Continuous electrocardiographic recording in Prinzmetal's variant angina pectoris: A report of four cases

Four patients with Prinzmetal''s variant angina pectoris were subjected to continuous electrocardiographic recording. In three of them several episodes of ST segment elevation unaccompanied by pain were recorded. In one patient, identical electrocardiographic alterations were observed both in presence or in absence of pain, while in the others a good correlation was evident between pain and severity of the electrocardiographic abnormalities. In two patients transmural myocardial infarction complicated the course of the angina. In contrast to the classical findings, in these patients the attacks of chest pain did not cease after the infarction, but became more frequent and severe. The electrocardiographic alterations of the anginal episodes occurred in the same myocardial areas involved by the infarction, so that a reversible superposition of electrocardiographic signs of acute ischaemia on those of recent necrosis was observed.Continuous electrocardiographic recording provided the best means of investigation of these patients with the variant form of angina pectoris.     

Clinical coronarographic characteristics and pathogenetic mechanism of angina pectoris with s-t elevation (author's transl)]

The study of 46 patients with frequent anginal episodes characterized by S-T elevation (so called "variant angina pectoris") demonstrated that this type of electrocardiographic pattern does not characterize a homogeneous group of patients. In fact, while in some patients angina occurred only at rest, in others it occurred also on exercise. Sometimes ecgraphic alterations characterized by S-T depression were observed on the same leads which on other occasions had shown S-T elevation. The angiographic picture revealed: absence of significant coronary alterations in 10% of cases, stenosis greater than 75% in one main branch in 29%, in two branches in 39% and in three branches in 22% of cases. The hemodynamic monitoring carried out on 14 of these patients demonstrated that the ecgraphic modifications occur before the onset of the hemodynamic parameters which control myocardial O2 consumption. This suggests a primitive reduction of regional myocardial blood supply as a cause of the ischaemic episodes. The study of the regional myocardial perfusion with 201Tl technique in 6 patients confirmed this hypothesis. Coronary angiography carried out during an ischemic episode showed that the reduction of myocardial blood supply was caused by a spasm of a large coronary artery involving a long segment of the vessel, reversible by nitroglycerin administration. Aorto-coronary by-pass operation performed on 6 patients was followed by the disappearance of pain in two patients, even though the "by-pass" patency was angiographically proved in two patients.     

Prognostic implications of silent myocardial ischemia: prediction of events?

In patients with stable and unstable angina pectoris, the occurrence of transient ST-T-wave alterations during ambulatory electrocardiographic monitoring is helpful in identifying a subgroup of patients who are especially likely to have severe atherosclerotic coronary artery disease and a guarded prognosis over the subsequent 1 to 12 months. Because the majority of these episodes are not accompanied by chest pain, it seems logical to conclude that recurrent episodes of silent myocardial ischemia signal a high likelihood of severe coronary artery disease and carry a poor short-term prognosis.     

Transient giant R waves in the early phase of acute myocardial infarction: Association with ventricular fibrillation

An unusual electrocardiographic (ECG) pattern was observed in five patients who suffered an acute anterior myocardial infarction. Early in their illness and following resuscitation from ventricular fibrillation (three patients), in the midst of recurrent ventricular irritability prior to development of ventricular fibrillation (one patient), and following a period of seizures (one patient), the ECG showed ST-segment elevation, marked increase in the R-wave amplitude, disappearance of S waves and merging of QRS complexes with the elevated ST segments. ECG patterns noted in these patients were similar to the ones recorded from dogs immediately after ligation of a large coronary artery, and from patients with severe episodes of variant angina. Although these early electrocardiographic changes probably reflect either marked regional transmural blood flow deprivation or its aftermath, they could not be taken as indices of eventual massive myocardial necrosis since in most of these patients the alterations were followed by development of nontransmural myocardial infarction. The possible mechanisms and the implications of such discrepancy between early and late electrocardiographic indicators of injury or necrosis is discussed.     

Coronary spasm and acute coronary insufficiency (author's transly)]

A series of cases illustrating a spectrum of acute coronary episodes associated with transient subepicardial injury, namely the variant form of angina, angina intermedia with electrocardiographic changes similar to those of the variant angina, acute myocardial infarction complicated by variant angina with electrocardiographic changes localized to the infarcted area, acute myocardial infarction preceded and followed by variant angina, is presented. The role of a coronary spasm as a common mechanism of the above mentioned episodes is postulated. Coronarographic demonstration of this mechanism is produced.     

