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At least 19 recordsLinked to original sources

PubMedDate not supplied

Angina patients' ratings of current health and health without angina: associations with severity of angina and comorbidity.

OBJECTIVE: To investigate the relationship between chronic stable angina patients' ratings of two health states (current health and health free of angina), the difference between these two ratings (the "anticipated gain"), and measures of anginal severity and comorbidity. DESIGN: Cross-sectional interviews and questionnaires. SETTING: Out-patient clinics and medical inpatient service of a Veterans Affairs Medical Center. PARTICIPANTS: Patients with chronic stable angina with no prior history of a revascularization procedure attending clinic appointments (n = 44) or electively admitted for cardiac catheterization (n = 11). Measurements. Ratings of current health and health free of angina using a verbal rating scale in which 0 = death and 100 = perfect health, the MOS SF-36, the Index of Coexistent Disease (a validated measure of comorbidity), and a question on the severity of anginal symptoms. RESULTS: Mean (95% CI) rating of current health was 61.8 (59.2, 64.4) and that of health free of angina was 77.0 (74.5, 79.5). Median anticipated gain between the two health ratings was 10.0 (range 0-80). Correlations between ratings for both health states and subscales of the SF-36 were positive, with some reaching statistical significance. In regression models with rating of current health, rating of life without angina, and anticipated gain as the dependent variables, severity of comorbidity was highly significant in all three, whereas severity of angina was significant only in the current-health rating model. Severity of comorbidity had much greater explanatory power in all three models than did severity of angina. CONCLUSIONS: Severity of comorbidity was a better predictor of patients' current health rating, rating for angina-free health, and anticipated gain from relief of angina than was severity of angina. Since patient perceptions of a symptom may be distinct from self-reported symptom severity, treatment-outcome studies should assess patient preferences in addition to symptom severity. Comorbidity should also be measured in such studies. Having patients rate current health and symptom-free health may be a useful measure of treatment effectiveness for specific symptoms in clinical trials and patient care, and may help patients and clinicians prioritize multiple health problems.

Activities of Daily Living↗

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↗

PubMed1975

Left and right heart haemodynamics during spontaneous angina pectoris. Comparison between angina with ST segment depression and angina with ST segment elevation.

The function of both right and left sides of the heart was studied during spontaneous attacks of angina pectoris at rest in 7 patients showing ST depression (type I) and 4 showing ST elevation (type II) during the attack. In none of the 44 type I attacks and 29 type II attacks which were recorded did circulatory changes; the latter were different in the two groups. Type I attacks showed: a) a brief fall in arterial pressure, accompanied by b) a rise of right atrial and pulmonary wedge pressures and c) a decrease of cardiac output, right and left stroke work, the mean rate of systolic ejection, and indirect left ventricular pre-ejection dP/dt. In the course of the attack a hypertensive phase followed, which was paralleled by an increase of heart rate, cardiac output, left and right stroke work, and mean systolic ejection rate, left dP/dt; right atrial pressure and wedge pressure remained raised. All of the circulatory functions started to revert towards the pre-attack levels coincident with the waning phase of the electrocardiographic alteration, the latter occurring either spontaneously or after nitroglycerin. Type II attacks for the entire duration of the electrocardiographic changes showed: a) a reduction of arterial pressure, cardiac output, right and left stroke work, mean systolic ejection rate, and left dP/dt, b) a rise of right atrial and wedge pressures, and c) quite small changes of heart rate. When the electrocardiogram started to revert to the pre-attack aspect, the cardiac function rapidly improved and, after a supernormal phase, returned to the basal levels in about 2 minutes. It is concluded: 1) that no circulatory factor interfering with the mechanical effort of the heart is responsible for eliciting spontaneous angina: 2) that in type I attacks right and left ventricular impairment occurs which recovers rapidly, possibly through a sympathetic compensation; 3) that in type II attachs dysfunction of both sides of the heart occurs and persists throughout the episode of electrocardiographic alteration; 4) that the dynamic impairment is probably more severe in type I than in type II angina.

Angina Pectoris↗

PubMed1994

Outcome of patients with diabetes and unstable angina. A subgroup analysis in the Spanish Multicentre Trial of trifusal in unstable angina. Grupo de Estudio del Trifusal en la Angina Inestable.

