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Biomedical subjects

M St John Sutton

Publications and source records attributed to M St John Sutton.

At least 37 records · Page 2Linked to original sources
PubMed1997

Cardiovascular death and left ventricular remodeling two years after myocardial infarction: baseline predictors and impact of long-term use of captopril: information from the Survival and Ventricular Enlargement (SAVE) trial.

BACKGROUND: We quantified cardiovascular death and/or left ventricular (LV) dilatation in patients from the SAVE trial to determine whether dilatation continued beyond 1 year, whether ACE inhibitor therapy attenuated late LV dilatation, and whether any baseline descriptors predicted late dilatation. METHODS AND RESULTS: Two-dimensional echocardiograms were obtained in 512 patients at 11+/-3 days and 1 and 2 years postinfarction to assess LV size, percentage of the LV that was akinetic/dyskinetic (%AD), and LV shape index. LV function was assessed by radionuclide ejection fraction. Two hundred sixty-three patients (51.4%) sustained cardiovascular death and/or LV diastolic dilatation; 279 (54.5%) had cardiovascular death and/or systolic dilatation. In 373 patients with serial echocardiograms, LV end-diastolic and end-systolic sizes increased progressively from baseline to 2 years (both P<.01). More patients with LV dilatation had a decrease in ejection fraction: 24.8% versus 6.8% (P<.001) (diastole) and 25.7% versus 5.3% (P<.001) (systole). Captopril attenuated diastolic LV dilatation at 2 years (P=.048), but this effect was carried over from the first year of therapy because changes in LV size with captopril beyond 1 year were similar to those with placebo. Predictors of cardiovascular death and/or dilatation were age (P=.023), prior infarction (P<.001), lower ejection fraction (P<.001), angina (P=.007), heart failure (P=.002), LV size (P<.001), and infarct size (%AD) (P<.001). CONCLUSIONS: Cardiovascular death and/or LV dilatation occurred in >50% of patients by 2 years. LV dilatation is progressive, associated with chamber distortion and deteriorating function that is unaffected by captopril beyond 1 year.

Captopril↗
PubMed1997

Stabilization of chronic remodeling by asynchronous cardiomyoplasty in dilated cardiomyopathy: effects of a conditioned muscle wrap.

BACKGROUND: Dynamic cardiomyoplasty is a promising new therapy for dilated cardiomyopathy. The girdling effects of a conditioned muscle wrap alone have recently been postulated to partly explain its mechanism. We investigated this effect in a canine model of chronic dilated cardiomyopathy. METHODS AND RESULTS: Twenty dogs underwent rapid ventricular pacing (RVP) for 4 weeks to create a model of dilated cardiomyopathy. Seven dogs were then randomly selected to undergo subsequent cardiomyoplasty, and all dogs had 6 weeks of additional RVP. The cardiomyoplasty group also received 6 weeks of concurrent skeletal muscle stimulation consisting of single twitches delivered asynchronously at 2 Hz to transform the wrap without active assistance. All dogs were studied by pressure-volume analysis and echocardiography at baseline and after 4 and 10 weeks of pacing. Systolic indices, including ejection fraction (EF), end-systolic elastance (Ees), and preload-recruitable stroke work (PRSW) were all increased at 10 weeks in the wrap versus controls (EF, 34.0 versus 27.1, P=.008; Ees, 1.65 versus 1.26, P=.09; PRSW, 35.9 versus 25.5, P=.001). Ventricular volumes, diastolic relaxation, and left ventricular end-diastolic pressures stabilized in the cardiomyoplasty group but continued to deteriorate in controls. Both the end-systolic and end-diastolic pressure-volume relationships shifted farther rightward in controls but remained stable in the cardiomyoplasty group. CONCLUSIONS: In addition to potential benefits from active systolic assistance, benefits from dynamic cardiomyoplasty appear to be partially accounted for by the presence of a conditioned muscle wrap alone. This conditioned wrap stabilizes the remodeling process of heart failure, arresting progressive deterioration of systolic and diastolic function.

Animals↗
PubMed1997

Accuracy and reproducibility of biplane two-dimensional echocardiographic measurements of left ventricular dimensions and function.

