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Journal articles on the topic 'Angian Pectoris'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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1

Abduljabbar, Ahmed Abduljalal, and Parween Abdulsamad Ismail. "Investigation of Malondialdehyde (MDA), Homocysteine (Hcy) and C- reactive protein (CRP) in sera of patients with Angina Pectoris." Al-Mustansiriyah Journal of Science 30, no. 1 (August 15, 2019): 68. http://dx.doi.org/10.23851/mjs.v30i1.463.

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Homocysteine (Hcy) has been considered as an independent risk factor for coronary artery disease (CAD Oxidative stress and free radicals are known to have important roles in the development ofAngina Pectoris. Oxidative stress is present in cardiovascular diseases (CVDs), and hyperhomocysteinemia, an independent risk factor for these diseases, may play a role in inducing production of oxygen free radicals. The aim of this study was to determine a possible relationship between blood serum Hcy levels and lipid peroxidation in patients suffering from Angina Pectoris (AP).To evaluate the possible role of homocysteine (Hcy) in inducing oxidative stress in Angina Pectoris(AP), plasma homocysteine( Hcy), plasma malondialdehyde (MDA) and C reactive protein (CRP) were measured in 60 unstable Angina Pectoris patients, we tested 30 healthy volunteers. Hcy was measured by an enzymatic colorimetric method and MDA, an index of lipid peroxidation, by spectrophotometer. Serum Hcy levels were significantly higher in angina pectories (AP) patients than the controls (23.2±8.0 vs 10.76 ± 2.55 micromol/L; P

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2

Chaloupka, Václav. "Angina, its diagnosis and treatment." Cor et Vasa 49, no. 9 (September 1, 2007): 334–40. http://dx.doi.org/10.33678/cor.2007.116.

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3

Rajanit, Sojitra, Mukesh Dungrani, Paras Virani, and Hasumati Raj. "A review on Nifedipine co-administered with Metoprolol succinate for the treatment of hypertension." International Journal of Advances in Scientific Research 1, no. 3 (April 30, 2015): 129. http://dx.doi.org/10.7439/ijasr.v1i3.1795.

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Hypertension and Angina pectoris area major public health problem in the developed Countries recently. Hypertension and Angina Pectoris are frequently treated with antihypertensive drugs like calcium-channel blockers, angiotensin-converting enzyme inhibitors, and angiotensin II (AT1) receptor blockers, and statins. Nifedipine is calcium-channel blockers and widely used in treatment of Angina pectoris condition. Metoprolol Succinate is Beta-adrenoreceptor blocker and widely used in treatment of hypertension condition. Combination of Nifedipine and Metoprolol Succinate is used in the treatment of cardiovascular diseases like hypertension and Angina Pectoris. So this combination therapy gives antihypertensive and Angina Pectoris effects in the treatment of cardiac diseases.

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4

Seyidov, V. G., A. Ya Fissun, V. V. Yevsyukov, I. V. Lyubchuk, S. Ye Bobyrev, and E. V. Arutyunov. "Long-term coronary shunting results for 5 years of observation. Factors influencing on angina pectoris recurrence after coronary shunting." Bulletin of Siberian Medicine 5, no. 3 (September 30, 2006): 105–11. http://dx.doi.org/10.20538/1682-0363-2006-3-105-111.

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Aimed at o comparing coronary shunting long-term results with drug treatment of angina pectoris as well as estimating influence of dyslipidemia, diabetes mellitus, hypoglycemic therapy nature, arterial hypertension and increased systemic inflammation on angina pectoris recurrence after the surgery, we examined 793 patients 5 years after coronary shunting and 81 patients who were treated by standard methods. Five years after the surgery, we noted decreased number of patients without angina pectoris symptoms and increased number of patients with angina pectoris. Increased levels of cholesterol, low density lipoproteins, α-lipoproteids, C-reactive proteins and diabetes mellitus of the 2-nd type II—III stage contribute to angina pectoris recurrence rate after the surgery. Operated on patients revealed angina pectoris recurrences, myocardial infarction frequency, repeated hospitalizations and annual mortality more seldom compared with patients who underwent drug treatment.

