Unstable Rest Research Articles

Early invasive tactics for treatment of patients with various forms of unstable angina

The paper presents immediate and long-term results of early invasive treatment tactics in 467 patients with various forms of unstable angina (UA), including 129 patients with unstable rest angina, 225 patients with unstable exertional angina, and 93 patients with a new onset angina. Percutaneous coronary interventions on a symptom-affected artery at a single procedure were performed in 213 cases (48%), indications for coronary artery bypass grafting were identified in 182 patients (41%), and only in 52 cases (11%) the treatment was limited to medicinal therapy. Coronary angiography performed in the initial 12–48 hours makes it possible to identify the indications to myocardial revascularization, to avoid inconsistencies in the choice of optimal treatment tactics and non-invasive risk assessment.

Potassium Metal as Reliable Reference Electrodes of Nonaqueous Potassium Cells.

Potassium metal electrochemical cells are widely utilized to examine potassium insertion materials for nonaqueous potassium-ion batteries. However, large polarization during K plating-stripping and unstable rest potential are found at the potassium electrodes, which leads to an underestimation of the electrochemical performance of insertion materials. In this study, the electrochemical behavior of K-metal electrodes is systematically investigated. Electrolyte salts, solvents, and additives influence the polarization of K metals. Although a highly concentrated electrolyte of 3.9 M KN(SO2F)2/1,2-dimethoxyethane realizes the smallest polarization of 25 mV among all the electrolytes investigated in this study, the polarization of K metals is still larger than those of Li and Na metals. The issue of inaccurate rest potential is solved by pretreating the K electrodes with a plating-stripping process, which is essential in evaluating the intrinsic electrode performance of potassium insertion materials.

Group size effects in social evolution

How the size of social groups affects the evolution of cooperative behaviors is a classic question in evolutionary biology. Here we investigate group size effects in the evolutionary dynamics of games in which individuals choose whether to cooperate or defect and payoffs do not depend directly on the size of the group. We find that increasing the group size decreases the proportion of cooperators at both stable and unstable rest points of the replicator dynamics. This implies that larger group sizes can have negative effects (by reducing the amount of cooperation at stable polymorphisms) and positive effects (by enlarging the basin of attraction of more cooperative outcomes) on the evolution of cooperation. These two effects can be simultaneously present in games whose evolutionary dynamics feature both stable and unstable rest points, such as public goods games with participation thresholds. Our theory recovers and generalizes previous results and is applicable to a broad variety of social interactions that have been studied in the literature.

Acoustic active two body clusters

Inspired from the stable bubble clustering phenomenon known as bubble grapes, and following the capabilities of recent novel concept of active carriers subjected to stimulating wave fields, we aim to propose the theory of noncontact clusters composed of harmonically activated spherical objects as the carriers. As the first step, the simplest case of two body cluster is considered which the sustaining field is due to self monopole (breathing mode) radiation of spherical components. The acoustic radiation forces on the bodies are analytically derived and it is shown that these interaction forces may have the nature of repulsive or attractive for each specific configuration (size), depending on the radiation characteristics (e.g., frequency and phase difference) and fluidic environment properties. In the rest states which the zero radiation force is exerted upon both bodies, the stability or instability of the cluster is examined. For the stable configurations, the frequency of oscillation of cluster is estimated O(10−3) of the frequency of operation. The instability situations may lead to two cases of dispersion (expansion) or bunching (contraction) of cluster's components. Due to existence of stable spatial configurations between each two successive unstable rest states, it is predicted that any deviation from the stable or unstable rest points, may guide the cluster to sustaining its stable rest state or migration toward another (probably closest) stable configuration. The proposed research will develop the advanced therapeutic agents, drug and material delivery systems and introduces a new configuration in active multi-body carrier design or remotely stable multi-body mechanism.

Group Size Effects in Social Evolution

How the size of social groups affects the evolution of cooperative behaviors is a classic question in evolutionary biology. Here we investigate group size effects in evolutionary games in which individuals choose whether to cooperate or defect. We find that increasing the group size decreases the proportion of cooperators at both stable and unstable rest points of the replicator dynamics. This implies that larger group sizes can have negative effects (by reducing the amount of cooperation at stable polymorphisms) and positive effects (by enlarging the basin of attraction of more cooperative outcomes) on the evolution of cooperation. These two effects can be simultaneously present in games whose evolutionary dynamics features both stable and unstable rest points, such as public goods games with participation thresholds. Our theory recovers and generalizes previous results and is applicable to a broad variety of social interactions that have been studied in the literature.

