Transient myocardial ischemia with minimal electrocardiographic changes: an echocardiographic study in patients with Prinzmetal's angina

Kn patients with Prinzmetal's angina, episodes of transient T wave abnormalities (T abn) are often documented in addition to the typical episodes of ST segment elevation (ST). As the interpretation of these minor ECG changes is still uncertain, we investigated if transient T abn are associated with reversible ventricular asynergies, similar to episodes with ST. For this purpose an ECG lead and a two-dimensional echocardiographic projection, which showed clear-cut changes during previous episodes of ST, were simultaneously monitored in five patients with Prinzmetal's angina for a total of 13 hours and 20 minutes. In all patients, the 30 episodes of ST recorded were all accompanied by reversible ventricular asynergies. Furthermore, in four of these patients, 14 episodes of T abn (peaking, flattening, or the appearance of a diphasic T wave) were recorded. All T abn were associated with reversible asynergies, as detected by three independent observers. The mechanical impairment occurred in the same ventricular wall both during ST and during T abn. During T abn the degree of mechanical impairment appeared less severe (hypokinesia in 12 and akinesia in two episodes) than during ST (hypokinesia in one, akinesia in 25, and dyskinesia in four episodes) (p less than 0.001). The duration of asynergies was less during T abn (107 +/- 76 seconds) than during ST (169 +/- 83 seconds) (p less than 0.05). Chest pain was reported in 5 of 14 episodes of T abn (36%) and in 20 of 30 (66%) episodes of ST (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventricular arrhythmias in patients with rest angina: correlation with ST segment changes and extent of coronary atherosclerosis

Major ventricular arrhythmias occurring concurrently with myocardial ischemia are presumed to be the most frequent mechanism for sudden cardiac death. Two hundred eighteen catheterized patients with angina pectoris at rest were reviewed to identify clinical, ECG, and arteriographic features that might correlate with the presence of serious ventricular arrhythmias occurring during episodes of rest pain. Ventricular arrhythmias during episodes of rest pain were significantly more common in patients who manifested transient ST segment elevation in the anterior leads and in patients with marked transient ST segment shifts (greater than 5 mm). Ventricular arrhythmias during episodes of rest pain were not more common in patients with extensive coronary artery disease.     

Perioperative myocardial ischemia in patients undergoing noncardiac surgery--I: Incidence and severity during the 4 day perioperative period. The Study of Perioperative Ischemia (SPI) Research Group

To determine the incidence and characteristics of perioperative myocardial ischemia, the electrocardiographic (ECG) changes consistent with ischemia during the 4 day perioperative period were documented and characterized in 100 patients with or at risk for coronary artery disease undergoing noncardiac surgery. Using continuous two channel ECG monitoring (leads CC5 and CM5), the frequency and severity of ECG ischemic episodes defined by ST segment depression greater than or equal to 1 mm or elevation greater than or equal to 2 mm during the preoperative (up to 2 days), intraoperative and early postoperative (first 2 days) periods were compared. Preoperatively, 28 patients (28%) exhibited 105 episodes of ischemia; intraoperatively, 27 patients exhibited 39 episodes and postoperatively, 42 patients exhibited 187 episodes. There was no difference between the pre- and intraoperative episode characteristics. However, postoperative ischemic episodes were the most severe. The mean ST change was 1.5, 2 and 2.6 mm for pre-, intra- and postoperative episodes, respectively (p less than 0.0001 postoperative versus pre- or intraoperative); duration of ischemic episodes was 69, 45 and 207 min, respectively (p less than 0.005 postoperative versus preoperative, p less than 0.001 versus intraoperative) and area under the ST curve was 88, 74 and 383 mm.min (p less than 0.009 postoperative versus preoperative, p less than 0.005 versus intraoperative). Ninety-four percent of all postoperative ischemic episodes were silent; 80% of all episodes occurred without acute change (+/- 20% of control) in heart rate and 77% of intraoperative episodes occurred without acute change in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical and angiographic findings in angina at rest

