Left Ventricular Midwall Mechanics Research Articles

Preoperative risk factors associated with left ventricular dysfunction after bariatric surgery

A large proportion of patients with severe obesity remain with left ventricular (LV) dysfunction after bariatric surgery. We assessed whether preoperative evaluation by echocardiography and inflammatory proteins can identify this high-risk group. In the Bariatric Surgery on the West Coast of Norway study, 75 patients (44 ± 10 years, body mass index [BMI] 41.5 ± 4.7 kg/m2) were prospectively evaluated by echocardiography and inflammatory proteins (high-sensitivity C-reactive protein [hsCRP], serum amyloid A [SAA] and calprotectin) before and one year after Roux-en-Y gastric bypass surgery. LV mechanics was assessed by the midwall shortening (MWS) and global longitudinal strain (GLS). Bariatric surgery improved BMI and GLS, and lowered hsCRP, calprotectin and SAA (p < 0.05). MWS remained unchanged and 35% of patients had impaired MWS at 1-year follow-up. A preoperative risk index including sex, hypertension, ejection fraction (EF) and high hsCRP (index 1) or SAA (index 2) predicted low 1-year MWS with 81% sensitivity/71% specificity (index 1), and 77% sensitivity/77% specificity (index 2) in ROC analyses (AUC 0.80 and 0.79, p < 0.001). Among individuals with severe obesity, women and patients with hypertension, increased serum levels of inflammatory proteins and reduced EF are at high risk of impaired LV midwall mechanics 1 year after bariatric surgery.ClinicalTrials.gov identifier NCT01533142 February 15, 2012.

Increased inflammatory proteins in patients with severe obesity is associated with persistent myocardial dysfunction one year after bariatric surgery. The FatWest study

Abstract Background Over half of patients with severe obesity have subclinical cardiac dysfunction and about 40% maintain impaired left ventricular (LV) mechanics one year after bariatric surgery despite impressive weight reduction. Purpose To investigate whether measurement of serum markers of chronic inflammation before bariatric surgery can help identify patients with persistent postoperative cardiac dysfunction. Methods In the prospective FatWest (Bariatric Surgery on the West Coast of Norway) study 75 patients with severe obesity (44±9 years, 72% women, body mass index [BMI] 41.5±4.7 kg/m², 56% with hypertension) underwent echocardiography before and 1 year after Roux-en-Y gastric bypass surgery. We assessed LV mechanics in the radial and longitudinal direction by the midwall shortening (MWS) and global longitudinal strain (GLS). Myocardial oxygen (O2) demand was derived from the LV mass-wall stress-heart rate product. Inflammation was assessed by high-sensitive C-reactive protein, serum amyloid A and calprotectin in biobank samples. Results Preoperatively, patients with low MWS (45% of the group) had increased high-sensitive C-reactive protein, total calprotectin, and several amyloid A isoforms, and patients with high myocardial O2 demand (20%) had high total calprotectin (all p&amp;lt;0.05). In the whole study population, bariatric surgery induced a significant improvement in both BMI (12.6±3.7 kg/m²), GLS (4.74±5.20%), myocardial O2 demand and inflammatory proteins (Figure A, all p&amp;lt;0.001). However, there were no significant improvement in MWS, and 33% of patients still had low MWS at the 1-year control. In logistic regression analyses, after adjustment for sex, BMI and hypertension, increased preoperative serum total calprotectin was independently associated with high myocardial O2 demand both pre- and postoperatively (Nagelkerke R² 0.47 and 0.51, p&amp;lt;0.05). In similar analyses, higher preoperative serum total amyloid A was related to low MWS and high myocardial O2 demand 1 year after surgery (Nagelkerke R² 0.55 and 0.51, p&amp;lt;0.05). A simple preoperative risk score based on sex, hypertension, biplane ejection fraction, and serum total amyloid A above 4.0 mg/ml predicted low 1-year MWS with 79% sensitivity and 75% specificity at a value of 1.75 in Receiver Operating Characteristic (ROC) analysis (AUC 0.80, p&amp;lt;0.001) (Figure B). Low GLS was not predicted by inflammatory biomarkers at any timepoint. Conclusion Increased serum concentration of inflammatory proteins in patients with severe obesity is linked to persistently elevated myocardial O2 demand and impaired LV midwall mechanics 1 year after bariatric surgery.Figure AFigure B

