Spontaneous Angina Research Articles

Randomised Placebo-Controlled Pilot Trial Evaluating the Anti-Anginal Efficacy of Ticagrelor in Patients with Angina with Nonobstructive Coronary Arteries and Coronary Slow Flow Phenomenon.

Background: The coronary slow flow phenomenon (CSFP) is an angiographic finding characterised by the delayed passage of contrast through the coronary arteries, despite the absence of obstructive coronary artery disease (defined as less than 50% narrowing of the vessel lumen). Patients with the CSFP experience recurrent angina, for which there are limited evidence-based therapies. Ticagrelor may serve as an effective anti-anginal therapy for these patients by increasing adenosine levels, which could alleviate coronary microvascular dysfunction and its associated angina due to its vasodilatory properties. This study aimed to determine the anti-anginal efficacy of ticagrelor 90 mg taken twice daily on spontaneous angina episodes in patients with refractory angina (i.e., episodes ≥3/week despite two anti-anginals) and documented CSFP. Methods: In a randomised, double-blind, placebo-controlled, cross-over trial, the anti-anginal efficacy of a 4-week ticagrelor therapy regimen was evaluated in 20 patients with refractory angina (mean age 61.5 ± 10.5 years; 40% women) who had documented slow coronary flow. The primary endpoint was the frequency of angina episodes, recorded using an angina diary. Secondary endpoints included the duration and severity of angina episodes, consumption of short-acting nitrates, and health status evaluations using the Seattle Angina Questionnaire (SAQ) and the Short Form-36 (SF-36) indices. Results: During the four weeks of therapy, ticagrelor did not significantly improve angina symptoms compared to the placebo (placebo 25.7 (16.7)) vs. ticagrelor 19.8 (18.1), p > 0.05). Furthermore, it did not impact other patient-related outcome measures, including angina severity, duration, frequency of prolonged angina episodes, nitrate consumption, or the SAQ/SF-36 health outcome indices. No serious adverse events related to the study drug were observed. Conclusions: In patients with documented CSFP who were unresponsive to standard anti-anginal therapy, ticagrelor did not reduce the frequency of spontaneous angina episodes or the consumption of nitrates. Further confirmation of the potential benefits of this therapy may be obtained through a larger clinical trial.

Anti-Anginal Efficacy of Zibotentan in the Coronary Slow-Flow Phenomenon.

Patients with coronary microvascular disorders often experience recurrent angina for which there are limited evidence-based therapies. These patients have been found to exhibit increased plasma levels of endothelin; thus, selective endothelin-A (Et-A) receptor blockers such as zibotentan may be an effective anti-anginal therapy in these patients. The study evaluated the impact of a 10 mg daily dose of zibotentan on spontaneous angina episodes in patients with the coronary slow-flow phenomenon who had refractory angina (i.e., experiencing angina at least three times/week despite current anti-anginal therapy). Using a randomized, double-blind, placebo-controlled, crossover trial design with 4-week treatment periods, 18 patients (63.2 ± 9.9 years, 33% females) were recruited. The primary endpoint was angina frequency as measured by an angina diary, with secondary endpoints including nitrate consumption, angina duration/severity and the Seattle Angina Questionnaire (SAQ) domains. During the 4 weeks of therapy, angina frequency significantly improved with zibotentan therapy (placebo 41.4 (58.5) vs. zibotentan 29.2 (31.6), p < 0.05), and sublingual nitrate consumption significantly reduced (placebo 11.8 (15.2) vs. zibotentan 8.8 (12.9), p < 0.05. Zibotentan improved the frequency of spontaneous angina episodes and reduced sublingual nitrate consumption in patients unresponsive to standard anti-anginal therapy.

