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Role of ischemia and infarction in late right ventricular dysfunction after atrial repair of transposition of the great arteries.

OBJECTIVES: This study was conducted to assess whether myocardial ischemia and/or infarction are involved in the pathogenesis of late right ventricular dysfunction in adult survivors of atrial baffle repair for transposition of the great arteries in infancy. BACKGROUND: The medium-term success of intraatrial baffle repair for transposition of the great arteries is good, with many patients surviving into adult life, but prognosis can be limited by progressive right ventricular dysfunction. We hypothesized that ongoing myocardial ischemia and/or infarction are important factors in the pathogenesis of this complication. Radionuclide techniques offer an opportunity to study both myocardial perfusion and concomitant ventricular wall motion. METHODS: Dipyridamole sestamibi single-photon emission computed tomography followed by rest sestamibi single-photon emission computed tomography was used to assess right ventricular myocardial perfusion, wall motion, wall thickening and ejection fraction in 22 adolescents/young adults who had undergone atrial baffle repair for simple transposition of the great arteries at median 6.7 (range 0.5 to 54) months of age. The patients were aged 10 to 25 (median 15.5) years; 19 in New York Heart Association class I, 2 in class II and 1 in class III. All were in a regular cardiac rhythm during the studies. The right ventricular tomographic images were examined in three parallel and two orthogonal planes, analyzed in 12 segments. RESULTS: Perfusion defects were evident in all patients in at least one segment, in either the rest or stress images. Twelve patients (55%) demonstrated fixed defects only, nine (41%) had fixed and reversible defects and one (4.5%) had reversible defects only. Concomitant wall-thickening abnormalities occurred in 83% of segments with fixed perfusion defects, mirrored by a reduction in wall motion in 91% of segments analyzed. Right ventricular ejection fraction was correlated with age (R = 0.62; p = 0.002), and with wall-thickening abnormalities (R = 0.60; p < 0.005). CONCLUSIONS: Reversible and fixed perfusion defects with concordant regional wall motion abnormalities occur in the right (systemic) ventricle 10 to 20 years after Mustard repair for transposition of the great arteries; this may be important in the pathogenesis of late right ventricular dysfunction in this group.

Adolescent↗

Synergism between infarct-borne left ventricular dysfunction and cardiomegaly in increasing the risk of coronary bypass surgery.

The effect of cardiomegaly on operative and late mortality in patients with left ventricular dysfunction undergoing coronary bypass operation was investigated. The study group consisted of 178 patients whose left ventricular ejection fraction was below 45% and who were operated on from 1978 through 1985. Forty-five patients (group A) had severe left ventricular dysfunction (ejection fraction < 30%) and 133 (group B) had moderate dysfunction (30% > ejection fraction > 45%). Twenty-four of group A (53%) and 54 of group B (41%) patients had cardiomegaly (cardiothoracic ratio on chest x-ray films > 0.5). There were 10 (6%) hospital deaths, four in group A (9%) and six in group B (4.5%). All four deaths in group A and the six deaths in group B were patients who had cardiomegaly. Regardless of the severity of the left ventricular dysfunction, there was no operative death among patients with normal heart size (p < 0.001). Age over 65, bypass time longer than 2 hours, and incomplete revascularization emerged as risk factors. Follow-up ranged from 5 to 13 years (mean 7.8 years). Overall 5-year actuarial survival, including hospital mortality, was 80% +/- 3%. Reduced 5-year survival was observed in patients with cardiomegaly (67% +/- 5% versus 91% +/- 3%, p < 0.05). Five- and 10-year survival of patients from group A with cardiomegaly was 53% +/- 7% and 18% +/- 13%, respectively.

Cardiomegaly↗

A reexamination of the hemodynamic effects of digitalis relative to ventricular dysfunction.

The available data suggest that digitalis improves symptoms of a failing heart in the presence of sinus rhythm as well as supraventricular arrhythmias. Intravenous digitalis administration in patients with chronic heart failure and baseline hemodynamic deterioration increases cardiac index and reduces heart rate. These beneficial effects are maintained with long-term oral therapy and are comparable with those obtained using dobutamine in patients with chronic severe heart failure. The addition of digoxin to therapy with vasodilators and diuretics confers clinical benefit in patients with moderate to severe heart failure symptoms because of systolic ventricular dysfunction. Digoxin effects on diastolic function appear to be different in patients with preserved systolic function in comparison to patients with overt heart failure and systodiastolic dysfunction. In patients with right ventricular dysfunction digoxin does not appear to influence hemodynamic measurements unless concomitant left ventricular dysfunction is present.

