Repetitive
Myocardial
lschemia of Prinzmetal
Type
Without Angina Pectoris
MAURIZIO GUAZZI, MARIA T. OLIVARI,
MD MD
ALVISE POLESE, MD CESARE FIORENTINI, MD FABIO
MAGRINI,
MD
Milan, Italy
In a patient with a normal electrocardiogram, normal treadmill exercise test, normal coronary arteriogram and no symptoms to suggest angina pectoris, continuous monitoring during several days exhibited repetitive (one to two per hour) S-T segment elevations in the precordial electrocardiographic leads and hemodynamic changes typical of Prinzmetal’s angina (reduction in arterial pressure and cardiac index and increase in systemic peripheral resistance and pulmonary wedge pressure). This case demonstrates that electrical and dynamic cardiac alterations of Prinzmetal’s angina can occur even in the absence of angina pectoris.
Transient electrocardiographic changes of myocardial ischemia occurring without angina have been described in patients with angina pectoris at rest, showing either the commoni or the Prinzmetal’s electrocardiographic pattern.1-5 In a patient with a normal electrocardiogram, not complaining of angina pectoris or other pain at rest or during exercise, transient S-T segment elevation in the left precordial leads was detected casually during a routine electrocardiographic test. Many such episodes were subsequently documented by continuous electrocardiographic recordings on several consecutive days, but none was perceived by the patient. The origin and the clinical meaning of these changes became more interesting in light of the patient’s normal coronary arteriograms. A continuous hemodynamic monitoring revealed that the phasic electrocardiographic alterations were accompanied by unequivocal circulatory signs of cardiac failure that subsided concomitantly with the reversion to normal concluded that the heart dynamic pattern typical subjective symptoms that
of the electrocardiogram. It was therefore of this patient exhibited an electrical and of Prinzmetal’s angina1s4 in the absence of could reveal the existence of the disorder. Case
From Clinica Medica II, Centro Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, lstituto Ricerche Cardiovascolari, University of Milan, Milan, Italy. Manuscript accepted January 3. 1975. Address for reprints: Maurizio Guazzi, MD, Istituto Ricerche Cardiovascolari. Via Francesco Sforza, 35, 20122 Milano, Italy.
Report
A 46 year old workman was hospitalized because of an attack of dyspnea and palpitation that occurred while at home, when he awoke in the morning, and that subsided within 10 minutes without any therapeutic intervention. He had been fully active and in excellent health until the preceding day. There was no history of hypertension, cardiac or lung diseases, or chest pain or discomfort at rest or on effort. Physical examination revealed an intelligent alert man in no distress; the blood pressure was 150/80 mm Hg in both arms; the pulse rate was 80/min and regular. No murmurs or gallop rhythms were audible. X-ray examination of the chest and cardiac fluoroscopy revealed a heart of normal size and configuration, with normal pulsations and without intracardiac calcifications. An electrocardiogram (Fig. 1A) was normal. A hemogram, urinalysis, serum electrolyte determinations, serum enzyme levels (glutamic oxaloacetic transaminase [GOT] and lactic dehydrogenase [LDH]) and protein-bound iodine levels were within normal limits. A maximal exercise
May 1976
The American
Journal
of CARDIOLOGY
Volume
37
923
MYOCARDIAL
ISCHEMA
WITHOUT
ANGINA-GUAZZI
ET
AL.
test performed on a motorized treadmill did not provoke either angina pectoris or arrhythmias, and no remarkable S-T segment shifts were noted. The patient remained asymptomatic in the hospital, and two subsequent electrocardiograms were normal and unchanged. On the morning of the 7th hospital day, when he was to be discharged, a casual electrocardiogram taken in the absence of symptoms revealed marked S-T segment elevation in leads Vz to Vs with reciprocal depression in leads II, III and aVF (Fig. 1B). Within a few minutes the electrocardiogram reverted spontaneously to its control appearance (Fig. 1C). The patient stated that he had no pain or other discomfort during the recording. Continuous 3 hour electrocardiographic recordings were obtained on 6 subsequent days during different hours each day, according to a method described previously.3 Transient S-T segment displacements of 3 to 5 minutes’ duration, such as those shown in Figure 1, were recorded with an average frequency of 1 to S/hour. The patient never had chest pain or other discomfort, and only in conjunction with one episode lasting longer than usual did he report mild respiratory distress. From these findings, it was assumed that an average of at least 20, and possibly more, episodes of transient S-T segment alteration occurred each 24 hours. In view of their prognostic and therapeutic implications, an effort was made to achieve a correct interpretation of these findings.
