Unstable Symptoms Research Articles

Prior aspirin use in unstable angina predisposes to higher risk: the aspirin paradox

Background: Aspirin is the most widely prescribed agent used in prevention of coronary thrombosis. Thus, many patients presenting with acute coronary syndromes have a history of aspirin usage. Methods: To assess response to medical therapy in patients taking aspirin prior to admission with an acute coronary syndrome, we reviewed outcomes data from the Efficacy and Safety of Subcutaneous Enoxaparin in Non-Q-wave Coronary Events (ESSENCE) and Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS) studies. Results: Patients with acute coronary syndromes who had taken aspirin prior to enrolment were less likely to have non-Q-wave myocardial infarction on admission (ESSENCE: 16.0% vs. 29.2%, p<0.001; PRISM-PLUS: 34.2% vs. 57.7%, p<0.001). However, prior aspirin users were more likely to be failed by standard medical therapy with unfractionated heparin than non-prior aspirin users (ESSENCE: 21.5% vs. 16.5%, p=0.017; PRISM-PLUS: 23.5% vs. 12.1%, p<0.001). Prior aspirin users received greater benefit from both enoxaparin (21.5% vs. 16.8%, p=0.009) and tirofiban with unfractionated heparin (23.5% vs. 16.0%, p=0.007) than from unfractionated heparin alone. Non-prior aspirin users presented with higher rates of non-Q-wave myocardial infarction. Conclusions: Prior aspirin users admitted with acute coronary syndromes may have a more benign presentation, but are more likely to be failed by medical therapy with unfractionated heparin and should be considered as a high-risk group. Enoxaparin or the combination of tirofiban and unfractionated heparin are both more effective than unfractionated heparin in this group.

A risk score system for predicting adverse outcomes and magnitude of benefit with glycoprotein IIb/IIIa inhibitor therapy in patients with unstable angina pectoris

Clinical outcomes of patients with unstable angina are variable. We sought to identify predictors of adverse clinical outcomes in patients with unstable angina and to investigate whether these factors would predict the magnitude of benefit achieved with platelet glycoprotein IIb/IIIa inhibition. We analyzed 20 variables in the 1,915 patients enrolled in the Platelet Receptor Inhibition for Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms trial. Five independent predictors were identified: age >65 years, prior coronary artery bypass grafting, antecedent aspirin use, antecedent β-blocker use, and ST depressions on the presenting electrocardiogram. A risk score system was created using these predictors in which patients were assigned 1 point for the presence of each risk factor. There was a progressive increase in the rate of the composite end point of death, myocardial infarction, or refractory ischemia at 7 days with an increasing number of risk factors. For patients treated with heparin alone, the composite end point event rate was 6.5% in the group with 0 or 1 predictor, 14.6% in the group with 2 predictors, 22.7% in the group with 3 predictors, and 37.1% in the group with 4 or 5 predictors (p <0.00001). When dividing patients into low- (0 or 1 point), medium- (2 or 3 points), and high-risk (4 or 5 points) groups, the addition of tirofiban to heparin therapy was associated with no significant benefit in the low-risk group, a 5.2% absolute reduction in the medium-risk group (p = 0.05), and a 16% absolute reduction in the high-risk group (p = 0.0055). Thus, we have developed a risk score system using 5 variables that can be used to identify patients at high risk for death and cardiac ischemic events and who experience the greatest benefit from the addition of a glycoprotein IIb/IIIa inhibitor to their treatment regimen.