Digoxin↗

Effects of long-term enalapril therapy on cardiac structure and function in patients with left ventricular dysfunction. Results of the SOLVD echocardiography substudy.

BACKGROUND: Studies of Left Ventricular Dysfunction (SOLVD) demonstrated that enalapril therapy significantly improved the clinical course of patients with left ventricular (LV) dysfunction. The goals of this substudy were to evaluate changes in LV structure and function in SOLVD patients and to test the hypothesis that enalapril inhibits remodeling in patients with LV dysfunction. METHODS AND RESULTS: Patients entering both the prevention and treatment arms of SOLVD from 5 of the 23 clinical centers were recruited for this substudy. The 301 patients who participated underwent Doppler-echocardiographic evaluation according to standard protocol before randomization to either enalapril or placebo and again after 4 and 12 months of therapy. Recorded data were analyzed in a blinded fashion at a central core laboratory. Analysis of baseline clinical characteristics showed that patients enrolled in the substudy were generally representative of the SOLVD population, although prevention arm patients were slightly overrepresented in the substudy group (69.8% compared with 61.9% of remaining SOLVD patients). The enalapril group demonstrated significant reductions in the mitral annular E-wave-to-A-wave velocity ratio (due predominantly to a reduction in E-wave velocity), and this response was different from that seen in the placebo group (P = .030). Changes in the E-to-A ratio in the enalapril group correlated significantly with changes in plasma atrial natriuretic peptide (r = .56; P < or = .01). LV end-diastolic and end-systolic volumes increased in placebo but not enalapril-treated patients, and the differences in response between the treatment groups were significant (P = .025 and .019, respectively). LV mass tended to increase in placebo patients and to be reduced in enalapril-treated patients, and the difference in response between the groups was highly significant (P < or = .001). CONCLUSIONS: These data demonstrate that enalapril attenuates progressive increases in LV dilatation and hypertrophy in patients with LV dysfunction. The results support the possibility that the favorable effects of enalapril reported in the SOLVD trials were related to inhibition of LV remodeling.

Adult↗

Diuretics and risk of arrhythmic death in patients with left ventricular dysfunction.

Background-Treatment with diuretics has been reported to increase the risk of arrhythmic death in patients with hypertension. The effect of diuretic therapy on arrhythmic death in patients with left ventricular dysfunction is unknown. Methods and Results-We conducted a retrospective analysis of 6797 patients with an ejection fraction <0.36 enrolled in the Studies Of Left Ventricular Dysfunction (SOLVD) to assess the relation between diuretic use at baseline and the subsequent risk of arrhythmic death. Participants receiving a diuretic at baseline were more likely to have an arrhythmic death than those not receiving a diuretic (3.1 vs 1.7 arrhythmic deaths per 100 person-years, P=0.001). On univariate analysis, diuretic use was associated with an increased risk of arrhythmic death (relative risk [RR] 1.85, P=0.0001). After controlling for important covariates, diuretic use remained significantly associated with an increased risk of arrhythmic death (RR 1.37, P=0.009). Only non-potassium-sparing diuretic use was independently associated with arrhythmic death (RR 1.33, P=0.02). Use of a potassium-sparing diuretic, alone or in combination with a non-potassium-sparing diuretic, was not independently associated with an increased risk of arrhythmic death (RR 0.90, P=0.6). Conclusions-In SOLVD, baseline use of a non-potassium-sparing diuretic was associated with an increased risk of arrhythmic death, whereas baseline use of a potassium-sparing diuretic was not. These data suggest that diuretic-induced electrolyte disturbances may result in fatal arrhythmias in patients with systolic left ventricular dysfunction.

Analysis of Variance↗

The left ventricular dysfunction questionnaire (LVD-36): reliability, validity, and responsiveness.

