Significance of malperfusion syndromes prior to contemporary surgical repair for acute type A dissection: outcomes and need for additional revascularizations.

OBJECTIVE: The aim of this study was to assess the significance of malperfusion syndromes in patients with acute type A aortic dissection following a contemporary surgical management algorithm and the effects on morbidity, hospital mortality, and long-term survival. We believe that obliteration of the primary tear site with restoration of flow in the true aortic lumen results in decreased need for revascularization of malperfused organ systems. METHODS: Our operative approach aims at replacing the entire ascending aorta, resuspension of the aortic valve with repair or replacement of the sinus segment, and routine open replacement of the arch under hypothermic circulatory arrest with retrograde cerebral perfusion with obliteration of false lumen at the distal arch/proximal descending thoracic aorta, thus reestablishing normal flow in the descending thoracic true lumen. From January 1993 to December 2004, 221 consecutive patients underwent repair of acute type A aortic dissection at our institution. Data were collected retrospectively and prospectively. Various types of malperfusion syndromes were present in 26.7% of patients. The organ systems with malperfusion were as follows: cardiac, 7.2%; cerebral, 7.2%; ileofemoral, 12.7%; renal, 4.1%; mesenteric, 1.4%; innominate, 5.4%; and spine, 2.2%. RESULTS: Coronary malperfusion required coronary revascularization in 62.5% of cases. Distal revascularization was needed in 42.9% of patients with ileofemoral malperfusion. Patients with malperfusion were more likely to suffer perioperative myocardial infarction (p<0.001), postoperative coma (p=0.012), delirium (p=0.011), sepsis (p=0.006), acute renal failure (p=0.017), dialysis (p=0.018), and acute limb ischemia (p<0.001). The in-hospital mortality was 30.5% in patients presenting with any malperfusion syndrome while only 6.2% in patients without malperfusion syndrome (p<0.001). Both cardiac (p=0.020) and cerebral malperfusions (p<0.001) were risk factors for in-hospital mortality. The actuarial long-term survival in patients with malperfusion syndrome was estimated by Kaplan-Meier methods to be 67.8%+/-6.1% at 1 year, 54.0%+/-7.0% at 5 years, and 43.1%+/-8.0% at 10 years and for patient without malperfusion 82.7%+/-3.0% at 1 year, 66.3%+/-3.9% at 5 years, and 46.1%+/-6.7% at 10 years (log rank 2.55, p=0.110). Cerebral malperfusion was a significant risk factor for decreased long-term survival (p=0.0002). CONCLUSIONS: The occurrence of malperfusion in patients with acute type A dissection is associated with significant increased risk of in-hospital mortality and complications. Additional revascularization is generally needed in patients with coronary malperfusion and ileofemoral malperfusion. Patients presenting with cardiac and cerebral malperfusions have a high hospital mortality and preoperative cerebral malperfusion is associated with dismal long-term survival.     

The bladder cooling reflex and the use of cooling as stimulus to the lower urinary tract

PURPOSE: We review the physiology of bladder cooling response in experimental animals and humans, and present its clinical usefulness. MATERIALS AND METHODS: We describe experimental studies of the bladder cooling response, and more recent clinical retrospective and prospective studies of the bladder cooling test in adults and children. RESULTS: Studies indicate the existence of a segmental spinal bladder cooling reflex that originates from specific cold receptors in the bladder and urethral walls supplied by unmyelinated C-afferents. The reflex is positive in neurologically normal infants and children until about age 4 years. It becomes negative with further maturation of the nervous system but may be unmasked by pathological processes that disturb the descending neuronal control of normal voiding. A positive test in a patient with an overactive bladder requires further neurourological evaluation. CONCLUSIONS: The bladder cooling response originates from cold receptors within the walls of the lower urinary tract. The cooling response represents a neonatal reflex that may be unmasked by central neuropathology, analogous to the appearance of the Basbinki sign in pyramidal tract lesions. The bladder cooling test is a simple and valuable tool to support the diagnosis of neurourological disorders.     