The purpose of this study was to delineate the clinical, ECG, and angiographic features of a large series of consecutive patients with angina at rest. Transient ST segment elevation during pain was observed in 219 patients (group I), while 220 patients showed ST segment depression during pain (group II). Group II patients were found to have higher incidence of hypertension (p less than 0.001), prior myocardial infarction (p less than 0.0005), history of exertional angina (p less than 0.0005), and a progressive aggravation of symptoms before hospitalization (p less than 0.0005), while group I patients had a prevalence of recent onset angina (p less than 0.05) and more frequently developed severe ventricular arrhythmias during pain (p less than 0.0005). Furthermore, a larger number of patients showing ST segment depression during chest pain had multivessel disease (p less than 0.0005), left main involvement (p less than 0.005), and lower values of left ventricular ejection fraction (p less than 0.001) than patients with ST segment elevation during pain. Survival curves of medically treated patients showed a significantly better long-term prognosis in patients of group I (p less than 0.01). The direction of the ST segment shift during anginal attacks at rest may therefore allow a classification of patients included into the broad spectrum of unstable angina. This distinction should be taken into consideration in studies aimed at evaluating long-term prognosis or the results of medical and surgical therapy.     

ST segment shifts are poor predictors of subsequent Q wave evolution in acute myocardial infarction. A natural history study of early non-Q wave infarction

Acute ST segment elevation is regarded generally as the sine qua non of evolving Q wave myocardial infarction (MI) because such electrocardiographic (ECG) injury is believed to be a marker of transmural ischemia and a forerunner of transmural necrosis. Alternatively, ST segment depression with or without T wave inversion is viewed as the dominant ECG feature of non-Q wave MI. However, this hypothesis has not been assessed prospectively in an acute MI population. We analyzed 2,304 serial ECGs at study entry (admission), day 2, day 3, and predischarge (mean, 10.2 +/- 2 days) from 576 patients with creatine kinase MB confirmed acute non-Q wave MI to determine what percentage of patients with early ST segment elevation culminated in subsequent Q wave development. Of this group, 187 patients (32%) exhibited 1 mm or greater ST segment elevation in two or more contiguous entry ECG leads. Of those patients whose non-Q wave MI could be localized on the basis of diagnostic admission ST segment shifts, the prevalence of early ST segment elevation was 43% (187 of 439). The sum total mean (+/- SD) peak ST segment elevation by lead group (anterior, inferior, lateral) was 4.0 +/- 2.4, 4.5 +/- 2.4, and 2.5 +/- 0.6 mm, respectively. Despite this, only 20% of patients with ST segment elevation (37 of 187) developed Q waves. Of 252 patients who exhibited early ST segment depression or T wave inversion or both, 39 (15%) evolved subsequent Q waves. Thus, while the prevalence of early ST segment elevation in acute evolving non-Q wave MI was higher than previously reported, 80% of patients with and 85% of patients without ST segment elevation and absent Q waves on the admission ECG did not develop subsequent Q waves during a 2-week period of observation (p = NS). In addition, when patients with ST segment elevation were compared with patients with ST segment depression or T wave inversions or both, there were no between-group differences in log peak creatine kinase (404 vs. 383 IU), reinfarction (6% vs. 8%), postinfarction angina (50% vs. 42%), or early recurrent ischemia (49% vs. 45%), defined as postinfarction angina with transient ECG changes. Thus, in patients who present with initial acute non-Q wave MI, ST segment shifts on admission are unreliable predictors of subsequent Q wave evolution and do not discriminate significant differences in postinfarction outcome. In particular, ST segment elevation during the early hours of evolving infarction is not an invariable harbinger of subsequent Q wave development.     

