Neurally mediated syncope.

Neurally mediated syncope is a disorder of the autonomic regulation of postural tone, which results in hypotension, bradycardia, and loss of consciousness. A wide variety of stimuli can trigger this reflex, the most common stimulus being orthostatic stress. Typically, a patient with neurally mediated syncope experiences nausea, lightheadedness, a feeling of warmth, and pallor before abruptly losing consciousness. If the cause of syncope is unclear, a stepwise approach is necessary to arrive at the diagnosis. The diagnosis of neurally mediated syncope can be confirmed by a head-up tilt-table test. Treatment options include behavioral modification and several pharmacologic therapies. For severe recurrent syncope unresponsive to conventional treatment, a pacemaker can be implanted.

Predictors of conversion to sinus rhythm using ibutilide for atrial fibrillation or flutter.

To determine what factors can predict conversion to sinus rhythm, we retrospectively studied 201 consecutive patients who received ibutilide for treatment of atrial fibrillation or flutter. On multivariate analysis, the following factors were significantly associated with conversion: recent onset of arrhythmia, an underlying atrial flutter rhythm, lack of a history of congestive heart failure, and lack of concomitant digoxin therapy.

Endovascular exclusion of abdominal aortic aneurysms: initial experience with stent-grafts in cardiology practice.

The use of an endovascular stent-graft prosthesis for the treatment of infrarenal abdominal aortic aneurysms is receiving increasing attention as an option that may avoid the significant morbidity and mortality associated with open surgical treatment. We studied the clinical effectiveness of stent-grafts in patients with infrarenal abdominal aortic aneurysms. Between October 1995 and May 1998, 33 patients underwent infrarenal abdominal aortic aneurysm exclusion with a homemade polytetrafluoroethylene-covered stent, and between November 1998 and September 1999, 56 patients underwent abdominal aortic aneurysm exclusion with the Medtronic AneuRx stent-graft. Overall, these patients represented a high-risk surgical group. The technical success rate was 100% in both groups. No patient required immediate conversion to open repair. With the polytetrafluoroethylene-covered stent, the primary success rate was 33%, and the secondary success rate was 76%. In the AneuRx group, the primary success rate was 82.8%, and the secondary success rate was 85.3% at 6 months. There was no procedural or 1-month mortality or major morbidity in either group. By showing that infrarenal abdominal aortic aneurysms can be treated safely and successfully with an endoluminal stent-graft, our early results provide additional support for the endovascular treatment of abdominal aortic aneurysms. Further follow-up studies will determine the long-term ability of such treatment to prevent aneurysmal rupture and death.

Impact of the "stent-when-feasible" policy on in-hospital and 6-month success and complication rates after coronary angioplasty: single-center experience with 17,956 revascularization procedures (1993-1997).

This retrospective, observational, single-center study analyzed the results of a "stent-when-feasible" policy in a real-world setting. The study began in the "pre-stent" period (1993) and ended after the beginning of the "routine stent" period (1997). When the 1993 and 1997 global data were compared, the early and 6-month results included significant improvements in the rates of angiographic success (89.3% vs 97.1%), emergency surgical revascularization (1.0% vs 0.3%), freedom from in-hospital major events (91.2% vs 95.9%), and freedom from 6-month major events (77.2% vs 85.1%). The 6-month redo revascularization rate was reduced by almost half for "any catheter intervention" (19.6% vs 10.7%) and was lowest after stent use (7.7% in 1997).

Low-energy internal cardioversion of atrial fibrillation after failed external cardioversion: Texas Heart Institute experience and review of the literature.

In patients with atrial fibrillation, low-energy internal cardioversion may be used to restore sinus rhythm after external cardioversion fails. We used this method in 8 consecutive patients with a mean age of 69.5+/-8.3 (SD) years, 7 (87.5%) of whom were successfully treated with a mean 9.1 J (range, 4 to 14 J). No patient had ventricular arrhythmias at the time of cardioversion, or local groin complications afterward. One patient had recurrent atrial fibrillation the morning after cardioversion, and another patient had an embolus to the renal artery 20 days posttreatment. After 1 month, 5 patients were still in sinus rhythm, and 1 patient was lost to follow-up. This study confirms the efficacy of internal cardioversion in this setting and stresses the importance of a standard anticoagulation protocol before and after cardioversion.

Platelet glycoprotein IIb/IIIa receptor antagonists: current concepts and future directions.

Platelets play a key role in the development of thrombosis. Glycoprotein (GP) IIb/IIIa antagonists are a new class of potent drugs that profoundly inhibit platelet function by blocking the key receptor involved in platelet aggregation. Several antiplatelet agents with varying characteristics have emerged in the past few years and have been evaluated in a variety of potential clinical settings. Clinical trials have established the effectiveness of these drugs in conditions where thrombosis plays a major contributing role such as unstable angina pectoris, myocardial infarction, and high-risk coronary intervention. Despite their potent antiplatelet effects, GP IIb/IIIa antagonists appear to be remarkably well tolerated, provided that the concomitant use of other anticoagulants such as heparin is managed carefully. Ongoing and future studies will further refine the role of GP IIb/IIIa antagonists, explore new applications, and further test their safety and cost effectiveness in the short and long term.

Complications associated with combined use of abciximab and an intracoronary thrombolytic agent (urokinase or tissue-type plasminogen activator).

A potent platelet inhibitor combined with an intracoronary thrombolytic agent is aggressive therapy that may be used for high-risk, complex, refractory thrombotic coronary lesions. A retrospective review of the records of 56 patients who received abciximab plus an intracoronary thrombolytic agent during a coronary interventional procedure did not reveal a prohibitive incidence of major bleeding with this combination therapy.

Epidermal growth factor stimulates distinct diradylglycerol species generation in Swiss 3T3 fibroblasts: evidence for a potential phosphatidylcholine-specific phospholipase C-catalysed pathway.

Stimulation of 3T3 fibroblasts with epidermal growth factor (EGF) results in an increase in 1,2-diacylglycerol (DAG) mass which is maximal at 25 s, declining at 1 min and returning to basal levels by 30 min. No changes in alkylacylglycerol or alkenylacylglycerol were detected. Three species account for most of this mass increase: 18:0/20:5,n-3, 18:0/20:4,n-6 and 18:0/20:3,n-9. These species are characteristic of the phosphoinositides; however, previous work failed to detect any EGF-stimulated rise in inositol phosphates in these cells [Cook and Wakelam (1992) Biochem. J. 285, 247-253]. This ruled out phosphoinositide hydrolysis by phospholipase C, but raised the possibility of phospholipase D/phosphatidate phosphohydrolase-catalysed hydrolysis of phosphatidylinositol. The inclusion of butanol in the incubation medium failed to block the diacylglycerol changes, indicating that the phospholipase D pathway is not involved and that DAG must be derived from another source, probably via phospholipase C-catalysed hydrolysis of a phosphatidylcholine pool that is particularly rich in these species. The tyrosine kinase inhibitor ST-271 almost abolished the elevation in 18:0/20:5,n-3, 18:0/20:4, n-6 and 18:0/20:3,n-9 at 25 s, but only reduced the rise in total DAG mass by about 50%. The protein kinase C (PKC) inhibitor Ro-31-8220 increased DAG levels at all time points but had no effect on the species profiles. This provides additional evidence for PKC-mediated regulation of cell-surface EGF receptors, since the inhibition of PKC would increase the availability and/or ligand binding affinity of receptors at the plasma membrane and hence increase and prolong the response to EGF.