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Six patients with Wolff-Parkinson-White (WPW) syndrome were given long-term treatment with amiodarone. Symptomatic relief was obtained in all. Tolerance to the drug was good. Reversible corneal changes appeared after some weeks' treatment in five patients. No thyroid side-effects were noticed. Prior to treatment, dual atrioventricular (AV) conduction was demonstrated on His bundle electrograms in all six patients. Recordings were made at varied heart rates, using atrial and ventricular pacing. Reciprocating tachycardia was readily provoked by properly timed extra stimuli in all patients. When amiodarone treatment had become clinically effective, a second comparative study was made in four patients after 26--85 days' treatment. Amiodarone reduced heart rate and second degree AV block appeared at a lower atrial pacing rate. It increased the refractory periods of right atrium, AV node, and the accessory pathway in proportion to the duration of treatment. Induction of tachycardia was effectively prevented by the drug. It appears that amiodarone in chronic treatment has a predictable and unique depressant action on cardiac conduction, supporting the opinion that this compound, despite side-effects, has an important role to play in the treatment of refractory arrhythmias in patients with the WPW syndrome.

The usefulness and feasibility of recording atrial wall motion by M-mode echocardiography guided by two-dimensional examination was evaluated in three groups of consecutive patients: 7 with undefined tachyarrhythmias, 25 in sinus rhythm, and 20 with atrial flutter or fibrillation. Atrial systole was recorded in the left and right atrium in 58 and 98% of the patients, respectively (p less than 0.05). Six of the patients with undefined tachyarrhythmias exhibited electrocardiographic atrioventricular dissociation revealed by preceding echocardiography in all. The precise timing of left and right atrial systole could be recorded in patients in sinus rhythm; right atrial contraction preceded left atrial systole by 42 +/- 31 msec (mean +/- SD). Among patients with atrial flutter or fibrillation, one case of dissimilar atrial rhythms was revealed by echocardiography. Thus, recording of atrial wall motion is feasible in the majority of patients and provides information which is otherwise available only by esophagus ECG or by invasive means.

Background: QT dispersion is considered to reflect inhomogeneity of myocardial repolarization. Method: The circadian variation of QT interval dispersion was examined in 95 healthy subjects using 24‐hour Holter monitoring. Three different methods of lead selection were applied: all 12 leads (QTdisp 12), only precordial leads (QTdisp 6), and the pair of leads selected at 3 a.m. in which the longest and shortest QT intervals were found in each individual subject (QTdisp 2). Results: A preliminary methodological study including measurements from every minute in 10 subjects revealed no significant circadian variation using mean values of QTdisp 12, QTdisp 6, or QTdisp 2 obtained every hour, every 2, or every 4 hours, except in QTdisp 6, which demonstrated a significant circadian variation (P < 0.01) in 1‐hour measurements. Analysis of all 95 subjects using measurements obtained every 4 hours revealed a significant circadian variation in QTdisp 12 and QTdisp 6 (P < 0.0001), whereas no circadian variation was seen in QTdisp 2. A subdivision into 10‐year age groups revealed that subjects at age >50 years had a significant circadian variation in QTdisp 12 and QTdisp 6, but not in QTdisp 2. Only in males a significant circadian variation was seen in QTdisp 12 (P < 0.0001), whereas QTdisp 6 demonstrated a circadian variation both in females (P < 0.001) and in males (P < 0.0001). Conclusions: Selection of leads is of crucial importance for repetitive measurements of QT dispersion. Circadian variation was detected in subjects over 50 years of age, when all 12 or only the 6 precordial leads were taken into account.

