Mm Of ST-segment Depression Research Articles

Significance of ST segment depression during paroxysmal supraventricular tachycardia

During paroxysmal supraventricular tachycardia, patients frequently experience chest pain and marked ST segment depression suggesting acute myocardial ischemia. The purpose of this study was to assess whether ST depression during supraventricular tachycardia is caused by myocardial ischemia as reflected by net myocardial lactate production. Twenty-five patients (14 men, 11 women) who had a history of paroxysmal supraventricular tachycardia and a mean age (± SD) of 38 ± 14 years underwent electrophysiologic testing. Twenty-four of these patients had no evidence of coronary disease, whereas one patient had undergone previous coronary bypass surgery. Nineteen patients had orthodromic and six patients had atrioventricular node reentrant tachycardias.A 12 lead electrocardiogram and simultaneous femoral artery and coronary sinus blood samples for lactate determinations were obtained at baseline and at 5 and 10 min of supraventricular tachycardia. Mean baseline heart rate of 83 ± 12 beats/min increased to 180 ± 25 beats/min during supraventricular tachycardia. All patients had 1 to 8 mm of ST segment depression in 1 to 9 of the 12 leads. Chest pain occurred in 64% of patients during supraventricular tachycardia. Baseline myocardial lactate extraction was 28 ± 13% with no significant change at 5 or 10 min of tachycardia. In contrast, in a comparison group of seven patients with known coronary artery disease, atrial pacing at 168 ± 26 beats/min in five patients resulted in ≥ 1 mm ST depression in 2 to 7 of the 12 leads and a change in lactate extraction from a baseline of 29 ± 13% to −27 ± 20% (p < 0.05) indicating net myocardial lactate production.In conclusion, in patients with coronary artery disease, supraventricular tachycardia may be associated with chest pain or marked ST segment depression, or both, in the absence of acute myocardial ischemia.

Atenolol and celiprolol for stable angina pectoris

Once-daily atenolol and celiprolol were compared in a placebo-controlled crossover study of 16 patients with stable angina pectoris. Atenolol and celiprolol equally and significantly reduced frequency of angina and electrocardiographic evidence of cardiac ischemia. Celiprolol, however, produced less suppression of the double product at 1 mm of ST-segment depression than atenolol, suggesting that actions other than reduction of heart rate may contribute to its antianginal efficacy.

Sustained antianginal efficacy of transdermal nitroglycerin patches using an overnight 10-hour nitrate-free interval

The antianginal efficacy of the transdermal nitroglycerin patch may be limited by the rapid development of tolerance during uninterrupted exposure. To address this problem, we investigated the role of intermittent therapy was investigated, using a daily nitroglycerin patch-free Interval in 13 patients with chronic stable angina. Concomitant antianginal medications were permitted. Entry criteria required reproducible exercise times to both onset of angina and 1 mm of ST-segment depression. In each patient the highest tolerated nitroglycerin patch dose was determined by a dose-titration phase, which was then used in a double-blind crossover trial comprising 2 randomized treatment arms: 1 week of active nitroglycerin patch and 1 week of matching placebo. All patches were worn only from 8 a.m. to 10 p.m. daily. Exercise testing was repeated before patch application and then 4 and 8 hours after application on both the first and the last day of each treatment arm. Eleven patients completed the randomized crossover phase. Exercise time to the onset of angina and to the onset of 1 mm of ST-segment depression was significantly prolonged during the first day of therapy at both 4 and 8 hours after active nitroglycerin patch application compared with placebo (p < 0.01). During sustained use, the benefit at 4 and 8 hours after nitroglycerin patch application was still evident (p < 0.001 and p < 0.05, respectively). No evidence of a overnight rebound or withdrawal phenomenon was observed by history or by ambulatory Hotter monitoring calibrated for ST-segment analysis. The results suggest that tolerance to the antianginal effects of the nitroglycerin patch can be avoided by providing a dosing regimen using interrupted exposure to nitroglycerin.

