Coronary Care Cardiology 1992;80:392-398
Cardiovascular Division and Coronary Care Unit, Beilinson Medical Center, Petah-Tiqva and Tel-Aviv University Sadder School of Medicine, Tel-Aviv, Israel
Keywords Electrocardiogram Myocardial infarction Q-waves Thrombolysis
Electrocardiographic Q-W aves Inconstancy during Thrombolysis in Acute Anterior Wall Myocardial Infarction
Abstract It is the purpose of this paper to describe the electrocardio graphic inconstancy of Q-waves during administration of thrombolytic therapy. This was documented in four patients given streptokinase early in the course of anterior wall myo cardial infarction. Understanding the pathogenesis of sequen tial dynamic variations of Q-waves in this setting may offer important insights into coronary physiology and management of acute coronary events. We discuss the possible explanations for such changes with respect to tissue viability, dynamic vas cular changes and electrophysiological properties of the reper fused infarcted myocardium.
Evolution of Q-waves during acute myo cardial infarction (AMI) is variable, tends to begin within 2 h of the onset of symptoms and is completed within 4-48 h. In experimental studies, Q-waves were noted 15-30 min after the release of coronary ligation and they be came more significant while serum enzyme levels were rising steeply [ 1]. Successful reper fusion has been shown to accelerate the rate of ECG changes [2] whereas delay in Q-wave appearance has been attributed to sustained compromised perfusion of the infarcted area. Regression or inconstancy of Q-waves may be
Received: December 27, 1991 Accepted: after revision: March 16. 1992
seen even as early as one week post-MI [3]. Naturally evolving non-Q-wave Ml would be expected in up to 37% of patients admitted with chest pain and ST segment elevation [4] as compared with 43% of patients who are treated with thrombolytic therapy [5], To our knowledge, no material has been published so far on the dynamic nature of Qwaves during thrombolytic therapy given at the early stages of AMI. In this report, the clinical and electrocardiographic sequence of observations in 4 patients with anterior wall MI canceling preexisting Q-waves during
Eldad Rechavia, MD Cardiovascular Division Beilinson Medical Center Petah-Tiqva, 49100 (Israel)
© 1992 S. Karger AG. Basel 0008-6312/92/ 0806-0392$2.75/0
Downloaded by: Leiden University Medisch Centrum 132.229.13.63 - 11/6/2018 8:08:20 AM
Eldad Rechavia Arnon Blum Aviv Mager Yochai Birnbaum Boris Strasberg Samuel Sclarovsky
thrombolytic therapy are briefly presented. Following thrombolytic therapy and during the remainder of the hospitalization period, no further Q-wave changes were noted. In all patients, continuous 3-channel ECG or serial ECGs were recorded using permanent posi tions of the precordial leads and identical ECG standardization.
Case Reports Patient I
A 60-year-old male was admitted with a 2-week history of spontaneous and exercise-induced anginal pain unresponsive to medical therapy. Physical exami nation elicited no abnormal findings. An electrocar diogram on admission was normal. Cardiac enzyme
values were negative for infarction. Oral nitrates and aspirin therapy was instituted for treatment of angina and the patient remained asymptomatic until 24 h lat er, when chest pain recurred. He had been transferred to the coronary care unit with sharp precordial pain radiating to his left arm accompanied by electrocardio graphic finding of ST segment elevation in the precor dial leads (fig. 1). Intravenous heparin (5.000 U) was given followed by continuous streptokinase infusion (1.5 million U over 30 min). Fifteen minutes later, the ST segment almost returned to baseline and Q-waves were transiently apparent in leads V2-V3. An ECG towards the end of streptokinase infusion and later on disclosed R-waves and inverted T-waves in these leads. The Q-waves were no longer present. Serial ECG’s and creatine kinase assays were diagnostic of non-lransmural MI without formation of Q-waves and slight loss of R-waves amplitude. Coronary angiography performed 5 days postinfarction demonstrated a 90% stenosis of the proxi-
393
Downloaded by: Leiden University Medisch Centrum 132.229.13.63 - 11/6/2018 8:08:20 AM
Fig. 1. Case I. Serial 3-channel (VI-V3) ECG recording with the same lead placement showing evolution of anterior wall MI during streptokinase (STK) administration. A QS pat tern was transiently noted 15 min starting with STK infusion. Final tracing is consistent with a non-Q-wave MI.
