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Creatine kinase (CK), lactic dehydrogenase (LDH), and more recently their isoenzyme determinations (CK-MB and LDH1) have been useful adjuncts in verification of myocardial injury. To determine whether DC cardioversion affects these serum enzyme levels, we recorded total CK, total LDH, CK-MB, and LDH1levels serially during 24 hours following elective DC cardioversion in 18 patients without cardiac ischemia. New postcardioversion elevations in total CK and total LDH levels were small and occasional: CK (one of 18 patients), LDH (four of 18 patients). Elevations of CK-MB or LDH1following cardioversion did not develop in any of the patients. Therefore, new CK-MB or LDH1elevations associated with arrhythmias must result from myocardial damage to DC cardioversion. (JAMA239:122-124, 1978)

Excerpt The treatment of ventricular arrhythmias remains a major challenge. Ventricular arrhythmias may be symptomatic; ventricular arrhythmias after myocardial infarction have recently been correl...

The time course of the rise in serum digoxin concentration was followed in 18 patients treated with digoxin as quinidine treatment was started with a loading dose. The mean serum digoxin levels rose significantly during the first 24 hours after administration of quinidine was begun, and reached a new steady state concentration after about 48 hours. Digoxin kinetics were studied in two groups of normal volunteers: Group I (n = 7) received a small dose of quinidine, 800 mg/day, and group II (n = 8) received 1,600 mg/day. There was no significant mean change in the apparent volume of distribution of digoxin in either group. In group I (small dose), quinidine reduced the digoxin clearance values: total clearance by 30 percent, renal clearance by 32 percent and nonrenal clearance by 29 percent. In group II (large dose), quinidine reduced digoxin total clearance by 36 percent, renal clearance by 54 percent and nonrenal clearance by 22 percent. The reductions in digoxin volume of distribution and renal clearance during quinidine treatment were a function of the serum quinidine concentration. The change in nonrenal clearance of digoxin was independent of serum quinidine concentration.

Two of the most important treatable causes of death in patients with coronary artery disease are the cardiac arrhythmias and conduction abnormalities. They may be associated with acute myocardial infarction (AMI) or chronic ischemia. Detection of such rhythm and conduction abnormalities has been discussed in chapter 5, and their pathophysiology was commented on in chapter 2. For the purpose of discussing therapeutic approaches, AMI can be divided into four phases: (1) the prehospital phase, (2) the CCU phase, (3) the post-CCU phase, and (4) the post-hospital phase. The cardiac arrhythmias and conduction defects encountered in each of these phases will be discussed, as will their therapy. The management of arrhythmias encountered in the setting of chronic ischemic heart disease will also be discussed.

Excerpt Quinidine has been the prototype of antiarryhthmic drug since it was introduced into clinical practice in 1918, and it is widely used for treatment of both atrial and ventricular arrhythmia...