Upstream use of tirofiban in patients admitted for an acute coronary syndrome in hospitals with or without facilities for invasive management

Management and prognosis of acute coronary syndromes may be influenced by the availability of catheterization facilities at admitting hospitals. Treatment effects of tirofiban were examined in a Canadian cohort of 834 patients enrolled in the Canadian Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS) trial according to admission into hospitals without (n = 322) or with catheterization facilities (n = 512). Hospital transfers for cardiac catheterization were facilitated using preexisting networks accelerated for the purposes of the protocol. In hospitals without facilities, the relative risks for occurrence of death, infarction, or refractory ischemia among patients receiving tirofiban plus heparin compared with heparin alone were 0.52 at 7 days (p = 0.02), 0.59 at 30 days (p = 0.03), and 0.70 at 180 days (p = 0.09); and for death or infarction, 0.32 (p = 0.02), 0.46 (p = 0.04,) and 0.51 (p = 0.03), respectively. Benefit was seen regardless of transfer status, with no statistically significant interaction between treatment, hospital type, and catheterization for any end point at any time point. The incidence of Thrombolysis In Infarction defined major bleeding with respect to therapy was not significantly different between hospital types. Thus, upstream treatment with tirofiban plus heparin confers clinical benefits in unstable angina and/or non–ST-segment elevation infarction patients regardless of whether initial presentation is to a hospital without catheterization facilities or to a hospital with such facilities.

Safety profile of tolterodine as used in general practice in England: results of prescription-event monitoring.

Unstable bladder symptoms are a common problem in general practice. Drug therapy with anticholinergic drugs is frequently used in the management of this condition. However such drugs are associated with a high incidence of anticholinergic adverse effects. Tolterodine is a competitive anticholinergic agent, selective for the bladder as opposed to the salivary glands. To monitor the safety of tolterodine as used in general practice patients in England for the treatment of urinary frequency, urgency and incontinence. Prospective observational cohort study. 14,526 patients [mean age 62.7 (SD 16.4) years; 68.6% female]. Patients prescribed tolterodine in general practice, soon after the release of the drug in the UK, were followed up for a minimum of 6 months using the technique of prescription-event monitoring (PEM). The most common adverse events reported were dry mouth, headache, malaise, constipation, dyspepsia, nausea and vomiting and pain in abdomen. We identified some uncommon events as possible adverse drug reactions--notably hallucinations, tachycardia and palpitations. The prevalence of these events was compared with that in patient cohorts for other drugs on the PEM database. The age- and sex-adjusted relative risk of hallucinations on tolterodine compared with 10 drugs of other therapeutic classes, and with terodiline, another drug indicated for bladder instability, was 4.85 [95% confidence interval (CI) 2.72 to 8.66] and 1.25 (95% CI 0.62 to 2.53), respectively. There was no significant difference for tachycardia/palpitation in this comparison. Tolterodine is well tolerated in general practice at the recommended daily dose. Hallucinations, tachycardia and palpitations are infrequently associated with the drug.

Hyperinsulinemia, lipoprotein (a), and Chlamydia pneumoniae antibodies--are they risk factors or serologic predictors for progression of coronary artery disease?

The authors studied 134 patients with unstable angina pectoris symptoms and 32 subjects without coronary artery disease (CAD) for the presence of classical risk factors such as hypercholesterolemia, smoking, and family history of CAD. In addition they analyzed plasma insulin levels, lipoprotein (a) (Lp [a]) levels, and antibody titers against Chlamydia pneumoniae. All patients had a heart catheterization. Patients with diabetes mellitus were excluded from the study. Fasting insulin, low-density lipoprotein (LDL) cholesterol and Chlamydia pneumoniae immunoglobulin G (IgG) and IgA antibody titers did not show any difference in CAD from healthy control subjects, whereas Lp(a) was increased and high-density lipoprotein (HDL) decreased in CAD patients. These data indicate that lipoprotein (a), low HDL cholesterol, and smoking, but neither hyperinsulinemia nor elevated Chlamydia pneumoniae titers, are risk factors or predictors for CAD.

