with controls. A trend towards smaller end diastolic volumes was seen in the propranolol group (mean (SD) 151(42) ml) compared with controls (167(42) ml). Exercise duration and frequency of angina were not significantly different in the two groups. It is concluded that limitation of infarct size by propranolol does not lead to a significant improvement in ventricular systolic function, although left ventricular dilatation may be reduced. These findings are consistent with the known effect of early intravenous beta blockade which limits infarct size by preservation of subepicardial myocardium.
Adult↗
Sequence of mechanical and electrical changes during myocardial ischemia: assessment by an ambulatory left ventricular function monitor.
To investigate the relationship between left ventricular function and electrical changes during myocardial ischemia, ambulatory left ventricular function monitoring and ECG recording were made during the ergometer exercise test in 14 patients with coronary artery disease. An ambulatory ventricular function monitor consists of a small cadmium telluride (CdTe) radionuclide probe (250 g) affixed to the patient's chest wall, a preamplifer (10 g), and a portable data acquisition unit (600 g). Left ventricular time-activity curves were recorded continuously using this monitor, and the end-systolic count (volume), end-diastolic count (volume) and ejection fraction were calculated after background subtraction. Twenty-eight exercise tests were performed in the supine and upright positions. In 15 tests, left ventricular dysfunction, i.e., an increase in the end-systolic count (greater than or equal to 10%) and a decrease in ejection fraction (greater than or equal to 5%), and ST depression (greater than or equal to 0.1 mV) were observed. In these 15 tests, exercise duration was 362 +/- 27 sec. Left ventricular dysfunction occurred earlier than ST depression and the time difference was 97 +/- 19 sec. Left ventricular function recovered 33 +/- 8.5 sec after discontinuation of exercise, while ST depression continued for the additional 85 +/- 18.5 sec after recovery of left ventricular function. In conclusion, 1) left ventricular dysfunction occurs earlier than electrical changes during exercise-induced ischemia; 2) left ventricular dysfunction improves earlier than electrical changes after exercise; and 3) the same temporal sequence exists in the restoration from myocardial ischemia.
Coronary Disease↗
Effects of altered PaO2 and PaCO2 on left ventricular function and coronary hemodynamics in sheep.
The effects of acute changes in arterial carbon dioxide and oxygen tension, produced by altering the inspired gas mixtures while maintaining constant-volume intermittent positive pressure ventilation, on global function, regional left ventricular function, and coronary hemodynamics were studied in eight sheep during halothane anesthesia. Hypercapnia (Paco2, 73.5 +/- 2.3 mm Hg, mean +/- SD) increased heart rate, stroke volume, and cardiac output but decreased systolic shortening in the base of the left ventricle. Hypocapnia (PaO2, 24 +/- 1.5 mm Hg) decreased cardiac output and coronary flow below levels seen with hypercapnia but not below levels seen with normocapnia. Systolic shortening decreased in both apical and basal regions, and left ventricular relaxation was impaired as evidenced by a reduction of the nadir of LV dP/dt. Hypoxemia (PaO2, 39 +/- 1.5 mm Hg) elicited a hyperdynamic response of the circulation, increased coronary blood flow, and exhausted the coronary flow reserve. Neither changes in PaCO2 nor changes in PaO2 caused postsystolic shortening, although hypercapnia caused nonuniformity of contraction in the left ventricle. Thus, marked alterations in oxygen and carbon dioxide tensions do not cause left ventricular dysfunction, even though moderate hypoxia reduces the coronary flow reserve.
Anesthesia, Inhalation↗
Relationship between maximal oxygen uptake and left ventricular function in exercise.