Lack of diurnal variation in maximal symptom-limited exercise test response in chronic stable angina

Exercise testing is widely used to evaluate the effects of anti-ischemic drugs. Many studies have reported good reproducibility when it is performed in the morning, but little information is available regarding the diurnal variation of exercise test response in patients with chronic stable angina. With the advent of new long-acting anti-ischemic drugs, it has become necessary to perform the exercise testing at various times of the day to determine the duration of action of a given drug. To examine the diurnal variation, exercise tests were performed on 41 patients, aged 53 to 75 years, with established chronic stable angina on 2 occasions 5 days apart at 10 a.m. and 4 p.m. on each day. On day 1, the mean ± standard error of the mean exercise time was 5.0 ± 0.4 minutes at 10 a.m. and 5.1 ± 0.4 minutes at 4 p.m., and on day 5, it was 5.6 ± 0.4 minutes at 10 a.m. and 5.5 ± 0.4 minutes at 4 p.m. These values did not differ in statistical significance. Similarly, the time to the development of 1 mm of ST-segment depression did not show any statistically significant change during either test period on either day nor did maximal ST-segment depression. Heart rate at rest was 79 ± 3 beats/min at 10 a.m., 81 ± 3 beats/min at 4 p.m. on day 1 and 78 ± 2 beats/min at 10 a.m. and 80 ± 3 beats/min at 4 p.m. on day 5 (difference not significant). Similarly, no significant changes were observed in maximal heart rate or rate-pressure product at peak exercise. Thus, it appears that if exercise tests are performed under standardized conditions at the same times of day, no significant diurnal variations in cardiovascular function are likely in patients with chronic stable angina. The test, therefore, is reliable for the evaluation of anti-ischemic drugs.

Comparison of amplitude-modulated (direct) and frequency-modulated ambulatory techniques for recording ischemic electrocardiographic changes

Continuous ambulatory electrocardiographic monitoring of ST-segment configuration has become a useful technique for evaluation of myocardial ischemia. Concern that direct or amplitude-modulated (AM) recording and playback systems have inherent limitations that cause inaccurate ST-segment recordings has led to preference for frequency-modulated (FM) devices. To determine the accuracy of AM and FM ambulatory electrocardiographic systems, the signal was compared from the same set of 2 bipolar leads simultaneously recorded by standard electrocardiography and AM and FM recorders in 14 patients during treadmill exercise. Also, simultaneous AM and FM recorders were compared in 9 ambulatory patients in 16 monitoring sessions. The AM recording system accurately reproduced ST segments recorded during treadmill exercise (range 4.0 mm of ST-segment depression to 2.0 mm of ST elevation) when measured at the J point (r = 0.91, p <0.0001), and 0.08 second after the J point (r = 0.95, p <0.0001). FM recording was equally accurate (r = 0.89 and 0.95, respectively, p <0.0001). Similarly, during ambulatory recording, the AM technique accurately recorded maximal ST depression in each episode as recorded by the FM device (28 episodes, range 0 to 3 mm of ST depression, r = 0.85, p <0.0001). Both AM and FM ambulatory electrocardiographic systems can accurately reproduce ST-segment deviation associated with ischemia and can be used to monitor transient ST-segment changes in patients with coronary artery disease.

Comparison of carvedilol and atenolol for angina pectoris

The antianginal efficacy of carvedilol, a novel β-blocking agent with vasodilating action, and atenolol were compared in 12 patients with stable effort angina and a positive stress test response. All patients received single doses of placebo, carvedilol, 25 and 50 mg, and atenolol, 50 mg. Heart rate at rest was reduced by 11 and 12 beats/min with both drugs, but only carvedilol, 50 mg, reduced blood pressure at rest. Both carvedilol, 50 mg, and atenolol, 50 mg, increased mean exercise time (24% and 34%, respectively, compared with placebo), time to angina (35% and 51%, respectively), and time to 1 mm of ST-segment depression (54% and 102%, respectively, p < 0.05 carvedilol vs atenolol). Carvedilol, 25 mg, produced smaller, directionally similar changes in exercise performance, which did not reach statistical significance except for time to 1 mm of ST depression. Both drugs in the 50-mg dose reduced ST-segment depression similarly at maximal and submaximal work levels and lowered heart rate and rate-pressure product at maximal and submaximal work. Carvedilol, 50 mg alone, significantly lowered maximal systolic pressure and rate-pressure product at 1 mm of ST-segment depression. Despite some evidence of vasodilator activity for carvedilol, there was no significant difference in antianginal efficacy with a conventional β-blocking drug.