Psycho-emotional status and vegetative resistance in patients with chronic cerebral ischemia on the background of angina pectoris

Objective — to assess the psycho‑emotional status and autonomic resistance in patients with chronic cerebral ischemia (CCI) against the background of stable angina pectoris (SAP).Methods and subjects. A total of 90 patients (61 male and 29 female) were examined, the mean age was 60.6 ± 7.8 years with CCI against the background of SAP II (first group n = 45) and III FC (second group, n = 45) of functional type. Control group comprised 30 patients (10 male and 20 female, mean age 55.27 ± 5.47) with CCI without stable exertional angina or post stroke cardio sclerosis. All patients underwent a comprehensive study of vegetative status, which included a survey by A. M. Wayne’s scheme for assessing vegetative subjective and objective symptoms, Kerdo’s vegetative index, Hildebrant index, ortho‑clinostatic test, and vegetative samples for evaluating vegetative reactivity. The level of anxiety and depression was assessed using the HADS and Spielberger — Hanin scale.Results. In terms of the Hildebrant vegetative index, the prevalence of mixed vegetative tonus was found in both the main and control groups, but in the group of patients with HIM against the background of SAP III FC, sympathicotonia was almost 3.5 times more frequent than in the first group and 5 times more frequent than in the control group. It was found out that in patients with CCI with SAP III FC, there were statistically significantly more patients with a high level of both reactive and personal anxiety.Conclusions. In the group of patients with CCI against the background of SAP III FC, a high level of depression and anxiety, reactive and personal anxiety was revealed, which causes pronounced autonomic dysfunction, which was manifested by insufficient vegetative support and the predominance of sympathicotonia in these patients. Detected autonomic dysfunction is one of the mechanisms of progression of SAP in patients with CCI. In ischemic heart disease (IHD), a marked myocardial remodeling and restructuring of the heart’s ANS occurs, causing the activation of the sympathoadrenal system and a decrease in the activity of the parasympathetic ANS, and thereby reduces the duration of painless myocardial ischemia and increases the duration of spontaneous angina attacks.

Spontaneous angina bullosa hemorrhagica of tongue: An unusual problem following prosthodontic procedure

Introduction: Angina Bullosa Hemorrhagica (ABH) is the term used to describe benign subepitilial oral mucosal blood filled blisters, which are not attributed to any systemic disorder. It is a very uncommon condition, mostly seen in elderly patients. The exact etiopathogenesis of the ABH is not known. Herewith, we present a case of 50-year-old male patient who developed ABH on right lateral border of the tongue, following prosthodontics impression making for completely edentulous mouth. Methods: The case management method was topical application of chlorhexidine gel (1%) and lignocaine gel (2%) with avoidance of hot and spicy food. Result and discussion: After one week in treating with topical therapy, the lesion became normal. The diagnosis of ABH is difficult in patients because of its asymptomatic nature. The early diagnosis of the lesion is very important as a rapidly expanding blood-filled bulla in the oropharynx can cause upper airway obstruction. Therefore, a high level of suspicion is warranted on part of dentists who may the first to encounter the lesion. Conclusion: Spontaneous Angina Bullosa Hemorrhagica of tongue was an unusual problem that can occur following prosthodontic procedure. The management of the lession were intended to reduce pain or discomfort and prevent secondary infections.

Coronary Blood Flow and Myocardial Metabolism in Angina Pectoris

It is interesting to note on this centenary celebration that we still are uncertain about the nature of anginal pain; we discuss the nitrites, we carry out experiments, yielding new data, and yet we are still really not quite sure how these agents act. I think it is desirable to review with humility some f Lauder Brunton’s ideas about the actions of these drugs. At a major national meeting in America just one year ago, the observation was made that the blood pressure rises before pain occurs in attacks of spontaneous angina pectoris. Unfortunately the speaker failed to appreciate that Sir Lauder Brunton had suggested the use of amyl nitrite for this very reason, namely high blood pressure with angina. He thought that nitrites might reduce the pain of angina pectoris by lowering the pressure.

Clinical implications of provocation tests for coronary artery spasm: safety, arrhythmic complications, and prognostic impact: Multicentre Registry Study of the Japanese Coronary Spasm Association