Objective - To assess the risk of atrial fibrillation (AF) recurrence requiring hospitalisation or its transition to long-lasting AF in patients with earlier or present AF from the clinical characteristics, the duration of AF-disease, and the signal-averaged P wave duration (SAPWD). Design -We studied 111 consecutive patients (40 women; median age 65 years, range 30-85 years) with earlier or present AF. The SAPWD was measured on inclusion; the follow-up median follow-up time was 184 days (range 171-437). Endpoints were hospitalisation due to recurrent AF or transition to AF lasting longer than two days. Results -During follow-up 5 patients died, 33 patients were hospitalised with AF, and 9 patients developed long-lasting AF. Multiple logistic regression analysis showed three risk factors of interest: history of hypertension, OR=3.67 (95% CI 1.61 to 8.37), duration of AF disease longer than two years, OR=3.22 (95% CI 1.31 to 7.86), and non-significantly prolonged SAPWD above 140 ms, OR=1.87 (95% CI 0.60 to 5.82). The probability of relapse in patients without risk factors was 9%, with one risk factor 16-27%, with two risk factors 37-54%, and with three risk factors 74% (p=0.0005). Conclusions -Hypertension and long history of AF disease were associated with an increased risk of AF-relapse.

Myocardial ischaemia has been described during endoscopic retrograde cholangio-pancreatography (ERCP), but the pathogenesis remains unclear. The aim of the present study was to evaluate whether coronary artery disease was present in patients with ST-segment changes during ERCP.Forty patients were monitored with a Holter tape recorder during ERCP. Patients with ST-segment deviation during ERCP subsequently underwent a standard exercise ECG test.Twelve patients developed signs of myocardial ischaemia during ERCP (30%) and 9 had concomitant tachycardia. None had a cardiac history or cardiorespiratory symptoms. Ten of the 12 patients did an exercise test and one patient developed silent ischaemia. Subsequent coronary angiography showed no evidence of coronary artery disease.No signs of existing coronary artery disease were found in patients developing ST deviation during ERCP when evaluated with a 12-lead exercise ECG test. Further studies should evaluate other mechanisms responsible for myocardial ischaemia during ERCP.

Arterial hypertension is accompanied by increased morbidity and mortality and constitutes a substantial part of medical care. Antihypertensive intervention reduces the cardiovascular morbidity and mortality. The aims of the study were to evaluate the relationship between cardiovascular risk factors and the blood pressure (BP), and to evaluate the percentage of patients who had achieved a BP level as recommended by the sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI). BP was evaluated in relation to age, body mass index, duration of hypertension, cholesterol and triglyceride level, smoking status, information of regular exercise, a family history of ischemic heart disease (IHD) and drug treatment, in 220 men treated for arterial hypertension. In the univariate analyses we found a higher systolic blood pressure (SBP) with older age, higher SBP in smoking patients and lower SBP in patients with regular exercise. In a multivariate model age (p = 0.0004), smoking status (p = 0.01) and regular exercise (p= 0.06) were independently associated with SBP. There was a lower diastolic blood pressure (DBP) with older age, and age was independently associated with DBP. Office SBP was above 140 mmHg in 83% and above 160 mmHg in 44% of patients. During ambulatory blood pressure monitoring (AMBP), SBP was above 135 mmHg in 40% and above 155 mmHg in 15% of patients. In addition to male sex and hypertension there was a high percentage of other cardiovascular risk factors--43% was smoking, 21% had a family history of IHD, 77% had a se-cholesterol above 5.5 mmol/l and 48% had a se-triglyceride above 1.6 mmol/l. In a consecutive group of asymptomatic male treated hypertensive patients SBP is independently associated with age and smoking status, and DBP with age. A high percentage of the patients do not have a well controlled BP, and a high percentage have additional risk factors such as smoking, hypercholesterolaemia, hypertriglyceridaemia and a family history of IHD. This means that there is room for much improvement in the control of hypertension.