Incomplete functional reverse remodelling of the left ventricle one year after bariatric surgery. Insights from the prospective FatWest study

Abstract Background Patients with severe obesity are predisposed to development of left ventricular (LV) hypertrophy with subsequent increased myocardial oxygen demand and impaired myocardial function. Bariatric surgery leads to rapid weight loss and improves cardiovascular risk profile. Purpose To assess whether LV systolic function, wall mechanics, and cardiac power improve 1 year after bariatric surgery. Methods 91 severely obese patients (43±10 years, 70% women, body mass index [BMI] 41.7±4.9 kg/m2, 55% with hypertension, 17% with diabetes mellitus) underwent echocardiography before, 6 and 14 months after Roux-en-Y gastric bypass surgery in the prospective FatWest (Bariatric Surgery on the West Coast of Norway) study. We assessed LV systolic function by biplane ejection fraction (EF), LV wall mechanics by midwall shortening (MWS) and global longitudinal strain (GLS), and cardiac power normalized for LV mass by 0.222 x cardiac output x mean blood pressure (BP)/LV mass. Results Surgery induced a significant reduction in BMI, heart rate, systolic BP, and LV mass (Figure 1). Prevalence of LV hypertrophy fell from 34 to 20% 14 months after surgery (p&amp;lt;0.001), while that of concentric geometry remained stable: 8 vs 10% (p=0.36). GLS improved by 28%, however LV EF and MWS did not change (Figure 2). LV power at rest decreased postoperatively, reflecting the lower BP and heart rate, but was unaltered when normalized for LV mass (Figure 2). In backward stepwise multivariate regression analyses, 1 year improvement in GLS was predicted by the systolic BP reduction (p&amp;lt;0.05) (R2 0.73, p&amp;lt;0.001), while low 1-year MWS was independently associated with female gender, concentric geometry and higher myocardial oxygen demand (all p&amp;lt;0.01) (Nagelkerke R2 0.44, p&amp;lt;0.001), and lower 1-year LV power-mass with female gender and LV hypertrophy (p&amp;lt;0.01) (R2 0.24, p&amp;lt;0.001). Conclusion In severely obese patients, LV longitudinal function normalizes 1 year after bariatric surgery, mainly due to the BP reduction. LV midwall mechanics and power do not improve, especially in women and patients with persistent LV geometric abnormalities. Funding Acknowledgement Type of funding sources: None. Figure 1Figure 2

One-year impact of bariatric surgery on left ventricular mechanics: results from the prospective FatWest study.

AimsPatients with severe obesity are predisposed to left ventricular (LV) hypertrophy, increased myocardial oxygen demand, and impaired myocardial mechanics. Bariatric surgery leads to rapid weight loss and improves cardiovascular risk profile. The present prospective study assesses whether LV wall mechanics improve 1 year after bariatric surgery.Methods and resultsNinety-four severely obese patients [43 ± 10 years, 71% women, body mass index (BMI) 41.8 ± 4.9 kg/m2, 57% with hypertension] underwent echocardiography before, 6 months and 1 year after gastric bypass surgery in the FatWest (Bariatric Surgery on the West Coast of Norway) study. We assessed LV mechanics by midwall shortening (MWS) and global longitudinal strain (GLS), LV power/mass as 0.222 × cardiac output × mean blood pressure (BP)/LV mass, and myocardial oxygen demand as the LV mass-wall stress-heart rate product. Surgery induced a significant reduction in BMI, heart rate, and BP (P < 0.001). Prevalence of LV hypertrophy fell from 35% to 19% 1 year after surgery (P < 0.001). The absolute value of GLS improved by—4.6% (i.e. 29% increase in GLS) while LV ejection fraction, MWS, and LV power/mass remained unchanged. In multivariate regression analyses, 1 year improvement in GLS was predicted by lower preoperative GLS, larger mean BP, and BMI reduction (all P < 0.05). Low 1-year MWS was associated with female sex, preoperative hypertension, and higher 1-year LV relative wall thickness and myocardial oxygen demand (all P < 0.001).ConclusionIn severely obese patients, LV longitudinal function is largely recovered one year after bariatric surgery due to reduced afterload. LV midwall mechanics does not improve, particularly in women and patients with persistent LV geometric abnormalities.ClinicalTrials.gov identifierNCT01533142, 15 February 2012.

