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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ahj.2008.04.034 Byline: Jason C. Kovacic (a)(b)(c)(e), Peter Macdonald (a)(b)(c), Michael P. Feneley (a)(b)(c), David W.M. Muller (a)(b)(c), Judith Freund (b)(c), Anthony Dodds (b)(c), Sam Milliken (b)(c), Helen Tao (b)(c), Silviu Itescu (d), John Moore (b)(c), David Ma (b)(c), Robert M. Graham (a)(b)(c) Abstract: Preclinical studies suggest granulocyte-colony stimulating factor (G-CSF) holds promise for treating ischemic heart disease; however; its clinical safety and efficacy in this setting remain unclear. We elected to evaluate the safety and efficacy of G-CSF administration in patients with refractory 'no-option' ischemic heart disease. Author Affiliation: (a) Victor Chang Cardiac Research Institute, University of New South Wales, Sydney, New South Wales, Australia (b) St Vincent's Hospital, University of New South Wales, Sydney, New South Wales, Australia (c) Faculty of Medicine, University of New South Wales, Sydney, New South Wales, Australia (d) Columbia University, New York, New York (e) Current appointment: Translational Medicine Branch, National Heart, Lung and Blood Institute, Bethesda, MD Article History: Received 18 September 2007; Accepted 14 April 2008 Article Note: (footnote) The study was approved by the St Vincent's Hospital human research ethics committee, registered with the Australian Clinical Trials Registry (no. 12605000050651), supervised by an independent data and safety monitoring board (DSMB), and conducted with the informed consent of all subjects. Enrollment commenced January 2004, with the final follow-up scan performed July 2006.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ahj.2005.04.033 Byline: Carlo Briguori (a), Bernhard Reimers (b), Cristiano Sarais (a), Massimo Napodano (b), Pietro Pascotto (b), Giuseppe Azzarello (c), Marco Bregni (a), Adolfo Porcellini (c), Orazio Vinante (c), Pierluigi Zanco (d), Cesare Peschle (e), Gianluigi Condorelli (f), Antonio Colombo (a) Abstract: Intramyocardial injection of autologous bone marrow (ABM) may induce angiogenesis. We tested the safety and feasibility of catheter-based direct percutaneous intramyocardial delivery of ABM in patients with refractory angina pectoris. Author Affiliation: (a) 'Vita-Salute' University School of Medicine, San Raffaele Hospital, Milan, Italy (b) Department of Cardiology, Mirano, Italy (c) Department of Oncology and Hemato-Oncology, PF Calvi Hospital, Noale, Italy (d) Department of Nuclear Medicine, Vincenza, Italy (e) Department of Hemato-Oncology, Istituto Superiore di Sanita, Rome, Italy (f) 'La Sapienza' University School of Medicine, Rome, Italy Article History: Received 15 February 2005; Accepted 28 April 2005

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ahj.2005.01.054 Byline: Andrew D. Michaels (a), Ajit Raisinghani (b), Ozlem Soran (c), Paul-Andre de Lame (d), Michele L. Lemaire (d), Paul Kligfield (e), Denny D. Watson (f), C. Richard Conti (g), George Beller (f) Abstract: Enhanced external counterpulsation (EECP) reduces angina and extends time to exercise-induced ischemia in patients with symptomatic coronary disease. One- and two-center studies and a retrospective case series reported that EECP improves myocardial perfusion in stable angina pectoris. We sought to critically evaluate and quantify the effect of EECP on myocardial perfusion. Author Affiliation: (a) Division of Cardiology, University of California at San Francisco Medical Center, San Francisco, Calif (b) Division of Cardiology, University of California at San Diego Medical Center, San Diego, Calif (c) Cardiovascular Institute, University of Pittsburgh Medical Center Health System, Pittsburgh, Pa (d) Anabase International Corporation, Stockton, NJ (e) Division of Cardiology, Cornell Medical Center, New York, NY (f) Division of Cardiology, University of Virginia, Charlottesville, Va (g) University of Florida, Gainesville, Fla Article History: Received 5 November 2004; Accepted 15 January 2005 Article Note: (footnote) The study is sponsored by Vasomedical, Inc, Westbury, NY, and is supported by a National Institutes of Health Mentored Patient-oriented Research Career Development Award (K23 RR018319-01 A1; Dr Michaels).

