Silent myocardial ischemia in patients with variant angina

Twenty-four hour ambulatory electrocardiographic recording was performed in 56 patients with variant angina admitted to the coronary care unit in order to evaluate the incidence and pathophysiology of silent episodes of ST elevation. Of 696 episodes of ST elevation of more than 0.1 mV identified during a recording period of 141 days, 531 (76%) episodes were completely silent. The incidence of silent episodes increased as the number of total ischemic episodes per day increased. Silent ST elevation revealed a significantly shorter duration and a lower intensity than symptomatic ST elevation. However, there were wide overlaps in the duration and intensity of ST elevation between silent and symptomatic episodes. In some patients, silent and symptomatic episodes of similar duration and intensity were observed. Arrhythmias during ischemic episodes such as premature ventricular contractions, ventricular tachycardia, high grade atrioventricular block, and sinus arrest were observed in 32 of 56 patients, 57% of cases and 9% of the total episodes. Arrhythmias were more common during symptomatic episodes (29%) than during silent ones (9%, p less than 0.01), but serious arrhythmias such as ventricular tachycardia, high grade atrioventricular block and sinus arrest occurred even during silent episodes. In both silent and symptomatic episodes, the duration and intensity of ST elevation were significantly lower in ischemic episodes with arrhythmias than in those without arrhythmias. These results suggest that 1) the majority of ischemic events are silent in patients with variant angina; 2) the severity of ischemia seems to be an important factor as the cause of anginal pain, but additional factors may be involved; 3) arrhythmias were more common during sympatomatic than silent episodes.     

Prevalence, time course and malignancy of ventricular arrhythmia during spontaneous ischemic ST-segment depression

Ventricular arrhythmias during transient myocardial ischemia were studied in 60 patients with spontaneous angina and greater than or equal to 1 ischemic attack with ST-segment depression during 24-hour ambulatory electrocardiography. The patients were divided into 2 groups: group 1, 10 patients (17%) who developed ventricular arrhythmias during 26 of 92 (28%) ischemic attacks; and group 2, 50 patients who did not show this phenomenon. Daily ischemic attacks, total ischemic time and the proportion of symptomatic ischemic attacks were significantly greater (p less than 0.01) in group 1 versus group 2. In group 1 patients, ischemic attacks were found to have twice the duration in the presence of arrhythmias than in their absence (20.4 +/- 11.9 vs 9.1 +/- 8.4 minutes, p less than 0.01); arrhythmias were more common during symptomatic than during silent ischemic attacks (39 vs 13%, p less than 0.02). Arrhythmias occurred at the onset or peak of ST-segment depression (ischemia phase) in 6 cases (60%), during the resolution of ST-segment depression (recovery phase) in 2 cases (20%) and during both phases of ischemic attacks in the remaining 2 (20%). When compared to recovery phase arrhythmias, ischemia phase arrhythmias were characterized by a later onset time (173 +/- 144 vs 58 +/- 54 seconds, p less than 0.01) and a longer duration (105 +/- 107 vs 41 +/- 22 seconds, p less than 0.01). During the ischemia phase, 16 of 353 ventricular premature complexes initiated ventricular tachycardia, while during the recovery phase only 1 of 161 ventricular premature complexes resulted in ventricular tachycardia (4.5 vs 0.6%, p less than 0.02). Thus, ventricular arrhythmias may accompany spontaneous ischemic ST-segment depression, when the latter is recurrent, prolonged and symptomatic; arrhythmias are characterized by a greater frequency, duration and malignancy during the ischemia phase than during the recovery phase of ischemic attacks.     

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.     