Coronary angiography demonstrated excellent visualization of each major coronary artery; all vessels had optimal distribution and patency; no evidence of collateralization was detected. Left ventriculography revealed normal left ventricular contraction and no mitral regurgitation. The nitroglycerin test was unrevealing because of the short duration and spontaneous subsidence of the electrocardiographic alterations. Since unequivocal circulatory signs of cardiac impairment have been shown to accompany the S-T segment displacement of Prinzmetal’s angina,lp4 it was thought that circulatory monitoring would yield useful diagnostic information. Hemodynamic studies: Studies were carried out with the patient fasting, without premeditation, in the supine position, by techniques described elsewhere in detail.‘,* The following data were continuously recorded, at variable paper speed, on a Hewlett-Packard eight channel ink recorder: electrocardiogram, phonocardiogram, heart rate, carotid sphygmogram, brachial arterial pressure, pulmonary arterial or wedge pressure and right atria1 pressure. The electrocardiogram was also monitored on an oscilloscope, but the phasic electrocardiographic changes were so clear that they could consistently be detected even at a paper speed as slow as 0.5 mm/set (see examples in Fig. 2
wedge
6
AP
t
I v4
b/min
HR
160
FIGURE 2. Original strips of records of an episode of S-T alterations (the onset and conclusion are indicated by arrows). From top: time marker: pulmonary wedge (wedge), right atrial (rap), and arterial pressures (AP); heart sounds (HS); leads Vs and V4 of the electrocardiogram: and heart rate (HR). The progressive elevation of the S-T segment and peaking of the T wave are clear even at a recording speed of 0.5 mm/set.
FIGURE 1. Twelve lead electrocardiogram. A, control record. B, spontaneous episode of S-T segment elevation in leads V2 to Vs with reciprocal depression in leads II, Ill and aVF; C, return to control.
624
May 1676
The American
Journal
of CARDIOLOGY
Volume
37
MYOCARDIAL ISCHEMIA WITHOUT ANGINA-GUAZZI
and 3). Arterial and venous catheters were introduced percutaneously. A balloon-tipped catheter6 was floated under fluoroscopic guidance to the pulmonary artery and advanced, when necessary, to the wedge position. For the measurement of right atria1 pressure a polyethylene catheter was also introduced into an antecubital vein and positioned in the right atrium. Cardiac output was determined using indocyanine green dye and a Gilford densitometer, and the derived variables (cardiac index, stroke volume, left and right ventricular ejection rate index and total peripheral resistance) were calculated in the standard fashion. Beat to beat variations of heart rate were detected by a Cardio-Tach preamplifier. Left ventricular preejection period and ejection time were determined from the electrocardiogram, carotid sphygmogram and phonocardiogram recorded at a paper speed of 100 mm/set. The right ventricular ejection time was measured from the pulmonary arterial tracing. The left ventricular mean electromechanical rate of rise of pressure (dP/dt),7 right and left stroke work (index) and mean rate of systolic ejection (index) were calculated from the standard formulas. A total of eight episodes of S-T segment displacement were investigated. Brachial, right atrial, pulmonary arterial and wedge pressures, heart rate and left and right ventricular ejection times were measured during the four 20 second intervals that immediately preceded the onset of the electrocardiographic changes. Measurements were also taken while S-T segment elevation was increasing, during its
ET AL.
