Effects of nicardipine in silent myocardial ischemia

201Tl myocardial scintigraphy was performed in 29 patients with coronary heart diseases and silent myocardial ischemic episodes revealed during a long-term monitoring of ST segment. The painless ST segment depression episodes and long high-amplitude painless ST segment elevations were found to be indicative of a significant severity of pathological processes in the myocardium. A 12-day nicardipine monotherapy produced antianginal and hypotensive effects and contributed to decrease in the frequency, duration, and amplitude of silent ST-segment depressions and in the duration of silent ST-segment elevations.     

ST-segment depressions correlate in patients with hypertensive heart disease with spontaneous changes in blood pressure]

In 15 patients with essential hypertension, anginal pain, and angiographically excluded coronary artery disease 24-h monitoring of the ST-segment and blood pressure was performed. 26 episodes with ST-segment depressions 0400.1 mV were recorded in 11/15 patients. In 10/26 episodes with ST-segment depressions blood pressure was elevated above 150/95 mm Hg or by more than 20% as compared to three successive measurements before the ST-segment depressions. Heart rate was increased by more than 20% in 20/26 ST-segment depressions. During 9 periods with ST-segment depressions angina pectoris was reported; in addition 27 anginal attacks without ST-segment depressions were observed. A significant, positive correlation between the diastolic (p less than 0.005) and systolic (p less than 0.02) blood pressure and the extent of the ST-segment depression was observed. These correlations imply a patho-physiological meaning of ST-segment depressions in hypertensive patients.     

Primary vasospastic angina pectoris: relations between manifestations of ischemia and presence of ventricular arrhythmia

24-hour ECG monitoring was performed in 12 patients with primary vasospastic angina (PVA). Angiography revealed a predominant lesion to a single coronary vessel (83%). There were 64 episodes of ST-segment changes (46 elevations and 18 depressions) during the monitoring that lasted 388 hours and 54 minutes. Ventricular arrhythmias were concomitant in 34% of the episodes. Ventricular arrhythmia significantly more frequently occurred when an ischemic episode lasted more than 5 minutes. No significant relation was established between the presence of ventricular arrhythmia and other indicators of ischemic manifestation.     

Intravenous diltiazem versus nitroglycerin for silent and symptomatic myocardial ischemia in unstable angina pectoris

For 18 patients consecutively admitted to the coronary care unit for unstable angina, 48-hour electrocardiographic Holter monitoring was performed after they were randomly assigned in a single-blind fashion to 1 of 2 treatment groups. The first group was treated with acetylsalicylic acid (ASA) and intravenous nitroglycerin, the second with ASA and intravenous diltiazem. All of the patients treated with nitroglycerin still had ischemic episodes after 48 hours (33% were symptomatic), in contrast with 11% of the diltiazem group (11% asymptomatic). Maximal ST-segment depressions of symptomatic and asymptomatic episodes were significantly different; and no significant increases in heart rate were observed either during the 15 seconds before ischemia began or during the ischemic episode. During the 48 hours, the diltiazem group had significantly fewer ischemic episodes (17) than did the nitroglycerin group (145). We concluded that "on-line" ST-segment observation is of prime importance for monitoring unstable angina; that the majority of the ischemic episodes associated with unstable angina are silent; and that intravenous diltiazem could be an effective pretreatment for patients who must undergo mechanical or surgical therapy.     

Clinical characteristics and prognosis of patients with postinfarction angina caused by coronary artery spasm

