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Unstable Angina with Tachycardia: Clinical and Therapeutic Implications

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Unstable Angina with Tachycardia: Clinical and Therapeutic Implications Unstable angina with tachycardia: Clinical and therapeutic implications We prospectively evaluated 19 patients with prolonged chest pain not evolving to myocardiai infarction and accompanied with reversible ST-T changes and tachycardia (heart rate >lOO beats/min) in order to correlate heart rate reduction with ischemic electrocardiographic (ECG) changes. Fourteen patients (74%) received previous long-term combined treatment with nifedipine and nitrates. Continuous ECG monitoring was carried out until heart rate reduction and at least one of the following occurred: (1) relief of pain or (2) resolution of ischemic ECG changes. The study protocol consisted of carotid massage in three patients (IS%), intravenous propranolol in seven patients (37%), slow intravenous amiodarone infusion in two patients (lo%), and intravenous verapamil in four patients (21%) with atrial fibrillation. In three patients (16%) we observed a spontaneous heart rate reduction on admission. Patients responded with heart rate reduction from a mean of 126 + 10.4 beats/min to 64 k 7.5 beats/min (p < 0.005) and an ST segment shift of 4.3 k 2.13 mm to 0.89 k 0.74 mm (p < 0.005) within a mean interval of 13.2 + 12.7 minutes. Fifteen (79%) had complete response and the other four (21%) had partial relief of pain. A significant direct correlation was observed for heart rate reduction and ST segment deviation (depression or elevation) (f = 0.7527 and 0.8739, respectively). These patients represent a unique subgroup of unstable angina, in which the mechanism responsible for ischemia is excessive increase in heart rate. Conventional vasodilator therapy may be deleterious, and heart rate reduction Is mandatory. (AM HEART J 1988;116:1188.) Samuel Sclarovsky, MD, Roni Bassevich, MD, Boris Strasberg, MD, Eliezer Klainman, MD, Eldad Rechavia, MD, Alex Sagie, MD, and Jacob Agmon, MD. Petah Tikva and Tel Aviv, Israel Unstable angina is a syndrome encompassing a patients with unstable angina and tachycardia. The variety of clinical and pathophysiologic entities.’ purpose of the present study was to characterize this Features of instability are largely determined by group clinically and electrocardiographically and to dynamic obstructions superimposed on a widely correlate heart rate reduction with clinical presenta- variable fixed obstruction.2-6 Continuous hemody- tion and ischemic ECG changes. namic and electrocardiographic (ECG) monitoring METHODS indicate that most episodes of ischemia in patients with unstable angina are not triggered by increases Nineteen consecutive patients (14 men and 5 women) with unstable angina and tachycardia were selected for in the major determinants of myocardial oxygen study provided they fulfilled the following criteria: (1) consumption. 7,g We recently discussedlo the prog- prolonged typical chest pain lasting longer than 15 nostic implications of the various patterns of ische- minutes accompanied by reversible ST-T wave changes mic ECG changes in patients with unstable angina and (2) heart rate above 100 beats/min not related to without evidence of increased myocardial oxygen effort with careful clinical evaluation to assurethat it was demand. not secondary to underlying physiologic abnormalities Because heart rate is the best single index for (dehydration, fever, anemia, overt heart failure). Patients myocardial oxygen consumption,‘* we used this with complete left bundle branch block or with subse- parameter to evaluate prospectively a subgroup of quent development of a new Q wave or with diagnostic elevation in cardiac isoenzymes were excluded. ST seg- ment deviation was defined as a shift >l mm from the PR segment 80 msec after the J point. A 12-lead ECG was From the Israel and Ione Massada Center for Heart Diseases, Beilinson recorded on admission. All patients entered a protocol in Medical Center; and the Tel Aviv University Sackler School of Medi- CIIIC. -zhi& they r;xkrwsnt continuol;s ECG monitoring in the Received for publication Dec. 11, 1987; accepted June 15, 1988. lead presenting the maximal ST segment deviation until Reprint requests: S. Sclarovsky, MD, Massada Center for Heart Diseases, heart rate reduction to 100 beatslmin or less and at least Beilinson Medical Center, Petah Tikva 49100, Israel. one of the following: (1) relief of pain or (2) restoration of 1188 Volume 116 Number 5, Part 1 Unstable angina with tachycardia 1189 7.1.87 & Ln Lm AVR AVL AVF vt v2 v3 v4 cc- Fig. 1. Example of unstable angina with tachycardia and ST segment elevation (case No. 1). A, Sinus tachycardia (130 beats/min) with evidence of recent anteroseptal myocardial infarction. ST segment elevation and positive T wave in leads V, to V,. B, Ten minutes after administration of propranolol. Note heart rate reduction to 94 beats/min, isoelectric ST segment, and T wave inversion. Lr Ln Lrn AVR AVL AVF V, v2 v3 v4 v5 V6 I : Fig. 2. Example of unstable angina with tachycardia and ST segment depression (caseNo. 