Effects of tirofiban plus heparin versus heparin alone on troponin i levels in patients with acute coronary syndromes

Elevated serum troponins following an acute coronary syndrome (ACS) predict a poor clinical outcome. Glycoprotein (GP) IIb/IIIa inhibitors reduce adverse clinical outcomes in patients with ACS, although their effect on serum troponin I (TnI) in this setting has not been described. We therefore studied the effects of the GP IIb/IIIa inhibitor tirofiban on serum TnI levels in a group of patients in the Platelet Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms trial. Serial blood samples were obtained in 53 patients receiving the combination therapy of tirofiban/heparin and in 52 receiving heparin alone, and were analyzed for baseline, peak, and mean concentrations of TnI. Baseline TnI levels were not different between the combination therapy and heparin-only groups (1.6 ± 3.0 vs 3.1 ± 6.7 ng/ml, p = 0.15). The peak TnI level was significantly lower in the combination therapy group than in the heparin group (5.2 ± 8.3 vs 15.5 ± 29.1 ng/ml, p = 0.017), and mean levels over the initial 24-hour period were also significantly lower in the combination therapy group (3.2 ± 5.0 vs 8.5 ± 14.8 ng/ml, p = 0.016). In univariate analysis, combination therapy was associated with lower TnI levels, whereas in a multivariate model, the lower peak and mean TnI levels as a consequence of tirofiban/heparin compared with heparin monotherapy remained significant (peak, p = 0.029; mean, p = 0.035). Among patients with negative TnI at baseline, treatment with the combination of tirofiban/heparin compared with heparin monotherapy still resulted in significantly lower peak (2.5 ± 5.4 vs 14.6 ± 32.8 ng/ml, p = 0.024) and mean (1.2 ± 2.6 vs 6.9 ± 15.8 ng/ml, p = 0.029) TnI levels. In patients with ACS, therapy with the combination of tirofiban and heparin (compared with heparin treatment alone) resulted in lower serum TnI levels, suggesting reduced myocardial injury.

Endothelial dysfunction, subangiographic atheroma, and unstable symptoms in patients with chest pain and normal coronary arteriograms.

Patients with chest pain and normal coronary arteriograms (CPNA) may present with unstable symptoms and other evidence of ischemia during clinical follow-up. Although repeat angiography usually proves negative, functional assessment of coronary vasomotor abnormalities may provide additional pathophysiologic information. The study was undertaken to evaluate the relationship between endothelial dysfunction and subangiographic atheroma in patients with CPNA undergoing repeat angiography because of unstable symptoms. We investigated nine patients with CPNA (8 women, mean age 57 +/- 9 years) undergoing repeat angiography because of unstable anginal symptoms. After normal angiography, simultaneous coronary epicardial and microvascular vasomotor responses to intracoronary vasodilators [acetylcholine (10(-6) M), adenosine (18 micrograms) and nitroglycerin (300 micrograms)] were investigated in the left anterior descending artery using quantitative angiography and Doppler flow measurements. The presence of subangiographic atheroma was assessed by intravascular ultrasound. Three patients demonstrated proximal and distal epicardial vasoconstriction and a reduction in coronary flow in response to acetylcholine, indicating concordant epicardial and microvascular endothelial dysfunction. These changes were associated with chest pain and ischemic electrocardiographic changes in two patients. None of the remaining patients suffered chest pain in response to intracoronary acetylcholine. Six patients had significant subangiographic disease (intimal thickness > 0.3 mm) on intravascular ultrasound imaging, and multivariate analysis indicated a significant relationship (R2 = 0.89, overall p = 0.001) between the extent of subangiographic disease and both plasma cholesterol concentration and hypertensive history. No significant relationship was demonstrated between endothelial dysfunction and the extent of subangiographic disease. Concordant epicardial and microvascular endothelial dysfunction may be pathophysiologically and clinically significant in unstable patients with CPNA but does not appear to be directly related to the extent of subangiographic atheroma.

