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As an increasing number of patients with congenital heart disease reach adulthood, more information is needed regarding outcomes. The first signs of impaired heart function may appear during exercise testing. The aim of the present study was to establish mean values for maximal oxygen uptake in adults with various congenital heart diseases. Patients from 6 major diagnostic groups were identified, including patients with atrial septal defect (ASD, n = 93), transposition of the great arteries corrected with the Mustard procedure (n = 84), congenitally corrected transposition of the great arteries (CCTGA, n = 41), Tetralogy of Fallot (n = 168), Ebstein's anomaly (n = 37), and Modified Fontan procedure (n = 52). Diminished maximal oxygen uptake was found in all diagnostic groups across age compared with healthy subjects. A significant decrease in maximal oxygen uptake with aging was found in those with ASD (p <0.0001), CCTGA (p = 0.01), and Tetralogy of Fallot (p <0.0001). There was no significant decline, however, in Ebstein's anomaly (p = 0.270), Fontan procedure (p = 0.182), and in the Mustard patients (p = 0.188). All patients achieved significantly lower heart rates than predicted (mean for all groups, p <0.0001). Forced vital capacity values (3.51 L, mean SD +/- 1.02) were lower than predicted values (4.10 L, mean SD +/- 0.90, p <0.0001) for all patients groups except those with ASD. Mean values, however, were within the accepted 20% range of variance. This study showed diminished aerobic capacity in all diagnostic groups when compared with a healthy population. The maximal oxygen uptake values across age groups can be used as reference values in patients with similar diagnoses and as the basis for further research. [ABSTRACT FROM AUTHOR]

Improvement in exercise capacity is an important clinical effect of percutaneous transluminal coronary angioplasty (PTCA), and was assessed in patients with and without previous myocardial infarction (MI) undergoing PTCA. We prospectively followed patients with exercise testing before and 2 weeks after angioplasty in 415 patients, 170 (41%) of whom had a previous MI. A third exercise test was performed 20 +/- 2 weeks after PTCA in 403 patients. From left ventricular angiography obtained before PTCA, regional dyskinesia was classified into anterior or posterior locations. Both patients with and without previous MI had a significant increase in exercise capacity from before to 2 and 20 weeks after PTCA (previous MI: 31.9% and 29.3%; no MI: 50.7% and 38.2%; p <0.0001 [analysis of variance]). In patients with MI and anterior dyskinesia, in whom lesions on the left anterior descending artery were dilated or posterior dyskinesia in whom lesions on the right coronary artery were dilated, exercise capacity increased significantly from before to 2 and 20 weeks after PTCA (left anterior descending artery: 53.1% and 39.7%, p <0.0001; right coronary artery: 16.9% and 27.6%, p = 0.01 [analysis of variance]). Multivariate regression analysis revealed that male sex, no previous MI, and dilation of left anterior descending artery were significantly associated with increased exercise capacity after angioplasty adjusted for age and smoking habits, whereas left ventricular ejection fraction and end-diastolic pressure were not associated with increased exercise capacity. [ABSTRACT FROM AUTHOR]

Our study investigated the abnormal right ventricular systolic pressure response (RVPR) in young patients with isolated atrial septal defect (ASD) or ventricular septal defect (VSD). An abnormal RVPR >50 mm Hg during exercise has been identified as a precursor of pulmonary artery hypertension. The present study included a population-based selection of 44 patients (age 13 to 25 years) with either isolated VSD (n = 27) or ASD (n = 17) and without right ventricular outflow tract obstruction. Of the 44 defects, 28 had been surgically closed (17 ASDs and 11 VSDs); 16 minor VSDs were untreated. Cardiovascular exercise testing and echocardiography at rest and during exercise were performed for all patients and 88 healthy controls. The aerobic capacity was significantly reduced in all patient groups (open VSD, closed VSD, closed ASD). The measurements of right ventricular performance were significantly lower in patients with closed ASD or closed VSD compared to those of the controls and patients with open VSD. Finally, 5% of the controls, no patient with ASD, and 9 patients with VSD (33%), regardless of defect closure, had an abnormal RVPR during exercise. In conclusion, 1/3 of young patients with isolated VSD had an abnormal RVPR during exercise., (Copyright 2010 Elsevier Inc. All rights reserved.)

The study aim was to investigate ventricular function at long-term follow-up in patients operated with arterial switch for transposition of the great arteries (TGAs). Although midterm results for anatomic correction of TGA are promising, there are reported minor alterations in left ventricular (LV) function possibly indicating myocardial dysfunction. Twenty-two patients with TGAs 12.4 +/- 2.3 years old operated with arterial switch were studied by magnetic resonance imaging and echocardiography. Twenty-two age-matched healthy subjects served as controls. Myocardial deformation was described by longitudinal and circumferential shortening (measured as strain and strain rate) and ventricular torsion, measured by speckle-tracking echocardiography. Although standard measurements of global systolic LV function were normal in patients with TGAs, longitudinal shortening was decreased compared with controls. Longitudinal strain was decreased in all ventricular regions except the posterior wall and most pronounced in the apical segments. LV circumferential shortening was similar in the 2 groups. Also, in the right ventricular free wall patients displayed decreased longitudinal shortening in the mid and apical segment. Moreover, LV torsion was decreased in the TGA group. Although rotation was relatively homogenous at the apical and basal levels in controls, there was greater dispersion in rotation in the patient group, with basal rotation being greatest in the inferior wall and apical rotation being greatest in the anterior wall. In conclusion, there was slightly decreased longitudinal shortening in the 2 ventricles and decreased LV torsion in patients with TGAs, although standard measurements of global ventricular function were normal.