A Linear Active Disturbance Rejection Control for a Ball and Rigid Triangle System

This paper proposes an application of linear flatness control along with active disturbance rejection control (ADRC) for the local stabilization and trajectory tracking problems in the underactuated ball and rigid triangle system. To this end, an observer-based linear controller of the ADRC type is designed based on the flat tangent linearization of the system around its corresponding unstable equilibrium rest position. It was accomplished through two decoupled linear extended observers and a single linear output feedback controller, with disturbance cancelation features. The controller guarantees locally exponentially asymptotic stability for the stabilization problem and practical local stability in the solution of the tracking error. An advantage of combining the flatness and the ADRC methods is that it possible to perform online estimates and cancels the undesirable effects of the higher-order nonlinearities discarded by the linearization approximation. Simulation indicates that the proposed controller behaves remarkably well, having an acceptable domain of attraction.

Stability analysis of phonon transport equations derived via the Chapman-Enskog method and transformation of variables

Under the assumption of Callaway's model of the Boltzmann-Peierls equation, the Chapman-Enskog method for a phonon gas forms the basis to derive various hydrodynamic equations for the energy density and the drift velocity of interest when normal processes dominate over resistive ones. The first three levels of the expansion (i.e., the zeroth-, first-, and second-order approximations) are satisfactory in that they are entropy consistent and ensure linear stability of the rest state. However, the entropy density contains a weakly nonlocal term, the entropy production is a degenerate function of variables, and the next order in the Chapman-Enskog expansion gives the equations with linearly unstable rest solutions. In the context of Burnett and super-Burnett equations, a similar type of problem was recognized by several authors who proposed different ways to deal with it. Here we report on yet another possible device for obtaining more satisfactory equations. Namely, inspired by the fact that there exists no unique way to truncate the Chapman-Enskog expansion, we combine the Chapman-Enskog procedure with the method of variable transformation and subsequently find a class of epsilon -dependent transformations through which it is possible to derive the second-order equations possessing a local entropy density and nondegenerate expression for the entropy production. Regardless of this result, we also show that although the method cannot be used to construct linearly stable third-order equations, it can be used to make the originally stable first-order equations asymptotically stable.

Travelling wave solutions of the degenerate KolmogorovPetrovskiPiskunov equation

We prove the existence of a family of Travelling Wave (TW) solutions for a large class of scalar reaction-diffusion equations with degenerate, nonlinear diffusion coefficients and monostable nonlinear reaction terms. We also investigate stability. Specifically, we show that, as in the linear diffusion case [6], the slowest TW in the family yields the asymptotic rate of the propagation of disturbances from the unstable rest state in these systems. In addition, we give conditions on the reaction term and diffusion coefficient ensuring the existence of interfaces.

Unstable angina: current concepts of pathogenesis and treatment.

During the past 15 years, we have learned an enormous amount about the pathogenesis and treatment of unstable angina. In most cases of unstable rest angina, the pathogenesis is a mural thrombus formation on a ruptured or eroded atherosclerotic plaque. However, any process that acutely changes the supply-demand ratio (decreased supply or increased demand in the presence of a decrease in supply) can precipitate the clinical presentation of unstable angina. Standard acute antithrombotic drug therapy is effective in decreasing progression to infarction. Newer agents (low-molecular-weight heparin and platelet glycoprotein IIb/IIIa inhibitors) are more effective, and their use is evolving. Percutaneous intervention and bypass surgery can reduce symptoms and multiple hospitalizations, in most cases without a decrease in the long-term mortality rate. Because the cost of hospitalization is extremely high and the clinical presentation and outcome are heterogeneous, better triage methods are required.

Rotational atherectomy: improved procedural outcome with evolution of technique and equipment. Single-center results of first 1,000 patients.

We present our single-center experience of rotational atherectomy (RA) in the first 1,000 consecutive patients divided arbitrarily into three different time periods corresponding to significant changes in technique or equipment for RA. Period I (August 1994 to April 1995; 172 cases) is characterized by early experience, longer ablation, and frequent use of intra-aortic balloon pump; period II (May 1995 to January 1996; 254 cases) is characterized by short ablation runs (20-30 sec) and use of rotaflush; period III (February 1996 to February 1997; 574 cases) is characterized by ReoPro use, neosynephrine boluses to avoid hypotension, and rota floppy wire and flexible shaft burrs. The procedural success rate has improved and complication rates have progressively declined over these three time periods. The incidence of lesion complexity (long and type C lesions) and patients with unstable rest angina have increased over these time periods of RA. Therefore, modification in procedural techniques and equipment over time have made RA a safe technique despite its use in very complex lesion subsets.