OBJECTIVE: To examine the reliability, validity, and responsiveness of a new health status measure (LVD-36) for patients with left ventricular dysfunction which was designed with emphasis on content validity, clarity, brevity, and ease of use. DESIGN: At baseline, patients completed the LVD-36 and a range of measures reflecting general health and disease severity. The LVD-36 was repeated after one week. After six months, it was repeated again, along with a transition question to measure global changes in health. SETTING: Patients were recruited from the cardiology and general medical clinics at a south west London hospital. PATIENTS: 60 patients with chronic left ventricular dysfunction. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Short form 36 questionnaire (SF-36), Minnesota living with heart failure questionnaire (LIhFE), New York Heart Association criteria, and exercise performance and echocardiographic tests. RESULTS: The LVD-36 showed good internal consistency (kappa = 0.95) and repeatability (r(i) = 0.95). Its scores were significantly associated with SF-36 mental and physical component scores (r = -0. 48 and -0.75; p < 0.0001), with exercise capacity (r = -0.52; p < 0. 0001), and with systolic shortening fraction (r = -0.27; p < 0.05). Change in the LVD-36 over six months was associated with change in overall health (F = 5.7; p < 0.001). In tests of validity and responsiveness, the LVD-36 performed similarly to or marginally better than the LIhFE. CONCLUSIONS: The LVD-36 showed a high level of reliability and validity, and appears to measure changes in health. It provides a short, simple, valid, and reliable measure of health status in patients with left ventricular dysfunction.

Aged↗

Effects of nisoldipine therapy on myocardial perfusion and neuro-hormonal status in patients with severe ischaemic left ventricular dysfunction.

The effects of nisoldipine on regional myocardial perfusion and neuro-hormonal status were assessed in a double-blind, placebo-controlled study of 32 patients. All patients had ischaemic left ventricular dysfunction, with a left ventricular ejection fraction between 25% and 35%; per protocol, they were stratified according to concomitant use of ACE inhibitors. After baseline measurements at rest, including single photon emission computed tomography (SPECT) with Tc-MIBI, plasma neuro-hormones (norepinephrine, renin, arginine vasopressin, atrial natriuretic peptide) and echocardiography, the patients were randomized to nisoldipine (core coat tablet, 20 mg once daily; n = 16) or placebo (n = 16). Measurements were repeated after 8 weeks. SPECT data were analysed qualitatively (visual comparison by blinded observer) and quantitatively to derive an index of hypoperfusion representing the percentage of the left ventricular mass with Tc-MIBI activity below normal. At baseline, all patients had left ventricular areas with reduced Tc-MIBI uptake and 29 patients also had increases in plasma neuro-hormones. With nisoldipine, the extent of hypoperfusion (quantitative analysis) was reduced in 8/14 patients vs only 2/14 patients with placebo (P = 0.046, 2-tailed test). The benefit of nisoldipine was similar in patients with or without ACE inhibitor therapy and was also confirmed by the visual analysis of the data. Further, none of the neuro-hormones examined was significantly modified by nisoldipine. Thus, chronically underperfused areas are present at rest in patients with ischaemic left ventricular dysfunction, and nisoldipine significantly improved Tc-MIBI uptake in these areas without evidence of detrimental changes in plasma neuro-hormones.(ABSTRACT TRUNCATED AT 250 WORDS)

Arginine Vasopressin↗

Left ventricular dysfunction in the fetus: relation to aortic valve anomalies and endocardial fibroelastosis.

OBJECTIVE: To examine the relation between a characteristic form of left ventricular dysfunction in the fetus and abnormalities of the aortic valve and endocardial fibroelastosis of the left ventricle. DESIGN: A retrospective study to examine the correlation between echocardiographic findings in the fetus and postnatal or necropsy findings. SETTING: Tertiary referral centre for fetal echocardiography. PATIENTS: Thirty fetuses showing a characteristic echocardiographic picture of left ventricular dysfunction. MAIN OUTCOME MEASURES: The relation between the prenatal echocardiographic features and the postnatal and necropsy findings. RESULTS: At presentation the size of the left ventricular cavity was normal or enlarged in all cases. The measurements of the orifice of the aortic root and mitral valve were either normal or small for the gestational age. The echocardiographic diagnosis made at presentation was critical aortic stenosis in all cases. At necropsy or postnatal examination the aortic valve was dysplastic and stenotic in 15 cases and the left ventricle had become hypoplastic in one of these. Aortic atresia was present in seven patients, three of whom had a hypoplastic left ventricle. In six patients the aortic valve was bicuspid although not obstructive. One of these patients had hypoplasia of the aortic arch and one had a hypoplastic left ventricle but in the remaining four patients endocardial fibroelastosis of the left ventricle was the only abnormality found. No follow up information was available in two. Of 26 patients for whom there was postmortem information, 24 had evidence of some degree of endocardial fibroelastosis of the left ventricle. Sequential observations showed that five cases developed into the hypoplastic left heart syndrome. CONCLUSIONS: This type of left ventricular dysfunction in the fetus is the result of an overlap of diseases, including primary left ventricular endocardial fibroelastosis, critical aortic stenosis, and the hypoplastic left heart syndrome.

