Evidence Of Myocardial Ischemia Research Articles

Multidetector computed tomography-guided treatment strategy in patients with non-ST elevation acute coronary syndromes: a pilot study.

Patients with non-ST elevation acute coronary syndrome (ACS) and evidence of myocardial ischaemia are scheduled for coronary angiography (CAG). In most patients CAG remains a single diagnostic procedure only. A prospective study was performed to evaluate whether 16-slice multidetector CT (MDCT) could predict treatment of the patients and to determine how many CAGs could have been prevented by MDCT scanning prior to CAG. Twenty-two patients with ACS were scanned prior to CAG. Based on MDCT data, a fictive treatment was proposed and compared to CAG-based treatment. Excellent accuracy was observed to detect significant stenoses using MDCT (sensitivity 94%, specificity 96%). In 45%, no PCI was performed during CAG, because of the absence of significant coronary artery disease (27%) or severe coronary artery disease, demanding CABG (18%). MDCT predicted correct treatment in 86%. By using MDCT data, 32% of the CAGs could have been prevented.

Effect of quinapril on the attenuated heart rate recovery of type 2 diabetic subjects without known coronary artery disease

Heart rate (HR) recovery at 1 min is a measure of the vagal reactivation that occurs after cessation of exercise. Despite ample evidence about the association of attenuated HR recovery with increased mortality, pharmacologic modification of this predictor has not been shown. On the other hand, angiotensin-converting enzyme (ACE) inhibitors are known to have vagomimetic activity. We hypothesized that ACE inhibition would increase HR recovery in a group of subjects known to have reduced HR recovery, namely diabetics. Maximal treadmill exercise stress test was performed in 31 type 2 diabetic and 31 nondiabetic male subjects with similar age, body mass index, and hypertensive status. None of the subjects had known heart disease or evidence of myocardial ischemia during the test. The diabetic subjects, after 2 weeks of treatment with quinapril, underwent a second exercise test. A third test was performed 2 to 3 weeks after cessation of quinapril treatment. At baseline, despite similar exercise capacity, the diabetics had a lower HR recovery at 1 min than nondiabetics (25 +/- 8 vs. 31 +/- 8 beats/min, p < 0.01). Quinapril significantly increased HR recovery at 1 min in diabetics (25 +/- 8 beats/min at baseline vs. 28 +/- 8 beats/min with quinapril vs. 25 +/- 7 beats/min off-therapy, p < 0.01 by analysis of variance). The attenuated HR recovery of type 2 diabetics can be improved by quinapril. Whether the improvement in HR recovery with ACE inhibition can lead to decreased mortality is currently unknown.

Prognosis in women with myocardial ischemia in the absence of obstructive coronary disease: results from the National Institutes of Health-National Heart, Lung, and Blood Institute-Sponsored Women's Ischemia Syndrome Evaluation (WISE).

We previously reported that 20% of women with chest pain but without obstructive coronary artery disease (CAD) had stress-induced reduction in myocardial phosphocreatine-adenosine triphosphate ratio by phosphorus-31 nuclear magnetic resonance spectroscopy (abnormal MRS), consistent with myocardial ischemia. The prognostic implications of these findings are unknown. Women referred for coronary angiography for suspected myocardial ischemia underwent MRS handgrip stress testing and follow-up evaluation. These included (1) n=60 with no CAD/normal MRS, (2) n=14 with no CAD/abnormal MRS, and (3) n=352 a reference group with CAD. Cardiovascular events were death, myocardial infarction, heart failure, stroke, other vascular events, and hospitalization for unstable angina. Cumulative freedom from events at 3 years was 87%, 57%, and 52% for women with no CAD/normal MRS, no CAD/abnormal MRS, and CAD, respectively (P<0.01). After adjusting for CAD and cardiac risk factors, a phosphocreatine-adenosine triphosphate ratio decrease of 1% increased the risk of a cardiovascular event by 4% (P=0.02). The higher event rate in women with no CAD/abnormal MRS was primarily due to hospitalization for unstable angina, which is associated with repeat catheterization and higher healthcare costs. Among women without CAD, abnormal MRS consistent with myocardial ischemia predicted cardiovascular outcome, notably higher rates of anginal hospitalization, repeat catheterization, and greater treatment costs. Further evaluation into the underlying pathophysiology and possible treatment options for women with evidence of myocardial ischemia but without CAD is indicated.