Mechanisms of arrhythmias accompanying ST-segment depression on ambulatory monitoring in stable angina pectoris

To investigate the mechanisms of ischemic arrhythmias during daily life, 32 patients with stable angina pectoris and documented ischemic episodes were studied by 24-hour ambulatory electrocardiographic monitoring. The severity of arrhythmias observed at or before peak ST-segment depression (early arrhythmias) and arrhythmias presenting during or after resolution of the ST-segment changes (late arrhythmias) was graded according to a modified Lown classification. Eleven patients (34%) had ischemic arrhythmias and had a greater number of ischemic episodes (6.0 +/- 5.4 vs 2.3 +/- 1.5, p less than 0.001) than patients without ischemic arrhythmias. Ischemic episodes accompanied by arrhythmias had a greater ST-segment depression (2.8 +/- 1.6 mm vs 1.9 +/- 0.6 mm, p less than 0.001), and duration (18.2 +/- 14.8 minutes vs 5.7 +/- 2.6 minutes, p less than 0.001) than those without arrhythmias. Ventricular tachycardia was observed in 3 patients during the early phase of ischemia and in 2 during or after recovery. Early but not late ventricular tachycardias were preceded by prodromal ventricular ectopic activity. Late arrhythmias were more frequent and severe than early arrhythmias, with an increased incidence of R-on-T ectopic complexes. In patients with stable angina, potentially life-threatening arrhythmias are closely associated with severe repetitive episodes of ischemia, and different mechanisms produce early and late arrhythmias. Prevention or reduction of the severity of ischemic episodes occurring during daily life in patients with stable angina may be more effective than prophylactic antiarrhythmic therapy.     

Effectiveness of glibenclamide on myocardial ischemic ventricular arrhythmias in non-insulin-dependent diabetes mellitus.

Glibenclamide, a hypoglycemic sulfonylurea, is a blocker of the adenosine triphosphatase-modulated potassium ion channels. The opening of these channels in the myocardial cells, induced by acute myocardial hypoxia, can be responsible for ischemic ventricular arrhythmias. To evaluate the antiarrhythmic effects of this drug 19 non-insulin-dependent diabetic patients were selected. They had coronary artery disease and evidence on Holter monitoring of ventricular premature complexes or nonsustained ventricular tachycardia, or both, induced by transient myocardial ischemia. In all patients, 24-hour electrocardiographic monitoring was performed to evaluate the number and duration of myocardial ischemic events, the frequency of ventricular premature complexes and nonsustained ventricular tachycardia per minute of ischemia and the percentage of ventricular premature complexes versus total ischemic beats. Selected patients were classified in 2 groups: group A (9 patients) received metformin (placebo) and group B (10 patients) was treated with glibenclamide. On the fourteenth day patients underwent 24-hour control monitoring. Then a crossover between the 2 groups was made and a new Holter monitoring sequence was performed at the end of the second phase. Results indicate that glibenclamide significantly (p less than 0.001) reduced both the frequency of ventricular premature complexes and the episodes of nonsustained ventricular tachycardia during transient myocardial ischemia, but did not change the number and duration of acute myocardial ischemic attacks and did not reduce the spontaneous ventricular arrhythmias. Thus, glibenclamide appears to have an antiarrhythmic effect in preventing ventricular arrhythmias induced by transient myocardial ischemia.     

Evaluation of the informative value and safety of the transesophageal atrial electric stimulation test in patients with unstable stenocardia and myocardial infarction (data of 24-hour ECG monitoring)

The effect of the transesophageal pacing test (TEPT) on the occurrence of ventricular arrhythmias and ischemic episodes was examined on the basis of 24-hour ECG monitoring in patients with unstable angina (UA) and myocardial infarction (MI). It is demonstrated that TEPT is a relatively safe test for UA and MI patients (to be performed on day 10-14), which does not provoke severe arrhythmias during and after the testing, but for short paroxysms of ventricular tachycardia seen in 2-4% of the cases. Both painful and painless ST displacements were recorded during the test; ST elevation was only noted in MI patients. The time of ECG baseline recovery was longer in painful ischemic episodes, as compared to painless ones. The TEPT test is a valuable instrument for detecting latent atrioventricular conductivity disorders in UA and MI patients.     