Clinical features and the course of 15 patients with postinfarction angina caused by coronary artery spasm are described. Episodes of postinfarction angina in the patients recurred at rest in the early recovery phase and were accompanied by transient ST-segment elevation. The area where ST-segment elevations were demonstrated on a 12-lead ECG always included the leads with newly developed abnormal Q waves. Pain resolved spontaneously or after sublingual nitroglycerin in several minutes. Holter ECGs during a 24-h period demonstrated frequent episodes of ST-segment elevation that were not always associated with chest pain. Treatment with calcium antagonist and/or nitrates effectively suppressed angina, and only one patient developed reinfarction. The patient's subjective symptoms were abolished by diltiazem and isosorbide dinitrate. A Holter ECG of the patient revealed silent ST-segment elevations before and after the reinfarction and an increase of the drugs completely suppressed the recurrence of silent ischemic ECG changes. Coronary arteriograms were obtained from 8 patients, which demonstrated more than 75% segmental stenosis on one coronary artery in 5 patients and no significant obstruction in the remaining 3. All patients performed a treadmill exercise stress test before discharge and most demonstrated excellent tolerance. All patients experienced no form of chest pain for an average of 25 months follow-up under medication. We conclude that among patients with postinfarction angina, those cases caused by coronary artery spasm have a relatively good prognosis.     

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.     

Dynamic changes of the QRS complex in unstable angina pectoris.

Despite intensive medical treatment to control chest pain, about one-third of patients with unstable angina have an unfavourable outcome within a period of 1 to 2 months. Holter monitoring can identify patients with silent myocardial ischaemia that are at a high risk of sustaining a major cardiovascular event. The present paper describes the use of dynamic, continuous, computerized on-line vectorcardiography for real-time monitoring of QRS-complex and ST-segment changes in patients with unstable coronary disease. In many patients a pattern of frequent repetitive episodes of QRS change was observed, with or without concomitant ST change. Whereas no patient had episodes of ST-vector change without also having episodes of significant QRS change, 15 patients had several episodes of QRS changes without any episode of significant ST change. The number of episodes of significant increase of the QRS vector difference correlated weakly but significantly with the number of episodes of significant ST-vector magnitude change (r = 0.34, p less than 0.05). The present study suggests that myocardial ischaemia will influence the QRS complex as well as the ST segment. The mechanism behind the QRS changes observed is not clear but episodes of QRS change without ST change or chest pain, may reflect sudden depressions of left ventricular function, as has been reported by others to occur in patients with coronary artery disease. Dynamic vectorcardiography offers the opportunity to monitor all parts of the QRST complex in real time.     

Painless myocardial ischemia in patients with stable stenocardia

24-hour Holter monitoring was performed in 58 patients with stable angina pectoris. Out of them, 70.7% were recorded to have painless ischemic ST-segment depression episodes which made up some half (45.7%) of the total number of myocardial ischemic episodes. The episodes of silent myocardial ischemia were characterized by various length, depending on the conditions of their occurrence. They were far short-term with physical activity and long-term at rest. An increase in the number of diseased coronary vessels in the patients undergoing coronary angiography was followed by a rise in the amount of episodes and ST-segment displacement amplitude. In patients who had an bicycle ergometric loading of 100 Wt or greater, the episodes of silent myocardial ischemia were observed twice more frequently than in patients who had a threshold loading of 25 to 50 Wt. Some proportion of the patients exhibited variations in the Holter monitoring and paired bicycle ergometric tests when finoptin and obsidan were evaluated for their antianginal effect. There was a significant decrease in obsidan's effect following 2-month continuous therapy. Despite the persistent growth of exercise tolerance as evidenced by bicycle ergometry, finoptin proved to be inefficient in 46.2% of the patients.     

Characteristics of transient ischaemic episodes in patients with silent and symptomatic exercise-induced myocardial ischaemia

To evaluate transient ischaemic episodes during daily life inpatients with coronary artery disease and exercise-induced myocardialischaemia, 38 patients underwent ambulatory ST-segment monitoringover 48 h. Sixteen patients had painless ischaemia during exerciseand occasional angina, and 12 patients had symptomatic ischaemiaand frequent angina during daily life. Ten patients with provencoronary artery disease but normal exercise electrocardiogramsserved as controls. The extent of coronary artery lesions andthe prevalence of myocardial infarction were similar in allgroups. ST-segment monitoring revealed 817 min and 98 episodesof ST depression in 13/16 patients of the asymptomatic groupand 111 min and 21 episodes in 5/12 patients of the symptomaticgroup (P<0.03). Subjective scores for physical activity duringHolter monitoring were significantly higher in the first groupthan in the second. The majority of ischaemic episodes in bothgroups was asymptomatic. No ischaemic ST changes occurred incontrol patients. Results indicate a higher frequency of transientischaemic episodes related to a higher level of physical activityin patients with silent ischaemia than in patients with symptomaticexercise-induced ischaemia.     

