Coronary-subclavian steal: an unusual cause of angina pectoris after successful internal mammary-coronary artery bypass grafting.

Coronary-subclavian steal syndrome is a rare cause of angina pectoris after bypass grafting using the internal mammary artery. We report the 11th case in the literature and review the pathophysiology and treatment of this disorder. We also review appropriate screening for this possibly increasing, yet preventable disorder.     

Coronary-subclavian steal: An unusual cause of angina pectoris after successful internal mammary-coronary artery bypass grafting

Coronary-subclavian steal syndrome is a rare cause of angina pectoris after bypass grafting using the internal mammary artery. We report the 11th case in the literature and review the pathophysiology and treatment of this disorder. We also review appropriate screening for this possibly increasing, yet preventable disorder.     

Coronary-subclavian steal syndrome presenting with chest pain and syncope

The present case is a 68-year-old patient with complaints of chest pain and syncopal attacks during physical activity of the left arm, for the last six months. He had a coronary artery bypass graft operation 10 years ago. Angiographic examination demonstrated total occlusion of the subclavian artery. The subclavian artery was stealing blood from the left anterior descending artery via the left internal mammary artery and from the brain via the left vertebral artery, leading to the diagnosis of subclavian artery steal syndrome; a rare cause of coronary and cerebral ischaemia.     

Coronary-subclavian steal syndrome. A case report.

Coronary-subclavian steal is an unusual clinical syndrome after successful internal mammary-coronary artery bypass grafting. Proximal subclavian artery (SA) stenosis is present and atherosclerotic disease is the underlying pathophysiologic mechanism in the majority of cases. The authors report a case of a sixty-two-year old man with angina and ventricular fibrillation soon after myocardial revascularization with left internal mammary artery (LIMA) to left anterior descending coronary (LAD). Dobutamine stress echocardiography showed ischemia in the anterior myocardial territory with patent LIMA-LAD bypass in the angiographic evaluation. This procedure showed occlusion of the proximal SA with reversal of flow in the LIMA. The best therapeutic approach was discussed and a carotid-subclavian bypass was performed with restoration of antegrade blood flow and reversal of the clinical setting.     

Coronary-subclavian steal syndrome following coronary artery bypass grafting

Angina pectoris resulting from the coronary-subclavian steal syndrome is a rare phenomenon with only 10 previously reported cases. However, with the increasing use of the internal mammary artery in the coronary artery bypass graft (CABG) procedure it may be encountered more frequently in the future. We report our recent experience with coronary-subclavian steal syndrome after CABG with 2 patients in whom complete relief from angina pectoris was obtained following bypass of a proximal subclavian artery occlusion in one patient and improvement of angina in the other. A review of the relevant literature is also presented.     

Thrombolysis in refractory unstable angina

Multiple drug therapy, including nitrates, beta blockers, calcium antagonists, aspirin, and heparin, has been advocated as effective in the treatment of unstable angina, a syndrome with a multifactorial pathogenesis. Recently, plaque rupture and thrombosis have been demonstrated as the most important pathogenetic mechanisms. Nevertheless, clear-cut results on the effects of thrombolytic treatment in unstable angina are still lacking. Some possible explanations why the medical treatment of unstable angina has still not yet been standardized, whereas that of myocardial infarction has, are suggested. A review of randomized and nonrandomized studies published on this topic evaluating the role of different thrombolytic agents in unstable angina is presented. In addition the role of coronary angiography is discussed. In view of the disappointing results of coronary artery bypass surgery performed in the acute phase of the disease, one of the goals of clinical research is to identify subsets of patients at high and low risk and who undergo different types of therapeutic interventions. To support published data suggesting that total myocardial ischemia has a significant impact on prognosis, we present our results of a study carried out on patients with refractory unstable angina treated with thrombolytic therapy and evaluated with continuous electrocardiographic monitoring in the attempt to correlate total myocardial ischemia with short-term prognosis. Data in favor of the prognostic role of continuous electrocardiographic monitoring in unstable angina are also reviewed. Finally, we propose some suggestions that might be useful for future studies.     

Coronary-subclavian steal: presentation and management: two case reports

Subclavian stenosis is a highly prevalent and underrecognized clinical entity. In patients with a history of coronary artery bypass grafting utilizing a left internal mammary artery, subclavian artery stenosis can cause coronary-subclavian steal, leading to myocardial ischemia. Traditionally, this has been treated surgically with a vascular bypass operation. Two cases of coronary-subclavian steal syndrome are presented, 1 treated percutaneously with angioplasty and stent, and 1 treated with a combined endovascular-surgical procedure.     