Clinical significance of silent ischemia in unstable angina pectoris

In a prospective study the significance of silent ischemia was evaluated in 66 patients with a clinical diagnosis of unstable angina (no requirement for reversible ST-T changes during pain on 12-lead electrocardiograms before entry), and the results of continuous 2-channel electrocardiographic (ECG) recordings, begun within 24 hours of admission, were compared with other clinical and ECG predictors of adverse outcome. Ischemic changes were detected in 7 patients (11%) during a mean of 41 hours of recording. There were 37 episodes of transient ST-segment change (16 ST elevation, 21 ST depression) of which 11 (30%) were symptomatic and 26 (70%) were silent. All 7 patients had at least 1 silent episode and 5 also had symptomatic episodes during the recording but only 2 patients had exclusively silent episodes. During a mean follow-up of 13.3 months, 3 patients died, 5 had a nonfatal myocardial infarction and 32 required revascularization. Although transient myocardial ischemia during the continuous ECG recording, whether silent or symptomatic, was a specific predictor of subsequent nonfatal myocardial infarction or death (specificity 92%), its sensitivity for these events was low (25%). In contrast, recurrent rest pain (greater than or equal to 1 episode) occurred in all patients with these serious adverse events (sensitivity 100%, specificity 49%). Transient ischemia occurs infrequently during continuous ECG recordings in patients with unstable angina not selected by reversible ST-T changes on a 12-lead electrocardiogram at entry. Recurrent rest pain after hospital admission is a more sensitive predictor of serious events in this group.     

Comparison of plasma serotonin levels in patients with variant angina pectoris versus healed myocardial infarction

Patients with variant angina pectoris showed greater serotonin plasma levels than did control subjects and patients with healed myocardial infarction. The levels also tended to be greater in those with >1 episode/month than in those with fewer episodes. Moreover, patients with variant angina pectoris also had greater levels of nitrite and nitrate plasma levels than did control subjects or patients with healed myocardial infarction, partly, perhaps, as a compensatory mechanism.     

Extracardiac contributions to chest pain perception in patients 6 months after acute myocardial infarction

OBJECTIVES: The amount of perceived anginal pain in patients after infarction deserves the attention of the physician. This study sought to identify the modulating influence of extracardiac factors on persistent angina pectoris after myocardial infarction. METHODS AND RESULTS: A total of 552 male survivors of acute myocardial infarction (age 29 to 65 years, median 54 years) were followed for a period of 6 months; the affective state was assessed immediately after the acute event. The prognostic importance of postinfarction depression on chest pain perception was evaluated 6 months after the cardiac event in 376 patients. After the 6-month follow-up period, 199 (53%) of the patients with myocardial infarction had angina pectoris. Somatic risk factors and electrocardiographic data at initial testing did not contribute to the risk of having chest pain. However, patients with high levels of depression at initial testing had an almost 3-fold risk of having angina pectoris 6 months after the index event. Older age, lower social class status, and preinfarction angina were also significantly related to angina pectoris at the end of the study. Patients who were pain free before the index infarction reported significantly more symptoms of chest pain at the study end point (P 相似文献   

Anginal symptoms without ischemic electrocardiographic changes during ambulatory monitoring in men with coronary artery disease

Episodes of angina pectoris without electrocardiographic (ECG) signs of myocardial ischemia during 24-hour ambulatory monitoring were studied in 128 patients with a history of stable angina, angiographically proven coronary artery disease and positive exercise test results. In all, 341 episodes of ischemic ECG changes (ST-segment depression greater than 1 mm for greater than 1 minute) and 190 episodes of angina pectoris were observed: 86 episodes consisted of both ECG changes and angina pectoris, 255 episodes consisted only of ECG changes, and 104 episodes only of angina pectoris. Duration and magnitude of ST-segment deviation and heart rate at the onset of ischemia were similar in the 86 symptomatic and the 255 asymptomatic episodes with ECG changes. The 104 episodes of angina pectoris without ECG changes were detected in 44 patients (34%) (group A); 29 of them had only episodes with angina pectoris and 15 patients had both--episodes of angina pectoris with and without ECG changes. In 84 patients (66%) (group B) angina pectoris without ECG changes was not observed; all episodes were accompanied by ischemic ECG changes in these patients. No differences in the angiographic extent of coronary artery disease and in exercise test data were seen in both groups A and B; however, maximal ST-segment depression during exercise testing was significantly greater in group B than in group A patients (2.4 +/- 0.8 mm vs 1.9 +/- 0.9 mm; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular performance and related haemodynamic changes in Prinzmetal's variant angina pectoris

