A patient with non-q wave acute inferior myocardial infarction. Citation Hong Kong Practitioner, 1997, v. 19 n. 4, p

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Title A patient with non-q wave acute inferior myocardial infarction Author(s) Ng, W; Wong, CK; Lau, CP Citation Hong Kong Practitioner, 1997, v. 19 n. 4, p. 199-202 ssued Date 1997 URL http://hdl.handle.net/10722/45037 Rights This work is licensed under a Creative Commons Attribution- NonCommercial-NoDerivatives 4.0 nternational License.

A Patient With Non-Q Wave Acute nferior Myocardial nfarction W Ng, MBBS, MRCP C K Wong, MD, FRCP C P Lau,* MD, FRCP Department of Medicine The University of Hong Kong Summary The occurrences of atrioventricular (AV) nodal blockade or right ventricular (RV) infarction in acute inferior myocardial infarction (M) had been well recognised and signified a proximal right coronary artery (RCA) occlusion. However, they did not point out the extent of the RCA territory involved. We recently managed a patient with incomplete inferior M in which ECG on presentation already showed (he infarct-related RCA as the dominant vessel having proximal occlusion. Various aggressive treatments have been taken subsequently. (HK Pract 1997; 19: 199-202) B. if & is -V. «& %f t JL z*-,t, T %. " «i * S > 1=1 nf & is S, flfc ii ife S >&. Bfe n % n. ^ «^ & is *^ «ft 14 - & T^ ^ ^ T - -^ ^ *. %, jfc i4 ^ Pa S 51 &-^ R * t ' -S- «it - J^ ife ^ * 5i Pp * P^l -& ntroduction Acute inferior myocardial infarction (M) was once believed not to have serious sequele. Recently, new data support the contrary. We recently managed a patient with an acute inferior M and its manifested complications. New perspectives concerning the disease are discussed. Case A 65-years old female non-smoker who had history of hyperlipidaemia presented with sudden onset of severe chest pain to the Accidents and Emergencies Department. ECG showed ST segment elevation (> 1 mm) over Leads,, and avf; ST-depression/ T wave inversions over leads V2-V4 and inverted P waves associated with shortened PR interval over various chest and limbs leads (Figure 1). These findings were compatible with extensive acute inferior myocardial infarction (M) associated with conduction disorder. A right sided ECG was not available. There being no contraindication to thrombolytic therapy, streptokinase 1.5 megaunits was given Address for correspondence: Professor C P Lau, 4/F, Professorial Block, Queen Mary Hospital, Pokfulam Road, Hong Kong. 199

Non-Q Wave Acute nferior Myocardial nfarction LE Figure 1: ECG showing acute inferior M with ST elevation over leads, & avf, ST depression/t wave inversions over V2-V4, inverted P wave/shortened PR interval 10mm/mV 25mm/s Filter DN 1 11, V4 V5 V6 TeCH. Name,. ;..... :. '.! } i f i f,...,... :. f Q.M.H MB (over one-hour infusion) to this patient 5 hours after the onset of symptoms. t brought about resolution of chest pain and recovery of ST segments (Figure 2). The patient subsequently entered the Cardiac Rehabilitation Programme. On treadmill, she developed signs of cardiac ischaemia with horizontal ST depression over V2-V6 and angina at low workload capacity, which recovered with rest and sublingual nitrate. Cardiac catheterisation showed a critical proximal stenosis in a dominant right coronary artery (Figures 3-4). Left ventriculogram revealed overall good contractility apart from mild inferobasal hypokinesia. Adhoc angioplasty to this lesion was performed. She had an uneventful recovery. Discussion t is well known that acute inferior M can be associated with bradycardia and/or AV block. 1 These occurrences may be transient or require temporary pacing, but occasionally a permanent pacemaker will be needed. Conduction disorder did occur in our patient but reverted back to normal sinus conduction when the infarct-related artery (right coronary artery, RCA, in this case) reperfused. n addition, the finding of ST segment elevation of 1 mm or more in lead V4R (right-sided ECG) has a high sensitivity and specificity for detecting right ventricular (RV) infarction, pinpointing the site of occlusion in the proximal RCA. 2,3 When RV infarction occurs, its stiffness increases, thereby impeding diastolic filling and leads to potential haemodynamic embarrassment. When hypotension or shock occurs, expansion of vascular volume is generally employed as initial therapy. n nonresponders, dobutamine or similar inotropic agents may be helpful. 4, 5 The occurrences of AV nodal blockade or RV infarction in acute inferior M had been well recognised and signified a proximal RCA occlusion. However, they did not point out the extent of the RCA territory involved (i.e. whether the infarct-related RCA is dominant or not). Certainly, if a proximal occlusion in a dominant RCA 200