Prodromal unstable angina in acute myocardial infarction: Prognostic value of short- and long-term outcome and predictor of infarct size

Background An estimated 50% of patients with myocardial infarction have prodromal unstable angina. There is controversy over whether prodromal unstable angina identifies a group of patients at lower risk of short- and long-term death and the clinical importance of recording this event. Methods Of 207 patients enrolled at a single Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) site, 196 survived the 24 hours after presentation, achieved peak creatine kinase MB concentrations, and were classified as having either abrupt symptom onset or prodromal unstable angina in the 2 weeks before myocardial infarction. Creatine kinase MB peak was used to categorize infarct size as aborted myocardial infarction, minor myocardial damage, or extensive myocardial injury. Follow-up was performed at 24 hours, 30 days, 1 year, and 5 years. Multiple variables, including prodromal unstable angina, time to treatment, age, sex, previous infarction and infarct location, were analyzed for predicting infarct size. Also, these variables plus peak creatine kinase MB level and a combined variable of prodromal unstable angina and peak creatine kinase MB level were examined for predicting survival. Results Mortality rate was 2.5% within 24 hours, 9.0% at 30 days, 13.5% at 1 year, and 27.1% at 5 years. Patients categorized as either aborted infarction or minor myocardial damage were significantly more likely to have prodromal unstable symptoms (81.3% vs 51.2%, P <.001) and better survival at each follow-up period. Prodromal presentation was the most significant predictor of infarct size category (P =.001). Five-year survival was predicted by age (P <.0001), peak creatine kinase MB level (P =.007), infarct location (P =.009), the combined variables (P =.029), and prodromal unstable angina (P =.017). Prodromal unstable angina had the highest odds ratio for 5-year survival at 3.83 (95% confidence interval 1.27-11.47). Conclusions Prodromal unstable angina is a strong predictor of infarct size and survival. Recognizing prodromal unstable angina is important for clinically assessing prognosis. (Am Heart J 2000;140:126-33.)

Stenting the stent: initial results and long-term clinical and angiographic outcome of coronary stenting for patients with in-stent restenosis

Stent restenosis constitutes a therapeutic challenge affecting an increasing number of patients. Conventional angioplasty and debulking techniques are currently used in these patients. However, the potential role of a second stent implantation in this setting (stenting the stent) remains unknown. Therefore, 65 consecutive patients (12 women, aged 62 ± 11 years) undergoing stent implantation (42 elective and 23 unplanned) for the treatment of in-stent restenosis (diffuse [>10 mm] in 39 [60%]) were studied. Angiographic success was obtained in all patients. Three patients developed hospital complications: 1 died from refractory heart failure and 2 suffered non–Q-wave myocardial infarctions. During follow-up (mean 17 ± 11 months) 1 patient died (noncardiac cause) and only 9 (14%) required target vessel revascularization. Kaplan-Meier event-free survival (freedom from death, myocardial infarction, and target vessel revascularization) at 1 year was 84%. Using Cox analysis, patients with unstable symptoms, a short time to stent restenosis, nonelective stenting, and B2-C lesions tended to have poorer prognosis. After adjustment, nonelective stenting was associated (adjusted RR 2.9, 95% confidence interval [CI] 0.82 to 10.3, p = 0.09) with an adverse clinical outcome. On quantitative angiography (core lab) restenosis was found in 13 of 43 patients (30%) (75% of those eligible). Logistic regression analysis identify restenosis length (adjusted RR 1.43, 95% CI 1.04 to 2.14, p = 0.04), and time to restenosis (adjusted RR 0.67, 95% CI 0.47 to 0.94, p = 0.01) as the only independent predictors of recurrent restenosis. Thus, repeat coronary stenting is a safe and efficacious strategy for the treatment of patients with in-stent restenosis. Both elective and nonelective stenting provide excellent initial results. The long-term clinical and angiographic outcome of these patients is also favorable.

