The left ventricular end-systolic pressure-dimension relation in patients with thalassemia major. A new noninvasive method for assessing contractile state.

Borow, Kenneth M.; Propper, Richard D.; Bierman, Fredrick Z.; Grady, Stafford; Inati, Adlette

doi:10.1161/01.cir.66.5.980

Cited by 62 publications

(20 citation statements)

References 44 publications

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“…In our group of patients with TGA/IVS there was a striking inverse correlation between the age at anatomic correction and the slope value for the Pes-Des relationship ( figure 5) Potential limitations of our noninvasive method for assessing LV contractility have been noted previously. [3][4][5] In this study, we assumed that the LV minor-axis dimension measured from the M mode echocardiogram was representative of overall LV function and that there was no significant coronary artery narrowing after anatomic correction. These assumptions seem reasonable since no patients showed evidence of significant regional wall motion abnormality on two-dimensional echocardiographic study even under peak afterload conditions.…”

Section: Resultsmentioning

confidence: 99%

Assessment of left ventricular contractile state after anatomic correction of transposition of the great arteries.

Borow¹,

Arensman²,

Webb³

et al. 1984

Circulation

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When compared with intra-atrial baffle repairs for D-transposition of the great arteries (TGA), anatomic correction offers the theoretic advantage that it results in the use of the left ventricle (LV) as the systemic ventricle. Although the long-term success of this procedure depends on the function of the LV, little is known regarding LV postoperative contractile state. The LV end-systolic pressure-dimension and wall stress-shortening (%AD) relationships, sensitive indexes of contractility, were studied during methoxamine-induced increases in afterload in eight patients with TGA and intact ventricular septa and in four patients with TGA and associated lesions. The patients with TGA and intact ventricular septa underwent pulmonary artery banding when they were between the ages 0.1 and 1.1 years (mean 0.4) to prepare the LV for anatomic correction. Age at repair ranged from 0.3 to 1.8 years (mean 1.0) and that at study from 1.7 to 6.7 years (mean 3.3). The interval from correction to study was 0.4 to 4.8 years (mean 2.3). End-systolic pressure was estimated from a calibrated suprasternal notch tracing. End-systolic dimension, wall thickness, and %zXD were determined by M mode and two-dimensional echocardiography, and end-systolic wall stress was then calculated. Results were compared with previously reported normal values. The pressure-dimension and wall stress-%AD relationships were normal in 10 of 12 TGA patients. The two patients with abnormal study results had TGA with intact ventricular septa and they underwent correction after 1.5 years of age. There was no relationship between contractile state and either interval from repair to study or age at study. Thus, LV contractility is normal in most patients with TGA who undergo anatomic correction. Circulation 69, No. 1, 106-112, 1984 Patients and methodsOur patient population consisted of 12 children (10 boys and two girls) who had undergone anatomic correction for TGA (table 1). Only patients in close geographic proximity to the study site in Harefield, England were evaluated. Before surgery eight children had TGA with intact interventricular septa (IVSs) and four had additional defects (large ventricular septal defects in three, and aortopulmonary window in one). All of the children with TGA/IVSs underwent two-stage repair with initial pulmonary artery banding performed when they were from 0.1 to 1.1 years of age (mean 0.4). The patients' ages at repair ranged from 0.3 to 1.8 years (mean 1.0), and their ages at postoperative study ranged from 1.7 to 6.7 years (mean 3.3); the interval between definitive repair and study ranged from 0.4 to 4.8 years (mean 2.3). The technique used for anatomic correc- Subjects under 6 years of age were given light sedation with oral trimeprazine (2.5 mg/kg) followed in 1 hr by an intramuscular injection of papaveretum (0.33 mg/kg) and scopolamine (0.0067 mg/kg). All patients were premedicated with intravenous atropine (0.01 mg/kg) to abolish reflex cardiac slowing. Each subject underwent simultaneous recordings of syst...

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Section: Resultsmentioning

confidence: 99%

Assessment of left ventricular contractile state after anatomic correction of transposition of the great arteries.

Borow¹,

Arensman²,

Webb³

et al. 1984

Circulation

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“…17 Depression of intra-atrial conduction causes a lengthening of P-wave. 18 In addition, it is now well accepted that a new and simple electrocardiographic marker, PWD, also represents inhomogeneous and discontinuous atrial conduction and has predictive value especially for paroxysmal atrial fibrillation.…”

Section: Discussionmentioning

confidence: 99%

Electrocardiographic markers for the early detection of cardiac disease in patients with beta-thalassemia major

Nişli¹,

Yavuz²,

Öner³

et al. 2010

J Pediatr (Rio J)