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.     

Ventricular dysrhythmias in patients undergoing coronary artery bypass graft surgery: incidence, characteristics, and prognostic importance. Study of Perioperative Ischemia (SPI) Research Group.

To determine the incidence and characteristics of ventricular dysrhythmias (premature ventricular contractions greater than 30/min, ventricular tachycardia greater than or equal to 3 beats, and ventricular fibrillation) and whether a relationship exists between ventricular tachycardia and myocardial ischemia in patients undergoing coronary artery bypass graft surgery, we continuously monitored 50 patients for 10 perioperative days using two-lead electrocardiography. Electrocardiographic changes consistent with ischemia were defined as a reversible ST depression greater than or equal to 1.0 mm, or ST elevation greater than or equal to 2.0 mm from baseline, lasting at least 1 minute. Ventricular dysrhythmias developed in 10% of patients preoperatively and in 16% intraoperatively before bypass surgery. The highest incidence occurred postoperatively, with ventricular dysrhythmias developing in 66% of patients (22% to 44% of patients on any postoperative day 0 to 7). Premature ventricular contractions were greater than 30/hr in 6% of patients preoperatively, in 8% intraoperatively before bypass, and in 34% postoperatively (6% to 23% of patients on any postoperative day). Twenty-nine patients (58%) developed 76 verified episodes of greater than or equal to 3 beats of ventricular tachycardia. Ventricular tachycardia occurred in 6% of patients preoperatively (four episodes), in 8% of patients intraoperatively prior to bypass (four episodes), and 54% of patients postoperatively (5% to 21% on any postoperative day). No patient developed ventricular fibrillation. All postoperative ventricular tachycardia episodes (after tracheal extubation) were asymptomatic. Postoperatively, 48% of patients developed ischemia, compared with 12% preoperatively and 10% intraoperatively before bypass surgery. Only 5 of 68 (7%) postoperative ventricular tachycardia episodes occurred within 3 hours of an ischemia episode.(ABSTRACT TRUNCATED AT 250 WORDS)     

Incidence and kind of reperfusion arrhythmias in thrombolytic therapy of acute myocardial infarct

In 200 consecutive patients with acute myocardial infarction combined medical-mechanical recanalization was attempted. Coronary angiography revealed an occluded vessel in 150 patients. This vessel could be opened in 127 patients. There were 112 men and 15 women, aged 32 to 72 years (mean age 61.2 years); 60 patients had an anterior and 67 patients presented with an inferior myocardial infarction. 103 from 127 patients presented with arrhythmias during the ischemic phase and 112 from 127 patients during the reperfusion phase. The following arrhythmias had a significantly higher incidence in the reperfusion phase compared to the ischemic phase: sinus bradycardia (29 pts. - 22.8% - vs. 15 pts. - 11.8%; p less than 0.05), ventricular bigeminy (28 pts. - 29.9% - vs. 5 pts. - 3.9%; p less than 0.01), ventricular couplets (34 pts. - 26.8% - vs. 20 pts. - 15.7%; p less than 0.05) and accelerated idioventricular rhythm (32 pts. - 25.2% - vs. 5 pts. - 3.9%; p less than 0.01). Ventricular fibrillation occurred during the ischemic phase in 9 patients and during the reperfusion phase in 7 patients (n.s.). None of the patients presented with sustained ventricular tachycardia, neither in the ischemic, nor in the reperfusion phase. Conclusions: The following rhythm disturbances can be called reperfusion arrhythmias: sinus bradycardia, ventricular bigeminy, ventricular couplets and accelerated idioventricular rhythm. The observed reperfusion arrhythmias were short-living and did not need special therapeutic measures.     