The giant R wave of acute myocardial infarction

The common clinical electrocardiographic criteria for diagnosis of acute transmural myocardial infarction include ST segment elevation and tall, upright T waves, but do not include changes in QRS morphology. The purpose of this study was to show that development of a 50% or greater increase in R wave amplitude, the giant R wave, in patients with acute transmural myocardial infarction occurs, and also to characterize changes in QRS morphology which may aid the ECG diagnosis of acute transmural myocardial infarction. Over the past 6 years, 36 patients with an increase in R wave amplitude during acute transmural myocardial infarction were identified at the Strong Memorial Hospital Coronary Care Unit. A significant increase in R wave height (0.33 +/- 0.10 to 0.97 +/- 0.08 mV, p less than 0.05), width (0.03 +/- 0.00 to 0.08 +/- 0.01, p less than 0.05) and area (0.01 +/- 0.00 to 0.05 +/- 0.01 mV-msec, p less than 0.05) appeared in the same ECG lead demonstrating ST segment elevation and tall T waves during the acute phase of transmural myocardial infarction. Patients with diaphragmatic myocardial infarction showed a significant (p less than 0.05) rightward QRS frontal plane axis shift and patients with anterior wall myocardial infarctions developed an anterior QRS axis shift in the horizontal plane during occurrence of the giant R wave. We conclude from this preliminary study that the giant R wave may be observed during acute transmural myocardial infarction and may in part be caused by local intramyocardial conduction delay in acutely ischemic tissue as supported by an increase in the R wave width along with shifts in the frontal and horizontal plane QRS axis toward the area of acute ischemia. The giant R wave occurs in conjunction with ST segment elevation and tall T waves and may aid the ECG diagnosis of acute transmural myocardial infarction.     

Clinical evaluation of transient myocardial ischemia

Out of 432 patients with coronary heart disease, 106 (24.5%) were found to have transient myocardial infarction during ECG monitoring of ST segment for 10 hours of daily activity. High-grade ventricular arrhythmias were revealed in 74.6% of mainly male and middle-aged subjects. 63.4% of the patients exhibited congestive heart failure, 48.1% had postinfarct cardiosclerosis, and 25.5% presented with diabetes mellitus. Transient myocardial ischemia was more frequently detected during exercise and more rarely during emotional stress (21.7%), meal (19.8%), and smoking (7.8%). Asymptomatic episodes of ST segment elevation were recorded in 36.8%, while asymptomatic episodes of ST segment depression, in 29.2%. The duration of asymptomatic episodes of ST segment elevation and depression was twice and 1.5 times, respectively, less than that of symptomatic ones. Substantial myocardial perfusion and metabolic impairments were revealed with an asymptomatic ST segment depression frequency of at least one an hour, an amplitude of more than 2 mm, and a duration of no less than 40 min.     

Inferior ST segment depression during acute anterior myocardial infarction: clinical and angiographic correlations

This study was performed to determine whether inferior ST segment depression during early stages of acute transmural anterior myocardial infarction identifies patients with multivessel coronary artery disease and additional inferior ischemia. Coronary and left ventricular angiography were performed within 3.4 months in 33 patients with acute transmural anterior infarction. Initial electrocardiograms, 2 to 5 hours after onset of chest pain, revealed significant ST segment depression (greater than or equal to 0.1 mV) in at least two of leads II, III and a VF in 15 patients (45%) (group B); in 18 patients (group A) this finding was absent. Compared with group A, patients in group B had greater anterior ST elevation (1.2 versus 0.7 mV, p less than 0.025); higher serum peak creatine kinase (2,475 versus 1,147 IU/liter, p less than 0.005); higher Killip scores (2.1 versus 1.3, p less than 0.001); more in-hospital complications (60 versus 17%, p less than 0.05); lower mean left ventricular ejection fraction (34 versus 55%, p less than 0.001); more frequent regional left ventricular dysfunction in anterolateral (91 versus 44%, p less than 0.05), posterolateral (36 versus 0%, p less than 0.05) and inferior (100 versus 6%, p less than 0.005) regions; greater wall motion abnormality scores (10.0 versus 5.5, p less than 0.005); higher frequency of concomitant left circumflex or right coronary artery disease, or both (80 versus 28%, p less than 0.01); more frequent postinfarction angina (100 versus 39%, p less than 0.001) and lower New York Heart Association functional classification scores (1.7 versus 2.4, p less than 0.05) at 6 month follow-up. The time course of inferior ST depression differed from that of anterior ST elevation. Thus, inferior ST depression was maximal in the first 48 hours and decreased (p less than 0.05) thereafter. In contrast, ST elevation in leads V1 to V6 and I appeared to decrease (p = NS) between days 4 and 7. However, inferior ST depression "mirrored" ST elevation in lead aVL, which also decreased (p less than 0.05) after 48 hours. Thus, inferior ST depression during anterior infarction is associated with more extensive infarction, greater morbidity and higher frequency of multivessel coronary disease. Such inferior ST depression might reflect not only "reciprocal change," but also ischemia in adjacent lateral and remote inferior regions.     