OBJECTIVE: To investigate sources of variability in serial echocardiographic recordings in a core laboratory we assessed the impact of repeated echo recordings, repeated video measurements and measurements made by different investigators. PATIENTS, METHODS: Two investigators each recorded and analysed two-dimensional echos in 12 individuals (n = 24 in total) three times at one week intervals. Left ventricular end-diastolic and end-systolic volumes were measured using the biplane modified Simpson's rule. Ejection fraction was derived from these volumes and left ventricular mass estimated using the area-length method. The left ventricular spherity index was expressed as the ratio of the short axis area and the long axis area at end-diastole. A video recording from each examination was reexamined twice by both investigators. RESULTS: Deviations between repeated echo recordings and repeated video measurements ranged from -5 to +5% between investigators. A three-way repeated analysis of variance indicated a small, but systematic difference between investigators. Reproducibility, measured by coefficients of variation, ranged from 3-9% for different investigators, 3-6% for repeated video measurements and 7-19% for repeated echo recordings across the different variables. The total variability of all three factors should be considered when the smallest detectable significant change in a variable is assessed. These ranged from 16-28% across the five variables studied, when a 10% error of classification was accepted for a one-sided change in a variable. CONCLUSION: Repeated echo recordings were the dominant component of variation. Two-dimensional echo measurements are reproducible and accurate, but the same investigator should follow the same patients.

Adult↗
PubMed1996

Which patient benefits from early angiotensin-converting enzyme inhibition after myocardial infarction? Results of one-year serial echocardiographic follow-up from the Captopril and Thrombolysis Study (CATS).

OBJECTIVES: In this study we sought to investigate the effect of intervention with captopril within 6 h of the onset of myocardial infarction on left ventricular volume and clinical symptoms of heart failure in relation to infarct size during a 1-year follow-up period. BACKGROUND: Remodeling of the heart starts in the early phase of myocardial infarction and is associated with an adverse prognosis. Angiotensin-converting enzyme inhibition started in the subacute or late phase after myocardial infarction has been shown to improve prognosis. METHODS: In the Captopril and Thrombolysis Study, 298 patients with a first anterior myocardial infarction treated with intravenous streptokinase were randomized to receive either oral captopril (25 mg three times a day) or placebo. The left ventricular volume index was assessed by two-dimensional echocardiography within 24 h, on days 3, 10 and 90 and after 1 year. RESULTS: A small but significant increase in left ventricular volume indexes was observed after 12 months. Using a random coefficient model, no significant treatment effect on left ventricular volumes could be detected. In contrast, when survival models were used, the occurrence of left ventricular dilation was significatnly lower in captopril-treated patients (p = 0.018). In addition, the incidence of heart failure was lower in the captopril group (p < 0.03). This effect appeared early and was most obvious in patients with a medium-sized infarct (p = 0.04) and was not present in large infarcts. CONCLUSIONS: Very early treatment with captopril after myocardial infarction significantly reduces the occurrence of early dilation and the progression to heart failure. These data underscore the importance of early treatment. Furthermore, patients with intermediate infarct size benefit the most from this treatment strategy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

A comparison of left ventricular myocardial velocity in diastole measured by magnetic resonance and left ventricular filling measured by Doppler echocardiography.

Abnormal diastolic left ventricular function is an early marker for myocardial disease and may be impaired even when global systolic function is normal. Subendocardial function is affected early in ischaemic heart disease and by altering left ventricular long axis motion, may contribute to abnormal transmitral pressure gradients. Regional myocardial long axis velocity in diastole measured by magnetic resonance was compared with left ventricular filling measured by Doppler echocardiography in 25 patients with coronary artery disease. Fifteen patients also underwent magnetic resonance assessment at the time of onset of early diastolic blood flow. The onset of diastolic long axis velocity preceded flow across the mitral valve by a mean of 46 ms. Mean long axis myocardial velocity correlated with peak early filling velocity (E) (r = 0.73, P < 0.001), early deceleration (r = -0.73, P < 0.001), and the early to late filling ratio (E/A) ratio (r = 0.6, P < 0.01). Maximum myocardial long axis velocity also correlated with peak early filling velocity (r = 0.56, P < 0.01), early deceleration rate (r = 0.63, P < 0.001), and the E/A ratio (r = 0.53, P < 0.01). The variability of long axis velocity around the ventricle correlated inversely with peak early filling, (r = -0.7, P < 0.001), early deceleration (r = -0.56, P < 0.01), and the E/A ratio (r = -0.48, P < 0.02). Peak atrial filling velocity did not correlate with any measure of long axis myocardial velocity. We conclude that early diastolic long axis myocardial velocity has a significant effect on left ventricular filling.