Transient myocardial ischemia in hypertensive patients

We wanted to determine whether there are episodes of myocardial ischemia in hypertensive patients with a normal coronary angiogram. ST-segment analysis on 24-h-Holter ECG was performed in 35 patients (18 males/17 females; mean age 54.6 +/- 10.4 years) with essential arterial hypertension (systolic/diastolic blood pressure 189.7 +/- 29/99.5 +/- 15 mm Hg). Left ventricular muscle mass (LVMM), enddiastolic volume (EDV), and the relation of mass to volume (M/V) were measured by ventriculography. Stenosis of coronary vessels was excluded by angiography in all patients. In 16 of 35 patients we observed 6.63 +/- 6.73 episodes of transient myocardial ischemia (ST-segment depressions greater than or equal to 1 mm, duration of the episode greater than or equal to 1 min). The duration of the episodes was 29.3 +/- 58.1 min, the maximal ST-segment depression 1.6 +/- 0.6 mm. In 95% of the episodes the patients did not experience any angina pectoris ("silent ischemia"). The degree of left ventricular muscle mass did not differ in hypertensive patients with and without transient myocardial ischemia (185.2 +/- 48.3 vs 227.1 +/- 71.5 g/m2). Systolic wall stress i.e. afterload was significantly higher in hypertensive patients with ST-segment depressions than in those without. In conclusion, these results demonstrate that transient myocardial ischemia often occurs in hypertensive patients. It seems that left ventricular hypertrophy by itself (myocardial factor) does not play a major role. Transient myocardial ischemia occurs mainly in hypertensive patients with eccentric myocardial hypertrophy i.e. low mass-volume ratio and high systolic wall stress. Accordingly, the occurrence of transient myocardial ischemia in hypertensive patients seems to be dependent on the myocardial energy demand.     

Surgery in patients with coronary artery disease—silent ischaemia during transurethral resection of tumors of prostate or bladder

Background: Asymptomatic episodes of myocardial ischemia in clinically stable patients seem to occur frequently and may hint at a worse prognosis. Hypothesis: This study was undertaken to determine whether surgical patients with coronary artery disease (CAD) have a higher risk of cardiac ischemia during the perioperative period compared with the late postoperative period and compared with patients without CAD. Methods: In all, 14 patients with and 14 patients without CAD were examined by Holter monitoring during the perioperative and three days later during the postoperative periods for the presence of ST-segment depression as a marker of silent myocardial ischemia. Results: While patients without CAD did not show ST-segment depression, patients with CAD were found to have had 143 episodes of ST-segment depression, 49% in the perioperative and 51% in postoperative recordings. Conclusion: Though patients were asymptomatic with antianginal therapy, there were episodes of ST-segment depression indicating silent myocardial ischemia in patients with CAD. Surgical interventions such as transurethral resection of tumors of prostate or bladder did not produce an increase of ischemic burden registered by Holter monitoring.     

Character of transient ischemia in angina pectoris

There is growing interest in the possible therapeutic and prognostic significance of silent myocardial ischemia in coronary artery disease (CAD) and its detection by ambulatory electrocardiographic (ECG) monitoring. In 100 apparently healthy normal subjects (20 with angiographically normal coronary arteries), Holter monitoring revealed significant ST-segment depression in only 2 (both over 40 years, one with positive treadmill test, the other with risk factor for CAD). No significant ECG changes were found in those with normal coronary vessels. In 30 patients with documented CAD, significant ST-segment depression during 1,934 episodes over 446 days of monitoring over 18 months was found. Only 24% of the episodes were associated with angina. Asymptomatic and symptomatic episodes were associated with comparable changes in perfusion detected by positron emission tomography. Heart rate increases greater than 10 beats/min preceding the onset of the ST-segment changes occurred in only 23% of the episodes. There was considerable variability in the ST-segment changes in the same patient monitored serially over long periods of time. The data indicate that it is extremely uncommon for patients without CAD to exhibit silent myocardial ischemia, whereas patients with stable angina exhibit frequent, variable and often asymptomatic ECG evidence of myocardial ischemia rarely triggered by increases in heart rate. These findings are likely to be of therapeutic and prognostic significance.     