Provocation tests of coronary artery spasm are useful for the diagnosis of vasospastic angina (VSA). However, these tests are thought to have a potential risk of arrhythmic complications, including ventricular tachycardia (VT), ventricular fibrillation (VF), and brady-arrhythmias. We aimed to elucidate the safety and the clinical implications of the spasm provocation tests in the nationwide multicentre registry study by the Japanese Coronary Spasm Association. A total of 1244 VSA patients (M/F, 938/306; median 66 years) who underwent the spasm provocation tests were enrolled from 47 institutes. The primary endpoint was defined as major adverse cardiac events (MACEs). The provocation tests were performed with either acetylcholine (ACh, 57%) or ergonovine (40%). During the provocation tests, VT/VF and brady-arrhythmias developed at a rate of 3.2 and 2.7%, respectively. Overall incidence of arrhythmic complications was 6.8%, a comparable incidence of those during spontaneous angina attack (7.0%). Multivariable logistic regression analysis demonstrated that diffuse right coronary artery spasm (P < 0.01) and the use of ACh (P < 0.05) had a significant correlation with provocation-related VT/VF. During the median follow-up of 32 months, 69 patients (5.5%) reached the primary endpoint. The multivariable Cox proportional hazard model revealed that mixed (focal plus diffuse) type multivessel spasm had an important association with MACEs (adjusted hazard ratio, 2.84; 95% confidence interval, 1.34-6.03; P < 0.01), whereas provocation-related arrhythmias did not. The spasm provocation tests have an acceptable level of safety and the evaluation of spasm type may provide useful information for the risk prediction of VSA patients.

Abstract 9477: Gender Differences in Clinical Characteristics and Risk Factors of Patients with Vasospastic Angina -A Report from the Nationwide Multi-Center Registry by the Japanese Coronary Spasm Association

Background: Recently, much attention has been paid to gender differences in cardiovascular medicine. Previous studies showed that vasospastic angina (VSA) is more common in male. However, the gender differences in clinical characteristics and outcomes of VSA patients remain to be fully elucidated. Thus, we addressed this important issue in the nationwide multi-center registry by the Japanese Coronary Spasm Association. Methods: We enrolled a total of 1,429 VSA patients (male/female, 1090/339; median 66 years) from 47 institutes in Japan between September 2007 and December 2008 with a median follow-up period of 32 months. The primary endpoint was defined as major adverse cardiac events (MACE), including cardiac death, non-fatal myocardial infarction (MI), unstable angina and heart failure. Results: In comparison with the female patients, the male patients were characterized by younger age (median 66 vs. 69 years, P&lt;0.001), higher incidence of smoking (72 vs. 20%, P&lt;0.001), previous MI (7 vs. 3%, P=0.003), organic coronary stenosis &gt;50% (16 vs. 9%, P=0.001) and ST elevation during spontaneous angina attacks (21 vs. 11%, P&lt;0.001). For the treatment of VSA, Ca channel blocker was used in more than 90% of patients in both genders, whereas antiplatelet was more frequently used in male than in female (50 vs. 38%, P&lt;0.001). Although 5-year MACE-free survival rate was comparable (male 91 vs. female 94%), Cox proportional hazard model demonstrated that the risk factors of MACE were considerably different between genders; male patients were more associated with structural abnormality (e.g., organic stenosis, previous MI), whereas female patients with electrical abnormality (e.g., VT/VF during spontaneous attack) ( Table ). Conclusions: These results indicate that there are substantial gender differences in the clinical characteristics and the risk factors of MACE in VSA patients, suggesting the importance of gender-specific management of the disorder.

Mechanisms of Coronary Artery Spasm

The term coronary artery spasm (CAS) refers to a sudden, intense vasoconstriction of an epicardial coronary artery that causes vessel occlusion or near occlusion. Although CAS may be involved in other coronary syndromes, it represents the usual cause of variant angina. The variant form of angina was first described in 1959 by Prinzmetal et al,1 who used this term to indicate that angina attacks, unlike the most common form of effort angina, occurred at rest and were associated with ST-segment elevation, rather than ST-segment depression, on the ECG (Figure 1). Because myocardial ischemia occurred in the absence of any change in myocardial oxygen demand, the authors hypothesized that it was caused by an increased tonus of vessels at the level of coronary stenoses.1 Figure 1. (Top) ST-segment elevation in anterior leads, with reciprocal mild ST-segment depression in inferior leads and V6, during an angina attack in a patient with variant angina. (Bottom) Normalization of the ECG after spontaneous resolution of chest pain. Some years later, in fact, coronary angiography, performed during spontaneous angina attacks, demonstrated that CAS is the usual cause of variant angina.2–4 Coronary angiography also showed that CAS could occur at the site of a stenosis (either minor or severe) or in angiographically normal coronary arteries,5 usually at a localized segment of an epicardial artery (focal spasm) (Figure 2).6 However, sometimes CAS involves 2 or more segments of the same (multifocal spasm) or of different (multivessel spasm) epicardial coronary arteries, or may also involve diffusely one or multiple coronary branches.7 Figure 2. Occlusive spasm of the left circumflex coronary artery and near occlusive spasm of the left anterior descending coronary artery (arrows) during coronary angiography (left, top), associated with dramatic ST-segment elevation at monitoring ECG leads (left, bottom). Complete resolution of spasm (right, …