Depressed systemic arterial compliance and impaired left ventricular midwall performance in aortic stenosis with concomitant type 2 diabetes: a retrospective cross-sectional study

BackgroundDegenerative aortic stenosis (AS), a disease of the elderly, frequently coexists with concomitant diseases, including type 2 diabetes (T2DM) which amplifies the cardiovascular (CV) risk. T2DM affects left ventricular (LV) structure and function via hemodynamic and metabolic factors. In concentric LV geometry, typical for AS, indices of LV midwall mechanics are better estimates of LV function than ejection fraction (EF). Effects of T2DM coexisting with AS on circumferential LV midwall systolic function and large artery properties have not been reported so far. Our aim was to compare characteristics of AS patients with and without T2DM, with a focus on LV midwall systolic function and arterial compliance.MethodsMedical records of 130 electively hospitalized patients with moderate or severe isolated degenerative AS were retrospectively analyzed. Exclusion criteria included clinical instability, atrial fibrillation, coronary artery disease and relevant non-cardiac diseases. From in-hospital echocardiography and blood pressure, we calculated LV midwall fractional shortening (mwFS), circumferential end-systolic LV wall stress (cESS) and valvulo-arterial impedance (Zva), estimates of LV afterload, as well as systemic arterial compliance.ResultsPatients with (n = 50) and without T2DM (n = 80) did not differ in age, AS severity, LV mass and LV diastolic diameter. T2DM patients exhibited elevated cESS (247 ± 105 vs. 209 ± 84 hPa, p = 0.025) and Zva (5.8 ± 2.2 vs. 5.1 ± 1.8 mmHg per mL/m2, p = 0.04), and lower stroke volume index (33 ± 10 vs. 38 ± 12 mL/m2, p = 0.01) and systemic arterial compliance (0.53 ± 0.16 vs. 0.62 ± 0.22 mL/m2 per mmHg, p = 0.01). mwFS (11.9 ± 3.9 vs. 14.1 ± 3.7%, p = 0.001), but not EF (51 ± 14 vs. 54 ± 13%, p = n.s.), was reduced in T2DM. mwFS and cESS were inversely interrelated in patients both with (r = − 0.59, p < 0.001) and without T2DM (r = − 0.53, p < 0.001) By multiple regression, higher cESS (p < 0.001) and T2DM (p = 0.02) were independent predictors of depressed mwFS.ConclusionsIn AS, coexistent T2DM appears associated with reduced systemic arterial compliance and LV dysfunction at the midwall level, corresponding to slightly depressed myocardial contractility.

P2849Independent association between left ventricular midwall mechanics and global longitudinal strain in native hypertensive patients

P2849Independent association between left ventricular midwall mechanics and global longitudinal strain in native hypertensive patients

Left ventricular midwall mechanics at 24 weeks' gestation in high‐risk normotensive pregnant women: relationship to placenta‐related complications of pregnancy

Most studies during pregnancy have assessed maternal left ventricular (LV) function by load-dependent indices, assessing only chamber function. The aim of this study was to assess afterload-adjusted LV myocardial and chamber systolic function at 24 weeks' gestation and 6 months postpartum in high-risk normotensive pregnant women. A group of 118 high-risk women with bilateral notching of the uterine arteries underwent an echocardiographic examination to evaluate midwall mechanics (midwall shortening (mFS%) and stress-corrected midwall shortening (SCmFS%)) of the LV at 24 weeks' gestation and 6 months postpartum. Patients were followed until delivery and pregnancies were classified retrospectively as uneventful (uncomplicated outcome) or complicated. A control group of 54 low-risk women with uneventful pregnancies without bilateral notching was also enrolled. The pregnancy was uneventful in 74 (62.7%) women, whereas 44 (37.3%) developed complications. At 24 weeks' gestation, mFS% and SCmFS% were greater in the uncomplicated-outcome compared with the complicated-outcome group (25.9 ± 4.8 vs 18.8 ± 5.0%, P < 0.001 and 107.9 ± 18.4 vs 77.9 ± 20.7%, P < 0.001, respectively). At 6 months postpartum, SCmFS% remained greater in the uncomplicated-outcome compared with the complicated-outcome group (100.4 ± 21.6 vs 87.8 ± 19.1, P < 0.05). In the uncomplicated-outcome group, SCmFS% was higher during pregnancy than it was postpartum, whereas in the complicated-outcome group, it was lower during pregnancy than it was postpartum (P < 0.05). Maternal cardiac midwall mechanics appear to be enhanced (SCmFS% increased compared with controls) during pregnancy compared with postpartum in high-risk patients with uncomplicated pregnancy, whereas midwall mechanics are depressed both during pregnancy and postpartum in patients with pregnancy complications.