Background Although ST-segment deviation has been evaluated and used during many years both on continuous electrocardiographic Holter monitoring and during exercise stress testing, considerable controversy still remains concerning the prevalence and diagnostic significance of fortuitously discovered ST-segment deviation in asymptomatic healthy persons. Methods and Results The occurrence of ST-segment deviation was studied in a population of 63 clinically healthy male subjects 51 to 75 years of age, with the use of 24-hour Holter monitoring and exercise stress testing. The subjects were recruited from the Copenhagen City Heart Study and were without cardiovascular risk factors, chronic diseases, or medication and without cardiovascular events during 5 to 12 years before and 3 to 5 years after admission. The specificity, that is, the probability of displaying a negative test result in healthy subjects without disease, was 1.0 when using as criterion for significant ST-segment deviation a horizontal or descending ST-segment depression of >0.20 mV or ST-segment elevation ≥0.15 mV during Holter monitoring, and acceptable, for example, 0.95, when using as criterion a horizontal or descending ST-segment depression of ≥0.15 mV during Holter monitoring or at the exercise test, respectively. Furthermore, the specificity was 0.95 when a horizontal or downsloping ST-segment depression of 0.1 mV was displayed in both the Holter and exercise electrocardiographic recording system. Conclusions Thus in asymptomatic persons, the usual criterion for significant ST-segment depression of 0.1 mV can be applied when occurring in both electrocardiographic recording systems. However, if one test alone is used, the criterion of significant ST-segment depression should be 0.15 mV. Absence of ST-segment deviation during Holter monitoring and exercise stress testing, indicated with a specificity of 1.0 or 0.95 according to choice of criterion, implies that the person is in a healthy state. (Am Heart J 1999;137:1070-4.)

Background: Ventricular ectopy early after an acute myocardial infarction (AMI) has previously been demonstrated to predict mortality. Less information is available about the prognostic implications of ventricular ectopy occurring late after an AMI, and no information is available about the prognostic implication of the development of ventricular ectopy during the first year after an AMI. Hypothesis: The purpose of the present prospectively conducted trial, a part of the Danish Verapamil Infarction Trial II (DAVIT II), was to evaluate the prognostic implication of (1) ventricular premature complexes (VPCs) recorded by 24-h Holter monitoring 1 week, 1 month, and 16 months after an AMI; and (2) development of > 10 VPCs/h or of any complex ventricular ectopy, that is, pairs, more than two types of VPCs, ventricular tachycardia, or > 10 VPCs/h during follow-up after an AMI. Methods: Patients were monitored 1 week (n = 250), 1 month (n = 210), and 16 months (n = 201) after AMI. Results: Multivariate analyses based on history, clinical findings, and ventricular ectopy showed the following results: After 1 week, > 10 VPCs/h (p = 0.0006) and heart failure (p 10 VPCs/h (p = 0.003) and resting heart rate (p 10 VPCs/h from 1 week to 1 month (p = 0.003) and 16 months (p = 0.03), and from 1 to 16 months (p = 0.007) after AMI, as well as by the development of any complex ventricular ectopy from 1 week to 1 month (p = 0.02) and 16 months (p = 0.01), and from 1 to 16 months (p = 0.04) after AMI. Conclusion: The present study demonstrated that 1 week and 1 month after an AMI the quantity of VPCs, that is, >10 VPCs/h, predicted mortality, whereas 16 months after an AMI the quality of VPCs, that is, ventricular tachycardia, predicted mortality.

Objective: Criteria for detection of late potentials have not yet been standardized, but the criteria recommended by ESC/AHA/ACC are widely used. In this investigation, the prevalence of late potentials is studied in an age stratified healthy population with likelihood of coronary artery disease < 5%. Relation between signal-averaged variables and clinical variables was studied. Methods: Signal-averaged ECGs were recorded using Butterworth filters at 40 and 250 Hz. The following three time-domain parameters were evaluated: QRS duration (duration of the amplified, filtered QRS complex); LPD (duration of the late potentials, i.e., duration from the point of time when the magnitude of the main complex becomes lower than 40 μV); and RMS40 (root mean square of the activity within the last 40 ms of the amplified, filtered QRS complex). Results: QRS duration was significantly longer in men than in women, and was correlated to the mass of the left ventricle (LVM). The combination LPD and RMS40 gave the highest prevalence of late potentials. The prevalence of late potentials was 25%. Conclusion: Standard criteria should be used with great caution, and normal limits should be established in each laboratory to a preselected noise level. QRSD should be included within the definition of reference limits and should be gender matched. Even though there is correlation between LVM and the QRSD, the upper normal limit of QRSD based on LVM matching is unchanged.