Adult↗
PubMed1994

Regional myocardial velocity imaged by magnetic resonance in patients with ischaemic heart disease.

OBJECTIVE: To assess the pattern of global and regional left ventricular long axis motion during early diastole in patients with ischaemic heart disease with and without myocardial infarction using magnetic resonance velocity mapping. DESIGN: Prospective study of 26 patients with a history of myocardial infarction (age 29-78, mean 55 years) and 21 patients with coronary artery disease without infarction (age range 39-71, mean 58 years). Values were compared with a control group (19 controls, age 35-76, mean 52 years) with a low likelihood of cardiovascular disease. RESULTS: Regional long axis velocity varied with time and position around the ventricle. All measurements were taken at the time of maximum early diastolic long axis velocity. Patients with coronary artery disease without infarction had lower values for maximum (mean (SD)) (99 (30) v 125 (33) mm/s, P < 0.05) and mean peak early diastolic wall motion (63 (13) v 82 (22) mm/s, P < 0.05) than controls. The coefficient of variation showed greater inhomogeneity of relaxation in patients than in controls (38 (18)% v 27 (10)%). All values were lower in patients with previous infarction than in patients with coronary artery disease without infarction and normal subjects. In patients with previous myocardial infarction the maximum (mean (SD)) early diastolic velocity was 80 (22) mm/s (P < 0.01 compared with controls and P < 0.05 compared with patients without infarction) and the mean (SD) velocity was 47 (18) mm/s (P < 0.01 compared with controls). The coefficient of variation was greater (52 (33)%) than for controls (P < 0.05) and patients with coronary artery disease without infarction. 18 of 26 patients with previous myocardial infarction and 13 of 21 patients with coronary artery disease without infarction had regional abnormalities corresponding to areas of fixed or reversible ischaemia on exercise electrocardiography or thallium myocardial perfusion tomography. CONCLUSIONS: Magnetic resonance velocity mapping can be used to assess regional long axis myocardial velocity. Ischaemic heart disease causes alterations in the patterns of left ventricular long axis velocity during early diastole.

Adult↗
PubMed1994

Quantitative two-dimensional echocardiographic measurements are major predictors of adverse cardiovascular events after acute myocardial infarction. The protective effects of captopril.

BACKGROUND: Left ventricular enlargement after myocardial infarction increases the likelihood of an adverse outcome. In an echocardiographic substudy of the Survival and Ventricular Enlargement (SAVE) Trial, we assessed whether captopril would attenuate progressive left ventricular enlargement in patients with left ventricular dysfunction after acute myocardial infarction and, if so, whether this would be associated with improved clinical outcome. METHODS AND RESULTS: Two-dimensional transthoracic echocardiograms were obtained in 512 patients at a mean of 11.1 +/- 3.2 days after infarction and were repeated at 1 year in 420 survivors. Left ventricular size was assessed as left ventricular cavity areas at end diastole and end systole and left ventricular function as percent change in cavity area from end diastole to end systole. Patients were randomly assigned to placebo or captopril, and the incidence of adverse cardiovascular events consisting of cardiovascular death, heart failure requiring either hospitalization or open-label angiotensin-converting enzyme inhibitor therapy, and recurrent infarction were determined over a follow-up period averaging 3.0 +/- 0.6 years. Irrespective of treatment assignment, baseline left ventricular systolic area and percent change in area were strong predictors of cardiovascular mortality and adverse cardiovascular events. At 1 year, left ventricular end-diastolic and end-systolic areas were larger in the placebo than in the captopril group (P = .038, P = .015, respectively), and percent change in cavity area was greater in the captopril group (P = .005). One hundred eleven of the 420 1-year survivors with 1-year echo measurements (26.4%) experienced a major adverse cardiovascular event, and these patients had more than a threefold greater increase in left ventricular cavity areas than those with an uncomplicated course. Sixty-nine patients with adverse cardiovascular events were in the placebo group compared with 42 patients in the captopril-treated group (a risk reduction of 35%, P = .010). CONCLUSIONS: Two-dimensional echocardiography provides important and independent prognostic information in patients after infarction. Left ventricular enlargement and function after infarction are associated with the development of adverse cardiac events. Attenuation of ventricular enlargement with captopril in these patients was associated with a reduction in adverse events. This study demonstrates the linkage between attenuation of left ventricular enlargement by captopril after infarction and improved clinical outcome.