Left ventricular systolic time intervals (STI's), cardiac output, and arterial blood pressures were measured during bicycle ergometer work in three groups of 10 young men (aged 20-33 yr) who represented average (VO2max = 42-45 ml.kg-1.min-1), moderate (VO2max = 50-56 ml.kg-1.min-1), and high (VO2max = 59-72 ml.kg-1.min-1) levels of cardiovascular fitness. The subjects were studied using noninvasive procedures at steady-state heart rate of approximately 110, 130, and 150 beats.min-1. At all exercise levels, the fitter subjects displayed slightly shorter values for the preejection period (PEP) compared with less fit groups. Significantly (P less than 0.05) larger stroke volumes, longer left ventricular ejection times (LVET), faster mean systolic ejection rates and lower PEP/LVET ratios were found in the group with the highest aerobic capacity. Although these observations appear to indicate a superior mean level of left ventricular performance in groups who represent high levels of cardiovascular fitness, it was concluded that the use of STI values by themselves to describe the cardiovascular fitness of an individual would not be warranted.
Adult↗
Left ventricular function in chronic renal failure.
Left ventricular function was studied in 14 patients with end-stage chronic renal failure using non-invasive methods (echocardiography and systolic time intervals). Patients were divided into 3 groups. Group 1 consisted of 5 patients who were normotensive at the time of study and group 2 of 7 patients who were hypertensive when studied. Group 3 consisted of 2 patients: one was receiving propranolol and the other, studied 302 days after renal transplantation, was receiving digitalis for recurrent episodes of cardiac failure. All except the patient receiving propranolol had normal left ventricular function in systole with normal measurements of fractional fibre shortening (% delta S, EF) and normal measurements relating to the velocity of ventricular contraction (mean Vcf, mean velocity of posterior wall motion). Stroke volume and cardiac output were normal in some patients but were increased in patients with fluid overload. Early diastolic compliance of the left ventricle seemed to be normal except in the patient with recurrent cardiac failure. The study provided no evidence for the existence of a specific uraemic cardiomyopathy.
Adult↗
Effects of left ventricular systolic function on left ventricular diastolic filling patterns in severe mitral regurgitation.
Significant mitral regurgitation (MR) may alter the normal pattern of Doppler detected left ventricular (LV) filling by causing a prominent early filling (E) wave velocity. The manner and extent to which the typical filling pattern of uncomplicated MR is affected by concomitant impaired LV systolic function has not been characterized. Twenty patients with severe LV systolic dysfunction (2-dimensional echocardiographic estimation of ejection fraction < or = 30%) and 21 age- and sex-matched case controls with normal systolic function (ejection fraction > or = 55%) were selected. In addition, 20 subjects with normal LV systolic function and no MR were analyzed as a reference group. Maximal E-wave velocity was increased and highest among MR patients with preserved LV systolic function (124 +/- 37 cm/s) than among those with LV systolic dysfunction (101 +/- 25 cm/s; p <0.05) and normal controls (74 +/- 18 cm/s; p <0.001). Concurrently, A-wave velocity was lowest in patients with systolic dysfunction and MR (47 +/- 23 cm/s; p <0.001) than in patients with normal systolic function and MR (79 +/- 33 cm/s) and normal controls (74 +/- 20 cm/s). Deceleration time of the E wave was longest among those with normal systolic function and MR (203 +/- 41 ms) than among those with systolic dysfunction and MR (152 +/- 35 ms; p <0.001) and normal controls (167 +/- 53 ms; p <0.05). Thus, systolic LV dysfunction in patients with severe MR, compared to patients with MR and normal LV systolic function, is associated with important changes in diastolic inflow velocities, including reduction of the maximal A-wave velocity to a greater extent than the E wave, resulting in an increased E/A ratio and shortening of deceleration time of the E wave.
Aged↗
Recovery of systolic and diastolic left ventricular function early after cardiopulmonary bypass.
