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PubMed2000

[New thrombocyte aggregation inhibitor in therapy of unstable angina].

Unstable angina is a critical phase of coronary heart disease with a risk for myocardial infarction or death of up to 20% within 30 days. Glycoprotein IIb/IIIa antagonists are a new class of potent antiplatelet drugs. In several large randomized trials, it has been well established that the antibody abciximab, and the low molecular synthetic compounds tirofiban and eptifibatide, reduce the cardiac event rate by 10 to 70% in patients with and without percutaneous interventions. This effect was found to be predominately present in patients with elevated troponins. Accordingly, glycoprotein IIb/IIIa antagonists represent a major achievement for the treatment regimen of patients with unstable angina.

Abciximab↗

PubMed2002

Low molecular weight heparins in the treatment of unstable angina.

Unstable angina is in most cases caused by partial or complete coronary artery occlusion due to the disruption of an atherosclerotic plaque and resultant thrombus formation. Platelet aggregation and thrombin formation are key events in the development of acute coronary syndromes. An immediate antithrombotic approach is essential to prevent fatal and non-fatal myocardial infarction, and the combination of aspirin and unfractionated heparin has been the treatment of choice in the past years. Low molecular weight heparins have improved pharmacokinetic and pharmacodynamic properties over unfractionated heparin that have resulted in greater efficacy and safety in the field of venous thromboembolism. Low molecular weight heparins can be administered by subcutaneous injections at fixed, weight adjusted doses without need for monitoring. Three low molecular weight heparins have been tested in adequately sized clinical trials in patients with unstable angina and non-Q-wave myocardial infarction: nadroparin, dalteparin and enoxaparin. The results of the published trials have confirmed that the newer compounds are at least as safe and effective as unfractionated heparin offering considerable practical and clinical advantages. Low molecular weight heparins are currently recommended as alternative to unfractionated heparin in the acute management of acute coronary syndromes. Nevertheless, the different properties of these compounds and possibly the different designs of the clinical trials have resulted in apparent differences in clinical outcomes with the different agents. Direct comparisons are now required to determine the superiority of one compound over another.

Angina, Unstable↗

PubMed1986

Therapeutic choices in unstable angina.

Unstable angina pectoris is a high-risk ischemic syndrome with complex, interacting pathophysiologic mechanisms that include coronary atherosclerosis, coronary vasoconstriction, and thrombosis. The roles of various medical strategies, including nitrates, beta blockers, calcium antagonists, and antiplatelet, anticoagulant, and thrombolytic agents, are discussed in conjunction with revascularization procedures such as coronary angioplasty and bypass surgery.

Adrenergic beta-Antagonists↗

PubMed1989

Calcium antagonists in the treatment of Prinzmetal's angina and unstable angina pectoris.

Calcium antagonists block the entry of calcium into vascular smooth muscle cells, producing pharmacological vasodilation. Thus, it is not surprising that these drugs are effective in treating unstable angina that is often characterized by increased vasomotion and dynamic obstruction at the site of atheromatous plaques. Nifedipine, diltiazem, and verapamil are all highly and equally effective in reducing painful and painless ischemic episodes in Prinzmetal's variant angina. In patients with unstable angina who have known or suspected significant underlying coronary artery disease, a multipharmacological approach to therapy is warranted. Nifedipine used with beta-blocker drugs is more effective than nifedipine as monotherapy. Diltiazem and verapamil have been shown to be effective when given without beta-blockers in unstable angina patients. In many patients, thrombus formation rather than vasospasm is the major pathophysiological event resulting in progression of the syndrome to infarction or sudden death. In these patients, antiplatelet, antithrombotic, or antiplatelet and antithrombotic therapy is of utmost importance to maintain adequate coronary flow. Nonresponders to medical therapy with unstable angina have a high prevalence of eccentric and multiple coronary stenoses with a high incidence of thrombi. The best responders to calcium antagonist therapy are patients with concentric coronary stenoses. In summary, calcium antagonists are highly effective in reducing ischemic episodes in patients with Prinzmetal's angina and effective for therapy for unstable angina when used in conjunction with other forms of medical treatment aimed at the processes of platelet activation and thrombus formation.