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5

YASUE, HIROFUMI. "Angina pectoris." Nihon Naika Gakkai Zasshi 86, no. 2 (1997): 189–90. http://dx.doi.org/10.2169/naika.86.189.

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6

O'Rourke, M. F. "ANGINA PECTORIS." Australian and New Zealand Journal of Medicine 15, no. 4 (August 1985): 409. http://dx.doi.org/10.1111/j.1445-5994.1985.tb02760.x.

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7

NEWTON, JANICE L. "Angina pectoris." Nursing 28, no. 8 (August 1998): 58–60. http://dx.doi.org/10.1097/00152193-199808000-00025.

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8

McGoon, Michael D. "Angina Pectoris." Mayo Clinic Proceedings 61, no. 1 (January 1986): 83. http://dx.doi.org/10.1016/s0025-6196(12)61416-5.

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9

Bittner, Vera. "Angina Pectoris." Circulation 117, no. 12 (March 25, 2008): 1505–7. http://dx.doi.org/10.1161/circulationaha.108.764217.

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10

Seim, Sigurd. "Angina Pectoris." Acta Medica Scandinavica 166, no. 4 (April 24, 2009): 255–67. http://dx.doi.org/10.1111/j.0954-6820.1960.tb17377.x.

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11

Aldana B., Jairo, and Alberto Suárez N. "Angina pectoris." Universitas Médica 53, no. 4 (September 9, 2012): 431–42. http://dx.doi.org/10.11144/javeriana.umed53-4.anpe.

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Se cumplen 200 años de la descripción de la angina de pecho, publicada en el New England Journal of Medicine. En este articulo se ha traducido el artículo original “Remarks on Angina Pectoris”, publicado en 1812, por el dr. John Warren.

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12

Goldschlager, Nora. "Angina pectoris." Postgraduate Medicine 80, no. 6 (November 1986): 147. http://dx.doi.org/10.1080/00325481.1986.11699596.

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13

. "Angina pectoris." Huisarts en Wetenschap 47, no. 4 (April 2004): 776. http://dx.doi.org/10.1007/bf03083974.

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14

MALIK, ISHTIAQ AHMED, KHALID MAHMOOD, and ALI NAWAZ KHAN. "ANGINA PECTORIS." Professional Medical Journal 16, no. 02 (June 10, 2009): 202–8. http://dx.doi.org/10.29309/tpmj/2009.16.02.2902.

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Objective: To assess the clinical efficacy, cost effectiveness and side effect profile of trimetazidine in the managementof stable angina pectoris. Patients a n d M e t h o d s : An open label, uncontrolled study was conducted in 200 patients with stable angina inarmed forces institute of cardiology, Rawalpindi Pakistan. Patients were treated for 4weeks with modified release trimetazidine tablet (35mg)twice daily in addition to their conventional therapy. R e s u l t s : As compared to base line trimetazidine significantly reduced the number ofanginal episodes per week from 10 to 3 (p<0.005), improved exercise duration time on standard exercise tolerance test (ETT) (410 vs. 370sec; p<0.01), time to onset of typical angina (380 vs, 290sec; p<0.05), time to 1mm or more ST segment depression (340 vs. 290 sec;p<0.01)).There was no drop out of patients due to side effects or non compliance. C o n c l u s i o n : These results indicate that trimetazidineis effective and well tolerated when used in combination with existing antianginal therapy in patients with angina pectoris

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15

Mathenge, Njambi, Wenjun Fan, Nathan D. Wong, Calvin Hirsch, Chris (Joseph) Delaney, Ezra A. Amsterdam, Bruce Koch, Rico Calara, and Julius M. Gardin. "Pre-diabetes, diabetes and predictors of incident angina among older women and men in the Cardiovascular Health Study." Diabetes and Vascular Disease Research 17, no. 1 (November 28, 2019): 147916411988847. http://dx.doi.org/10.1177/1479164119888476.