Ischaemia related ventricular arrhythmias in patients with variant angina pectoris

Twenty-three patients with variant angina were studied by Holtermonitoring both to assess the incidence of serious ventriculararrhythmias (a risk factor of sudden death in variant angina),during ischaemic episodes and to examine the time-relation ofthe arrhythmias to ST changes. Serious ventricular arrhythmias were observed in 12/23 patients(52%). In the 23 patients, a total of 491 episodes of ST segmentelevation were recorded during 954 h of Holter monitoring; seriousventricular arrhythmias were found in only 46 ischaemic episodes(9.4%). Six out of 12 patients showed serious ventricular arrhythmiasat the onset of ischaemic episodes or during maximal ST elevation(phase 1), one patient during return or immediately after returnof ST to baseline (phase 2) and five patients during both phases.Thirty-three out of 46 ischaemic episodes (76%) showed seriousventricular arrhythmias during phase 1, eight (17%) during phase2, and five (11%) during both phases. Serious ventricular arrhythmias were neither related to previousmyocardial infarction nor to the presence of serious ventriculararrhythmias during inter-crisis periods, whereas a good relationshipwith severity of ischaemic episodes, as assessed by the magnitudeand duration of ST elevation, was found. A modest relationshipwith anterior ST elevation was also found. In conclusion: (1) serious ventricular arrhythmias occur ina high percentage of variant angina patients, but in only asmall proportion of ischaemic episodes; (2) serious ventriculararrhythmias are related to the severity of ischaemia and occurpredominantly at the onset of ischaemic episodes and/or duringmaximal ST elevation; in only a few cases do they occur duringresolution of ischaemic episodes.     

Incidence of ventricular arrhythmias during transient myocardial ischemia in patients with stable coronary artery disease

To determine the incidence of ventricular arrhythmias related to episodes of transient myocardial ischemia during ambulatory electrocardiographic (ECG) monitoring, 97 patients with stable angina pectoris, angiographically proved coronary artery disease and an abnormal exercise test were studied. A total of 573 episodes with ST segment depression were documented: in 118 episodes (21%) the patients were symptomatic and in 455 (79%) they remained asymptomatic. Ventricular arrhythmias (greater than 5 premature ventricular beats/min, bigeminy, couplets or salvos of premature ventricular beats) occurred during 27 (5%) ischemic episodes in a subset of 10 patients (10%) (group A). The other 87 patients (90%) (group B) showed exclusively ischemic episodes without ventricular arrhythmias. Comparison of patients in group A and group B showed no differences in hemodynamic, angiographic, exercise testing and ambulatory ECG monitoring data. Ischemic episodes with and without ventricular arrhythmias showed a similar duration and amplitude of ST segment depression and a comparable heart rate at the onset of ischemia. Both types of ischemic episodes, with and without arrhythmias, occurred predominantly during the morning hours between 6:00 AM and noon, and both types remained asymptomatic to within similar percentages. The data demonstrate that ventricular arrhythmias are related to transient myocardial ischemia in only a few patients with stable angina pectoris; these arrhythmias are related neither to the degree of ischemia during ambulatory ECG monitoring nor to the occurrence of anginal symptoms.     

Effects of restored coronary circulation on nature and character of arrhythmia during attacks of angina pectoris in patients with ischemic heart disease]

The nature and frequency of cardiac arrhythmias were studied in 23 patients with coronary heart disease during anginal episodes accompanied by ECG ST-segment depression and elevation. All the ischemic episodes were divided into 2 periods: (1) that from the onset of ST-segment displacement to its maximum; (2) that from the first period to the return of ST segment to the baseline position. The predictive poor ventricular arrhythmias were more frequently recorded in the second period of ST-segment displacement. The occurrence of arrhythmias was demonstrated to be related to the degree of ST-segment elevation (depression) and the duration of the first period of ischemic episode in the second period of ST-segment displacement.     