Adrenergic beta-Antagonists↗

PubMed2000

Contemporary diagnosis and management of unstable angina.

Unstable angina (UA) is one of the acute coronary syndromes, a group of conditions that also includes non-ST elevation myocardial infarction (MI) and ST elevation MI. The underlying pathogenic substrate of all these entities is the unstable coronary plaque with an overlying intracoronary thrombus. Initial management for the patient with suspected UA includes a resting electrocardiogram and oral administration of aspirin. ST-segment elevation indicates acute MI with the need for urgent reperfusion therapy. Patients without ST-segment elevation commonly have a mixture of UA and non-ST elevation MI; initial management is similar with assessment of near-term risk of MI or death as the next step. Features of UA indicating high risk include persistent ST-segment depression, persistent ischemic pain, elevated troponin level, or features of heart failure. Such patients undergo intensive medical therapy with heparin (unfractionated or low-molecular-weight), beta-blockade, and IIb/IIa antiplatelet agents, usually followed by coronary angiography and percutaneous intervention. The timing of intervention depends on the patient's response to therapy. Intermediate- or low-risk patients (including those presenting to the emergency department) can be managed with a chest pain unit strategy, and those with normal results on serial electrocardiograms, cardiac marker studies, and functional testing can be safely discharged home. Others are admitted for elective angiography, intensive medical therapy, or both. Assessment of coronary risk factors and their modification is an important component of long-term therapy for both high-risk and low-risk patients with UA, as well as those determined to have had non-ST elevation MI.

Abciximab↗

PubMed2002

Coagulation indicators in chronic stable effort angina and unstable angina: relationship with acute phase reactants and clinical outcome.

The aim of the study was to evaluate which pattern of coagulation indicators characterizes unstable angina and, particularly, its relationship with short-term prognosis. Forty patients with unstable angina (UA Group) at admission in the intensive care unit, 40 patients with chronic stable effort angina (SEA Group), and 20 age- and sex-matched healthy controls were studied. Blood coagulation indicators were fibrinogen, prothrombin fragment F1 + 2 (F1 + 2), thrombus precursor protein (TpP), and D-dimer. C reactive protein (CRP) and cardiac Troponin I (cTnI) have also been determined and compared. Patients in the UA Group were followed for in-hospital adverse events (sudden death, acute myocardial infarction and angina refractory to medical therapy). CRP, D-dimer and cTnI plasma levels were significantly lower in the SEA Group than in the UA Group; the same trend was found for fibrinogen and F1 + 2 plasma levels, although not statistically significant. The TpP was similar in all groups. The control group showed the lowest levels for all indicators. Within the UA Group, 17 patients developed adverse events during hospitalization; F1 + 2, D-dimer, cTnI and CRP plasma levels were higher in these patients than in those with good outcome. Relative risks for adverse events associated with the highest tertile of D-dimer, cTnI, and CRP plasma levels were 8.4 (95% confidence interval, 1.5-48.9), 6.7 (95% confidence interval, 1.1-38.6) and 5.2 (95% confidence interval, 1.1-25.2), respectively. D-Dimer is significantly increased in patients with unstable angina and, in particular, in those who develop an adverse event.

Acute-Phase Proteins↗

PubMed1996

Medical management of stable angina and unstable angina in the elderly with coronary artery disease.

Coronary artery disease is a major clinical problem in the elderly. This article discusses the medical management of stable and unstable angina pectoris. A review of the general measures and drug therapy used to treat these disorders, especially as they relate to the elderly patient are presented. In addition, new insights into the pathophysiologic mechanisms of chronic stable angina and unstable angina are reviewed.

Adrenergic beta-Antagonists↗

PubMed1995

Optimizing the Treatment of Unstable Angina.