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Diabetes mellitus and angina pectoris are important conditions in older persons. The utility of pre-diabetes mellitus, diabetes mellitus and other risk factors as predictors of incident angina pectoris among older adults has not been characterized. We examined incident angina pectoris rates by sex and diabetes mellitus status in 4511 adults aged ⩾65 years without coronary heart disease at baseline from the Cardiovascular Health Study. Cox regression examined predictors of incident angina pectoris, including pre-diabetes mellitus or diabetes mellitus adjusted for sociodemographic characteristics and other risk factors, over 12.2 ± 6.9 years of follow-up. Overall, 39.1% of participants had pre-diabetes mellitus, 14.0% had diabetes mellitus and 532 (11.8%) had incident angina pectoris. Incident angina pectoris rates per 1000 person-years in those with neither condition, pre-diabetes mellitus, and diabetes mellitus were 7.9, 9.0 and 12.3 in women and 10.3, 11.2 and 14.5 in men, respectively. Pre-diabetes mellitus and diabetes mellitus were not independently associated with incident AP; however, key predictors of AP were male sex, low-density lipoprotein-cholesterol, triglycerides, systolic blood pressure, antihypertensive medication and difficulty performing at least one instrumental activity of daily living (all p < 0.05 to p < 0.01). In our cohort of older adult participants, while the incidence of AP is greater in those with diabetes mellitus, neither diabetes mellitus nor pre-diabetes mellitus independently predicted incident angina pectoris.

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16

S., V. "To the pathogenesis and treatment of true angina pectoris. Palya (Wien. Klin. Woch., 1926, No. 22)." Kazan medical journal 22, no. 7 (September 4, 2021): 865. http://dx.doi.org/10.17816/kazmj79534.

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17

Tiwari, Ishwar, Raphael M. Herr, Adrian Loerbroks, and Shelby S. Yamamoto. "Household Air Pollution and Angina Pectoris in Low- and Middle-Income Countries: Cross-Sectional Evidence from the World Health Survey 2002–2003." International Journal of Environmental Research and Public Health 17, no. 16 (August 11, 2020): 5802. http://dx.doi.org/10.3390/ijerph17165802.

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The evidence regarding the effects of household air pollution on angina pectoris is limited in low-and middle-income countries (LMICs). We sought to examine the association between household air pollution and angina pectoris across several countries. We analyzed data of individuals from 46 selected countries participating in the cross-sectional World Health Survey (WHS) 2002–2003. Pooled and stratified (sex, continent) logistic regression with sampling weights was used to estimate adjusted odds ratios (ORs) and 95% confidence intervals (CIs) to quantify associations between the use of different household fuels with angina pectoris. In the pooled sample, we observed lower odds of angina pectoris with electricity use (OR: 0.68, 95% CI: 0.56–0.83) compared to those households reporting the use of gas as a household fuel. Increased odds of angina pectoris were observed with the use of agriculture/dung/shrub/other (OR: 1.65, 95% CI: 1.30–2.09), mixed (solid and non-solid fuels) (OR: 1.31, 95% CI: 1.09–1.56), and mixed solid fuel use (OR: 1.59, 95% CI: 1.12–2.25). Higher odds of angina pectoris were observed mainly with solid fuel use. The results highlight the importance of addressing these issues, especially in regions with a high proportion of solid fuel users and increasing levels of cardiovascular disease.

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18

Shang, Qinghua, Hao Xu, Zhaolan Liu, Keji Chen, and Jianping Liu. "OralPanax notoginsengPreparation for Coronary Heart Disease: A Systematic Review of Randomized Controlled Trials." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/940125.

