Analysis of transthoracic echocardiographic data in major vascular surgery from a prospective randomised trial comparing sevoflurane and fentanyl with propofol and remifentanil anaesthesia.

The aim of this study was to define pre-operative echocardiographic data and explore if postoperative indices of cardiac function after open abdominal aortic surgery were affected by the anaesthetic regimen. We hypothesised that volatile anaesthesia would improve indices of cardiac function compared with total intravenous anaesthesia. Transthoracic echocardiography was performed pre-operatively in 78 patients randomly assigned to volatile anaesthesia and 76 to total intravenous anaesthesia, and compared with postoperative data. Pre-operatively, 16 patients (10%) had left ventricular ejection fraction < 46%. In 138 patients with normal left ventricular ejection fraction, 5/8 (62%) with left ventricular dilatation and 41/130 (33%) without left ventricular dilatation had evidence of left ventricular diastolic dysfunction (p < 0.001). Compared with pre-operative findings, significant increases in left ventricular end-diastolic volume, left atrial maximal volume, cardiac output, velocity of early mitral flow and early myocardial relaxation occurred postoperatively (all p < 0.001). The ratio of the velocity of early mitral flow to early myocardial relaxation remained unchanged. There were no significant differences in postoperative echocardiographic findings between patients anaesthetised with volatile anaesthesia or total intravenous anaesthesia. Patients had an iatrogenic surplus of approximately 4.1 l of fluid volume by the first postoperative day. N-terminal prohormone of brain natriuretic peptide increased on the first postoperative day (p < 0.001) and remained elevated after 30 days (p < 0.001) in both groups. Although postoperative echocardiographic alterations were most likely to be related to increased preload due to a substantial iatrogenic surplus of fluid, a component of peri-operative myocardial ischaemia cannot be excluded. Our hypothesis that volatile anaesthesia improved indices of cardiac function compared with total intravenous anaesthesia could not be verified.

Differences between echocardiographic measurements of left ventricular dimensions and function by local investigators and a core laboratory in a 2-year follow-up study of patients with an acute myocardial infarction.

AIMS: To examine differences in measurements of left ventricular dimensions and function, and prognostic value between local investigators and a core laboratory in a multicentre serial echocardiographic study. METHODS AND RESULTS: Seven hundred and fifty-six patients with acute myocardial infarction and preserved left ventricular function were examined at baseline and after 3 months with measurements by the biplane Simpson's method, and followed prospectively from 3 to 24 months. At baseline and 3 months local investigators relative to the core laboratory measured lesser end-diastolic volume by 8 and 6 ml (P<0.001), end-systolic volume by 3 and 2 ml (P<0.01), and ejection fraction by 0.0 and 0.6% (P<0.01), respectively. Local investigators and the core laboratory measured an increase in left ventricular end-diastolic volume of 8.6 and 6.9 ml, and in left ventricular end-systolic volume of 5.2 and 4.3 ml, and a decrease in left ventricular ejection fraction of 0.6 and 0.0%. Using the Cox proportionate hazards model, the prognostic value for subsequent clinical endpoints was significant both for the 3-month values (P<0.05) and changes (P<0.005) measured by the core laboratory, but not by local investigators. CONCLUSION: Only measurements in the core laboratory had significant prognostic value for subsequent clinical endpoints. These results strongly support the use of a core laboratory in studies employing echocardiographic measurements.

Are changes in left ventricular volume as measured with the biplane Simpson's method predominantly related to changes in its area or long axis in the prognostic evaluation of remodelling following a myocardial infarction?

