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Cardiac dysfunction in patients with systemic lupus erythematosus and antiphospholipid syndrome.

OBJECTIVE: To comparatively assess the parameters of systolic and diastolic cardiac function in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). METHODS: Consecutive patients (n=74) who were free of cardiovascular symptoms were divided into four groups: (1) SLE (n=23); (2) SLE with antiphospholipid antibodies (aPL; n=18); (3) SLE with APS (n=20); and (4) primary antiphospholipid syndrome (PAPS; n=13). Pulsed, continuous, colour Doppler echocardiography, and M-mode and B-mode studies were performed. RESULTS: Left ventricular end diastolic and end systolic dimensions were higher in SLE as compared with patients with PAPS (p=0.022 and 0.022, respectively), with a trend towards a lower fractional shortening in SLE (p=0.07), suggesting systolic dysfunction. Parameters of diastolic function were more impaired in patients with APS, reflected by lower left ventricular and right ventricular E wave to A wave (E:A) ratios in patients with APS (groups 3, 4) compared with those without APS (groups 1, 2; 1.15 (0.40) v 1.49 (0.43), p=0.001 and 1.19 (0.31) v 1.49 (0.41), p=0.001, respectively) and a more prolonged left ventricular isovolumic relaxation time (IVRT; 94.2 (24.6) v 84.4 (17) ms, respectively, p=0.055). Patients with APS were older than those without APS (47.12 (14.86) v 34.29 (12.6), p=0.0001). Patients with SLE were younger than those with PAPS (38.19 (14.68) v 48.53 (13.97), p=0.023). CONCLUSION: Abnormal echocardiographic findings were detected frequently in asymptomatic patients with SLE or PAPS. Although patients with SLE were younger, left ventricular systolic function was more impaired in patients with SLE compared with those with PAPS, whereas left ventricular and right ventricular diastolic function, as reflected by IVRT and E:A ratios, were significantly more impaired in patients with APS.

Adult↗

New index of combined systolic and diastolic myocardial performance: a simple and reproducible measure of cardiac function--a study in normals and dilated cardiomyopathy.

BACKGROUND: Because systolic and diastolic dysfunction frequently coexist, it is hypothesized that a combined measure of left ventricular chamber performance may be more reflective of overall cardiac dysfunction than systolic or diastolic measures alone. METHODS Study patients consisted of 170 subjects: 70 normals, 47 patients with severe dilated cardiomyopathy in NYHA class III-IV awaiting cardiac transplantation and 53 patients with idiopathic dilated cardiomyopathy of intermediate severity [NYHA class II, ejection fractions (EF) 30-50%]. EF, stroke volume and cardiac indexes were measured using conventional echo-Doppler methods. Pre-ejection period/ejection time (PEP/ET), isovolumetric relaxation time (IRT), isovolumetric contraction time/ET (ICT/ET) were also measured. A new derived index of myocardial performance: (ICT+IRT)/ET, was obtained by subtracting ET from the interval between cessation and onset of the mitral inflow velocity to give the sum of ICT and IRT. RESULTS The index was easily measured, reproducible, and had a narrow range in normals. The mean value of the index was significantly different between normal, intermediate and pre-transplant subjects (0.39 +/- 0.05, 0.59 +/- 0.10 and 1.06 +/- 0.24, respectively, p < 0.001 for all comparisons). The degree of inter-group overlap was smaller for the index compared to PEP/ET, ICT/ET and other parameters. Within functional groups, the value of the index did not appear to be related to heart rate, mean arterial pressure and the degree of mitral regurgitation. CONCLUSION (ICT+IRT)/ET is a conceptually new, simple and reproducible Doppler index of combined systolic and diastolic myocardial performance in patients with primary myocardial systolic dysfunction.

Adult↗

The prognostic value of QTc interval and QT dispersion following myocardial infarction in patients treated with or without dofetilide.

