Vrelo?
>>PALO ALTO, Calif., Nov 19, 2001 /PRNewswire via COMTEX/ -- CV Therapeutics, Inc. (Nasdaq: CVTX chart, msgs) announced today that in an open-label, dose-ranging Phase II clinical trial in patients with atrial fibrillation or flutter, CVT-510 consistently reduced heart rate from baseline (p<0.05) without decreasing blood pressure. The Company is therefore embarking on a broad Phase IIb development program aimed at defining an optimized dosage regimen in patients with this complex cardiac disease. Current clinical trials for CVT-510 include a Phase III trial in patients with PSVT and Phase II trials in patients with atrial fibrillation.
"We are pleased that the CVT-510 program has successfully established proof of concept for reduction of heart rate in atrial fibrillation, and is now committed to a broader Phase IIb program," said Louis G. Lange, M.D., Ph.D., Chairman and Chief Executive Officer of CV Therapeutics, Inc. "With our strong balance sheet of approximately $350 million in cash, we can continue to move our clinical programs forward."
Over 2.6 million times per year, patients are admitted to U.S. hospitals and emergency rooms with a primary or secondary diagnosis of atrial arrhythmias. Atrial arrhythmias, such as atrial fibrillation, atrial flutter and paroxysmal supraventricular tachycardia (PSVT), can cause potentially life-threatening low blood pressure, and may also result in stroke or heart attack.
Atrial arrhythmias occur when electrical signals in the atria cause the heart to beat too rapidly or uncontrollably. The AV node controls the transmission of electrical impulses from the atria to the ventricles. When the frequency of signals passing through the AV node is too high, the ventricles, in turn, begin to beat too rapidly. This results in insufficient time for filling and emptying the left ventricle, which causes low blood pressure (hypotension) and reduced blood flow to the brain and other vital organs. Therefore, the heart rate needs to be controlled urgently.
Clinical studies conducted with intravenous CVT-510 suggest that it may slow the speed of AV nodal conduction by selectively stimulating the A1 adenosine receptor, and could avoid blood pressure lowering because it does not stimulate the A2 adenosine receptor. Thus, it may be possible to use intravenous CVT-510 for rapid intervention in the control of atrial arrhythmias without lowering blood pressure.<<
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Cheers, Tuck (who made a few bucks on the recent drop and is thinking of reloading) |