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ahj.2004.07.039 Byline: Nawsad Saleh (a), Bertil Svane (b), Jens Jensen (a), Lars-Olof Hansson (d), Margareta Nordin (c), Per Tornvall (a) Abstract: The systemic inflammatory response to percutaneous coronary intervention (PCI) is associated with recurrent cardiac events; however, the pathophysiology of this inflammatory response is not well understood. The present study was performed to investigate the role of pathogen burden of infection in determining the magnitude of C-reactive protein (CRP) and interleukin 6 (IL-6) response to PCI. Author Affiliation: (a) Department of Cardiology, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden (b) Department of Physiology and Thoracic Radiology, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden (c) Clinical Microbiology, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden (d) Clinical Chemistry and Pharmacology, Uppsala University Hospital, Uppsala, Sweden Article History: Received 19 January 2004; Accepted 27 July 2004

Byline: HA[yen]kan Emanuelsson, Kenneth Egstrup, Kjell Nikus, Jan Ellstrom, Torben Glud, Cornel Pater, Morten Scheibel, Anders Tisell, Karl-Johan Totterman, Mikael Forsby Abstract: Objective The primary objective of this randomized, double-blind, parallel group trial was to compare the antianginal and antiischemic efficacy of a combination tablet of felodipine-metoprolol 10/100 mg once daily with both drugs given separately once daily in patients with stable effort-induced angina pectoris. The secondary objective was to compare the tolerability of the 3 treatments. Methods The main criteria for inclusion were stable effort-induced angina pectoris for at least 2 months before the enrollment and a positive bicycle exercise test result. Patients were allocated to once-daily treatment with either felodipine-metoprolol 10/100 mg, felodipine 10 mg, or metoprolol 100 mg. The duration of active double-blind treatment was 4 weeks. There were 3 primary efficacy variables in the study; time until end of exercise, time until onset of chest discomfort, and time until 1-mm ST depression during a standardized exercise test. Results The number of patients randomized was 397. There was a statistically significant improvement in time until end of exercise with felodipine-metoprolol 10/100 mg compared with metoprolol 100 mg (P = .04) and felodipine 10 mg compared with metoprolol 100 mg (P = .03). However, for time until onset of pain or time until 1-mm ST-depression there were no significant differences among the treatment groups. At highest comparable workload, ST depression was less pronounced with felodipine-metoprolol than with metoprolol alone (P = .04), and the rate-pressure product was significantly lower in the groups receiving felodipine-metoprolol and metoprolol than in the group receiving felodipine alone. The combination and metoprolol were better tolerated than felodipine alone. Conclusions In stable angina pectoris, the combination felodipine-metoprolol 10/100 mg and felodipine 10 mg alone increased exercise time compared with metoprolol 100 mg. The combination tablet and metoprolol 100 mg alone showed a more favorable tolerability profile than felodipine 10 mg alone. (Am Heart J 1999;137:854-62.) Author Affiliation: Goteborg, Sandviken, Hasselholm, Vetlanda, and Molndal, Sweden; Helsinki and Jakobstad, Finland; and Svendborg, Middelfart, and Kjenerup, Denmark From.sup.aSahlgrenska Hospital, Goteborg;.sup.bSvendborg Hospital, Denmark,.sup.cJakobstad Hospital, Finland,.sup.dSandviken Hospital, Sweden,.sup.eMiddelfart Hospital, Denmark,.sup.fHassleholm Hospital, Sweden,.sup.gKjellerup Hospital, Denmark,.sup.hVetlanda Hospital, Sweden,.sup.iThe Deaconess Hospital, Helsinki, Finland, and.sup.jHassle Lakemedel AB, Sweden Article History: Received 16 March 1998; Accepted 28 July 1998 Article Note: (footnote) [star] Funded by Astra Denmark A/S, Denmark, Suomen Astra Oy, Finland, and Hassle Lakemedel AB, Sweden., [star][star] Reprint requests: HA[yen]kan Emanuelsson, Division of Cardiology, Arebro Medical Center Hospital, S-70185 Arebro, Sweden., a 0002-8703/99/$8.00 + 0 4/1/93933