We analyzed the clinical characteristics of the 58 diabetic and 218 nondiabetic patients enrolled in the Spanish multicentre trial of trifusal in unstable angina. After 6 months of follow-up, 25 suffered from myocardial infarction or death, 10 of which were diabetics (17.2%) and 15 nondiabetics (6.9%) (P = 0.0146). This difference remained significant after multivariate analysis. We conclude that diabetes is an independent predictor of adverse outcome in patients with medically treated unstable angina.

Aged↗

PubMed1991

Ticlopidine treatment for patients with unstable angina at rest. A further analysis of the study of ticlopidine in unstable angina. Studio della Ticlopidina nell'Angina Instabile Group.

Data collected to investigate the effects of ticlopidine in a subset of 489 patients with angina at rest accompanied by transient ischaemic electrocardiographic changes have been analysed. Of the 489 patients, 255 received conventional treatment including beta-blockers, nitrates, or calcium antagonists (control group); 234 received conventional treatment plus ticlopidine 250 mg b.i.d. (ticlopidine group). The predefined end-points were vascular death and acute myocardial infarction (AMI). The incidence of end-points was assessed according to the intention-to-treat principle. The post-hoc estimated statistical power was 80%. The rate of death or AMI in the 6-month follow-up period was reduced from 14.9 to 6.8% (-54.4%) (odds ratio: 0.42; confidence intervals: 0.22, 0.80). The incidence of fatal or nonfatal AMI was reduced from 12.2 to 4.3% (-65%) (odds ratio: 0.32; confidence intervals: 0.14, 0.70) and of nonfatal AMI from 10.2 to 3.8% (-63%) (odds ratio: 0.35; confidence intervals: 0.15, 0.80). Nineteen patients died; 12 in the control group (4.7%) and seven in the ticlopidine group (83%) (-36%) (odds ratio: 0.62; confidence intervals: 0.21, 1.74); five patients in the control group and only one in the ticlopidine group died of an AMI. The post-hoc estimated statistical power was 80%. However, we cannot draw definitive conclusions about the clinical effect of ticlopidine treatment in the patients with angina at rest accompanied by transient ischaemic electrocardiographic changes because the subgroup analysis was not planned a priori. Nevertheless, this report strongly suggests that such patients can benefit from antiplatelet treatment with ticlopidine; the benefit mainly depends on the protective effect against myocardial infarction.

Aged↗

PubMed1995

Comparative study of left ventricular function in patients with unstable angina, non-Q wave myocardial infarction and stable angina pectoris: assessment with atrial pacing and digital ventriculography.

To compare left ventricular global and segmental function at rest and during right atrial pacing in patients with unstable angina, non-Q wave myocardial infarction, and stable angina (class III angina), low-dose digital subtraction ventriculography was performed at rest and after abrupt cessation of pacing in 42 patients with unstable angina, 8 patients with non-Q wave myocardial infarction and 15 patients with stable angina during selective coronary arteriography. Left ventricular ejection fraction was significantly lower at rest in patients with unstable angina (P < 0.01) and non-Q wave myocardial infarction (P < 0.05) and during pacing (P < 0.01). These two groups of patients had significantly higher values of left ventricular end-diastolic and end-systolic volumes at rest and during pacing as compared with stable angina group. In comparing various clinical patterns of unstable angina, ejection fraction was significantly (P < 0.05) lower during pacing in patients with crescendo angina than in new-onset angina. However, ejection fraction was significantly (P < 0.01) lower in crescendo angina only at rest as compared with rest angina. The length of zone of severe hypokinesia was greater in unstable angina (P < 0.01) as well as in non-Q wave myocardial infarction (P < 0.05) both at rest and during pacing as compared with stable angina. Contractility of region of hypokinesia during pacing was higher (P < 0.01) in stable angina than in unstable angina and non-Q wave myocardial infarction. In analyzing segmental function in various subgroups of unstable angina, the authors found that the length of total hypokinesia was significantly higher (P < 0.05) during pacing in crescendo angina than in new-onset angina. Contractility of region of hypokinesia was lowest at rest and during pacing in patients with crescendo angina. This study demonstrates that patients with unstable angina as well as non-Q wave myocardial infarction were characterized by more pronounced global and segmental left ventricular dysfunction at rest and during pacing as compared with patients with stable angina, which may explain the poorer prognosis in the former two groups. This study also shows that patients with crescendo angina have more profound left ventricular global and regional dysfunction as compared with patients with new-onset as well as rest angina.

