Cardiac events in patients with silent myocardial ischemia.

The clinical implications of silent myocardial ischemic (SMI) episodes in patients with coronary artery disease were assessed in 253 patients whose angina symptoms were resolved by antianginal drugs. This population included 93 patients without a history of myocardial infarction (angina group) and 160 patients with myocardial infarction (infarction group). These patients were further divided into 2 subgroups according to whether or not SMI was detected by Holter monitoring immediately before discharge. The incidence of cardiac events was 19% for the angina group and 18% for the infarction group. The incidence of cardiac events did not differ between the 2 groups, but the cardiac event profile did. Briefly, 14 angina patients experiencing cardiac events needed coronary revascularization for worsening symptoms, while 18 myocardial infarction patients experiencing cardiac events had another infarction. In both angina and myocardial infarction patients, the cumulative rates of cardiac events were significantly higher in the subgroups with SMI (p less than 0.01 in either group). The significant prognostic factors as determined in the Cox regression model were multivessel disease, asynergy score, and SMI on Holter monitoring for angina patients, and SMI on Holter monitoring and multivessel disease for myocardial infarction patients. In conclusion, the cardiac event rate is significantly elevated in the subgroups with SMI, regardless of whether the patient had previous myocardial infarction; patients with SMI carry a poor prognosis, especially when they have a history of myocardial infarction.     

Unstable angina: Relationship of clinical presentation,coronary artery pathology,and clinical outcome

Patients with unstable angina are heterogeneous with respect to presentation, coronary artery morphology, and clinical outcome. Subclassification of these patients based on clinical history has been proposed as a means of identifying individuals at increased cardiac risk. We applied such a classification system to 129 patients discharged from a coronary care unit with a diagnosis of acute myocardial ischemia. Patients were then assessed for cardiac events (recurrent angina requiring revascularization, myocardial infarction, death) 12 months following hospital discharge. Patients were classified as recent onset unstable angina preinfarction (n = 42), crescendo unstable angina preinfarction (n = 48), and unstable angina postinfarction (n = 39). Within each of these groups, the patients were further subclassified based on the occurrence of angina on effort, at rest, or both. No attempt was made to subset patients taking antiischemic drugs at the time of clinical presentation to the physician. Coronary angiographic pathology (morphology and number of vessels involved) was similar in the subgroups, but coronary artery thrombus was statistically more likely to be found in patients with crescendo rest angina preinfarction or with frequent anginal episodes at rest postinfarction. Mortality was significantly higher for patients with unstable angina postinfarction (7.7%) than preinfarction (1.1%). No statistical differences were noted between the subgroups with respect to the occurrence of myocardial infarction or recurrent unstable angina requiring revascularization. These data suggest that subclassification of unstable angina patients based on clinical characteristics at presentation is not useful to predict subsequent myocardial infarction or recurrent angina requiring revascularization. However, as one might expect, patients with recurrent angina postinfarction have a higher mortality rate than patients with unstable angina preinfarction, and patients with recurrent rest angina, either pre- or postinfarction, are more likely to have intracoronary thrombus than patients with new onset angina or crescendo effort angina; however, the presence of thrombus did not predict a poor clinical outcome.     

Relations of the duration of pre-existing angina pectoris, collateral circulation and left ventricular function after isolated coronary occlusion with or without myocardial infarction

The aim of this retrospective study was to determine the relationship between the duration of preceding angina pectoris, collateral circulation and left ventricular function after isolated coronary occlusion with or without myocardial infarction. Coronary angiography of 138 consecutive patients showed isolated and complete occlusions of the left anterior descending (58 patients) or right coronary artery (80 patients). One hundred and four patients had myocardial infarction with (Group A, n = 21) or without (Group B, n = 83) preceding angina pectoris and 34 had angina without myocardial infarction (Group C). The left ventricular ejection fraction was measured by ventriculography in the 30 degrees right anterior oblique projection. The collateral circulation was assessed by coronary angiography and evaluated as follows: no flow or flow limited to collateral branches (subgroup 1) and partial or complete filling of the epicardial arterial segment (subgroup 2). In the global population the left ventricular ejection fraction was higher and the duration of preceding angina pectoris was longer in the subgroups with a well developed collateral circulation. There was no difference in ejection fraction between Groups A and B (presence of myocardial infarction), on the other hand, within each of the groups, a good collateral circulation (subgroup 2) was associated with a significantly higher ejection fraction. Group C (without infarction) patients had better ejection fractions than Groups A or B, especially when the collateral circulation was poorly developed. Within Group C, the quality of the collateral circulation did not seem to affect the ejection fraction. The left ventricular ejection fraction is lower in patients with isolated coronary occlusion and myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Irregular coronary lesion morphology after thrombolysis predicts early clinical instability.