冠心病患者的无症状性心肌缺血

本文报道冠心病患者108例在日常活动情况下,采用Holter 24小时监测,发现60例(55.6%)有心肌缺血发作,总计发作244次,其中无症状性心肌缺血198次(81%)。心肌缺血发作时与发作前的心率比较无明显差异。无症状性心肌缺血发作时ST段下降程度与伴随有胸痛发作时比较,亦无明显差异。在上午6时至12时,无症状性心肌缺血发作频率最高,占55.1%。内服缓释硝酸异山梨酯(消心痛)可以减少心肌缺血发作。     

Hemodynamic and electrocardiographic correlates of symptomatic and silent myocardial ischemia: pathophysiologic and therapeutic implications

Numerous hemodynamic, electrocardiographic, metabolic and radionuclide measurements in various subsets of patients with coronary artery disease (CAD) reveal that ischemia does not always occur on the basis of increases in myocardial oxygen consumption. Continuous hemodynamic monitoring indicates that most episodes of myocardial ischemia are not preceded by increases in such major determinants of oxygen consumption as heart rate or blood pressure, but that these usually increase in response to the development of ischemia. The development of pain during ischemia is a late feature and most episodes are silent. There are no significant differences in the hemodynamic characteristics of symptomatic versus asymptomatic episodes of myocardial ischemia in patients with angina at rest or between those associated with ST-segment depression and those with ST-segment elevation. Continuous Holter recordings analyzed by compact analog technique in hospitalized and ambulatory patients with ischemic heart disease indicate that in both unstable and chronic stable angina, over two-thirds of myocardial ischemic episodes are clinically silent. Symptomatic and silent episodes do not differ significantly with respect to duration. Most symptomatic and asymptomatic episodes are not triggered by increases in the determinants of oxygen demand. Such episodes may arise on the basis of a critical reduction in the lumen of the diseased coronary artery leading to a primary reduction in blood flow. Intermittent obstruction due to changes in coronary vasomobility or possibly formation of thrombi may be a common mechanism for the pathogenesis of myocardial ischemia in patients with a varying spectrum of coronary artery lesions. At present, the precise clinical and prognostic significance of silent ischemia in CAD is not completely defined.(ABSTRACT TRUNCATED AT 250 WORDS)     

Efficacy of a single dose of slow-release isosorbide dinitrate in the treatment of silent or painful myocardial ischemia in stable angina pectoris.

A double-blind study was performed in 32 patients with stable angina pectoris to assess the effects of slow-release isosorbide dinitrate (ISDN) (a single dose of 120 mg/day) on the frequency and duration of painless and painful ischemic episodes, and on electrocardiographic changes and exercise tolerance. Forty-eight-hour electrocardiographic monitoring and treadmill exercise tests were performed before, and at 20 and 21 days of therapy. Holter monitoring showed a significant decrease in the frequency of painful and silent episodes (p less than 0.001), and in the duration of painful (1,623 +/- 664 seconds vs 323 +/- 161 seconds; p less than 0.001) and silent episodes (2,818 +/- 1,496 seconds vs 223 +/- 102 seconds; p less than 0.001). The magnitude of painful and silent ST-segment depression was significantly reduced (2.7 +/- 0.9 mm to 0.7 +/- 0.7 mm and 2.0 +/- 1.1 mm to 0.7 +/- 0.5 mm, respectively; p less than 0.001). Time of exercise testing to the onset of ST-segment depression (442 +/- 137 seconds vs 858 +/- 110 seconds; p less than 0.001) or anginal pain was doubled (461 +/- 128 seconds vs 830 +/- 130 seconds; p less than 0.001). The work load increased from 6 to 10 METs (p less than 0.001). ISDN in a single dose of 120 mg/day is a valuable drug for stable angina pectoris, decreasing the frequency of silent and painful ischemic episodes and the magnitude of ST-segment depressions, and increasing exercise tolerance. It particularly shortened the duration of silent episodes. For patients' compliance, a once-daily dose of ISDN could be advantageous.     