Adult↗

PubMed1995

Arteriographic morphology and intracoronary thrombus in patients with unstable angina, non-Q wave myocardial infarction and stable angina pectoris.

Coronary artery lesions were compared in 71 patients with unstable angina, 15 patients with non-Q wave myocardial infarction (MI), and 40 patients with stable angina. In the unstable angina group, 29 patients had new-onset angina, 31 had crescendo angina, and 11 had rest angina. In a subgroup of patients with unstable angina, three-vessel disease was less frequently (P < 0.05) seen in patients with new-onset angina (10.3%) than in the patients with crescendo angina (51.6%) or rest angina (54.5%). An angina-producing artery could be identified in 59 patients with unstable angina, in 11 with non-Q wave MI, and in 30 with stable angina. Type II eccentric stenosis (asymmetric narrowing with narrow neck and overhanging irregular edges) was present in 31 patients (52.5%; P < 0.01) with unstable angina, in 7 (63.6%; P < 0.01) with non-Q wave MI, and in only 2 (6.7%) with stable angina. Abrupt occlusion of a vessel was observed in 7 patients (11.9%) with unstable angina and in 2 (18.2%) with non-Q wave MI. None of the patients with stable angina had this type of occlusion. In the group of unstable angina and non-Q wave MI, angiographic evidence of intracoronary thrombi was present in 16 (27.1%) and 3 patients (27.3%), respectively, but in stable angina in only 1 patient (3.3%; P < 0.05). Intracoronary thrombi were most frequently found in rest angina (88%; P < 0.001) and crescendo angina (33.3%; P < 0.01) compared with new-onset angina (3.7%).(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

PubMed1995

Coronary artery plaque morphology in stable angina and subsets of unstable angina: an in vivo intracoronary ultrasound study.

Little information is available regarding the in vivo composition of angina producing culprit atherosclerotic lesions in various anginal syndromes. In this study we used intracoronary ultrasound to determine the composition of culprit lesions in various subsets of anginal syndromes and correlated this composition with the patient's clinical presentation. One hundred and forty six patients referred for angioplasty or atherectomy were classified as having either chronic stable angina (angina which was clinically unchanged for > 2 months), crescendo angina (an accelerating pattern of frequent or prolonged anginal episodes), severe rest angina (abrupt onset of prolonged angina) or post-infarction angina (angina within 2 weeks of acute myocardial infarction). Intracoronary ultrasound imaging of the culprit lesion was performed before intervention. Lesions were classified as soft, mixed fibrous without calcium, mixed fibrous with calcium or calcified. Analysis of the ultrasound images revealed that the majority of culprit lesions were soft in severe rest (71%) and post-infarction angina (73%) whereas, the majority of culprit lesions were mixed fibrous or calcified in chronic stable (69%) and crescendo (53%) angina (X2 = 22.73, p = 0.007). In addition, the frequency of intralesional calcium in chronic stable or crescendo angina was significantly higher than that in severe rest or stable angina. We conclude that the composition of culprit lesions in various anginal subsets are different. The lesion morphology in crescendo angina frequently resembles that in chronic stable angina; while those in severe rest and post-infarction angina are frequently similar. These findings may have implications for medical or interventional treatment of patients with angina.

Aged↗

PubMed1993

Relation between clinical presentation and angiographic findings in unstable angina pectoris, and comparison with that in stable angina.