BACKGROUND: Acute myocardial infarction (MI) is associated with an increased risk of death, with a 1-year mortality close to 10% in patients discharged from hospital alive. During the first year following MI, close to 50% of deaths are assumed to be due to arrhythmic events. HYPOTHESIS: The study was undertaken to determine the interaction between dofetilide treatment and pretreatment QTc interval and QT dispersion regarding mortality in patients with left ventricular (LV) dysfunction and a recent MI. METHODS: The study population consisted of 894 patients with a recent MI and LV systolic dysfunction, who were randomized to receive dofetilide or placebo. The study was a substudy of the Danish Investigations of Arrhythmia and Mortality on Dofetilide-MI (DIAMOND-MI). RESULTS: During a minimum of 1-year follow-up, 261 (29%) patients died. Baseline QTc interval did not hold any prognostic value on mortality for placebo-treated patients. When pretreatment QTc interval was <429 ms, dofetilide resulted in a 45% reduction of mortality (hazard ratio 0.55, 95% confidence limits 0.34-0.88, p<0.02) compared with placebo. When QTc interval was >429 ms, dofetilide did not influence mortality significantly. This study revealed no statistically significant relation between QT dispersion, dofetilide treatment, and mortality. CONCLUSION: In patients with a recent MI, LV dysfunction, and a short baseline QTc interval, dofetilide is associated with significant survival benefit. This benefit is not seen with a longer QTc interval. QT dispersion is not a risk factor in this population.

Aged↗

Diminished contractile reserve in patients with left ventricular hypertrophy and increased end-systolic stress during Dobutamine stress echocardiography.

Left ventricular hypertrophy (LVH) is associated with decreased contractile response to inotropic stimulation in animal models, but this has not been documented in humans. To determine whether LVH is associated with decreased myocardial contractile reserve, we measured left ventricular mass, heart rate-corrected velocity of circumferential fiber shortening (Vcfc), end-systolic stress, and LV ejection fraction (LVEF) in patients with LVH and increased end-systolic stress (n = 6) and in patients without LVH (n = 7) who had a normal response to dobutamine stress echocardiography (increased LVEF and no wall motion abnormalities). The afterload-dependent indexes of left ventricular systolic performance were normal at baseline and showed significant increases at peak dobutamine dose (LVH group: Vcfc 0.91 +/- 0.11 to 1.76 +/- 0.59, p = 0.006; LVEF 49 +/- 5 to 65 +/- 6, p = 0.001; group without LVH: Vcfc 1.16 +/- 0.24 to 1.99 +/- 0.36, p = 0.001; LVEF 61 +/- 6 to 68 +/- 6, p = 0.05). The Vcfc/ end-systolic stress relation, a load-independent index of myocardial contractility, rose in a dose-dependent fashion in both groups, but the increment was significantly less for patients with LVH (p < 0.02), suggesting a blunted myocardial contractile reserve to inotropic stimulation. The change in heart rate-corrected velocity of circumferential fiber shortening per unit of change in end-systolic stress in each patient at each dobutamine dose showed a linear and inverse relationship. The increment in heart rate-corrected velocity of circumferential fiber shortening for a given reduction in end-systolic stress was larger in patients without LVH than in patients with LVH (p = 0.01). These results suggest that in patients with LVH and increased end-systolic stress, ventricular performance is maintained at the expense of limited myocardial contractile reserve, and that inotropic stimulation unmasks this abnormality, despite a normal response in LVEF and velocity of circumferential fiber shortening. This approach may identify patients with LVH at risk of developing systolic dysfunction and heart failure.

Adult↗

Geometric changes of mitral annulus assessed by real-time 3-dimensional echocardiography: becoming enlarged and less nonplanar in the anteroposterior direction during systole in proportion to global left ventricular systolic function.

OBJECTIVE: We sought to investigate the geometric changes of the mitral annulus during systole in relation to global left ventricular (LV) systolic function using real-time 3-dimensional (3D) echocardiography. METHODS: Real-time 3D echocardiography was performed in 23 patients with global LV systolic dysfunction with ejection fraction of 37 +/- 19% and 9 control subjects with ejection fraction of 62 +/- 4%. Volumetric data were divided into 9 rotational apical planes (angle increment = 20 degrees) using 3D software. Nine rotational annular dimensions (ADs) were measured in all planes in early and late systole. Nonplanar angle (NPA) of the annulus between two vectors from two hinge points of the annulus in the anteroposterior plane to the center between two commissures in the commissure-commissure plane was measured during early and late systole. Fractional changes of NPA and AD were defined as changes in percentage during systole. RESULTS: NPA significantly increased during systole (early, 145 +/- 12 degrees; late, 160 +/- 9 degrees; P < .01). Among 9 ADs, 3 anteroposteriorly directed ADs showed the most prominent fractional increases during systole in all patients. Both fractional changes of NPA ( R 2 = 0.87, P < .01) and the anteroposterior dimension, AD 1 ( R 2 = 0.85, P < .01) showed significant positive correlation with global LV systolic function. CONCLUSIONS: Real-time 3D echocardiography demonstrated that saddle shape of the mitral annulus was getting enlarged and less nonplanar mainly in the anteroposterior direction during systole. These geometric changes were proportional to the global LV systolic function.

