The purpose of this study was to determine right ventricular (RV) function from 16-detector-row CT by using two different software tools in comparison with MRI. Nineteen patients underwent cardiac CT. (1) With semiautomated contour detection software end-diastolic and end-systolic RV volumes were determined from short-axis CT reformations (MPR) created at every 10% of the RR-interval. (2) End-systolic and end-diastolic axial images were transformed to 3D to determine the volumes by using a threshold-supported reconstruction algorithm. Steady-state free-precession cine-MRI of the heart was done in short-axis orientation. RV function could not be analyzed in one patient because of sternal wire artifacts in MRI. Mean end-diastolic (155.4+/-54.6 ml) and end-systolic (79.1+/-37.0 ml) RV volumes determined with MPR correlated well with MRI [151.9+/-53.7 ml (r=0.98) and 75.0+/-36.0 ml (r=0.96), respectively (P<0.001)]. RV stroke volume (76.2+/-20.2 ml for MPR-CT, 76.9+/-20.7 ml for MRI, r=0.93) showed a good correlation and RV ejection fraction (50.8+/-8.4% for MPR-CT, 51.9+/-7.4% for MRI, r=0.74) only a moderate one. Threshold supported 3D reconstructions revealed insufficient correlations with MRI (r=0.31-0.59). MPR-based semiautomated analysis of cardiac 16 detector-row CT allows for RV functional analysis. The results correlate well with MRI findings. Threshold value-supported 3D reconstructions did not show satisfying results because of inhomogeneities of RV contrast enhancement.

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Early diagnosis of primary pulmonary artery sarcomas can be improved by computed tomography and magnetic resonance scanning. Radical surgical resection probably presents the only chance for cure. The role of neoadjuvant or adjuvant treatment modalities has to be defined. Pulmonary artery sarcoma need not necessarily be a fatal diagnosis.

Nine patients with obstruction of coronary artery blood flow caused by myocardial bridging underwent surgery after failure of medical treatment. The diagnoses were made angiographically at rest or during beta-stimulation. Impaired blood flow was found only in the left anterior descending artery in seven patients and additionally in the diagonal branch in two. The operations, performed with cardiopulmonary bypass consisted of complete dissection of the overlying myocardium. All patients survived the operation. Major intraoperative complications were accidental opening of the right ventricle in two patients. Postoperative scintigraphic and angiographic studies demonstrated restoration of coronary flow and myocardial perfusion without residual myocardial bridges under beta-stimulation. Surgical relief of myocardial ischemia due to systolic compression of intramyocardial coronary arteries can be accomplished with low operative risk and with excellent functional results.

No abstract

CTnI after minimal invasive surgery shows a characteristic pattern with a maximum at 24h after the operation. The measurement of postoperative biochemical marker concentrations, specially cTnI, reflects myocardial injury incurred during the procedure. It is an accurate method for confirming or excluding a perioperative myocardial injury diagnosis after OPCAB surgery.

No abstract

Following cardiac surgery, electrocardiography and creatine kinase isoenzyme MB (CK-MB) activities are of limited value in diagnosing a non-transmural infarction. With the recent availability of an assay to detect serial levels of the specific cardiocyte contractile protein troponin T the possibility has been increased of closing a diagnostic gap among cardiosurgical patients. Ninety patients with severe diffuse three-vessel disease undergoing myocardial revascularization were grouped by their postoperative electrocardiographic (ECG) findings (group I--unchanged ECG; group II--new Q-waves representing perioperative myocardial infarction (PMI)). Serial levels of troponin T and the activity of CK-MB were measured 6, 12, 24 and 48 h after aortic unclamping. The course of CK-MB activity was compared to a profile and values derived from patients with unchanged (n = 1312) or new Q-wave ECGS (n = 89). In 72 patients (80.0%) with unchanged postoperative ECG (group I) serial troponin T levels remained constantly low and reached a median peak value of 0.37 microgram/l (quartile 0.13-0.50 microgram/l) after 24 h. Serial CK-MB activities demonstrated the typical non-ischemic course with a monoexponential decline from an initial median peak value of 15.5 U/l (quartile 12.0-21.0 U/l) to 7.0 U/l (quartile 6.0-9.0 U/l). In seven patients (7.8%) with new Q-waves and a pathologic CK-MB profile (group II) troponin T reached median levels of 10.47 micrograms/l (quartile 6.34-12.50 micrograms/l) (P < 0.001 I vs II). Four of five patients with a new right bundle branch block demonstrated low troponin T levels below 1 microgram/l and a normal CK-MB profile. Among six patients with unchanged QRS-configuration and elevated troponin T levels between 0.84 and 4.99 micrograms/l CK-MB activity showed a characteristic PMI pattern in two patients. Troponin T is characterized by a very narrow margin of normal values represented by a maximum third quartile of 0.50 microgram/l. A singular value of troponin after 6 h or 24 h may be sufficient evidence to confirm the diagnosis of a PMI.