STK 043° 0435 3 10mm/mV
04«)
04«
04“
05°°
0530
O630
r pi
« : I
Fig. 2. Case 2. Serial 3-channel (V1-V3) ECG recording taken immediately before and during streptokinase (STK) infusion. Note that Q-waves disappeared whereas ST segment displacement becomes more prominent. Final tracing is consistent with a Q-wave MI.
Patient 2 A 56-year-old man with no previous history of car diac disease or risk factors was admitted because of chest tightness lasting for 2 h. On admission, physical examination was normal. The blood pressure was 130/80 mm Hg; the pulse was 70/min and regular. The ECG recorded on admission showed Q-waves in leads VI-V3 and ST segment elevation with peaked positive T-waves extending from VI to V5 (fig. 2). A bolus injection of heparin (5,000 U) was given and a continous infusion of streptokinase (1.5 million U) was promptly started. Continuous bedside 3-lead ECG was recorded starting with streptokinase infusion for 2 h. Ten minutes starting with streptokinase infusion, elec trocardiographic monitoring revealed accentuation of ST segment displacement. This was accompanied by cancellation of preexisting Q-waves. ST segment eleva tion gradually subsided giving rise to Q-wave infarc
394
tion. Creatine kinase peaked at 2,930 U/l. Coronary1 arteriography performed 1 week post-infarction re vealed a severe narrowing (95%) of the left anterior descending in its second part with slow antegrade fill ing of the distal portion of the vessel. PTCA success fully recanalized the stenotic artery.
Patient 3 A 63-year-old man with long-standing hyperten sion and no history of cardiac disease was admitted within 2 h from symptom onset of AMI. On admis sion, vital signs were normal. Physical examination revealed a loud 4th heart sound and a grade 1/6 apical systolic murmur. On admission ECG. Q-waves were already documented in leads VI and V2 (fig. 3). Within 5 min of streptokinase infusion an abrupt widening of QRS complex was noted. Q-waves were not recorded at this stage and reappeared when QRS widening was subsiding. The peak serum creatine kinase level rose to 2,410 U/l (MB fraction of 15%). Coronary angiography demonstrated equivalent left main disease consisting of circumflex and left anterior descending proximal stenotic lesions.
Rechavia/Blum/Mager/Birnbaum/ Strasberg/Sclarovsky
Electrocardiographic Q-Waves Inconstancy
Downloaded by: Leiden University Medisch Centrum 132.229.13.63 - 11/6/2018 8:08:20 AM
mal portion of the left anterior descending with good collateral filling of the distal segment by the right coro nary artery. The stenotic lesion was successfully di lated to a 20% residual stenosis.
395
Downloaded by: Leiden University Medisch Centrum 132.229.13.63 - 11/6/2018 8:08:20 AM
Fig. 3. Case 3. A serial 12-lead ECG recording during streptokinase (STK.) infusion. An abrupt widening of QRS complex is accompanied by transient loss of Q-waves. Note that no significant axis deviation could be recognized.
Fig. 4. Case 4. Serial 3-channel (V1-V3) ECG showing an initial QS pattern. The gradual disappearance of Q-wave in V3 and partial resolution in V2 is accompanied by progressive upwards displacement of ST segment.