BACKGROUND: Impairment of left ventricular function after cardiopulmonary bypass (CPB) is well recognized, but little is known about the time course of recovery of cardiac function early after separation from CPB. Therefore, recovery of left ventricular function was evaluated early after separation from CPB in patients undergoing coronary artery surgery. The authors tried to determine whether this recovery might be attributed to autoregulation of function by preload. METHODS: Left ventricular pressure was measured with fluid-filled catheters. Data were digitally recorded during increased pressure induced by elevating the legs. Transgastric short-axis echocardiographic views of the left ventricle were simultaneously recorded on videotape. Systolic function was evaluated with the slope (Ees, mmHg/ml) of the systolic pressure-volume relation. Diastolic function was evaluated with the chamber stiffness constant (Kc, ml-1) of the diastolic pressure-volume relation. Cardiac function was assessed before CPB, after termination of CPB, and 5, 10, and 15 min later. Two different separation procedures from CPB were compared: in protocol 1, left ventricular function was documented during the standard procedure (n = 24); in protocol 2, the heart was optimally filled 10 min before separation from CPB (n = 12). RESULTS: In protocol 1, Ees was 2.88 +/- 0.21 mmHg/ml (mean +/- SEM) and Kc was 0.012 +/- 0.001 ml-1 before CPB. Within 10 min after separation from CPB, Ees increased from 1.10 +/- 0.32 to 2.92 +/- 0.34 (P = 0.001) and Kc decreased from 0.022 +/- 0.002 to 0.011 +/- 0.001 (P = 0.001). The parameters remained stable thereafter. In protocol 2, Ees was 2.92 +/- 0.51 mmHg/ ml and Kc was 0.011 +/- 0.002 ml-1 before CPB. Depression of systolic and diastolic function was not observed in these patients. At time 0, Ees was 2.46 +/- 0.16 and Kc was 0.012 +/- 0.002. These values remained stable throughout the entire observation period. CONCLUSIONS: Significant functional recovery was observed early after separation from CPB, which was suggestive of time-dependent changes in both systolic and diastolic left ventricular function induced by preload restoration.
Anesthesia↗
Influence of right ventricular stimulation site on left ventricular function in atrial synchronous ventricular pacing.
OBJECTIVES: The study investigates the correlation between left ventricular function and QRS duration obtained by alternate right ventricular pacing sites. BACKGROUND: 1. Right ventricular apical pacing is associated with alterations of left ventricular contraction sequence. 2. A stimulation producing narrow QRS complexes is supposed to provide for better left ventricular contraction patterns. METHODS: Fourteen patients with third degree AV block received one ventricular pacing lead in apical position. The alternate lead was attached to that site on the septum that produced the smallest QRS complex as measured from the earliest to the last deflection in any of the orthogonal Frank leads (xyz). During atrial synchronous ventricular pacing, the AV delay was optimized individually and for each stimulation site using mitral valve doppler or impedance cardiography. By radionuclide ventriculography, the phase distribution histogram of left ventricular contraction was evaluated as area under the curve (AuC); systolic function was determined as ejection fraction (EF) and as absolute ejected counts (EC) in random order. The difference (delta) in QRS duration between apical and septal stimulation (deltaxyz) was correlated with the difference in phase distribution (deltaAuC) and ejection parameters (deltaEF, deltaEC). RESULTS: QRS duration was shorter with septal than with apical pacing in 9 out of 14 patients (64%); it was longer in 4 (29%), and no difference was seen in 1 patient. There was a significant positive correlation between the change in QRS duration (deltaxvz) and phase distribution (deltaAuC: r = 0.66393, p = 0.010) and a significant negative correlation to systolic function (deltaEF: r = 0.70931, p = 0.004; deltaEC: r = 0.74368, p = 0.002). CONCLUSIONS: In atrial synchronous right ventricular pacing, if the AV delay is adapted individually, decreased QRS duration obtained by alternate pacing sites is significantly correlated with homogenization of left ventricular contraction and with increased systolic function in acute tests.
Aged↗
[Left ventricular function in chronic obstructive lung disease (author's transl)].
Left ventricular function was studied at rest and during post-extrasystolic potentiation in 18 patients with chronic obstructive lung disease. The contractility indices used were obtained from pressures recorded in the isovolumetric period (left ventricular end-diastolic pressure, Vmax., VECmax., dP/dtmax.) and from volume variations during ejection (end-diastolic volume, ejection fraction, VCF). Left ventricular diastolic compliance was also evaluated. All patients were hypoxic (PaO2 = 58 +/- 7 torr); six of them had cor pulmonale (group B); the remaining 12 patients constituted group A. Left ventricular function of groups A and B was similar; we conclude that right cardiac failure, in cor pulmonale, is not secondary to left ventricular failure. However, left ventricular dysfunction exists; the left ventricle is hypertrophied (probably resulting from chronic hypoxia). Pump function is altered (abnormal ventricular function points are found), but left ventricular kinetics is normal or exaggerated (ejection fraction and VCF are increased). Isovolumetric phase contractility indices are diminished; however, they may increase normally during post-extrasystolic potentiation. Left ventricular compliance is abnormal due to left and right ventricular hypertrophy and to paradoxical movement of the interventricular septum which impedes diastolic expansion of the left ventricle. These changes are responsible for decreased left ventricular output. There seems to exist an impairment of left ventricular function related to both intrinsic (secondary to hypoxia, hypercapnia, left ventricular hypertrophy) and extrinsic factors (right ventricula hypertrophy deviating interventricular septum, lowering of left ventricular preload).