Adult↗

Heart failure from diastolic dysfunction.

Heart failure from diastolic dysfunction is a clinical syndrome similar to, but distinct from, failure from systolic dysfunction. Because the standard cardiac diagnostic tools may not be helpful, the advance practice nurse and physician collaborate on the diagnosis. Interventions are aimed toward improving diastolic filling and reducing hemodynamic compromise for these patients.

Critical Care↗

Treatment of congestive heart failure--state of the art and future trends.

1. Cardiac failure is a clinical syndrome of symptoms and signs, which can be confirmed by imaging or invasive haemodynamic techniques. It may be caused by systolic or diastolic dysfunction, but systolic dysfunction rarely occurs alone. It is important to ascertain the degree to which each contributes, and the precise aetiology of the condition, particularly in relation to surgically correctable lesions. 2. Non-pharmacological approaches including weight loss, salt restriction and lifestyle changes may be beneficial in some patients, and diuretics, which reduce the load on the heart, are the traditional baseline therapy. 3. Digitalis has been used where problems with contractility predominate, but its beneficial effect has been disputed, and expectations of improvement in patients in sinus rhythm should not be too high. 4. Vasodilators have been considered as the next line of treatment. Arteriolar dilators tend to increase cardiac output, but have little effect on pulmonary artery wedge pressure, and venodilators tend to have the opposite effect. Probably both actions are necessary and angiotensin converting enzyme (ACE) inhibitors, which have both, have proved effective in terms of symptoms and survival. 5. Various other inotropic agents have been tried. Phosphodiesterase inhibitors improve exercise tolerance, but may increase the probability of serious arrhythmias, already a significant cause of sudden death. beta 1-partial adrenoceptor agonists such as xamoterol have shown some promise, and anti-arrhythmic therapy has also been considered. 6. Drugs which prevent progression of myocardial damage would prove a great advance, and beta-adrenoceptor antagonists and calcium channel blockers appear to have considerable potential in this area.

Adrenergic beta-Agonists↗

From hypertension to heart failure.

The prevalence of heart failure is increasing in modern societies. Hypertension is a major contributor to the development of heart failure, whether through the development of left ventricular hypertrophy and diastolic dysfunction or by promoting atherosclerosis and myocardial infarction, which eventually leads to systolic dysfunction and left ventricular dysfunction. Effective therapy for hypertension can prevent more than 50% of heart failure events. Most studies done in the last three decades have used b blockers with diuretics as the modality of therapy. These agents have been shown to effectively prevent the development of heart failure. More recent comparative studies have shown that use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are also effective in preventing heart failure. Calcium channel blockers, however, seem to be less effective in preventing development of heart failure in patients with hypertension. It needs to be emphasized that the most important variable in preventing heart failure is the appropriate treatment of hypertension.

Adrenergic beta-Antagonists↗

Transient Ca2+ overload alters Ca2+ handling in rat cardiomyocytes: effects on shortening and relaxation.

Transient Ca2+ overload in cardiomyocytes occurs during pathophysiological conditions. The aim of the present study was to investigate the effects of transient Ca2+ overload on shortening and relaxation in isolated rat cardiomyocytes electrically stimulated at 0.5 Hz and to examine whether transient Ca2+ overload induces alterations in Ca2+ handling and myofilament sensitivity. Fractional shortening and shortening velocity fell to 79 +/- 5% (P < 0.05) and 78 +/- 4% (P < 0.01) 2 min after exposure to high Ca2+. A transient decrease in resting length, a reduction in relaxation velocity to 86 +/- 7% (P < 0.05), and a prolonged time of relaxation with 8.3 +/- 4.3% (P < 0.05) were also observed. Systolic fluorescence ratio using fura 2 as the Ca2+ indicator fell by 11.0%, and the decline of the fluorescence ratio was prolonged by 29.8%. By applying caffeine, we observed a significant reduction in sarcoplasmic reticulum Ca2+ content after transient Ca2+ overload. A significant reduction in myofilament sensitivity was also observed. In conclusion, the systolic dysfunction observed after transient Ca2+ overload is the result of both decreased systolic Ca2+ and reduced myofilament sensitivity. The relaxation abnormalities are most likely caused by altered Ca2+ handling, since we observed a reduction in the sarcoplasmic reticulum Ca2+ content and a prolongation of the decline of the fura 2 transient.