396
Discussion A number of previous reports have de scribed the fleeting nature of Q-waves in pa tients with effort angina [6], prinzmetal an gina [7], myocardial ischemia [8-10], co caine-associated MI [12], open-heart surgery [13], metabolic abnormalities [14], shock [15], myocarditis [16], cerebral hemorrhage [15], bronchial asthma [18], pulmonary em bolism [19], phosphorus intoxication [20] and acute pancreatitis [21], Reversibility of Qwaves has also been reported following PTCA [22], Although Q-waves appearance in left precordial leads has been highly regarded as the most,reliable ECG marker of myocardial necrosis affecting the left anterior descending distribution territory, on theoretical and clini
Rechavia/Blum/Mager/Birnbaum/ Strasbcrg/Sclarovsky
Electrocardiographic Q-Wavcs Inconstancy
Downloaded by: Leiden University Medisch Centrum 132.229.13.63 - 11/6/2018 8:08:20 AM
Patient 4 A 48-year-old previously healthy man was admit ted to the coronary care unit with clinical and electro cardiographic evidence of AMI. On admission, the pulse was regular. 75 beats/min. and blood pressure was 110/65 mm Hg. Twelve leads ECG was compat ible with acute phase of anterior wall Ml, demonstrat ing marked ST segment elevation from VI-V5. The patient was placed under continuous 3-channel ECG recording and streptokinase infusion was started. Ad ministration of streptokinase transiently increased the magnitude of ischemia as reflected by subsequent ST segment elevation accompanied by gradual resolution of Q-wave in V3 and decreased Q-wave amplitude in V2 (fig. 4). Continuous ECG recording and serial crea tine kinase assays were compatible with AMI. There was a maximal CK rise of 1.760 U/l. Cardiac catheter ization revealed subtotal occlusion in the mid left ante rior descending coronary artery'. The patient under went PTCA with successful reopening of the occluded anterior descending.
physiological ischemic insult to the jeopar dized myocardium. This report emphasizes that detection of Q-waves during thrombolysis can easily be missed because of its dynamic nature. How ever, at the same time, the presence of Qwaves might be misleading and do not pre clude the possibility of a transient finding reflecting reversible pathological changes, namely preserved tissue viability. This se quence of observations is pertinent to patient management. In view of the instability of Qwaves, thrombolytic therapy should not be restricted to patients demonstrating non-Qwave electrocardiographic pattern during on going ischemia. Obviously, in cases where intermiltency of Q-waves is aparent on the ECG, thrombolytic therapy is recommended in an effort to preserve tissue viability.
Conclusion Although the dynamic nature of Q-waves remains poorly understood, in the critical set ting of acute coronary events, understanding the pathogenesis could aid in therapy for atte nuating the degree of ventricular impairment. In this clinical context, one may also speculate the presence of Q-waves as a valuable crite rion for patient enrollment to thrombolytic therapy.
397
Downloaded by: Leiden University Medisch Centrum 132.229.13.63 - 11/6/2018 8:08:20 AM
cal grounds, it is appealing to accept that this finding can no longer be solely attributed to purely irreversible necrosis. Current thinking on the pathogenesis of Q-wave inlcrmittency involves either vascular or tissue related fac tors such as ischemia, myocardial hemor rhage and edema, dynamic changes in coro nary vascular tone of the infarct related ar tery, local reversible loss of electrical activity in severly hypoperfused ischemic but still via ble myocardial tissue [23] and interference with impulse conduction through the left bun dle branch responsible for septal activation [24], However, in patients with hypertrophic cardiomyopathy Q-waves variation could not be related to any recognized form of special ized conduction block. Abnormal electrophysiologic properties of the hypertrophic myo pathic myocardium has been ascribed to this phenomenon [25], The electrocardiographic patterns, time course and sequence of events in our 4 pa tients differed. Reviewing the sequence of ECG changes in patients 2 and 4, there is increasing evidence supporting that dynamic variation of Q-waves is influenced by the con temporaneous behavior of ST segment and consequently depending on the intensity of coronary flow reduction and the severity of ischemic insult. As long as the magnitude of ischemia as reflected by the degree of ST seg ment displacement tends to increase, preex isting Q-waves gradually disappear and vice versa (fig. 2. 4). This observation finds sup port in a previous study where a rapid evolu tionary pattern of QRS complex was associ ated with a rapid decline of ST vector magni tude to normal levels following thrombolytic therapy [26]. A unique aspect of patient 3 relates to the abrupt widening of QRS com plex, resulting in transient resolution of Qwaves. When no significant axis deviation is noted (fig. 3), one is tempted to postulate that this ECG recording coincides with the electro