Spontaneous Echocardiographic Wall Motion Abnormalities in Variant Angina

Variant angina, defined as spontaneous angina pectoris associated with transient ST-segment elevation, is usually caused by episodic coronary spasm. At present, coronary artery spasm is a reversible coronary stenosis that limits coronary blood flow under resting conditions. Prinzmetal first described this type of angina pectoris as a distinct entity in 1959.1 Although several hypotheses have been suggested, the precise mechanism for coronary vasospastic disease remains unclear. Natural history of variant angina is heterogeneous. In most of the cases, the prognosis is good; however, it can lead to myocardial infarction (MI), life-threatening ventricular arrhythmias, and sudden death. A 51-year-old man, a smoker, who had no history of cardiac disease and who was affected by hepatitis C positive-related cryoglobulinemic glomerulonephritis with mild renal failure, was admitted to the emergency department for sudden, typical chest pain that occurred during a routine nephrologic visit. The 12-lead ECG showed a significant ST-segment elevation in …

Inflammation in variant angina: Is there any evidence?

Variant angina, defined as spontaneous angina pectoris associated with transient ST-segment elevation, has proved to be caused usually by episodic coronary spasm since Prinzmetal and his associates described a form of angina quite different from classic Heberden angina pectoris in 1959. Currently, coronary artery spasm is defined as reversible coronary stenosis, which limits coronary blood flow under resting conditions, and it plays an important role in ischemic heart disease, particularly in variant angina. Data available in respect of coronary vasospasm showed that it is closely related to atherosclerotic coronary artery disease, since intravascular ultrasound studies reveal atherosclerotic plaques in almost any spastic segment. Risk factors for coronary artery disease and coronary vasospasm, however, differ profoundly. Cigarette smoking is the only established risk factor. Although several candidates and predisposing factors, such as serotonin, histamine, thromboxane, and endothelin, have been described, the mediators and the pathogenesis of the disease remain unknown. There are abundant studies that inflammation plays an important role in the initiation, development as well as evolution of atherosclerosis, suggesting that atherosclerosis is an inflammation disease. The evidence regarding the role of inflammatory pathways in different clinical entities of coronary artery disease has significantly been accumulated. And also, primary studies have showed that inflammation may be a contributor for variant angina or vasospastic coronary disease is at least partially driven by inflammation. Although much more research is obviously needed, primary evidence provide us with some direction for that research.

Interpreting new treatment guidelines for non-ST-segment elevation acute coronary syndromes

The American College of Cardiology/American Heart Association Task Force on Practice Guidelines has published recommendations on the diagnosis and treatment of patients with known or suspected unstable angina and non-ST-segment elevation myocardial infarction. The acute ischemia pathway presented in these guidelines encompasses both an early invasive strategy and an early conservative strategy. There are now 4 randomized, controlled trials that have compared the routine early invasive strategy with the selective-invasive or ischemia-guided strategy (Thrombolysis in Myocardial Infarction [TIMI] IIIB, Veterans Affairs Non-Q-Wave Infarction Strategies in Hospital [VANQWISH], Fragmin and Fast Revascularization During Instability in Coronary Artery Disease [FRISC] II, and Treat Angina with Aggrastat and Determine Cost of Therapy with an Invasive or Conservative Strategy [TACTICS]-TIMI 18). The most relevant of these studies to current clinical practice are the FRISC II and TACTICS-TIMI 18 studies. The data from these studies indicate that ST-segment depression or elevated levels of troponin or the MB isoenzyme of creatinine kinase are markers of increased risk and that such patients would benefit from early revascularization. However, the data further suggest that aggressive antiplatelet, antithrombin, and anti-ischemic therapies are also important. Although FRISC II and TACTICS-TIMI 18 support an early invasive approach in most patients (ie, intermediate- and high-risk patients) with non-ST-segment elevation acute coronary syndromes (ACS), all 4 trials support a more conservative approach in those without electrocardiographic changes or enzyme elevations, notably the use of intensive antiplatelet, antithrombotic, and anti-ischemic therapy combined with careful clinical assessment and provocative testing. Patients then undergo catheterization and revascularization only if spontaneous angina occurs or if there is electrocardiographic, enzymatic, or other objective evidence of stress-induced myocardial ischemia. We conclude that tailoring the early initial therapy in hospital to the level of risk is essential to optimizing efficacy and clinical outcomes in this challenging, but common group of ACS patients.