The diagnosis of unstable angina encompasses a broad spectrum of patients with myocardial ischemia, varying widely in cause, prognosis and responsiveness to therapy. A new clinical classification of unstable angina is based on the following 2 components: severity, and the clinical setting in which unstable angina develops. The hypothesis that this clinical classification correlates with the underlying coronary artery anatomy was tested. In 238 consecutive patients, an unstable angina score ranging from 2 to 6 was determined by adding the scores for severity (1 = unstable angina without pain at rest; 2 = pain at rest > 48 hours before angiography; and 3 = pain at rest < or = 48 hours before angiographic evaluation) and the clinical setting of unstable angina (1 = unstable angina secondary to a noncardiac condition; 2 = primary unstable angina; and 3 = early postinfarction unstable angina). Fifty concurrently studied consecutive patients with stable angina were assigned a score of 0. Patients with unstable angina averaged 63 +/- 11 years of age, and 165 were men (69%). Pain at rest occurred in 202 of 238 patients (85%), and angiography was performed < or = 48 hours in 139 of these patients (69%). Among patients with unstable angina, 5 (2%) had secondary unstable angina, 143 (60%) had primary unstable angina, and 90 (38%) had postinfarction unstable angina. Multivariable regression analysis identified the unstable angina score as the most important predictor of intracoronary thrombus (p = 0.011) and lesion complexity (p = 0.004) in the ischemia-related artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1998

Changes in platelet size and count in unstable angina compared to stable angina or non-cardiac chest pain.

AIMS: An increase in platelet aggregability is associated with unstable angina and myocardial infarction. Platelet size and activity correlate and mean platelet volume was found to be increased before acute myocardial infarction. We measured the mean platelet volume and platelet count in patients with stable angina, unstable angina and non-cardiac chest pain. METHODS AND RESULTS: We studied 981 patients (734 men; 247 women) defined clinically as stable angina (n = 688), unstable angina (n = 108) and unstable angina requiring immediate angioplasty (n = 52). After coronary angiography the patients were subdivided into single (n = 269), double (n = 304) and triple-vessel disease (n = 311) and the control group of non-cardiac chest pain (n = 97). There was no significant difference in platelet count between the control group and patients with 1, 2, or 3-vessel disease. However, the platelet size in patients with coronary artery disease was significantly larger (single: 8.7 +/- 1.19 fl; double: 8.7 +/- 1.12 fl; triple-vessel disease: 8.8 +/- 1.18 fl) than the control group (8.2 +/- 0.95 fl) (P < 0.01). Patients with stable angina similarly had no, significant difference in platelet count compared to the control group but did have a significantly increased mean platelet volume (8.7 +/- 1.13; P < 0.01). In contrast, patients with unstable angina had a decreased platelet count (245 +/- 56 x 10/l) compared to either stable angina (262 +/- 62 x 10/l; P < 0.05) or the control group (261 +/- 58 x 10/l; P < 0.05); furthermore, the mean platelet volume (9.4 +/- 1.23 fl) was significantly greater than for stable angina (P < 0.01). Patients with unstable angina requiring immediate PTCA had an even lower platelet count (231 +/- 55 x 10/l) and higher mean platelet volume (10.4 +/- 1.03 fl) (P < 0.01) than the rest of the population with unstable angina. CONCLUSIONS: In stable angina the platelet count is unchanged compared to patients with normal coronary arteries but the platelet size is increased. However, in unstable angina there is a decrease in platelet count and an even larger increase in platelet size. We interpret this as meaning that unstable angina might be associated or preceded by an increase in platelet destruction rate that is not completely compensated for by an increase in platelet production rate. The large, more reactive platelets might be causally related to an ongoing coronary artery obstruction in unstable angina.

Adult↗

PubMed1998

Fasting and postprandial ischemic threshold in patients with unstable angina with and without postprandial angina at rest.