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This systematic review aims to evaluate current evidence for the benefit and side effect of oralPanax notoginsengpreparation for coronary heart disease (CHD). We included 17 randomized clinical trials (17 papers and 1747 participants). Comparing with no intervention on the basis of conventional therapy, oralPanax notoginsengdid not show significant effect on reducing cardiovascular events, but it could alleviate angina pectoris (including improving the symptoms of angina pectoris [RR 1.20; 95% CI 1.12 to 1.28; 7 trials,n=791], improving electrocardiogram [RR 1.35; 95% CI 1.19 to 1.53; 8 trials,n=727], decreasing the recurrence of angina pectoris [RR 0.38; 95% CI 0.16 to 0.94; 1 trials,n=60], duration of angina pectoris [RR −1.88; 95% CI −2.08 to −1.69; 2 trials,n=292], and dosage of nitroglycerin [MD −1.13; 95% CI −1.70 to −0.56; 2 trials,n=212]); oralPanax notoginsenghad no significant difference compared with isosorbide dinitrate on immediate effect for angina pectoris [RR 0.96; 95% CI 0.81 to 1.15; 1 trial,n=80]. In conclusion, oralPanax notoginsengpreparation could relieve angina pectoris related symptoms. However, the small sample size and potential bias of most trials influence the convincingness of this conclusion. More rigorous trials with high quality are needed to give high level of evidence, especially for the potential benefit of cardiovascular events.

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19

Laederach-Hofmann, Kurt, Clemens Turniger, Lutz Mussgay, and Ralph Jürgensen. "Sensorische und affektive Komponenten im Gebrauch von Schmerzwörtern bei Patienten mit Angina Pectoris und koronarer Herzkrankheit oder Syndrom-X." Zeitschrift für Klinische Psychologie und Psychotherapie 30, no. 3 (July 2001): 182–88. http://dx.doi.org/10.1026/0084-5345.30.3.182.

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Zusammenfassung. Ziel: Untersuchung von Patienten mit Syndrom-X im Vergleich zu solchen mit koronarstenotisch bedingter Angina pectoris im Hinblick auf Unterschiede in verbal-inhaltlichen Aspekten der Schmerzbeschreibung. Methode: Einundsechzig Patienten mit Angina pectoris wurden untersucht, 32 davon mit Syndrom-X (Angina pectoris, abnorme Ergometrie und normale Koronarangiographie) und 29 mit koronarer Herzkrankheit (Angina Pectoris, abnorme Ergometrie, angiographisch dokumentierte koronare 1-3-Gefässerkrankung, kein vorgängiger Myokardinfarkt). Neben einem klinisch semi-strukturierten Interview werden dafür die Hamburger Schmerz Adjektiv Liste, die Schmerzempfindungsskala und die Berner Version des McGill Pain Questionnaire verwendet. Ergebnisse: Patienten mit Syndrom-X weisen bei sensorischen Adjektiven in der Hamburger Schmerz Adjektiv Liste und in der Schmerzempfindungsskala signifikant geringere Werte auf als solche mit koronare Herzkrankheit. Für die affektiven Adjektive gibt es lediglich signifikante Unterschiede in der Hamburger Schmerz Adjektiv Liste zwischen beiden Patientengruppen. Im McGill Pain Questionnaire erwiesen sich die Unterschiede zwischen den Gruppen sowie zwischen den Fragebögen als nicht signifikant. Schlußfolgerungen: Die Unterschiede in den Fragebogendaten erlauben zwar keine diagnostische Trennung der beiden Gruppen, zeigen jedoch eine höhere affektive Schmerzbewertung bei Angina pectoris mit koronarer Herzkrankheit.

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20

BORTOLOTTI, M. "Angina pectoris and oesophageal angina." Gut 45, no. 4 (October 1, 1999): 630. http://dx.doi.org/10.1136/gut.45.4.630.