One hundred and ninety consecutive patients discharged with congestive heart failure were examined with clinical evaluation, blood chemistry, 24 h Holter monitoring, exercise test and radionuclide angiography. Median left ventricular ejection fraction was 0.30, 46% were in New York Heart Association class II and 44% in III. Total mortality after 1 year was 21%, after 2 years 32%. Of 60 deaths, 33% were sudden and 49% due to pump failure. Multivariate analyses identified totally different risk factors for sudden death: ventricular tachycardia, s-sodiumor = 137 mmol/l, s-magnesiumor = 0.80 mmol/l, s-creatinine121 mumol/l, and maximal change in heart rate during exerciseor = 35 min-1, and for death from progressive pump failure: New York Heart Association class III + IV, delta heart rate over 24 hor = 50 min-1, low ejection fraction, high resting p-noradrenaline, s-urea7.6 mmol/l, s-potassium3.5 mmol/l, and maximal exercise durationor = 4 min. In conclusion, this study demonstrated different risk factors for sudden death and for death from progressive pump failure.

The present study was a prospectively planned subset of the postinfarction, double blind, randomized, multicenter, placebo controlled trial of verapamil, DAVIT II. Patients had 24 hours of Holter monitoring before randomization, i.e., second week after infarction (placebo, n=122; verapamil, n=128), after 1 month (placebo, n=108; verapamil, n=94) and after 16 months (placebo, n=75; verapamil, n = 63) of treatment. The purpose was to evaluate the effect of verapamil on the prevalence and changes over time of arrhythmias and heart rate. In patients monitored twice, a significant increase of average ventricular premature complexes (VPC) per hour from before to 1 month (p=0.0007) and 16 months (p=0.02) after was demonstrated in the placebo group, and from before to 1 months (p=0.01) after in the verapamil group. Average VPC/hr did not change from 1 to 16 months of treatment. A significant increment of >10 VPC/hr was found after 1 (p=0.03) and 16 months (p=0.05) compared to prerandomization in the placebo, but not in the verapamil group. A significant increase of supraventricular arrhythmias after 1 month compared with prerandomization was found in the placebo group (p=0.003) but not in the verapamil group. The prevalence of VPC and supraventricular tachycardia was significantly lower in the verapamil compared with the placebo group after 1 month of treatment. At 16 months no significant difference was found between the two groups. The 24 hour mean heart rate was significantly lower, 3 beats/min, in the verapamil compared with placebo after 1 and 16 months of treatment. Thus a significant increase of ventricular and supraventricular arrhythmias during the first postinfarction month, without change the following year, was seen in the placebo group. Verapamil significantly lowered heart rate, prevented supraventricular tachycardia, and reduced VPC early after an AMI. This rather limited effect of verapamil on postinfarction arrhythmias cannot explain the beneficial effect of verapamil on mortality and major events in patients without heart failure.

The purpose of this study was to examine the 24-hour antiischemic efficacy of once-a-day anipamil compared to placebo in the treatment of patients with stable angina. The study was designed as a double-blind, placebo-controlled crossover study with an initial 3 week single-blind placebo period. The patients received anipamil 80 mg once daily, anipamil 160 mg once daily, and placebo in a randomized order. At the end of each treatment period the patients underwent 24-hour ambulatory ECG recording. Nineteen patients were included, all with typical stable angina pectoris for at least 2 months, exercise test withor = 0.10 mV horizontal or down-sloping ST-segment depression and limited by angina pectoris, and at least 10 attacks of angina pectoris in the initial single-blind placebo period. During the placebo period, a total duration of transient myocardial ischemiaor = 0.10 mV during the 24-hour ambulatory ECG monitoring period was 2263 minutes, 75% of which were asymptomatic. Anipamil 80 mg and 160 mg significantly reduced the duration of episodes to 712 minutes (p0.001), with 87% asymptomatic, and to 913 minutes (p0.001), with 92% asymptomatic, respectively. In conclusion, anipamil given once a day is an effective 24-hour antiischemic drug in the treatment of transient myocardial ischemia.