The effect of valsartan on left ventricular myocardial functions in hypertensive patients with left ventricular hypertrophy

It has been shown by various diagnostic methodologies that angiotensin receptor blockage reduces left ventricular mass, improves diastolic function and increases contractility in hypertensive left ventricular hypertrophy (LVH). We planned to detect the effect of angiotensin receptor blockage on midwall mechanics and myocardial dynamics in hypertensive patients with LVH. Angiotensin 2 type 1 receptor blocker (valsartan 80-160 mg) was administered to 38 previously untreated hypertensive patients with LVH for 6 months. Left ventricular midwall mechanics and tissue Doppler velocities were measured at baseline and at the end of the study. Mean blood pressure was reduced from 152 ± 14/92 ± 8 to 131 ± 14/83 ± 9 mmHg (P < 0.05). Left ventricular mass index was decreased from 135 ± 15 to 114 ± 14 g/m(2) (P < 0.001). Midwall fractional shortening was increased from 19.0 ± 4 to 22.4 ± 3% (P < 0.05). Circumferential end-systolic wall stress was decreased from 131 ± 44 to 119 ± 37 × 10(3) dyn/cm(2) (P < 0.05). Left ventricular interventricular septal myocardial tissue peak systolic velocity was increased from 6.7 ± 1 to 8.1 ± 0.9 cm/s (P < 0.001) and lateral wall myocardial tissue peak systolic velocity was increased from 7.5 ± 1 to 9.0 ± 1 cm/s (P < 0.001), and E/E(m) ratio was significantly decreased (11.0 ± 0.3 to 8.90 ± 0.1, P < 0.05) with 6-month valsartan therapy. This study suggests that valsartan exhibits not only blood pressure-lowering qualities but also cardioprotective actions in patients with hypertension because it enhances regression of LVH and improves left ventricular myocardial contractility and relaxation.

Adaptive and Maladaptive Cardiac Hypertrophy: What Is the Effective Role of Heat Shock Transcription Factor 1?

To the Editor: In the recent interesting article by Sakamoto et al,1 the authors found that rats undergoing exercise training showed lower degree of left ventricular (LV) hypertrophy, higher expression and activity of heat shock transcription factor 1 (HSF1), and preserved LV systolic function in comparison with rats exposed to sustained pressure overload by surgical constriction of the transverse aorta (TAC). They also observed that transgenic mice expressing constitutively active HSF1 showed less evident hypertrophic response and better systolic function than their wild-type littermates 5 weeks after TAC. Conversely, HSF1-deficient mice showed similar degree of LV hypertrophy but worse systolic function in comparison with their wild-type littermates after 4 weeks of exercise or 1 week after TAC. These data support the intriguing hypothesis that HSF1 upregulation in cardiac myocytes may play a key role in preventing LV systolic impairment in the exercise-induced hypertrophy model, and in determining the adaptive or maladaptive nature of the hypertrophic response. An important …

The Transition From Hypertrophy to Failure

Hypertensive heart disease is a major contributor to cardiovascular morbidity and mortality, especially in African Americans, in whom LV hypertrophy is 2 to 3-fold more common in the general population as compared with whites.1 In the classic paradigm of hypertensive heart disease, concentric hypertrophy (a nondilated, thick-walled left ventricle typically with a normal left ventricular ejection fraction [LVEF]) is a common precursor to LV failure (an increased LV volume with reduced LVEF).2 Although molecular triggers of this transition from concentric hypertrophy to failure have been the subject of intense investigation, there are no previous large, longitudinal cohort studies in humans demonstrating that this progression occurs frequently. The transition from concentric LV hypertrophy to failure has been well demonstrated in animal models including the spontaneously hypertensive rat,3 or after aortic banding4 or transgenic manipulation,5 and also in humans with aortic stenosis6 or familial hypertrophic cardiomyopathy.7 Whether this paradigm faithfully represents the natural history of hypertensive heart disease is not yet known (Figure). An alternative paradigm is that the LV response to elevated blood pressure is either hypertrophy or failure, with transition between the 2 uncommon in the absence of an interval cardiac injury. Potential pathways in progression of hypertensive heart disease. Hypertension can lead to concentric left ventricular hypertrophy (LVH), characterized by nondilated, thick-walled left ventricle (arrow, top left). After “transition to failure,” the LV is dilated with reduced LVEF. Coronary artery disease often via MI is a common contributor to this transition (first horizontal arrow). Whether concentric LVH commonly leads to low EF in absence of an interval MI or significant coronary artery disease is uncertain (second horizontal arrow). If LVH is not common precursor to LV …