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21

Tobing, Erna R., Jusak Nugraha, and Muhammad Amminuddin. "DIAGNOSTIC CONCORDANCE BETWEEN NEXT-GENERATION AND HIGH SENSITIVE TROPONIN-I IN ANGINA PECTORIS PATIENTS." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 24, no. 1 (March 29, 2018): 64. http://dx.doi.org/10.24293/ijcpml.v24i1.1158.

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Angina pectoris merupakan gejala klinis Sindrom Koroner Akut (SKA) yang mengarah pada penyakit jantung koroner. Sindromkoroner akut terdiri dari Unstable Angina dan Infark Miokard Akut (IMA). Kadar Troponin I (TnI) dapat mendukung penegakkandiagnosis IMA di pasien angina pectoris. Beberapa metode pemeriksaan TnI semakin berkembang diantaranya TnI high sensitive (TnI hs)dan TnI next-generation (TnI ng). Tujuan penelitian ini adalah menganalisis kesesuaian diagnostik antara kadar TnI ng yang diperiksamenggunakan metode Fluorescent Enzyme Transfer Latex (FETL) [Alere Triage MeterPro®] dan TnI hs dengan metode ChemiluminescentImmunoassay (CLEIA) [Mitsubishi PathFast®] di pasien angina pectoris. Penelitian dilaksanakan di RSUD Dr.Soetomo Surabaya masawaktu Maret-Juli 2016 dengan rancangan penelitian potong lintang. Sebanyak 82 subjek penelitian dengan gejala angina pectorisdiperiksakan kadar Troponin-I menggunakan kedua metode. Subjek penelitian sebanyak 44% didiagnosis SKA, dan 56% non SKA. Nilaikesesuaian koefisien kappa antara TnI ng dan TnI hs di pasien angina pectoris adalah 0,738 (p<0,01). Kepekaan dan kekhasan TnI ngterhadap TnI hs untuk diagnosis IMA dengan cut off 0,02 ng/mL adalah 94% dan 78%. Analisis kenasaban antara kadar TnI ng danTnI hs dengan koefisien kenasaban Spearman rho (ρ) adalah 0,826 (p<0,01). Terdapat kesesuaian diagnostik antara TnI ng dan TnI hsdi pasien angina pectoris. Kedua metode pemeriksaan TnI dapat digunakan untuk membantu menegakkan diagnosis di pasien anginapectoris. Penelitian lebih lanjut diperlukan untuk mengetahui nilai prognosis TnI.

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22

Kim, Michael C., Annapoorna Kini, and Samin K. Sharma. "Refractory angina pectoris." Journal of the American College of Cardiology 39, no. 6 (March 2002): 923–34. http://dx.doi.org/10.1016/s0735-1097(02)01716-3.

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23

Yeghiazarians, Yerem, Joel B. Braunstein, Arman Askari, and Peter H. Stone. "Unstable Angina Pectoris." New England Journal of Medicine 342, no. 2 (January 13, 2000): 101–14. http://dx.doi.org/10.1056/nejm200001133420207.

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24

Bankwala, Zehyani, and Lyle J. Swenson. "Unstable angina pectoris." Postgraduate Medicine 98, no. 6 (December 1995): 155–65. http://dx.doi.org/10.1080/00325481.1995.11946092.

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25

Becker, Richard C., and Joseph S. Alpert. "Variant Angina Pectoris." Chest 92, no. 6 (December 1987): 963–65. http://dx.doi.org/10.1378/chest.92.6.963b.

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26

Pfisterer, M. E., and Ch Kaiser. "Instabile Angina pectoris." Hämostaseologie 20, no. 01 (2000): 53–58. http://dx.doi.org/10.1055/s-0037-1619469.