CIRCADIAN RHYTHM IN PEAK EXPIRATORY FLOW: ALTERATION WITH NOCTURNAL ASTHMA AND THEOPHYLLINE CHRONOTHERAPY*

We investigated changes in the circadian rhythm of peak expiratory flow (PEF) in seven persons with nocturnal asthma for a 24h span when (1) they were symptom free and their disease was stable, (2) their asthma deteriorated and nocturnal symptoms were frequent, and (3) they were treated with theophylline chronotherapy. Subjects recorded their PEF every 4h between 07:00 and 23:00 one day each period. Circadian rhythms in PEF were assessed using the group-mean cosinor method. The circadian rhythm in PEF varied according to asthma severity. Significant circadian rhythms in PEF were detected during the period when asthma was stable and when it was unstable and nocturnal symptoms were frequent. When nocturnal symptoms were present, the bathyphase (trough time) of the PEF rhythm narrowed to around 04:00; during this time of unstable asthma, the amplitude of the PEF pattern increased 3.9-fold compared to the symptom-free period. No significant group circadian rhythm was detected during theophylline chronotherapy. Evening theophylline chronotherapy proved to be prophylactic for persons whose symptoms before treatment had occurred between midnight and early morning. Changes in the characteristics of the circadian rhythm of PEF, particularly amplitude and time of bathyphase, proved useful in determining when to institute theophylline chronotherapy to avert nocturnal asthma symptoms. (Chronobiology International, 17(4), 513–519, 2000)

Chest pain centers: moving toward proactive acute coronary care

Ischemic heart disease is the major cause of death, disability and lost productivity in the developed countries of the world. The evolution of cardiac care units has improved patient survival from myocardial infarctions, but requires a high-tech, very expensive treatment facility. Chest pain centers, located in emergency departments, present an efficient alternative to triage patients with chest pain, providing prompt and accurate diagnosis, risk evaluation and appropriate treatments. Hospitals benefit from this cost-effective approach as resources are used more efficiently, and patients benefit from a supportive treatment facility that focuses on early intervention. Early recognition of prodromal unstable angina symptoms and intercession with newly developed treatment can help move the cardiologist toward a more proactive role that minimizes or avoids myocardial infarctions rather than reacting to the acute event.

Newer antiplatelet agents in acute coronary syndromes

Aspirin is accepted as standard therapy in the management of acute coronary syndromes, but has significant limitations, including intolerance, allergy, resistance, peptic ulceration, and intracranial hemorrhage. Recent trials involving approximately 18,000 patients with unstable angina have investigated the efficacy and safety of glycoprotein IIb/IIIa receptor antagonists, which block the final common pathway of platelet aggregation. The Platelet Receptor Inhibition in Ischemic Syndrome Management (PRISM) trial compared tirofiban with heparin and found a 33% reduction in the composite end point of death, myocardial infarction, or refractory ischemia at 48 hours. In the Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS) trial, patients were randomly assigned to receive either heparin, tirofiban, or both. At 7 days, the patients who had received heparin and tirofiban had a 34% lower incidence of the composite end point of death, myocardial infarction, or refractory ischemia than those treated with heparin alone. The Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial randomly assigned patients to receive either eptifibatide or placebo. At 30 days, the rate of death or myocardial infarction was reduced by 9.6% in the eptifibatide group compared with the placebo group. In the Platelet IIb/IIIa Antagonism for the Reduction of Acute Coronary Syndrome Events in a Global Organization Network (PARAGON) trial, patients were randomly assigned to receive either low- or high-dose lamifiban with or without heparin, or heparin alone. There were no differences between the treatment groups at 30 days, but at 6 months the patients randomly assigned to receive low-dose lamifiban had a 23% lower incidence of death or myocardial infarction, perhaps because of long-term passivation of the plaque. Overall, IIb/IIIa antagonists have been shown to be safe and beneficial in patients with unstable angina, particularly during the infusion period. However, there remain a number of unanswered questions concerning treatment with these agents, such as the appropriate dosing regimens and the safety and efficacy of combining intravenous antiplatelet therapy with other agents such as low-molecular-weight heparin, thrombolytic agents, and oral agents. (Am Heart J 1999;138:S570-S576.)