Attacks of Prinzmetal's variant form of angina pectoris are spontaneous, recur cyclically, and present unequivocal electrocardiographic alterations: they are ideal for a detailed haemodynamic study.Four patients with this form of angina were investigated. In each of them episodes occurred of electrocardiographic abnormalities either accompanied or unaccompanied by pain. During the same session, the cardiogram, heart rate, arterial pressure, and right atrial pressure were continuously recorded during periods ranging from 5 to 7 hours in each patient. Cardiac output was measured at selected times. Left ventricular ejection time, isovolumic contraction time, mean rate of isovolumic pressure development, and mean systolic ejection rate were also determined.In the 38 recorded anginal episodes, no circulatory change preceded the cardiographic modifications. From the onset of the electrocardiographic abnormalities to the beginning of their reversion, the following circulatory events were observed: (1) obvious reduction of cardiac output; (2) arterial hypotension; (3) lengthening of isovolumic contraction time and mean rate of isovolumic pressure development; (5) reduction of mean systolic ejection rate. It is concluded: (1) that no circulatory factor interfering with work or oxygen consumption of the heart is responsible for eliciting these anginal episodes; (2) that conspicuous left ventricular impairment occurs during the increasing and steady period of the electrocardiographic abnormalities.As the electrocardiogram started reverting to the pre-attack aspect, cardiac performance rapidly improved and, after a ;supernormal' phase, returned in about 2 minutes to basal levels. It is possible that this phase is dependent on a temporary sympathetic compensatory mechanism.No significant qualitative differences were detected between the circulatory pattern of various anginal episodes. The difference was mainly quantitative and the magnitude of the haemodynamic changes correlated well with the degree of the electrocardiographic abnormalities. Pain, when present, seemed just a concomitant symptom not significantly interfering with the circulatory changes associated with the episodes of this form of angina pectoris.     

Transient ST-segment depression as a marker of myocardial ischemia during daily life

Patients with angina and coronary artery disease (CAD) have many episodes of transient ST-segment depression during ordinary daily life, and these are often asymptomatic. To investigate this signal as a marker of myocardial ischemia, 30 patients with chronic stable angina and CAD underwent positron tomography, recording the regional myocardial uptake of rubidium-82, pain and ST-segment changes before, during and after 59 technically satisfactory exercise tests, 35 cold pressor tests and 22 episodes of unprovoked ST depression. Exercise resulted in 53 episodes of ST depression with angina and in 5 episodes without pain. After cold pressor tests, there were 3 episodes of ST depression and pain and 12 of painless ST depression. Only 9 episodes of unprovoked ST depression were accompanied by pain. Tomography showed independent evidence of ischemia in 63 (97%) of the total 65 episodes of ST depression with angina and in all 30 episodes of painless ST depression. In each patient perfusion defects occurred in the same myocardial segment during painful and painless ST depression and responses were significantly different from those in 16 normal subjects studied in the same way. These findings support the use of transient ST depression in continuous monitoring to assess the activity of CAD, but only in patients with typical angina pectoris, ST depression during exercise and proved CAD. They strengthen the evidence derived from ambulatory monitoring for a wider picture of the disease than is generally appreciated, with more frequent episodes of silent myocardial ischemia than of angina pectoris.     