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ZusammenfassungIn den letzten Jahren wurden bei der instabilen Angina pectoris sowohl im Bereich des pathophysiologischen Verständnisses, der Risikostratifizierung als auch der Therapie große Fortschritte unternommen. Nebst besserer klinischer Risikostratifizierung stehen uns heute ebenfalls biochemische Marker wie z.B. das Troponin zur initialen Risikoabschätzung zur Verfügung. Zusätzlich zur Standardtherapie mit Azetylsalizylsäure und der intravenösen Vollheparinisierung verfügen wir über neuere Medikamente wie die niedermolekularen Heparine sowie die GPIIb/IIIa-Rezeptorantagonisten, welche in größeren Studien mit oder ohne koronare Intervention ihre Wirksamkeit bewiesen haben, vorerst jedoch vor allem den Hochrisikopatienten vorbehalten sein sollten. Die interventionelle Therapie wurde insbesondere durch die Entwicklung von koronaren Stents verbessert, die Wahl des richtigen Zeitpunkts der Intervention bleibt jedoch kontrovers.

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Tijssen, J. G. P., M. L. Simoons, P. J. De Feijter, P. G. Hugenholtz, and J. Lubsen. "Unstable angina pectoris." European Heart Journal 8, suppl H (October 2, 1987): 3–15. http://dx.doi.org/10.1093/eurheartj/8.suppl_h.3.

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Strauer, Bodo. "Stabile Angina pectoris." Der Klinikarzt 37, no. 10 (October 2008): 457. http://dx.doi.org/10.1055/s-0028-1103380.

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Wallace, W. A., J. F. Richeson, and P. N. Yu. "Unstable angina pectoris." Clinical Cardiology 13, no. 10 (October 1990): 679–86. http://dx.doi.org/10.1002/clc.4960131002.

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RIDDERVOLD, FRIDTJOV, OTTO A. SMISETH, KOLBJØRN FORFANG, and TOR FRØYSAKER. "Unstable Angina Pectoris." Acta Medica Scandinavica 224, no. 1 (April 24, 2009): 19–23. http://dx.doi.org/10.1111/j.0954-6820.1988.tb16733.x.

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YEGHIAZARIANS, YEREM, JOEL B. BRAUNSTEIN, ARMAN ASKARI, and PETER H. STONE. "Unstable Angina Pectoris." Survey of Anesthesiology 44, no. 6 (December 2000): 327–28. http://dx.doi.org/10.1097/00132586-200012000-00007.

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Garratt, Kirk N. "Stable angina pectoris." Current Treatment Options in Cardiovascular Medicine 2, no. 2 (April 2000): 161–72. http://dx.doi.org/10.1007/s11936-000-0009-y.

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. "angina pectorisAngina pectoris." Medisch-Farmaceutische Mededelingen 38, no. 4 (April 2000): 86. http://dx.doi.org/10.1007/bf03057527.

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. "Instabiele angina pectoris." Medisch-Farmaceutische Mededelingen 39, no. 1 (January 2001): 20. http://dx.doi.org/10.1007/bf03057666.

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Maseri, Attilio, Sergio Chierchia, and Juan Carlos Kaski. "Mixed angina pectoris." American Journal of Cardiology 56, no. 9 (September 1985): E30—E33. http://dx.doi.org/10.1016/0002-9149(85)91173-7.

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Dörr, Rolf. "Stabile Angina pectoris." Herz Kardiovaskuläre Erkrankungen 31, no. 9 (December 2006): 827–35. http://dx.doi.org/10.1007/s00059-006-2938-z.

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Henderson, Robert, and Adam Timmis. "Stable angina pectoris." Srce i krvni sudovi 31, no. 4 (2012): 38–47. http://dx.doi.org/10.5937/siks1201038h.

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Mazur, E. S., V. V. Mazur, R. M. Rabinovich, K. S. Myasnikov, and M. A. Bachurina. "On the Causes of Angina Pectoris in Patients With Pulmonary Embolism." Kardiologiia 60, no. 1 (February 6, 2020): 28–34. http://dx.doi.org/10.18087/cardio.2020.1.n729.