BACKGROUND: Postprandial angina develops within minutes after a meal in patients with unstable angina, but the clinical characteristics of these patients and why it develops in only some of those with advanced coronary artery disease remain largely unknown. A severely reduced coronary reserve associated with postprandial increases in heart rate could be a contributory mechanism. METHODS: The clinical and angiographic characteristics of 277 patients with unstable angina with (23) or without (254) postprandial angina were analyzed. The coronary reserve was also analyzed by measuring the ischemic threshold by atrial pacing in a fasting state in all patients and 15 minutes after a 900-calorie meal in 54. RESULTS: Patients with postprandial angina were older, more likely to be women, and had a higher incidence of hypertension and three-vessel disease than those without (p < 0.005) and had a lower fasting ischemic threshold (131.8 [SD 13.0] vs 147.5 [SD 23.4] beats/min, p < 0.0001). However, 67 of the 79 patients with the lowest fasting thresholds (< or =130 beats/min) (84.8%) had no postprandial angina. Moreover, among patients with and without postprandial angina who were matched for age, sex, and extent of coronary disease, the ischemic threshold was also lower in those with postprandial angina (p < 0.005) and there were no differences in left ventricular end-diastolic pressure or volume. Postprandial pacing was positive in 37 patients but postprandial ischemic threshold was comparable to fasting threshold (132 [SD 14] vs 132 [SD 16] beats/min). Moreover, in the 10 patients who experienced in-hospital postprandial angina, heart rate during postprandial angina was similar to nonpostprandial angina (93.1 [SD 14.7] vs 90.3 [SD 17.6]) and lower than the fasting ischemic threshold (132.0 [SD 10.8] beats/min, p < 0.0001). CONCLUSIONS: Thus postprandial angina tends to occur among elderly and hypertensive patients with advanced coronary disease and severely reduced ischemic threshold. The fact that the postprandial ischemic threshold was clearly higher than the heart rate attained during postprandial angina suggest that factors others than increases in heart rate account for postprandial angina. Furthermore, the lack of a decline in the postprandial ischemic threshold suggests that, in the absence of postprandial angina, there is not a consistent postprandial change in coronary tone or that the increases in myocardial oxygen demands due to increased myocardial contractility-wall tension do not seem to play a major role in postprandial ischemia.

Adult↗

PubMed1996

[Histopathologic features in atherectomy samples obtained from patient with unstable angina, stable angina and restenosis. Directional Atherectomy Lombardi Group].

BACKGROUND: The present study was aimed at investigating the pathologic features of directional coronary atherectomy (DCA) samples obtained from 194 patients (14 females) with stable (n = 68) and unstable (n = 95) angina, and with restenosis (n = 27). METHODS: DCA samples were obtained from culprit lesions, using the Simpson technique. Unstable angina was classified according to E. Braunwald criteria. Stable angina was grouped according to the presence or absence of a prior myocardial infarction (MI). DCA samples were fixed, processed, serially cut and stained with hematoxilin-eosin and with Movat pentachrome stain. RESULTS: The major pathologic findings were thrombosis, inflammation of the superficial plaque layers, and neointimal hyperplasia which often coexisted within a same sample. Their frequencies, in that order, were distributed in the differing groups of patients as follows: 21% (n = 9), 29.2% (n = 12) and 51% (n = 21) of the 41 cases with stable angina without prior MI. 40.7% (n = 11), 40.7% (n = 11), and 51.8% (n = 14) of the 27 cases with stable angina with prior MI. 25% (n = 4), 56.2% (n = 9) and 68.7% (n = 11), of the 16 cases with BI unstable angina. 35.3% (n = 14), 55.8% (n = 19) and 44% (n = 15), of the 34 cases with BII unstable angina. 44.4% (n = 4), 33.3% (n = 3) and 33.3% (n = 3), of the 9 cases with BIII unstable angina. 48.2% (n = 14), 48.2% (n = 14) and 51.8% (n = 15), of the 29 cases with CII unstable angina at 35.8 days after MI. 60% (n = 3), 60% (n = 3) and 40% (n = 2), of the 5 cases with CIII unstable angina at 8.3 days after MI. 26% (n = 7), 48% (n = 13) and 85.1% (n = 23), of the 27 cases with restenosis. According to above observation, the frequency of coronary thrombosis increases with the increase of the severity of myocardial ischemia. However, thrombosis is not found in most unstable angina without prior MI (63% of BI-II-III unstable angina cases do not have thrombus). In addition, thrombus is not a specific finding of unstable angina, given its occurrence, although in a much lower percentage of cases, in stable angina and in restenosis. CONCLUSIONS: Present data show that different ischemic and plaque lesions. This observation questions on the pathogenetic role of thrombus in unstable angina and calls for further investigations on inflammation and neointimal hyperplasia, as well as on the the reciprocal relation between these findings which are often combined within a same lesion.