steady state, while it was beginning to revert to control levels and 30 and 90 seconds after full normalization. Cardiac output was determined before, during and after the S-T segment displacement. The averages of the hemodynamic functions at the various time intervals are summarized in Table I. The electrocardiographic alterations were not preceded by changes in heart rate, systemic, pulmonary arterial wedge or right atria1 pressures, cardiac output or right or left ventricular ejection time. With the onset of S-T segment changes there was a progressive reduction in arterial pressure accompanied by a conspicuous reduction in cardiac index and increase in systemic peripheral resistance. The following changes were simultaneously seen: increase in right atria1 and pulmonary wedge pressures, mild increase in heart rate and definite reductions in right and left stroke work, mean rate of systolic ejection and left mean electromechanical dP/dt. All the circulatory functions reverted toward control levels within 1 to 2 minutes after complete disappearance of the electrocardiographic abnormalities. Figures 2 and 3 reproduce original strips of records of two such episodes. During the S-T alterations in Figure 3, the patient had junctional extrasystoles with aberrant ventricular conduction but no symptoms. The pulse pressure of the postextrasystolic beats did not exceed that of the control beats. Treatment and course: Treatment with propranolol was started at a daily dose of 160 mg with subsequent in-
wedge
w
HS
FIGURE 3. Original records during an episode of ST-T alterations (indicated by arrowheads) accompanied by cardiac arrhythmias. III = lead 3 of the electrocardiogram: other abbreviations as in Figure 2.
60
HR
bhr(n
May 1976
The American Journal of CARDIOLOGY
Volume 37
925
MYOCARDIAL ISCHEMIA WITHOUT ANGINA-GUAZZI
TABLE
I
Average
Circulatory
SAP (mm Hg) DAP (mm Hg) HR (beats/mln) mRAP (mm Hg) mWP (mm Hg) RSW (g.m/m’) LSW (g.nl/rnl) RMSEJR (ml/set per m’) LMSEJR Iml/sec per m”) dP/dt (mm Hg/msec) Cl (mlimin per m’)
Values
at Various
Periods*
A
8
165
164 90 81 4 7
4 7 5 75 150
ET AL
During C 163
4 7
S-T
Segment
Displacement
D
E
164 90 81 4 7
172 0.9 3950
0.95
F
G
150
145
8835 7 10 3 50 122
10 15 2 40 115
148 87 80 10 15
147
135
0.72 2920
0.6 2800
H
I
158 88 80
90” 148
4 7 5 72 152
172
168
0.92 4050
0.91 3990
Measurements were taken during the four 20 second Intervals immediately preceding the electrocardiographic changes (A, B, C, D), during the Increase in S-T segment elevation (El, during the steady state period (F), at the onset of reversion to control level IG) and 30 (H) and 90 seconds (I) after full normalization. Cl = cardiac index; DAP = diastolic arterial pressure; dP/dt = left mean electromechanical dP/dt; HR = heart rate; LMSEJR = left mean systolic ejection rate (index); LSW = left stroke work (index); mRAP = mean right atrial pressure: mWP = mean wedge pressure; RMSEJR = right mean systolic ejection rate (Index); RSW = right stroke work; SAP = svstolic arterial oressure. l
crements of’ 80 mg every other day, according to the patient’s response, which was evaluated daily with 3 hour continuous electrocardiographic recordings. Full disappearance of the phasic electrocardiographic alterations was consistently found at a dose of 800 mg/day, and he was discharged at this dosage. For 2 months he has returned weekly to our Cardiology Clinic for follow-up studies including 3 hour continuous recordings of the electrocardiogram; the electrocardiogram has remained normal, and the patient is asymptomatic and has returned to work.