Aortic Valve↗

Verapamil responsive incessant ventricular tachycardia resulting in severe ventricular dysfunction in a young child: successful management with oral verapamil.

In young children with incessant ventricular tachycardia and severe ventricular dysfunction, the management of tachycardia with conventional antiarrhythmic drugs remains a major therapeutic challenge because most of these drugs can further depress myocardial function. We report a four year old boy with verapamil responsive incessant ventricular tachycardia and severe ventricular dysfunction in whom oral verapamil treatment eliminated both the arrhythmia and the picture of dilated cardiomyopathy. On oral verapamil, the patient remains asymptomatic without recurrence of the ventricular tachycardia over a follow up period of 10 months.

Administration, Oral↗

QT dispersion and viable myocardium in patients with prior myocardial infarction and severe left ventricular dysfunction.

BACKGROUND: QT dispersion (QTd) has been found to correlate to the amount of viable myocardium in patients with Q-wave myocardial infarction and well-preserved LV function. However, this relationship is unknown in patients with severe left ventricular dysfunction. METHODS: Thirty-four patients with prior large myocardial infarction and severe left ventricular dysfunction underwent Tc-99m sestamibi single photon emission cardiac tomography (SPECT) and F-18 fluorodeoxyglucose (FDG) SPECT. Viability was defined as a defect relative count density (DCD) of at least 20% greater on FDG SPECT. QTd, corrected QT dispersion (QTcd), and QT coefficient of variation (cv) in patients with viable myocardium was compared to those without viable myocardium in the infarct area. RESULTS: Thirteen patients were excluded from analysis for poor FDG images or inadequate ECG tracings. Of the remaining patients, 10 (48%) were found to have viability on FDG SPECT. QTd, QTcd, and QTcv in patients with viability were: 58 +/- 22 ms, 61 +/- 23 ms, and 4.81 +/- 1.76%, respectively, which did not differ significantly from those in patients without viability (QTd = 56 +/- 14 ms, QTcd = 70 +/- 16 ms and Qtcv = 5.06 +/- 1.20% [P = NS]). Moreover, neither FDG defect size, nor LVEF correlated with QTd. CONCLUSIONS: This study indicates no relationship between QTd and viability in patients with myocardial infarction and severe left ventricular dysfunction.

Aged↗

Reversible left ventricular dysfunction associated with raised troponin I after subarachnoid haemorrhage does not preclude successful heart transplantation.

Transient abnormalities in ECGs, echocardiograms, and cardiac enzymes have been described in the acute setting of subarachnoid haemorrhage. In addition, left ventricular dysfunction has been reported at the time of brain death. A patient with an acute subarachnoid haemorrhage who presented with raised troponin I (TnI) concentrations and diffuse left ventricular dysfunction is described. After declaration of brain death 32 hours later, the heart was felt initially not suitable for transplantation. A normal cardiac catheterisation, however, lead to successful transplantation of the donor heart. Raised catecholamine concentrations and metabolic perturbations have been proposed as the mechanisms leading to the cardiac dysfunction seen with brain death. This may be a biphasic process, allowing time for myocardial recovery and reversal of the left ventricular dysfunction. Awareness of this phenomenon in the acutely ill neurologic population needs to be raised in order to prevent the unnecessary rejection of donor hearts.

Biomarkers↗

Prognostic value of coronary angiography in patients with chronic ischemic left ventricular dysfunction and evidence of viable myocardium on thallium reinjection imaging.