Unstable angina and non--Q-wave myocardial infarction (MI) are at the center of the spectrum of myocardial ischemia, which ranges from stable angina to acute Q-wave MI. In addition to clinical evaluation, cardiac specific markers such as troponin T or I can assist in early diagnosis, triage, and risk stratification. Antithrombotic therapy with aspirin and heparin have been shown to improve the outcome of patients with acute ischemic syndromes. Thrombolytic therapy does not appear to be beneficial in these syndromes. Antiischemic therapy remains an important component of the overall therapy. A strategy of early coronary angiography and revascularization leads to a similar long-term outcome as compared with a more conservative strategy of revascularization for recurrent ischemia, but the early invasive strategy is more expeditious as a large number of conservatively treated patients have recurrent ischemia. At present, many new antithrombotic agents are under active investigation, with the hope that they will lead to further improvement in the clinical outcome of patients with acute ischemic syndromes.

Journal Article↗

PubMed1997

Nitrate tolerance, rebound, and their clinical relevance in stable angina pectoris, unstable angina, and heart failure.

Vascular tolerance develops rapidly in isolated vascular strips exposed to millimolar concentrations of nitroglycerin. Several mechanisms, including depletion of sulfhydryl groups, reduced biotransformation of nitrates to NO or nitrosothiols, oxygen free radical injury, and downregulation of a membrane-bound enzyme or a nitrate receptor, have been proposed, but the exact mechanism responsible for in-vitro tolerance remains unknown. In-vivo tolerance of the beneficial effects of nitrates on hemodynamics, myocardial ischemia, and exercise performance develops rapidly. It has been suggested, but remains to be proven, that development of venous tolerance and not arterial tolerance is responsible for the attenuation of nitrate effects during long-term nitrate therapy. Several mechanisms, including neurohormonal activation, depletion of sulfhdryl groups, and the shift of fluid from the extravascular to intravascular compartment have been implicated. However, the use of agents to counteract these mechanisms (ACE inhibitors, sulfhydryl donors, diuretics) has produced conflicting results. Thus, at present the mechanism responsible for in vivo tolerance to nitrates remains unknown. Both in vitro and in vivo vascular tolerance to nitrates can be prevented or minimized by providing nitrate-free or low-nitrate intervals. However, during nitrate-free periods, rebound phenomena (rest angina in patients with ischemic heart disease or a deterioration in exercise performance prior to the renewal of the morning dose in patients with stable angina) remain a clinical concern. When treating patients with stable angina pectoris, it must be recognized that none of the nitrate preparations or formulations can provide round-the-clock antianginal or antiischemic prophylaxis. In these patients, beneficial antianginal and antiischemic effects of nitrates for 10-14 hours during the daytime can be maintained by using formulations and dosing regimens that avoid or minimize the development of tolerance (standard formulation of isosorbide-5-mononitrate, 20 mg in the morning and 7 hours later; slow-release formulation of isosorbide-5-mononitrate, 120-240 mg once a day; or nitroglycerin patch delivering 0.6 nitroglycerin per hour for 10-12 hours each day). Only the patch on and off treatment is associated with nitrate rebound. Although intermittent nitrate therapy is not associated with the development of tolerance, this strategy cannot be recommended for treating unstable angina because rebound angina during nitrate-free periods complicates clinical decision making. In the acute phase of unstable angina, continuous treatment with intravenous nitroglycerin is recommended because it permits rapid up- or down-titration. Tolerance towards antianginal and antiischemic effects does develop in a substantial number of patients with 24 hours, but this can be overridden by dose escalation and restoration of the therapeutic effectiveness of nitroglycerin. Tolerance towards the beneficial effects of nitrates on hemodynamics and on exercise performance also develops rapidly during continuous or long-term nitrate therapy, and for these reasons nitrates are not used as first-line therapy to treat chronic heart failure. In combination with hydralazine, high-dose isosorbide dinitrate (30-40 mg four times a day) improves survival, but this combination therapy is inferior to ACE inhibitors.