Echocardiographic assessment of left ventricular midwall mechanics in spontaneously hypertensive rats

Echocardiographic assessment of left ventricular midwall mechanics in spontaneously hypertensive rats

Instantaneous assessment of left ventricular midwall mechanics with tissue Doppler tracking technique

BackgroundLeft ventricular (LV) systolic function is better characterized by midwall mechanics in patients with LV hypertrophy than by endocardial LV function, and the midwall mechanics is an independent predictor of prognosis. However, a complex calculation is currently required to assess it, and it is not routinely assessable in clinical practice. Tissue Doppler imaging enables tracking of a point within the LV wall though a cardiac cycle; we tested our hypothesis that the tissue Doppler tracking technique provides an instantaneous and reliable evaluation of midwall mechanics. MethodsLV M-mode echocardiogram was recorded in 18 subjects with conventional echocardiography and with tissue Doppler imaging. The midwall shortening was calculated from the data obtained with conventional echocardiography for the comparison with that measured with the tissue Doppler tracking technique. The tissue Doppler-determined midwall shortening correlated well with conventionally calculated value (r=.84, P<.0001), and their difference was small irrespective of absolute value of the midwall shortening. ConclusionsThe midwall mechanics can be instantaneously and accurately evaluated with the tissue Doppler tracking technique.

The relation between left ventricular geometric patterns and left ventricular midwall mechanics in hypertensive patients.

To evaluate the alteration of myocardial contractility in hypertensive patients with different left ventricular geometric patterns by the end-systolic stress-midwall fractional shortening relation. Echocardiography was applied to study the left ventricular geometry and cardiac function among 117 cases of essential hypertension, with 45 normal cases as control(s). Left ventricular mass index (LVMI) and relative wall thickness (RWT) were calculated using echocardiographic data. All patients were divided into four kinds of left ventricular geometry pattern based on LVMI and RWT. Patients of the eccentric hypertrophy group suffered the most serious damage of left ventricular systolic function. Myocardial contractility shown by end-systolic stress-midwall fractional shortening relation was significantly decreased in the concentric remodeling group, eccentric hypertrophy group and concentric hypertrophy group, and those with concentric hypertrophy showed the worst contractility. The degree of myocardial contractility damage was different in patients with different left ventricular geometric patterns. Geometric changes may have compensated for the reduction of myocardial contractility in some phases in order to maintain the normal pump function.

Relationship between left ventricular midwall mechanics and natriuretic peptide in patients with hypertension

Relationship between left ventricular midwall mechanics and natriuretic peptide in patients with hypertension

Ventricular and myocardial function following treatment of hypertension

This study assesses and evaluates left ventricular (LV) contractile function after treatment of hypertension, with an emphasis on LV midwall mechanics. Although prior studies have assessed cardiac function after hypertension treatment, none has performed an analysis of LV midwall mechanics. The Veterans Affairs Study of monotherapy in hypertension was a study large enough to permit analysis of midwall mechanics across a wide spectrum of mass changes accompanying hypertension treatment. LV chamber function was assessed by computing fractional shortening at the endocardial surface; LV midwall shortening was used to define myocardial function. Both shortening indexes were related to end-systolic circumferential stress in the entire population by partitioning values of mass and relative wall thickness changes. Two hundred sixty-eight patients were studied at baseline and again after a 1- or 2-year period. In the entire group, there was no significant change in circumferential shortening either at the endocardium (38 ± 8% at baseline vs 37 ± 7% at follow up, p = 0.29) or in shortening at the midwall (20 ± 3% vs 20 ± 3%, p = 0.53). However, 83 patients had a reduction in relative wall thickness and an increase in midwall shortening. The change in midwall shortening was significantly related to changes in relative wall thickness (r = −0.53, p = 0.0001). Thus, reductions in LV mass associated with antihypertensive therapy are generally not accompanied by a decrement in LV chamber or myocardial function. Improvement in midwall shortening is more closely related to normalization of LV geometry than to reduction in LV mass.