AIMS: Two-dimensional (2D) echocardiography has been widely applied to measure left ventricular volumes with the biplane Simpson's method in the assessment of left ventricular remodelling following an acute myocardial infarction. This volume formula is based upon tracings of endocardium and measurement of long axis on left ventricular images. In the present follow-up study of post-myocardial infarction patients we evaluated the prognostic impact of changes in left ventricular areas and geometry versus long axis to determine if only long-axis measurements may be used for prognostic purposes. METHODS AND RESULTS: Two-dimensional echocardiographic video recordings of the apical four-chamber and long-axis views were obtained in 756 patients 2--7 days and 3 months following an acute myocardial infarction. All videotapes were sent to a core laboratory and left ventricular volumes were measured with the biplane Simpson's method in end-diastole and end-systole. During the first 3 months 44 patients had suffered one of the following end-points and were excluded: cardiac death, recurrent myocardial infarction, heart failure or chronic arrhythmia. Over a period of 3--24 months 58 such end-points occurred. With the Cox proportional hazards model the increase in left ventricular systolic volume was the strongest predictor for such events (Chi-square 18.5, P<0.0001), followed by an increase in end-systolic area (Chi-square 17.0, P<0.0001) and end-systolic spherity index (Chi-square 8.74,P =0.003). The increase in end-systolic long axis had only a borderline predictive value (Chi-square 4.3, P=0.04). The change in long-axis shortening from end-diastole to end-systole had no significant predictive value at all. CONCLUSION: In the studied population changes in left ventricular area and geometry, but not in the long axis, were mainly related to cardiac morbidity. The proper assessment of changes in left ventricular dimensions should therefore be based upon tracings of the area and not on long axis measurements only.

Outcome of congenital heart defects--a population-based study.

UNLABELLED: In a population-based study including 35,218 infants born alive during the 15-y period 1982-96, 360 (1%) were diagnosed as having a congenital heart defect (CHD). At a follow-up 3-18 y after birth (median 9.5 y) 154 patients (42.8%) were spontaneously cured; of these, 142 (92.2%) had ventricular septal defects (VSDs). Forty-two patients (11.7%) died, 22 of these (52.4%) during the neonatal period (0-28 d after birth). A total of 119 patients (33.1%) underwent therapeutic procedures (surgery, catheter interventions), 24 (20.2%) of whom died. Of the 95 children surviving therapeutic procedures, 54 (56.8%) had their defects completely repaired, while 41 (43.2%) had residual defects or cardiac sequelae, often of minor importance. In 69 children (19.2%) with persistent non-operated defects, 43 (62.3%) had VSDs. A chromosomal disorder, syndrome or associated extracardiac malformation occurred in 72 children (20%). CONCLUSIONS: The study underlines the broad variety in severity of CHDs, with a high neonatal mortality rate as well as a high rate of spontaneous cure. It is estimated that 25% of infants born with a CHD will grow into adult age with persistent non-operated defects, residual defects or cardiac sequelae after therapeutic procedures.

Early clinical screening of neonates for congenital heart defects: the cases we miss.

In a population-based study of 35,218 infants born alive during the 15 years from 1982 to 1996, 353 (1%) were diagnosed as having a congenital heart defect, of whom 84 (24%) were diagnosed subsequent to discharge from hospital after birth (2.4/1000). Of these, 40 (48%) had a ventricular septal defect, 14 (17%) an atrial septal defect, 9 (11%) a patent arterial duct, 8 (10%) an aortic stenosis and 13 (15%) other defects. Compared with those in whom diagnosis was made before discharge, the group of patients with defects detected late had an increased prevalence of atrial septal defects, patent arterial duct and aortic stenosis, but less decreased prevalence of ventricular septal defects (p < 0.05). Median age at detection of the defects subsequent to discharge was 6 months (range 2 weeks-11 years). Seven patients (8%) presented with clinical symptoms of cardiac decompensation. The mortality rate was significantly lower in those in whom defects were detected late (1/84; 1%) as compared with those detected immediately after birth (37/269; 14%) (p < 0.05). The total rate for early detection was the same after using one clinical examination (8.2/1000) of newborns as our basic routine instead of two (7.1/1000) (p > 0.05). A substantial proportion of congenital cardiac malformations are detected after discharge from hospital after birth. Some patients with these lesions present with cardiac decompensation and are in need of medication and surgery. One clinical examination of newborns detects congenital malformations of the heart as efficient as two.