Gastrointestinal Bleeding on Oral Anticoagulation: What is Currently Known

Drug Safety - Gastrointestinal bleeding (GIB) is the most common type of bleeding occurring in patients on oral anticoagulation. A meta-analysis of the landmark randomized controlled trials (RCTs)...     

Low mannose binding lectin predicts poor prognosis in patients with early rheumatoid arthritis. A prospective study

OBJECTIVE: To determine whether low mannose binding lectin (MBL) is associated with poor prognosis in rheumatoid arthritis (RA) and whether patients with RA have increased frequency of MBL deficiency. METHODS: Patients with recent onset symmetric polyarthritis (< 1 year, median 3 mo) were recruited if they had not been treated longer than 2 weeks with disease modifying drugs. They were reevaluated after 6 months and their disease activity and progression were correlated with their MBL concentration, rheumatoid factor (RF) isotypes, and C-reactive protein (CRP). Sixty-three female patients with advanced RA were also analyzed. RESULTS: Sixty-five patients with early arthritis fulfilled American College of Rheumatology criteria for RA and 52 were followed for 6 months or longer. Low MBL was associated with raised RF, IgA RF in particular (p = 0.02). and also with a combined elevation of IgM and IgA RF (p = 0.035). Patients with low MBL (lowest 25th percentile) showed less improvement after 6 months of treatment than patients in the highest MBL quartile. This applied to the Thompson joint score (p = 0.03) and grip strength (p = 0.004). Low MBL was also significantly associated with radiological joint erosions at recruitment and at 6 month followup (p = 0.039); and the group with advanced RA also showed a significant association between low MBL concentration and radiological damage (p = 0.036). However. neither patient group had increased frequency of MBL deficiency compared to healthy controls. CONCLUSION: Low MBL predicts poor prognosis in patients with early RA.     

Genetics of cardiovascular diseases: lessons learned from a decade of genomics research in Iceland

Abstract

In the past 10 years, large-scale genotyping has led to discoveries of sequence variants that confer the risk of many common and complex diseases. Due to pioneering work done, in large part, at deCODE genetics in Reykjavik, discoveries from Iceland have contributed substantially to key advances in population genetics. In cardiovascular medicine, a number of discoveries have been made, uncovering sequence variants that are associated with disorders such as coronary artery disease, atrial fibrillation, sick sinus syndrome, peripheral vascular disease, aortic aneurysm, and ischemic stroke. Thus, a wealth of genetic data has been accumulated in cardiology and has enhanced our understanding of a number of diseases. In many cases, these findings offer new mechanistic clues into the pathophysiology of complex cardiovascular diseases and may point toward novel therapeutic approaches in drug therapy. The next important step is to begin to transform these findings into practical clinical knowledge with the aim of improving the delivery of cardiovascular health care.     

Deficiency of complement-dependent prevention of immune precipitation in systemic sclerosis

BACKGROUND: Previous studies have indicated that complement may be activated or inherently abnormal in systemic sclerosis (SSc), and it has been suggested that immune complex deposition plays a part in the microvascular damage of this disease. OBJECTIVE: To study several aspects of the complement system in 24 patients with SSc. METHODS: Complement dependent prevention of immune precipitation (PIP) was measured by a sensitive enzyme immunoassay, levels of C1q, C4, and C3 by rocket immunoelectrophoresis, C4 allotypes by high voltage agarose electrophoresis, and C4A, C4B, and C3d by an enzyme linked immunosorbent assay (ELISA). RESULTS: PIP was markedly decreased in the patients with SSc (p<0.001). Abnormal complement activation was detected in nine patients as raised levels of the complement split product C3d. However, a relation between low PIP and complement activation was not seen. PIP was significantly lower in patients who carried the C4A*Q0 allotype (p=0.03), and a strong correlation was found between PIP and C4A concentration (p<0.00001). The PIP defect may, at least in some patients, be associated with the initial phase of the disease. CONCLUSIONS: The results show a previously unrecognised functional defect of complement in SSc; the defect correlates with low levels of classical pathway components and, in particular, C4A.