After successful thrombolytic treatment for acute myocardial infarction, recurrent ischemia and infarction may occur with little warning. Coronary lesion morphology was analyzed from angiograms performed in 72 consecutive patients at 1 to 8 days after streptokinase treatment for acute myocardial infarction and the data were evaluated in relation to the subsequent clinical course. All patients were clinically stable at the time of angiography and continued to receive heparin infusion for greater than or equal to 4 days after thrombolysis. The infarct-related artery was patent in 55 patients (76%). In the 10 days after angiography, 15 patients developed prolonged episodes of angina at rest; the condition of 4 stabilized with medical treatment, but 11 required urgent medical intervention (coronary angioplasty in 8 and bypass surgery in 3). There were no differences in age, gender, left ventricular function or extent of coronary artery disease between those patients who developed unstable angina and those who had a stable in-hospital course. However, the median plaque ulceration index of the infarct-related lesion was 6.7 (95% confidence limits 6.3, 10) in the 15 patients with an unstable course versus 3.3 (2, 4.4) in those with a stable course (p less than 0.001). There were no differences between the two patient groups in the severity of stenosis, length of diseased segment, symmetry/eccentricity, presence of a shoulder, location at branch point or bend, presence of globular or linear filling defects, contrast staining or collateral supply. These data show that after thrombolysis, the degree of irregularity of the infarct-related artery is a critical determinant of early clinical instability.(ABSTRACT TRUNCATED AT 250 WORDS)     

Arteriographic patterns early in the onset of the coronary syndromes.

Coronary arteriography in 300 patients within one year of onset of symptoms of coronary arterial disease revealed already severe anatomical coronary disease in three patient groups: those with angina pectoris alone (164 patients), with subendocardial myocardial infarction (63 patients), and with transmural myocardial infarction (73 patients). The number of vessels diseased (larger than or equal to 50% obstruction), distribution of obstruction, and degree of stenosis were similar in the three groups. However, total occlusion of at least one artery was much more common in transmural myocardial infarction and in subendocardial myocardial infarction with elevation of enzyme levels. We suggest that such occlusions occurred at the time of the infarction. Similarities in coronary anatomy between patient subgroups with angina (on exercise or at rest and nocturnal) indicate that factors other than coronary anatomy intervene in precipitating the different types of angina. Vessel disease was not related to smoking, hyperlipidaemia, or hypertension but coronary disease was manifest earlier in life in smokers or those with hyperlipidaemia.     

Intracoronary thrombolysis 3 to 13 days after acute myocardial infarction for postinfarction angina pectoris

The restoration of anterograde coronary flow long after coronary thrombosis may be of benefit to patients with continuing ischemia. To determine whether “old” intracoronary thrombi are susceptible to lysis with thrombolytic agents, 18 patients with angina at rest during evolving acute myocardial infarction (AMI) and total occlusion of the infarct vessel were treated with Intracoronary streptokinase 3 to 13 days after onset of AMI. In 12 of the 18 patients (67%), successful recanalization of the artery was achieved 6.9 ± 2.7 days after AMI. Thrombolysis was followed by coronary angioplasty in 2 patients. To evaluate the efficacy of this approach in reducing post-AMI Ischemia, the number of episodes of angina at rest was compared in patients with successful and unsuccessful attempts at recanalization. Even in patients without angioplasty, the mean number of daily episodes decreased from 1.02 ± 0.6 to 0.09 ± 0.2 in patients In whom reperfusion was achieved, and from 1.07 ± 0.8 to 0.88 ± 0.8 in those in whom it was not (p = 0.027 for the difference between the groups). Thus, in patients with early post-AMI angina, intracoronary streptokinase can restore flow in the occluded artery, may decrease the frequency of angina, and allows angioplasty to be performed.     