Myocardial ischemia in patients awaiting coronary artery bypass grafting

The results of ambulatory ECG monitoring are described in a group of patients that have not previously been characterized. Fifty men who were initially seen for elective CABG surgery underwent 48 hours of continuous ambulatory ECG monitoring. ST segment deviation from baseline, trended every 15 seconds, was quantified for duration, maximum ST segment change, area under the ST segment-time curve (AUC), and average ST segment change for the episode (AUC/duration). Ischemic episodes, 87% of which were silent, occurred in 42% of the patients. Symptomatic episodes had greater maximum ST segment change than silent episodes (-2.4 vs -1.9 mm; p less than 0.05) but were shorter in duration (11 vs 18 minutes; p less than 0.05). Episodes that were unrelated to heart rate, that is, episodes with less than 20% increase in heart rate over the baseline rate at the onset of ischemia, made up 75% of all ischemic events and occurred in 90% of patients (19 of 21). Heart rate-related and unrelated ischemic episodes did not differ in duration, maximum ST segment change, AUC, or average ST segment change. It was concluded that: (1) as with patients with unstable angina, patients with severe coronary artery disease continue to have frequent episodes of silent myocardial ischemia despite intensive medical therapy; (2) painful episodes have greater maximum ST segment change but are shorter than silent ones; (3) most ischemic episodes (75%) occur without an initial increase in heart rate; and (4) heart rate-related and unrelated episodes are quantitatively similar.     

Effect of metaraminol during acute inferior wall myocardial infarction accompanied by hypotension: preliminary study

This study was designed to evaluate the effects of metaraminol (Aramine) in six patients with evolving acute inferior wall myocardial infarction accompanied by hypotension and warm limbs. There were 16 episodes of acute inferior wall ischemia, and the response to therapy was judged by evaluating blood pressure and ST segment and T wave abnormalities. Three patients received intravenous isosorbide dinitrate and two received streptokinase as the initial therapy. The mean ST segment elevation was significantly reduced (from 4.94 +/- 1 to 0.5 +/- 0.7 [p less than 0.0001]) after metaraminol infusion was initiated. The average T wave height also decreased (from 6.8 +/- 2 to -1.3 +/- 2.5 mm [p less than 0.0005]). The average heart rate decreased from 82 +/- 11 to 69 +/- 9 beats/min (p less than 0.05) and the mean arterial blood pressure increased from 81 +/- 12 mm Hg before metaraminol treatment to 126 +/- 8 mm Hg after treatment. All these changes occurred within a few minutes after metaraminol therapy was instituted. In 12 episodes, accelerated idioventricular rhythm appeared concomitantly with the resolution of ST segment elevation. Coronary angiography performed between 4 and 10 days after admission demonstrated significant obstruction in all infarct-related arteries, but none was totally occluded. Left ventricular function was normal in three patients and slightly hypokinetic in the inferior wall in two. These results indicate that in a selected group of patients with acute inferior myocardial infarction, metaraminol administration (in certain hemodynamic circumstances) can alleviate acute ischemia within a few minutes and thereby reduce ischemic injury.     

Ventricular arrhythmias during ergonovine-induced episodes of variant angina

Of 95 consecutive patients with active variant angina who underwent ergonovine testing in the coronary care unit while off treatment, 24 (25%) developed serious ventricular arrhythmias: ventricular tachycardia in eight, bigeminy in seven, pairs in five, and frequent ventricular extrasystoles in four. Ergonovine-induced arrhythmias were observed more often in patients with anterior than inferior ST segment elevation (p less than 0.05). ST segment elevation was significantly higher (10.3 +/- 8.1 vs 3.1 +/- 2.1 mm) in patients who developed arrhythmias. All ventricular arrhythmias began within 3 minutes after the onset of ST segment elevation. The intravenous administration of nitroglycerin eliminated arrhythmias in 22 of 24 cases; in only two patients did ventricular arrhythmias develop after the administration of nitroglycerin. Serious ventricular arrhythmias were found during spontaneous variant angina attacks in 14 of 24 patients with ergonovine-induced arrhythmias compared to 16 of 71 patients without ergonovine-induced arrhythmias (p less than 0.001). We conclude that arrhythmias during ergonovine testing are most often caused by ischemia and not reperfusion. Patients with arrhythmias during ergonovine-induced attacks are more likely to have arrhythmias during spontaneous attacks.     