BACKGROUND: We evaluated the independent and incremental prognostic value of cardiac catheterization and coronary angiographic data over thallium reinjection after stress redistribution imaging in patients with myocardial infarction and left ventricular dysfunction. METHODS AND RESULTS: Sixty-nine patients with a first myocardial infarction (> 8 weeks) and left ventricular ejection fraction < or = 40% underwent thallium-201 reinjection after stress redistribution tomographic imaging and cardiac catheterization. During follow-up (mean 26 months) 11 cardiac events (8 cardiac deaths and 3 nonfatal myocardial infarctions) occurred. On Cox regression analysis independent predictors of cardiac events were the sum of reversible and moderately irreversible defects at thallium reinjection (chi 2, 16.4, p < 0.005) and the number of reversible defects at stress redistribution (chi 2, 5.1, p < 0.05). Moreover, thallium reinjection imaging improved the prognostic power of clinical, exercise, and stress redistribution data (p < 0.01). The inclusion of left ventricular ejection fraction produced a borderline improvement (p = 0.06), whereas the number of vessels with coronary disease did not. In contrast, in patients at high risk such as those with at least 25% of viable myocardium at reinjection, the number of diseased vessels provided additional prognostic information (p < 0.05). CONCLUSIONS: In patients with chronic ischemic left ventricular dysfunction, left ventricular ejection fraction, but not the number of diseased vessels, provides additional prognostic information to thallium imaging. Therefore coronary angiography seems unnecessary in these patients, unless a significative amount of viable myocardium is detectable.

Chronic Disease↗

Exercise is superior to pacing for T wave alternans measurement in subjects with chronic coronary artery disease and left ventricular dysfunction.

INTRODUCTION: T wave alternans (TWA) is a heart rate-dependent marker of vulnerability to ventricular arrhythmias. Atrial pacing and exercise both are used as provocative stimuli to elicit TWA. However, the prognostic value of the two testing methods has not been compared. The aim of this prospective study was to compare the prognostic value of TWA measured during bicycle exercise and atrial pacing in a large cohort of high-risk patients with ischemic heart disease and left ventricular dysfunction. METHODS AND RESULTS: This was a prospective study of 251 patients with coronary artery disease and left ventricular dysfunction who were referred for electrophysiologic studies (EPS) for standard clinical indications. Patients underwent TWA testing using bicycle ergometry (exercise TWA, n = 144) and/or atrial pacing (pacing TWA, n = 178). The primary endpoint was the combined incidence of death, sustained ventricular arrhythmias, and appropriate implantable cardioverter defibrillator therapy. The predictive value of exercise and pacing TWA for EPS results and for endpoint events was determined. Exercise and pacing TWA both were significant predictors of EPS results (odds ratios 3.0 and 2.9 respectively, P < 0.02). Kaplan-Meier survival analysis of the primary endpoint revealed that exercise TWA was a significant predictor of events (hazard ratio 2.2, P = 0.03). In contrast, pacing TWA had no prognostic value for endpoint events (hazard ratio 1.1, P = 0.8). CONCLUSION: TWA should be measured during exercise when it is used for clinical risk stratification. EPS results may not be an adequate surrogate for spontaneous events when evaluating new risk stratification tests.

Aged↗

Prognostic importance of the quantification of myocardial viability in revascularized patients with coronary artery disease and moderate-to-severe left ventricular dysfunction.

The aim of this study was to assess the prognostic value of the amount of dysfunctional but viable myocardium in revascularized patients with coronary artery disease and left ventricular dysfunction. To quantify the amount of dysfunctional but viable myocardium, low-dose dobutamine echocardiography was performed. The wall motion was scored using a 16-segment model. The dysfunctional segments were defined as viable if they exhibited functional improvement of at least 1 grade with any dose of dobutamine, or only worsening with dobutamine infusion. Two hundred and twenty patients were revascularized and followed-up for a mean period of 33+/-23 months (range, 0-86) for cardiac-related death and hospitalization for heart failure. Standard follow-up echocardiography was performed 3-6 months after revascularization. Receiver operating characteristic curve analysis identified six dysfunctional but viable segments as the optimal cutoff value for discriminating patients with and without risk of cardiac events. Thirty-eight patients exhibited a large amount of dysfunctional but viable myocardium (>or=6 segments, group A), 103 patients had a small amount of dysfunctional but viable myocardium (2-5 segments, group B), and 79 patients were found to have dysfunctional myocardium irreversibly damaged (group C). Similar baseline left ventricular ejection fractions of 36+/-4, 34+/-5, 35+/-5% in groups A, B, and C increased to 46+/-6% (P<0.01 versus baseline and versus groups B and C), to 39+/-5% (P<0.01 versus baseline and group C), and to 36+/-7% (P<0.01 versus baseline), respectively, after revascularization. The greatest functional improvement after revascularization in group A patients was accompanied by a lower frequency of cardiac events during follow-up (1 vs. 27 in group B, P<0.01, and versus 18 in group C, P<0.01) and by a better cardiac event-free survival according to Kaplan-Meier survival analysis (P<0.01 versus groups B and C, respectively). In conclusion, in revascularized patients with coronary artery disease and moderate-to-severe left ventricular dysfunction, the presence of >or=6 dysfunctional but viable segments identifies patients with the best prognosis.