Adenosine Triphosphate↗

Influence of coronary occlusion during PTCA on end-systolic and end-diastolic pressure-volume relations in humans.

The influence of acute coronary occlusion on systolic and diastolic left ventricular pressure-volume relations was studied in 10 patients undergoing percutaneous transluminal coronary angioplasty (PTCA). Pressure-volume relations were obtained by conductance catheter and micromanometer techniques and with volume load altered by transient inferior vena caval occlusion. End-systolic and end-diastolic pressure-volume relations were obtained at baseline, during 60-90 seconds of ischemia, and at return to baseline after angioplasty balloon deflation. Coronary occlusion significantly altered systolic and diastolic chamber function. Systolic dysfunction was characterized by a reproducible rightward shift of the end-systolic pressure-volume relation (+25.4 +/- 18.4 ml) that was greater for proximal left anterior descending and circumflex coronary artery occlusions (+41 ml) than for distal or right coronary artery occlusions (+15.4 ml, p less than 0.05). Occlusion also lowered chamber systolic function indexes, such as the end-systolic pressure-volume relation slope (from 4.2 to 2.8 mm Hg/ml) and preload recruitable stroke work (from 97 to 78.6 mm Hg). All systolic (and diastolic) changes were resolved with successful angioplasty. Diastolic abnormalities during angioplasty were characterized by prolonged pressure relaxation and an upward shift of the resting diastolic pressure-volume data and by an apparent increase in chamber elastic stiffness. However, when end-diastolic data from multiple beats during inferior vena caval occlusion were compared, control and ischemic end-diastolic pressure-volume relations displayed little or no difference. Thus, elevations in resting diastolic pressure-volume relations and apparent increase in chamber elastic stiffness during coronary occlusion in humans appear dominated by altered right ventricular or pericardial loading. These data indicate that pressure-volume analysis is useful in assessing the functional significance of coronary lesions and reperfusion.

Angioplasty, Balloon, Coronary↗

Cardiac function of patients with essential hypertension during exercise and isoproterenol infusion.

The left ventricular function of patients with essential hypertension was examined during exercise and isoproterenol (ISP) infusion echocardiography. Twenty-eight hypertensive patients without cardiac hypertrophy (Group NH), 20 patients with cardiac hypertrophy (Group HH), 7 patients with cardiac dilatation (Group D), and 13 normotensives (Group N), were studied during multistage exercise using a supine bicycle ergometer. In addition, 23 hypertensives (Group NH: 13 patients, Group HH: 10 patients) and 10 normotensives were studied during ISP infusion (0.005 microgram/kg/min, and 0.01 microgram/kg/min, respectively, for 5 min). To assess the left ventricular function, an M-mode echocardiogram was utilized at rest and during exercise and ISP infusion. At rest, the isovolumic relaxation time (IRT) of each hypertensive group was significantly longer than that of Group N. IRT of Group HH and Group D was significantly longer than that of Group NH. Only the shortening fraction (SF) of Group D was significantly smaller than that of Group N. During exercise the SF increased in all groups, and only the SF of Group D was significantly smaller than that of Group N at a load of 75 W as well as at rest. The SF of Group HH tended to be smaller. There was no significant difference in peak negative dD/dt (-dD/dt) between any of the groups at rest; however, the -dD/dt of Group HH was significantly smaller than that of Group N during ISP infusion. We concluded that left ventricular diastolic function was disturbed in each hypertensive group at rest. Diastolic dysfunction worsened in Group HH and Group D. Only the left ventricular systolic function of Group D was already depressed at rest. Furthermore, unmanifested systolic dysfunction of the left ventricle seemed to be present in Group HH, because SF during exercise tended to be smaller and -dD/dt during ISP infusion was significantly smaller than that of Group N.

Adult↗

Prevalence and implications of diastolic dysfunction after subarachnoid hemorrhage.