Angina Pectoris↗

PubMed1995

[Usefulness of 123I-BMIPP myocardial imaging in patients with stable effort angina and unstable angina].

We evaluated the clinical significance of myocardial imaging using 123I-15-(p-iodophenyl)-3-methyl pentadecanoic acid (BMIPP) scintigraphy in patients with stable effort angina pectoris (SAP) and unstable angina pectoris (UAP). Thirty-three patients with SAP were studied using rest BMIPP and stress 201TlCl (Tl) myocardial scintigraphy, and 13 patients with worsening effort type of UAP were also examined using both rest BMIPP and Tl scintigraphy. We compared those BMIPP findings with myocardial perfusion images obtained with Tl and the regional wall motion determined by left ventriculography. In 45% of 282 segments of myocardial ischemia of SAP, the degree of myocardial uptake of BMIPP was concordant with that of stress Tl and the defect score of Tl was higher than that of BMIPP. On the other hand, in 32% of 62 segments of ischemia of UAP, the degree of myocardial BMIPP and Tl uptake was concordant and BMIPP defect score was higher than Tl score. In SAP, the decrease in regional wall motion agreed better with the decrease in myocardial uptake of BMIPP than that of Tl. These results suggest that myocardial ischemic regions decreased BMIPP uptake show the disturbance of fatty acid metabolism and lead to abnormal wall motions. Such ischemic regions may be clinically severe state in patients with angina pectoris.

Aged↗

PubMed1995

Comparison of coronary angiographic narrowing in stable angina pectoris, unstable angina pectoris, and in acute myocardial infarction.

Coronary angiographic findings were compared in patients who presented with acute myocardial infarction (AMI, n = 75), unstable angina pectoris (UAP, n = 36), or stable angina pectoris (SAP, n = 36) for > or = 2 years without evidence of any previous acute event and with an angiogram within 2 years of the initial symptoms. Angiograms were evaluated blindly for severity, extent (depending on the percentage of each coronary segment showing atherosclerosis), and pattern (discrete, < 3 loci of narrowings involving < 50% of any segment; diffuse, anything exceeding this). Patients in the SAP group had more narrowed arteries (2.4 +/- 0.7 vs 1.3 +/- 0.6 [p < 0.02] and 1.4 +/- 0.6 [p < 0.02]), more stenoses (6.0 +/- 3.3 vs 2.1 +/- 1.5 [p < 0.01] and 2.6 +/- 1.7 [p < 0.05]) and occlusions (1.3 +/- 1.1 vs 0.7 +/- 0.6 [p = 0.05] and 0.3 +/- 0.5 [p < 0.02]), and a greater extent index (0.9 +/- 0.5 vs 0.5 +/- 0.3 [p < 0.02] and 0.5 +/- 0.3 [p < 0.02]) than those in the AMI and UAP groups. Furthermore, a discrete pattern was less prevalent in patients with UAP than in those with SAP or AMI (3% vs 40% [p < 0.02] and 25% [p < 0.05], respectively). In conclusion, patients who present with acute coronary syndromes have less extensive atherosclerosis than those who present with chronic stable angina. Therefore, in the former group, coronary atherosclerosis appears to be more susceptible to ischemic stimuli responsible for acute coronary syndromes.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

PubMed1991

Coronary bypass surgery for stable angina and unstable angina pectoris.

Large randomized trials have shown that surgical revascularization is more effective than medical therapy in relieving angina and improving exercise tolerance. Development of atherosclerosis in the vein grafts plus progression of disease in the native vessels, however, results in a return of angina in a substantial proportion of patients 5 to 10 years after the procedure. The better myocardial protection, more complete revascularization, and improved graft patency rates that have occurred in the last decade imply that survival following coronary artery bypass may be improved in a broader spectrum of coronary artery disease patients than documented in the randomized trials. Patients with unstable angina have higher operative mortality but clearly benefit symptomatically from revascularization. There is a need for randomized trials to compare the relative risks and benefits of angioplasty versus surgical revascularization.