Effects of nicardipine on exercise- and pacing-induced myocardial ischemia in angina pectoris

To define the effects of nicardipine, a new dihydropyridine calcium antagonist drug, on exercise- and pacing-induced myocardial ischemia, 15 men with coronary artery disease were studied during cardiac catheterization. Nicardipine was administered intravenously as a 2-mg bolus followed by an infusion titrated to maintain a 10- to 20-mm Hg decrease in systolic arterial pressure. At rest, nicardipine decreased systemic and coronary vascular resistances, left ventricular end-diastolic pressure and increased coronary blood flow, heart rate and myocardial oxygen consumption. During bicycle exercise-induced myocardial ischemia, nicardipine significantly prolonged exercise duration and time to 1 mm of ST-segment depression. These changes were associated with no alteration in the product of systolic pressure and heart rate, decreased left ventricular end-diastolic pressure, systemic and coronary vascular resistances and increased coronary blood flow, as well as myocardial oxygen consumption. During atrial pacing, the heart rate threshold for myocardial ischemia was not changed by nicardipine administration, despite improvement in the ratio of coronary blood flow to myocardial oxygen consumption and hemodynamic changes otherwise similar to those during exercise. Nicardipine favorably influenced myocardial metabolic state, as indexed by lactate extraction during pacing-induced ischemia. Nicardipine is a potent coronary and systemic vasodilating drug that improves exercise tolerance and myocardial metabolic response to pacing stress, the mechanism for which appears to be partially mediated through increased coronary blood flow.

Effects of titrated beta blockade (metoprolol) on silent myocardial ischemia in ambulatory patients with coronary artery disease

This study investigates effects of β-adrenergic blockade on total silent ischemic time assessed by ambulatory electrocardiographs monitoring and its relation to heart rate and time of day in ambulatory men with coronary artery disease. Metoprolol, when titrated to optimal dose in a controlled trial in 9 patients, reduced both total silent ischemic time (from 156 ± 65 to 20 ± 15 minutes, p = 0.04) and frequency of silent ischemic episodes (from 8 ± 2 to 2 ± 2 episodes, p = 0.03) compared with placebo. Mean daily heart rate was reduced, from 82 ± 2 beats/min during placebo to 58 ± 1 beats/min, as was heart rate at onset of 1 mm of ST-segment depression (106 ± 2 to 74 ± 4 beats/min, both p < 0.001). Heart rate increased 10 ± 1 beats/min during silent ischemia with placebo therapy, but increased only 4 ± 1 beats/min during metoprolol treatment (p < 0.03). During placebo administration the largest proportion of silent ischemic time occurred between 0600 and 1200 hours. Metoprolol attenuated this circadian variation in silent ischemia while reducing (p < 0.05) total silent ischemic time in all periods. Thus, β-adrenergic blockade reduces the frequency of silent myocardial ischemic episodes and total silent ischemic time, while mean daily heart rate and heart rate at onset of ischemia and maximal ischemia decrease. Metoprolol treatment also attenuates circadian variation of silent ischemia. These data may be interpreted to suggest that β-adrenergic activation operates in the pathogenesis of silent myocardial ischemia and its circadian variation.

