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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↗

Left ventricular function and hemodynamic features of inappropriate left ventricular hypertrophy in patients with systemic hypertension: the LIFE study.

BACKGROUND: Predicted left ventricular (LV) mass for sex, height (2.7), and hemodynamic load can be used as an intrapatient reference for the observed LV mass. The ratio of observed/predicted LV mass may allow more physiologically correct comparisons of LV geometry, systolic and diastolic functions, and hemodynamics among hypertensive patients. METHODS: We studied 659 participants in the LIFE (Losartan Intervention for Endpoint Reduction in Hypertension) study with both electrocardiographic and echocardiographic LV hypertrophy (68% of the echocardiographic cohort) without previous myocardial infarction. LV mass was predicted by an equation including sex, stroke work, and height (2.7). Observed/predicted LV mass > 128% defined inappropriate LV hypertrophy (iLVH). Relative wall thickness > or = 0.43 defined concentric LV geometry. Systolic myocardial dysfunction was assessed by midwall mechanics and abnormal LV relaxation by isovolumic relaxation time (IVRT). RESULTS: Compared with patients with appropriate LV hypertrophy (aLVH), those with iLVH had higher body mass index, LV mass index, relative wall thickness, prevalences of systolic myocardial dysfunction and prolonged IVRT and lower end-systolic stress and cardiac index. Patients with eccentric iLVH had the highest wall stress and lowest ejection fraction; 43% had systolic myocardial dysfunction. Of patients with concentric iLVH, 79% had systolic myocardial dysfunction but normal ejection fraction and the lowest wall stress. Systolic myocardial dysfunction was present in 12% with concentric aLVH and none with eccentric aLVH. Prevalence of prolonged IVRT was high in all 4 groups (65% to 77%). Cardiac index was similarly lower with concentric or eccentric iLVH than with aLVH. CONCLUSIONS: Among hypertensives with LV hypertrophy, iLVH identified cardiac phenotypes with a high prevalence of myocardial systolic dysfunction.

Aged↗

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↗

Haemodynamic and catecholamine response to simulated ventricular tachycardia in man: effect of baseline left ventricular function.

OBJECTIVE: To examine the effects of baseline left ventricular function on the haemodynamic and catecholamine responses to ventricular tachycardia. DESIGN: Experimental cohort study. SETTING: Cardiac catheterisation laboratory in tertiary referral centre. SUBJECTS: 24 patients (19 male, 5 female; mean (SD) age, 59 (10) years) without coronary artery disease, divided into two groups with normal or impaired left ventricular function: group A, ejection fraction > 65% (n = 10); group B, ejection fraction < 45% (n = 14). Other medical and demographic factors were similar in the two groups. INTERVENTIONS: Ventricular tachycardia was simulated with rapid pacing at 150 beats/min for 10 minutes. MAIN OUTCOME MEASURES: Arterial blood pressure; venous plasma catecholamine concentrations. RESULTS: During rapid pacing, blood pressure was lower in group B (with impaired left ventricular function) than in group A: systolic blood pressure, 102 (11) v 115 (9) mm Hg (p = 0.005); mean blood pressure, 79 (6) v 85 (6) mm Hg (p = 0.02). The ejection fraction correlated with the lowest systolic blood pressure (r = 0.64, p = 0.0006). Although the rise in adrenaline was comparable between the two groups, the rise in noradrenaline was more pronounced (p < 0.05) in patients in group B. CONCLUSION: At low rates and in selected patients, the underlying state of left ventricular function affects haemodynamic tolerance of ventricular tachycardia. Patients with impaired left ventricular function have a lower blood pressure during ventricular tachycardia, despite an exaggerated noradrenaline release.

Blood Pressure↗

[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↗

Left ventricular outflow tract presystolic flow velocity--another marker of left ventricular diastolic function.