Arteriographic patterns early in the onset of the coronary syndromes.

Coronary arteriography in 300 patients within one year of onset of symptoms of coronary arterial disease revealed already severe anatomical coronary disease in three patient groups: those with angina pectoris alone (164 patients), with subendocardial myocardial infarction (63 patients), and with transmural myocardial infarction (73 patients). The number of vessels diseased (larger than or equal to 50% obstruction), distribution of obstruction, and degree of stenosis were similar in the three groups. However, total occlusion of at least one artery was much more common in transmural myocardial infarction and in subendocardial myocardial infarction with elevation of enzyme levels. We suggest that such occlusions occurred at the time of the infarction. Similarities in coronary anatomy between patient subgroups with angina (on exercise or at rest and nocturnal) indicate that factors other than coronary anatomy intervene in precipitating the different types of angina. Vessel disease was not related to smoking, hyperlipidaemia, or hypertension but coronary disease was manifest earlier in life in smokers or those with hyperlipidaemia.     

Evolution of myocardial ischemia and left ventricular function in patients with angina pectoris without myocardial infarction and total occlusion of the left anterior descending coronary artery and collaterals from other coronary arteries

Repeated episodes of myocardial ischemia might lead to progressive impairment of left ventricular (LV) function. This radionuclide study assessed myocardial ischemia and LV function several years after documented coronary occlusion without myocardial infarction. Over 5 years, 24 consecutive patients, who underwent cardiac catheterization for angina pectoris without myocardial infarction, had isolated total occlusion of the left anterior descending coronary artery with well-developed collateral vessels. Five patients were successfully treated by coronary bypass grafting and 3 by coronary angioplasty. Among the 16 medically treated patients, 1 was lost to follow-up and 1 died (extracardiac death). The mean (+/- standard deviation) follow-up (14 patients) was 48 +/- 15 months. At follow-up, 8 patients still had clinical chest pain, 11 received antianginal therapy, 4 patients had no stress ischemia and the other 10 had greater than or equal to 1 sign of stress ischemia. All patients had a normal LV ejection fraction at rest (mean 60 +/- 3%; range 55 to 65%). Collateral circulation preserves LV function at the time of occlusion and, in some cases, prevents the development of myocardial ischemia; in patients with persisting myocardial ischemia after well-collateralized coronary occlusion, LV function is not impaired at long-term follow-up.     

Role of coronary artery spasm in ischemic heart disease. Therapeutic implications

The term coronary artery spasm should not be used interchangeably with the specific clinical syndrome "variant angina" since it does occur in other acute and chronic ischemic heart disease syndromes. The term coronary artery spasm should not be applied to patients with ischemic heart disease unless there is clinical, angiographic, and physiologic evidence of its presence. The diagnosis of coronary artery spasm is confirmed by angiography, i.e. change in caliber of the coronary arteries plus evidence of ischemia. Probable diagnosis is in patients who have the syndrome of variant angina, i.e. rest angina associated with ST segment elevation on the electrocardiogram. One can be highly suspicious that the spasm is at work in patients who have rest angina, especially those with unstable angina. One can be suspicious of patients who have variable effort angina or walk-through angina. Coronary artery spasm is a possibility in patients with an acute myocardial infarction or acute re-infarction and is also possible that sudden death in patients with normal coronary arteries can be related to coronary artery spasm. Coronary artery spasm is the usual cause of myocardial ischemia in patients with rest angina without effort angina. This has also commonly been documented in patients with rest and effort angina. There are isolated reports suggesting that patients with effort angina pectoris also develop coronary artery spasm. Coronary artery spasm has been documented to occur in association with acute myocardial infarction. Whether coronary artery spasm is the cause or the result of myocardial infarction has not been determined at this time. However, the recent combined use of intracoronary nitroglycerin and intracoronary streptokinase in patients with acute myocardial infarction has shown reversal of totally obstructed arteries and suggests the relationship between coronary artery disease, coronary artery spasm, and in situ coronary thrombosis. The incidence of sudden death in patients with documented coronary artery spasm is unknown. But, since complete heart block and/or ventricular tachycardia occur during episodes of coronary artery spasm, it is not unreasonable to assume that some patients have died as a result of these rhythm disturbances. The prognosis of patients with coronary artery spasm seems to depend on the presence or absence of severe coronary atherosclerosis, i.e. those with severe disease have a worse prognosis. Current therapy of patients with coronary artery spasm involves the use of nitrates and calcium antagonists.(ABSTRACT TRUNCATED AT 400 WORDS)     