Avoidance of routine revascularization in the management of patients with non-ST-segment elevation acute coronary syndromes

A debate continues over whether a routine invasive or a conservative strategy is the best treatment approach for patients with non–ST-segment elevation acute coronary syndrome. The fundamental question underlying this debate is whether risk stratification should be an anatomy-driven or an ischemia-driven process. An early routine invasive or “drive-through” strategy, which consists of cardiac catheterization followed by percutaneous coronary intervention within 24 hours of the onset of angina, has not been shown to result in improved outcomes. In fact, investigators in the Veterans Affairs Non–Q-Wave Infarction Strategies in Hospital (VANQWISH) trial found that aggressively treated patients had significantly worse outcomes during the first year of follow-up than did those treated with a conservative strategy. In this overview, a conservative (ischemia-guided) strategy with aggressive medical therapy is recommended for patients with non–ST-segment elevation acute coronary syndrome. This conservative treatment includes intensive antiplatelet, antithrombotic, and anti-ischemic therapy combined with careful clinical assessment and provocative testing. Patients undergo catheterization and revascularization only if spontaneous angina occurs or there is objective evidence of stress-induced myocardial ischemia. In the future, it may be revealed that only patients at high risk have real benefit from early aggressive therapy, but the same approach may result in harm to patients at low risk. Tailoring therapy to the level of risk is essential to optimizing efficacy and clinical outcomes.

Effects of ischemia on P wave dispersion and maximum P wave duration during spontaneous anginal episodes.

P wave dispersion (P dispersion), defined as the difference between the maximum and the minimum P wave duration, and maximum P wave duration (P maximum) are electrocardiographic (ECG) markers that have been used to evaluate the discontinuous propagation of sinus impulses and the prolongation of atrial conduction time, respectively. To study the effects of myocardial ischemia on P dispersion and P maximum, 95 patients with coronary artery disease (CAD) and typical angina pectoris and 15 controls with angina like symptoms underwent 12-lead surface ECG during and after the relief of pain. During pain and during the asymptomatic period, P maximum and P dispersion were calculated from the averaged complexes of all 12 leads. P dispersion increased significantly during spontaneous angina (45+/-17 ms) compared to the asymptomatic period (40+/-15 ms), P < 0.001 only in the patient group. Both P maximum and P dispersion showed higher values during angina in those patients who developed diffuse ischemia, as estimated with ST segment changes in multiple ECG leads. P dispersion showed higher values during the anginal episode in patients with left ventricular dysfunction, independently of the presence of a previous myocardial infarction. Atrial conduction abnormalities, as estimated with P maximum and particularly P dispersion, are significantly influenced by myocardial ischemia in patients with CAD and spontaneous angina.

Effects of ischemia on QT dispersion during spontaneous anginal episodes

Myocardial ischemia induced by pacing, angioplasty, or stress results in a significant increase in QT dispersion (QTd = QT maximum - QT minimum). This study investigated the effects of ischemia on QTd and the rate-corrected QTd (QT cd) during spontaneous anginal episodes in patients with coronary artery disease (CAD). Ninety-five patients with CAD and typical angina pectoris and 15 control subjects complaining of anginalike symptoms were studied. QTd and QT cd were calculated from 12-lead surface electrocardiograms recorded during and after the relief of pain. QTd and QT cd were significantly higher during the anginal episode (84 ± 31 ms and 98 ± 51 ms) compared to the painless conditions (69 ± 24 ms and 71 ± 24 ms) ( P = .003 and P = .001 for QTd and QT cd, respectively) only in the 57 CAD patients who had a history of an old previous myocardial infarction. QTd and QT cd are significantly increased during spontaneous angina in patients with documented CAD and history of previous myocardial infarction.

