Davinder S. Jassal

Comprehensive Assessment of Myocardial Perfusion Defects, Regional Wall Motion, and Left Ventricular Function by Using 64-Section Multidetector CT

PURPOSE To evaluate the accuracy of 64-section multidetector computed tomography (CT) for the assessment of perfusion defects (PDs), regional wall motion (RWM), and global left ventricular (LV) function. MATERIALS AND METHODS All myocardial infarction (MI) patients signed informed consent. The IRB approved the study and it was HIPAA-compliant. Cardiac multidetector CT was performed in 102 patients (34 with recent acute MI and 68 without). Multidetector CT images were analyzed for myocardial PD, RWM abnormalities, and LV function. Global LV function and RWM were compared with transthoracic echocardiography (TTE) by using multidetector CT. PD was detected by using multidetector CT and was correlated with cardiac biomarkers and single photon emission CT (SPECT) myocardial perfusion imaging. Multidetector CT diagnosis of acute MI was made on the basis of matching the presence of PD with RWM abnormalities compared with clinical evaluation. RESULTS Correlation between multidetector CT and TTE for global function (r = 0.68) and RWM (kappa = 0.79) was good. The size of PD on multidetector CT had a moderate correlation against SPECT (r = 0.48, -7% +/- 9). There was good to excellent correlation between cardiac biomarkers and the percentage infarct size by using multidetector CT (r = 0.82 for creatinine phosphokinase, r = 0.76 for creatinine phosphokinase of the muscle band, and r = 0.75 for troponin). For detection of acute MI in patients, multidetector CT sensitivity was 94% (32 of 34) and specificity was 97% (66 of 68). Multidetector CT had an excellent interobserver reliability for ejection fraction quantification (r = 0.83), as compared with TTE (r = 0.68). CONCLUSION Patients with acute MI can be identified by using multidetector CT on the basis of RWM abnormalities and PD.

Multidetector computed tomography for the detection of left atrial appendage thrombus: A comparative study with transesophageal echocardiography

Objective: To determine the diagnostic performance of multidetector computed tomography (MDCT) for the detection of left atrial appendage (LAA) thrombus as compared with transesophageal echocardiography. Methods: Multidetector computed tomography was evaluated in 43 patients qualitatively for the presence or absence of a filling defect in the LAA and compared with transesophageal echocardiography. Additionally, a ratio of the mean computed tomographic attenuation in the LAA apex to the mean computed tomographic attenuation in the aortic root was used for quantitative evaluation. Results: A filling defect visualized in the LAA by MDCT corresponded to a sensitivity of 70% (7/10), a specificity of 82% (27/33), and a negative predictive value of 90% (27/30) for detection of LAA thrombus. When using quantitative parameters, MDCT demonstrated a sensitivity of 80% (8/10), a specificity of 73% (24/33), and a negative predictive value of 92% (24/26). Multidetector computed tomography was not able to differentiate LAA thrombus from spontaneous echo contrast by either visual evaluation or by quantitative parameters. Conclusions: Multidetector computed tomography remains limited for the detection of LAA thrombus. However, a subgroup of patients at very high risk for LAA thrombus may benefit from the high negative predictive value of cardiac MDCT.

64-Slice multidetector computed tomography (MDCT) for detection of aortic regurgitation and quantification of severity