1 Blumcnthal MR. Wang HH. Liu LMP: Experimental coronary ar terial occlusion and release: Effects on en/vmes. electrocardiograms, myocardial contractility and reac tive hyperemia. Am J Cardiol 1975; 36:225-233. 2 Hackworthv R. Sorensen S. Fitzpa trick P. Barry WH. Mcnlove RL. Rothbard RL. Anderson JL for the APSAC investigators: Effect of re perfusion on electrocardiographic and enzymatic infarct size: Results of a randomized multicenter study of intravenous plasminogen strepto kinase activator complex (APSAC) versus intracoronary streptokinase in acute myocardial infarction. Am Heart J 1988:116:903-914. 3 Chuang MY. Spodick DH: Electro cardiographic Q-wave inconstancy in inferior wall myocardial infarc tion. Am J Cardiol 1990:66:1144— 1146. 4 Huey BL. Gheorghiade M. Crampton RS. Bellcr GA. Kaiser DL. Wat son DD. Nygaard TW. Craddock GB. Sayre SL. Gibson RS: Acute non-Q-wave myocardial infarction associated with early ST segment el evation: Evidence for spontaneous coronary reperfusion and implica tions for thrombolytic trials. J Am Coll Cardiol 1987:9:18-25. 5 Chouhan L. Hajar HA. George T. Pomposiello JC: Non-Q- and Qwave infarction after thrombolytic therapy with intravenous streptoki nase for chest pain and anterior STsegment elevation. Am J Cardiol 1991:68:446-450. 6 Bateman T. Gray R. Maddahi J. Rozanski A. Raymond M, Berman D: Transient appearance of Q waves in coronary disease during exercise el ectrocardiography: Consideration of mechanisms and clinical impor tance. Am Heart J 1982:104:192195.
398
7 Meller J. Conde CA. Donoso E. Dack S: Transient Q waves in prinzmetal's angina. Am J Cardiol 1975: 35:691-695. 8 Roesler H, Dressier W: Transient el ectrocardiographic changes identi cal with those of acute myocardial infarction accompanying attacks of angina pectoris. Am Heart J 1954: 47:520-526. 9 Goldman AG, Gross H. Rubin IL: Transitory Q waves simulating the Q wave of myocardial infarction. Am Heart J 1960;60:61-72. 10 Rubin IL. Gross H, Vigiliano EM: Transient abnormal Q waves during coronary insufficiency. Am Heart J 1966:71:254-259. 11 Haiat R. Chiche P: Transient abnor mal Q waves in the course of isch emic heart disease. Chest 1974:65: 140-143. 12 Ascher EK. Stauffer JCE, Gaasch WH: Coronary artery spasm, car diac arrest, transient electrocardio graphic Q waves and stunned myo cardium in cocaine-associated acute myocardial infarction. Am J Cardiol 1988;61:939-941. 13 Klein HO. Gross H. Rubin IL: Tran sient electrocardiographic changes simulating myocardial infarction during open-heart surgery. Am Heart J 1970:79:463-470. 14 Nora JR. Pilz CG: Pseudoinfarction pattern associated with electrolyte disturbance. Arch Intern Med 1959: 104:300-310. 15 Shugoll GI: Transient QRS changes simulating myocardial infarction as sociated with shock and severe met abolic stress. Am Heart J 1967;74: 402-409. 16 Spodick DH: Infection and infarc tion: Acute viral (and other) infec tion in the onset, pathogenesis and mimicry of acute mvocardiai infarc tion. Am J Med 1986:81:661-668.
t7 Srivastava SC. Robson AO: Electro cardiographic abnormalities associ ated with subarachnoid hemor rhage. Lancet 1964;ii:431— 433. 18 Rosenfeld I. Silverblatl MD. Grishman A: Allergic shock in humans: Reports of two cases with electrocar diographic findings. Am Heart J 1957:463-471. 19 Romhill D, Susilavorn B. Chou TC: Unusual electrocardiographic mani festation of pulmonary embolism. Am Heart J 1970:80:237-241. 20 Pietras RJ. Stavrakos C. Gunnar RM. Tobin JR: Phosphorus poison ing simulating acute myocardial in farction. Arch Intern Med 1968; 122:430-434. 21 Fulton MC. Marriot HJL: Acute pancreatitis simulating myocardial infarction in the electrocardiogram. Ann Intern Med 1963:59:730—732. 22 Ibba GV. Terrosu P. Franceschino V, Contini GM. Frau G. Sannia L: Disappearance of pathologic Q wave after PTCA in evolving myo cardial infarction. Am Heart J 1984: 108:1538-1540. 23 DePasquale NP, Burch GE. Phillips Jli: Electrocardiographic alterations associated with electrically ‘silent’ areas of myocardium. Am Heart J 1964:68:697-709. 24 Gambetta M. Childers R: Rate-de pendent right precordial Q waves: "Septal focal block’. Am J Cardiol 1973:32:196-201. 25 Cosio FG. Moro C, Alonso M, Calzada CS. Liovet A: The Q waves of hypertrophic cardiomyopathy. N Engl J Med 1980;302:96-99. 26 Dellborg M. Riha M, Swcdberg K for the TEAHAT Study Group: Dy namic QRS-complex and ST-segment monitoring in acute myocar dial infarction during recombinant tissue-type plasminogen activator therapy. Am J Cardiol 1991:67: 343-349.
