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PubMed1995

[Drug treatment of angina pectoris. Study Group on Angina Pectoris of the Ischemic Cardiopathy and Coronary Units Section of the Spanish Society of Cardiology].

Medical treatment in angina pectoris is supported by: 1) slowing in coronary artery disease progression; 2) control of the angina episodes and the enhanced of the functional status, and, 3) prognosis improvement. The authors describe in this review, inside the own experience and the large body of evidence, the general measures and pharmacological treatment of both stable and unstable angina. There are included some therapeutic options in associated clinical conditions.

Angina Pectoris↗
PubMed1993

Discordance between effects of anti-ischemic therapy on ambulatory ischemia, exercise performance and anginal symptoms in patients with stable angina pectoris. The Angina and Silent Ischemia Study Group (ASIS).

OBJECTIVES: We sought to define the extent to which the therapeutic efficacy of three single-drug regimens on ambulatory ischemia paralleled efficacy on other clinical manifestations of ischemia, specifically exercise test performance and anginal symptoms. BACKGROUND: Some studies have shown that the presence and severity of ambulatory ischemia are predictive of anginal symptoms and exercise test performance, whereas other studies have not. Less is known about effects of antianginal treatment and whether response to therapy for one clinical manifestation reflects therapeutic responses for other clinical manifestations. METHODS: We studied 50 patients in the Angina and Silent Ischemia Study who had documented coronary disease, an exercise test positive for ischemia, the presence of ambulatory and asymptomatic ischemia on ambulatory electrocardiographic (ECG) Holter monitoring and stable anginal symptoms. Patients received maximally tolerated doses of sustained release propranolol (mean 293 mg/day), sustained release diltiazem (mean 350 mg/day), nifedipine (mean 79 mg/day) and placebo, each for 2-week periods in a double-blind, crossover fashion. Patients' responses to treatment were assessed by 48-h ambulatory ECG monitoring, exercise test (standard Bruce protocol) and diaries of angina. Levels of efficacy for each agent and for each clinical measure were compared using Spearman correlation analysis. RESULTS: With placebo there was no correlation among the frequency of ischemic episodes by ambulatory ECG monitoring, exercise time to 1.0-mm ST segment depression or frequency of anginal episodes. Furthermore, for a given patient the efficacy of each active medication in reducing ambulatory ischemia was not correlated with response in anginal symptoms or exercise test performance (r = -0.21 to 0.24, p = NS). Within each of these clinical measures, efficacy of one drug was more strongly correlated with efficacy of another drug (r = 0.64 to 0.81 for ambulatory ischemia, 0.48 to 0.56 for exercise test performance and 0.16 to 0.54 for anginal symptoms). CONCLUSIONS: Different measures of ischemia, specifically ambulatory ischemia assessed by ambulatory ECG monitoring, exercise performance on exercise test and anginal symptoms, are independent. Efficacy for each clinical end point must be assessed separately when considering response to drug treatment.

Aged↗
PubMed1991

The circadian rhythm of angina pectoris. Amlodipine Angina Studies Group.

A clear circadian rhythm exists for angina, with the frequency of attacks increasing during the mid-morning and mid-afternoon hours. This pattern is comparable to circadian rhythms previously reported for the incidence of myocardial infarction and sudden cardiac death. The frequency of angina attacks precipitated by physical exertion showed a more pronounced circadian pattern compared to non-exertional angina. Beta-adrenergic blocking agents did not abolish the circadian rhythm of total angina and exertional angina attacks.

Angina Pectoris↗
PubMed1989

[Echocardiography detection of reversible regional disorders of contraction in patients with unstable angina pectoris and Prinzmetal angina during an attack].

We studied seven patients with Prinzmetal's angina and three patients with unstable angina pectoris type III (according to the criteria of Conti) during and after a spontaneous attack of angina pectoris by two-dimensional echocardiography. All patients underwent coronary angiography. The echocardiographic studies were performed during the attack (phase I), immediately after the attack (phase II), and 24 h after the attack (control). Left ventricular ejection fraction was significantly decreased during the attack (38.1 +/- 11% vs 59.8 +/- 7%), while left ventricular end-diastolic volume was increased (71.9 +/- 28 ml/m2 vs 50.3 +/- 13 ml/m2). The double product of heart rate and systolic blood pressure was equal at the 3 different examination times. In all patients transient regional disturbances of left ventricular contraction could be observed. In six patients the wall motion disturbances had already disappeared at phase II, while in four patients hypokinetic regions could still be found. At control, nine patients showed a normal left ventricular contraction pattern, while one patient with previous anterior myocardial infarction showed a small region of anterior akinesia. In all patients coronary artery obstructions were found in the same region of the left ventricle, where transient wall motion abnormalities occurred. Thus, two-dimensional echocardiography performed during an attack of angina pectoris in patients with Prinzmetal's angina and unstable angina pectoris type III can evaluate the localization, as well as the extent of transient myocardial wall motion abnormalities.