Results of percutaneous transluminal coronary angioplasty for unstable angina pectoris in patients 70 years of age and older

Between November 1980 and November 1985, 54 patients ages greater than or equal to 70 years underwent percutaneous transluminal coronary angioplasty for unstable angina, defined as recent-onset (less than 1 month) angina, new onset of rest angina (greater than or equal to 2 episodes) or accelerating class III or IV angina. In these 20 men and 34 women, disease was 1-vessel in 34 (63%) and multivessel in 20 (37%). The mean (+/- standard deviation) ejection fraction was 0.62 +/- 0.12. Angioplasty was successful in 43 patients (80%). In the 11 unsuccessful cases, emergency coronary artery bypass grafting for acute occlusion was performed in 3 and elective coronary artery bypass surgery in 8. There were no deaths. Two patients (4%) sustained Q-wave myocardial infarctions. The mean duration of follow-up for the total group was 37 months (6 to 73 months). Of the 43 patients with successful dilation, 4 died, 1 had an non-Q-wave myocardial infarction and 8 had symptomatic restenosis (4 underwent successful repeat angioplasty, 1 had repeat percutaneous transluminal coronary angioplasty and then bypass surgery, 1 had repeat bypass surgery alone and 2 had medical therapy). At last follow-up, 3 patients had stable class III or IV angina and 31 patients (72%) were angina-free.     

Intra-aortic balloon pumping in coronary artery disease

Cardiogenic shock and severe left ventricular failure after acute myocardial infarction, refractory angina pectoris at rest either of new onset or superimposed on stable angina pectoris, or occurring in the post infarct (less than 2 weeks) period, and the suspicion of a slowly evolving infarction are the main indications for intra-aortic balloon pumping at the Thoraxcenter. 76 patients were treated with intra-aortic balloon pumping for cardiogenic shock after acute myocardial infarction and left ventricular failure, 42/76 (55%) could be weaned, 9 (12%) died within 3 months, 33 (43%) survived over 3 months, to date 29 are alive. 42 patients with refractory angina at rest were treated with intra-aortic balloon pumping. Pain relief was prompt in 41 (98%), who subsequently underwent coronary artery bypass grafting. Total myocardial infarction rate was 11% (5/42), total mortality rate was 7%. Perioperative myocardial infarction rate was 8% (4/42) and perioperative mortality was 7% (3/42). Pain relief was prompt in 14/17 patients (82%) with post infarct refractory angina. In 3 patients pain persisted despite intra-aortic balloon pumping, all sustained a myocardial infarction, 1 died, 2 other patients were excluded for surgery. 12 patients underwent coronary artery bypass grafting, none died, none developed acute myocardial infarction, 3 have mild stable angina. In 8 patients a slowly evolving myocardial infarction was suspected. Pain relief was prompt in 7/8 (88%) after institution of intra-aortic balloon pumping. Intra-aortic balloon pumping improves prognosis in cardiogenic shock after myocardial infarction, and abolishes refractory ischemic pain.     