Rechavia/Blum/Mager/Birnbaum/ Strasberg/Sclarovsky
Electrocardiographic Q-Wavcs Inconstancy
Downloaded by: Leiden University Medisch Centrum 132.229.13.63 - 11/6/2018 8:08:20 AM
References
Cardiovascular Division and Coronary Care Unit, Beilinson Medical Center, Petah-Tiqva and Tel-Aviv University Sadder School of Medicine, Tel-Aviv, Israel
Keywords Electrocardiogram Myocardial infarction Q-waves Thrombolysis
Electrocardiographic Q-W aves Inconstancy during Thrombolysis in Acute Anterior Wall Myocardial Infarction
Abstract It is the purpose of this paper to describe the electrocardio graphic inconstancy of Q-waves during administration of thrombolytic therapy. This was documented in four patients given streptokinase early in the course of anterior wall myo cardial infarction. Understanding the pathogenesis of sequen tial dynamic variations of Q-waves in this setting may offer important insights into coronary physiology and management of acute coronary events. We discuss the possible explanations for such changes with respect to tissue viability, dynamic vas cular changes and electrophysiological properties of the reper fused infarcted myocardium.
Evolution of Q-waves during acute myo cardial infarction (AMI) is variable, tends to begin within 2 h of the onset of symptoms and is completed within 4-48 h. In experimental studies, Q-waves were noted 15-30 min after the release of coronary ligation and they be came more significant while serum enzyme levels were rising steeply [ 1]. Successful reper fusion has been shown to accelerate the rate of ECG changes [2] whereas delay in Q-wave appearance has been attributed to sustained compromised perfusion of the infarcted area. Regression or inconstancy of Q-waves may be
Received: December 27, 1991 Accepted: after revision: March 16. 1992
seen even as early as one week post-MI [3]. Naturally evolving non-Q-wave Ml would be expected in up to 37% of patients admitted with chest pain and ST segment elevation [4] as compared with 43% of patients who are treated with thrombolytic therapy [5], To our knowledge, no material has been published so far on the dynamic nature of Qwaves during thrombolytic therapy given at the early stages of AMI. In this report, the clinical and electrocardiographic sequence of observations in 4 patients with anterior wall MI canceling preexisting Q-waves during
Eldad Rechavia, MD Cardiovascular Division Beilinson Medical Center Petah-Tiqva, 49100 (Israel)
© 1992 S. Karger AG. Basel 0008-6312/92/ 0806-0392$2.75/0
Downloaded by: Leiden University Medisch Centrum 132.229.13.63 - 11/6/2018 8:08:20 AM
Eldad Rechavia Arnon Blum Aviv Mager Yochai Birnbaum Boris Strasberg Samuel Sclarovsky
thrombolytic therapy are briefly presented. Following thrombolytic therapy and during the remainder of the hospitalization period, no further Q-wave changes were noted. In all patients, continuous 3-channel ECG or serial ECGs were recorded using permanent posi tions of the precordial leads and identical ECG standardization.