Left Ventricular Midwall Mechanics in Healthy Children and Adolescents

The assessment of left ventricular function in pediatric age generally has been made by measuring the extent and velocity of fiber shortening at the endocardium and relating these parameters to systolic wall stress. It has been suggested from animal and human studies that this “endocardial method” can result in an overestimation of myocardial function when healthy hearts and those with hypertrophy are compared. Thus an assessment of left ventricular pump function and contractility that takes into account the epicardial migration of the midwall circumferential fibers during systole (midwall analysis) is warranted. Although the normal range for midwall indexes of left ventricular mechanics has been established in adult subjects, up to now it has not been studied in pediatric subjects. To establish normal values for left ventricular midwall mechanics, 70 healthy children ranging in age from 3 days to 18 years were evaluated with 2-dimensional and M-mode echocardiography. Midwall fractional shortening (FSmw), rate-corrected mean velocity of circumferential fiber shortening (VCFcmw), and the relation between these indexes and left ventricular end-systolic wall stress (ESS) were calculated separately for the children younger than 2 (group 1, 20 subjects) and older than 2 (group 2, 50 subjects) years of age. Group 1 had significantly higher FSmw and VCFcmw compared with group 2. An inverse linear relation between FSmw and ESS and between VCFcmw and ESS was found in both age groups. The y-intercept was higher in group 1, and the slope of the mean regression line was steeper than in group 2 for both the relationships, suggesting an age-dependent midwall left ventricular pump function and contractility. These normative data can be used to assess the left ventricular midwall mechanics in pediatric patients with pressure or volume overload. (J Am Soc Echocardiogr 1999;13:932-40.)

Left ventricular midwall mechanics in systemic arterial hypertension. Myocardial function is depressed in pressure-overload hypertrophy.

Left ventricular (LV) midwall geometry has been described conventionally as the sum of the chamber radius and half of the wall thickness; this convention is based on the assumption of uniform transmural thickening during systole. However, theoretical considerations and experimental data indicate that the inner half (inner shell) of the LV wall thickens more than the outer half (outer shell). Thus, an end-diastolic circumferential midwall fiber exhibits a relative migration toward the epicardium during systole. As a result, the conventional method provides an overestimate of the extent of the midwall fiber shortening. We developed an ellipsoidal model with a concentric two-shell geometry (nonuniform thickening) to assess midwall fiber length transients throughout the cardiac cycle. This modified midwall method was used in the analysis of LV cineangiograms from 15 patients with systemic arterial hypertension and 14 normal subjects. Study groups were classified according to LV mass index (LVMI): 14 normal subjects (group I), eight hypertensive patients with a normal LVMI (group II), and seven hypertensive patients with an increased LVMI (group III). There were no significant differences in LV end-diastolic pressure or volume among the three groups; the ejection fraction was slightly greater in group II (70 +/- 5%) than in groups I (65 +/- 8%) and III (66 +/- 4%), but this trend did not achieve statistical significance. Values for endocardial and conventional midwall fractional shortening (FS) were also similar in the three groups. By contrast, FS by the concentric two-shell geometry (modified midwall method) in group III (16 +/- 2%) was significantly less than that seen in groups I and II (21 +/- 4% and 21 +/- 5%, respectively; both p less than 0.05). This difference achieves greater importance when it is recognized that mean systolic circumferential stress was lower in group III (151 +/- 22 g/cm2) than in groups I and II (244 +/- 37 g/cm2 and 213 +/- 38 g/cm2, respectively; both p less than 0.01). The midwall stress-shortening coordinates in six of the seven group III patients were outside the 95% confidence limits for the normal (group I) subjects. Thus, despite a normal ejection fraction, systolic function is subnormal in hypertensive patients with LV hypertrophy. Chamber dynamics provide an overestimate of myocardial function, especially when LV wall thickness is increased. This is due to a relatively greater contribution of inner shell thickening in pressure-overload hypertrophy.