Rotational atherectomy: Improved procedural outcome with evolution of technique and equipment. single‐center results of first 1,000 patients

We present our single-center experience of rotational atherectomy (RA) in the first 1,000 consecutive patients divided arbitrarily into three different time periods corresponding to significant changes in technique or equipment for RA. Period I (August 1994 to April 1995; 172 cases) is characterized by early experience, longer ablation, and frequent use of intra-aortic balloon pump; period II (May 1995 to January 1996; 254 cases) is characterized by short ablation runs (20–30 sec) and use of rotaflush; period III (February 1996 to February 1997; 574 cases) is characterized by ReoPro use, neosynephrine boluses to avoid hypotension, and rota floppy wire and flexible shaft burrs. The procedural success rate has improved and complication rates have progressively declined over these three time periods. The incidence of lesion complexity (long and type C lesions) and patients with unstable rest angina have increased over these time periods of RA. Therefore, modification in procedural techniques and equipment over time have made RA a safe technique despite its use in very complex lesion subsets. Cathet. Cardiovasc. Intervent. 46:305–311, 1999. © 1999 Wiley-Liss, Inc.

Lipoprotein(a) and inflammation in human coronary atheroma: association with the severity of clinical presentation.

The purpose of this study was the investigation of the in vivo role of lipoprotein(a) [Lp(a)] and inflammatory infiltrates in the human coronary atherosclerotic plaque and their correlation with the clinical syndrome of presentation. Lipoprotein(a) is an atherogenic and thrombogenic lipoprotein, and has been implicated in the pathogenesis of acute coronary syndromes. Lipoprotein(a) induces monocyte chemoattraction and smooth muscle cell activation in vitro. Macrophage infiltration is considered one of the mechanisms of plaque rupture. This study of atherectomy specimens investigated the in vivo role of Lp(a) at different stages of the atherogenic process, and its relationship with macrophage infiltration. We examined coronary atheroma removed from 72 patients with stable or unstable angina. Specimens were stained with antibodies specific for Lp(a), macrophages (KP-1), and smooth muscle cells (alpha-actin). Morphometric analysis was used to quantify the plaque areas occupied by each of the three antigens, and their colocalization. All specimens had localized Lp(a) staining; the mean fractional area was 58.2%. Ninety percent of the macrophage areas colocalized with Lp(a) positive areas, whereas 31.3% of the smooth muscle cell areas colocalized with Lp(a) positive areas. Patients with unstable angina (n = 46) had specimens with larger mean plaque Lp(a) areas than specimens from stable angina patients (n = 26): 64.4% versus 47.7% (p = 0.004). Unstable angina patients with rest pain (n = 28) had greater mean plaque Lp(a) area than unstable angina patients with crescendo exertional pain (n = 18): 71.1% versus 52.4% (p < 0.001). Mean KP-1 area was 31.2% in unstable rest angina versus 18.3% in stable angina (p = 0.05); alpha-actin area was greater in stable (48.5%) and crescendo exertional angina (48.8%) than in rest angina (30.4%). The strongest correlation between plaque KP-1 and Lp(a) area was in unstable rest angina (r = 0.88, p < 0.001), and between alpha-actin and Lp(a) areas in the crescendo exertional angina (r = 0.62, p < 0.01). Lipoprotein(a) is ubiquitous in human coronary atheroma. It is detected in larger amounts in tissue from culprit lesions in patients with unstable compared to stable syndromes, and has significant colocalization with plaque macrophages. A correlation of plaque alpha-actin and Lp(a) area suggests a role of Lp(a) in plaque growth.