To determine the best sites for ambulatory monitoring leads to detect myocardial ischaemia.50 consecutive patients recovering from myocardial infarction. Six patients were excluded because of unsatisfactory recordings or baseline electrocardiographic abnormalities that influenced the diagnostic accuracy of ST segment depression. In 38 patients important ST segment changes were seen before the study recordings.Reproducibility of detecting the electrocardiographic ST segment changes with 12 bipolar leads alone or in combination.The highest reproducibility rate was found in infarcts involving both the anterior and inferior left ventricular walls (80%). The reproducibility decreased as the extent of ventricular wall involvement decreased and was lowest in inferior infarcts (31%) (p0.001). For large infarcts the detection rate was almost equal for the 12 study leads, whereas disparity between leads increased as the infarct size decreased. The highest overall reproducibility was found in a transthoracic lead (V2, V9R) (76%). This lead was significantly better (p = 0.03) than lead CM5 (50%). When the transthoracic lead was combined with an inferior lead, the reproducibility increased (82%) and was significantly better than the combination of CM5 and an inferior lead (58%) (p = 0.02).Extensive ischaemic electrocardiographic changes are better detected than smaller ones and anterior infarcts better than inferior. A transthoracic lead (V2, V9R) was significantly better than CM5 both alone and when CM5 and the transthoracic lead were combined with an inferior lead.

The pathophysiological mechanisms responsible for increased cardiovascular mortality in diabetic autonomic neuropathy are unknown. To investigate the effect of autonomic neuropathy on myocardial function, we performed dynamic contrast-enhanced magnetic resonance perfusion imaging during baseline conditions and after Dipyridamole-induced vasodilatation in nine type 1 diabetic patients with autonomic neuropathy (AN+), defined by cardiovascular tests, as well as in 10 type 1 diabetic patients without autonomic neuropathy (AN−) and 10 healthy control subjects. Baseline myocardial perfusion index (Ki) was similar in the three groups (AN+ 88.6 ± 8.7 ml · 100 g−1 · min−1, AN− 82.6 ± 7.2, control subjects 93.7 ± 9.0) (means ± SE). Ki during Dipyridamole vasodilatation was significantly lower in the patients with autonomic neuropathy (P < 0.001) than in the other groups (AN+ 131.1 ± 13.0 ml · 100 g−1 · min−1, AN− 177.3 ± 8.6, control subjects 197.2 ± 8.9). Mean blood pressure was unchanged during Dipyridamole infusion in AN− and control subjects, whereas a significant blood pressure decrease was found in AN+ (15.6 ± 2.6 mmHg, P < 0.025). There was a significant correlation between blood pressure response to Dipyridamole and myocardial perfusion reserve index. We conclude that type 1 diabetic patients with autonomic neuropathy have a decreased myocardial perfusion reserve capacity when challenged with a vasodilatator, a finding that may in part be the pathophysiological substrate for the increase in mortality in these patients. The underlying mechanism may be defective myocardial sympathetic vasodilatation, a lack of ability to maintain blood pressure during vasodilatation, or both.