tative or qualitative electrocardiographic’” or circulaor tory differences lv4 between attacks accompanied unaccompanied by pain. In conclusion, the findings in our case do not shed light on the mechanisms or agents directly responsible for eliciting pain in myocardial ischemia. They do indicate (1) that these mechanisms are undetectable by electrocardiography, and (2) that pain and impaired cardiac function do not necessarily accompany each other, although each is probably a consequence of ischemia. Angiographic studies have indicated a transient spasm of the coronary vessels as the possible triggering mechanism of ischemia in patients with Prinzmetal’s angina.9-17 In our subject none of the circulatory factors that acutely increase the mechanical effort of the heart, and consequently its need for oxygen, such as tachycardia, increase in arterial pressure or lengthening of ventricular contraction, can be considered responsible for the episodic myocardial ischemia, which seems to be the event leading to impairment of cardiac function. These findings are in keeping with the interpretation that in such cases, ischemia is primarily due to an altered oxygen supply, possibly caused by coronary spasm, rather than to increased myocardial oxygen demand. Our observations further indicate that continuous electrocardiographic recording or monitoring provides the most direct and informative means for evaluating and recognizing patients with disturbances of the coronary circulation. This diagnostic tool was valuable in the diagnosis of our case, which probably represents a new facet of Prinzmetal’s angina that might be called “angina without angina.”
Discussion The reduction in cardiac output, arterial pressure, stroke work, mean rate of systolic ejection and dP/dt, as well as the increase in pulmonary wedge and right atria1 pressures, clearly indicates that heart failure occurred during the electrocardiographic alterations. It is therefore likely that the S-T segment displacement in this patient reflects myocardial ischemic changes that induced no pain but were severe enough to cause dynamic impairment of the heart as well as cardiac arrhythmias. The electrocardiographic8 and the circulatory featuresl,” in this case are typical of Prinzmetal’s angina; nonetheless, the total absence of pain is unusual and hard to interpret. This aspect deserves comment. Because the angiograms revealed no coronary arterial lesion, the absence of pain might be attributed to this finding. However, there have been many reports of patients with normal coronary arteriograms presenting with the classic symptoms of Prinzmetal’s angina.+‘” Since no pain-producing episode of ischemia was recorded, painful and nonpainful attacks cannot be compared in our subject. In reported cases, however, there were no definite quanti-
References 1. Guazzi M, Poise A, Fiorentini C, et al: Left and right heart haemodynamics during spontaneous angina pectoris. Comparison between angina with S-T segment depression and angina with S-T segment elevation. Br Heart J 37:1235-1245. 197.5 2. Robinson JS: Prinzmetal’s variant angina pectoris. Report of a
926
May 1976
The American
Journal
of CARDlOLOGY
Volume
case. Am Heart J 70:797-800, 1965 3. Guazzi M, Fiorentini C, Polese A, et al: Continuous electrocardiographic recording in Prinzmetal’s variant angina pectoris. A report of four cases. Br Heart J 32:611-616, 1970 4. Guazzi M, Polese A, Fiorentini C, et al: Left ventricular perfor-
37
MYOCARDIAL
5.
6.
7.
8.
9.
10.
mance and related haemodynamic changes in Prinzmetal’s variant angina pectoris. Br Heart J 33:84-94, 1971 Lasser RP, de la Paz NS: Repetitive transient myocardial ischemia, Prinzmetal type, without angina pectoris, presenting with Stokes-Adams attacks. Chest 641350-352.1973 Swan HJC, Ganr W, Forrester J, et al: Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter. N Engl J Med 283:447-451. 1970 Diamond G, Forrester JS, Chatterjee K, et al: Mean electromechanical AP/At. An indirect index of the peak rate of rise of left ventricular pressure. Am J Cardiol 30:338-342. 1972 Prinzmetai M, Ekmecki A, Kennamer R, et al: Variant form of angina pectoris. Previously undelineated syndrome. JAMA 174: 1794-1800, 1960 Likoff W, Segai BL, Kasparian H: Paradox of normal selective coronary arteriograms in patients considered to have unmistakable coronary artery disease. N Engl J Med 276:1063-1068, 1967 Whiting RB, Klein MD, Vander Veer J, et al: Variant angina
11.
12. 13.
14.
15. 16. 17.