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Objective Compare the distance between the pulmonary artery (PA) and the left coronary artery (LCA) using pulmonary angiography and the rate of detection of the signs of left ventricular myocardial ischemiain the first electrocardiogram (ECG) in pulmonary embolism (PE) patients with or without angina to detect possible causes of angina pectoris.Material and Methods Measurement of the minimum distance between the PA and LCA in multislice spiral computed tomography and analysis of the first ECG were performed in 55 PE patients. 15 (27.3%) patients had angina pectoris at the onset of the disease.Results Angina pectoris was observed in 14 (93.3%) of 15 patients with the distance between the PA andLCA less than 4.3 mm, and in one (2.5%) of 40 patients with the distance between these vessels equalto or exceeding the specified value (p<0.001). In the first ECG, the ST elevation in the aVR lead wasdetected in 10 (66.7%) patients with angina pectoris, and only in 3 (7.5%) patients without anginapectoris (p<0.001).Conclusions The findings suggest that angina pectoris in acute pulmonary embolism may be caused by compression of the LCA by the dilated PA.

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Cheng, Long, Yue Liu, and Xiao-bo Sun. "The Clinical Efficacy of Yindanxinnaotong Soft Capsule in the Treatment of Stroke and Angina Pectoris: A Meta-Analysis." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–14. http://dx.doi.org/10.1155/2017/2060549.

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Objective. To systematically evaluate the clinical efficacy of Yindanxinnaotong (YD) soft capsule in adult patients with cardiovascular diseases (stroke and angina pectoris). Methods. We electronically searched databases including Medline, PubMed, Chinese National Knowledge Infrastructure (CNKI), Cqvip Database (VIP), and Wanfang Database for published articles of randomized controlled trials (RCTs) of YD capsule in treating stroke and angina pectoris. The meta-analysis was performed using RevMan 5.3 software. Results. 49 RCTs involving 6195 subjects with cardiovascular diseases (angina pectoris and stroke) were included. Compared with western conventional medicine (WCM) and/or other Chinese medicines, YD plus WCM therapeutic regimen could significantly improve the efficacy rate (RR = 1.21, 95% CI (1.17, 1.25), P<0.00001 for angina pectoris, RR = 1.24, 95% CI (1.18, 1.31), P<0.00001 for stroke), showing the clinical value. In addition, the therapeutic efficiency of WCM plus YD capsule regimen is better than that of WCM alone in improving CRP (MD = −2.07, 95% CI (−3.97, −0.17), P=0.03 <0.05) and TG (MD = −0.37, 95% CI (−0.52, −0.23), P<0.0001). Conclusion. YD is effective in the treatment of cardiovascular diseases (angina pectoris and stroke) in adults, and WCM plus YD therapeutic regimen can significantly improve the effective rate in the clinic.

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Kieback, G., Lorbeer, Wallaschofski, Ittermann, Völzke, Felix, and Dörr. "Claudication, in contrast to angina pectoris, independently predicts mortality risk in the general population." Vasa 41, no. 2 (March 1, 2012): 105–13. http://dx.doi.org/10.1024/0301-1526/a000172.

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Background: The aim of our analyses was to investigate whether claudication and angina pectoris, each defined and based on the answer to a single question, are predictive of future mortality. Probands and methods: The study population consisted of 3995 subjects selected from the population-based Study of Health In Pomerania (SHIP). Kaplan-Meier analysis and multivariable Cox proportional hazards regression analysis were used to analyze the association of angina pectoris and claudication with all-cause and cardiovascular mortality adjusted for major cardiovascular risk factors. Results: At baseline, 417 individuals had symptoms of angina pectoris, and 323 had symptoms of claudication. During a median follow-up of 8.5 years, 277 individuals died. Individuals with claudication had a higher fully-adjusted all-cause mortality rate (Hazard Ratio (HR) 1.79; 95 % CI 1.34, 2.39, p < 0.001) and a higher sex- and age-adjusted cardiovascular mortality rate (HR 1.76; 95 % CI 1.03, 2.99, p = 0.038) compared to subjects without claudication. In contrast, subjects with angina pectoris had neither an elevated fully-adjusted all-cause mortality rate (HR 1.15; 95 % CI 0.82, 1.61, p = 0.413) nor sex- and age-adjusted cardiovascular mortality rate (HR 0.71; 95 % CI 0.34, 1.48, p = 0.363) compared to those without this symptom. Conclusions: Claudication, in contrast to angina pectoris, is a strong, independent predictor of all-cause mortality.