Additional molsidomine in refractory unstable angina pectoris

Summary In a prospective single-blind study we examined the effects of additional molsidomine in 20 patients (63±10 years; 15 males, 5 females) with unstable resting angina (3 attacks/24 hours) refractory to triple therapy (nitrates, calcium antagonists, and beta blockers) combined with heparin or aspirin. All but one patient had coronary artery disease documented by coronarography (n=17) or by recent myocardial infarction (n=3). Two patients had angiographically documented severe coronary spasms. Patients entered the study if coronary bypass surgery or PTCA could not be performed within 3 days after angiography (n=9) or was not feasible due to anatomical or technical reasons (n=6), concomitant malignant disease (n=2), or age greater than 75 years (n=3). All patients received molsidomine orally 12 to 24 mg/day. In 15 of the 20 patients molsidomine was given i.v. initially, starting with 20 mg i.v., followed by infusion of 1 to 4 mg/hour. Heart rate and blood pressure did not change significantly, and eight patients had a slight decrease of systolic and diastolic blood pressure. Severe adverse effects did not occur, and moderate headaches were reported by five patients. In 13 patients, unstable angina could be stabilized, and they remained free of resting angina; five had a marked reduction of the frequency of anginal attacks. In two patients, molsidomine was without demonstrable beneficial effects. After a follow-up of 4 weeks, nine patients were free of symptoms after bypass surgery or PTCA, 10 continued to have angina NYHA class II or III, and one patient died due to acute myocardial infarction and cardiogenic shock 4 days after starting additional molsidomine. We conclude that molsidomine is well tolerated and has a marked beneficial effect in patients with refractory unstable angina. Molsidomine should therefore be considered for routine therapy of unstable angina, especially in those patients who are suspected of tolerance to nitrate therapy.     

The elusive cause of instability in unstable angina

The causes of unstable angina are still largely unknown. However, some facts deriving from angiographic, postmortem, and pathophysiologic studies are well established. Angiographic findings: coronary thrombi and complicated stenoses are more frequent in unstable than in stable angina. Conversely, the severity of coronary atherosclerosis and the development of collateral circulation is similar in both coronary syndromes. Postmortem findings: the following features are more frequent in unstable than in stable angina: (1) mural thrombi, which often represent out-growth from the inside of a fissured plaque; (2) inflammatory cells at the site of plaques and in perivascular nerves; and (3) contraction bands in smooth muscle cells of the media surrounding plaques. However, fissured plaques can be found in 10% of individuals dying of noncardiac causes, and fissured plaque may occasionally be missing under the coronary thrombus in unstable angina. Pathophysiologic findings: patients with unstable angina compared with those with stable angina exhibit: (1) higher levels of serotonin in the coronary sinus; (2) higher systemic levels of fibrino-peptide A; (3) higher urinary levels of thromboxane A2 metabolites; and (4) a greater coronary reactivity to constrictor stimuli. A critical analysis of these established facts is required to set the stage for a better comprehension of the causes which can cause a coronary segment to progress in a stuttering way toward acute persistent coronary occlusion and myocardial infarction. Plaque fissure is likely to be an important background thrombogenic stimulus in many cases.(ABSTRACT TRUNCATED AT 250 WORDS)     

Tissue plasminogen activator in refractory unstable angina. A randomized double-blind placebo-controlled trial in patients with refractory unstable angina and subsequent angioplasty

To evaluate the effect of recombinant tissue plasminogen activator(alteplase) on the clinical course, angiographic changes andthe outcome of subsequent coronary angioplasty, 36 patientswith angina at rest, despite bedrest and medical treatment includingheparin, and with concomitant ECG changes, were studied. Afterdiagnostic angiography, patients were randomized to receiveeither alteplase 100mg in 3 h (19 patients), or placebo (17patients). The mean interval between qual anginal episode andinitial angiography was 10 and 9 h for the alteplase and placebogroup, respectively. Angiography was repeated and angioplastywas performed within 24 hours. Between the first and the second angiogram, five patients inthe alteplase and seven in the placebo group had recurrent ischaemicepisodes, while four alteplase and three placebo patients showedsigns of myocardial necrosis (creatine kinase (CK) rise twicethe upper limit for normal). Intracoronary clots were recognizedin three alteplase patients and one placebo patient at the firstangiograrn, while two alteplase patients and one placebo patientshowed total occlusion of the ischaemic-related vessel. Afterinfusion, thrombi were present in four alteplase patients andone placebo patient, and total occlusion in three alteplasepatients and one placebo patient. Quantitative coronary angiographyshowed no change in the percentage diameter stenosis of theischae, nia-related segment after drug infusion, (alteplase67±16 to 69±16%; placebo 65±11 to 63±12%).Angioplasty was successful in 14 of 19 alteplase and 14 of 16placebo patients. Three patients after alteplase and two placebopatients developed myocardial necrosis during percutaneous transluminalcoronary angioplasty (PTCA) and one alteplase patient requiredurgent bypass surgery. Minor bleeding complications were observedin six alteplase patients before the second angiogram and infive alteplase patients and one placebo patient after PTCA.One patient after alteplase developed a fatal retroperitonealhaemorrhage. In patients with unstable angina refractory to medical treatment,including heparin, alteplase has no beneficial effect on theseverity of coronary stenosis, on the clinical course, or onthe success of a subsequent angioplasty procedure. Thus thrombolytictherapy with alteplase for unstable angina cannot be recommendedon the basis of this investigation.     