13). A, Atria1 fibrillation (130 beats/min) with ST segment depression (9 mm in lead V,). B, Ten minutes after administration of verapamil. Conversion to sinus rhythm at a rate of 77 beats/min with only 1 mm ST segment depression. ECG changes.In order to assessthe net effect of heart rate tes, and three had both hypertension and diabetes. reduction on clinical features (pain) and ischemic ECG Fourteen patients (74 % ) received previous long- changes, no nitrates or analgesic treatment was given term treatment with nifedipine and nitrates in a throughout the study protocol. This protocol was as dose up to 60 mg and 160 mg, respectively; only one follows: (1) gentle carotid massagefor 3 minutes; (2) when of these patients received concomitant treatment carotid massage was ineffective or contraindicated (cervi- with beta blockers. One patient (No. 17) was admit- cal murmurs, previous TIA), intravenous propranolol up ted 24 hours after abrupt withdrawal of long-term t,o 0.1 mg/kg at the rate of 1 mg/min was administered; (3) when propranolol was contraindicated (bronchial asthma, beta blocker therapy. Eight patients received sublin- heart failure), amiodarone, 300 mg, was given in 30 gual nitrates for a short term (average dose 10 mg; minutes as a slow intravenous infusion; (4) in patients range, 5 to 20 mg) without clinical subjective with supraventricular tachycardia or atria1 fibrillation, improvement. verapamil was given intravenously up to 10 mg. Four patients (21% ) had ST segment elevation. Statistical analysis. All data are presented as the All had a recent myocardial infarction and the mean t standard deviation. Comparisonswere done by a maximal ECG changes occurred in the same lead paired t test. A p value <0.05 was considered signifi- demonstrating the previous infarction: two (50 % 1 cant. were in lead V, and the other two were in lead III (Fig. 1). Fifteen patients had ST segment depres- RESULTS sion. In 13 (87%) the maximal changes were The study group (Table I) consisted of 19 patients observed in leads V, and V, (Fig. 2). All patients had (14 or 74% were men) with a mean age of 65 -+ 9.8 typical chest pain lasting at least 15 minutes and years. Five patients had an old myocardial infarc- ranging from 15 to 420 minutes (mean 153 +- 130). tion, four had a recent (within 2 weeks) myocardial Three patients (16%) responded to carotid mas- infarction, seven had hypertension, five had diabe- sage. Seven patients (37%) were treated with beta November We8 1190 Sclarovsky et al. American Heart Journal Table I. Clinical data and therapeutic modalities in patients with unstable angina and tachycardia Interval Heart rate Pa- Type Lead with Duration till beatslmin tient Previous of tachy- ST segment max ST of pain effect No. Age Sex medical therapy cardia deviation changes min) Therapy (min) Pre Post 1 59 F N, NT ST Elevation V3 15 BB 10 130 94 2 50 M - ST Depression V, 90 BB 13 120 92 3 63 M N, NT, NTSL ST Elevation V3 120 CM 3 130 80 4 74 M N, NT, NTSL AF Depression V4 180 Verapamil 6 140 80 5 84 F N, NTSL ST Depression V4 360 CM 2 116 78 6 63 M N, NT ST Elevation L 180 BB 10 120 75 7 73 M N, NT, NTSL AF Depression V4 180 Verapamil 26 150 92 8 65 F NTIV ST Depression V5 15 BB 10 120 92 9 74 M AF Depression V5 420 Verapamil 20 140 75 10 58 F NTIV, N, NSL ST Depression V3 20 BB 10 120 90 11 49 M N, NT, I? ST Depression V, 90 CM 5 120 78 12 75 F - ST Elevation d 360 BB 15 135 96 13 71 M N, NT AF Depression V, 120 Verapamil 10 130 77 14 71 M N, NTSL ST Depression V, 180 Amiodarone 30 125 87 15 64 M N, NT ST Depression V4 120 Amiodarone 55 115 78 16 60 M N, NT, NTSL ST Depression V4 30 Spontaneous - 112 75 17 57 M BB withdrawal ST Depression VS 360 BB 12 120 90 18 63 M Diltiazem AF Depression V4 30 Spontaneous - 110 80 19 51 M N, NT, NTSL ST Depression V3 90 Spontaneous - 125 90 AF, atria1 fibrillation; BB, beta blockers; CM, carotid massage; IE, isoelectric; IV, intravenous; N, nifedipine; NT, nitrates; P, propranolol; SL, sublingual; ST, sinus tachycardia. *T wave inversion. blockers, four (21%) were treated with verapamil, patients can be classified into more homogeneous and two (10%) were treated with amiodarone. In groups by the use of more precise anatomic and three (16 % ) we observed spontaneous heart rate functional criteriaal We believe that such criteria reduction on arrival. Patients responded with heart must include the different patterns of ischemic ECG rate reduction from a mean of 125 +- 10.4 to 84 +- changes, and we recentlylO correlated those patterns 7.5 beats/min (p <0.005) and an ST segment shift of with prognosis and coronary anatomy.
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