Changes in Regional Adrenergic Tone During Sustained Ventricular Tachycardia Associated with Coronary Artery Disease or Idiopathic Dilated Cardiomyopathy Kenneth A. Ellenbogen, MD, Michael L. Smith, PhD, Marc D. Thames, MD, and Pramod K. Mohanty, MD The hemodynamk tokrance of an episode of ventrkular tachycardia (VT) can vary widety from no decrease in systotk bkod pressure to severe hy- potenston. Little is known about the factors respon- sible for these different responses In man. Previous animal stuc&s have suggested an important rots for vasownstriction mediated by the a-adrenergk nervous system. To detennine the magnitude and thne course of changes in a-adrenergk tone during symptomatk sustained monomo@tk VT, VT cyck length, mean and phask arterial pressure, forearm blood flow (by venous OCCIU&I p~~y-~~phy) and forearm vascular resistance were measured in 15 patients. Nine of these patients were studied be- fore and after regknal intraarterial a bkchade with phentotamine. After the induction of VT (350 f 68 ms), mean forearm bkod flow decreased from 32 f 1.1 to 2.2 f 0.8 ml/min/lOO ml (p = 0.0002) and the forearm vascular resistance increased from 32* 14t040*14units(p=0.01).Therewere no dgnificant differen~s for forearm vascular re- sktancedurbtgthefirstandlast3OsecondsofVT (41.3 f 14 VI 37 f 13 units). After the Infuskn of intraartertal phentolamine, there were no signifi- cant changes in the VT cycle length or mean arteri- al pressure, but the forearm vascular resistance in- crease during VT was blunted by 60 to 70%. Most patients with symptomatic VT demon- strate sympathetk v Biandthese changes are maximal during the first 30 seconds of VT. This sympathoexcttatory response is due iargeiy to sttmutatkn of a-adrenorecepton and may be mediated by arterial baroroflexes. (Am J Cardid 1990;65:1334-1338) From the Department of Medicine, Division of Cardiology, McGuire Veterans Administration Medical Center and the Medical College of Virginia, Richmond, Virginia. This study was supported in part by grant HL 30506 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland, and by funds from the Veterans Administration. Manuscript received November 13, 1989; revised manuscript received and accepted February 2,199O. Address for reprints: Kenneth A. Ellenbogen, MD, McGuire Veter- ans Administration Medical Center, Cardiology (111 J), 1201 Broad Rock Boulevard, Richmond, Virginia 23249. T he autonomic nervous system plays an important role in the genesis of ventricular arrhythmias.1-4 Hemodynamic tolerance and clinical symptom- atology during an episode of ventricular tachycardia (VT) vary widely from minimal symptoms to syncope resulting from severe hypotension. Little is known about the different factors responsible for these varying re- sponses. The baroreflexes mediate vasoconstrictor re- sponses during hypotension, and may play an important role in the modulation of the severity of hypotension during VT. Our understanding of the autonomic changes that occur during induced ventricular arrhythmias is based primarily on animal studies5v6 These studies demon- strate increases in cardiac and peripheral sympathetic nerve traffic as well as elevated plasma catecholamine levels after single premature ventricular complexes and couplets.7-9 The increase in sympathetic nerve traffic af- ter premature ventricular complexes is believed to be mediated largely by arterial baroreflexes. There is, how- ever, little information about changes in sympathetic outflow during sustained ventricular arrhythmias in humans. Venous occlusion plethysmography is a noninvasive technique for measurement of changes in forearm blood flow and calculation of changes in forearm vascular re- sistance. This measurement is an approximation of re gional changes in sympathetic outflow to a vascular bed and can detect rapid changes in sympathetic tone. We measured the magnitude and time course of changes in forearm vascular resistance during sustained monomor- phic VT, before and after CY blockade. MEW005 The study group consisted of 15 patients referred for evaluation of symptomatic VT due to coronary artery disease or idiopathic dilated cardiomyopathy. All pa- tients underwent angiography with left ventriculog- raphy to determine ejection fraction. No patient had symptoms of New York Heart Association class IV congestive heart failure. Patients with diabetes mellitus or inability to cooperate with the measurement of fore- arm blood flow because of other systemic diseases (e.g., Parkinson’s disease) or previous trauma to the arm or brachial arteries were also excluded from this study. All calcium antagonists, /3 blockers, angiotensin converting 1334 THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 65