Late Thrombosis After Radiation

Five years after Condado et al1 first treated human coronary arteries with brachytherapy, there is ongoing clinical investigation into its safety and efficacy in preventing restenosis. As with any novel technique, unexpected complications may dampen early high expectations and result in pessimism and skepticism. However, time, experience, and complete data analysis will determine the reality. Costa and coworkers2 may be reacting prematurely by reporting a new phenomenon in interventional cardiology entitled “late, sudden thrombosis after PTCA plus radiotherapy.” They report 6 (6.6%) of 91 patients who presented with late total occlusion/thrombosis at angiographic follow-up; these patients were enrolled into different radiation protocols using different β-emitters at different prescribed doses. Late total occlusion or late thrombosis is a valid concern, especially when associated with acute myocardial infarction (MI). However, can we really draw any conclusion from 6 heterogeneous case reports taken from a small cohort of patients in the absence of a control group? Is this announcement based on too few data, and is it premature? An editorial based on a Brief Rapid Communication mandates the editorialist to gather additional information, disclose his own insights, and provide the readers (the jury in this case) with as much information as possible. Acute thrombosis occurs during or early after intervention, and subacute thrombosis occurs within the subsequent 30 days. Both usually present with unstable symptoms and angiographic evidence of thrombus. However, the definition of late thrombosis may be problematic. It may not present with symptoms. It may be detected only when follow-up angiography shows a late total occlusion, which could also be the result of progressive intimal hyperplasia. Late total occlusion/thrombosis should be defined as any angiographically documented total occlusion >30 days after the procedure. For patients who have a patent treatment site at 6 months and subsequently develop a total …

Perioperative morbidity and mortality after transmyocardial laser revascularization: incidence and risk factors for adverse events

OBJECTIVESThe purpose of this study was to describe the incidence and spectrum of perioperative cardiac and noncardiac morbidity and mortality after transmyocardial laser revascularization (TMR) and to identify predictors of these adverse clinical events.BACKGROUNDClinical studies have demonstrated the efficacy of TMR for relieving angina pectoris, although no study to date has specifically addressed the associated perioperative morbidity and mortality.METHODSBetween October 1995 and August 1997, 34 consecutive patients with end-stage coronary artery disease (CAD) underwent isolated TMR. The majority of patients (94%) had class III or IV angina pectoris, and two patients (6%) had unstable symptoms preoperatively. Patient records were reviewed for fatal and nonfatal adverse cardiac and noncardiac events.RESULTSPerioperative death occurred in two patients (5.9%) due to cardiogenic shock complicating acute myocardial infarction. Perioperative cardiac morbidity occurred in 16 patients (47.1%); noncardiac morbidity was seen in 12 patients (35.3%). Preoperative unstable angina was the only variable predictive of perioperative death (p = 0.005). Cardiac (p = 0.005) and noncardiac (p < 0.001) morbidity rates were significantly higher for the initial 15 patients undergoing the procedure. Other predictors of perioperative complications included lack of postoperative treatment with a furosemide infusion (p ≤ 0.04) and preoperative unstable angina (p = 0.05).CONCLUSIONSPerioperative mortality in patients undergoing isolated TMR is low. Transmyocardial laser revascularization patients are at higher risk for adverse perioperative cardiac and noncardiac events, likely reflecting the lack of immediate benefit from the procedure in the setting of severe CAD. These patients merit vigilant surveillance for adverse events and aggressive medical management in the perioperative period.

Current Evidence For The Use Of Platelet Gpiib/iiia Receptor Inhibitors In Acute Coronary Syndromes

Current Evidence For The Use Of Platelet Gpiib/iiia Receptor Inhibitors In Acute Coronary Syndromes

Tirofiban plus heparin was more effective than heparin alone for unstable angina and non-Q-wave MI

Source Citation The Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS) Study Investigators. Inhibition of the platelet glyc...