Hong Kong Practitioner 19 (4) April 1997 Figure 2: ECG showing reperfusion of acute inferior M 10m/nV 2 r >mm/s Filter ON ' avr av. avk UM/.V V V2 V} V4 V5 V6 ^JL^- ~, Rhythm( ) 10mm/mV Figure 3: Right coronary artery in right anterior oblique view showing a critical lesion in its proximal segment (arrow) Figure 4: Right coronary artery in right anterior oblique view after successful PTCA (arrow) 201

Non-Q Wave Acute nferior Myocardial nfarction UPDATE ARTCLE Key messages 1. Proximal RCA occlusion in acute inferior M is suggested by the occurrences of AV nodal blockade and/or RV Presence of significant precordial ST depression (V1-V3) in acute inferior M reflects the involvement o -flc&^l^^ ' < ' '","*," ; ; -.'.', occurred, more aggressive treatments should be given in order to salvage more myocardium. Wong et al 6-10 reported that the presence of significant precordial ST depression (V1-V3) in acute inferior M reflects the size of a dominant RCA with large posterolateral and total left ventricular perfusion territory, and is not a benign reciprocal ECG change as previously believed. As exemplified in our case there was significant precordial ST segment depression during the acute event which recovered with reperfusion. Subsequent cardiac catheterisation reviewed a dominant RCA with large posterolateral distribution. n the thrombolytic era, when successful reperfusion in the infarct related artery occurs, it often results in incomplete M or Non-Q M. They merely predict a high one year coronary event rate and therefore necessitate cardiac catheterisation and revascularisation procedure accordingly as performed here. n summary, acute inferior Ms are not always benign and various clinical and ECG parameters can help identify those high risk cases for more aggressive treatment strategy. References Tans AC, Lie K: AV nodal block in acute myocardial infarction. The conduction system of the Heart, Leiden, 1976 Stenfert Kroese. BraatSH, GorgelsAPM, Bar FW, et al: Value of the ST-T segment in lead V4R in inferior wall acute myocardial infarction to predict the site of coronary arterial occlusion. Am J Cardio 1988; 62:140-142. Braat SH, Burgada P, de Zwaan C, et al: Value of electrocardiogram in diagnosing right ventricular 10. involvement in patients with an acute inferior wall myocardial infarction. Br Heart J 1983; 49: 368-372. Kinch JW, Ryan TJ: Right ventricular infarction. N Engl J Med 1994; 330:1211-1215. Williams JF: Right ventricular infarction. Clin Cardiol 1990; 13: 309-315. Wong CK, Freedman SB, Bautovich G, et al: Derivation & validation of a new angiographic score of right coronary artery perfusion. Eur Heart J 1993; 14:469-473. Wong CK, Freedman SB: mplications of ST changes in reperfusion management of acute inferior myocardial infarction. Eur Heart J 1994; 15: 1385-1390. Wong CK, Freedman SB, Bautovich G, et al: Mechanison & significance of precordial STsegment depression during inferior wall acute myocardial infarction associated with severe narrowing of the dominant right coronary artery. Am J Cardio 1993; 71: 1025-1030. Wong CK, Freedman SB: Usefulness of continuous ST monitoring in inferior wall acute myocardial infarction for describing the relation between precordial ST depression & inferior ST elevation. AmJCardio 1993; 72: 532-537. Wong CK, Freedman SB: Reperfusion in acute inferior myocardial infarction: could tailed therapy be based on precordial ST depression? Am Heart J (in press). 202