Arrhythmias in patients with repaired tetralogy of Fallot (ToF) might be due in part to altered autonomic heart rate control caused by altered right ventricle hemodynamics. This study investigated autonomic heart rate control in adolescents with ToF at rest and during unloading of the right ventricle. A total of 17 patients with ToF and 56 healthy controls aged 12 to 18 years underwent orthostatic stress with lower body negative pressure of -20 mm Hg. Heart rate, blood pressure, and stroke volume were recorded noninvasively. Indices of heart rate variability were computed in time and frequency domains. All patients with ToF also underwent cardiac magnetic resonance imaging, demonstrating pulmonary regurgitation and right ventricular dilation. At rest, heart rate variability indices of vagal heart rate control were nonsignificantly lower in the patients with ToF compared with controls. During lower body negative pressure, heart rate increased more in controls than patients with ToF (p

Hemodynamic dysfunction is documented in chronic fatigue syndrome (CFS). This study was conducted to investigate cardiovascular responses to orthostatic stress in adolescents with CFS, using a novel procedure for tilt-table testing. A total of 27 adolescents with CFS and 33 healthy control subjects with equal age and gender distribution underwent 15 minutes of 20 degrees head-up tilt testing. Heart rate, systolic blood pressure (BP), mean BP, diastolic BP, stroke index, total peripheral resistance index, end-diastolic volume index, and acceleration index were continuously and noninvasively recorded. At rest, patients with CFS had higher total peripheral resistance index values (p<0.01) and lower stroke index and end-diastolic volume index values (p<0.05) than controls. During 20 degrees head-up tilt testing, patients with CFS had greater increases in heart rate, diastolic BP (p<0.001), mean BP (p<0.01), and total peripheral resistance index (p<0.05) than controls and greater decreases in stroke index (p<0.05). Syncope or near syncope was not observed. In conclusion, this study found that adolescents with CFS have significant abnormalities of cardiovascular regulation in response to mild orthostatic stress, differentiating them from healthy controls.

Data concerning the natural history of asymptomatic coronary artery disease (CAD) has been limited to epidemiologic rather than angiographic studies, thus leading to uncertainty as to whether warning symptoms and signs will identify subjects with silent myocardial ischemia before morbid events. To address this issue, 50 apparently healthy men with angiographically proven CAD and asymptomatic exercise-induced ST depression have been followed prospectively for 15 years in the Oslo Ischemia Study. Fourteen men died. The initial presenting clinical event in these 14 men was chest pain in 4 (30%)--but in only 1 case was it recognized as typical angina--silent myocardial infarction in 5 (35%) and sudden death in 5 (35%). Thirty-six men survived, with 19 developing symptoms. Overall, chest pain was the first clinical event in 22 of the total of 33 men with symptoms (66%), whereas myocardial infarction occurred in 6 (18%) and sudden death in 5 (16%). Although chest pain occurred in 22 men, it was clinically diagnosed as typical angina pectoris in only 6. These observations suggest that there is an absence of clear-cut ischemic symptoms in many asymptomatic patients before morbid events.

Thromboxane A2 (TxA2) may aggravate myocardial ischemia by inducing vasoconstriction and platelet aggregation in small coronary vessels, whereas prostacyclin (PGI2) counteracts these effects. Acetylsalicylic acid (ASA) inhibits the formation of TxA2 as well as PGI2, whereas dazoxiben, a thromboxane synthetase inhibitor, reduces TxA2 formation selectively. In 25 patients with coronary artery disease, 2 identical atrial pacing stress tests were performed: before and after the administration of dazoxiben (200 mg) in 15 patients and before and after ASA (250 mg) in 10. The ischemic response, quantified by coronary sinus and aortic lactate levels and by ST depression, was significantly reduced after administration of dazoxiben (p less than 0.02) but not after ASA. Heart rate at rest, myocardial extraction of free fatty acids and the arteriovenous oxygen difference was unaffected by medication. Both drugs reduced TxB2 levels to the same extent, whereas collagen-induced aggregation was more reduced after ASA than after dazoxiben. The effect of dazoxiben on ischemia was probably a result of inhibited TxA2 and preserved PGI2 production, which increased blood flow to ischemic regions.

The function of blood platelets sampled from the coronary sinus and the superior vena cava was studied in 50 men with coronary artery disease at rest and during pacing-induced angina. At rest, a lower platelet aggregation and retention response was found in coronary sinus compared with vena caval blood. This may be due to refractoriness after previous platelet stimulation or to release of platelet inhibitors in the coronary circulation. During pacing-induced angina, lactate levels indicated that blood was sampled from ischemic myocardium in only 27 of the patients. Pacing-induced angina influenced platelet function differently in blood from ischemic and nonischemic regions. Adenosine diphosphate- and collagen-induced aggregation, platelet retention and plasma beta-thromboglobulin levels remained unchanged in blood from ischemic myocardium during pacing, but increased in blood from nonischemic regions. Thus, factors other than ischemia activated platelets in the coronary circulation during tachycardia-induced stress.