Adult↗

PubMed1988

The efficacy of the addition of nifedipine in patients with mixed angina compared to patients with classic exertional angina: a multicenter, randomized, double-blind, placebo-controlled clinical trial.

Episodes of myocardial ischemia in patients with coronary artery disease may be due to transient increases in coronary vasomotor tone superimposed on a fixed atherosclerotic obstruction. The purpose of this study was to determine whether identification of the clinical pattern of angina could predict the therapeutic response to the addition of nifedipine to a regimen of beta blockers and/or long-acting nitrates. Seventy-two patients with stable exertional angina were divided into two groups: "classic exertional angina" (17 patients), defined as exertional angina with a stable threshold; and "mixed angina" (55 patients), defined as exertional angina provoked by a variable threshold and/or at least two episodes of rest angina within the 3 months prior to screening. Patients were studied with nifedipine and placebo in a 6-week, double-blind, crossover design that used serial anginal diaries, exercise treadmill tests, and 24-hour ambulatory ECG monitoring. In patients with mixed angina, nifedipine reduced the frequency of angina compared to that during placebo treatment (13.1 vs 9.9 episodes/3 weeks, p less than 0.01) and reduced nitroglycerin consumption (11.7 vs 7.5 tablets/3 weeks, p less than 0.05); while in patients with classic exertional angina, nifedipine had no symptomatic effect (7.9 vs 6.8 anginal episodes/3 weeks, NS; 6.4 vs 5.8 nitroglycerin tablets/3 weeks, NS). Patients in both groups experienced a significant decrease in the manifestations of ischemia during exercise testing. Patients with mixed angina experienced a reduction in the daily frequency of painful episodes of ST segment depression during nifedipine treatment compared to placebo (0.6 vs 0.2 episodes, p less than 0.05), but there was no effect on the frequency of episodes of silent ischemia (4.2 vs 3.4 episodes, NS). In patients with classic exertional angina, the addition of nifedipine had no effect on any measure of ambulatory ischemia. We conclude that patients with mixed angina are more likely to benefit symptomatically from the addition of nifedipine therapy than patients with classic exertional angina. The lack of a consistently preferential response to nifedipine in patients with mixed angina, however, suggests that episodic coronary vasoconstriction may not be the only mechanism responsible for ischemia in these patients, and/or that nifedipine may not necessarily provide additional therapeutic benefit beyond that conferred by a regimen of beta blockers and/or nitrates.

Adrenergic beta-Antagonists↗

PubMed1996

Early and six-month outcome in patients with angina pectoris early after acute myocardial infarction (the GISSI-3 APPI [angina precoce post-infarto] study).

There is conflicting evidence whether or not early postinfarction angina implies an unfavorable prognosis. This prospective study assessed the significance and natural history of early angina in a broad population of patients conservatively managed after acute myocardial infarction (AMI) and enrolled in the third Gruppo Italiano per lo Studio della Sopravvivenza nel Infarto Miocardico (GISSI-3) trial. Out of 2,363 consecutive patients (age 63 +/- 11; first AMI in 86%; thrombolysis in 74%) admitted in 31 centers lacking on-site revascularization facilities, early angina associated with transient electrocardiographic (ECG) changes was documented in 332 (14%). At multivariate analysis, preinfarction angina, age > or = 70 years, female gender, and history of infarct were significant predictors of early angina. Though the in-hospital course was free from major cardiac events in 78% of patients after the first anginal episode, reinfarction was more common after early angina (7% vs 2% in patients without, RR 3.1, 95% confidence interval [CI] 1.9 to 5.6; p <0.001), and death occurred in 7% of patients with early angina (vs 5% of patients without, RR 1.4, CI 0.9 to 2.4, p = NS). No demographic or clinical characteristics identified patients who suffered nonfatal reinfarction after angina, and neither the ECG location (infarct zone or remote) nor patterns of ECG changes during angina proved significant predictors of in-hospital reinfarction or death. Early angina emerged as the sole independent predictor of 6-month cumulative reinfarction (12% vs 5% of patients without, RR 2.9, CI 2.0 to 4.4; p <0.0001) and an independent predictor of death (13% vs 7% of patients without early angina, RR 2.3, CI 1.6 to 3.3; p <0.0001). Early postinfarction angina is a powerful prognostic marker. Patients with early postinfarction angina had an unfavourable in-hospital outcome, but the prospective identification of patients at greater risk of major events after angina remains elusive. Although in-hospital stabilization was achieved by medical treatment in the majority of patients with early angina, their increased 6-month risk of reinfarction and death suggests that a more aggressive management is warranted.