Ischemic Preconditioning in Unstable Coronary Syndromes: Evidence for Time Dependence

Objectives. We hypothesized a time-dependent relation between angina occurring spontaneously before percutaneous transluminal coronary angioplasty (PTCA) and the likelihood of an ischemic response during initial balloon occlusion. We further hypothesized that the ability to elicit the “classic” mode of PTCA-related preconditioning would vary with the interval from clinical angina to PTCA.Background. Antecedent angina represents a potential for myocardial preconditioning in unstable ischemic coronary syndromes.Methods. We studied 67 patients with Braunwald class III unstable coronary syndromes undergoing PTCA. The interval between the last spontaneous episode of angina preceding PTCA and initial balloon inflation was categorized as follows: 0 to 6 h; 6 to 12 h; 12 to 24 h; and >24 h.Results. Across the various intervals, there was a significant difference (p = 0.004) in the proportion of patients with an absent ischemic response during the first balloon inflation (0 to 6 h, 50%; 6 to 12 h, 35%; 12 to 24 h, 23%; and >24 h, 4%). There was, however, no difference between the first and second inflations in the proportion of patients with a diminished ischemic response until 6 to 12 h (p = 0.017) had elapsed since the last spontaneous episode of angina. Patients whose angina last occurred >24 h before the first inflation showed the greatest inducibility of PTCA-related preconditioning.Conclusions. Strong evidence exists for the occurrence of ischemic preconditioning in unstable coronary syndromes. Although the protective effect of spontaneous angina appears to wane beyond 6 h, recovery of preconditioning occurs from 6 to 12 h. Thus, preconditioning can be reinduced during PTCA with a marked potentiation of the effect at 24 h. This suggests an underlying time-dependent mechanism with a physiologic “half-life” of 6 to 12 h.

F42. Ultrasound: An unexplored tool for studying hemorheology

Thirty-seven patients affected by spontaneous angina and 15 comparable control subjects were enrolled in a 12-month prospective study to evaluate the relationship between blood clotting activation (assessed by fibrinopeptide A [FPA] plasma concentration) and the occurrence of myocardial ischemic attacks. FPA measurements and clinical examinations in patients were performed every 2 weeks. In control subjects blood sampling was performed every 4 weeks. Data from 28 patients who completed the study and from the 15 control subjects were analyzed. The clinical activity of angina was divided into three classes (asymptomatic, mildly symptomatic, and severely symptomatic) on the basis of the number and time-concentration of the ischemic attacks and ECG changes during the 15 days preceding each clinical examination. In all but one patient, a cyclic pattern of activity of coronary artery disease was observed. During follow-up studies, 624 FPA measurements were performed in patients and 173 in control subjects. Mean values were 4.68 ± 4.53 and 1.32 ± 0.60 ng/ml, respectively (p < 0.001). FPA levels differed markedly in relation to the activity of angina. A relationship between FPA levels and activity of disease (r = 0.54, p < 0.01) was found in time course. Bolus heparin administration (100 IU/kg) during the active phase of angina sharply but incompletely lowered FPA plasma levels, indicating thrombin formation both intravascularly and extravascularly. Present results indicate that a marked blood clotting activation occurs simultaneously with the outbursts of clinical activity of spontaneous angina.