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Objective: To comparatively evaluate P-wave dispersion (PWD) in patients with β-thalassemia major (TM) and healthy control subjects for the early prediction of arrhythmia risk.Methods: Eighty-one children with β-TM, aged 4-19 years, and 74 healthy children (control group) underwent routine electrocardiography and transthoracic echocardiography for cardiac evaluation. PWD was calculated as the difference between the maximum and the minimum P-wave duration.Results: There was a statistically significant difference between study and control groups in peak early (E) mitral inflow velocity and E/late (A) velocity ratio. Maximum P-wave duration and PWD were found to be significantly higher in β-TM patients than in control subjects. Conclusions:Increased PWD in our β-TM patients might be related to depression of intra-atrial conduction due to atrial dilatation and increased sympathetic activity. These patients should be closely followed up for risk of lifethreatening arrhythmias.J Pediatr (Rio J). 2010;86(2):159-162: Thalassemia major, P-wave dispersion, ferritin, cardiac involvement. Original article0021-7557/10/86-02/159 Jornal de PediatriaCopyright © 2010 by Sociedade Brasileira de Pediatria IntroductionCardiac failure and sudden death, the latter probably due to arrhythmias, remain the major causes of death in β-thalassemia major (TM). 1 Disease prognosis, however, has been modified with regular blood transfusions and iron chelation therapy with deferoxamine. 2 P-wave dispersion (PWD) is a simple electrocardiographic marker that has been reported to be associated with inhomogeneous and discontinuous propagation of sinus impulses. It has been defined as the difference between the maximum and the minimum P-wave duration. 3-4 Prolonged P-wave duration and increased PWD have been shown to carry an increased risk for atrial fibrillation. 4 Cardiomyopathy is associated with a four-to six-fold increase in the risk of developing atrial fibrillation. 5 The present study aimed to comparatively investigate these electrocardiographic markers in patients with β-TM and healthy control subjects for the early prediction of arrhythmia risk. MethodsThe study population consisted of two groups: Group I -81 children with β-TM; and group II -74 healthy children Peak mitral inflow velocities in early diastole (E) and after atrial contraction (A) were expressed as cm/s. Deceleration time of peak E filling velocity was measured in milliseconds.Overall LV diastolic dysfunction was defined as the presence of any abnormality of the mitral valve. Twelve-lead electrocardiogram (ECG) was recordedfor each patient and control subject at a rate of 50 mm/s.At the time of electrocardiographic recording, all subjects were in sinus rhythm and none were taking any type of antiarrhythmic agent. P-wave duration was measured manually by two of the investigators who were blinded to the participants' clinical status. All measurements were performed using calipers and magnifying lens to improve accuracy. The onset of P-wave was defined as the junctio...

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“…However, there is a large body of experimental and clinical data showing that the LV ESPVR is relatively load independent and sensitive to changes in LV contractility and, hence, can serve as a clinically useful index of LV function. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] In the isolated heart, the right ven-tricular (RV) ESPVR also appears to be load independent and responsive to inotropic changes. 16 However, there have been few studies of the RV ESPVR in humans.…”

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Human right ventricular end-systolic pressure-volume relation defined by maximal elastance.

Brown

Ditchey

1988

Circulation

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This study was undertaken to determine 1) whether a combined radionuclide-hemodynamic technique could define the right ventricular end-systolic pressure-volume relation (RV ESPVR) in the clinical setting, 2) whether the human RV ESPVR defined by maximal elastance is linear and responsive to inotropic interventions, and 3) whether more easily measured modifications of the ESPVR are reliable substitutes as an index of RV function. Eight patients with normal RV function were studied with simultaneous micromanometer RV pressure measurements and radionuclide ventriculography to construct RV pressure-volume loops. Data were collected at baseline and after at least two alterations in loading conditions with nitroglycerin, phenylephrine, or saline. End systole was defined by maximal elastance (E(t) = P(t)I [V(t) -VO]). Data were also obtained during administration of dobutamine in four patients and after atrial pacing tachycardia in one patient. The RV ESPVR defined by maximal elastance was highly linear (r=0.988-0.999) throughout the range of pressures and volumes tested. Furthermore, the linear correlations were significantly higher (p<0.005), and the linear regression standard error of the estimate (SEE) was significantly lower (p<0.005) for the RV ESPVR defined by maximal elastance compared with modifications of the ESPVR with the ratio of pulmonary artery-dicrotic notch pressure or RV peak pressure to end-ejection volume. Dobutamine or atrial pacing tachycardia produced a leftward shift of the entire RV pressure-volume loop, and in each patient (five of five), the point of maximal elastance fell outside the 95% confidence interval defined by the baseline ESPVR. However, because of the larger SEE, the leftward shift with modifications of the ESPVR was not statistically significant in any patient by the pulmonary artery-dicrotic notch pressure: end-ejection volume ratio and was significant in only one of five patients by the RV peak pressure: end-ejection volume ratio (p<0.03). Therefore, it appears that the steady-state RV ESPVR defined by maximal elastance in patients with normal RV function is responsive to alterations in inotropic state and is more sensitive to alterations in RV function than the frequently used, more easily measured modifications of the RV ESPVR. (Circulation 1988;78:81-91) T he concept of the left ventricular (LV) endsystolic pressure-volume relation (ESPVR) has evolved substantially in complexity in recent years. However, there is a large body of experimental and clinical data showing that the LV ESPVR is relatively load independent and sensitive to changes in LV contractility and, hence, can serve as a clinically useful index of LV function. 1-15 In the isolated heart, the right ven-

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The left ventricular end-systolic pressure-dimension relation in patients with thalassemia major. A new noninvasive method for assessing contractile state.

Cited by 62 publications

References 44 publications

Assessment of left ventricular contractile state after anatomic correction of transposition of the great arteries.

Assessment of left ventricular contractile state after anatomic correction of transposition of the great arteries.

Electrocardiographic markers for the early detection of cardiac disease in patients with beta-thalassemia major

Human right ventricular end-systolic pressure-volume relation defined by maximal elastance.

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