Programmed electric stimulation following acute myocardial infarct. Significance of stimulation timing

To assess the influence of time on the inducibility by programmed electrical stimulation of ventricular arrhythmias after acute myocardial infarction, we studied 18 patients on the 5th and 24th day after infarction with a stimulation protocol employing a maximum of 3 right ventricular extrastimuli during sinus rhythm and at 3 paced cycle lengths. All patients were without documented sustained ventricular arrhythmias (sustained ventricular tachycardia or ventricular fibrillation) prior to the investigation. Sustained ventricular arrhythmias were induced in 2 patients on day 5, but in 9 on day 24 after infarction. This difference in incidence was statistically significant (p less than 0.05), as was the change in the distribution ratio of induced sustained ventricular arrhythmias from day 5 to day 24 (p less than 0.05). The types of arrhythmia induced on day 24 were sustained ventricular tachycardia with a mean cycle length of 207 ms in 6 cases (5 monomorphic, 1 polymorphic), and ventricular fibrillation in 3 cases. These 9 patients did not differ from the remaining 9 patients in maximal CPK, infarct site, number of stenosed coronary arteries, global left ventricular ejection fraction, and in the results of 24-hour Holter monitoring, but they had a significantly shorter right ventricular effective refractory period (223 +/- 10 ms versus 259 +/- 28 ms; p less than 0.05). During the follow-up period of 24 +/- 5 months no patient died, had syncopal attacks, or developed spontaneous episodes of sustained ventricular arrhythmia. The timing of programmed electrical stimulation with a maximum of 3 right ventricular extrastimuli strongly influences the inducibility of sustained ventricular arrhythmias after acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Inducible multiform ventricular tachycardia in Wolff-Parkinson-White syndrome.

The induction of ventricular tachycardia by ventricular stimulation was investigated in 46 patients with isolated Wolff-Parkinson-White syndrome (10 concealed) and 36 control patients with normal electrocardiograms and conduction systems. None of those studied had spontaneous ventricular arrhythmias or myocardial or valve disease. Single and double ventricular extrastimuli were delivered at 3 cycle lengths (sinus, 600 ms, 400 ms). In the controls ventricular simulation induced one episode (3%) of non-sustained ventricular tachycardia. Ventricular stimulation in patients with Wolff-Parkinson-White syndrome induced two episodes of ventricular fibrillation and 15 episodes of non-sustained multiform ventricular tachycardia (37%). Ventricular arrhythmias were induced only in patients with overt Wolff-Parkinson-White syndrome. In 14 patients the conformation of the electrocardiogram at the start of ventricular tachycardia resembled that of major pre-excitation. The absence of inducible ventricular tachycardia in patients with concealed Wolff-Parkinson-White syndrome suggests that anterograde conduction via an atrioventricular accessory pathway is required to initiate the ventricular arrhythmias: the ventricular tachycardia may be associated with reentry of impulses via atrioventricular connection during the phase of ventricular vulnerability. The similarity between the start of ventricular tachycardia and pre-excitatory complexes may also indicate local reentry into the ventricular area occupied by the bypass tracts. Patients with Wolff-Parkinson-White syndrome and anterograde pre-excitation are more likely to have inducible multiform ventricular tachycardia than individuals without Wolff-Parkinson-White syndrome.     

Ventricular arrhythmias and local electrograms after chronic regional denervation of the ischemic area in the pig heart