Vasotonic angina: A spectrum of ischemic sysdroms involving function abnormalities of the epicardial and microvascular coronary circulation

Objectives. The present study was undertaken to investigate the response of large and small coronary arteries in a subgroup of patients with no or minimal coronary artery disease found to have objective signs of myocardial ischemia.Background. Many patients apparently have normal coronary arteries despite abnormal electrocardiographic (ECG) changes during spontaneous angina attacks or exercise stress testing.Methods. Twenty-five patients with no or minimal (<30% stenosis) coronary artery disease were chosen from a pool initially selected on the basis of spontaneous anginal attacks and ST segment shifts in the anterior leads. Of these, 10 were grouped as having variant angina (at least one episode of ST elevation) and the remaining 15 as having syndrome X (exercise-induced anginal pain, ST depression and reversible thallium abnormalities). Data were compared with those obtained in 10 patients with stable angina and documented coronary artery disease. Eighteen patients with supraventricular arrhythmias and normal coronary arteries served as control patients. Patients showing focal spasm during ergonovine testing were not included in the subsequent angiographic analysis. Great cardiac vein blood flow, aortic pressure and changes in coronary artery diameter were measured at rest and 2 to 4 min after hyperventilation in the remaining study group. The same procedure was repeated after sublingual administration of 0.3 mg of nitroglycerin in eight patients (four with syndrome X and four with variant angina).Results. Hyperventilation induced diffuse epicardial coronary diameter reduction, which was marginal in control patients (9 ± 4%) and those with coronary artery disease (5 ± 3%) but severe (p < 0.001) in those with variant angina (28 ± 14%) or syndrome × (25 ± 13%). Concomitant determination of coronary flow showed significant (p < 0.001) decreases in those with variant angina (25 ± 11%) and syndrome × (28 ± 10%) but not in control patients (5 ± 8%) or those with coronary artery disease (4 ± 5%), Changes in great cardiac vein blood flow during hyperventilation were similar before and after nitroglycerin.Conclusions. These indicate vasoconstrictor stimuli may trigger a diffuse abnormal response of both epicardial and resistance vessels in some patients with chest pain and angiographicaily normal coronary arteries. Patients showing such diffuse vasoconstrictor abnormalities are suggested to have a single pathogenetic entity with a spectrum of ECG manifestations ranging from ST depression to ST elevation.

Risk stratification in unstable angina: how to select patients who need emergency revascularization.

Patients considered to have unstable angina have a varying prognosis depending on their clinical presentation. Prognosis can be influenced by several factors including persistent pain, transient ST segment shifts, left main coronary artery stenosis, and silent myocardial ischemia. Most patients who present with unstable angina have their symptoms controlled initially with pharmacological management. If symptoms persist, coronary angioplasty or heart surgery can be performed but morbidity and mortality is slightly higher than in patients who are stable. Patients who will benefit from early revascularization include those with persistent myocardial ischemia as manifested by spontaneous angina, spontaneous ST segment shifts on ambulatory ECG, a positive exercise test at a low cardiac workload, or a markedly positive radionuclide or cardiac ultrasound imaging test.

The sensitivity of intracoronary injection of acetylcholine in inducing coronary spasm differs in patients with stable and unstable angina

In an attempt to clarify the role of coronary artery spasm in the pathogenesis of unstable angina, acetylcholine (20 and 50 μg) was injected directly into the coronary arteries of 19 patients with unstable effort angina (group 1), 30 patients with unstable spontaneous angina (group 2), and 15 patients with stable effort angina due to coronary artery organic stenosis (≧ 75%) (group 3). Coronary spasm was defined as severe vasoconstriction (≧ 90% of luminal diameter) with chest pain and/or ischemic ST-segment changes. Intracoronary injection of acetylcholine induced spasm of at least one coronary artery in 19 patients (100%) of group 1 and 28 (93%) of group 2 but only 3 (20%) of group 3 ( p < 0.01). When acetylcholine was injected into the left and right coronary arteries separately, multivessel spasm (spasm of both coronary arteries) was induced in 5 of 12 (42%) patients of group 1 and in 9 of 23 (39%) patients of group 2. In contrast, intracoronary acetylcholine did not cause multivessel coronary spasm in any of 15 patients of group 3 (0%). These results suggest that coronary arteries in patients with unstable effort angina as well as spontaneous angina are susceptible to spasm and that coronary artery spasm may be responsible at least in part for the genesis of attacks in these patients.

Long term IV infusion of gallopamil reduces ischaemic episodes in spontaneous angina

Long term IV infusion of gallopamil reduces ischaemic episodes in spontaneous angina