“Variant” angina: One aspect of a continuous spectrum of vasospastic myocardial ischemia: Pathogenetic Mechanisms, Estimated Incidence and Clinical and Coronary Arteriographic Findings in 138 Patients

From January 1970 to December 1977, transient reversible episodes of S-T segment elevation were documented in 138 patients (80 with angina only at rest, 58 with angina both on exertion and at rest). Electrocardiographic monitoring in 33 patients with hemodynamic monitoring revealed that (1) during 6,009 transient episodes of myocardial ischemia, pain was always a late phenomenon and, in some patients, often did not occur; (2) during such transient episodes, ST-T wave behavior was often variable in the same patient with alternation of elevation, depression or only T wave changes with or without pain; (3) independent of the direction of the S-T segment and T wave changes, the episodes were never preceded by an increase of the hemodynamic determinants of myocardial demand but were associated with obvious impairment of left ventricular function. Thallium scintigraphy in 32 patients revealed a regional massive and localized reduction of myocardial perfusion during S-T segment elevation and pseudonormalization of T waves. During S-T segment depression the reduction of thallium uptake was diffuse with fuzzy limits. Coronary angiography revealed no significant stenosis in 8 patients and single, double and triple vessel disease in 38, 34 and 26 patients, respectively. Angiography in all 37 patients studied during angina revealed a severe coronary vasospasm involving vessels with extremely variable extent of atherosclerosis. Severe arrhythmias were recorded in 27 patients, and a myocardial infarction occurred in 28. A total of five patients died within 1 month of hospital admission. Thus, variable intensity and extension of coronary vasospasm and the presence of collateral vessels may result in different degrees of ischemia and various electrocardiographic patterns with or without anginal pain. Vasospastic angina can occur in the presence of extremely variable degrees of coronary atherosclerosis and in any phase of ischemie heart disease. It may evolve into acute myocardial infarction and sudden death: Variant angina appears to be only its most striking electrocardiographic manifestation. When vasospastic angina is appropriately searched for, its incidence rate appears to be high.     

Nifedipine therapy for recurrent ischemic pain following myocardial infarction

The efficacy of nifedipine in relieving recurrent ischemic episodes following acute myocardial infarction was studied in 11 patients a mean of 9.2 days post infarction (range 2–42 days). Prior to infarction, all of the patients had a history of exertional angina only, yet following the infarction, episodes of recurrent ischemia occurred at rest in spite of maximal medical management with beta-blockers and/or nitrate preparations, which lowered the heart rate to a mean of 65 beats/min, and the blood pressure to a mean of 109/70 mmHg. Ischemic episodes were associated with ST-segment elevation in 7 patients and ST-segment depression or T-wave inversion in 4 patients. Coronary angiography was performed in 8 patients, and demonstrated multivessel coronary disease in 7. The episodes of rest ischemia were prevented in all but one patient by the addition of nifedipine (mean daily dose 60 mg, range 40–120 mg) without causing a change in heart rate or blood pressure. Two patients continued to have myocardial ischemia with minimal exertion, although rest pains were abolished, and they underwent coronary bypass surgery for relief of exertional pain. Only one patient continued to have episodes of ischemia at rest, although the frequency of ischemic episodes was decreased, and bypass surgery was necessary for pain relief. The other 8 patients have been managed medically for a mean of 5.4 months (range 1–12 months) and have remained pain free on combined regimens of nifedipine, beta blockers, and/or nitrate preparations. We conclude that nifedipine may be efficacious for the relief of recurrent myocardial ischemia at rest following acute infarction. In some patients nifedipine may eliminate the need for coronary artery bypass surgery and in others it may provide clinical stability prior to operation.     

Diagnostic value of ambulatory Holter monitoring for the detection of coronary artery disease in patients with variable threshold angina pectoris

Patients with chronic stable angina pectoris may present with either fixed or variable threshold symptoms. To evaluate the diagnostic value of ambulatory Holter monitoring for the detection of coronary artery disease (CAD) in patients with variable threshold angina, 216 consecutive candidates for coronary angiography were investigated prospectively. For comparison, a group of 55 consecutive patients with fixed threshold angina was studied under the same conditions. Patients with prior myocardial infarction or angiographically documented CAD were excluded. Within 4 months of Holter monitoring, the advised coronary angiography was performed in 77% of the patients with variable threshold angina and in 89% of the patients with fixed threshold angina (p less than 0.05). The prevalence of CAD was markedly lower in patients with variable threshold angina compared to patients with fixed threshold angina (54 vs 90%, p less than 0.001). CAD patients of both subgroups, however, did not differ significantly with respect to the number of obstructed vessels, the Gensini coronary score, the number with impaired left ventricular function (ejection fraction less than 50%) or the duration of ischemic episodes during Holter monitoring. Diagnostic accuracy of Holter monitoring did not differ between variable and fixed threshold angina groups (67 vs 78%). In 91% of the patients results obtained by Holter monitoring could be compared to the results of a bicycle stress test. In patients with fixed threshold angina the diagnostic accuracy was similar for both tests (80 vs 80%). In patients with variable threshold angina, the diagnostic accuracy of Holter monitoring exceeded that of the exercise stress test (68 vs 55%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Follow up results of treatment of unstable angina by coronary angioplasty.