INTRODUCTION: Electrocardiographic changes, troponin release, and reduced left ventricular ejection fraction have been described after subarachnoid hemorrhage (SAH). Little is known about the occurrence of diastolic dysfunction in this setting. The purpose of this study was to determine the prevalence of diastolic dysfunction and its association with cardiac outcomes after SAH. METHODS: SAH patients were prospectively enrolled into the study, and echocardiographic, clinical, chest X-ray, and cardiac troponin I data were obtained on days 1, 3, and 6 after enrollment. Each echocardiogram included Doppler recordings of mitral inflow and pulmonary venous flow. For each study, diastolic function was categorized as normal, impaired relaxation, pseudonormal, or restrictive. The relationships between diastolic dysfunction and pulmonary edema-elevated cardiac troponin I and left ventricular contractile dysfunction were quantified using both univariate and multivariate statistical methods. Clinical predictors of diastolic dysfunction were defined by multivariate logistic regression. RESULTS: Of 223 enrolled subjects, 207 had technically adequate Doppler data. Diastolic dysfunction was observed in 71% of subjects. The prevalence of diastolic versus systolic dysfunction in 44 patients with pulmonary edema was 91 versus 37%, respectively (p=0.001). After multivariate statistical adjustment, diastolic dysfunction remained a significant predictor of pulmonary edema (odds ratio [OR] 3.34, 95% CI=1.05-10.59). Diastolic dysfunction also was associated with troponin release (p=0.02). A history of hypertension and increasing age were predictive of diastolic dysfunction. CONCLUSION: Diastolic dysfunction is common after SAH. It is associated with history of hypertension and older age and may explain the development of pulmonary edema in many SAH patients.

Adult↗

Thermal therapy for congestive heart failure: estimation by TEI index.

Systolic dysfunction commonly coexists with diastolic dysfunction in patients with congestive heart failure due to myocardial disease. Also, right ventricular dysfunction is frequently associated with left ventricular dysfunction. The Doppler total ejection isovolume (TEI) index, a combined measurement of systolic and diastolic myocardial performance, is more reflective of overall cardiac function than systolic or diastolic function alone in both ventricles, and provides a conceptually new measure of global cardiac function. Single sauna bathing improves acute hemodynamics and repeated sauna therapy improves cardiac function and clinical symptoms in patients with heart failure. More recently, improvement of vascular endothelial function were observed by repeated sauna therapy in patients with heart failure. The TEI index, combining systolic and diastolic myocardial function, is a promising tool for the quantitative assessment of global cardiac function before and after thermal therapy.

Diastole↗

[Incidence of myocarditis in patients with dilated cardiomyopathy].

We performed right ventricular endomyocardial biopsies in 23 patients with dilated cardiomyopathy aged 45 +/- 14 years. All patients had congestive heart failure of unknown etiology dating up to one year before the procedure (57% less than 3 months). NYHA functional class was II in 5, III in 12 and IV in 6 patients. All patients had evidence of systolic dysfunction and a dilated left ventricle (LV diastolic dimension 68 +/- 11 and systolic dimension 55 +/- 11). Definite evidence of myocarditis, based on findings of inflammatory infiltrate and cellular damage, was found in 6 patients (26%), borderline myocarditis in 9 and abnormalities consistent with dilated cardiomyopathy in 8. The incidence of myocarditis here reported is lower than previously figures based on findings of more than 5 lymphocytes per high power field. In this series, clinical and functional aspects of heart failure did not differ in patients with or without evidence of myocarditis.

Adolescent↗

Brief communication: Outcomes of subsequent pregnancy after peripartum cardiomyopathy: a case series from Haiti.

BACKGROUND: Maternal risks with pregnancies after an index diagnosis of peripartum cardiomyopathy (PPCM) are inadequately understood. OBJECTIVE: To describe the clinical outcomes of subsequent pregnancy in Haitian women with PPCM. DESIGN: Prospectively identified cases from a defined population base, 2000-2005. SETTING: Hôpital Albert Schweitzer, Deschapelles, Haiti. PATIENTS: 15 patients with PPCM and subsequent pregnancies among 99 prospectively identified patients with PPCM. MEASUREMENTS: Clinical and echocardiographic parameters. RESULTS: Fifteen women with PPCM had 16 subsequent pregnancies after the index pregnancies. Eight of these patients experienced worsening heart failure; of these, 1 died and 1 regained normal left ventricular systolic function. Seven patients tolerated pregnancy without worsening heart failure, and ventricular function recovered in these patients within 30 months after the subsequent pregnancy. LIMITATIONS: The results may not apply to non-Haitian women, and power was insufficient to identify factors that might predict recovery (n = 15). CONCLUSIONS: Half of the women with subsequent pregnancy after PPCM experienced worsening heart failure and long-term systolic dysfunction, while the other half experienced no deterioration and regained normal left ventricular systolic function.