Asymptomatic Giant Coronary Aneurysm Presented as Cardiac Murmur

A 27-year-old man presented with cardiac murmur detected on routine examination. He has no history of the illness consistent with Kawasaki disease on his childhood. On admission, his blood pressure was 120/80 mmHg and heart rate was 78 beats per minute. On the chest auscultation, heart beat was regular, and early systolic murmur and thrill was detected on left side of mid sternal border. The intensity of murmur aggravated on expiration and attenuated on inspiration. The electrocardiogram and the plain chest X-ray revealed no definite abnormal findings. Transthoracic and transesophageal echocardiogram showed enlarged left main coronary artery (maximal diameter of 54 mm) with enlarged left anterior descending coronary artery and left circumflex artery. The patient underwent left and right heart catheterization with coronary angiography. The coronary angiography revealed diffuse ectatic change on three coronary arteries with sluggish antegrade flow. Thrill was aggravated with forced hand injection of dye to the left coronary artery. On the exercise treadmill test, there was no evidence of myocardial ischemia, arrhythmia or symptoms even at the stage 4 by Bruce protocol. The patient discharged with the medication of antiplatelet and anticoagulant agent. He got along without any complications and remained free of symptoms for the entire 3-year follow-up period.

Impairment of coronary microvascular function in patients with neurally mediated syncope.

Recent evidence suggests that myocardial ischemia may occur in patients with neurally mediated syncope and normal coronary angiograms. This study was conducted to evaluate if coronary microvascular function is impaired in such patients. Coronary hemodynamic studies and head-up tilt table tests (HUTs) were performed on 30 consecutive patients with normal coronary angiograms and recurrent syncope. Another ten subjects with atypical chest pain and no evidence of myocardial ischemia or syncope served as a control. Great cardiac vein flow (GCVF) and coronary sinus flow (CSF) were measured by the thermodilution method at baseline and after dipyridamole infusion (0.56 mg/kg i.v. for 4 minutes). Coronary flow reserve (CFR), derived from CSF and GCVF, was significantly lower in the 15 patients with positive HUT than in the other 15 patients with negative HUT (1.75 +/- 0.48 vs 2.64 +/- 0.8, P < 0.01 and 2.29 +/- 0.45 vs 3.07 +/- 0.63, P < 0.01, respectively). Ischemic-like ECG was noted during treadmill exercise test in 40% of the former and in 7% of the latter group (P = 0.01). There was no significant difference in CFR between patients with negative HUT and control subjects. Coronary microvascular function was impaired in syncopal patients with positive HUT and relatively preserved in those with negative HUT, suggesting the possible linkage between coronary microvascular dysfunction and the development of neurally mediated syncope.

A Pharmacoeconomic Evaluation of the Myocardial Ischaemia Reduction with Aggressive Cholesterol Lowering (MIRACL) Study in the United Kingdom

To determine the short-term healthcare costs associated with intensive lipid lowering with atorvastatin initiated within 24-96 hours of the occurrence of acute coronary syndrome (ACS) in patients in the UK. Patient-level clinical outcome data from the Myocardial Ischaemia Reduction with Aggressive Cholesterol Lowering (MIRACL) trial and standard cost data were used to compare the total expected 16-week cost per patient on atorvastatin 80 mg/day versus placebo. Clinical outcomes assessed included the following: death; cardiac arrest with resuscitation; nonfatal myocardial infarction; worsening angina pectoris with objective evidence of myocardial ischaemia requiring rehospitalisation; surgical or percutaneous coronary revascularisation; nonfatal stroke; hospitalisation for angina without objective evidence of myocardial ischaemia; and new or worsening congestive heart failure requiring rehospitalisation. All relevant direct medical costs from the perspective of the NHS were considered. The total expected cost was pound 784.05 per patient in the placebo cohort and pound 851.59 per patient in the atorvastatin cohort, resulting in an incremental cost of pound 67.54 per patient in the atorvastatin group. The cost per event avoided was pound 1762.04. A third of the cost of atorvastatin treatment was offset within 16 weeks by the cost savings resulting from the reduction in the number of events in the atorvastatin cohort compared with the placebo cohort. The clinical benefits of short-term intensive atorvastatin treatment administered after ACS is attainable through a marginal increase in 'upfront' costs.

