Exercise-induced st segment elevation in a patient with effort angina pectoris and normal coronary arteries

A 32 year old woman who complained of exercise-induced chest pain was found to have widespread elevation of the ST segment of the electrocardiogram during exercise testing. Coronary angiography demonstrated no obstructive lesions and no evidence of coronary artery spasm despite ergonovine administration, bicycle ergo-metry and rapid atrial pacing. Exercise thallium-201 cintigraphy demonstrated no perfusion defects despite ST segment elevation. Radionuclide blood pool imaging revealed a slight decrease in ejection fraction with exercise. The available evidence raises the possibility of small vessel coronary artery disease, either structural or vasotonic, as a cause of this patient's symptoms

Left Ventricular Function by Pressure‐Volume Loop Analysis before and after Percutaneous Repair of Large Atrial Septal Defects

Aim The intent of the present study was to evaluate changes in ventricular function with percutaneous closure of atrial septal defect (ASD), as it is associated with alterations in ventricular loading and function. Transcatheter occlusion of ASD imparts acute changes in volume loading of the left ventricle (LV) that obscures measurement of ventricular function by load‐dependent indices. To differentiate between changes in ventricular loading and function, load‐independent indices of ventricular function must be utilized . Methods During transcatheter occlusion of ASD, subjects underwent measurement of LV pressure and volume by the conductance catheter method. Load‐dependent indices of ventricular function included: systolic and diastolic pressures, +dP/dt max , and −dP/dt max . Load‐independent indices included: elastance and tau, the preload‐independent time constant ofisovolumic relaxation. To obtain elastance, afterload was augmented by phenylephrine bolus pre‐ and post‐device occlusion . Results In total, 29 patients (age 2–79 years) underwent ASD device occlusion (device size 12–38 mm, median 28 mm). Load‐dependent indices were obtained in all, and satisfactory pressure‐volume loops in 11. At baseline, LV end‐diastolic pressure was 5–23 mmHg (13 ± 5 mmHg) and tau was 31 ± 6 ms. Postclosure of the ASD, LV systolic and diastolic pressures rose by 10 ± 11 mmHg and 5 ± 3 mmHg, respectively (P < 0.05), and +dP/dt max rose from 1,288 ± 313 mmHg/sec to 1,415 ± 465 mmHg/sec (P < 0.05), but −dP/dt max was unchanged. Elastance significantly improved (9.4 ± 8.3 mmHg/mL vs. 13.0 ± 7.3 mmHg/mL, P < 0.05) and tau was unchanged . Conclusions Transcatheter occlusion of ASD is associated with acute improvement in load‐independent indices of systolic function in this cohort, without significant worsening of the preload‐independent index of diastolic function . (J Interven Cardiol 2014;27:204–211)Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/106889/1/joic334.pd

Percutaneous closure of atrial septal defects leads to normalisation of atrial and ventricular volumes

Background: Percutaneous closure of atrial septal defects (ASDs) should potentially reduce right heart volumes by removing left-to-right shunting. Due to ventricular interdependence, this may be associated with impaired left ventricular filling and potentially function. Furthermore, atrial changes post-ASD closure have been poorly understood and may be important for understanding risk of atrial arrhythmia post-ASD closure. Cardiovascular magnetic resonance (CMR) is an accurate and reproducible imaging modality for the assessment of cardiac function and volumes. We assessed cardiac volumes pre- and post-percutaneous ASD closure using CMR. Methods: Consecutive patients (n = 23) underwent CMR pre- and 6 months post-ASD closure. Steady state free precession cine CMR was performed using contiguous slices in both short and long axis views through the ASD. Data was collected for assessment of left and right atrial, ventricular end diastolic volumes (EDV) and end systolic volumes (ESV). Data is presented as mean ± SD, volumes as mL, and paired t-testing performed between groups. Statistical significance was taken as p &lt; 0.05. Results: There was a significant reduction in right ventricular volumes at 6 months post-ASD closure (RVEDV: 208.7 ± 76.7 vs. 140.6 ± 60.4 mL, p &lt; 0.0001) and RVEF was significantly increased (RVEF 35.5 ± 15.5 vs. 42.0 ± 15.2%, p = 0.025). There was a significant increase in the left ventricular volumes (LVEDV 84.8 ± 32.3 vs. 106.3 ± 38.1 mL, p = 0.003 and LVESV 37.4 ± 20.9 vs. 46.8 ± 18.5 mL, p = 0.016). However, there was no significant difference in LVEF and LV mass post-ASD closure. There was a significant reduction in right atrial volumes at 6 months post-ASD closure (pre-closure 110.5 ± 55.7 vs. post-closure 90.7 ± 69.3 mL, p = 0.019). Although there was a trend to a decrease in left atrial volumes post-ASD closure, this was not statistically significant (84.5 ± 34.8 mL to 81.8 ± 44.2 mL, p = NS). Conclusion: ASD closure leads to normalisation of ventricular volumes and also a reduction in right atrial volume. Further follow-up is required to assess how this predicts outcomes such as risk of atrial arrhythmias after such procedures.Karen SL Teo, Benjamin K Dundon, Payman Molaee, Kerry F Williams, Angelo Carbone, Michael A Brown, Matthew I Worthley, Patrick J Disney, Prashanthan Sanders and Stephen G Worthle