A single-blind, placebo-controlled study of effects of atenolol on transient ischemia in “mixed” angina

The efficacy of atenolol in preventing episodes of transient ischemia during daily life was evaluated in 10 patients with “mixed” angina who underwent a 4-week, single-blind, double-crossover placebocontrolled trial. On day 6 and 7 of each treatment phase, continuous ambulatory electrocardiographic monitoring was performed for 48 hours. On day 7 an exercise test was also performed. Two-hundred and sixty-four ischemic episodes (79% “silent”) were recorded during placebo treatment; 98 were recorded during atenolol treatment (63% decrease, p < 0.01). In agreement with previous observations, most ischemic episodes observed during placebo (156 or 59%) were not preceded by an increase in heart rate. Surprisingly, the beneficial effects of atenolol were more pronounced for these episodes than for those preceded by an increase in heart rate and apparently caused by an increase in myocardial demand (decreases of 72% and 48%, respectively). Painful and painless episodes were decreased by a similar extent. In all patients, the heart rate recorded at the beginning of ST-segment depression was widely variable and significantly lower with atenolol (64 ± 14 beats/min) than with placebo (81 ± 13 beats/min, p < 0.05). During both placebo and atenolol treatment, the highest incidence of ischemic events was observed between 6 A.M. and 9 P.M., in coincidence with the highest levels of the heart rate resting. During placebo, exercise testing was consistently positive, with angina and ST-segment depression in all 20 tests; this became negative in 7 patients during atenolol treatment. The rate-pressure product at 1 mm of ST-segment depression was significantly lower with atenolol (12,638 ± 2,997 beats/min × mm Hg) than during control (17,807 ± 3,777 beats/min × mm Hg). It is concluded that atenolol is highly effective in patients with mixed angina, especially for suppressing episodes that are not preceded by an increase in heart rate. In such patients high levels of myocardial oxygen demand represent a predisposing rather than a causative factor for the development of myocardial ischemia, which, in most instances, is precipitated by a transient impairment of regional myocardial perfusion.

Exercise thallium testing in ventricular preexcitation

Ventricular preexcitation, as seen in Wolff-Parkinson-White syndrome, results in a high frequency of positive exercise electrocardiographic responses. Why this occurs is unknown but is not believed to reflect myocardial ischemia. Exercise thallium testing is often used for noninvasive assessment of coronary artery disease in patients with conditions known to result in false-positive electrocardiographic responses. To assess the effects of ventricular preexcitation on exercise thallium testing, 8 men (aged 42 ± 4 years) with this finding were studied. No subject had signs or symptoms of coronary artery disease. Subjects exercised on a bicycle ergometer to a double product of 26,000 ± 2,000 (± standard error of mean). All but one of the subjects had at least 1 mm of ST-segment depression. Tests were terminated because of fatigue or dyspnea and no patient had chest pain. Thallium test results were abnormal in 5 patients, 2 of whom had stress defects as well as abnormally delayed thallium washout. One of these subjects had normal coronary arteries on angiography with a negative ergonovine challenge, and both had normal exercise radionuclide ventriculographic studies. Delayed thallium washout was noted in 3 of the subjects with ventricular preexcitation and normal stress images. This study suggests that exercise thallium testing is frequently abnormal in subjects with ventricular preexcitation. Ventricular preexcitation may cause dys-synergy of ventricular activation, which could alter myocardial thallium handling, much as occurs with left bundle branch block. Exercise radionuclide ventriculography may be a better test for noninvasive assessment of coronary artery disease in patients with ventricular preexcitation.

Characteristics of silent myocardial ischemia during out-of-hospital activities in asymptomatic angiographically documented coronary artery disease

Ambulatory electrocardiographic monitoring is useful in documenting characteristics of both painful and silent myocardial ischemia occurring during out-of-hospital activities in patients with angina and coronary artery disease (CAD), but few data are available concerning silent myocardial ischemia during ambulatory electrocardiographic monitoring in asymptomatic patients with CAD. Accordingly, 480 hours of ambulatory electrocardiographic monitoring were recorded in 10 asymptomatic patients with CAD not receiving cardiac drugs (48 hours/patient). All 10 patients had silent myocardial ischemia on treadmill exercise testing, with initial ST-segment depression at 2 to 6 minutes in 7 patients and more than 6 minutes In 3 patients. During ambulatory electrocardiographic monitoring, 64 episodes of silent myocardial ischemia (1 mm of ST-segment depression for at least 1 minute) were recorded, ranging from 1 to 17 episodes/patient/48 hours. Of the 64 silent myocardial ischemic episodes, 30 (47%) occurred between 6 AM and noon. Duration of silent myocardial ischemia was 798 minutes (range 1 to 80). ST-segment depression ranged from 1 to 4.5 mm. Heart rate at onset of the episodes on ambulatory electrocardiographic monitoring ranged from 65 to 150 beats/min (mean 98), which was significantly less than that during treadmill exercise testing in the same patients (mean 120). At cardiac catheterization, 7 patients had 2- or 3-vessel CAD and 3 had 1-vessel CAD. Thus, silent myocardial ischemia is common during daily life in asymptomatic CAD patients with positive treadmill exercise tests.