May 1976
ISCHEMIA WITHOUT ANGINA-GUAZZI
ET AL.
pectoris. N Engi J Med 282:709-712, 1970 Christian N, Botti RE: Prinzmetal’s variant angina pectoris with prolonged electrocardiographic changes in the absence of obstructive coronary disease. Am J Med Sci 263:225-232, 1972 Cosby RS, Giddings JA, See JR, et al: Variant angina. Case reports and critique. Am J Med 53:739-742. 1972 Cheng TO, Bashour T, Kaiser GA Jr, et al: Variant angina of Prinzmetal with normal coronary arteriograms. A variant of the variant. Circulation 47:476-485, 1973 Oiiva PB, Potts DE, Piuss RG: Coronary arterial spasm in Prinzmetal angina. Documentation by coronary angiography. N Engl J Med 2881745-751, 1973 MacAipin R: Coronary spasm as a cause of angina. N Engl J Med 288:788-789, 1973 Linhart JW: Prinzmetal variant angina pectoris. JAMA 288: 342-343, 1974 Bodenheimer M, Lipski J, Donoso E, et al: Prinzmetal’s variant angina: a clinical and electrocardiographic study. Am Heart J 871304-313, 1974
The American
Journal
of CARDIOLOGY
Volume
37
927
Myocardial
lschemia of Prinzmetal
Type
Without Angina Pectoris
MAURIZIO GUAZZI, MARIA T. OLIVARI,
MD MD
ALVISE POLESE, MD CESARE FIORENTINI, MD FABIO
MAGRINI,
MD
Milan, Italy
In a patient with a normal electrocardiogram, normal treadmill exercise test, normal coronary arteriogram and no symptoms to suggest angina pectoris, continuous monitoring during several days exhibited repetitive (one to two per hour) S-T segment elevations in the precordial electrocardiographic leads and hemodynamic changes typical of Prinzmetal’s angina (reduction in arterial pressure and cardiac index and increase in systemic peripheral resistance and pulmonary wedge pressure). This case demonstrates that electrical and dynamic cardiac alterations of Prinzmetal’s angina can occur even in the absence of angina pectoris.
Transient electrocardiographic changes of myocardial ischemia occurring without angina have been described in patients with angina pectoris at rest, showing either the commoni or the Prinzmetal’s electrocardiographic pattern.1-5 In a patient with a normal electrocardiogram, not complaining of angina pectoris or other pain at rest or during exercise, transient S-T segment elevation in the left precordial leads was detected casually during a routine electrocardiographic test. Many such episodes were subsequently documented by continuous electrocardiographic recordings on several consecutive days, but none was perceived by the patient. The origin and the clinical meaning of these changes became more interesting in light of the patient’s normal coronary arteriograms. A continuous hemodynamic monitoring revealed that the phasic electrocardiographic alterations were accompanied by unequivocal circulatory signs of cardiac failure that subsided concomitantly with the reversion to normal concluded that the heart dynamic pattern typical subjective symptoms that
of the electrocardiogram. It was therefore of this patient exhibited an electrical and of Prinzmetal’s angina1s4 in the absence of could reveal the existence of the disorder. Case
From Clinica Medica II, Centro Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, lstituto Ricerche Cardiovascolari, University of Milan, Milan, Italy. Manuscript accepted January 3. 1975. Address for reprints: Maurizio Guazzi, MD, Istituto Ricerche Cardiovascolari. Via Francesco Sforza, 35, 20122 Milano, Italy.