OBJECTIVE Post-menopausal hormone replacement (HRT) might protect against cardiovascular disease, possibly by arterial vasodilation and reduced blood pressure. Progestogens are needed to avoid endometrial disease but vascular effects are controversial. The objective was to assess temporal changes in blood pressure (BP) by two measurement techniques during a cyclic hormone replacement regimen. DESIGN AND METHODS Sixteen healthy and normotensive post-menopausal women (age 55 +/- 3 years) were studied in a placebo-controlled, randomized crossover study, and were randomized to 17beta-oestradiol plus cyclic norethisterone acetate (NETA) or placebo in two 12-week periods separated by a 3-month washout Clinic blood pressure was measured sitting by the same observer with a mercury manometer at four visits in each period. Twenty-four hour ambulatory blood pressure was measured at baseline and in the ninth weeks of treatment in both periods. RESULTS Clinic systolic and diastolic BP were reduced after 10 days of oestradiol (-5.1 and -3.2 mmHg respectively, P < or = 0.05). After 9 weeks of cyclic HRT, prior to progestogen addition, clinic BP returned to baseline. During addition of NETA, diastolic blood pressure was again reduced (-3.6 mmHg, P= 0.037). Mean 24 h ambulatory systolic and diastolic blood pressures were significantly lower than clinic measurements (-15.7 and -5.9 mmHg, P < 0.001) but were unaffected by HRT. CONCLUSIONS Clinic blood pressure is reduced during a cyclic HRT regimen but the reduction varies with the HRT regimen, which might explain the diversity in previous BP findings during HRT. Norethisterone acetate might possess additive blood pressure-lowering effects in postmenopausal women.

Myocardial ischaemia (defined as ST-segment deviation on electrocardiogram (ECG)) may occur during colonoscopy, but the pathogenic mechanisms are unknown. We have evaluated the occurrence of arterial hypoxaemia, tachycardia, and myocardial ischaemia during routine colonoscopy.Eighteen patients underwent colonoscopy under conscious sedation and without supplementary oxygen. Arterial oxygen saturation was measured by continuous pulse oximetry, and ECG was monitored continuously with a Holter tape recorder during the procedure.Arterial oxygen desaturation and tachycardia were common during colonoscopy and occurred in 45% and 35% of patients, respectively. Two patients developed signs of myocardial ischaemia during the colonoscopy: one case of ST depression (1.7 mV) and one case of ST elevation (4.3 mV). In both patients the ST deviation disappeared when the colonoscope was retracted. Myocardial ischaemia occurred in both patients simultaneously with tachycardia, and in one of these arterial hypoxaemia was also present.Myocardial ischaemia occurs during routine colonoscopy, but with a lower incidence than previously reported during upper endoscopy. Myocardial ischaemia during colonoscopy may be associated with tachycardia and/or hypoxaemia. Further studies should clarify the relative role of tachycardia, hypoxaemia, and viscerocardiac reflexes in the pathogenesis of myocardial ischaemia during colonoscopy.

Objective: To evaluate the effect of metoprolol, a s adrenergic blocking drug, on the occurrence of myocardial ischaemia during endoscopic cholangiopancreatography. Design: Double blind, randomised, controlled trial. Setting: University Hospital. Subjects: 38 (two groups of 19) patients scheduled for endoscopic cholangiopancreatography. Interventions: Metoprolol 100 mg or placebo as premedication two hours before endoscopy. Main outcome measures: Heart rate, arterial oxygen saturation by continuous pulse oximetry, ST segment changes during endoscopic cholangiopancreatography (an ST segment deviation >1 mV was defined as myocardial ischaemia), electrocardiogram monitored continuously with a Holter tape recorder. Results: All patients had increased heart rate during endoscopy compared with rate before endoscopy, but heart rate during endoscopy was significantly lower in the metoprolol group compared with the placebo group (P = 0.0002). Twenty one patients (16 placebo, 5 metoprolol; P = 0.0008) developed tachycardia (heart rate > 100/min) during the procedure, and 11 patients (10 placebo, 1 metoprolol; P = 0.003) developed myocardial ischaemia. One patient in the placebo group had an acute inferolateral myocardial infarction. In the 10 other patients with signs of myocardial ischaemia during endoscopy the ST deviation disappeared when the endoscope was retracted. In all patients myocardial ischaemia was related to increases in heart rate, and 10 of the 11 patients had tachycardia coherent with myocardial ischaemia. Conclusions: Metoprolol prevented myocardial ischaemia during endoscopic cholangiopancreatography, probably through lowering the heart rate. Thus, tachycardia seems to be a key pathogenic factor in the development of myocardial ischaemia during endoscopy. Key messages Metoprolol prevented myocardial ischaemia during endoscopy Myocardial ischaemia was related to tachycardia more than to concomitant hypoxaemia Tachycardia seems to be a key pathogenic factor in the development of myocardial ischaemia during endoscopy