Rho-kinase inhibition with intracoronary fasudil prevents myocardial ischemia in patients with coronary microvascular spasm

ObjectivesWe sought to determine whether a potent Rho-kinase inhibitor fasudil prevents the occurrence of myocardial ischemia in patients with microvascular angina attributable to coronary microvascular spasm. BackgroundEffective treatment of patients with angina who have normal coronary arteriograms (microvascular angina) has not yet been established. Rho-kinase–mediated calcium sensitization of the myosin light chain in smooth muscle cells has been implicated as substantially contributing to vascular hyperconstriction. MethodsWe studied consecutive 18 patients with angina and normal epicardial coronaries in whom intracoronary acetylcholine (ACh) induced myocardial ischemia (ischemic electrocardiographic changes, myocardial lactate production, or both) without angiographically demonstrable epicardial coronary vasospasm. All patients underwent a second ACh challenge test after pretreatment with either saline (n = 5) or fasudil (4.5 mg intracoronarily, n = 13). ResultsMyocardial ischemia was reproducibly induced by ACh in the saline group. In contrast, 11 of the 13 patients pretreated with fasudil had no evidence of myocardial ischemia during the second infusion of ACh (p < 0.01). The lactate extraction ratio (median value [interquartile range]) during ACh infusion was improved by fasudil pretreatment, from −0.16 (−0.25 to 0.04) to 0.09 (0.05 to 0.18) (p = 0.0125). ConclusionsFasudil ameliorated myocardial ischemia in patients who were most likely having coronary microvascular spasm. The inhibition of Rho-kinase may be a novel therapeutic strategy for this group of patients with microvascular angina.

Chest pain: an update

Chest pain is one of the most common symptoms for seeking acute medical care. Evidence of myocardial ischemia, however, can only be established in a minority of patients. The establishment or ruling out of myocardial ischemia is difficult and the cost is high. An effective rationale for ischemia detection, without unnecessary hospital admission, is needed. The development of chest pain units potentially offers a rapid, effective way of identifying patients at high risk for acute coronary syndromes, as well as those with a low probability of ischemia. Other cardiac or noncardiac causes of chest pain should also be considered. Recent developments in chest pain, including the ruling in or out of ischemic pain by triage and different ischemia detection methods, are discussed. Other causes of chest pain such as esophageal, drug related, psychiatric and post-coronary bypass surgery pain are also discussed. Recent findings on syndrome X are reviewed and patients with myocardial infarction presenting without chest pain are discussed. The possibility of safely and quickly ruling out myocardial ischemia by point-of-care biochemical analyses is reviewed, which might influence our clinical handling of chest pain patients. The importance of biopsychosocial factors, pain perception, esophageal dysfunction, drugs and the coronary artery bypass procedure in itself, is discussed and vital clinical information is provided for the handling of our chest pain patients.

Inflammatory markers and coronary interventions: a potentially useful follow-up modality after stenting.

Periprocedural levels of various inflammatory markers have been correlated with prognosis in patients undergoing percutaneous coronary interventions. However, long-term variations of interleukin-1 receptor antagonist (IL-1Ra) or C-reactive protein (CRP) during follow-up after coronary interventions were not previously investigated. The aim of our study was to perform serial evaluations of these markers before and after coronary stenting and to correlate them with clinical status. Plasma levels of IL-1Ra and CRP were measured at baseline and 3 and 6 months after the procedure in 31 patients with symptomatic coronary artery disease undergoing stent implantation, who had no evidence of myocardial ischemia at 6-month follow-up. While at 3 months there were no significant variations of baseline values, 6 months after the procedure a significant decrease from baseline was observed both in IL-1Ra and CRP levels (median -24 pg/ml, P = 0.048, and -0.13 mg/dl, P = 0.017, respectively). Six-month reduction in both IL-1Ra and CRP levels was significant in patients with unstable angina (n = 18; IL-1Ra: from 175 to 119 pg/ml, P = 0.001; CRP: from 0.52 to 0.18 mg/dl, P = 0.002) and nonsignificant in those with stable angina (n = 13) on admission (IL-1Ra: from 123 to 158 pg/ml, P = 0.22; CRP: from 0.19 to 0.10 mg/dl, P = 0.44). In conclusion, a significant reduction of IL-1Ra and CRP levels is observed 6 months after stent implantation in patients with preprocedural unstable angina who remain free of ischemia. This decrease suggests a stabilization of the inflammatory process and may be associated with a favorable prognosis after coronary interventions.