Angina Pectoris↗
PubMed1976

Clinical analysis of angina pectoris and angina-like pain --With special reference to ECG during attack, "cervical spondylosis" and selective coronary arteriography.

In a series of 63 patients, 60 with angina pectoris and 3 with cervical spondylosis and "thoracic spondylosis" showing angina like pain detailed assessments were made of the mode of onset of attack, including electrocardiography during attacks, X-ray examination of the thoracic and cervical vertebrae and neurological examinations, along with coronary arteriography in some cases, with the following results: 1. The cases of angina pectoris were classifiable grossly into two groups according to mode of onset of chest pain: Group A: Angina began with pain in the anterior chest (39 cases); Group B: Angina in the anterior chest was preceded by "pain" occurred elsewhere in the chest (21 cases). The cases in group B were further classified under two categories, types BI and BII, the former being characterized by a sudden onset of "pain" in a somatic area or areas other than the anterior chest where there is usually no dysesthesia, followed by development of retrosternal or precordial pain (6 cases), while the latter type of angina began with paroxysmal exacerbation of preexistent dysesthesia in the nape, shoulder and arms and eventuated in pain in the anterior chest (15 cases). There were two subtypes in the type BII angina viz. types BIIa and BIIb. There was no ECG evidence of ischemic changes at exacerbation of the nucha-omo-brachial dysesthesia in type BIIa while significant ischemic ECG changes were evident in association of aggravation of dysesthesia in the type BIIb patients. 2. Concomitant "cervical spondylosis" with radiographic evidence of abnormalities in cervical vertebrae and associated subjective symptoms accounted for 22.9% of group A and for 71.4% of group B. In no case of type BI was there evidence of such complication whilst all the cases of type BII had this complication. 3. The mode of appearance of pain in patients with cervical spondylosis showing angina like pain resembled to that of angina pectoris in type BII but ECG during attack did not reveal any significant ischemic changes. 4. As for interrelation between findings by selective coronary angiography (26 cases of angina pectoris) and complication of "cervical spondylosis", the complication of "cervical spondylosis" was higher in incidence in the group of cases with low-grade coronary arterial changes (degree of occlusion less than 50%) than in the group with greater arterial changes (degree of occlusion over 50%). The findings described suggest the possibility that the mode of manifestation of anginal attack may be modified by the concomitant presence of "cervical spondylosis".

Adult↗
PubMed1999

Coronary artery stenting in unstable angina pectoris: a comparison with stable angina pectoris.

OBJECTIVE: To compare early complication rates in unselected cases of coronary artery stenting in patients with stable v unstable angina. SETTING: Tertiary referral centre. PATIENTS: 390 patients with stable angina pectoris (SAP) and 306 with unstable angina (UAP). Patients treated for acute myocardial infarction (primary angioplasty) or cardiogenic shock were excluded. INTERVENTIONS: 268 coronary stents were attempted in 211 patients (30.3%). Stents used included AVE (63%), Freedom (14%), NIR (7%), Palmaz-Schatz (5%), JO (5%), and Multilink (4%). Intravascular ultrasound was not used in any of the cases. All stented patients were treated with ticlopidine and aspirin together with periprocedural unfractionated heparin. RESULTS: 123 stents were successfully deployed in 99 SAP patients v 132 stents in 103 UAP patients. Failed deployment occurred with nine stents in SAP patients, v four in UAP patients (NS). Stent thrombosis occurred in four SAP patients and 11 UAP patients. Multivariate analysis showed no relation between stent thrombosis and clinical presentation (SAP v UAP), age, sex, target vessel, stent length, or make of stent. Stent thrombosis was associated with small vessel size (p < 0.001) and bailout stenting (p = 0.01) compared with elective stenting and stenting for suboptimal PTCA, with strong trends toward smaller stent diameter (p = 0.052) and number of stents deployed (p = 0.06). Most stent thromboses occurred in vessels < 3 mm diameter. CONCLUSIONS: Coronary artery stenting in unstable angina is safe in vessels >/= 3 mm diameter, with comparable initial success and stent thrombosis rates to stenting in stable angina.