Adult↗

PubMed1982

Effects of calcium antagonists, especially nifedipine, on variant angina, resting angina, and unstable angina.

The effects of drugs were evaluated in 47 cases with variant angina (VA), 19 with resting angina showing ST depression (RA), and 84 with unstable angina (UA). In VA patients, calcium antagonists were effective in 87.1% of the cases, while other drugs were effective in 56.3%. The difference was statistically significant. In RA patients, calcium antagonists were effective in 80.0% of the cases and other drugs in 44.4%. Nifedipine was effective in all 5 cases with coronary stenosis of more than 75.0%. All cases of RA had multiple vessel disease and nifedipine was effective in 80.0% of the patients. Nifedipine was effective in 83.3% of VA cases showing ST elevation during an exercise test, and was particularly effective in all patients having attacks only at rest. The effects of nifedipine were confirmed in 83.3% of UA cases. These results indicate that calcium antagonists are effective in VA, RA, and UA.

Aged↗

PubMed1991

Gradation of unstable angina based on a sensitive immunoassay for serum creatine kinase MB.

A newly developed, highly sensitive immunoassay for creatine kinase MB isoenzyme was evaluated in 68 patients with or without different types of ischaemic heart disease. Patients were classified on the basis of clinical criteria in four groups: no ischaemic heart disease, stable angina, unstable angina, and acute myocardial infarction. Enzyme concentration in patients with stable angina was the same (even during exercise) as seen in the patients without ischaemic heart disease. Patients with unstable angina, however, could be divided into two groups. One group showed clear evidence of severe myocardial ischaemia by serial changes and higher mean values of creatine kinase MB up to 40 hours after the onset of symptoms, whereas in the remainder values were stable and resembled those seen in the patients without ischaemic heart disease. The changes in concentration correlated with signs of repetitive ischaemic episodes deduced from continuous ST segment monitoring during the first 24 hours after admission. These findings indicate that patients with unstable angina are a heterogenous group. In some, severe and prolonged ischaemia can be detected by a serological assay with high sensitivity.

Angina Pectoris↗

PubMed1998

Neovascularization in atherectomy specimens from patients with unstable angina: implications for pathogenesis of unstable angina.

Although neovascularization has been noted in atherosclerotic plaque, the presence of neovascularization has not been correlated with clinical syndromes. This study examined the relation between neovascularization in atherosclerotic plaque removed during directional coronary atherectomy and clinical status in 28 patients. Neovascularization was determined by immunohistochemistry with endothelial cell-specific monoclonal antibodies and was found in nine (50%) of 18 specimens from patients with unstable angina and in only one (10%) of 10 specimens from patients with stable angina (p < 0.05). There was no significant relation between neovascularization and other clinical factors (age, sex, race, hypertension, diabetes, tobacco use, hypercholesterolemia, positive family history of coronary artery disease, history of myocardial infarction, or stenosis severity). These results suggest that neovoscularization may play a role in the pathogenesis of unstable angina.

Angina Pectoris↗

PubMed1983

Coronary angiographic findings in various types of unstable angina--study on the pathophysiology of unstable angina.

Coronary angiographic findings were studied in 129 patients with various types of unstable angina in order to clarify the pathophysiology of unstable angina. The subjects were divided into 3 types: effort angina (E), rest angina (R), and effort and rest angina (E+R), and each of these 3 types was subdivided into group I (new onset), II (recurrent) and III (changing pattern). 1) R had less severe coronary lesions than E or E+R. 2) Severity and distribution of coronary atherosclerotic lesions in unstable angina were similar to those in stable angina. 3) Incidence of coronary spasm is higher in unstable R and E+R than in stable R and E+R, respectively. 4) Unstable R and E+R with frequent attacks were associated with a higher frequency of coronary spasm and severe proximal coronary stenosis than those without frequent attacks, respectively. 5) Among unstable E+R-III (changing pattern), the patients who developed E+R from E showed significantly higher incidence of multiple vessel disease than those who developed E+R from R and significantly lower incidence of spontaneous spasm than those with E+R, who remained with the same pattern but in whom the frequency and/or the intensity of the attack increased, without any significant difference in the severity of coronary stenosis from other 2 subgroups. It is concluded that coronary spasm as well as severe coronary atherosclerotic lesions may be responsible for the unstable state of angina. Especially in R and E+R, coronary spasm is the most important factor responsible for the unstabilization of angina.