Adult↗
Ultrastructural pathological study of left ventricular myocardium in patients with isolated rheumatic mitral stenosis with normal or abnormal left ventricular function.
An electron microscopic study of left ventricular myocardium was carried out in 15 patients who had isolated rheumatic mitral stenosis, with particular reference to the relation among ultrastructural pathological findings, the severity of mitral stenosis and left ventricular function. They were divided into 2 groups based on left ventricular performance evaluated by 2-dimensional echocardiography and angiocardiography. The severity of mitral stenosis was determined by hemodynamic data and mitral valve areas measured by 2-dimensional echocardiography. Regardless of the level of left ventricular contractile function we consistently demonstrated varying degrees of ultrastructural pathological alterations of left ventricular muscle cells, involving the myofibrils, mitochondria, nuclei and other elements of the sarcoplasm and membranes surrounding the myocardial cells in all specimens examined. The ultrastructural pathological findings did not correlate with the severity of mitral stenosis reflected in the echocardiographic and hemodynamic data. However, those patients with abnormal left ventricular function always exhibited more extensive loss of myofibrils resulting from either disproportion of the mitochondria-to-myofibril ratio or myofibrillar degeneration. The present investigation provides the morphological data at the ultrastructural level to support the widely held concept of a myocardial factor i.e., the extent of myocardial involvement by the rheumatic process as the basic pathogenetic mechanism responsible for left ventricular dysfunction in patients with isolated rheumatic mitral stenosis. Furthermore, it is suggested that pathological alterations of myocardial ultrastructure were related to the extent of myocardial involvement by the rheumatic process rather than being structural adaptations in response to the hemodynamic derangement.
Adult↗
Effects of nisoldipine on systolic and diastolic function in postinfarction patients with reduced left ventricular function: a randomized, double-blind, placebo controlled study.
The long-term effects of oral nisoldipine or placebo on clinical variables, exercise test results and echo Doppler-determined systolic and diastolic functions were studied in 30 consecutive patients with reduced left ventricular function (predischarge echocardiographic wall motion score greater than or equal to 8) following myocardial infarction. Groups were comparable in clinical variables, exercise results, echo Doppler measurements and coronary anatomy. During 6 months follow-up, death, reinfarction and bypass surgery or balloon angioplasty were equally distributed. A significant increase in exercise duration and time to onset of ST-depression was found in the nisoldipine treatment group, compared to the placebo group after 3 and 6 months. Time to onset of angina was not significantly different. Echocardiographic indices of left ventricular systolic function (ejection fraction and wall motion score) were unaltered; however, the time-velocity integral of the early diastolic filling phase and the early vs late diastolic flow velocity ratio were significantly increased while the atrial time-velocity integral vs total time-velocity integral was significantly decreased in the nisoldipine treatment group after 3 and 6 months of follow-up. In conclusion, nisoldipine reduced exercise-induced ischaemia, improved exercise capacity and diastolic left ventricular function in postinfarction patients with reduced left ventricular function.
Cardiac Catheterization↗
[The induction of ventricular fibrillation by transesophageal pacing in subjects with atrial flutter and compromised left ventricular functioning].
In patients with depressed left ventricular function, the normal precautions during transesophageal atrial pacing may not be sufficient to prevent life threatening arrhythmias. In this article two cases of ventricular fibrillation induced during this technique, aimed at treating atrial flutter, are described.
Atrial Flutter↗