prolonged H-V conduction and increased refractoriness within the VSCS suggests that patients with LBBB have conduction abnormalities in the right bundle as well. Metabolic Consequences of Increased Peripheral Arteriolar Stiffness in Active Skeletal Muscle in Clinical Congestive Heart Failure ROBERT CAPONE, MD; EDWARD MANSOUR, MD; JOHN LONGHURST; DEAN T. MASON, MD, FACC; EZRA A. AMSTERDAM, MD; ROBERT ZELIS, MD, Davis, California Patients with congestive heart failure (CHF) exhibit 2 major peripheral circulatory compensatory mechanisms: increased arteriolar stiffness resulting in reduced blood flow to metabolically active tissues and augmented sympathetic tone limiting flow to metabolically inactive tissues. To determine the physiologic consequences of CHF arteriolar stiffness, forearm blood flow (FBF) was measured plethysmographically at rest and during relaxation between 5 second isotonic hand-grip exercises to 25, 50 and 100 mm Hg (4/min for 6 min). Resting FBF was depressed in 5 patients with severe CHF (2.02 ml/min per 100 ml) and during each level of exercise (exercise, 3.95, 5.17, 6.68) when compared with 19 normal subjects (rest, 3.27, P and potassium balance (K+, A CS mEq/liter). In 2 subjects angina did not develop, and they had a normal electrocardiogram and hemodynamits. Angina was induced in 12 patients before GTN, with S-T segment depression (-2.4 + 1.7 mm, mean + SD) and elevation of the post-pacing left ventricular end-diastolic pressure (PP-LVEDP, 23.6 t 7.2 mm Hg). Mean lactate production and myocardial K+ loss were -17.8 + 31.9% and -0.27 2 0.21 mEq/liter, respectively. During sinus rhythm, GTN did not alter myocardial lactate metabolism or K+ balance, although uptake of this cation was seen at this time. During pacing after GTN, angina was absent in 10 patients with less S-T segment depression (-0.83 f 1.2 mm, P = 0.016) and lower PP-LVEDP (11.5 2 5.2 mm Hg, P <O.Ol). Despite variability in individual responses mean lactate production and myocardial K+ loss did not occur although lactate uptake was seen in only 2 patients. In summary, after GTN administration there was improvement of clinical, electrocardiographic, hemodynamic and metabolic responses during atria1 pacing. Aberrant Atrial Conduction-Unrecognized Electrocardiographic Entity EDWARD K. CHUNG, MD, FACC, Morgantown, West Virginia The bizarre configuration of the P wave of a sinus beat immediately following an atria1 premature contraction (APC), atrioventricular (A-V) nodal or ventricular premature contraction (NPC or VPC) or parasystolic beat is termed “aberrant atria1 conduction” (AAC) ; and is analogous to aberrant ventricular conduction. This paper describes the incidence, diagnostic criteria and clinical correlation of this heretofore unrecognized electrocardiographic finding. In patients whose ages ranged from 40 to 89 years, 120 instances (0.1%) of AAC were found among 120,000 tracings. The incidences of AAC after APC, NPC, VPC and parasystolic beat were, respectively, 72 (60%), 20 (16.6%), 12 (10%) and 16 (13.3%). An AAC tends to occur after a long post-ectopic pause, (i.e., nonconducted APC or a retrograde P wave of an NPC or VPC), and it is not directly related to the coupling interval or to the length of the cardiac cycle just preceding or following this interval. AAC may rarely occur in 2 or more consecutive sinus beats. An alteration of atria1 depolarization due to a prolonged refractory period influenced by an ectopic impulse is considered to be the cause of AAC. In 97.3% of cases organic heart disease was present, most commonly ischemic or hypertensive, or both (80 cases; 66.6%). In 75% the patients were 60 years or older. Half had evidence of heart failure, 6 had digitalis intoxication, and a small number had other heart diseases. AAC is to be differentiated from wandering atria1 pacemaker, atria1 fusion beats, A-V nodal escape beats and artifacts. The author proposes “AAC” as a new electrocardiographic entity indicating significant organic heart disease. 628 The American Journal of CARDIOLOGY