Transient changes in left ventricular mechanics during attacks of Prinzmetal's angina: an M-mode echocardiographic study

M-mode echocardiograms were recorded in 12 patients with Prinzmetal's angina during 29 episodes of transient myocardial ischemia at rest (18 spontaneous and 11 ergonovine-induced). At peak ST segment elevation a regional mechanical impairment was observed in the interventricular septum during 23 episodes of angina and in the posterior wall during six episodes. In the 18 spontaneous episodes the left ventricular ischemic wall, when compared to the basal state, was found to have a significant reduction in motion (-76.3 +/- 9.1%) (mean +/- SEM), in diastolic thickness (-11.7 +/- 2.5%), and in percent systolic thickening (-88.0 +/- 5.6%). Increase in left ventricular end-diastolic diameter (+13.1 +/- 2.1%) and decrease in percent fractional shortening (-38.1 +/- 3.7%) were also observed. When ST segment was back to the isoelectric line, a transient overshoot in regional left ventricular function was observed. In induced episodes statistically significant changes could be detected by M-mode echocardiography even before appearance of ST segment elevation and anginal pain. No significant difference was found in type or degree of mechanical impairment between induced and spontaneous episodes. Therefore, in patients with Prinzmetal's angina: (1) M-mode echocardiography allows detection of mechanical changes due to transient myocardial ischemia; and (2) mechanical impairment occurs earlier than clinical (pain) and electrocardiographic (ST segment elevation) signs of transmural ischemia.     

The haemodynamic response to myocardial ischaemia in ambulant patients with variant angina

The haemodynamic response to myocardial ischaemia in patients with variant angina during ambulatory activity is unknown. Ambulatory pulmonary artery pressure monitoring with a transducer tipped catheter and simultaneous frequency modulated electrocardiograms was used to assess changes in left ventricular function in five male patients (mean age 51.8 years) during variant angina; four patients had coronary artery stenosis and one had normal coronary arteries. Two hundred and seventy hours of ambulatory recordings were analysed. Twenty episodes (12 painful, 8 silent) of ST segment change greater than 1 mm occurred. Episodes tended to occur more frequently in the early morning hours. Six episodes of painful ST elevation were associated with a rise in pulmonary artery diastolic pressure. In the remaining episodes ST segment elevation was of shorter duration and there was no rise in pulmonary artery diastolic pressure. Pain was usually a late feature. Silent ST segment elevation occurred at rest and pulmonary artery diastolic pressure increased in all but one episode. Silent exertional ST segment depression was associated with a greater increase in pulmonary artery diastolic pressure than that seen during ST segment elevation. ST segment depression preceded or followed ST segment elevation in two episodes. The onset of ST segment elevation nearly always preceded the onset of a rise in pulmonary artery diastolic pressure. Ergometrine maleate provocation produced a rise in pulmonary artery diastolic pressure in three patients. In one there was no response to 1000 micrograms but spontaneous episodes of ST segment elevation were recorded during ambulatory monitoring. Treadmill exercise resulted in both ST segment elevation and depression with a similar haemodynamic response during both types of electrocardiographic change. When there is important coronary artery disease in two or more vessels ST segment changes may occur in different territories during treadmill exercise and during spontaneous episodes. Ambulatory pulmonary artery diastolic pressure monitoring is a useful technique for the investigation of variant angina.     

The haemodynamic response to myocardial ischaemia in ambulant patients with variant angina.