Report
A 46 year old workman was hospitalized because of an attack of dyspnea and palpitation that occurred while at home, when he awoke in the morning, and that subsided within 10 minutes without any therapeutic intervention. He had been fully active and in excellent health until the preceding day. There was no history of hypertension, cardiac or lung diseases, or chest pain or discomfort at rest or on effort. Physical examination revealed an intelligent alert man in no distress; the blood pressure was 150/80 mm Hg in both arms; the pulse rate was 80/min and regular. No murmurs or gallop rhythms were audible. X-ray examination of the chest and cardiac fluoroscopy revealed a heart of normal size and configuration, with normal pulsations and without intracardiac calcifications. An electrocardiogram (Fig. 1A) was normal. A hemogram, urinalysis, serum electrolyte determinations, serum enzyme levels (glutamic oxaloacetic transaminase [GOT] and lactic dehydrogenase [LDH]) and protein-bound iodine levels were within normal limits. A maximal exercise
May 1976
The American
Journal
of CARDIOLOGY
Volume
37
923
MYOCARDIAL
ISCHEMA
WITHOUT
ANGINA-GUAZZI
ET
AL.
test performed on a motorized treadmill did not provoke either angina pectoris or arrhythmias, and no remarkable S-T segment shifts were noted. The patient remained asymptomatic in the hospital, and two subsequent electrocardiograms were normal and unchanged. On the morning of the 7th hospital day, when he was to be discharged, a casual electrocardiogram taken in the absence of symptoms revealed marked S-T segment elevation in leads Vz to Vs with reciprocal depression in leads II, III and aVF (Fig. 1B). Within a few minutes the electrocardiogram reverted spontaneously to its control appearance (Fig. 1C). The patient stated that he had no pain or other discomfort during the recording. Continuous 3 hour electrocardiographic recordings were obtained on 6 subsequent days during different hours each day, according to a method described previously.3 Transient S-T segment displacements of 3 to 5 minutes’ duration, such as those shown in Figure 1, were recorded with an average frequency of 1 to S/hour. The patient never had chest pain or other discomfort, and only in conjunction with one episode lasting longer than usual did he report mild respiratory distress. From these findings, it was assumed that an average of at least 20, and possibly more, episodes of transient S-T segment alteration occurred each 24 hours. In view of their prognostic and therapeutic implications, an effort was made to achieve a correct interpretation of these findings.
Coronary angiography demonstrated excellent visualization of each major coronary artery; all vessels had optimal distribution and patency; no evidence of collateralization was detected. Left ventriculography revealed normal left ventricular contraction and no mitral regurgitation. The nitroglycerin test was unrevealing because of the short duration and spontaneous subsidence of the electrocardiographic alterations. Since unequivocal circulatory signs of cardiac impairment have been shown to accompany the S-T segment displacement of Prinzmetal’s angina,lp4 it was thought that circulatory monitoring would yield useful diagnostic information. Hemodynamic studies: Studies were carried out with the patient fasting, without premeditation, in the supine position, by techniques described elsewhere in detail.‘,* The following data were continuously recorded, at variable paper speed, on a Hewlett-Packard eight channel ink recorder: electrocardiogram, phonocardiogram, heart rate, carotid sphygmogram, brachial arterial pressure, pulmonary arterial or wedge pressure and right atria1 pressure. The electrocardiogram was also monitored on an oscilloscope, but the phasic electrocardiographic changes were so clear that they could consistently be detected even at a paper speed as slow as 0.5 mm/set (see examples in Fig. 2
wedge
6
AP
t
I v4
b/min
HR
160
FIGURE 2. Original strips of records of an episode of S-T alterations (the onset and conclusion are indicated by arrows). From top: time marker: pulmonary wedge (wedge), right atrial (rap), and arterial pressures (AP); heart sounds (HS); leads Vs and V4 of the electrocardiogram: and heart rate (HR). The progressive elevation of the S-T segment and peaking of the T wave are clear even at a recording speed of 0.5 mm/set.
FIGURE 1. Twelve lead electrocardiogram. A, control record. B, spontaneous episode of S-T segment elevation in leads V2 to Vs with reciprocal depression in leads II, Ill and aVF; C, return to control.