Significance of silent myocardial ischemia during exercise testing in patients with coronary artery disease

To evaluate the significance of ischemic ST-segment depression without associated chest pain during exercise testing, data were analyzed from 2,982 patients from the Coronary Artery Surgery Study (CASS) registry who underwent coronary arteriography and exercise testing and were followed up for 7 years. Patients with proved coronary artery disease (CAD) (at least 70% diameter narrowing) were grouped according to whether they had at least 1 mm of ST-segment depression or anginal chest pain during exercise testing. Four hundred twenty-four had ischemic ST depression without angina (group 1); 232 had angina but no ischemic ST depression (group 2); 456 had both ischemic ST depression and angina (group 3); and 471 had neither ischemic ST depression nor angina (group 4). Sixty-three percent of patients in group 1 and 55% in group 2 had multivessel CAD (difference not significant). The 7-year survival rates were similar for patients in groups 1 (76%), 2 (77%), and 3 (78%), but were significantly better for patients in group 4 (88%, p <0.001). Among group 1 patients, survival was related to severity of CAD (p <0.001). The 7-year survival rate in group 1 was significantly worse than that in a separate group of 282 patients with ischemic ST depression without angina during exercise testing who had no CAD (95% survival, p <0.001). Thus, in patients with silent myocardial ischemia during exercise testing, the extent of CAD and the 7-year survival rate are similar to those of patients with angina during exercise testing. Prognosis is determined primarily by the severity of CAD. In patients without CAD, the survival rate is excellent.

Effect of Nicorandil on Exercise Performance in Patients with Effort Angina

The effects of a single oral dose (20 mg) of a new vasodilator, nicorandil, on exercise performance were assessed in 29 patients with stable effort angina using a symptom-limited treadmill exercise test. A single-blind, placebo-controlled, randomized, crossover design was employed. Compared with placebo, 20 mg of nicorandil significantly increased maximal exercise duration and time to 1 mm of ST-segment depression at 1, 3, and 6 h after administration. Systolic blood pressure was reduced both at rest and during exercise. Heart rate increase during exercise did not differ significantly compared with control, though resting heart rate was increased. The maximal pressure-rate product at peak exercise was increased in association with increased exercise time in about half of the patients, while it was unchanged or decreased in the others. It was suggested that nicorandil may act by either reducing myocardial oxygen demand and/or increasing myocardial oxygen supply.

Effect of Nicorandil on Exercise Performance in Patients with Effort Angina

The effects of a single oral dose (20 mg) of a new vasodilator, nicorandil, on exercise performance were assessed in 29 patients with stable effort angina using a symptom-limited treadmill exercise test. A single-blind, placebo-controlled, randomized, crossover design was employed. Compared with placebo, 20 mg of nicorandil significantly increased maximal exercise duration and time to 1 mm of ST-segment depression at 1, 3, and 6 h after administration. Systolic blood pressure was reduced both at rest and during exercise. Heart rate increase during exercise did not differ significantly compared with control, though resting heart rate was increased. The maximal pressure-rate product at peak exercise was increased in association with increased exercise time in about half of the patients, while it was unchanged or decreased in the others. It was suggested that nicorandil may act by either reducing myocardial oxygen demand and/or increasing myocardial oxygen supply.

