Three-dimensional echocardiographic quantitative evaluation of left ventricular diastolic function using analysis of chamber volume and myocardial deformation

Currently, no real-time three-dimensional echocardiographic (RT3DE) indices are recommended by the official guidelines for the assessment of diastolic dysfunction (DD). We hypothesized that recent developments in RT3DE imaging technology that allow dynamic quantification of both left ventricular (LV) volume and 3D myocardial deformation, could be utilized to objectively assess DD. Transthoracic RT3DE datasets were acquired (Philips iE33, X5 transducer, frame rate 19 ± 4) in 76 subjects, including 20 normal controls (NL), 16 mild DD, 20 moderate DD and 20 severe DD (grade 1, 2 and 3, respectively, using ASE guideline). Images were analyzed using prototype software (TomTec) that performs 3D speckle tracking to generate time curves of LV volume and segmental myocardial strain. Indices of diastolic LV function were calculated: volume at 25, 50 and 75 % of filling duration (FD) in percent of end-diastolic volume (volume index, LVVi), and rapid filling volume (RFV) fraction. Temporal indices included: FD in % of RR, and rapid filling duration (RFD) in % of FD. Additionally, longitudinal, radial and circumferential strains at 25, 50 and 75 % of FD were calculated. Inter-groups differences were tested using ANOVA. LVVi and RFV fraction showed a biphasic pattern with the severity of DD characterized by an initial decrease (grade 1), a pseudo-normalization (grade 2), and then an increase above normal (grade 3). FD progressively decreased with severity of DD. RFD was significantly increased in all 3 groups compared to NL. After normalization by peak systolic values, all three strain components showed a linear pattern with the severity of DD, suggesting potential clinical usefulness. This is the first study to show that current RT3DE technology allows combined quantitative analysis of LV volume and 3D myocardial strain, which is sensitive enough to demonstrate differences in myocardial relaxation in patients with different degrees of DD.     

Considerations when measuring myocardial perfusion reserve by cardiovascular magnetic resonance using regadenoson

Background

Adenosine cardiovascular magnetic resonance (CMR) can accurately quantify myocardial perfusion reserve. While regadenoson is increasingly employed due to ease of use, imaging protocols have not been standardized. We sought to determine the optimal regadenoson CMR protocol for quantifying myocardial perfusion reserve index (MPRi) – more specifically, whether regadenoson stress imaging should be performed before or after rest imaging.

Methods

Twenty healthy subjects underwent CMR perfusion imaging during resting conditions, during regadenoson-induced hyperemia (0.4 mg), and after 15 min of recovery. In 10/20 subjects, recovery was facilitated with aminophylline (125 mg). Myocardial time-intensity curves were used to obtain left ventricular cavity-normalized myocardial up-slopes. MPRi was calculated in two different ways: as the up-slope ratio of stress to rest (MPRi-rest), and the up-slope ratio of stress to recovery (MPRi-recov).

Results

In all 20 subjects, MPRi-rest was 1.78 ± 0.60. Recovery up-slope did not return to resting levels, regardless of aminophylline use. Among patients not receiving aminophylline, MPRi-recov was 36 ± 16% lower than MPRi-rest (1.13 ± 0.38 vs. 1.82 ± 0.73, P = 0.001). In the 10 patients whose recovery was facilitated with aminophylline, MPRi-recov was 20 ± 24% lower than MPRi-rest (1.40 ± 0.35 vs. 1.73 ± 0.43, P = 0.04), indicating incomplete reversal. In 3 subjects not receiving aminophylline and 4 subjects receiving aminophylline, up-slope at recovery was greater than at stress, suggesting delayed maximal hyperemia.

Conclusions

MPRi measurements from regadenoson CMR are underestimated if recovery perfusion is used as a substitute for resting perfusion, even when recovery is facilitated with aminophylline. True resting images should be used to allow accurate MPRi quantification. The delayed maximal hyperemia observed in some subjects deserves further study.