624
May 1676
The American
Journal
of CARDIOLOGY
Volume
37
MYOCARDIAL ISCHEMIA WITHOUT ANGINA-GUAZZI
and 3). Arterial and venous catheters were introduced percutaneously. A balloon-tipped catheter6 was floated under fluoroscopic guidance to the pulmonary artery and advanced, when necessary, to the wedge position. For the measurement of right atria1 pressure a polyethylene catheter was also introduced into an antecubital vein and positioned in the right atrium. Cardiac output was determined using indocyanine green dye and a Gilford densitometer, and the derived variables (cardiac index, stroke volume, left and right ventricular ejection rate index and total peripheral resistance) were calculated in the standard fashion. Beat to beat variations of heart rate were detected by a Cardio-Tach preamplifier. Left ventricular preejection period and ejection time were determined from the electrocardiogram, carotid sphygmogram and phonocardiogram recorded at a paper speed of 100 mm/set. The right ventricular ejection time was measured from the pulmonary arterial tracing. The left ventricular mean electromechanical rate of rise of pressure (dP/dt),7 right and left stroke work (index) and mean rate of systolic ejection (index) were calculated from the standard formulas. A total of eight episodes of S-T segment displacement were investigated. Brachial, right atrial, pulmonary arterial and wedge pressures, heart rate and left and right ventricular ejection times were measured during the four 20 second intervals that immediately preceded the onset of the electrocardiographic changes. Measurements were also taken while S-T segment elevation was increasing, during its
ET AL.
steady state, while it was beginning to revert to control levels and 30 and 90 seconds after full normalization. Cardiac output was determined before, during and after the S-T segment displacement. The averages of the hemodynamic functions at the various time intervals are summarized in Table I. The electrocardiographic alterations were not preceded by changes in heart rate, systemic, pulmonary arterial wedge or right atria1 pressures, cardiac output or right or left ventricular ejection time. With the onset of S-T segment changes there was a progressive reduction in arterial pressure accompanied by a conspicuous reduction in cardiac index and increase in systemic peripheral resistance. The following changes were simultaneously seen: increase in right atria1 and pulmonary wedge pressures, mild increase in heart rate and definite reductions in right and left stroke work, mean rate of systolic ejection and left mean electromechanical dP/dt. All the circulatory functions reverted toward control levels within 1 to 2 minutes after complete disappearance of the electrocardiographic abnormalities. Figures 2 and 3 reproduce original strips of records of two such episodes. During the S-T alterations in Figure 3, the patient had junctional extrasystoles with aberrant ventricular conduction but no symptoms. The pulse pressure of the postextrasystolic beats did not exceed that of the control beats. Treatment and course: Treatment with propranolol was started at a daily dose of 160 mg with subsequent in-
wedge
w
HS
FIGURE 3. Original records during an episode of ST-T alterations (indicated by arrowheads) accompanied by cardiac arrhythmias. III = lead 3 of the electrocardiogram: other abbreviations as in Figure 2.
60
HR
bhr(n
May 1976
The American Journal of CARDIOLOGY
Volume 37
925
MYOCARDIAL ISCHEMIA WITHOUT ANGINA-GUAZZI
TABLE
I
Average
Circulatory
SAP (mm Hg) DAP (mm Hg) HR (beats/mln) mRAP (mm Hg) mWP (mm Hg) RSW (g.m/m’) LSW (g.nl/rnl) RMSEJR (ml/set per m’) LMSEJR Iml/sec per m”) dP/dt (mm Hg/msec) Cl (mlimin per m’)
Values
at Various
Periods*
A
8
165
164 90 81 4 7
4 7 5 75 150
ET AL
During C 163
4 7
S-T
Segment
Displacement
D
E
164 90 81 4 7
172 0.9 3950
0.95
F
G
150
145
8835 7 10 3 50 122
10 15 2 40 115
148 87 80 10 15
147
135
0.72 2920
0.6 2800
H
I
158 88 80
90” 148
4 7 5 72 152
172
168
0.92 4050
0.91 3990
Measurements were taken during the four 20 second Intervals immediately preceding the electrocardiographic changes (A, B, C, D), during the Increase in S-T segment elevation (El, during the steady state period (F), at the onset of reversion to control level IG) and 30 (H) and 90 seconds (I) after full normalization. Cl = cardiac index; DAP = diastolic arterial pressure; dP/dt = left mean electromechanical dP/dt; HR = heart rate; LMSEJR = left mean systolic ejection rate (index); LSW = left stroke work (index); mRAP = mean right atrial pressure: mWP = mean wedge pressure; RMSEJR = right mean systolic ejection rate (Index); RSW = right stroke work; SAP = svstolic arterial oressure. l
crements of’ 80 mg every other day, according to the patient’s response, which was evaluated daily with 3 hour continuous electrocardiographic recordings. Full disappearance of the phasic electrocardiographic alterations was consistently found at a dose of 800 mg/day, and he was discharged at this dosage. For 2 months he has returned weekly to our Cardiology Clinic for follow-up studies including 3 hour continuous recordings of the electrocardiogram; the electrocardiogram has remained normal, and the patient is asymptomatic and has returned to work.