Background:Recent advances in 64-slice multidetector computed tomography (MDCT) provide an opportunity to assess coronary artery disease, left ventricular function and, potentially, valvular heart disease. Objective:To determine the ability of 64-MDCT to both detect and to quantify the severity of aortic regurgitation (AR), as compared with transthoracic echocardiography (TTE). Methods:We evaluated a total of 64 patients (43 males, mean age 63 ± 11 years), 30 with varying severities of AR as assessed by TTE and 34 matched controls. The severity of AR by TTE was determined using the vena contracta, the ratio of jet to left ventricular outflow tract (LVOT) height, and the ratio of the jet to LVOT cross-sectional area. AR by MDCT was defined as a lack of coaptation of the aortic valve leaflets in diastole and, if detected, the maximum anatomic aortic regurgitant orifice was determined. Results:All 34 control patients without AR were correctly identified by MDCT. There were 14 patients with mild AR, 10 with moderate AR, and 6 with severe AR by TTE. Of these patients, MDCT correctly identified 21 patients with AR (sensitivity 70%, specificity 100%, positive predictive value [PPV] 100%, and negative predictive value [NPV] 79%). Anatomic regurgitant orifice area measured by MDCT correlated well with the TTE-derived vena contracta (r = 0.79, P < 0.001), ratio of jet to LVOT height (r = 0.79, P < 0.001), and ratio of jet to LVOT cross-sectional area (r = 0.75, P < 0.001). Conclusions:Direct planimetric measurement of the aortic valve anatomic regurgitant orifice area on 64-MDCT provides an accurate, noninvasive technique for detecting and quantifying AR.

Delayed Enhancement Cardiac MR Imaging in Noncompaction of Left Ventricular Myocardium

A 49-year-old female with a history of paroxysmal atrial fibrillation, presented with worsening dyspnea on minimal exertion. During the follow-up period, transthoracic echocardiography and cardiac magnetic resonance imaging (CMR) were consistent with the diagnosis of noncompaction of the left ventricle. Delayed-enhancement CMR demonstrated hyperenhancement of the prominent trabeculations located at the mid and apical portions of the left ventricle, suggesting areas of fibrosis. Although previous cases of left ventricular noncompaction diagnosed with CMR have been described in the literature, this is the first case to describe the utility of delayed-enhancement imaging in the pathohistological confirmation of myocardial fibrosis and scarring in the hypertrabeculated myocardium.

Iloprost attenuates doxorubicin-induced cardiac injury in a murine model without compromising tumour suppression

AIMS The use of doxorubicin (DOX) as a chemotherapeutic agent is limited by cardiac injury. Iloprost, a stable synthetic analogue of prostacyclin, has previously been shown to protect against DOX-induced cardiomyocyte injury in vitro. Here, we addressed whether iloprost is cardioprotective in vivo and whether it compromises the anti-tumour efficacy of DOX. METHODS AND RESULTS Lewis Lung Carcinoma cells were implanted subcutaneously in the flank of C57BL/6 mice. DOX treatment was commenced from when tumours became visible. Iloprost was administered from prior to DOX treatment until sacrifice. Echocardiography and invasive haemodynamic measurements were performed immediately before sacrifice. As expected, DOX induced cardiac cell apoptosis and cardiac dysfunction, both of which were attenuated by iloprost. Also, iloprost alone had no effect on tumor growth and indeed, did not alter the DOX-induced suppression of this growth. CONCLUSION In a murine model, iloprost attenuated the acute cardiac injury and dysfunction induced by DOX therapy without compromising its chemotherapeutic effect.

Cor triatriatum: The utility of cardiovascular imaging

A 44-year-old man with no known cardiac history presented with worsening dyspnea on minimal exertion. During follow-up, computed tomography angiography and echocardiography confirmed the incidental finding of cor triatriatum. As improvements in spatial and temporal resolution continue, cardiac computed tomography may become better suited to the dynamic imaging of anatomical defects in the heart, including, but not limited to, coronary artery disease.

A continuous murmur.

A 61‐year‐old male with a history of a mechanical Bjork‐Shiley aortic valve replacement in 1977 and repair of an ascending aortic root dissection in 1993, presented with a 2‐week history of fatigue and exertional dyspnea. Echocardiography confirmed the presence of an aortic pseudoaneurysm with a fistulous connection between the aorta and right atrium, which subsequently underwent successful repair. Although there have been several cases describing the development of an aortic pseudoaneurysm after aortic dissection repair, our case is the first to describe an aorta‐atrial fistula as a long‐term complication of a previous aortic dissection repair.