Adult↗

Tissue Doppler imaging predicts left ventricular dysfunction and mortality in a murine model of cardiac injury.

AIMS: Currently available non-invasive imaging methods frequently fail to detect alterations in left ventricular (LV) function despite histological evidence of injury. Tissue Doppler imaging (TDI) can detect subtle LV dysfunction. The aim of this study was to investigate whether TDI indices can predict LV systolic dysfunction and mortality following exposure to doxorubicin (DOX) in mice. METHODS AND RESULTS: TDI-derived peak endocardial systolic velocity (V(ENDO)) and strain rate (SR), as well as M-mode and two-dimensional indices of LV systolic function, were measured serially in mice after receiving DOX as a single dose (20 mg/kg). Haemodynamic measurements were obtained invasively before and at 1, 2, 4, and 5 days after the single DOX dose. Cardiac apoptosis was measured before and at 1 day after DOX. V(ENDO) and SR decreased after 1 and 2 days, respectively, whereas changes in fractional shortening (FS) and LV ejection fraction (LVEF) were not detected before 5 days. The reduction in both V(ENDO) and SR correlated with the decrease in dP/dt(MAX), and the change in V(ENDO) correlated with the early increase in cardiac cell apoptosis. In a subsequent experiment, DOX was administered at 4 mg/kg/week for 5 weeks, and LV function was followed serially for 16 weeks. In this chronic experiment, TDI indices decreased before FS and LVEF, correlated with late LV dysfunction, and predicted DOX-induced mortality. CONCLUSION: In a murine model of DOX-induced cardiac injury, TDI detects LV dysfunction prior to alterations in conventional echocardiographic indices and predicts mortality. This study suggests that TDI may be a reliable tool to detect early subtle changes in DOX-induced cardiac dysfunction.

Animals↗

Effect of revascularization on left ventricular remodeling in patients with heart failure from severe chronic ischemic left ventricular dysfunction.

Few data exist regarding the effect of revascularization on left ventricular (LV) geometry in patients with severe LV systolic dysfunction and viable myocardium. We hypothesized that patients with chronic ischemic LV dysfunction but viable myocardium will have improved LV geometry after revascularization, which in turn will improve long-term outcome. Accordingly, 70 patients with severe ischemic LV dysfunction (LV ejection fraction <0.35) were studied at rest. They then either underwent revascularization (n = 36) or were treated medically (n = 34). Fifty-four patients had viable myocardium, and 16 did not. They were evaluated for change in LV function and geometry (size and shape) a mean of 21 months later. Further follow-up was performed for a mean of 3.5 years to determine outcome. Patients with viable myocardium had improvement not only in regional and global function, but also in LV geometry (shape and size), which was independent of and incremental to the improvement in function. On long-term follow-up, change in LV end-systolic volume was the only multivariate discriminator between 15 patients who died and 55 who did not, irrespective of whether they had undergone revascularization. Thus, measurement of the effect of revascularization of viable myocardium in chronic ischemic heart disease should not only include improvement in resting regional and global LV function, but also LV geometry. Improvement in LV geometry contributes to better LV systolic function, which in turn is the best predictor of survival after revascularization.

Cohort Studies↗

Pulmonary stenosis and severe biventricular dysfunction: improvement following percutaneous valvuloplasty.

A 15-year-old boy with severe pulmonary stenosis associated with severe right and left ventricular systolic dysfunction is reported. After successful percutaneous pulmonary valvuloplasty, there was an initial and early improvement in right ventricular (RV) function, followed by a delayed and more gradual improvement in left ventricular (LV) function. At long-term follow up, both RV and LV systolic functions were nearly normalized. Several mechanisms may be implicated, including ventricular interdependence, geometric factors, altered compliance and intrinsic alteration in the LV muscle. A delayed, but sustained, improvement in LV systolic function following relief of RV pressure overload suggests that the latter mechanism must have played an important role in the genesis of the LV dysfunction. Pulmonary stenosis associated with severe biventricular dysfunction may be treated primarily by percutaneous pulmonary balloon valvuloplasty with near-total recovery of the ventricular function.

Adolescent↗