tative or qualitative electrocardiographic’” or circulaor tory differences lv4 between attacks accompanied unaccompanied by pain. In conclusion, the findings in our case do not shed light on the mechanisms or agents directly responsible for eliciting pain in myocardial ischemia. They do indicate (1) that these mechanisms are undetectable by electrocardiography, and (2) that pain and impaired cardiac function do not necessarily accompany each other, although each is probably a consequence of ischemia. Angiographic studies have indicated a transient spasm of the coronary vessels as the possible triggering mechanism of ischemia in patients with Prinzmetal’s angina.9-17 In our subject none of the circulatory factors that acutely increase the mechanical effort of the heart, and consequently its need for oxygen, such as tachycardia, increase in arterial pressure or lengthening of ventricular contraction, can be considered responsible for the episodic myocardial ischemia, which seems to be the event leading to impairment of cardiac function. These findings are in keeping with the interpretation that in such cases, ischemia is primarily due to an altered oxygen supply, possibly caused by coronary spasm, rather than to increased myocardial oxygen demand. Our observations further indicate that continuous electrocardiographic recording or monitoring provides the most direct and informative means for evaluating and recognizing patients with disturbances of the coronary circulation. This diagnostic tool was valuable in the diagnosis of our case, which probably represents a new facet of Prinzmetal’s angina that might be called “angina without angina.”
Discussion The reduction in cardiac output, arterial pressure, stroke work, mean rate of systolic ejection and dP/dt, as well as the increase in pulmonary wedge and right atria1 pressures, clearly indicates that heart failure occurred during the electrocardiographic alterations. It is therefore likely that the S-T segment displacement in this patient reflects myocardial ischemic changes that induced no pain but were severe enough to cause dynamic impairment of the heart as well as cardiac arrhythmias. The electrocardiographic8 and the circulatory featuresl,” in this case are typical of Prinzmetal’s angina; nonetheless, the total absence of pain is unusual and hard to interpret. This aspect deserves comment. Because the angiograms revealed no coronary arterial lesion, the absence of pain might be attributed to this finding. However, there have been many reports of patients with normal coronary arteriograms presenting with the classic symptoms of Prinzmetal’s angina.+‘” Since no pain-producing episode of ischemia was recorded, painful and nonpainful attacks cannot be compared in our subject. In reported cases, however, there were no definite quanti-
References 1. Guazzi M, Poise A, Fiorentini C, et al: Left and right heart haemodynamics during spontaneous angina pectoris. Comparison between angina with S-T segment depression and angina with S-T segment elevation. Br Heart J 37:1235-1245. 197.5 2. Robinson JS: Prinzmetal’s variant angina pectoris. Report of a
926
May 1976
The American
Journal
of CARDlOLOGY
Volume
case. Am Heart J 70:797-800, 1965 3. Guazzi M, Fiorentini C, Polese A, et al: Continuous electrocardiographic recording in Prinzmetal’s variant angina pectoris. A report of four cases. Br Heart J 32:611-616, 1970 4. Guazzi M, Polese A, Fiorentini C, et al: Left ventricular perfor-
37
MYOCARDIAL
5.
6.
7.
8.
9.
10.
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