Asymptomatic myocardial ischemia

Silent (asymptomatic) myocardial ischemia (SMI) is defined as a transient alteration in myocardial perfusion in the absence of chest pain or the usual anginal equivalents. Patients may be classified as having one of the three types of SMI: type A--totally asymptomatic patients with no history of angina or myocardial infarction; type B--asymptomatic patients with previous myocardial infarction; type C--patients with angina and asymptomatic ischemic episodes. SMI has been found in 2.5% of all healthy males aged 40-59 and in 20% of all postinfarction patients. In type C-patients, 80% has been found to have asymptomatic ischemic episodes in addition to typical angina pectoris. The frequency of SMI may be up to three or four times that of anginal attacks. SMI patients have generally reduced sensitivity to pain an differences in severity an duration of ischemic episodes. Diagnosis is based on screening by means of exercise testing in patients working in specific professions (like pilots, busdrivers etc.), in postinfarction patients and in patients after unstable angina pectoris and after coronary bypass surgery or coronary angioplasty. Prognosis is the same as in asymptomatic ischemia. SMI is an indicator of instability in certain groups of patients (post infarction, after unstable angina pectoris). SMI persisting after medical therapy of unstable angina is associated with adverse short-term-prognosis, therefore coronary surgery or angioplasty is indicated.     

Myocardial ischemia induced by the cold pressor test in patients with exertion angina. Case contribution

The aim of the present study was to assess the incidence of myocardial ischemia during cold pressor test in patients with stable exertional angina pectoris. Thirty-seven patients with proven coronary artery disease were submitted to cold pressor and exercise stress testing; computer assisted electrocardiographic recordings were obtained throughout the examinations. Cold stimulation provoked electrocardiographic signs of subendocardial ischemia only in 3 patients. They had suffered of a previous myocardial infarction and showed low exercise tolerance and severe coronary lesions (one with triple vessel and 2 with left main disease). Interestingly, only one of these patients gave an history of angina during cold exposure. Thus these data indicate that chest pain and electrocardiographic signs of ischemia are an uncommon event during cold pressor stimulation which occurs more likely in patients with fairly severe coronary narrowings. More sensitive markers of ischemia and/or different modalities of cold application are required for studies concerning the relationship between cold exposure and angina pectoris.     

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

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

Painless ST-segment depression in patients with angina pectoris. Correlation with daily activities and cigarette smoking.

Ambulatory electrocardiographic monitoring was employed in 33 patients with angina pectoris and abnormal stress tests to determine the frequency with which myocardial ischemia manifested by painless ST-segment depression occurred during normal activity. ST-segment depression occurred in 24 patients during the monitoring period; and in 21, it occurred either solely in the absence of pain or both with and without pain. Of 109 recorded episodes of ST-segment depression, 61 percent were painless. The frequency of painless ST-segment depression was independent of activity other than automobile driving, during which all episodes were painless. In patients who smoked cigarettes, ST-segment depression was more common while smoking, but the incidence of painless ST-segment depression was not altered. The study indicates that ST-segment depression occurs more commonly in the absence than in the presence of chest pain and that ambulatory electrocardiographic monitoring is a useful method of determining the frequency of myocardial ischemia during normal daily activity.     

Effect of exercise training on the total ischaemic burden: an assessment by 24 hour ambulatory electrocardiographic monitoring.

OBJECTIVE--To examine the effect of prolonged high intensity exercise training on total ischaemic burden in men with chronic stable angina pectoris. DESIGN--A randomised controlled trial based on 24 hour ambulatory electrocardiographic monitoring of patients on two occasions a year apart. SETTING--Cardiology department of a large general hospital. SUBJECTS--40 men under 60 years of age with chronic stable angina pectoris and no previous myocardial infarction. RESULTS--After training the exercise group showed a 30% reduction in frequency of ST segment depression. There were significant reductions in painful episodes of ischaemia and those triggered by changes in heart rate. There was also a trend towards a reduction in silent ischaemia and episodes not triggered by changes in heart rate. The duration of ischaemic episodes was also reduced. No significant change in frequency or severity of dysrhythmia was shown. CONCLUSIONS--Exercise training reduces total ischaemic burden in patients with angina pectoris by reducing the frequency and duration of all types of ischaemic episode.     

Myocardial infarction after exercise-induced electrocardiographic changes in a patient with variant angina pectoris

The electrocardiographic response to stress testing varies considerably in patients with variant angina pectoris: no change in the S-T segment as well as S-T segment depression and elevation have been observed. This report describes a patient with a resting ST-T abnormality that reverted to normal appearance with exercise. However, the patient experienced severe chest pain shortly after discontinuing exercise testing, and an electrocardiogram showed evidence of acute anterolateral infarction. The possible implications of such electrocardiographic changes are discussed.     