Age Factors↗

PubMed1987

Calcium antagonists for Prinzmetal's variant angina, unstable angina and silent myocardial ischemia: therapeutic tool and probe for identification of pathophysiologic mechanisms.

The calcium antagonists provide a unique tool to reduce myocardial oxygen demand and prevent increases in coronary vasomotor tone. For patients with Prinzmetal's variant angina, diltiazem, nifedipine and verapamil are extremely effective in preventing episodes of coronary vasospasm and symptoms of ischemia. Unstable angina pectoris is a more complex pathophysiologic syndrome with episodes of ischemia due to increases in coronary vasomotor tone, intermittent platelet aggregation or alterations in the underlying atherosclerotic plaque. Each of the calcium antagonists is effective as monotherapy in decreasing the frequency of angina at rest. Nifedipine is the only calcium antagonist that has been studied in a combination regimen with beta blockers and nitrates for patients with unstable angina, and control of angina is better with the combination regimen than with either form of therapy alone. Although symptoms of myocardial ischemia in unstable angina are reduced by calcium antagonists, these agents do not seem to decrease the incidence of adverse outcomes. Antiplatelet therapy appears to improve morbidity and mortality in patients with unstable angina, suggesting that thrombus formation may play a central role in that disorder. Episodes of silent or asymptomatic myocardial ischemia, identified by ST-segment monitoring, occur in a variety of disorders of coronary disease. Among patients with Prinzmetal's variant angina and unstable angina, episodes of silent ischemia appear to be as frequent as episodes of angina and the calcium antagonists are effective in decreasing episodes of ischemia regardless of the presence or absence of symptoms. Persisting episodes of silent ischemia among patients with unstable angina despite maximal medical therapy identify patients at high risk for an early unfavorable outcome. Among patients with stable exertional angina, episodes of silent ischemia may be up to 5 times as frequent as episodes of angina, and may be due to increases in coronary vasomotor tone, transient platelet aggregation or increases in myocardial oxygen demand. Preliminary experience suggests that calcium antagonists and beta blockers are effective in decreasing episodes of silent ischemia in patients with stable exertional angina and that a combination regimen may be more effective than either form of therapy alone.

Angina Pectoris↗

PubMed1978

Relationship of myocardial infarction to presence of angina pectoris in patients with coronary heart disease: lack of abolition of angina by infarction.

To evaluate the relationship between myocardial infarction and angina pectoris, history of symptomatic coronary heart disease was analyzed in 146 patients who had had documented myocardial infarction. There were 126 males and 70 females of mean age 55 years (range 32 to 70 years). Infarction had occurred 6 to 63 months prior to the study (mean: 30 months). Angina pectoris occurred at some time during the clinical course of 75 patients (51%), and 71 patients (49%) had not experienced angina. In the majority of the group with angina (n = 39; 52%) the symptom had not been present before infarction, appearing initially thereafter. Angina was present both before and after infarction in 31 patients (41%). In only 5 patients (7%) was precedent angina lost after infarction. Angina was, therefore, present in 70 of 146 patients (48%) after, compared to 36 patients (25%) before, infarction and in 86% (31/36) of patients with angina before infarction it persisted following the attack. Prior angina following myocardial infarction was not related to increased activity since in the majority of patients activity level was less after than before infarction. Post-infarction cardiac failure, which developed in 9 patients who had prior angina, was not associated with abolition of angina in any of this group. It is concluded that: 1. angina is frequent after myocardial infarction, 2. when present before infarction it usually persists thereafter, 3. angina commonly appears as a new symptom after infarction when not previously present and 4. disappearance of angina after infarction is distinctly uncommon.

Adult↗

PubMed1992

Plasma plasminogen activator inhibitor activity and tissue plasminogen activator levels in patients with unstable angina and those with coronary spastic angina.