Captopril↗
PubMed1994

Prevention of post-infarction left ventricular remodeling by ACE-inhibitors.

Left ventricular remodeling post-infarction occurs in at least a third of patients post-infarction and is associated with diminished survival and an increased incidence of adverse cardiovascular events. This process, which has been well described in recent years, can be largely attenuated with the use of ACE-inhibitors and with it survival improved and adverse events minimized. Since it is currently not possible to identify people at risk from left ventricular remodeling, ACE-inhibitors should be administered to all patients within the first 48 hours of infarction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

Serial assessment of left ventricular function and mass after orthotopic heart transplantation: a 4-year longitudinal study.

Long-term changes in left ventricular performance and geometry in the transplanted human heart have been incompletely described. Therefore, two-dimensional echocardiograms were performed on 22 recipients of an orthotopic heart transplant at 1 month (32 +/- 20 days), 1 year (11 +/- 3 months) and 4 years (54 +/- 9 months) after transplantation. All studies were performed at a time when the patient had no pathologic evidence of rejection. Ten healthy men served as a normal control group. Over 4 years of follow-up, mean systolic blood pressure in the study patients increased from 121 +/- 12 (p = NS vs. values in the control group) to 139 +/- 11 mm Hg (p less than 0.05 vs. both control values and values at 1 month); mean diastolic blood pressure increased from 72 +/- 7 (p = NS vs. normal values in the control group) to 93 +/- 8 mm Hg (p less than 0.05 vs. both control values and values at 1 month). Left ventricular end-systolic volume increased from 42 +/- 10 (p = NS vs. control values) to 51 +/- 14 ml (p less than 0.05 vs. both control values and values at 1 month) and end-diastolic volume increased from 103 +/- 28 (p = NS vs. control values) to 112 +/- 27 ml (p less than 0.05 vs. control values) over 4 years. Left ventricular mass and ejection fraction did not change significantly within the patient cohort and remained similar to that found in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1987

Longitudinal changes in left ventricular architecture and function in peripartum cardiomyopathy.

Left ventricular (LV) function was quantitated in 14 patients with peripartum cardiomyopathy, in 10 using 2-dimensional (2-D) echocardiography and in 4 radionuclide ventriculography, and values were compared with those in 11 normal women in the immediate postpartum period. LV end-diastolic and end-systolic volume indexes, LV wall mass index and ejection fraction were calculated during the acute phase of the illness and serially through long-term follow-up (mean 24 months). During the acute phase of illness there was marked LV dilatation: mean end-diastolic volume index was 95 +/- 22 ml/m2, vs 67 +/- 9 ml/m2 in control subjects (p less than 0.005), and mean end-systolic volume index was 66 +/- 18 ml/m2, compared to 27 +/- 5 ml/m2 in control subjects (p less than 0.001). Mean heart rates and mean systolic pressures in the patients with peripartum cardiomyopathy and the control subjects were similar, 91 +/- 24 vs 79 +/- 14 beats/min and 120 +/- 14 vs 117 +/- 10 mm Hg, respectively. LV wall mass index was higher, 139 +/- 38 vs 96 +/- 8 g/m2 (p less than 0.005), and ejection fraction much lower, 29 +/- 5% vs 67 +/- 5% (p less than 0.001), in control subjects. Five patients underwent endomyocardial biopsy during the acute illness, which showed interstitial fibrosis but no evidence of active inflammation. There was rapid and early improvement in LV function in 13 of 14 patients. Changes in LV volume, mass and ejection fraction all followed an exponential time course during LV remodeling.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Matching of myocardial oxygen consumption to mechanical load in human left ventricular hypertrophy and dysfunction.

