An 81-year-old marathon runner-internist
developed syncope followed by myocardial stunning two hours after conversion to
normal sinus rhythm and 4 hours after adding a single 150mg dose of propafenone
to 650mg of quinidine gluconate which he had ingested 3 hours earlier. Cardiac isoenzyme, electrolyte, CBC, TSH and
EKG were normal. Echocardiogram one week
later revealed left ventricular hypertrophy with an enlarged left atrium
typical of men with habitual endurance-associated atrial fibrillation. Over the previous 24 years he had
successfully converted more than 100 episodes of PAF with PIP oral quinidine
sulfate (200mg-600mg) or quinidine gluconate (650-975mg) without utilizing
other cardiac, anti-arrhythmic, or anti-coagulation therapy. Several months
after we published his adverse event (37) CYP2D6 analysis demonstrated alleles
4 and 41, identifying him as an IM/PM 2D6-deficient subject.
Within the next year, he successfully converted episodes of PAF on 2
occasions with 100mg of oral flecainide, but both were accompanied by mildly symptomatic EKG-documented atrial
flutter with 2/1 AV block and a ventricular rate of 120-140 beats per minute,
resulting in a return to PIP quinidine and successful conversion of over 60
additional mildly symptomatic but increasingly frequent episodes of PAF over
the next 3 years by utilizing 200-600mg of oral quinidine sulfate each
resolving within 4-8 hours, during which he was able to continue his daily
exercise and other daily activities without interruption.
Credits: Harry W. Daniell, MD