Angina Pectoris↗
PubMed2004

[Comparison between unstable angina pectoris and stable effort angina pectoris by using 123I-BMIPP and 201Tl myocardial SPECT].

We performed BMIPP myocardial SPECT and Tl myocardial SPECT in patients with unstable angina (UAP) and stable effort angina (SAP), and compared the results for the two groups. Our subjects were 30 patients with the UAP and 25 patients with the SAP. The early and delayed images of the BMIPP were obtained with patients at rest. The early image of the Tl alone was obtained with patients at rest. We calculated severity score (SS) using the polar map based on SPECT short-axis image on the both myocardial SPECT. And, we calculated % uptake of the responsible coronary lesion and regional washout rate (WR) on myocardial SPECT with BMIPP. On coronary angiogram, no difference in % diameter stenosis was seen between the two groups. On myocardial SPECT with Tl, no difference in the SS was seen between the two groups. However, on myocardial SPECT with BMIPP, the SS was significantly higher score in the UAP group than in the SAP group. And, on myocardial SPECT with BMIPP, the % uptake and the WR were significant lower values in the UAP group than in the SAP group. Even if the two groups have almost the same level of myocardial perfusion disorder, the UAP group may have severer myocardial fatty-acid metabolic disorder than the SAP group, because the defects in BMIPP were significantly severer in the UAP group.

Angina Pectoris↗
PubMed1994

Low dose acetylsalicylic acid in the antithrombotic treatment of patients with stable angina pectoris and acute coronary syndromes (unstable angina pectoris and acute myocardial infarction).

Acetylsalicylic acid has an antithrombotic effect by inhibition of thromboxane A2 synthesis in platelets. Thromboxane A2 is a potent stimulator of platelet aggregation and vasoconstriction and synthesis may be completely inhibited by a single oral dose of 150 mg acetylsalicylic acid or an intravenous dose of 100 mg. A daily maintenance dose of 75 mg acetylsalicylic acid is sufficient to effectively inhibit thromboxane A2 synthesis in long-term treatment. Acetylsalicylic acid therapy reduces acute myocardial infarction and sudden death in patients with stable angina pectoris and the drug is equally effective in patients with symptomatic and 'silent' angina pectoris. Early intervention with acetylsalicylic acid in patients with unstable angina pectoris reduces the risk of acute myocardial infarction and death. In patients with acute myocardial infarction, acute therapy with acetylsalicylic acid significantly reduces mortality both in monotherapy and in combination with thrombolytics. In the secondary prophylaxis following acute myocardial infarction, acetylsalicylic acid reduces the incidence of reinfarction and coronary death. Treatment of 100 patients with acute coronary syndrome (unstable angina pectoris or acute myocardial infarction) for 2 years may hinder the development of 3-4 fatal and 4 non-fatal vascular events. The risk of gastrointestinal side-effects and bleeding during acetylsalicylic acid therapy is dose-dependent and the incidence is low with a daily dose of 75-150 mg.

Administration, Oral↗
PubMed2005

Treatment of refractory angina pectoris.

Refractory angina pectoris is defined as Canadian Cardiovascular Society class III or IV angina, where there is marked limitation of ordinary physical activity or inability to perform ordinary physical activity without discomfort, with an objective evidence of myocardial ischemia and persistence of symptoms despite optimal medical therapy, life style modification treatments, and revascularization therapies. The patients with refractory angina pectoris may have diffuse coronary artery disease, multiple distal coronary stenoses, and or small coronary arteries. In addition, a substantial portion of these patients cannot achieve complete revascularization and continue to experience residual anginal symptoms that may impair quality of their life and increase morbidity. This represents an end-stage coronary artery disease characterized by a severe myocardial insufficiency usually with impaired left ventricular function. As the life expectancy is increasing, patients with angina pectoris refractory to conventional antianginal therapeutics are a challenging problem. We review the nonconventional therapies to treat the refractory angina pectoris, including pharmacotherapy, therapeutic angiogenesis, transcutaneus electrical nerve and spinal cord stimulation, enhanced external counterpulsation, surgical transmyocardial laser revascularization, percutaneous transmyocardial laser revascularization, percutaneous in situ coronary venous arterializations, and percutaneous in situ coronary artery bypass. These therapies are not supported by a large body of data and have only a complementary role; therefore, the aggressive traditional and proven treatment of angina pectoris should be continued along with these therapies, used on an individual basis.

Angina Pectoris↗