Case Reports Patient I
A 60-year-old male was admitted with a 2-week history of spontaneous and exercise-induced anginal pain unresponsive to medical therapy. Physical exami nation elicited no abnormal findings. An electrocar diogram on admission was normal. Cardiac enzyme
values were negative for infarction. Oral nitrates and aspirin therapy was instituted for treatment of angina and the patient remained asymptomatic until 24 h lat er, when chest pain recurred. He had been transferred to the coronary care unit with sharp precordial pain radiating to his left arm accompanied by electrocardio graphic finding of ST segment elevation in the precor dial leads (fig. 1). Intravenous heparin (5.000 U) was given followed by continuous streptokinase infusion (1.5 million U over 30 min). Fifteen minutes later, the ST segment almost returned to baseline and Q-waves were transiently apparent in leads V2-V3. An ECG towards the end of streptokinase infusion and later on disclosed R-waves and inverted T-waves in these leads. The Q-waves were no longer present. Serial ECG’s and creatine kinase assays were diagnostic of non-lransmural MI without formation of Q-waves and slight loss of R-waves amplitude. Coronary angiography performed 5 days postinfarction demonstrated a 90% stenosis of the proxi-
393
Downloaded by: Leiden University Medisch Centrum 132.229.13.63 - 11/6/2018 8:08:20 AM
Fig. 1. Case I. Serial 3-channel (VI-V3) ECG recording with the same lead placement showing evolution of anterior wall MI during streptokinase (STK) administration. A QS pat tern was transiently noted 15 min starting with STK infusion. Final tracing is consistent with a non-Q-wave MI.
STK 043° 0435 3 10mm/mV
04«)
04«
04“
05°°
0530
O630
r pi
« : I
Fig. 2. Case 2. Serial 3-channel (V1-V3) ECG recording taken immediately before and during streptokinase (STK) infusion. Note that Q-waves disappeared whereas ST segment displacement becomes more prominent. Final tracing is consistent with a Q-wave MI.
Patient 2 A 56-year-old man with no previous history of car diac disease or risk factors was admitted because of chest tightness lasting for 2 h. On admission, physical examination was normal. The blood pressure was 130/80 mm Hg; the pulse was 70/min and regular. The ECG recorded on admission showed Q-waves in leads VI-V3 and ST segment elevation with peaked positive T-waves extending from VI to V5 (fig. 2). A bolus injection of heparin (5,000 U) was given and a continous infusion of streptokinase (1.5 million U) was promptly started. Continuous bedside 3-lead ECG was recorded starting with streptokinase infusion for 2 h. Ten minutes starting with streptokinase infusion, elec trocardiographic monitoring revealed accentuation of ST segment displacement. This was accompanied by cancellation of preexisting Q-waves. ST segment eleva tion gradually subsided giving rise to Q-wave infarc
394
tion. Creatine kinase peaked at 2,930 U/l. Coronary1 arteriography performed 1 week post-infarction re vealed a severe narrowing (95%) of the left anterior descending in its second part with slow antegrade fill ing of the distal portion of the vessel. PTCA success fully recanalized the stenotic artery.
Patient 3 A 63-year-old man with long-standing hyperten sion and no history of cardiac disease was admitted within 2 h from symptom onset of AMI. On admis sion, vital signs were normal. Physical examination revealed a loud 4th heart sound and a grade 1/6 apical systolic murmur. On admission ECG. Q-waves were already documented in leads VI and V2 (fig. 3). Within 5 min of streptokinase infusion an abrupt widening of QRS complex was noted. Q-waves were not recorded at this stage and reappeared when QRS widening was subsiding. The peak serum creatine kinase level rose to 2,410 U/l (MB fraction of 15%). Coronary angiography demonstrated equivalent left main disease consisting of circumflex and left anterior descending proximal stenotic lesions.
Rechavia/Blum/Mager/Birnbaum/ Strasberg/Sclarovsky
Electrocardiographic Q-Waves Inconstancy
Downloaded by: Leiden University Medisch Centrum 132.229.13.63 - 11/6/2018 8:08:20 AM
mal portion of the left anterior descending with good collateral filling of the distal segment by the right coro nary artery. The stenotic lesion was successfully di lated to a 20% residual stenosis.
395
Downloaded by: Leiden University Medisch Centrum 132.229.13.63 - 11/6/2018 8:08:20 AM
Fig. 3. Case 3. A serial 12-lead ECG recording during streptokinase (STK.) infusion. An abrupt widening of QRS complex is accompanied by transient loss of Q-waves. Note that no significant axis deviation could be recognized.
Fig. 4. Case 4. Serial 3-channel (V1-V3) ECG showing an initial QS pattern. The gradual disappearance of Q-wave in V3 and partial resolution in V2 is accompanied by progressive upwards displacement of ST segment.