768-6 Lipid Rich Plaques with Thrombus are Common in Unstable Rest Angina: Observations from Atherectomy Tissue Analysis

Several autopsy studies indicate that disrupted atherosclerotic plaques particularly those rich in lipid with associated thrombus. are the cause of acute MI. Other plaques without disruption are fibrocellular without lipid. Although unstable rest angina (UA) shares a common pathogenesis to acute MI, there are little pathological data on plaque composition in UA. Directional Coronary Atherectomy (DCA) provides the opportunity to study plaque composition in UA. We prospectively analyzed the DCA tissue specimens of 60 pts with de novo culprit lesions for fibrocellular and lipid constituents by hematoxylin &amp; eosin and oil red O stains. A fibrous plaque (FP) was defined as one which had predominantly fibrous and sclerotic tissue with no or minimallipid (0 or 1 + on scale of 3). A lipid plaque (LP) was defined as one with moderate or high lipid (2 or 3+) content. The presence of inflammatory cells and thrombus were also noted. Histopathology was analyzed independent of clinical presentation. Clinical syndrome FP(%) LP(%) P Stable/asymptomatic (10) 9(90) 1(10) New or Crescendo (16) 9 (56) 7 (44) Rest Angina (21) 4 (19) 17 (81) Post-MI (13) 2 (15) 11 (85) Coronary thrombus on histologic analysis was present in 23/36 (64%) of LP vs. in 5/24 (21%) of FP (p &lt; 0.01). Coronary thrombus was present in 88% and 82% of LP in rest angina and post MI respectively. Inflammatory cells were noted in 12 LP and 2 FP (p = 0.02) — in 38% of both rest angina and post MI specimens. Lipid rich plaque are very common in rest angina and post MI, moderately common in crescendo or new onset and rare in stable angina. LP are usually associated with thrombus and inflammation particularly in rest angina and post MI pts. These DCA tissue analyses confirm and expanded on prior autopsy studies in acute syndromes and support the pathogenetic link between unstable rest angina and acute MI.

Combination antithrombotic therapy in unstable rest angina and non-Q-wave infarction in nonprior aspirin users. Primary end points analysis from the ATACS trial. Antithrombotic Therapy in Acute Coronary Syndromes Research Group.

The purpose of this study was to compare combination antithrombotic therapy with aspirin plus anticoagulation versus aspirin alone, when added to conventional antianginal therapy in patients with unstable rest angina or non-Q-wave myocardial infarction who were nonprior aspirin users. Two hundred fourteen patients were randomized; 109 were randomized to receive aspirin alone (162.5 mg daily) and 105 to receive a combination of aspirin plus anticoagulation, ie, aspirin 162.5 mg daily plus heparin (activated partial thromboplastin time, two times control) followed by aspirin 162.5 mg daily plus warfarin (international normalized ratio, 2 to 3). Trial therapy was begun by 9.5 +/- 8.8 hours of qualifying pain and was continued for 12 weeks. Primary end points were recurrent angina with ECG changes, myocardial infarction, and/or death. Analysis by intention to treat of primary events at 12 weeks was performed. At 14 days, there was a significant reduction in total ischemic events in the combination group versus aspirin alone (10.5% versus 27%, P = .004). An efficacy analysis of primary events at 12 weeks also revealed a large reduction in total ischemic events in the combination group versus aspirin alone (13% versus 25%, P = .06). Bleeding complications were slightly more common with combination therapy. In nonprior aspirin users, combination antithrombotic therapy with aspirin plus anticoagulation significantly reduces recurrent ischemic events in the early phase of unstable angina.

Daily life ischemia and nitrate therapy

Daily life ischemia has generated considerable interest because most of it is silent and associated with increased risk of adverse outcome. Coronary vasomotion, as well as increases in myocardial oxygen demand, seem important in the pathogenesis of this form of ischemia, so treatment with nitrates seems rational. Administration of sublingual nitroglycerin hourly, over 12 hours, was shown to decrease both silent and painful ischemic episodes in patients with effort angina. Subsequently, isosorbide dinitrate or mononitrate, given either as an intravenous infusion or orally, was shown to decrease both silent and painful ischemic episodes in patients with unstable rest angina and in those with severe angina. More recently, 6 studies have reported using transdermal nitroglycerin for daily life ischemia. Three of these reported open-label uncontrolled observations and suggested that ischemia frequency may be reduced approximately 60–80% during treatment with doses of 10–30 mg/ day, with a duration of treatment ranging from 1 hour to 14 days. In 2 of these reports the duration of ischemia also decreased. The other 3 studies were randomized, double-blind, placebo-controlled studies with a total enrollment of 86 patients. These studies provided mked results. One suggested that evidence for partial tolerance develops within 1 day of treatment, using large continuous or intermittent doses (mean, 52 mg/ day). Another suggested that no tolerance develops to intermittent dosing (18 mg/16 hr out of 24 hr) during exercise testing but no effect is seen on daily life ischemia. The remaining study suggested that tolerance does not develop using small doses (15 mg/day) continuously over 14 days for ischemia during daily life, and that this response is different from that observed using the calcium antagonist nifedipine. These limited observations and conflicting results underscore a need for additional larger controlled trials, employing topical nitrate therapy in low intermittent doses for daily life ischemia.