Angiographic progression in patients with angina pectoris and normal or near normal coronary angiograms who are restudied due to unstable symptoms.

Syndrome X patients commonly remain symptomatic during follow-up and may be readmitted with unstable anginal symptoms. Angiographic disease progression must be considered as a possible mechanism for instability, particularly where multiple coronary risk factors are present and an interval of several years has elapsed since previous angiography. We reviewed data from 139 consecutive patients with chest pain and normal or near normal coronary angiograms (101 patients with completely normal angiograms and 38 patients with minimal lumenal irregularities). During a 5-year period, 24 patients (19 women, median age 56 years) underwent repeat angiography due to primary unstable angina (median interval between angiograms 58 months (range 8-130 months)). This group included three patients with minimal lumenal irregularities and four patients with left bundle branch block. Only two patients had progression to significant angiographic stenosis (> 30% diameter reduction); both were male patients with minimal irregularities at baseline angiography, left bundle branch block and multiple coronary risk factors. However, overall only two of 18 (11%) patients with one or more conventional coronary risk factors had angiographic progression. Unstable symptoms in patients with chest pain and previously normal or near normal coronary arteriograms are rarely due to angiographic disease progression. However, the presence of minimal lumenal irregularities at baseline angiography and LBBB may identify a sub-group at increased risk.

Acute coronary syndromes: unstable angina and non-Q-wave myocardial infarction.

Ischemic heart disease includes a wide spectrum of conditions, ranging from silent ischemia and exertion-induced angina, through unstable angina, to acute MI. Unstable angina occupies the center of this spectrum, causing disability and risk greater than that of chronic stable angina but less than that of acute MI1 (Fig 1⇓). Although non–Q-wave MI for many years was considered prognostically similar to unstable angina, recent longitudinal studies indicate that it is similar to Q-wave infarction2 3 (Fig 2⇓). Figure 1. Cumulative 6-month mortality from ischemic heart disease. Diagnosis on admission to hospital (n=21 761; 1985 to 1992). From Duke Cardiovascular Database. Reproduced with permission from Reference 1. Figure 2. Top, Cumulative 1-year combined death or MI among patients with Q-wave and non–Q-wave MI treated with fibrinolysis. Reproduced with permission from Reference 2. Bottom, Risk of subsequent cardiac events in stable convalescing patients after first non–Q-wave and Q-wave MI. Reproduced with permission from Reference 3. The concept of unstable angina has emerged from observations of frequent symptoms preceding acute MI, followed by prospective documentation that unstable symptoms frequently culminated in acute MI. The syndrome was rapidly accepted as a well-defined clinical entity as specific clinical manifestations, pathophysiological mechanisms, laboratory findings, and treatment became better characterized. Unstable angina is currently one of the leading causes of hospital admission for CAD, and non–Q-wave MI accounts for >30% of admissions for acute MI.1 4 Yet, the diagnosis of unstable angina remains clinical, based on symptom recognition. The physician caring for patients with unstable angina is in a privileged position of recognizing rapidly evolving CAD and being able to intervene to prevent irreversible left ventricular damage and progression of CAD. Unstable angina is classically described as a heterogeneous disease, referring to a wide spectrum of clinical manifestations from stable angina to MI, of disease …

Angiographic Disease Progression in Patients With Angina Pectoris and Normal Coronary Angiograms who Are Restudied due to Unstable Symptoms

Angiographic Disease Progression in Patients With Angina Pectoris and Normal Coronary Angiograms who Are Restudied due to Unstable Symptoms

Angiographic disease progression in patients with angina pectoris and normal coronary angiograms who are restudied due to unstable symptoms

Angiographic disease progression in patients with angina pectoris and normal coronary angiograms who are restudied due to unstable symptoms