Plasminogen activator inhibitor (PAI) activity and tissue plasminogen activator (TPA) antigen were measured in venous samples in 14 patients with unstable angina consisting of eight patients with organic stenosed coronary arteries and six patients with coronary spastic angina (unstable angina group); in 14 patients with stable exertional angina (stable exertional angina group); and in 14 patients with chest pain syndrome (chest pain syndrome group). The plasma levels of PAI activity were higher (p less than 0.01) in the unstable angina group than in the stable exertional angina group and the chest pain syndrome group (12.3 +/- 1.0 versus 5.1 +/- 0.7 and 4.8 +/- 0.6 IU/ml). The plasma levels of TPA antigen were also higher (p less than 0.05) in the unstable angina group than in the stable exertional angina group and the chest pain syndrome group (10.2 +/- 1.3 versus 6.5 +/- 0.8 and 6.0 +/- 0.7 ng/ml). There were no significant differences in PAI activity and TPA antigen levels between the stable exertional angina group and the chest pain syndrome group. Furthermore, both PAI activity and TPA antigen levels in the unstable angina group decreased to the levels in the stable exertional angina group and the chest pain syndrome group after treatment (p less than 0.01). In conclusion, the increased plasma PAI activity in patients with unstable angina and in those with coronary spastic angina indicates that the fibrinolytic system is impaired in these patients.

Angina, Unstable↗

PubMed2004

Effects of ranolazine with atenolol, amlodipine, or diltiazem on exercise tolerance and angina frequency in patients with severe chronic angina: a randomized controlled trial.

CONTEXT: Many patients with chronic angina experience anginal episodes despite revascularization and antianginal medications. In a previous trial, antianginal monotherapy with ranolazine, a drug believed to partially inhibit fatty acid oxidation, increased treadmill exercise performance; however, its long-term efficacy and safety have not been studied in combination with beta-blockers or calcium antagonists in a large patient population with severe chronic angina. OBJECTIVES: To determine whether, at trough levels, ranolazine improves the total exercise time of patients who have symptoms of chronic angina and who experience angina and ischemia at low workloads despite taking standard doses of atenolol, amlodipine, or diltiazem and to determine times to angina onset and to electrocardiographic evidence of myocardial ischemia, effect on angina attacks and nitroglycerin use, and effect on long-term survival in an open-label observational study extension. DESIGN, SETTING, AND PATIENTS: A randomized, 3-group parallel, double-blind, placebo-controlled trial of 823 eligible adults with symptomatic chronic angina who were randomly assigned to receive placebo or 1 of 2 doses of ranolazine. Patients treated at the 118 participating ambulatory outpatient settings in several countries were enrolled in the Combination Assessment of Ranolazine In Stable Angina (CARISA) trial from July 1999 to August 2001 and followed up through October 31, 2002. INTERVENTION: Patients received twice-daily placebo or 750 mg or 1000 mg of ranolazine. Treadmill exercise 12 hours (trough) and 4 hours (peak) after dosing was assessed after 2, 6 (trough only), and 12 weeks of treatment. MAIN OUTCOME MEASURES: Change in exercise duration, time to onset of angina, time to onset of ischemia, nitroglycerin use, and number of angina attacks. RESULTS: Trough exercise duration increased by 115.6 seconds from baseline in both ranolazine groups (pooled) vs 91.7 seconds in the placebo group (P =.01). The times to angina and to electrocardiographic ischemia also increased in the ranolazine groups, at peak more than at trough. The increases did not depend on changes in blood pressure, heart rate, or background antianginal therapy and persisted throughout 12 weeks. Ranolazine reduced angina attacks and nitroglycerin use by about 1 per week vs placebo (P<.02). Survival of 750 patients taking ranolazine during the CARISA trial or its associated long-term open-label study was 98.4% in the first year and 95.9% in the second year. CONCLUSION: Twice-daily doses of ranolazine increased exercise capacity and provided additional antianginal relief to symptomatic patients with severe chronic angina taking standard doses of atenolol, amlodipine, or diltiazem, without evident adverse, long-term survival consequences over 1 to 2 years of therapy.

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