Management of acute coronary occlusion during percutaneous transluminal coronary angioplasty: experience of complications in a hospital without on site facilities for cardiac surgery.

To determine whether percutaneous transluminal coronary angioplasty may be safely performed in cardiology centres in the United Kingdom without immediate on site cardiac surgical cover for complications arising at angioplasty. Retrospective review of coronary angioplasties and complications in a hospital without on site cardiac surgical cover. All angioplasties were performed in the catheterisation laboratory of the Belfast City Hospital. Revascularisation surgery for complicated coronary angioplasty was performed in the cardiac surgical unit of the Royal Victoria Hospital, 2.4 km away from the catheterisation laboratory. 540 Coronary angioplasties were performed on 512 patients between late 1982 and November 1988. Indications included stable angina, unstable rest angina, and suitable coronary disease at coronary arteriography after myocardial infarction. In hospital mortality after complicated coronary angioplasty and delay to surgical revascularisation after acute coronary occlusion at angioplasty. Coronary angioplasty was successful in 444 cases (82%). Acute coronary occlusion occurred in 35 cases (6.5%). Twelve patients required urgent revascularisation surgery and were transferred safely to the surgical unit; none of these patients died. A mean delay of 268 minutes (range 180-390 minutes) occurred before revascularisation compared with 273 minutes (range 108-420 minutes) in the Royal Victoria Hospital, where on site surgical cover was available. The principal cause of delay was the wait for a cardiac operating theatre to become available and not the transfer time between hospitals. Five deaths occurred after coronary angioplasty, a mortality of 0.9%. Three deaths were related to acute coronary occlusion. The absence of immediate surgical help did not influence the outcome in any patient. With careful selection of patients coronary angioplasty may be safely performed in a hospital without on site cardiac surgical facilities, provided that these are available at a nearby centre.

Silent Myocardial Ischemia During Daily Activities: Studies in Asymptomatic Patients and Those with Various Forms of Angina

Asymptomatic subjects with proven coronary artery disease, including those with no previous manifestations of coronary heart disease and those with previous myocardial infarction, have silent ischemic episodes during daily activity. Patients with all forms of angina, stable effort and unstable rest angina, and those with coronary artery spasm have very frequent episodes of silent myocardial ischemia during ordinary activity. Characteristics of these episodes and evidence for these findings are reviewed.