Eighty nine of 327 consecutive patients undergoing coronary angioplasty at a centre had unstable angina--defined as either a worsening of the frequency or the severity of chest pain or severe episodes of chest pain at rest with no evidence of acute myocardial infarction. Multivessel disease was present in 31 of these patients. Two or more vessels were dilated in the same procedure in one fifth of the patients. Primary success was obtained in 80 (90%) patients. Acute myocardial infarction was a complication in four (5%) patients, including two of four patients who needed emergency coronary bypass grafting. Follow up coronary angiography at a mean (SD) of 10 (6) months in 57 patients showed restenosis in 21 (37%): of these, 13 patients had repeat coronary angioplasty and three had elective coronary bypass grafting. All patients in whom angioplasty was initially successful were followed up for 10 (6) months after the last angioplasty procedure. There were no deaths. One patient had sustained a myocardial infarction unrelated to the dilated vessel. Clinically, 74 patients improved by at least one New York Heart Association class and 40 (50%) were symptom free and with no signs or symptoms of myocardial ischaemia on a stress test. Coronary angioplasty offers long term symptomatic improvement at an acceptable risk in the majority of patients with unstable angina.     

Segmental analysis of coronary arterial stenoses in patients presenting with angina or first myocardial infarction.

The segmental distribution of stenoses within the coronary arteries was analysed in a population of 258 patients with a first myocardial infarction undergoing coronary angiography to evaluate the effect of thrombolytic therapy, and in a population of 466 patients undergoing elective coronary angiography for stable angina. Mean ages were 53.7 and 56.7 years respectively (P = NS). As judged angiographically, coronary arterial disease was more extensive in the group suffering angina, with a greater proportion of patients with two- or three-vessel disease (odds ratio 2.56, 95% confidence interval 1.87 to 3.52) and more patients having stenoses in two or more coronary arterial segments (odds ratio 1.52, 95% confidence interval 1.12 to 2.08). For each coronary vessel, the probability of finding a stenosis greater than 50% in an individual segment was greater in the group presenting with angina. There was a relative deficiency of stenoses within the main stem of the left coronary artery or its proximal left anterior descending branch among the patients suffering myocardial infarction. Within those having angina, subgroups were identified with "isolated" and "diffuse" coronary arterial disease: the latter patients tended to have a lower concentration of total cholesterol in the serum, but an increased prevalence of diabetes mellitus. Patients presenting clinically with a first myocardial infarction, and patients with severe angina, constitute distinct populations selected by different mechanisms from the overall pool of patients with atheromatous coronary arterial disease.     

Repeat coronary angioplasty as treatment for restenosis.