396
Discussion A number of previous reports have de scribed the fleeting nature of Q-waves in pa tients with effort angina [6], prinzmetal an gina [7], myocardial ischemia [8-10], co caine-associated MI [12], open-heart surgery [13], metabolic abnormalities [14], shock [15], myocarditis [16], cerebral hemorrhage [15], bronchial asthma [18], pulmonary em bolism [19], phosphorus intoxication [20] and acute pancreatitis [21], Reversibility of Qwaves has also been reported following PTCA [22], Although Q-waves appearance in left precordial leads has been highly regarded as the most,reliable ECG marker of myocardial necrosis affecting the left anterior descending distribution territory, on theoretical and clini
Rechavia/Blum/Mager/Birnbaum/ Strasbcrg/Sclarovsky
Electrocardiographic Q-Wavcs Inconstancy
Downloaded by: Leiden University Medisch Centrum 132.229.13.63 - 11/6/2018 8:08:20 AM
Patient 4 A 48-year-old previously healthy man was admit ted to the coronary care unit with clinical and electro cardiographic evidence of AMI. On admission, the pulse was regular. 75 beats/min. and blood pressure was 110/65 mm Hg. Twelve leads ECG was compat ible with acute phase of anterior wall Ml, demonstrat ing marked ST segment elevation from VI-V5. The patient was placed under continuous 3-channel ECG recording and streptokinase infusion was started. Ad ministration of streptokinase transiently increased the magnitude of ischemia as reflected by subsequent ST segment elevation accompanied by gradual resolution of Q-wave in V3 and decreased Q-wave amplitude in V2 (fig. 4). Continuous ECG recording and serial crea tine kinase assays were compatible with AMI. There was a maximal CK rise of 1.760 U/l. Cardiac catheter ization revealed subtotal occlusion in the mid left ante rior descending coronary artery'. The patient under went PTCA with successful reopening of the occluded anterior descending.
physiological ischemic insult to the jeopar dized myocardium. This report emphasizes that detection of Q-waves during thrombolysis can easily be missed because of its dynamic nature. How ever, at the same time, the presence of Qwaves might be misleading and do not pre clude the possibility of a transient finding reflecting reversible pathological changes, namely preserved tissue viability. This se quence of observations is pertinent to patient management. In view of the instability of Qwaves, thrombolytic therapy should not be restricted to patients demonstrating non-Qwave electrocardiographic pattern during on going ischemia. Obviously, in cases where intermiltency of Q-waves is aparent on the ECG, thrombolytic therapy is recommended in an effort to preserve tissue viability.
Conclusion Although the dynamic nature of Q-waves remains poorly understood, in the critical set ting of acute coronary events, understanding the pathogenesis could aid in therapy for atte nuating the degree of ventricular impairment. In this clinical context, one may also speculate the presence of Q-waves as a valuable crite rion for patient enrollment to thrombolytic therapy.
