Left ventricular aneurysm repair: early survival.

BACKGROUND: The aim of this study was to evaluate the early survival in patients submitted to left ventricular (LV) repair and concomitant myocardial revascularization. METHODS: We retrospectively reviewed the records of 51 patients who were submitted to LV repair and concomitant myocardial revascularization between January 1998 and June 2003. Of 51 patients (44 males with a mean age of 60+/-9.2 years, and 7 females with a mean age of 61+/-6.5 years), 29 (56.9 %) were submitted to the McCarthy technique, 16 (31.3 %) to the technique that was described by Jatene and modified by Dor, and 6 (11.8%) to the Cooley technique (linear repair). The mean preoperative LV ejection fraction was 36.5+/-7.7 %, the mean preoperative LV end-diastolic diameter was 61.8+/-3.9 mm, the mean preoperative LV end-systolic diameter was 49.9+/-5.1 mm, the mean preoperative interventricular septal thickness was 9.7+/-1.7 mm, and finally, the mean posterior wall thickness was 8.9+/-1 mm. The mean follow-up was 30.7+/-23.4 months (range 11-82 months). RESULTS: One patient died during surgery (1.9%) and one early postoperatively (1.9%). The causes of death were respectively irreversible ventricular fibrillation and low cardiac output syndrome. The overall survival at follow-up was 98% (49 patients). One patient died during follow-up of myocardial infarction. At follow-up, all patients presented with improved clinical symptoms, and had a better mean NYHA functional class with respect to the preoperative value (3.3+/-0.3 vs 2.0+/-0.5, p < 0.05). Besides, the mean CCS angina class decreased in all patients (3.4+/-0.2 vs 1.9+/-0.3, p < 0.05). The average LV ejection fraction increased from 36.3+/-7.7 to 44.3+/-4.9% (p < 0.001), the average LV end-diastolic diameter decreased from 61.7+/-3.9 to 55.5+/-5.6 mm (p < 0.001), and the average LV end-systolic diameter decreased from 49.9+/-5.1 to 40.4+/-5.1 mm (p < 0.001). No statistically significant difference was found between the preoperative and postoperative data regarding the interventricular septal thickness (9.7+/-1.7 vs 10.3+/-1.6 mm, p = NS), and the posterior wall thickness (9.7+/-1 vs 8.8+/-1.3 mm, p = NS). CONCLUSIONS: LV aneurysm repair and concomitant myocardial revascularization may be performed with an acceptable surgical risk and a good early survival.     

Source of exhaled nitric oxide in primary biliary cirrhosis

BACKGROUND: Exhaled nitric oxide (NO) levels may be elevated in patients with liver cirrhosis and autoimmune diseases. Primary biliary cirrhosis (PBC) is often associated with keratoconjunctivitis sicca (Sjogren syndrome [SS]), an extrahepatic autoimmune manifestation. The aim of this study was to evaluate the source of increased exhaled NO (ie, alveolar vs airway) in patients with PBC, whether associated with SS or not, and to evaluate its impact on oxygenation abnormalities. DESIGN: Observational controlled study. SETTING: University hospital. METHODS: The fractional alveolar NO concentration (FANO) and airway flux of NO (QbrNO) were measured by the multiple flows technique in 34 patients with PBC, 12 with associated SS, and were compared to 20 control subjects and 12 patients with primary SS. RESULTS: FANO was significantly higher in patients with PBC, associated with SS (mean [+/- SEM], 8.9 +/- 0.8 parts per billion [ppb]) or not (mean, 7.7 +/- 0.7 ppb) compared to healthy control subjects (mean, 4.6 +/- 0.5 ppb; p < 0.001) and to patients with primary SS (mean, 4.3 +/- 0.5 ppb; p < 0.001). FANO was significantly higher in cirrhotic patients with increased alveolar-arterial oxygen pressure difference (P[A-a]O(2)) compared to patients with normal P(A-a)O(2) values (9.8 +/- 0.8 vs 7.3 +/- 0.7, respectively; p = 0.018). When compared with control subjects and with patients with PBC not associated with SS, QbrNO was significantly increased in patients with both primary SS and SS associated with PBC. CONCLUSIONS: Increased exhaled NO levels found in PBC are from both alveolar and airway sources in patients with associated SS, but only FANO is associated with oxygenation impairment.     