Quality of life in children with congenital heart defects.

Quality of life was measured in children with congenital heart defects (CHDs) registered in a total population of infants born live in the period 1982-91 (n = 22,810), using essential life spheres: external living conditions, interpersonal and personal conditions. In 200 children with CHD alive at the time the investigation was performed, 164 (82%) of the families answered a questionnaire addressing different dimensions of these quality of life spheres. Three subgroups of CHDs were investigated: CHDs spontaneously cured (n = 80), CHDs treated by surgery (n = 56), and CHDs with associated syndromes/malformations (n = 29). 301 (75%) out of 400 controls, matched for age and habitat (county), answered the same questionnaire. The children's ages at investigation were 2 y 2 months-12 y 2 months (median 6 y 1 month). There were no statistically significant differences between the CHD groups and the controls for overall quality of life for any of the three life spheres (p > 0.05). In children with operated CHDs and CHDs associated with syndromes/malformations, quality of life was influenced at some aspects of the external as well as at the interpersonal and personal levels. A trend existed for a higher subjective experience of quality of life in the total CHD group as well as in all the subgroups. It is speculated that this may represent development of coping mechanisms and recalibration of values of life.

Does an early neonatal diagnosis of a later spontaneously closed ventricular septal defect impair quality of life?

The hypothesis that early diagnosis of a ventricular septal defect (VSD) with spontaneous closure later on may impair the parental-infant bonding process, with consequences for the child's quality of life in the longer term, was tested in 51 children born in 1986-1991 (gestational age > or = 37-42 weeks) with VSDs diagnosed in the early neonatal period and closing spontaneously during the first 24 months of life. The results were compared to 83 healthy controls matched for gestational age, time and place of birth. A method (questionnaire) taking into consideration the quality of life spheres of external living conditions and the interpersonal and personal conditions of the child was used. Except for a lower satisfaction with family network in the VSD group (p < 0.05), no differences were found between the VSD group and the controls for any of the parameters tested or for overall quality of life (p>0.05).

Increasing incidence of ventricular septal defects caused by improved detection rate.

In a population-based study in children born alive during the 10-year period from 1982 to 1991 (n = 22,810), ventricular septal defects (VSDs) were diagnosed in 127 cases, an incidence of 5.6 per 1000. The incidence was significantly higher in the cohort of children born during the 6-year period from 1986 to 1991 than among those born in the preceding 4-year period, 1982-1985 (6.5 and 4.0 per 1000 respectively; p < 0.05). The increase was caused entirely by an increased detection rate of small defects in the muscular part of the interventricular septum after introducing echocardiography as a standard method for investigating suspect congenital heart defects in the neonatal period. This also explained entirely an increase in the total incidence of congenital heart defects to 10.6 per 1000 in the last period from 8.4 per 1000 in the first, although this increase was not significant (p > 0.05). More children born in 1986-1991 had spontaneous closure of their VSDs (75.5%) than those born in 1982-1985 (51.5%) (p < 0.05). In 69.3% of patients the VSDs closed during the first year of life. For the cohort born in 1986-1991, 84.6% of the defects located in the muscular part of the septum closed spontaneously. Small defects in the muscular part of the interventricular septum with spontaneous closure in early life may represent the tail of a normal developmental process, and not defects in the sense of malformations.

Correlations between left ventricular mass and systolic blood pressure at rest and during maximal exercise in moderately hypertensive men.

We examined 87 men with moderate hypertension (diastolic blood pressure, DPB, greater than or equal to 95 and less than 110 mmHg) (mean age 45, range 22-64, years) with echocardiography and maximal ergometer bicycle test. Left ventricular mass index (LVMI) was calculated according to the Penn convention. Mean LVMI was 126 (60-210) g/m2. The maximal systolic blood pressure (SBP) during exercise was on average 217 (155-260) mmHg. Linear regression analysis revealed a significant correlation between LVMI and SBP at rest (r = 0.48, P less than 0.001) and during exercise (r = 0.39, P less than 0.001). Multiple regression analysis correcting for differences in age, cumulative work and cholesterol level revealed a significant correlation between LVMI and SBP at rest (t = 4.07, P less than 0.0001) and during exercise (t = 3.25, P = 0.002). Thus in patients with established, moderate hypertension exercise SBP is not more predictable for LVMI than is SBP at rest.