Verapamil is effective as antianginal medication but contraindicated in patients with congestive heart failure. Angiotensin-converting enzyme (ACE) inhibitors improve survival in patients with congestive heart failure but have limited effect on patients with angina pectoris. No studies have been published on the combined treatment with verapamil and ACE inhibitors in patients with stable angina pectoris and left ventricular dysfunction. We performed an open study in 14 patients with angina pectoris and ejection fraction < 40%. The patients received verapamil 180 mg and trandolapril 2 mg twice daily for 3 months. We found a significant increase in ejection fraction from 28 +/- 6 to 35 +/- 11 (p < 0.03), wall motion index from 1.0 +/- 0.3 to 1.2 +/- 0.3 (p < 0.03), exercise duration from 6.9 +/- 2.5 to 7.7 +/- 2.9 minutes (p < 0.01), and ratio of exercise to rest rate-pressure product from 2.2 +/- 0.4 to 2.5 +/- 0.6 (p < 0.02). Use of nitroglycerin and number of angina pectoris attacks were both significantly reduced after 3 months of treatment. These findings support the hypothesis that the combination of verapamil and trandolapril is useful in patients with attenuated left ventricular function and angina pectoris.

Once-daily administration of 10 mg amlodipine has been compared with two daily doses of 40 mg sustained-release isosorbiddinitrate (ISDN) in 59 patients with stable angina, using a randomized, double-blind, double-placebo, crossover study design. Nine patients dropped out due to side effects (3 during amlodipine and 6 during ISDN therapy), and one patient was excluded for technical reasons. A maximal symptom limited supine bicycle tolerance test and a 48 h ambulatory ECG monitoring were performed at the end of each 5 week period of therapy. During exercise, exercise time, time to onset of angina, and time to onset of ischaemia, i.e., 1 mm ST segment depression were measured. During ambulatory monitoring, number of anginal episodes and duration per hour of ST deviation were assessed. Amlodipine significantly prolonged time to angina (320 ± 155 vs 304 ± 126 sec; p l 0.05) and time to ischaemia (292 ± 153 vs 232 ± 126 sec; p l 0.001). when compared with ISDN, while exercise time was similar for both treatments. Furthermore, amlodipine reduced anginal episodes (1.2 ± 1.6 vs 2.4 ± 3.0 attacks/48 h; p l 0.001), whereas, no difference was found between amlodipine and ISDN in duration of ST deviation during ambulatory monitoring. In conclusions, addressing the long-term treatment of patients with stable angina pectoris, once-daily dosing of amlodipine appears to be more effective than ISDN, as determined by its anti-anginal and anti-ischaemic effects during exercise tolerance testing and ambulatory ECG monitoring.