The coupling of myocardial oxygen consumption (MVO2) with its determinants in left ventricular hypertrophy in human beings is poorly understood. Therefore, thermodilution-derived coronary blood flow, MVO2 and left ventricular wall stress, obtained from simultaneous left ventricular M-mode echogram and pressure, were compared in 32 patients with various degrees of left ventricular hypertrophy. Patients were studied at rest and after mechanical load alteration with nitroglycerin or phenylephrine. Decreases in MVO2 (-5.7 +/- 0.8 ml/min; p less than 0.001) and the time integral of meridional ejection stress or shortening load (-1,297 +/- 152 X 10(3) dynes X s/cm2; p less than 0.001) were observed after nitroglycerin administration while increases in MVO2 (+5.5 +/- 0.7 ml/min; p less than 0.001) and shortening load (+1,412 +/- 137 X 10(3) dynes X s/cm2; p less than 0.001) were noted after phenylephrine. An index relating the change in MVO2 to the corresponding change in shortening load (SL), % delta MVO2/% delta SL, was significantly different in patients without (Group 1) and with (Group 2) clinical left ventricular failure. Left ventricular mass was similar in both groups. The mean % delta MVO2/% delta SL with phenylephrine in Group 1 (79.6 +/- 9.6) was greater than the index for Group 2 (35.5 +/- 6.1; p less than 0.005). With nitroglycerin, Group 2 patients exhibited a greater reduction in % delta MVO2/% delta SL (110.5 +/- 17.8) than Group 1 (54.0 +/- 9.4; p less than 0.01). In conclusion, in patients with left ventricular hypertrophy and dysfunction there appears to be a state of diminished coronary flow response to load augmentation. However, load reduction in patients with clinical left ventricular failure results in a more balanced relation between oxygen uptake and ejection stress.

Adult↗
PubMed1983

Mechanics of pulsus alternans in aortic valve stenosis.

Differences in the mechanics of strong and weak contractions during sustained pulsus alternans were studied in 4 patients with aortic valve stenosis (AS). No significant difference was observed between strong (S) and weak (W) beats in M-mode echographic end-diastolic minor-axis dimension or end-diastolic meridional wall stress. Peak systolic meridional stress (S:225 X 10(3) dynes/cm2; W:205 X 10(3) dynes/cm2), the time integral of left ventricular (LV) meridional systolic stress (S:5,000 X 10(3) dynes/cm2; W:4,500 X 10(3) dynes/cm2) and the area of a stress dimension loop (S:202 X 10(3) dyne/cm; W 165 X 10(3) dyne/cm) were all greater for strong beats. However, end-systolic meridional stress (S:100 X 10(3) dynes/cm2; W:115 X 10(3) dynes/cm2) and end-systolic minor-axis dimension (S:4.75 cm; W:5.0 cm) were significantly greater for weak beats. Stress-length relations, derived from resting and postnitroglycerin determinations, revealed higher end-systolic dimensions for weak beats at any level of limiting afterload, suggesting diminished contractile performance of weak beats. Additionally, fractional minor-axis shortening for weak beats was diminished, at any level of end-systolic stress, in comparison with that for strong beats. The results are supportive of theories suggesting alternating contractile performance during pulsus alternans.

Aortic Valve Stenosis↗
PubMed1983

Myocardial oxygen consumption in left ventricular hypertrophy and its relation to left ventricular mechanics.

Alterations in left ventricular (LV) mechanics have significant effects on myocardial oxygen consumption (MVO2) as a result of changing LV pressure and dimensions. However, the effects of load alteration on MVO2 in the setting of LV hypertrophy and LV dysfunction have not been well characterized. Therefore, we examined changes in LV mechanics and MVO2 in 32 patients with varying degrees of LV hypertrophy and LV dysfunction before and after pharmacologic alteration of load. With phenylephrine or nitroglycerin-induced load alteration, changes in peak systolic meridional stress, mean systolic stress and the area of a stress-dimension loop all correlated modestly with changes in MVO2 (r = 0.66, 0.62, 0.63, respectively). However, changes in the time integral of LV ejection stress, or shortening load, were significantly correlated with changes in MVO2 (r = 0.88, p less than 0.001). In particular, load reduction results in a beneficial effect on MVO2. In addition, for a given change in LV systolic pressure, changes in shortening load (38 +/- 3.7%) were significantly greater than changes in tension-time index (13 +/- 1.4%), thus providing a sensitive marker of alteration of mechanical load. We conclude that physiologic alterations in mechanical load in normal persons as well as patients with LV hypertrophy are reflected in significant changes in the time integral of LV ejection stress. These changes in shortening load, mediated by changing LV pressure and dimension, are significantly related to changes in MVO2.

Adult↗
PubMed1983

Determinants of circulatory response to intravenous hydralazine in congestive heart failure.