Assessing the results of surgery for congenital heart disease: a continuing process.

HomeCirculationVol. 65, No. 6Assessing the results of surgery for congenital heart disease: a continuing process. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBAssessing the results of surgery for congenital heart disease: a continuing process. T P GrahamJr T P GrahamJrT P GrahamJr Search for more papers by this author Originally published1 Jun 1982https://doi.org/10.1161/01.CIR.65.6.1049Circulation. 1982;65:1049–1051 Previous Back to top Next FiguresReferencesRelatedDetailsCited By McManus A and Leung M (2000) Maximising the Clinical Use of Exercise Gaseous Exchange Testing in Children With Repaired Cyanotic Congenital Heart Defects, Sports Medicine, 10.2165/00007256-200029040-00002, 29:4, (229-244), . Calabrò R, Pisacane C, Pacileo G and Russo M (1999) Left Ventricular Midwall Mechanics in Healthy Children and Adolescents, Journal of the American Society of Echocardiography, 10.1016/S0894-7317(99)70146-X, 12:11, (932-940), Online publication date: 1-Nov-1999. Abe T, Morikawa M, Komatsu S, Morita K, Kubota M and Tsuda T (2011) Noninvasive evaluations of pulmonary circulation, cardiac function, and liver excreting rate at late follow-up following the modified Fontan operation, International Journal of Angiology, 10.1007/BF01616276, 7:01, (46-51) Norgård G, Andersen K and Vik-Mo H (2008) Echocardiographic assessment of left ventricular function at rest and during exercise in postoperative patients with tetralogy of Fallot, Cardiology in the Young, 10.1017/S1047951100011173, 4:3, (267-276), Online publication date: 1-Jul-1994. Franklin R, Wyse R, Graham T, Gooch V and Deanfield J (1990) Normal values for noninvasive estimation of left ventricular contractile state and afterload in children, The American Journal of Cardiology, 10.1016/0002-9149(90)90819-M, 65:7, (505-510), Online publication date: 1-Feb-1990. Moreau G and Graham T (1989) Clinical Assessment of Ventricular Function After Surgical Treatment of Congenital Heart Defects, Cardiology Clinics, 10.1016/S0733-8651(18)30447-8, 7:2, (439-452), Online publication date: 1-May-1989. Sandor G, Puterman M, Patterson M, Tipple M and Vince D (1986) Effect of pressure loading, volume loading and surgery on left ventricular chamber and myocardial stiffness in congenital heart disease, with a reevaluation of normal pediatric values, Journal of the American College of Cardiology, 10.1016/S0735-1097(86)80053-5, 8:2, (371-378), Online publication date: 1-Aug-1986. Del Torso S, Kelly M, Kalff V and Venables A (1985) Radionuclide assessment of ventricular contraction at rest and during exercise following the fontan procedure for either tricuspid atresia or single ventricle, The American Journal of Cardiology, 10.1016/0002-9149(85)90649-6, 55:9, (1127-1132), Online publication date: 1-Apr-1985. Ishikawa T, Neutze J, Brandt P and Barratt-Boyes B (1984) Hemodynamics following the Kreutzer procedure for tricuspid atresia in patients under two years of age, The Journal of Thoracic and Cardiovascular Surgery, 10.1016/S0022-5223(19)38324-2, 88:3, (373-379), Online publication date: 1-Sep-1984. Ramsay J, Venables A, Kelly M and Kalff V (1984) Right and left ventricular function at rest and with exercise after the Mustard operation for transposition of the great arteries., Heart, 10.1136/hrt.51.4.364, 51:4, (364-370), Online publication date: 1-Apr-1984. Peterson R, Franch R, Fajman W, Jennings J and Jones R (1984) Noninvasive determination of exercise cardiac function following Fontan operation, The Journal of Thoracic and Cardiovascular Surgery, 10.1016/S0022-5223(19)38362-X, 88:2, (263-272), Online publication date: 1-Aug-1984. June 1, 1982Vol 65, Issue 6 Advertisement Article InformationMetrics Copyright © 1982 by American Heart Associationhttps://doi.org/10.1161/01.CIR.65.6.1049 Originally publishedJune 1, 1982 PDF download Advertisement