Comparison of effect of intensive lipid lowering with atorvastatin to less intensive lowering with lovastatin on C-reactive protein in patients with stable angina pectoris and inducible myocardial ischemia

In patients with stable angina pectoris and evidence of myocardial ischemia, intensive therapy with atorvastatin was associated with a more rapid decline in CRP than low-dose lovastatin. In the atorvastatin group, half of the long-term decrease occurred within 4 weeks of intensive therapy. Intensive therapy with statins to reach low LDL targets (<80 mg/dl) may offer greater plaque stabilization in higher-risk patients.

Cardiopulmonary responses to exercise in women with sickle cell anemia.

Multiple factors contribute to exercise intolerance in patients with sickle cell anemia, but little information exists regarding the safety of maximal cardiopulmonary exercise testing (CPET) or the mechanisms of exercise limitation in these patients. The purpose of the present study was to examine these issues. Seventeen adult women with sickle cell anemia underwent symptom-limited maximal CPET using cycle ergometry and ramp protocols; blood gases and lactate concentrations were measured every 2 minutes. All patients completed CPET without complications. No patient demonstrated a mechanical ventilatory limitation to exercise or had evidence of myocardial ischemia. However, we observed three pathophysiologic patterns of response to exercise in these patients. Eleven patients had low peak VO2, low anaerobic threshold (AT), gas exchange abnormalities, and high ventilatory reserve; this pattern is consistent with exercise limitation due to pulmonary vascular disease in this patient subgroup. Three patients had low peak VO2, low AT, no gas exchange abnormalities, and a high heart rate reserve, a pattern consistent with peripheral vascular disease and/or a myopathy. The remaining three patients had low peak VO2, low AT, no gas exchange abnormalities, and a low heart rate reserve; this pattern of exercise limitation is best explained by anemia.

Coronary microvascular spasm causes myocardial ischemia in patients with vasospastic angina

ObjectivesWe aimed to test the hypothesis that coronary microvascular spasm (MVS) alone causes myocardial ischemia in patients with angina attributable to epicardial coronary spasm, and to determine whether there is a difference in clinical characteristics between those with and without microvascular spasm. BackgroundPatients with “vasospastic angina” have epicardial coronary artery spasm, but it is unknown whether coronary microvessel disease also contributes to the occurrence of angina in these patients. MethodsWe studied 55 consecutive patients with angina in whom epicardial coronary spasm was provoked by intracoronary acetylcholine (ACH). ResultsIn 14 patients (25.5%, Group 1), submaximal dose of ACH induced myocardial ischemia (chest pain, ischemic electrocardiogram changes, lactate production) without large epicardial spasm, suggesting the occurrence of coronary microvascular spasm. By contrast, the remaining 41 patients (Group 2) had evidence of myocardial ischemia only when epicardial spasm was angiographically demonstrated. The Group 1 patients were predominantly women (p < 0.05) and had a history of prolonged (>30 min) chest pain (p < 0.05), whereas the Group 2 patients were more likely men and smokers (p < 0.01). ConclusionsMyocardial ischemia most probably due to coronary MVS was demonstrated in a sizable portion of patients with epicardial vasospasm, preferentially in women having both typical and prolonged anginal pain. The result suggests that coronary microvascular disease may also contribute to angina in patients with “vasospastic angina.”

Inflammation and coagulation factors in persons >65 years of age with symptoms of depression but without evidence of myocardial ischemia

Depression is associated with increased cardiovascular disease, but the underlying mechanisms are not well understood. This study examines associations of depressive symptoms with inflammation and coagulation factors in persons aged >65 years. Blood samples were obtained from 4,268 subjects free of cardiovascular disease (age 72.4 ± 5.5 years, 2,623 women). Inflammation markers were C-reactive protein (CRP), white blood cell (WBC) count, total platelet count, and albumin; coagulation factors included factors VIIc and VIIIc and fibrinogen. Depression was assessed with the Center for Epidemiologic Studies Depression scale, and states of energy depletion with a validated exhaustion index. Statistical adjustments were made for risk factors (age, sex, race, systolic blood pressure, smoking status, diabetes mellitus) and physical measures of frailty (isometric handgrip, timed 15-feet walk test, activity level). Depression was associated with elevated CRP (3.31 ± 0.10 vs 3.51 ± 0.21 mg/L), WBC (6.14 ± 0.03 vs 6.43 ± 0.11 10 6/L), fibrinogen (319 ± 1 vs 326 ± 3 mg/dl), and factor VIIc (124.6 ± 0.6% vs 127.2 ± 1.3%; all p <0.05). Exhaustion also was related to elevated inflammation and coagulation markers (p <0.05). Exhausted men had markedly elevated CRP levels (6.82 ± 2.10 mg/L) versus nonexhausted men (3.05 ± 0.16: p = 0.007). After adjustment for control variables, exhaustion remained associated with albumin (p = 0.033), fibrinogen (p = 0.017), CRP (p = 0.066), and WBC (p = 0.060), whereas associations of depressive symptoms with biochemistry measures lost statistical significance. Thus, depression and exhaustion are associated with low-grade inflammation and elevated coagulation factors in persons aged >65 years.