Left ventricular outflow tract (LVOT) presystolic flow velocities were studied using pulse doppler echocardiography in 30 normal persons. Thirty patients of mild hypertension with transmitral flow velocity pattern suggestive of impaired relaxation were also studied. Transmitral flow velocity pattern was correlated with LVOT presystolic flow velocities in the two groups. Hypertensive patients had significantly higher transmitral A wave velocity (p < 0.001) and significantly lower transmitral E wave/A wave velocity ratio (p < 0.001) as compared to normal group. LVOT presystolic flow velocities had significant direct correlation with transmitral A wave velocity (p < 0.01) and significant inverse relation with transmitral E wave/A wave velocity ratio (p < 0.05). Our observations suggest that increased LVOT presystolic flow peak velocity can also be used as another marker of impaired left ventriCular compliance during atrial contraction. More work is needed to establish exact status of this preliminary observation.

Blood Flow Velocity↗

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↗

The effect of vitamin E on endothelial function of micro- and macrocirculation and left ventricular function in type 1 and type 2 diabetic patients.

We examined the effects of high-dosage vitamin E treatment over a 12-month period on the vascular reactivity of micro- and macrocirculation and left ventricular function in diabetic patients. Subjects (n = 89) were randomized to vitamin E (1,800 IU daily) or placebo and were followed for 12 months. High-resolution ultrasound images were used to measure the flow-mediated dilation (FMD; endothelium dependent) and nitroglycerin-induced dilation (NID; endothelium independent) of the brachial artery. Laser Doppler perfusion imaging was used to measure vascular reactivity in the forearm skin. Left ventricular function was evaluated using transthoracic echocardiogram. At the end of the 6-month period, a worsening in endothelium-dependent skin vasodilation (P = 0.02) and rise in endothelin levels (P = 0.01) were found in the vitamin E compared with the placebo group. At the end of the 12-month period, a worsening was observed in NID (P = 0.02) and a marginal worsening was seen in systolic blood pressure (P = 0.04) and FMD (P = 0.04) in the vitamin E compared with the placebo group. In addition C-reactive protein levels decreased marginally in the vitamin E compared with the placebo group (P = 0.05). No changes were observed in left ventricular function. We concluded that long-term treatment with 1,800 IU of vitamin E has no beneficial effects on endothelial or left ventricular function in diabetic patients. Because vitamin E-treated patients had a worsening in some vascular reactivity measurements when compared with control subjects, the use of high dosages of vitamin E cannot be recommended.

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↗

Inhibition of collagen synthesis with prolyl 4-hydroxylase inhibitor improves left ventricular function and alters the pattern of left ventricular dilatation after myocardial infarction.

Background- Left ventricular (LV) remodeling after myocardial infarction (MI) is associated with fibrosis, dilatation, and dysfunction. We postulated that prevention of fibrosis after MI with a prolyl 4-hydroxylase inhibitor (P4HI) would preserve LV function and attenuate LV enlargement. Methods and Results- Adult female rats (200 to 250 g) had experimental MI and were then randomized to treatment with P4HI (MI-FG041, n=29) or vehicle (MI-control, n=29) 48 hours after MI for 4 weeks in 2 phases. Echocardiograms were performed weekly with a 15-MHz linear transducer, and at 4 weeks, collagen isoform determinations and in vivo hemodynamics were performed. At randomization, the infarct size and LV function and size were similar in MI-FG041 and MI-control but significantly different from shams (n=9). At week 4, the LV function in MI-FG041 was significantly better than in MI-controls (fractional shortening 21% versus 16%, P=0.01; fractional area change 30% versus 19%, P=0.002; ejection fraction 35% versus 23%, P=0.001). In the FG041 group, LV area in systole was less (P<0.05), the dP/dt(max) after isoproterenol was higher (P<0.05), and types I and III collagen in noninfarcted LV were less than in MI-control. The hydroxyproline/proline ratio was increased by 64% in MI-control and reduced to the sham value in MI-FG041 rats. In the scar tissue, it was reduced by 24% in MI-FG041. Conclusions- This study demonstrates that prevention of interstitial fibrosis with a P4H inhibitor alters the pattern of LV enlargement and produces partial recovery of LV function after MI.

Animals↗