Cardiac denervation has been proved to reduce the incidence of coronary occlusion arrhythmias in digs, but the effect of limiting the extent of sympathectomy to the ischemic area, particularly in hearts with sparse coronary collateral circulation, as in the human heart, needs further investigation. Ventricular arrhythmias and changes in epicardial direct current electrograms induced during acute left anterior descending coronary artery occlusion were recorded in 14 pigs subjected to regional denervation of the ischemic area 2 weeks before; these were compared with findings in 14 sham-operated control pigs. Regional denervation was induced by pericoronary application of phenol above the occlusion site and it was confirmed by the loss of myocardial catecholamine histofluorescence. During 35 min of ischemia, significant differences in occurrence of ventricular premature beats, ventricular tachycardia, ST segment elevation, TQ segment depression and epicardial activation delays were observed between the two groups of experiments, with lower values of each variable in the denervated hearts. Ventricular fibrillation occurred 32 times in 11 control pigs and only 15 times in eight denervated hearts. In contrast, programmed ventricular extrastimuli delivered during 35 to 50 min of ischemia induced 39 fibrillatory episodes in 13 denervated hearts and only 14 episodes in seven control pigs. Thus, denervation limited to the ischemic area in hearts with a human-like coronary artery pattern was associated with a decrease in the magnitude of early ischemic arrhythmias and electrocardiographic alterations, but the procedure was unable to prevent early induction of ventricular fibrillation.     

Inducible multiform ventricular tachycardia in Wolff-Parkinson-White syndrome

The induction of ventricular tachycardia by ventricular stimulation was investigated in 46 patients with isolated Wolff-Parkinson-White syndrome (10 concealed) and 36 control patients with normal electrocardiograms and conduction systems. None of those studied had spontaneous ventricular arrhythmias or myocardial or valve disease. Single and double ventricular extrastimuli were delivered at 3 cycle lengths (sinus, 600 ms, 400 ms). In the controls ventricular simulation induced one episode (3%) of non-sustained ventricular tachycardia. Ventricular stimulation in patients with Wolff-Parkinson-White syndrome induced two episodes of ventricular fibrillation and 15 episodes of non-sustained multiform ventricular tachycardia (37%). Ventricular arrhythmias were induced only in patients with overt Wolff-Parkinson-White syndrome. In 14 patients the conformation of the electrocardiogram at the start of ventricular tachycardia resembled that of major pre-excitation. The absence of inducible ventricular tachycardia in patients with concealed Wolff-Parkinson-White syndrome suggests that anterograde conduction via an atrioventricular accessory pathway is required to initiate the ventricular arrhythmias: the ventricular tachycardia may be associated with reentry of impulses via atrioventricular connection during the phase of ventricular vulnerability. The similarity between the start of ventricular tachycardia and pre-excitatory complexes may also indicate local reentry into the ventricular area occupied by the bypass tracts. Patients with Wolff-Parkinson-White syndrome and anterograde pre-excitation are more likely to have inducible multiform ventricular tachycardia than individuals without Wolff-Parkinson-White syndrome.     

Troponin-I elevation in a young man with arrhythmogenic right ventricular dysplasia/cardiomyopathy

Ventricular arrhythmias occur frequently in patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) as well as those with ischemic heart disease. We present the case of a 29-year-old man with ARVD/C and multiple episodes of symptomatic ventricular tachycardia terminated by implantable cardioverter defibrillator (ICD) discharges. Phasic elevation of troponin-I prompted repeated coronary angiograms, all of which were normal. The patient was successfully treated with radiofrequency ablation. This case illustrates that ARVD/C may result in elevated cardiac enzymes in the absence of coronary artery disease.     

Transient myocardial ischaemia after acute myocardial infarction does not induce ventricular arrhythmias.