Tissue plasminogen activator in refractory unstable angina. A randomized double-blind placebo-controlled trial in patients with refractory unstable angina and subsequent angioplasty.

To evaluate the effect of recombinant tissue plasminogen activator (alteplase) on the clinical course, angiographic changes and the outcome of subsequent coronary angioplasty, 36 patients with angina at rest, despite bedrest and medical treatment including heparin, and with concomitant ECG changes, were studied. After diagnostic angiography, patients were randomized to receive either alteplase 100 mg in 3 h (19 patients), or placebo (17 patients). The mean interval between qualifying anginal episode and initial angiography was 10 and 9 h for the alteplase and placebo group, respectively. Angiography was repeated and angioplasty was performed within 24 hours. Between the first and the second angiogram, five patients in the alteplase and seven in the placebo group had recurrent ischaemic episodes, while four alteplase and three placebo patients showed signs of myocardial necrosis (creatine kinase (CK) rise greater than or equal to twice the upper limit for normal). Intracoronary clots were recognized in three alteplase patients and one placebo patient at the first angiogram, while two alteplase patients and one placebo patient showed total occlusion of the ischaemic-related vessel. After infusion, thrombi were present in four alteplase patients and one placebo patient, and total occlusion in three alteplase patients and one placebo patient. Quantitative coronary angiography showed no change in the percentage diameter stenosis of the ischaemia-related segment after drug infusion, (alteplase 67 +/- 16 to 69 +/- 16%; placebo 65 +/- 11 to 63 +/- 12%). Angioplasty was successful in 14 of 19 alteplase and 14 of 16 placebo patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

最大限度内科治疗对难治性不稳定心绞痛的作用

目的探讨最大限度内科治疗对难治性不稳定心绞痛的作用。方法回顾性分析了我院老年及老年前期不稳定心绞痛患者８８例，将这些患者分成药物难治组和药物治疗稳定组。结果经用４～５种药物最大限度内科治疗，８１例胸痛缓解，７例（８．０％）最后被证实为难治性不稳定心绞痛。难治性不稳定心绞痛组胸痛时多伴有前壁心电图变化，ＳＴ段压低６例，需用肝素６例、β阻滞剂６例，均显著多于药物治疗稳定组，院内发生急性心肌梗死２例。院内死亡１例以及进行经皮冠状动脉腔内成形术（ＰＴＣＡ）治疗者３例，也均显著高于药物治疗稳定组。结论应用最大限度内科治疗有利于降低难治性不稳定心绞痛的发生率。     

Thrombolytic therapy in refractory unstable angina: the role of Holter monitoring.

We tested the safety and the usefulness of intravenous urokinase (2 million units administered over 30 min) in 44 patients with refractory unstable angina, defined as persistence of ischemic episodes during 48-h Holter monitoring (Phase 1) despite maximal medical therapy. After thrombolysis, recurrence of ischemia was observed during a week of observation in the CCU, including two 24-h Holter monitorings at the beginning and the end of the week (Phase 2). Seventeen patients completed the observation period without either symptomatic or asymptomatic ischemic episodes (Group A); the remaining 27 continued to manifest ischemia (Group B). No bleeding complications occurred. Within a 6-month follow-up, 2 patients of Group A had recurrence of unstable angina while in Group B, 19 patients had refractory angina or a major cardiac event [10 patients underwent coronary artery bypass surgery (CABG) or percutaneous transluminal coronary angioplasty (PTCA) for refractory angina (p less than 0.001), 6 other patients with refractory angina continued medical therapy, one patient had a myocardial infarction, and two patients died]. In Phase 1 the duration of total ischemia (min/24 h) was a relevant prognostic marker: higher duration correlated with adverse clinical outcome (p less than 0.01). In comparison to Phase 1, duration of total ischemia in Phase 2 was significantly reduced in both groups (16.9 +/- 19.6 vs. 25.4 +/- 17.7; p less than .001). A percent value expressing this variation was calculated for each patient: the variation thus obtained again gave information on the clinical outcome--the greater the reduction, the lower the risk of cardiac events (p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)