Silent myocardial ischemia: diagnosis, clinical significance and management

With the inception of continuous ECG monitoring with high-fidelity reproduction of the ST-segment, silent myocardial ischemia has been regarded with increasing importance in the detection and management of coronary artery disease. With the aid of a variety of invasive and noninvasive methods, the validity of ST-segment depression as indicative of myocardial ischemia, even in the absence of symptoms, has been adequately documented. In completely asymptomatic subjects with positive evidence of silent ischemia in the exercise ECG or Holter monitoring, the risk of developing a future manifestation of coronary artery disease may be up to ten-fold higher than in individuals with negative tests In patients with established coronary artery disease, concomitant use of continuous ECG monitoring and exercise testing, methods which complement each other rather than being mutually exclusive, a substantial number of patients with otherwise typical angina pectoris may be found to have silent ischemic episodes. An adequate differentiation between those with symptomatic and those who are asymptomatic based on characterization with respect to age, sex, hypertension, coronary anatomy, etc., has not been successful. Patients with silent ischemia during exercise may also exhibit more episodes of silent ischemia during daily activities and up to 75% of ischemic episodes may be asymptomatic. In general, however, silent ischemia during exercise appears more common than silent ischemia only during daily activities. In the latter case, since there is usually no increase in heart rate, the pathophysiology is regarded as dissimilar from that associated with exercise-induced ischemia. While the presence of silent ischemia appears quite common in patients after acute myocardial infarction, its occurrence, to date, has not been confirmed to carry additional risk, whereas in unstable angina, the association of silent ischemia is indicative of a higher probability of subsequent cardiac events.     

Transient myocardial ischemia during daily life in patients with syndrome X

Nineteen patients with syndrome X (typical exertional angina, positive exercise test response [at least 0.1 mV of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries) underwent continuous 48-hour electrocardiographic (ECG) monitoring during unrestricted daily life. Fifty-eight ischemic episodes of at least 0.1 mV of ST-segment depression were observed in the same ECG leads that showed ST depression during stress testing: 28 (48%) were accompanied by anginal pain and 30 (52%) were asymptomatic. No significant differences were found between painful and silent ST-segment depression with regard to the number of episodes, their temporal distribution, magnitude, duration or heart rate (HR) at onset of ST-segment depression. In the minute preceding ischemic ST shifts, HR did not change in 33% of episodes or increased by less than 10 beats/min in 28%. HR at onset of ST depression was significantly lower during ambulatory ECG monitoring than during exercise testing (98 ± 18 vs 117 ± 18 beats/min, p < 0.01). During ambulatory monitoring, 85 episodes of sinus tachycardia (exceeding by 10 to 80 beats/min the HR that triggered ischemia during exercise testing) occurred in the absence of angina or ST-segment shifts. The results of this study suggest that in patients with syndrome X, (1) myocardial ischemia frequently develops during daily life; (2) silent ischemia is an important component of this syndrome; and (3) increased oxygen demand in the presence of impaired coronary vasodilatory capacity is not the only cause of myocardial ischemia. Active mechanisms that transiently reduce coronary flow may act and explain occurrence of angina at rest and with minimal exertion.     