Usefulness of noninvasive doppler measurement of ascending aortic blood velocity and acceleration in detecting impairment of the left ventricular functional response to exercise three weeks after acute myocardial infarction

Left ventricular (LV) function was assessed by Doppler ultrasound measurement of ascending aortic blood velocity and maximal acceleration in 165 patients 3 to 4 weeks after acute myocardial infarction (AMI); all were undergoing routine 12-lead electrocardiogram exercise stress testing. Patients were grouped according to electrocardiographic stress test response; a positive response was defined as at least 1 mm of ST-segment depression in any lead. The Doppler velocity signal yielded 3 variables of interest: peak velocity, maximal acceleration (an index of inotropic state) and the systolic velocity integral (an index of stroke volume). All 3 Doppler ejection variables were significantly lower at peak exercise in patients with a positive electrocardiographic stress test response than in those with negative response, with maximal acceleration showing the most significance (p less than or equal to 0.001). Coronary angiography was performed in 63 of the 67 patients with positive responses, and patients were separated into 2 groups according to extent of coronary artery disease (CAD): 1- and 2-vessel or 3-vessel CAD. Peak velocity and maximal acceleration were significantly lower in patients with 3-vessel CAD than in those with 1- and 2-vessel CAD (p less than or equal to 0.01 and p less than or equal to 0.01). Discriminant analysis showed maximal acceleration and peak velocity values at peak exercise to be 65% predictive of 3-vessel CAD, onset time to ST-segment depression was 74% predictive and the combination of Doppler and electrocardiographic variables increased 3-vessel CAD predictive value to 80%.(ABSTRACT TRUNCATED AT 250 WORDS)

The role of exercise testing in identifying patients with improved survival after coronary artery bypass surgery

To determine whether exercise testing can identify patients whose survival might be prolonged by coronary artery bypass surgery, the results of bypass surgery were compared with those of medical therapy alone in 5,303 nonrandomized patients from the Coronary Artery Surgery Study registry who underwent exercise testing. Patients in the two treatment groups differed substantially with regard to important baseline variables. Analysis of 32 variables by Cox's regression model for survival revealed an independent beneficial effect of bypass surgery on survival (p less than 0.00001). Patients were then stratified into subsets according to the results of exercise testing. Surgical benefit was greatest in the 789 patients who exhibited at least 1 mm of ST segment depression and who could exercise only into stage 1 or less. Among the 398 patients with three vessel coronary disease showing these characteristics, 7 year survival was 58% for the medical group and 81% for the surgical group (p less than 0.001). There was no difference in survival between the surgical and medical groups among the 1,545 patients without ischemic ST segment depression who were able to exercise into stage 3 or greater. Thus, in patients who demonstrate ischemia on exercise testing and whose exercise capacity is limited, coronary bypass surgery appears to improve survival in comparison with medical therapy alone.

Comparison of nifedipine alone with propranolol alone for stable angina pectoris including hemodynamics at rest and during exercise

The effects of nifedipine (60 to 90 mg/day) and propranolol (240 mg/day) on symptoms, angina threshold and cardiac function were compared in a placebo-controlled, double-blind, crossover study. Five-week treatment periods with nifedipine and propranolol were compared with 2 weeks of placebo treatment in 21 men with chronic stable angina pectoris, 13 of whom had symptoms both at rest and on exertion. Compared with placebo, New York Heart Association functional class improved in patients equally with nifedipine (p = 0.001) and propranolol (p = 0.006). Frequency of chest pain decreased with nifedipine (p = 0.001) and propranolol (p = 0.01), and nitroglycerin consumption similarly decreased with both treatments. Nifedipine significantly delayed the onset of chest pain (p = 0.01) and 1 mm of ST-segment depression (p = 0.002) during bicycle exercise; smaller increases with propranolol were not statistically significant. A preferential clinical response to nifedipine (9 patients) or propranolol (6 patients) was unrelated to the presence or absence of pain at rest or to any baseline hemodynamic finding. Nifedipine and propranolol were equally effective in relieving exertional ischemia as shown by improvements in ejection fraction at identical workloads, from 0.48 ± 0.11 to 0.58 ± 0.12 (p < 0.001) and 0.56 ± 0.14 (p < 0.001), respectively. Exercise wall motion, assessed by a semiquantitative wall motion score, also improved with both drugs. Propranolol treatment decreased exercise cardiac output by 14% (p = 0.01) through its effect on heart rate. In contrast, nifedipine treatment had no effect on cardiac output. Thus, nifedipine is as effective as propranolol when administered as single drug therapy in stable angina and has the potential advantage of preserving cardiac output during exercise.