[Tricuspid valve endocarditis with pulmonary embolism]. / Trikuspidalendokarditt med lungeembolier.

We describe two patients suffering from bacterial endocarditis with tricuspid valve envolvement. Both had pulmonary embolism, revealed by scintigraphic lung perfusion examination. The diagnosis was made by transthoracic echocardiography in one patient and transoesophageal echocardiography in the other. Both received therapy with antibiotics and heparin given intravenously. In one patient the vegetation disappeared. We discuss the epidemiology, diagnosis and treatment of the condition, with special focus on the possible role of heparin.

[Children with congenital heart defects in Vestfold 1982-88. Increase in the incidence resulting from improved diagnostics methods]. / Barn med medfødt hjertefeil i Vestfold 1982-88. Insidensøkning som følge av bedret diagnostikk.

In the population of live born children in the County of Vestfold, Norway, during the seven-year period 1982-88 (N = 15,307), 138 cases of congenital heart defects were diagnosed (patent ductus arteriosus in preterm infants excluded), an incidence of 0.9%. In 114 infants (83%) the defect was diagnosed before discharge from hospital after birth (nursery, neonatal unit), in 20 infants (14%) it was diagnosed later during the first year of life, and in four (3%) during the second year of life. In 24 children (17%) congenital heart defect was associated with a syndrome (Down syndrome eight, Edwards syndrome three, other syndromes three), or other congenital malformations (single eight, multiple two). Diagnosis was made clinically only (including ECG, phonocardiography and X-ray pictures) in 15 patients (11%). 13 were classified as having ventricular septal defects, and two were unclassified. Echocardiography was performed in 120 children (87%), heart catheterization in 44 (32%), surgery in 47 (34%), and autopsy in 12 (9%). 15 children (11%) died, all during the first year after birth. 45 children (33%) are healthy after spontaneous closure of a ventricular (41 children) or atrial septal defect (four children), and 15 (11%) after surgical repair. 63 (46%) are alive with a defect. We found a tendency towards increasing incidence of congenital heart defects. This increase was explained by echocardiographic diagnosis of small muscular ventricular septal defects in the early neonatal period, with spontaneous closure of the defect during the first year of life.(ABSTRACT TRUNCATED AT 250 WORDS)

Evolution of infarct size during the early use of nifedipine in patients with acute myocardial infarction: the Norwegian Nifedipine Multicenter Trial.

In a multicenter double-blind study, 227 patients with suspected acute myocardial infarction (AMI) were randomized within 12 hr from onset of symptoms to treatment with nifedipine (112 patients) or placebo (115 patients). AMI was confirmed in 74 patients on nifedipine and in 83 on placebo. Patients with AMI received nifedipine 5.5 +/- 2.9 hr (mean +/- SD) after onset of symptoms. Infarct size was assessed by the release of creatine kinase isoenzyme MB (CK-MB). Infarct size index (CK-MB geq/m2) was 25 +/- 16 (n = 71) in the nifedipine group and 23 +/- 13 (n = 77) in the placebo group (NS). After the first 10 mg of nifedipine systolic blood pressure fell from 147 +/- 30 to 135 +/- 28 mm Hg (p less than .01) and heart rate rose from 75 +/- 18 to 79 +/- 19 beats/min (p less than .01). No change was observed after the first placebo dose. The treatment was continued for 6 weeks. Over this period there were 10 deaths in each group. Early treatment with nifedipine in patients with AMI does not seem to reduce infarct size as determined by enzyme level.