Adult↗

PubMed1996

[Cardiac troponin I in unstable angina].

BACKGROUND: Unstable angina implies high risk of myocardial infarction and sudden death. Increased levels of cytoplasmatic enzymes and proteins (creatine phosphokinase, MB creatine phosphokinase troponin T, etc.) were described in unstable angina, providing information about incoming major coronary events. Cardiac troponin I (cTn-I) is a structural protein inhibiting the actinomyosine ATPase; it is only found in myocardial cells. Serum titration of cTn-I has been recently introduced into clinical practice as a sensitive and specific marker of myocardial cellular necrosis. OBJECTIVES: The aim of our prospective study was to assess the presence of cTn-I in blood samples of patients with unstable angina and no signs of myocardial necrosis. Furthermore we intended to test the possible use of cTn-I in unstable angina as a prognostic marker of major coronary events on short and middle term. METHODS: We studied 33 consecutive patients admitted to our CCU for unstable angina. According to unstable angina Braunwald's classification, 6 patients were included in the first class, 4 patients in the second class and 23 patients in the third class. We excluded patients with acute or recent myocardial infarction. Blood samples of all patients were obtained at the time of CCU admission and every eight hours in the first and second day. Serum cTn-I titration was performed with the sandwich immunoenzymometric method, recently introduced by Diagnostic Pasteur. Two months follow-up was carried out in order to survey major coronary events and revascularization procedures, either angioplasty or coronary artery bypass surgery. RESULTS: No patients with unstable angina exhibited cTn-I in their blood samples; accordingly, cTn-I was not found in the first blood sample of a patient who underwent myocardial infarction during hospitalization. During the follow-up 2 patients died of myocardial infarction, 9 patients had surgical revascularization and 5 patients angioplasty. CONCLUSIONS: CTn-I is a sensitive and specific marker of myocardial necrosis. It is not found in patients with unstable angina; therefore it has no role as a prognostic marker of major coronary events.

Adult↗

PubMed2001

"Hot" unstable angina--is it worse than subacute unstable angina? Results from the GUARANTEE Registry.

BACKGROUND AND METHODS: Because time to presentation to the hospital affects time to treatment and is known to be important in acute myocardial infarction, we evaluated this variable in patients with unstable angina/non-ST segment elevation myocardial infarction (UA/NSTEMI). Among 2909 consecutive patients with UA/NSTEMI admitted to 35 hospitals in 6 geographic regions of the United States, we compared patients with acute (onset of pain <12 hours before admission) and subacute (onset >12 hours) unstable angina. RESULTS: Patients with "hot" (acute) unstable angina presented more often to the emergency department and were subsequently admitted more often to an intensive care unit. Hospital administration of medications did not differ between the two groups, with the exception of heparin, which was paradoxically used more often in subacute patients (p<0.001). All cardiac invasive procedures were undertaken less often in the acute patients (catheterization, 41.4% vs. 58.7%, p=0.001; percutaneous coronary intervention, 11.3% vs. 21.1%, p=0.001; coronary artery bypass grafting, 5.6% vs. 12.0%, p=0.001). A greater percentage of acute patients were found to have no significant coronary artery disease at cardiac catheterization (20.1% vs. 15.0%, p=0.006). Mortality did not differ between the two groups; however, the composite endpoint of death and MI favored the acute patients (1.3% vs. 2.2%, p=0.032). CONCLUSIONS: Contrary to our initial hypothesis, "hot" UA patients tended to be at lower risk than patients with subacute presentation, highlighting the fact that patients with UA/NSTEMI remain at high risk even after the initial 12-hour period.

Acute Disease↗