OBJECTIVE--To see whether transient myocardial ischaemia on ambulatory monitoring after myocardial infarction is associated with ventricular arrhythmias. DESIGN--A prospective study. SETTING--The coronary care unit, general medical wards, and cardiorespiratory department of a major teaching hospital. PATIENTS--203 consecutive patients without specific exclusion criteria admitted with acute myocardial infarction. INTERVENTIONS--24 hour ambulatory electrocardiographic monitoring for ventricular arrhythmias and ST depression both early (mean 6.3 days after infarction, n = 201) and late (mean 38 days, n = 177). MAIN OUTCOME MEASURES--Episodes of myocardial ischaemia were identified during ambulatory monitoring by transient ST depression of > or = 1.0 mm lasting for > or = 30 s. Ventricular arrhythmias were single extrasystoles, couplets, or ventricular tachycardia. RESULTS--All ventricular arrhythmias were significantly more frequent in late than early monitoring. The arrhythmias included couplets (in 83/174 (48%) v 49/200 (25%) of patients, p = 0.0000028) and ventricular tachycardia (29/174 (17%) v 15/199 (8%), p = 0.0064). Patients with ST depression (29 early; 56 late), compared with those without ischaemia, did not experience a significant increase in single extrasystoles, couplets (31% v 23% early; 47% v 48% late), or ventricular tachycardia (3% v 8% early; 18% v 16% late). Even patients with frequent (> or = 3 episodes), and deep (> or = 1.5 mm) or prolonged (> or = 20 min) ST depression had no increase in arrhythmias. CONCLUSIONS--Ventricular arrhythmias after myocardial infarction are not associated with transient myocardial ischaemia during daily activities. This study does not support the belief that to abolish silent ischaemia would reduce the incidence of sudden death due to uncontrollable ventricular arrhythmias after myocardial infarction.     

Diurnal distribution of ST-segment elevation and related arrhythmias in patients with variant angina: a study by ambulatory ECG monitoring

Twenty-four-hour ambulatory ECG recording was performed in 26 patients with variant angina to evaluate the diurnal distribution of ST-segment elevation in relation to chest pain and the incidence of arrhythmias during the episodes. During a recording period of 52 days, 364 ST-segment elevations of 1 mm or greater were observed and 79% were asymptomatic. ST-segment elevation frequently occurred between 0:00 and 9:00 hours (72%) and most frequently between 5:00 and 6:00 hours (13%). Only a few episodes occurred between 10:00 and 18:00 hours. Premature atrial contractions, premature ventricular contractions (PVCs), ventricular tachycardia (VT) and complete atrioventricular block occurred during 12% of the episodes and were more common during painful episodes (32%) than during painless ones (6%). However, VT and severe forms of PVCs (couplets and bigeminy) appeared eight times during painless episodes and nine times during painful ones. Arrhythmias occurred more frequently when the elevated ST segment started to return or was returning to the control level (n = 38) than when the ST segment was rising (n = 8). The incidence of arrhythmias was lower when the daily frequency of ischemic episodes was high. This study shows that episodes of asymptomatic coronary artery spasm predominantly occur early in the morning as symptomatic episodes; complex dysrhythmias appear during the asymptomatic episodes; arrhythmias occur predominantly during a "reperfusion period;" and more arrhythmias accompany infrequent daily episodes of ischemia than frequent ones.     

Efficacy of slow-release nifedipine on myocardial ischemic episodes in variant angina pectoris

To evaluate the efficacy of slow-release nifedipine (a single dose of 20 mg given at 10 P.M. or 2 doses of 20 mg at 10 P.M. and 6 A.M.) on ischemic episodes in patients with variant angina, a single-blind crossover study with ambulatory electrocardiographic monitoring was performed in 15 patients (13 men and 2 women, mean age 63 years). In all, there were 646 ischemic episodes detected with ambulatory electrocardiographic monitoring during the study period, and 618 episodes of them occurred during placebo periods with a circadian variation. Sixty-nine percent of the episodes in placebo periods were asymptomatic. The number of anginal attacks, nitroglycerin tablets taken, ST-segment elevation and the total ischemic duration significantly decreased during nifedipine therapy compared with results after the placebo therapy period, respectively (p less than 0.01 or 0.05). Twenty-eight ischemic episodes occurred during nifedipine therapy when the plasma level of nifedipine was low. Thus, asymptomatic ischemic episodes more frequently occur than symptomatic episodes and the administration of slow-release nifedipine is highly effective in suppressing not only symptomatic but also asymptomatic myocardial ischemia in patients with variant angina. The timing of the administration of slow-release nifedipine is an important factor in suppressing ischemic episodes.