Byline: Oscar A. Salomone, J.Robert Crook, Mojgan Hossein-Nia, David Holt, Juan Carlos Kaski Abstract: Background Total serum sialic acid concentration has been reported to predict death from cardiovascular disease. This study was performed to assess the relation between serum sialic acid concentration and the angiographic extent and severity of coronary atheroma in patients with stable angina. Methods Quantitative coronary angiography was performed in 40 patients with stable angina with either triple-vessel disease (23 patients) or normal/nearly normal coronary arteries (17 patients). A colorimetric assay for the enzymatic determination of serum sialic acid was used. Results Serum sialic acid concentration was not significantly different in patients with normal or nearly normal coronary angiograms compared with those with triple-vessel disease (68 [+ or -] 10 mg/100 mL and 68 [+ or -] 11 mg/100 mL, respectively). Neither was there any association between the extent or severity of coronary disease and serum sialic acid levels. Conclusions Serum sialic acid concentration does not appear to be associated with the extent or severity of coronary artery disease in patients with stable angina pectoris. Thus the previously described association between serum sialic acid and cardiovascular death may reflect the role of mechanisms other than the severity of coronary artery narrowings. (Am Heart J 1998;136:620-3.) Author Affiliation: London, United Kingdom Article Note: (footnote) [star] From the Department of Cardiological Sciences, St. George's Hospital., [star][star] Reprint requests: J.C. Kaski, MD, Department of Cardiological Sciences, St. George's Hospital Medical School, Cranmer Terrace, London SW17 ORE, United Kingdom., a E-mail: jkaski@sghms.ac.uk, aa 4/1/92420

Byline: Enrico Hoffmann, Pasquale Assennato, Maria Donatelli, Isabella Colletti, Teresa M. Valenti Abstract: Background Some patients with typical angina and electrocardiographic evidence of ischemia have normal coronary angiograms. These patients have a reduced coronary flow reserve and abnormal endothelium-dependent vasodilator responses; this syndrome is known as microvascular angina. Among endothelium-derived peptides, endothelin-1 (ET-1) is a potent vasoconstrictor and an important modulator of microvascular function. Methods Plasma ET-1 was measured in 13 patients with typical angina, instrumental evidence of ischemia, and normal arteriograms and in 20 normal control subjects. Results Mean concentration of ET-1 was 2.89 [+ or -] 1.24 pmol/L in patients with angina and normal angiograms and 1.99 [+ or -] 0.81 pmol/L in normal control subjects (p < 0.02). Plasma levels of ET-1 values were significantly higher in patients with angina, positive exercise test results for ischemia, and normal coronary arteriograms compared with the group of patients with no clinical or instrumental evidence of ischemia. Conclusions This is consistent with the hypothesis that in patients with microvascular angina, an endothelial dysfunction in the coronary vascular area caused by impaired endothelium-derived ET-1 could play an active role in the disease process. (Am Heart J 1998;135:684-8.) Author Affiliation: Palermo, Italy Article History: Received 20 May 1997; Accepted 2 October 1997 Article Note: (footnote) [star] From Cattedra di Cardiologia, bIstituto di Clinica Medica, Facolta di Medicina e Chirurgia, aUniversita degli Studi di Palermo., [star][star] Reprints requests: Prof. Pasquale Assennato, Via A. Salinas n.56, 90141 Palermo, Italy., a 4/1/87783

Byline: Yoshito Inobe, Kiyotaka Kugiyama, Hiroo Miyagi, Masamichi Ohgushi, Seiji Tomiguchi, Mutsumasa Takahashi, Hirofumi Yasue Abstract: Quantitative analysis of iodine 123 metaiodobenzylguanidine (MIBG) myocardial tomographic imaging showed that the regional uptake reduction and abnormally high washout of MIBG in the myocardial territories of the coronary artery with spasm were observed in 33 (75%) and in 30 (68%) of 44 patients with coronary spastic angina, whereas it was observed in two (7%) and in four (15%) of 27 control subjects, respectively. The patients with higher disease activity of the anginal attack and those with life-threatening ventricular arrhythmias were frequently associated with either the uptake reduction or the abnormally high washout of MIBG (91% in patients with high disease activity, 100% in patients with ventricular arrhythmias). The repeated studies of MIBG myocardial tomographic imaging at 2 and 6 months after suppression of anginal attacks by medical treatments showed that the scintigraphic abnormalities still remained in 85% of the patients at 2 months and 32% at 6 months. Thus the abnormalities in sympathetic nervous system assessed with MIBG scintigraphy has been shown to be highly associated with patients with coronary arteries with spasm, particularly high-risk patients, and lasted for several months despite suppression of anginal attack. (Am Heart J 1997;134:112-118.) Author Affiliation: Kumamoto, Japan Article Note: (footnote) [star] From the Division of Cardiology and Department of Radiology, Kumamoto University School of Medicine., [star][star] Reprint requests: Kiyotaka Kugiyama, MD, Division of Cardiology, Kumamoto University School of Medicine, 1-1-1 Honjo, Kumamoto, 860, Japan., a 0002-8703/97/$5.00 + 0 4/1/82101