Repeat coronary angioplasty has become the standard approach to a first restenosis. However, the long-term outcome of such a strategy is not well defined. In the present study, 465 patients (mean age 58 years [range 27 to 79], 53% with multivessel disease) underwent a second angioplasty procedure at the same site. The procedure was successful in 96.8% with a 1.5% rate of in-hospital bypass surgery, a 0.9% incidence rate of myocardial infarction and no procedural deaths. Four hundred sixty-three patients (99.6%) were followed up for a mean of 40.5 months. Forty-nine patients (10.6%) underwent a third angioplasty procedure at the same site, 55 (11.8%) had coronary bypass surgery and 33 (7.1%) underwent angioplasty at a different site. During follow-up, 12 patients (2.6%) sustained a myocardial infarction and 21 (4.5%) died including 13 (2.8%) with cardiac death. Of the 442 surviving patients, 88% experienced sustained functional improvement and 78% were free of angina. The actuarial 5-year cardiac survival rate was 96% and the rate of freedom from cardiac death and myocardial infarction was 92%. For the subgroup of 49 patients who had a third angioplasty procedure at the same site, the success rate was 93.9% with a 2% incidence rate of myocardial infarction. There were no in-hospital deaths or coronary artery bypass operations. The mean follow-up interval for this subgroup was 30.5 months with a 22.4% cross-over rate to coronary bypass surgery, a 4.1% incidence rate of myocardial infarction and a 2% cardiac mortality rate. At last follow-up, 89% of patients had sustained functional improvement and 76% were free of angina. The combined angiographic and clinical restenosis rate was 48%. Repeat angioplasty as treatment for restenosis is an effective approach associated with a high success rate, low incidence of procedural complications, and sustained functional improvement in combination with an acceptable rate of bypass surgery. However, there is a trend toward diminished angioplasty efficacy after a second restenosis. Thus, decisions for further revascularization should be made after careful review of available options.     

The value of amiodarone for the treatment of unstable angina

Amiodarone is a potent coronary vasodilator; it has alpha and beta receptor-antagonist activity and is well-known for its marked antiarrhythmic efficacy. This report describes the results of a randomized study of amiodarone in unstable angina. 40 patients (33 male, 7 female; mean age: 55) with unstable angina entered the study. They were randomized into two treatment groups. In group I (20 cases), amiodarone was the first drug applied (during the first 3 days; 1500 mg/24 hours IV + 200 mg orally every 8th hour; from day 4 onwards: 200 mg orally 3 times daily). If, after 8 hours following initiation of treatment, the symptoms were still present or recurred, nifedipine was added at a dose of 10 mg 4 times daily. In case of failure of the combined medical treatment, coronary angiography and, if needed, surgery was performed after 16 hours. In group II (20 cases), nifedipine was given as the first drug and at a dose of 10 mg every 6th hour. If, after 8 hours, this therapy failed, amiodarone was added according to the scheme previously described. In case of failure of the combined therapy, coronary angiography and surgery were performed. In group I, amiodarone was successful within 8 hours in 12 cases. None of the non-responders was improved by the addition of nifedipine. In group II, nifedipine was successful within 8 hours in 6 cases (p = 0.086). Among the 14 non-responders, amiodarone controlled the anginal episodes in 11 instances (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Relative contributions of a single-admission 12-lead electrocardiogram and early 24-hour continuous electrocardiographic monitoring for early risk stratification in patients with unstable coronary artery disease

Patients with unstable coronary syndromes are a heterogeneous group with varying degrees of ischemia and prognosis. The present study compares the prognostic value of a standard electrocardiogram (ECG) obtained at admission to the hospital with the information from 24-hour continuous electrocardiographic monitoring obtained immediately after admission. The admission ECGs and 24 hours of vectorcardiographic (VCG) monitoring from 308 patients admitted with unstable coronary artery disease were analyzed centrally regarding standard electrocardiographic ST-T changes, ST-vector magnitude (ST-VM), and ST change vector magnitude episodes. End points were death, acute myocardial infarction, and refractory angina pectoris within a 30-day follow-up period. ST-VM episodes (> or = 50 microV for > or = 1 minute) during VCG monitoring was the only independent predictor of death or acute myocardial infarction by multivariate analysis. ST-VM episodes during vectorcardiography was associated with a relative risk of 12.7 for having a cardiac event, hypertension was associated with a relative risk of 1.7, and ST depression on the admission ECG was associated with a relative risk of 5.7. Patients with ST depression at admission had an event rate (death or acute myocardial infarction) of 17% at 30-day follow-up. Patients without ST depression could further be risk stratified by 24 hours of VCG monitoring into a subgroup with ST-VM episodes at similar (8%) risk and a subgroup without ST-VM episodes at low (1%) risk (p = 0.00005). Continuous VCG monitoring provides important information for evaluating patients with unstable coronary artery disease. It is recommended that patients not initially estimated at high risk based on the admission ECG are referred for 24 hours of VCG monitoring for further risk stratification.