Does placebo improve indexes of effort-induced myocardial ischemia? An objective study in 150 patients with chronic stable angina pectoris

The effects of placebo were studied in 150 patients (135 men, 15 women) aged 42 to 75 years with stable exertional angina pectoris, using multistage graded exercise testing. Treadmill exercise, using on-line computer analysis of the electrocardiogram, was performed after a basal period, during which time the patients had no treatment for 2 weeks, and after 2 weeks of placebo therapy. Mean exercise time during no treatment was 6.0 ± 0.2 minutes and during placebo was 6.1 ± 0.2 minutes (difference not significant). Similarly, time to development of 1 mm of ST-segment depression of 4.0 ± 0.2 minutes without treatment was 4.1 ± 0.2 minutes after 2 weeks of placebo therapy (difference not significant). Placebo failed to show any effect on rest or maximal heart rate or on maximal ST-segment depression. It also failed to increase exercise tolerance or to improve other objective indexes of effort-induced myocardial ischemia in both single-and double-blind protocols in patients with stable exertional angina pectoris. Therefore, placebo control of antianginal drug trials that use exercise testing for evaluation of effect is unnecessary and can be omitted.

Clinical Evaluation of Bisoprolol in Patients with Stable Angina Pectoris: A Preliminary Report

Efficacy and safety of the new beta-adrenoceptor antagonist, bisoprolol, in treatment of stable angina pectoris were studied in 36 patients using two types of single-blind design. After 2 weeks of therapy with bisoprolol in doses of 5 mg to 10 mg a day, exercise duration and time to 1 mm of ST-segment depression were significantly prolonged in 7 out of 10 patients who had a positive treadmill exercise test before bisoprolol. Bisoprolol significantly reduced heart rate (HR), systolic blood pressure (SBP), and rate-pressure product (RPP) at peak exercise, which would account for the beneficial effect of bisoprolol on exercise tolerance. Bisoprolol also produced improvement in symptoms for 26 patients with stable effort angina, as indicated by decreased frequency of anginal attacks and nitroglycerin consumption with a once-a-day regimen. Ten patients had no attacks after 5 mg of bisoprolol, and three more did not develop angina after increasing the dose to 10 mg a day. These results suggest that bisoprolol will be a promising, efficacious, and safe drug for the treatment of stable angina pectoris.

Effects of coenzyme Q 10 on exercise tolerance in chronic stable angina pectoris

The effects of coenzyme Q 10(CoQ 10) on exercise performance were studied in 12 patients, average age 56 years, with stable angina pectoris. The study involved a double-blind, placebo-controlled, randomized, crossover protocol, using multistage treadmill exercise tests. CoQ 10(150 mg/day in 3 daily doses) was administered orally for 4 weeks, tended to reduce anginal frequency from 5.3 ± 4.9 to 2.5 ± 3.3 attacks for 2 weeks and nitroglycerin consumption from 2.6 ± 2.8 to 1.3 ± 1.7 tablets for 2 weeks compared with patients receiving the placebo, but the reduction was not statistically significant. Exercise time increased from 345 ± 102 seconds with placebo to 406 ± 114 seconds during CoQ 10 treatment (p < 0.05). The time until 1 mm of ST-segment depression occurred increased from 196 ± 76 seconds with placebo to 284 ± 104 seconds during CoQ 10 treatment (p < 0.01). During the exercise test, ST-segment depression, heart rate and pressure-rate product at the same and at the maximal workload showed no significant difference between patients after placebo and CoQ 10 administration. The average CoQ 10 plasma concentration increased from 0.95 ± 0.48 μg/ml to 2.20 ± 0.98 μg/ml after CoQ 10 treatment. This increase was significantly related to the increase in exercise duration (r = 0.68, p < 0.001). Only 1 patient had a loss of appetite, but continued therapy. This study suggests that CoQ 10 is a safe and promising treatment for angina pectoris.