Unstable Angina Associated with Factor VIII Concentrate Therapy for Hemophilia A

Brief Report1 August 1986Unstable Angina Associated with Factor VIII Concentrate Therapy for Hemophilia AROBERT G. KOPITSKY, M.D., EDWARD M. GELTMAN, M.D.ROBERT G. KOPITSKY, M.D.Search for more papers by this author, EDWARD M. GELTMAN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-105-2-215 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe importance of intracoronary thrombosis in patients with atherosclerotic coronary stenosis has been well established in the pathogenesis of acute transmural myocardial infarction (1). Recent angiographic studies have shown that intracoronary thrombi also occur in many patients who have unstable angina without myocardial infarction (2-5). In patients with severe atherosclerotic coronary obstruction, it is conceivable that a severe coagulation defect could partially protect against unstable angina or acute myocardial infarction by impairing the ability to form intracoronary thrombi; correction of the defect could negate this protection. We describe a case of severe unstable angina associated with the use of factor...References1 DEWOODSPORESNOTSKE MJR. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N Engl J Med. 1980;303:897-902. CrossrefMedlineGoogle Scholar2. HOLMESHARTZLERSMITHFUSTER DGHV. Coronary artery thrombosis in patients with unstable angina. Br Heart J. 1981; 45:411-6. CrossrefMedlineGoogle Scholar3. VETROVECLEINBACHGOLDCOWLEY GRHM. Intracoronary thrombolysis in syndromes of unstable ischemia: angiographic and clinical results. Am Heart J. 1982;104(4 pt 2):946-52. CrossrefMedlineGoogle Scholar4. MANDELKORNWOLFSINGH JNS. Intracoronary thrombus in nontransmural myocardial infarction and in unstable angina pectoris. Am J Cardiol. 1983;52:1-6. CrossrefMedlineGoogle Scholar5. ZACKISCHINGERAKERDINCERKENNEDY PTUBH. The occurrence of angiographically detected intracoronary thrombus in patients with unstable angina pectoris. Am Heart J. 1984;108:1408-12. CrossrefMedlineGoogle Scholar6. BUJAWILLERSON LJ. Clinicopathologic correlates of acute ischemic heart disease syndromes. Am J Cardiol. 1981;47:343-56. CrossrefMedlineGoogle Scholar7. GALLINOHAEBERLIBAURSTRAUB AAHP. Fibrin formation and platelet aggregation in patients with severe coronary artery disease: relationship with the degree of myocardial ischemia. Circulation. 1985;72:27-30. CrossrefMedlineGoogle Scholar8. OLIVA P. Unstable rest angina with ST-segment depression: pathophysiologic considerations and therapeutic implications. Ann Intern Med. 1984;100:424-40. LinkGoogle Scholar9. FUERTHMAHRER JP. Myocardial infarction after factor IX therapy. JAMA. 1981;245:1455-6. CrossrefMedlineGoogle Scholar10. SULLIVANPURDYBILLINGHAMGLADER DLMB. Fatal myocardial infarction following therapy with prothrombin complex concentrates in a young man with hemophilia A. Pediatrics. 1984;74:279-81. MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: ROBERT G. KOPITSKY, M.D.; EDWARD M. GELTMAN, M.D.Affiliations: Washington University School of Medicine St. Louis, Missouri PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byParadoxical thrombosis part 1: factor replacement therapy, inherited clotting factor deficiencies and prolonged APTTEndothelial dysfunction in haemophilia patientsClassic Polyarteritis Nodosa Presenting Rare Clinical Manifestations in a Patient with Hemophilia APotential role for rFVIIa in transfusion medicineAcute left anterior descending artery occlusion in a hemophiliac A patient during recombinant factor VIII infusion: Treatment with coronary angioplastySevere Haemophilia A Patient with Factor V Leiden Homozygosity Associated with Portal Vein Thrombosis and Myocardial InfarctionCerebral infarct associated with factor V Leiden mutation in a boy with hemophilia AFactor VIII, HIV and AIDS in haemophiliacs: an analysis of their relationshipAssociation of severe haemophilia A and factor V Leiden: report of three casesFatal complication of desmopressinFactor VIII, HIV and AIDS in haemophiliacs: An analysis of their relationshipDeep venous thrombosis in hemophilia A 1 August 1986Volume 105, Issue 2Page: 215-216KeywordsAcute myocardial infarctionCardiology and cardiovascular diseasesHemophilia AMyocardial infarctionPathogenesisStable coronary artery diseaseStenosisThrombosisUnstable angina ePublished: 1 December 2008 Issue Published: 1 August 1986 PDF downloadLoading ...

Unstable rest angina with ST-segment depression. Pathophysiologic considerations and therapeutic implications.

Because of recent findings, a reassessment is needed of the concept that rest angina associated with ST-segment depression is due to a spontaneous, transient increase of blood pressure or heart rate, or both, in the presence of critical coronary artery stenosis. Continuous hemodynamic and electrocardiographic recordings done before and during attacks of rest angina and thallium-201 scintigrams done during pain indicate that a transient reduction of flow is the immediate cause of ischemia in most, but not all, instances. Flow reduction, in turn, appears to be due to coronary arterial spasm or platelet aggregation, or both, acting at a site of atherosclerotic narrowing. Therapy for unstable rest angina should include measures to prevent both transient reductions of flow and increases of myocardial oxygen consumption. A combination of long-acting nitrates, a beta-blocker, a calcium-channel blocker, and aspirin or heparin is suggested for this purpose. Intravenous nitroglycerin is useful when angina occurs despite this therapy or when frequent attacks of ischemia are occurring at the time of admission.

The Spectrum of Coronary Artery Spasm

Angina from coronary artery spasm is not rare. Because new and effective medical therapy is now available, it is imperative that the physician recognize this syndrome when it occurs. Coronary artery spasm can present clinically as unstable rest angina with reversible ST-segment elevation and bradyarrhythmias and tachyarrhythmias. In this setting, Prinzmetal's variant angina is generally promptly recognized and appropriately treated. The diagnosis is variant angina, however, often is not so obvious. Chest pain may be exertional or seem noncardiac in origin. The chest pain syndrome may be chronic and stable as well as unstable. The ECG may show ST-segment depression, rather than elevation. Five cases of coronary artery spasm that emphasize the variable features of variant angina and offer aid for the prompt diagnosis and treatment of the syndrome are presented here.