Byline: Patricia Gramling-Babb, Michael J. Miller, Scott T. Reeves, Raymond C. Roy, Michael R. Zile Abstract: Surgical sympathectomy can relieve symptoms of angina in patients with refractory angina. However, in these high-risk patients this thoracic surgery may result in significant morbidity and mortality rates. Similar sympathetic blockade can now be produced with high thoracic epidural analgesia (HTEA). From September 1995 to August 1996, we treated 10 consecutive patients with HTEA. These eight men and two women, aged 58 [+ or -] 5 years, with extensive three-vessel coronary disease and ejection fractions of 40% [+ or -] 5%, had New York Heart Association (NYHA) class IV angina despite medical therapy, including nitrates, [beta]-blockade, calcium channel blockade, and narcotics. HTEA was performed at the T1 through T4 levels with a catheter placed either percutaneously or surgically, with radiographic confirmation of catheter placement with an epidurogram or computed tomography scan. Bupivacaine (0.25% to 0.5%), an amide local anesthetic, was given as a bolus through the epidural catheter and then maintained either as a continuous infusion or an intermittent rebolus. The epidural catheter remained in place for 7 days in four patients, 14 days in three patients, and [greater than or equal to]90 days in three patients. Before consideration for HTEA, each patient was deemed unsuitable for or refused coronary bypass surgery and percutaneous coronary angioplasty and had NYHA class IV symptoms of angina. Seven of 10 patients required intravenous nitroglycerin and heparin and were unable to be discharged from the intensive care unit because of anginal symptoms. Two of these seven patients also required an intraaortic balloon pump for symptom control. After HTEA, all 10 patients had improved symptoms, with five patients improving to NYHA class II symptoms and five improving to NYHA class III. All seven patients receiving intravenous nitroglycerin, heparin, or intraaortic balloon pump support had these modalities discontinued. Six of these seven patients were subsequently discharged from the hospital. One patient died from a non-HTEA related cause. There were no HTEA-related deaths. There were three catheter-related complications necessitating catheter removal during 12 months of HTEA use. Local infection developed in one patient, one had catheter occlusion caused by fibrosis, and one patient had chronic back pain exacerbation from a paraspinous muscle spasm. No patient had a myocardial infarction or a significant arrhythmia. In patients with otherwise intractable angina pectoris, HTEA is an effective modality that produces symptomatic relief of angina pectoris and allows increased activity level. (Am Heart J 1997; 134:648-55.) Author Affiliation: Charleston, S.C Article History: Received 20 December 1996; Accepted 26 March 1997 Article Note: (footnote) [star] Patricia Gramling-Babb, MD, Department of Anesthesia and Perioperative Medicine, Medical University of South Carolina, 171 Ashley Ave., Charleston, SC 29425., [star][star] E-mail: gramlipm@musc.edu, a 4/1/82104

Byline: Takeshi Motoyama, Hiroaki Kawano, Kiyotaka Kugiyama, Ken Okumura, Masamichi Ohgushi, Michihiro Yoshimura, Osamu Hirashima, Hirofumi Yasue Abstract: Coronary spasm is induced by acetylcholine, serotonin, ergonovine, or histamine, all of which cause vasodilation when the endothelium is intact, and is promptly relieved by nitroglycerin, which vasodilates through the direct action on smooth muscle. Endothelial dysfunction is therefore possibly involved in the pathogenesis of coronary artery spasm. The aim of this study was to determine whether endothelium-dependent vasodilation is impaired in the peripheral arteries of patients with coronary spastic angina. Flow-dependent vasodilation of the brachial arteries during reactive hyperemia after the transient arterial occlusion was examined by using the high-resolution ultrasound technique in 35 patients with coronary spastic angina and 35 controls. Flow-dependent vasodilation of the brachial arteries was impaired in patients with coronary spastic angina compared with controls (5.9% [+ or -] 4.2% vs 9.6% [+ or -] 3.4%, p < 0.001) although the percent increase in blood flow during reactive hyperemia was not different between the two groups. The dilator response to nitroglycerin was preserved in patients with coronary spastic angina compared with controls (18.6% [+ or -] 5.1% vs 16.2% [+ or -] 3.9%, p < 0.04). The results indicate that endothelium-dependent vasodilation of the brachial arteries is impaired in patients with coronary spastic angina. Thus endothelial vasomotor dysregulation may also be present in the systemic arteries as well as coronary arteries in patients with coronary spastic angina. (Am Heart J 1997;133:263-7.) Author Affiliation: Kumamoto, Japan Division of Cardiology, Kumamoto University School of Medicine Article History: Received 14 May 1996; Accepted 8 August 1996 Article Note: (footnote) [star] Supported in part by grants-in-aid for Scientific Research on Priority Area (03268107), B03454257, and C3670460 from the Ministry of Education, Science, and Culture in Japan, and the Smoking Research Foundation, Tokyo, Japan., [star][star] Reprint requests: Hirofumi Yasue, MD, Division of Cardiology, Kumamoto University School of Medicine, Honjo 1-1-1, Kumamoto City, Japan 860., a 0002-8703/97/$5.00 + 0 4/1/78084

