INEFFICACY OF "THEHAPEuTIC" SERUM LEVELS OF DIGOXIN IN CONTROLLING THE VENTRICULAR RATE IN ATRIAL FIBRILLATION Steven Goldman, MD, Peter Probst, MD, Margot Green, MD, and Keith Cohn, MD, FACC, Presbyterian Hospital, Pacific Medical Center, San Francisco, California Although therapeutic and toxic serum concentrations of digoxin have been established, there is sparse information permitting correlation of drug level with clinical effect. This study was undertaken to assess the radioimnunoassay serum digoxin levels (DL) in 30 pts with acute atria1 fibrillation (AAF, 39 determinations) and 30 pts with chronic The chronic fibrillators AF (CAF, 54 determinations). were subdivided into those who were clinically stable (14 pts), and those unstable with a superimposed illness Slowing of ventricular response (VR) (65 - 95 (16 pts). beats/min) at "therapeutic" levels of digoxin (0.8-z ng/ml) was achieved in only 5/39 with AAF and 7/38 clinically unstable pts with CA??. However, 10/16 with stable CAF slowed adequately with therapeutic or 39 of these were in pts who were subtherapeutic DL's. ill with conditions such as infection, hypoxia or recent Slowing of the VH required potentially thoracotomy. Concl; 1) DL's toxic DL (2.5-6 ng/&) in 14 instances. below 2 ng/ml are usually sufficient to control VH in stable pts with CAF; 2) These levels often fail to lower VR appreciably when a complicating illness coexists; and 3) Even high concentrations of digoxin, > 2.5 ng/ml, often fail both to produce adequate AV blockade and to elicit signs and symptoms of toxicity in pts with atria1 fibrillation and rapid ventricular response.
THE VALUE OF ECG TELEMETRY IN DETECTING ARRHYTHMIAS DURING THE CONVALESCENT PHASE OF ACUTE MYOCARDIAL INFARCTION. H. Joel Gorfinkel, MD, FACC, Lois Kercher, RN, Joseph Lindsay, Jr., MD, FACC, The George Washington University Medical Center, Washington, D. C. In recent years large amounts of time and money have been spent in equipping progressive coronary care units with ECG telemetry (T) equipment, and in training personnel to interpret arrhythmias (A). Currently many hospitals are monitoring the ECG rhythm of patients convalescing from acute myocardial infarction (MI) after their transfer from the CCU. Others are making However, the value of this approach plans to do so. to patient care has not been established. Therefore, we assessed the value of T in a group of 100 patients recovering from acute MI after their transfer from the ecu. The patients' ages covered a span of the 4th through the 9th decade. There were 73 men and 27 women. Patients were monitored from 1 to 15 days, mean, 4 days. Arrhythmias were detected in 66/100 patients (66%), 46% detected within the first 2 days. Thirty-eight patients (38%) had PVCs, 2 had ventricular tachycardia, and 3 had ventricular fibrillation (VF). In 27/66 patients with A (41%) treatment was changed as a direct result In 1 case T was life saving. Three patients died of T. who had experienced irreversible brain damage as a result of VF prior to CCU admission, and 1 died secondary to ventricular rupture. There were no complications attributable to A in any patient in whom no A was observed by T. T also detected early digitalis toxic A in 1 patient. Because of the 41% rate of change in therapy due to A detection with T, T is of value in treating patients recovering from MI.
The American Journal of CARDIOLOGY
1 HOUR FOLLOWING
OCCLUSION: EFFECT OF COLLATERAL BLOOD FLOW Martin G. Gottwik, MD; Edward S. Kirk, PhD; Sylvia Hoffstein, PhD; William B. Weglicki, MD, Peter Bent Brigham Hospital, Harvard Medical School, Boston, Mass. Early changes in lysosomal enzymes must occur, if their role is significant in irreversible myocardial injury. We therefore ligated the anterior descending coronary artery in 12 dogs and after 60 min excised epicardial and endocardial samples from the ischemic and adjacent normal heart. The muscle was disrupted and fractionated by ultracentrifugation into nuclear pellet (NP) heavy lysosoma1 pellet (HL), light lysosomal pellet (LL), microsomal pellet (M) and supernatants (S). Electron microscopy demonstrated changes characteristic of ischemia in tissues and sedimented fractions. Acid hydrolase stains indicated abundance of residual bodies in the HI fraction and membrane bound material in the LL fraction. Significant decreases in the specific activity (n moles/mg-min) of N-acetylglucoseamindase (NAG) and S-Glucuronidase (B-GLUC) occurred in the endocardial LL fraction: (NAG from .64 to .45, B-GLUC from .80 to .41, ~.005), while increases in both were found in supernatants (NAG from .46 to .62, B-GLUC from .56 to .70). josses of p-nitrophenylphosphatase occurred in both LL and S (from 2.10 to 1.50 in LL, from 1.30 to 1.08 in S, p>.Ol). Moreover, a decrease of NAG in HI.was positively correlated to the degree of ischemia, measured with radioactive microspheres (r = .9, x.001) and the enzyme appeared normal when collateral flow (CF) was 40%. CF in endocardial samples averaged 19% of control. Ischemia and enzyme changes were less significant in epicardial samples. The early loss of enzymes from the lysosomal fractions in severe ischemia strongly suggests a role for lysosomal hydrolases in the necrosis that follows coronary occlusion.
SALUTARY EFFECTS OF EXTERNAL COUNTERPULSATION IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION K.S. Gowda, MD; Robert Roberts, MD; H. Dieter Ambos; Burton E. Sobel, MD, FACC, Washington University, St. Louis, Missouri. To determine whether external counterpulsation (ECP) protects myocardium we studied 13 patients with myocardial infarction treated with ECP, 13 conventionally managed patients matched for estimated infarct size and 13 normal subjects. Ventricular premature complexes (WCs) on '20 hour continuous ECG recordings were quantified with the Argus/H computer system. Infarct size was predicted from projected serum CPK values on best fit curves derived from early CPK values as previously described. Observed infarct size was estimated from 48 hr serial CPK changes. ECP was performed for 30 min with 15 min rest periods for 18 hrs beginning as soon as infarct size had been predicted. It augmented intra-arterial diastolic pressure by at least 30 mm Hg in all patients. ECP did not release substantial amounts of CPK from skeletal muscle in normal subjects (mean peak CPK = .067 IU/ml). ECP decreased the frequency of VPCs within one hr in all but one patient (av. decrease from 160 to 89 VPCs/hr, p<.Ol), with the reduction persisting throughout the 20 hr recording interval. VPC frequency remained constant in controls during corresponding intervals (av. increase = 2 VPCs/hr). Although ECP decreased pulmonary artery occlusive pressure (mean decrease = 7 mm Hg), it did not preserve jeopardized myocardium. Average predicted and observed infarct size ware similar (91 and 90 CPK-g-eq) in treated patients, as well as in controls. In three patients treated with ECP, frank extension of infarction (averaging 134%) accompanied termination of the intervention. Thus, ECP decreases the frequency of VPCs after infarction. However, although it may slow the evolution of infarction, it does not salvage ischemic myocardium.