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Rada, Feryal H. "ASSOCIATION OF LIPID FRACTIONS LEVELS WITH CARDIOVASCULAR DISEASE." Asian Journal of Pharmaceutical and Clinical Research 10, no. 3 (March 1, 2017): 180. http://dx.doi.org/10.22159/ajpcr.2017.v10i3.15984.

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ABSTRACTObjective: The aim of this study is to analyze the association of serum lipids and lipoproteins in patients with angina pectoris.Methods: A total of 110 patients (60 males and 50 females) with angina pectoris aged (55±5) years and 80 healthy controls (43 males and37 females) aged (45±4) years were enrolled in this case-control study from the clinic of Al Yarmouk Hospital. Serum lipids, lipoprotein(a) [Lp(a)],apolipoprotein-A1, and apolipoprotein-B levels were measured and studied.Results: The results of this study showed that increased odds of angina pectoris were associated with increased serum levels of Lp(a) more thanserum levels of apolipoprotein-B.Conclusions: Analysis of Lp(a) may be an important determinant of cardiovascular disease diagnosis.Keywords: Lipoprotein(a), Apolipoprotein-A1, Apo lipoprotein-B, Angina pectoris.

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GERHOLD, WALTER M. "Surgery for Angina Pectoris." Annals of Internal Medicine 103, no. 3 (September 1, 1985): 477. http://dx.doi.org/10.7326/0003-4819-103-3-477_2.

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Kaplinsky, Elieser. "Management of Angina Pectoris." Drugs 43, Supplement 1 (1992): 9–14. http://dx.doi.org/10.2165/00003495-199200431-00004.

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&NA;. "Chronic stable angina pectoris." Inpharma Weekly &NA;, no. 1193 (June 1999): 4. http://dx.doi.org/10.2165/00128413-199911930-00006.

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Hubert, Michael. "Angina pectoris ernst nehmen!" CardioVasc 17, no. 6 (December 2017): 74. http://dx.doi.org/10.1007/s15027-017-1285-8.

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Hubert, Michael. "Angina pectoris ernst nehmen!" Info Diabetologie 11, no. 6 (December 2017): 54. http://dx.doi.org/10.1007/s15034-017-1234-8.

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Lanza, Gaetano Antonio, Alessandro Sciahbasi, Alfonso Sestito, and Attilio Maseri. "Angina pectoris: a headache." Lancet 356, no. 9234 (September 2000): 998. http://dx.doi.org/10.1016/s0140-6736(00)02718-5.

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Eff, Jack, John Godfrey, Ronald Garutti, and Paolo Capone. "Celiprolol in Angina Pectoris." Journal of Cardiovascular Pharmacology 8, Supplement 4 (1986): S132—S134. http://dx.doi.org/10.1097/00005344-198608004-00030.

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Müller, Carl. "Xanthomata, Hypercholesterolemia, Angina Pectoris." Acta Medica Scandinavica 95, S89 (April 24, 2009): 75–84. http://dx.doi.org/10.1111/j.0954-6820.1938.tb19279.x.

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Thadani, Udho, and Asim Chohan. "Chronic stable angina pectoris." Postgraduate Medicine 98, no. 6 (December 1995): 175–88. http://dx.doi.org/10.1080/00325481.1995.11946093.

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