Byline: Koji Tamura, Hisako Tsuji, Takashi Nishiue, Satoshi Tokunaga, Toshiji Iwasaka Abstract: We studied 140 patients with a first acute myocardial infarction to examine the effect of preceding angina as a marker of ischemic preconditioning on clinical ventricular arrhythmias and late potentials. Preceding angina was defined as the presence of ischemic chest pain within 24 hours before onset of myocardial infarction lasting no longer than 30 minutes and seen three or more times per day or at rest. Clinical features, angiographic findings, and late potentials were compared between patients with and without preceding angina. Thirty-four (24%) patients had preceding angina. Although the incidence of life-threatening ventricular tachyarrhythmias significantly differed (p = 0.0219), other clinical findings, including presence of late potentials, were not different between the two groups. Of 14 patients with life-threatening ventricular tachyarrhythmias, five events were considered as reperfusion arrhythmias. In patients who had successful reperfusion therapy, the incidence of life-threatening ventricular tachyarrhythmias had a tendency to be lower in patients with preceding angina than in those without preceding angina (p = 0.0586). Severe angina within 24 hours of onset of acute myocardial infarction is suggested to reduce occurrence of life-threatening ventricular tachyarrhythmias mainly associated with reperfusion during hospitalization. (Am Heart J 1997;133:297-301.) Author Affiliation: Osaka, Japan Article History: Received 18 April 1996; Accepted 7 August 1996 Article Note: (footnote) [star] From the Cardiovascular Center, Kansai Medical University., [star][star] Reprint requests: Koji Tamura, MD, Internal Medicine, Keihanna Hospital, 1-2-1 Fujisakahigashimachi, Hirakata City, Osaka, 573-01, Japan., a 0002-8703/97/$5.00 + 0 4/1/78085

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ahj.2006.07.018 Byline: Saskia L.M.A. Beeres (a), Jeroen J. Bax (a), Petra Dibbets-Schneider (b), Marcel P.M. Stokkel (b), Willem E. Fibbe (c), Ernst E. van der Wall (a), Martin J. Schalij (a), Douwe E. Atsma (a) Abstract: Cell therapy has recently been introduced to treat patients with refractory angina. Because most studies have only included short-term follow-up, the effects of cell therapy over a longer period are unknown. Author Affiliation: (a) Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands (b) Department of Nuclear Medicine, Leiden University Medical Center, Leiden, The Netherlands (c) Department of Hematology, Leiden University Medical Center, Leiden, The Netherlands Article History: Received 16 May 2006; Accepted 19 July 2006

Byline: JA[cedilla]rgen F. Hansen, Leif Hagerup, Bjarne Sigurd, Flemming Pedersen, Kresten Mellemgaard, Ole Pedersen Bjergaard Abstract: In a double-blind, randomized trial in a consecutive group of postinfarct patients in treatment with diuretic agents for congestive heart failure, the 3 month rate of cardiac events (i.e., death, repeat infarction, unstable angina pectoris, or repeat admission because of heart failure) was 14% in patients treated with verapamil and trandolapril and 35% in patients treated with trandolapril (p = 0.01). In another study of patients with angina pectoris and left ventricular ejection fraction less than 40%, trandolapril plus verapamil improved exercise duration and left ventricular ejection fraction. These findings indicate that combined treatment with verapamil and trandolapril may be beneficial in patients with congestive heart failure. (Am Heart J 1997;134:S48-S52) Author Affiliation: Hvidovre, Holstebro, NykA[cedilla]bing, HillerA[cedilla]d, and Nyborg Denmark Article Note: (footnote) [star] From the Department of Cardiology, Hvidovre University Hospital, Holstebro,a NykA[cedilla]bing F,b Hilleroslash;d,c and Nyborgd Hospitals, Denmark., [star][star] Reprint requests: J. Fischer Hansen, MD, Department of Cardiovascular Medicine, Bispebjerg University Hospital, Bispebjerg Bakke 23, DK-2400 Copenhagen NV, Denmark., a 0002-8703/97/$5.00 + 0 4/0/84183