Adult↗

Non-cardioplegic coronary surgery in patients with severe left ventricular dysfunction.

OBJECTIVES: Although most surgeons use cardioplegia for myocardial protection during coronary artery bypass grafting (CABG), some still use non-cardioplegic methods with very good early and long-term outcome. However, the results in patients with severe left ventricular dysfunction remain unproved. This study evaluates the perioperative mortality and morbidity in patients with severe left ventricular dysfunction submitted to CABG using non-cardioplegic methods. METHODS: From April 1990 through December 1997, 3,180 patients were consecutively subjected to isolated CABG using non-cardioplegic methods, for construction of the distal anastomoses. This prospective study is based on the 107 (3.4%) patients with severe impairment of the left ventricular function (ejection fraction < 30%). The mean age at operation was 57.0 +/- 9.2 years and 95.3% of patients were male. Fifty three patients (49.5%) were in class CCS III/IV and 12 (11.2%) were subjected to urgent surgery. A history of previous myocardial infarction was recorded in 99 (92.5%) patients. Ninety seven (90.6%) patients had triple vessel and 17 (15.9%) left main stem disease, and 77 (71.9%) had a left ventricular end-diastolic pressure > 20 mmHg. Cardiopulmonary bypass time was 73.1 +/- 21.7 min. The mean number of grafts per patient was 3.2. At least one internal mammary artery was used in all cases and 16 patients (14.9%) had bilateral internal mammary artery grafts (1.2 arterial grafts/patient). Endarterectomies were performed in 23 (21.5%) patients. RESULTS: Perioperative mortality was 2.8% (respiratory-1; cardiac-2). Forty one (38.3%) patients required inotropes, but for longer than 24 h in only 12 (11.2%), and two (1.9%) needed intra-aortic counterpulsation. The incidence of myocardial infarction was 2.8%. Two (1.9%) patients had reintervention for haemorrhage and another five (4.6%) for sternal complications. The incidences of supraventricular arrhythmias, renal failure and cerebrovascular accident were 16.8%, 3.6% and 2.8%, respectively. The mean time of hospital stay was 9.3 +/- 6.4 days. CONCLUSION: These results appear to demonstrate that non-cardioplegic methods afford good myocardial protection and operating conditions with excellent applicability, even in patients with severe left ventricular dysfunction.

Aged↗

Increased brain and atrial natriuretic peptides in patients with chronic right ventricular pressure overload: correlation between plasma neurohormones and right ventricular dysfunction.

OBJECTIVE: To evaluate the role of plasma neurohormones in the diagnosis of asymptomatic or minimally symptomatic right ventricular dysfunction. SETTING: Tertiary cardiovascular referral centre. METHODS: Plasma brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) concentrations were measured in 21 asymptomatic or minimally symptomatic patients with chronic right ventricular pressure overload caused by congenital heart disease, and in seven healthy volunteers. Right ventricular ejection fraction was determined using magnetic resonance imaging. RESULTS: Right ventricular ejection fraction in the volunteers was higher than in the patients (69.0 (8.2)% v 58.0(12.0)%, respectively; p < 0.006). Left ventricular ejection fraction was 72.3(7.8)% in volunteers and 68.1(11.0)% in patients (NS). There was a significant difference between patients and volunteers in the plasma concentrations of BNP (5.3 (3.5) v 2.3 (1.7) pmol/l, respectively; p < 0.009) and ANP (7.3 (4.5) v 3.6 (1.4) pmol/l; p < 0.05). In both patients and volunteers, mean plasma ANP was higher than mean plasma BNP. Right ventricular ejection fraction was inversely correlated with BNP and ANP (respectively, r = 0.65; p < 0.0002 and r = 0.61; p < 0.002). There was no correlation between left ventricular ejection fraction and BNP (r = 0.2; NS) or ANP (r = 0.52; NS). Similarly, no correlation was shown between the level of right ventricular systolic pressure and either plasma BNP (r = 0.20) or plasma ANP (r = 0.07). CONCLUSIONS: There was a significant inverse correlation between right ventricular ejection fraction and the plasma neurohormones BNP and ANP in asymptomatic or minimally symptomatic patients with right ventricular pressure overload and congenital heart disease. Monitoring changes in BNP and ANP may provide quantitative follow up of right ventricular dysfunction in these patients.

Adult↗