Trial registration

ClinicalTrials.gov {"type":"clinical-trial","attrs":{"text":"NCT00871260","term_id":"NCT00871260"}}NCT00871260     

Cerebrospinal fluid adenosine deaminase activity for the diagnosis of tuberculous meningitis in adults

We studied adenosine deaminase (ADA) activity in cerebrospinal fluid (CSF) of 16 cases of tuberculous meningitis, 4 cases of cryptococcal meningitis, 5 cases of bacterial meningitis, 12 cases of eosinophilic meningitis, 26 cases of aseptic meningitis, 6 cases of carcinomatous meningitis and 108 cases with normal CSF. The mean CSF ADA values for the different groups were: 39.44 +/- 41.46, 13.00 +/- 7.43, 34.20 +/- 40.81, 3.17 +/- 4.82, 10.03 +/- 9.23, 8.67 +/- 13.60, and 2.58 +/- 2.90 U/I, respectively. Comparing the ADA activity between patients with tuberculous meningitis and non-tuberculous meningitis, the receiver-operating characteristic (ROC) curve identified a CSF ADA level of 15.5 U/I as the best cut-off value to differentiate between the two, with a sensitivity of 75% and a specificity of 93%, with an area under the curve of 0.92. When tuberculous meningitis was compared with aseptic and carcinomatous meningitis, the ROC curve identified a CSF ADA level of 19.0 U/I as the best cut-off value for differentiation, with a sensitivity of 69% and a specificity of 94%, with an area under the curve of 0.83. The level of CSF ADA may be useful as a complementary tool in the early diagnosis of tuberculous meningitis.     

Ceftazidime overdose-related nonconvulsive status epilepticus after intraperitoneal instillation

We report a case of ceftazidime-related nonconvulsive status epilepticus (NCSE) in a 70-year-old female patient with continuous ambulatory peritoneal dialysis (CAPD)-related peritonitis. She was given ceftazidime intravenously which was then changed to intraperitoneal installation after clinical improvement. She received 11 g of ceftazidime via intraperitoneal installation for two days after being discharged from the hospital. Her consciousness was altered with mutism, asterisxis, and horizontal nystagmus. Her EEG showed continuous generalized three spikes-and-wave per second that were abolished after intravenous diazepam. Ceftazidime-related NCSE was suggested and ceftazidime therapy was stopped. Hemodialysis was done while phenytoin was also given to control the convulsions. Her consciousness improved after hemodialysis. Serum ceftazidime measured before and after hemodialysis on the second and third day were 105.2/39.4, 36.2/5.2 microg/mL (normal peak level 55 microg/mL), respectively. Repeated evaluation on day 6 showed normal EEG without epileptiform activity. She was later discharged with full recovery.     

Evaluation of myocardial deformation in patients with sickle cell disease and preserved ejection fraction using three-dimensional speckle tracking echocardiography

Background: Sickle cell disease (SCD) is a hemoglobinopathy that affects one in 500 African Americans. Although it is well established that patients with SCD have left ventricular (LV) diastolic dysfunction, it is not clear whether they have subtle LV systolic dysfunction despite preserved ejection fraction (EF). We used three-dimensional speckle tracking echocardiography (3DSTE) to assess changes in both systolic and diastolic LV function in SCD. Methods: Transthoracic real time 3D images were obtained (Philips iE33) in 56 subjects, including 28 stable outpatients with SCD (age 33 ± 7 years) and 28 normal controls (age 35 ± 9 years). 3DSTE was performed using prototype software (4DLV Analysis, TomTec) to obtain LV volume and deformation time curves, from which indices of systolic and diastolic LV function were calculated. Results: In SCD patients, 3DSTE-derived LV filling parameters were significantly different from normal controls, reflecting an increase in both rapid and atrial filling volumes and prolonged active relaxation, depicted by a decrease in filling volume fractions at fixed times and an increase in rapid filling duration. Global LV systolic function was not only preserved but increased compared to controls, as reflected by significantly increased global longitudinal strain. Importantly, twist angle and torsion as well as radial and circumferential components of 3D strain were similar in both groups. Conclusions: 3DSTE was able to confirm diastolic dysfunction, as expected in some patients with SCD. However, 3DSTE strain analysis did not reveal any changes in LV systolic function. These findings provide novel insight into the pathophysiology of the cardiovascular complications of SCD.