Usefulness of intravenous myocardial contrast echoardiography in the early left ventricular remodeling in acute myocardial infarction

The aim of this study was to assess the role of intravenous myocardial contrast echocardiography (IMCE) in the prediction of left ventricular (LV) remodeling in patients with acute myocardial infarction (AMI). Sixty-three patients with AMI, who were successfully treated with acute coronary angioplasty, underwent IMCE and low-dose dobutamine echocardiography during hospital admission. IMCE was graded semiquantitatively on a score of 0 (no visible contrast effect), 0.5 (patchy myocardial contrast enhancement), and 1 (homogenous contrast effect). Patients were considered to have microvascular impairment if <50% of segments within the infarct-related area had score of 1. A mean perfusion score index was calculated for each patient. Patients with a good perfusion at IMCE (IMCE+) showed a lower creatine kinase peak (p = 0.001) and lower creatine kinase-MB (p = 0.01), and a better baseline regional contractile function compared with patients who had negative results at IMCE (IMCE-) (p <0.0001) and a higher amount of myocardial viability at low-dose dobutamine echocardiography (p = 0.03). At follow-up, a higher improvement in regional systolic function (p = 0.0006) was observed in IMCE+ patients, whereas IMCE- patients showed an evident increase in LV end-diastolic volume from baseline to 6-month follow-up (p <0.0001), implying LV remodeling, which has been associated with a higher incidence of adverse cardiac events (p = 0.005). By stepwise multiple regression analysis, microvascular impairment at IMCE was a significant independent predictor of LV remodeling (p <0.0001). Thus, IMCE seems to be an important diagnostic tool, able to predict LV remodeling in patients with AMI.     

The dangers of the “Head Down” position in patients with untreated pituitary macroadenomas: case series and review of literature

Purpose

Cavernous sinus syndrome is a rare phenomenon, characterized by simultaneous neuropathies of cranial nerves III–VI. Various pathological processes have been reported as precipitating etiologies, including infection, inflammation, vascular lesions, and neoplasms.

Purpose

We report a unique case series of cavernous sinus syndrome attributable to prolonged Trendelenburg or prone positioning during non-cranial procedures and review the pertinent literature to enlighten on this rare but catastrophic phenomenon.

Methods

Retrospective case series.

Results

In the past year we encountered two patients who presented with acute cavernous sinus syndrome upon awakening from non-cranial operations. One patient underwent an extensive urologic resection of a bladder malignancy positioned in Trendelenburg for approximately 4 h. The second patient underwent a lumbar laminectomy and discectomy in prone position. Both patients were discovered to have infarcted large pituitary macroadenomas as the etiology of their acute ophthalmoplegias, and transnasal, transsphenoidal resection was performed acutely to decompress the cavernous sinus contents. Pathologic analysis of the resected specimens in each case confirmed necrotic, infarcted pituitary adenoma. Both patients made a complete recovery with no evidence of residual or recurrent tumor in short term follow-up.

Conclusion

We report a brief case series of acute cavernous sinus syndrome resulting from dependent positioning during non-cranial operations in patients with pituitary macroadenoma. Although rare, this highlights a potential danger of “head down” positioning in patients with intracranial pathology—particularly in or around the sella and cavernous sinus. Despite multiple cranial neuropathies upon presentation, both patients made complete recovery following surgical decompression of the cavernous sinuses.

     

Serum and Bile Lipids in Young Women with Radiolucent Gallstones

To investigate the relationship between blood and bile lipids, serum cholesterol, high density lipoprotein cholesterol, and triglycerides were correlated with cholesterol saturation index of bile in 21 women-10 with radiolucent gallstones and 11 without stones. All of the women had regular menstrual cycles, were normolipidemic, and on a hospital diet. On the same morning, blood and the darkest duodenal bile were taken after cholecystokinin (CCK) stimulation. Standard laboratory procedures were used to analyze serum and bile lipids. We found: 1) statistically significant (t test, p less than 0.05) but only slight hypercholesterolemia (+ 12%) in patients with gallstones; 2) a negative correlation of serum cholesterol with cholesterol saturation index of bile, both in the control group (r = -0.654, p less than 0.05) and in gallstone patients (r = -0.665, p less than 0.05); 3) a correlation of high density lipoprotein cholesterol with cholesterol saturation index only in normal women (r = -0.619, p less than 0.05); 4) conversely, a correlation of triglycerides with the same index in only gallstone patients (r = 0.641, p less than 0.05). With the stepwise multiple regression analysis (independent variables: diagnosis of gallstones, serum cholesterol, HDL cholesterol, triglycerides; dependent variable: biliary cholesterol saturation index), only gallstone diagnosis and serum cholesterol influenced significantly (F test, p less than 0.05) the biliary cholesterol saturation index. These findings suggest that young women with radiolucent gallstones are slightly hypercholesterolemic, that in women both with and without gallstones there is a negative correlation between serum cholesterol and biliary cholesterol saturation, but women with gallstones have a higher cholesterol saturation index of the bile than women without gallstones with the same level of cholesterol in the blood.     