To determine whether the circulatory response to hydralazine in heart failure is influenced by initial hemodynamic status or left ventricular (LV) chamber size, 28 patients with chronic LV dysfunction were studied. Hemodynamic measurements and echocardiographic LV end-diastolic dimension were correlated with the response to 20 mg of intravenous hydralazine and to a dose titrated in each patient to reduce systemic resistance by greater than or equal to 20%. Hydralazine, 20 mg, decreased systemic resistance from 23 +/- 8 to 18 +/- 8 U (p less than 0.01) and increased the cardiac index from 2.0 +/- 0.5 to 2.5 +/- 0.6 liters/min/m2 (p less than 0.01) and the stroke work index from 21 +/- 11 to 24 +/- 9 g . m/m2 (p less than 0.05). Titrating the dose to decrease systemic resistance by greater than or equal to 20% increased the cardiac index further to 2.7 +/- 0.6 liters/min/m2 and the stroke work index to 32 +/- 9 g . m/m2. The change in systemic resistance produced by 20 mg of hydralazine correlated only with initial systemic resistance (r = 0.53), suggesting that vascular response to hydralazine is a direct function of initial vascular resistance. The percentage change in stroke work index produced by 20 mg of hydralazine correlated directly with indexes of LV preload-end-diastolic wall stress (r = 0.69) and pulmonary wedge pressure (r = 0.43) and inversely with stroke work index (r = -0.49), an index of ventricular work. Similar but less close correlations were observed when the dose of hydralazine was titrated. The hemodynamic response to hydralazine did not correlate with LV end-diastolic dimension or right atrial pressure. Thus, vascular response to moderate doses of hydralazine is related to initial systemic vascular resistance. LV pump response is related to the level of initial LV pump dysfunction but not to LV chamber size or right atrial pressure.

Female↗
PubMed1982

Epicardial mapping of segmental myocardial function: an echocardiographic method applicable in man.

A technique for epicardial mapping of segmental myocardial function at multiple sites over both right and left ventricles was developed using a high-resolution, 7.5-MHz, short-focus, miniaturized, M-mode echocardiographic transducer worn on the fingertip. Myocardial function was determined from the extent and time course of systolic thickening and diastolic thinning at each site mapped. The technique was characterized in an open-chest canine model of myocardial ischemia. Ischemia was induced by transient or permanent coronary occlusion in 17 dogs. Acute occlusions produced reduced segmental thickening within 10-15 seconds and, often, overt systolic thinning of ischemic myocardium. Rhodamine fluorescence perfusion maps were compared with echocardiographic maps in nine dogs. Segmental thickening was reduced in perfused segments adjacent to, but not involved by, ischemia, as well as ischemic segments. Reproducibility appeared satisfactory for quantitative analysis of grouped data on multiple segments, and qualitative analysis in individual segments. Initial human studies performed during coronary bypass surgery in 11 subjects showed echocardiographic abnormalities in the six patients with ventriculographic abnormalities and in four with normal ventriculograms. Transmural infarctions were akinetic, showing no change in thickness throughout the cardiac cycle. Hypokinetic segments distal to high-grade coronary stenosis were common, although most segments distal to stenosis contracted normally. Reversal of segmental contraction abnormalities by coronary bypass grafting was shown in three subjects, while worsening of function was seen in previously abnormal segments in two and in a previously normal segment in one subject. Epicardial echocardiographic mapping is a practical method for intraoperative assessment of myocardial function during coronary surgery in man that may enhance our understanding of the pathophysiology of coronary disease and the effects of coronary surgery.

Animals↗
PubMed1981

Valve replacement without preoperative cardiac catheterization.

During the year 1978, the decision to perform cardiac catheterization in patients with valvular heart disease was delayed until clinical and noninvasive assessment have been completed. As a result, 184 patient underwent operation without invasive studies, and 59 had elective catheterization. Another 62 patients were referred during the same period for valve replacement after routine catheterization had been performed elsewhere. Age, sex distribution, symptoms, and cause of valve disease were similar in all three groups, although we managed emergencies and second operations more frequently without catheterization. In all patients, the preoperative diagnosis was confirmed, and no unexpected pathologic process was encountered. Operative mortality was the same in all three groups, and after two years of follow-up there was no difference in survival or symptoms. No uncorrected valve lesions became apparent in uncatheterized patients. We conclude that routine catheterization is unnecessary before valve replacement but can be reserved for specific indications in some patients.

Adolescent↗