The haemodynamic response to myocardial ischaemia in patients with variant angina during ambulatory activity is unknown. Ambulatory pulmonary artery pressure monitoring with a transducer tipped catheter and simultaneous frequency modulated electrocardiograms was used to assess changes in left ventricular function in five male patients (mean age 51.8 years) during variant angina; four patients had coronary artery stenosis and one had normal coronary arteries. Two hundred and seventy hours of ambulatory recordings were analysed. Twenty episodes (12 painful, 8 silent) of ST segment change greater than 1 mm occurred. Episodes tended to occur more frequently in the early morning hours. Six episodes of painful ST elevation were associated with a rise in pulmonary artery diastolic pressure. In the remaining episodes ST segment elevation was of shorter duration and there was no rise in pulmonary artery diastolic pressure. Pain was usually a late feature. Silent ST segment elevation occurred at rest and pulmonary artery diastolic pressure increased in all but one episode. Silent exertional ST segment depression was associated with a greater increase in pulmonary artery diastolic pressure than that seen during ST segment elevation. ST segment depression preceded or followed ST segment elevation in two episodes. The onset of ST segment elevation nearly always preceded the onset of a rise in pulmonary artery diastolic pressure. Ergometrine maleate provocation produced a rise in pulmonary artery diastolic pressure in three patients. In one there was no response to 1000 micrograms but spontaneous episodes of ST segment elevation were recorded during ambulatory monitoring. Treadmill exercise resulted in both ST segment elevation and depression with a similar haemodynamic response during both types of electrocardiographic change. When there is important coronary artery disease in two or more vessels ST segment changes may occur in different territories during treadmill exercise and during spontaneous episodes. Ambulatory pulmonary artery diastolic pressure monitoring is a useful technique for the investigation of variant angina.     

Electrocardiographic findings in acute right ventricular infarction: sensitivity and specificity of electrocardiographic alterations in right precordial leads V4R, V3R, V1, V2, and V3

To determine the sensitivity, specificity, predictive value and diagnostic efficiency of electrocardiographic alterations in the diagnosis of acute right ventricular infarction, 43 autopsy patients with acute myocardial infarction and an electrocardiogram including 12 leads plus leads V3R and V4R were studied. Group A included 21 patients with right ventricular infarction, of whom 14 (group AI) had posterior and 7 (group AII) had anterior right ventricular infarction. Group B included 22 patients without right ventricular infarction. Excluding group AII patients, the sensitivity of the presence of a Q wave reached 78.6% in lead V4R and decreased in leads V1 to V3; its specificity was low in all the leads. The sensitivity of ST segment elevation reached 100% in lead V4R and decreased in leads V1 to V3; its specificity was highest (68.2%) in leads V4R and V3R, its negative predictive value was 100% and its diagnostic efficiency was 80.6%. The criterion of ST segment elevation in lead V4R being higher than that in leads V1 to V3 was less sensitive (78.6%) than ST segment elevation in lead V4R alone, but its specificity reached 100%, its positive predictive value 100% and its diagnostic efficiency 91.7%. In conclusion, there are no electrocardiographic criteria to identify anterior right ventricular necrosis, but posterior right ventricular necrosis may be identified by the presence of a Q wave or ST segment elevation in the right precordial leads, reaching the highest sensitivity and specificity in lead V4R. The criterion of ST segment elevation in lead V4R being higher than that in leads V1 to V3 offers the highest specificity and efficiency in the diagnosis.     

Diltiazem in spontaneous angina: double-blind cross-over study with Holter monitoring

Using Holter monitoring the Authors compared the effectiveness of diltiazem 120 mg every 8 hours for three consecutive days with the results of a placebo administered with the same regimen, following a double-blind completely balanced cross-over trial in 20 patients with angina at rest. During treatment with diltiazem the total number of recorded ischemic episodes was 100, during treatment with placebo the total number was 357 (Tab. I); P less than 0.01 at analysis of variance (Tab. II). Ischemic episodes during treatment with diltiazem had a shorter duration (3.9 versus 5.1 min.), less marked ST segment shifts (1.3 versus 2 mm), and were less symptomatic (20% versus 29%) than ischemic episodes during placebo (Tab. III). No significant differences at a paired t test were noted. Diltiazem was more effective in the morning (12 p.m. - 12 a.m.: from 187 to 34 ischemic episodes) than in the evening (12 a.m. - 12 p.m.: from 170 to 66 ischemic episodes) (Fig. 1); P less than 0.01 at the chi-square test (Tab. IV). Diltiazem reduced the number of ischemic episodes with ST segment elevation, peaking of T waves and negative T wave inversion (from 188 to 39) more than the number of episodes with ST segment depression (from 169 to 61) (Tab. V); P less than 0.05 at the chi-square test. In conclusion, in patients with angina at rest, diltiazem reduces the incidence and seems to reduce the severity of ischemic episodes, too.(ABSTRACT TRUNCATED AT 250 WORDS)     