miR-15b/16-2 deletion promotes B-cell malignancies

The central role of the microRNA (miR) 15a/16-1 cluster in B-cell oncogenesis has been extensively demonstrated, with over two-thirds of B-cell chronic lymphocytic leukemia characterized by the deletion of the miR-15a/16-1 locus at 13q14. Despite the well-established understanding of the molecular mechanisms occurring during miR-15a/16-1 dysregulation, the oncogenic role of other miR-15/16 family members, such as the miR-15b/16-2 cluster (3q25), is still far from being elucidated. Whereas miR-15a is highly similar to miR-15b, miR-16-1 is identical to miR-16-2; thus, it could be speculated that both clusters control a similar set of target genes and may have overlapping functions. However, the biological role of miR-15b/16-2 is still controversial. We generated miR-15b/16-2 knockout mice to better understand the cluster’s role in vivo. These mice developed B-cell malignancy by age 15–18 mo with a penetrance of 60%. At this stage, mice showed significantly enlarged spleens with abnormal B cell-derived white pulp enlargement. Flow cytometric analysis demonstrated an expanded CD19+ CD5+ population in the spleen of 40% knockout mice, a characteristic of the chronic lymphocytic leukemia-associated phenotype found in humans. Of note, miR-15b/16-2 modulates the CCND2 (Cyclin D2), CCND1 (Cyclin D1), and IGF1R (insulin-like growth factor 1 receptor) genes involved in proliferation and antiapoptotic pathways in mouse B cells. These results are the first, to our knowledge, to suggest an important role of miR-15b/16-2 loss in the pathogenesis of B-cell chronic lymphocytic leukemia.MicroRNAs (miRNAs) are a class of small noncoding RNAs that modulate gene expression in many physiological and pathological conditions (1). Altered miRNA expression has been reported in several human cancers, and miRNA expression profiles vary according to the considered tumor (2).A role for miRNAs in tumorigenesis and progression was originally documented for the miR-15/16 family (2–5). This group of miRNAs encompasses the miR-15a/16-1 cluster (on chromosome 13q14,) the miR-15b/16-2 cluster (on chromosome 3q25), and the miR-195/497 cluster (on chromosome 17p13).The role of the miR-15a/16-1 cluster in B-cell pathology has been extensively demonstrated (5). The deletion of the miR-15a/16-1 cluster has been reported in over two-thirds of B-cell chronic lymphocytic leukemias (B-CLLs) (5). Our group has demonstrated that the loss of miR-15a/16-1 expression induces higher levels of the antiapoptotic proteins BCL2 and myeloid cell leukemia sequence 1 (BCL2-related) (MCL1) (3, 6). Moreover, this deletion promotes mature B-cell expansion by deregulating the transition from G1 to S phase (7).On the other hand, the biological role of miR-15b/16-2 is still controversial, as this cluster has been reported to behave as either a tumor suppressor [acute promyelocytic leukemia (8, 9) and osteosarcoma (10)] or an oncogene [melanoma (11), up-regulated in the plasma of colorectal cancer (12) and head and neck carcinoma (13)].Because the miR-15a/16-1 and miR-15b/16-2 clusters share miRNAs that are highly similar or, in the case of miR-16, identical, it is possible that they control a similar set of target genes and have overlapping functions.To better characterize the role of miR-15b/16-2 in tumorigenesis and tumor progression, we generated a conventional miR-15b/16-2 knockout mouse model. By the age of 15–18 mo, miR-15b/16-2 knockout mice developed lymphoproliferative disorders closely resembling human B-CLL, with diffuse lymph node enlargement and severe splenomegaly due to the expansion of a CD19+ CD5+ double positive population of neoplastic B cells.