The purpose of this prospectively conducted study was to determine the prevalence of transient myocardial ischemia, evaluated from 24 h continuous ECG monitoring and exercise test, 6 months after inclusion in the Anglo Scandinavian Study of Early Thrombolysis (the ASSET trial, a randomised, placebo controlled study of alteplase for survival in patients with suspected acute myocardial infarction (AMI)), and to relate these findings to development of cardiac events. Of the 58 consecutively studied patients ischemic responses were found in 13 (45%) of 29 patients initially treated with placebo, and in 21 (72%) of 29 alteplase treated patients (P = 0.03). After another 6 months, i.e. 12 months after the acute event, two patients were dead, two had non-fatal reinfarctions and three had coronary artery by-pass surgery in the group with ischemic response; no events were recorded in patients without ischemia (P0.05). Alteplase treated patients more often had late myocardial ischemia, and cardiac events were found in patients with ischemia. Since the ASSET trial has demonstrated significantly higher short- and long-term survival rate in the alteplase treated group, it was indicated (1) that alteplase treated patients were better positioned for sustaining subsequent ischemia and thus cardiac events due to preservation of viable myocardial tissue, and (2) that late ischemia in the setting of initial alteplase treatment may convey other information than ischemia occurring in placebo treated patients.

Aims We aimed to determine the prevalence and prognostic significance of daily-life silent myocardial ischaemia (SMI) in healthy middle-aged and elderly subjects with no previous heart disease. Methods and results Six hundred and seventy-eight healthy men and women between 55 and 75 years of age and with no history of cardiovascular disease or stroke were included. Baseline examinations included physical examination, fasting laboratory testing, and 48 h ambulatory electrocardiogram monitoring. An episode of ischaemia was defined by a down-sloped or horizontal ST depression of at least 1 mm at a duration of at least 1 min. Seventy-seven subjects (11.4%) had SMI. All participants were followed for up to 5 years. In 77 subjects with SMI, 16 (20.7%) had an event (death or myocardial infarction). In 601 subjects without SMI, 50 (8.3%) had an event. The hazard ratios for SMI in relation to cardiac and combined events after correction for conventional risk factors were 3.1 [(1.24-7.97), P=0.016] and 1.97 [(1.06-3.69), P=0.033], respectively. Conclusion SMI as detected by Holter monitoring was detected in 11.4% of these subjects and was associated with more than three-fold increase in the cardiac event rate after correction for risk factors, implying that this test could be used to identify high-risk individuals among these subjects.

Four young healthy men (17–25 years old) experienced life-threatening arrhythmias during physical exertion. All were successfully resuscitated. One died later. Electrophysiological studies disclosed a lack of normal conduction delay and abnormal His-Purkinje properties indicating congenital malformation of the atrioventricular (AV) node in one patient and the rare and potentially dangerous combination of an accessory AV pathway and intraatrial conduction delay with liability to dissimilar rhythms and fibrillation in the atria in another. The conduction system functioned normally in the other two. One of the latter two patients had cerebral damage during prolonged resuscitation and experienced repeated epileptic spells until he died unexpectedly. Autopsy revealed scarring of unknown origin in the interventricular septum. The other had stress-induced ventricular ectopy, which gradually diminished and disappeared in a few weeks. The etiology of the latter two is suggested to be ischemia. It is warranted to point out the possible danger of maximal physical strain even in young people.

Holter monitoring of 51 patients on the 4th to 6th day after acute myocardial infarction (AMI) disclosed complex ventricular ectopic beats in 17 (35%), nine of whom (53%) died in the following 26 months. Of the remaining patients with no or only non-complex ectopic beats, five (15%) died. The difference was significant using Gehan's test of censored data (p less than 0.01). Multivariate analysis demonstrated a significant increase of death risk associated with complex ventricular ectopic beats as well as with heart failure (relative risk 3.6 and 5.9, respectively). Age, gender, number of ventricular ectopic beats, cardiac enlargement on X-ray and angina pectoris had no significant effect on mortality. The prevalence of ventricular ectopy was 84% (n = 43) irrespective of age and sex and equal to the finding in the late hospital phase reported by other investigators, and in healthy subjects. Complex ventricular ectopic beats appeared in 35% (n = 17). The prevalence increased significantly with age and was significantly higher in post-infarction patients (38%) than in healthy individuals (8%). The present results indicate that a subgroup containing most of the high-risk patients may be identified early after AMI by detecting complex premature ventricular beats in continuous electrocardiographic recordings.