Calcium antagonists for Prinzmetal's variant angina, unstable angina and silent myocardial ischemia: therapeutic tool and probe for identification of pathophysiologic mechanisms

The calcium antagonists provide a unique tool to reduce myocardial oxygen demand and prevent increases in coronary vasomotor tone. For patients with Prinzmetal's variant angina, diltiazem, nifedipine and verapamil are extremely effective in preventing episodes of coronary vasospasm and symptoms of ischemia. Unstable angina pectoris is a more complex pathophysiologic syndrome with episodes of ischemia due to increases in coronary vasomotor tone, intermittent platelet aggregation or alterations in the underlying atherosclerotic plaque. Each of the calcium antagonists is effective as monotherapy in decreasing the frequency of angina at rest. Nifedipine is the only calcium antagonist that has been studied in a combination regimen with beta blockers and nitrates for patients with unstable angina, and control of angina is better with the combination regimen than with either form of therapy alone. Although symptoms of myocardial ischemia in unstable angina are reduced by calcium antagonists, these agents do not seem to decrease the incidence of adverse outcomes. Antiplatelet therapy appears to improve morbidity and mortality in patients with unstable angina, suggesting that thrombus formation may play a central role in that disorder. Episodes of silent or asymptomatic myocardial ischemia, identified by ST-segment monitoring, occur in a variety of disorders of coronary disease. Among patients with Prinzmetal's variant angina and unstable angina, episodes of silent ischemia appear to be as frequent as episodes of angina and the calcium antagonists are effective in decreasing episodes of ischemia regardless of the presence or absence of symptoms. Persisting episodes of silent ischemia among patients with unstable angina despite maximal medical therapy identify patients at high risk for an early unfavorable outcome. Among patients with stable exertional angina, episodes of silent ischemia may be up to 5 times as frequent as episodes of angina, and may be due to increases in coronary vasomotor tone, transient platelet aggregation or increases in myocardial oxygen demand. Preliminary experience suggests that calcium antagonists and beta blockers are effective in decreasing episodes of silent ischemia in patients with stable exertional angina and that a combination regimen may be more effective than either form of therapy alone.     

Holter monitoring before, during and after percutaneous transluminal coronary angioplasty for evaluation of high-resolution trend recordings of leads CM5 and CC5 for ST-segment analysis

Frequency-modulated Holter monitoring of leads CM5 and CC5 was performed before, during and after percutaneous transluminal coronary angioplasty (PTCA) in 16 patients with stenosis of the left anterior descending coronary artery, in 5 patients with stenosis of the left circumflex coronary artery, and in 5 patients with stenosis of the right coronary artery. All patients presented with 1-vessel coronary artery disease and stable or unstable angina pectoris. ST-segment analysis was based on high-resolution trend recordings. During balloon inflations all patients had significant (at least 0.1 mV) ST-segment changes in lead CM5. In lead CC5, associated ST-segment deviations were found in 22 of 26 patients. During 29.2 +/- 13.6 hours before PTCA, 90 spontaneous episodes with significant ST-segment deviations were detected in 10 patients. Of these episodes, 17% were characterized by ST-segment deviations in lead CC5 only, 57% by ST-segment deviations in lead CM5 only, and 27% by simultaneous ST-segment deviations in both leads. Asymptomatic episodes occurred twice as frequently as symptomatic episodes (66 vs 34%). Symptomatic episodes were more often characterized by ST-segment deviations of at least 0.15 mV (48 vs 9%, p less than 0.001) and by ST-segment deviations observed in both leads simultaneously (48 vs 15%, p less than 0.001). During 34.8 +/- 10.6 hours after successful PTCA, 5 spontaneous asymptomatic episodes with significant ST-segment deviations were detected in 2 patients.     

ST segment changes in long-term ECG in healthy heart probands

100 healthy medical students were studied with 24-h Holter monitoring for ST-segment evaluation. Six recordings (1.8% of males and 11.6% of females) contained at least one episode of horizontal or downsloping ST-segment depression of at least 0.1 mV or more and 1 min duration in the V-5-like lead. Since ST-segment elevations (in 73% of the recordings in the V-5-like lead, and in 40% in the V-2-like lead) and discordant (negative) T-waves associated with ST-segment depressions (in 31% of the recordings in the V-2-like lead) were commonly seen, these ECG findings have to be considered as nonspecific. During exercise tests using a protocol of maximal work load, not one of these healthy individuals displayed typical ST-segment depressions indicative of myocardial ischemia. Therefore, typical documented ST-segment alterations in Holter-ECG recordings should be used with caution when observed in individuals with suspected coronary heart disease, particularly when they are female.