Contribution of creatine kinase MB mass concentration at admission to early diagnosis of acute myocardial infarction.

OBJECTIVE--To assess the diagnostic value at admission of creatine kinase MB mass concentration, alone or in combination with electrocardiographic changes, in suspected myocardial infarction. DESIGN--Prospective study of all consecutive patients admitted within 12 hours after onset of chest pain to a coronary care unit for evaluation of suspected myocardial infarction. SETTING--Large regional hospital. PATIENTS--In 297 patients creatine kinase and creatine kinase MB activities and creatine kinase MB mass concentration were determined. Myocardial infarction according to the criteria of the World Health Organisation was diagnosed in 154 patients and excluded in 143 patients (including 70 with unstable angina pectoris). RESULTS--Sensitivity/specificity for creatine kinase MB mass concentration in patients admitted within 4 hours and 4-12 hours after onset of chest pain were 45%/94% and 76%/79% respectively. Corresponding values for creatine kinase activity were 20%/89% and 59%/83%, and for creatine kinase MB activity 16%/87% and 53%/87%. Raised creatine kinase MB mass concentration was seen in 17% of patients with unstable angina pectoris. Stepwise logistic regression analysis showed that independent predictors of acute myocardial infarction in patients admitted within 4 hours after onset of chest pain were electrocardiographic changes and creatine kinase MB mass concentration on admission; in patients admitted 4-12 hours after the onset of pain independent predictors were electrocardiographic changes and creatine kinase MB mass concentration and activity. CONCLUSION--Creatine kinase MB mass concentration is a more sensitive marker for myocardial infarction than the activity of creatine kinase and its MB isoenzyme. Electrocardiographic changes on admission in combination with creatine kinase MB mass concentration (instead of creatine kinase and creatine kinase MB activities) are best in diagnosing myocardial infarction.     

Association between silent myocardial ischemia and prognosis: Insensitivity of angina pectoris as a marker of coronary artery disease activity

The clinical syndrome of angina pectoris was accurately described over 200 years ago by Sir William Heberden. However, in recent years, we have learned that many episodes of myocardial ischemia occur that are not accompanied by symptoms of angina pectoris. These silent ischemic episodes may be detected either during exercise testing, using electrocardiographic criteria that can be combined with scintigraphic studies evaluating myocardial blood flow (thallium perfusion studies) or left ventricular function (gated blood pool scans). In addition, continuous electrocardiographic (Holter) monitoring can be used for the detection of transient ST-segment changes; these changes on Holter monitoring have been correlated with abnormalities of myocardial perfusion and function, indicating that they represent true ischemic events.

Studies have shown that patients with coronary artery disease who have evidence of ongoing ischemia, whether symptomatic or silent, have an increased risk for experiencing subsequent cardiac events than patients without evidence of ischemia. Many studies have demonstrated that ischemia during an exercise study after myocardial infarction identifies patients at high risk for recurrent cardiac events, whether or not the ischemia is associated with angina pectoris. Holter monitoring has allowed for the detection of ischemic events out of hospital in ambulatory patients. Studies in stable angina patients have shown that there are many asymptomatic episodes in this setting, which are often occurring at low heart rates during activities of everyday life, without an apparent significant increase in myocardial oxygen demands, and these episodes may even be precipitated by mental stress. Several studies have suggested that the presence of ongoing silent ischemia in unstable angina patients and postinfarction patients can identify those at higher risk for cardiac events. The results of these studies will be discussed.

The treatment of coronary artery disease has been for the most part symptomatic, with the primary goal of relieving symptoms of angina pectoris. Several exceptions include patients with left main disease or severe proximal 3-vessel disease, who have extensive amounts of myocardium at risk and who are generally referred for bypass surgery.

These new data indicating that the presence and severity of asymptomatic ischemia have adverse prognostic implications suggest that therapy should be directed at reducing the total ischemic profile, i.e., symptomatic and asymptomatic episodes. Guidelines for appropriate screening and therapeutic strategies will be discussed.