Incidence of coronary-subclavian steal syndrome in patients undergoing noncardiac surgery

Objective: To identify the incidence of coronary-subclavian steal syndrome in patients undergoing noncardiac surgery. Design: Prospective. Setting: Veterans Affairs Medical Center and university-affiliated medical center. Participants: Adult patients with prior coronary artery bypass graft surgery and documented use of an internal mammary artery. Interventions: Bilateral simultaneous brachial blood pressures were determined noninvasively. The presumptive diagnosis of ipsilateral subclavian artery stenosis and coronary-subclavian steal syndrome was made if the systolic blood pressure differential was >20 mmHg. Measurements and Main Results: The presumptive diagnosis of ipsilateral subclavian artery stenosis based on a blood pressure differential was made in 6 of 86 (5%) patients screened. The diagnosis of coronary-subclavian steal syndrome was confirmed at cardiac catheterization by observing retrograde internal mammary artery flow in 3 patients or lack of internal mammary artery flow in 1 patient (3.4%). All 4 patients with angiographic confirmation had either angina or silent ischemia. Three patients had successful carotid subclavian bypass, and 1 patient refused surgery. Two patients had no evidence of myocardial ischemia and underwent their planned procedure without incident. Conclusion: Coronary-subclavian steal syndrome occurs with relative frequency in noncardiac surgery patients with prior coronary artery bypass graft surgery using internal mammary artery conduits. Bilateral blood pressure measurements should be routinely performed during the preoperative evaluation. A pressure differential >20 mmHg should suggest the possibility of coronary-subclavian steal syndrome. Copyright © 2001 by W.B. Saunders Company

Differential Coronary Calcification on Electron-Beam CT Between Syndrome X and Coronary Artery Disease in Patients With Chronic Stable Angina Pectoris

The differential diagnosis of syndrome X and coronary artery disease (CAD) in patients with evidence of myocardial ischemia may be difficult. The possible difference in coronary calcium detected by electron-beam CT (EBCT) between syndrome X and CAD is rarely evaluated, especially in aged patients with chronic, stable angina. Prospective, controlled study at a tertiary referral medical center. Forty patients with syndrome X (85% male) and 53 patients with CAD (89% male) were enrolled. Ten control subjects (90% male) with negative exercise treadmill test results and normal coronary angiographic findings served as control subjects. EBCT determined the coronary calcium scores (CCSs), and standard cardiovascular risk factors of all study subjects were analyzed. The 93 study patients had CCSs that ranged from 0 to 1,857. Coronary calcification was seen in 2 of the 10 control subjects (20%), 21 of the 40 syndrome X patients (52.5%), and 51 of the 53 CAD patients (96.2%) [p < 0.01]. The CCS (median [range]) was significantly lower in syndrome X patients than in CAD patients: 1 (0 to 117) vs 202 (0 to 1,857) [p < 0.001]. Receiver operating characteristic curve analyses also demonstrated that coronary calcification differentiated syndrome X from CAD (area under curve, 0.891; 95% confidence interval, 0.806 to 0.947). Of the CAD patients whose CCSs were < 117 and overlapped with CCSs of syndrome X, multivariate analyses determined CCS > 5 (odds ratio, 13.1; 95% confidence interval, 2.86 to 59.7), hypertension (odds ratio, 6.4; 95% confidence interval, 1.5 to 27.4), and hypercholesterolemia (odds ratio, 6.7; 95% confidence interval, 1.5 to 30.5) to be independent discriminators to differentiate CAD from syndrome X. Patients with CAD had more frequent hypertension than patients with syndrome X. The coronary calcium detected noninvasively by EBCT was different, though with some overlapping, between patients with syndrome X and CAD. In addition to standard cardiovascular risk factors, CCS determined by EBCT (especially > 117 or = 0) could differentiate between syndrome X and CAD in patients with chronic, stable angina with evidence of myocardial ischemia. Larger trials would be useful to validate CCS on EBCT as a predictor of clinical outcome in these patients.