397
Downloaded by: Leiden University Medisch Centrum 132.229.13.63 - 11/6/2018 8:08:20 AM
cal grounds, it is appealing to accept that this finding can no longer be solely attributed to purely irreversible necrosis. Current thinking on the pathogenesis of Q-wave inlcrmittency involves either vascular or tissue related fac tors such as ischemia, myocardial hemor rhage and edema, dynamic changes in coro nary vascular tone of the infarct related ar tery, local reversible loss of electrical activity in severly hypoperfused ischemic but still via ble myocardial tissue [23] and interference with impulse conduction through the left bun dle branch responsible for septal activation [24], However, in patients with hypertrophic cardiomyopathy Q-waves variation could not be related to any recognized form of special ized conduction block. Abnormal electrophysiologic properties of the hypertrophic myo pathic myocardium has been ascribed to this phenomenon [25], The electrocardiographic patterns, time course and sequence of events in our 4 pa tients differed. Reviewing the sequence of ECG changes in patients 2 and 4, there is increasing evidence supporting that dynamic variation of Q-waves is influenced by the con temporaneous behavior of ST segment and consequently depending on the intensity of coronary flow reduction and the severity of ischemic insult. As long as the magnitude of ischemia as reflected by the degree of ST seg ment displacement tends to increase, preex isting Q-waves gradually disappear and vice versa (fig. 2. 4). This observation finds sup port in a previous study where a rapid evolu tionary pattern of QRS complex was associ ated with a rapid decline of ST vector magni tude to normal levels following thrombolytic therapy [26]. A unique aspect of patient 3 relates to the abrupt widening of QRS com plex, resulting in transient resolution of Qwaves. When no significant axis deviation is noted (fig. 3), one is tempted to postulate that this ECG recording coincides with the electro
1 Blumcnthal MR. Wang HH. Liu LMP: Experimental coronary ar terial occlusion and release: Effects on en/vmes. electrocardiograms, myocardial contractility and reac tive hyperemia. Am J Cardiol 1975; 36:225-233. 2 Hackworthv R. Sorensen S. Fitzpa trick P. Barry WH. Mcnlove RL. Rothbard RL. Anderson JL for the APSAC investigators: Effect of re perfusion on electrocardiographic and enzymatic infarct size: Results of a randomized multicenter study of intravenous plasminogen strepto kinase activator complex (APSAC) versus intracoronary streptokinase in acute myocardial infarction. Am Heart J 1988:116:903-914. 3 Chuang MY. Spodick DH: Electro cardiographic Q-wave inconstancy in inferior wall myocardial infarc tion. Am J Cardiol 1990:66:1144— 1146. 4 Huey BL. Gheorghiade M. Crampton RS. Bellcr GA. Kaiser DL. Wat son DD. Nygaard TW. Craddock GB. Sayre SL. Gibson RS: Acute non-Q-wave myocardial infarction associated with early ST segment el evation: Evidence for spontaneous coronary reperfusion and implica tions for thrombolytic trials. J Am Coll Cardiol 1987:9:18-25. 5 Chouhan L. Hajar HA. George T. Pomposiello JC: Non-Q- and Qwave infarction after thrombolytic therapy with intravenous streptoki nase for chest pain and anterior STsegment elevation. Am J Cardiol 1991:68:446-450. 6 Bateman T. Gray R. Maddahi J. Rozanski A. Raymond M, Berman D: Transient appearance of Q waves in coronary disease during exercise el ectrocardiography: Consideration of mechanisms and clinical impor tance. Am Heart J 1982:104:192195.
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7 Meller J. Conde CA. Donoso E. Dack S: Transient Q waves in prinzmetal's angina. Am J Cardiol 1975: 35:691-695. 8 Roesler H, Dressier W: Transient el ectrocardiographic changes identi cal with those of acute myocardial infarction accompanying attacks of angina pectoris. Am Heart J 1954: 47:520-526. 9 Goldman AG, Gross H. Rubin IL: Transitory Q waves simulating the Q wave of myocardial infarction. Am Heart J 1960;60:61-72. 10 Rubin IL. Gross H, Vigiliano EM: Transient abnormal Q waves during coronary insufficiency. Am Heart J 1966:71:254-259. 11 Haiat R. Chiche P: Transient abnor mal Q waves in the course of isch emic heart disease. Chest 1974:65: 140-143. 12 Ascher EK. Stauffer JCE, Gaasch WH: Coronary artery spasm, car diac arrest, transient electrocardio graphic Q waves and stunned myo cardium in cocaine-associated acute myocardial infarction. Am J Cardiol 1988;61:939-941. 13 Klein HO. Gross H. Rubin IL: Tran sient electrocardiographic changes simulating myocardial infarction during open-heart surgery. Am Heart J 1970:79:463-470. 14 Nora JR. Pilz CG: Pseudoinfarction pattern associated with electrolyte disturbance. Arch Intern Med 1959: 104:300-310. 15 Shugoll GI: Transient QRS changes simulating myocardial infarction as sociated with shock and severe met abolic stress. Am Heart J 1967;74: 402-409. 16 Spodick DH: Infection and infarc tion: Acute viral (and other) infec tion in the onset, pathogenesis and mimicry of acute mvocardiai infarc tion. Am J Med 1986:81:661-668.
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Rechavia/Blum/Mager/Birnbaum/ Strasberg/Sclarovsky
Electrocardiographic Q-Wavcs Inconstancy
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