Arrhythmias in relation to transient ST elevations in Prinzmetal angina: induction by occlusion and reperfusion

To study the temporal relationship of occlusion and reperfusion we examined 16 patients (14 m, 2f) with variant angina for the occurrence and time course of arrhythmias with episodes of ST-elevation (n = 82). The patients underwent frequency-modulated ambulatory ECG recording, episodes of ST elevation were defined, and the arrhythmias were counted before, during and after each episode. In 10 patients (group A) no or only infrequent extrasystoles occurred. Of the other 6 patients (group B), one had a-v block II degree, 5 had frequent (greater than 2/min) ventricular or supraventricular premature beats, 3 with couplets or runs of VPB. Patients of group A and B did not differ in age, severity of fixed coronary stenoses and ventricular ejection fraction. There was a tendency towards a greater incidence of higher ST-elevations (greater than 2 mm) in group B (4 of 6 patients versus 2 of 10 in group A, p = 0.09). The relationship of arrhythmias and ST changes showed different patterns: the maximum of arrhythmias occurred during the episode in 3 patients, during and after the episode in 2 patients and only after the episode in 1 patient. Potentially dangerous arrhythmias are frequent in patients with variant angina and persist beyond the ST segment changes in one half of the affected patients.     

Transient ST segment elevation occurring without anginal pain. Correlations with Prinzmetal's angina.

Two cases presenting with episodes of marked ST segment elevation occurring with, but most often without, anginal pain are reported. The changes were recorded through continuous ECG monitoring during Prinzmetal's angina and in the course of myocardial infarction. Such transient asymptomatic ECG abnormalities reveal silent acute myocardial ischemia and are often unrecognized. However, they may lead to severe arrhythmias or myocardial infarction, and sudden deaths occurring in the course of ischemic heart disease are likely to be explained on this basis. Transient episodes of silent ST segment elevation similar to those occurring in Prinztal's angina have been reported in various circumstances. They bring into discussion the delimitations of variant angina pectoris.     

Value of the intracoronary electrocardiogram to monitor myocardial ischemia during percutaneous transluminal coronary angioplasty

To enhance detection of ischemia during percutaneous transluminal coronary angioplasty (PTCA), unipolar intracoronary electrocardiograms (ECGs) were recorded during PTCA in 25 patients from the tips of guidewires positioned distal to stenoses being dilated. Surface electrocardiographic leads chosen to reflect likely areas of reversible ischemia during PTCA were recorded simultaneously. In 21 of 29 stenoses dilated (72%), ST segment elevation and/or T wave peaking in intracoronary ECG appeared during balloon inflation and disappeared after deflation, accompanied by transient angina on 19 occasions. Two patients had transient ST segment elevation in intracoronary ECGs during PTCA without associated angina. ST changes in the surface ECG during PTCA were seen on only nine occasions (31%), always accompanied by ST segment elevation in the intracoronary ECG that appeared earlier and was of much greater magnitude. Five patients with prior myocardial infarction and aneurysm formation had fixed ST segment elevation in the intracoronary ECG unrelated to balloon inflation. Myocardial ischemia during PTCA can be detected easily with intracoronary ECGs and with greater sensitivity than that of the surface ECG. Furthermore, intracoronary ECGs may help to clarify the nature of chest pain during balloon inflation or during suspected complications.     

Electrocardiographic alterations in leads V1 to V3 in the diagnosis of right and left ventricular infarction

As Q wave and ST segment elevation in leads V1 to V3 may be due either to right ventricular infarction (RVI) or to anterior left ventricular infarction (ALVI), 72 autopsy patients with acute myocardial infarction who had had conventional 12-lead ECG records were studied to determine the accuracy of these ECG criteria, both for the diagnosis of RVI (29 patients, group A) and of ALVI (43 patients, group B). The accuracy of three ECG criteria (Q wave, ST segment elevation greater than or equal to 0.05 mV, and ST segment elevation greater than or equal to 0.1 mV) in diagnosing group A and group B patients was determined in each precordial lead (V1, V2, and V3) and the three criteria were found to be significantly more accurate in diagnosing group B than group A patients. In conclusion, although Q wave and ST segment elevation in leads V1, V2, and V3 may be present in some cases of RVI, their accuracy is too low to be considered useful diagnostic criteria in these patients.