Accelerated Atherosclerosis, Aortic Aneurysm Formation, and Ischemic Heart Disease in Apolipoprotein E/Endothelial Nitric Oxide Synthase Double-Knockout Mice

To test whether deficiency in endothelial nitric oxide synthase (eNOS) affects atherosclerosis development, we compared lesion formation in apolipoprotein E (apoE)/eNOS-double knockout (DKO) and apoE-knockout (KO) control animals. After 16 weeks of "Western-type" diet, apoE/eNOS-DKO males and females showed significant increases in lesion area of 93.6% and 59.2% compared with apoE-KO mice. All apoE/eNOS-DKO animals studied developed peripheral coronary arteriosclerosis, associated with perivascular and myocardial fibrosis, whereas none of the apoE-KO mice did. Transthoracic echocardiography showed a significantly increased left ventricular wall thickness and decreased fractional shortening in DKO animals. Mean arterial pressure was increased in DKO mice and was comparable in degree to eNOS-KO animals. Male DKO animals developed atherosclerotic abdominal aneurysms and aortic dissection. eNOS deficiency increases atherosclerosis in Western-type diet-fed apoE-KO animals and introduces coronary disease and an array of cardiovascular complications, including spontaneous aortic aneurysm and dissection. This phenotype constitutes the first murine model to demonstrate distal coronary arteriosclerosis associated with evidence of myocardial ischemia, infarction, and heart failure. Hypertrophy and reduced left ventricular function cannot be explained by increased blood pressure alone, because eNOS-KO animals do not develop these complications.

Feasibility of percutaneous transluminal coronary angioplasty to patients with Kawasaki Disease as an early management strategy.

We successfully performed percutaneous transluminal coronary angioplasty (PTCA) in three infants with Kawasaki disease ages 11 to 29 months. The time from the onset of disease to PTCA ranged from 6 to 21 months. On period reevaluation 12 to 40 months after PTCA, they had no evidence of myocardial ischemia or restenosis. As an early management strategy, PTCA could be a good palliation to control myocardial ischemia associated with Kawasaki disease. From our study and a literature review, we suggest that PTCA may be more effective if it is performed earlier, even in young patients.

A basic approach to the interpretation of the exercise test

To interpret the exercise test, the following parameters need to be evaluated: the heart rate and blood pressure response, symptoms, dysrhythmias, aerobic capacity, and evidence for myocardial ischemia. When analyzing the ST segment for ischemia, the amount and type of ST depression and the time of onset and resolution are examined. The exercise test results are best used to determine a post-test probability that the patient has significant coronary disease, predict its severity, and provide a prognosis of the patient. The test allows primary care physicians to decide which patients with coronary artery disease can be safely managed medically and which high-risk patients need further evaluation and consideration for revascularization.

Coronary artery fistulas: long-term results of surgical correction

Background. Opinions vary as to whether operation should be offered patients with coronary artery fistula, particularly to those who are asymptomatic. Published studies lacked long-term follow-up data. Methods. We studied 41 patients with coronary artery fistula operated in our unit in the past 30 years with restudies including coronary angiograms in those who agreed to the investigation. Results. There was no operative mortality and operative morbidity was low. The mean duration of follow-up was 9.1 years and 96.9% of the patients were asymptomatic. Twenty-one patients had a coronary angiogram. The native coronary artery either remained dilated and tortuous, or more frequently had thromboses with a short proximal stump. (None of these patients had evidence of myocardial ischemia.) Four patients had demonstrable recurrence fistula but without hemodynamic disturbance. Conclusions. We advocate operation for all patients with coronary artery fistulas and demonstrable shunting in view of minimal operative risks. Small asymptomatic fistulas without demonstrable shunting should be left alone. The relatively high incidence of residual or recurrent fistula makes long-term follow-up mandatory.

The TIMI risk score for unstable angina/non–ST-elevation MI: a method for prognostication and therapeutic decision making

Epithelioid hemangioma (EH) is a benign vascular lesion. It is generally found in the dermis, subcutis, and rarely in visceral organs. We identified incidental EHs of the right coronary artery and right ventricle during an autopsy of Japanese female whose cause of death was liver cirrhosis. The tumor of the coronary artery originated from the tunica media of the artery and proliferated into the intima and out of the vascular wall. It resulted in marked luminal narrowing of approximately 50%–75% stenosis. However, no evidence of myocardial ischemia was found. Cardiac EH is rare and this is the first report of EH arising in the coronary artery, to our knowledge.