1. Angina pectoris is chest pain caused by reduced blood flow to the heart muscle due to an imbalance between the heart's oxygen supply and demand. It is a common symptom of coronary artery disease.
2. The main causes of reduced blood flow are blockages in the coronary arteries from atherosclerosis and spasms of the arteries. Other potential causes include abnormalities in the microcirculation of the heart and reduced oxygen-carrying capacity of the blood.
3. Angina affects millions of Americans each year and is more common in women, blacks, and older individuals. It is an important cause of mortality and morbidity from heart disease.
Myocardial infraction or Heart attack are terms used anonymously, but the preferred term is MI.
In an MI an area of the myocardium is permanently destroyed.
MI is usually caused by reduced or decreased blood flow in a coronary artery due to rupture of an atherosclerotic plaque and subsequent occlusion of the artery by a thrombus.
Myocardial infarction (MI) death of the cells of an area of the heart muscle (myocardium) as a result of oxygen deprivation, which in turn is caused by obstruction of the blood supply; commonly referred to as a “heart attack.”
MI refers to the processes by which myocardial tissue is destroyed in regions of the heart that are deprived of an adequate blood supply because of reduced coronary artery blood flow.
Eighty percent to 90% of all acute MI are secondary to thrombus formation. When thrombus develops , perfusion to the myocardium distal to the occlusion is halted, resulting in necrosis.The myocardium receives its blood supply from the two large coronary arteries and their branches.
Occlusion of one or more of these blood vessels (coronary occlusion) is one of the major causes of myocardial infarction.
The occlusion may result from the formation of a clot that develops suddenly when an athermanous plaque ruptures through the sub layers of a blood vessel, or when the narrow, roughened inner lining of a scleroses artery leads to complete thrombosis.
The acute MI process takes time. Cardiac cells can withstand in ischemic conditions for approximately 20 minutes before cellular death begins.
The earliest tissue to become ischemic is the sub endocardium (the innermost layer of tissue in the cardiac muscle)
If ischemia persists, it takes approximately 4 to 6 hours for the entire thickness if the heart muscle to become necrosis.
Myocardial infraction or Heart attack are terms used anonymously, but the preferred term is MI.
In an MI an area of the myocardium is permanently destroyed.
MI is usually caused by reduced or decreased blood flow in a coronary artery due to rupture of an atherosclerotic plaque and subsequent occlusion of the artery by a thrombus.
Myocardial infarction (MI) death of the cells of an area of the heart muscle (myocardium) as a result of oxygen deprivation, which in turn is caused by obstruction of the blood supply; commonly referred to as a “heart attack.”
MI refers to the processes by which myocardial tissue is destroyed in regions of the heart that are deprived of an adequate blood supply because of reduced coronary artery blood flow.
Eighty percent to 90% of all acute MI are secondary to thrombus formation. When thrombus develops , perfusion to the myocardium distal to the occlusion is halted, resulting in necrosis.The myocardium receives its blood supply from the two large coronary arteries and their branches.
Occlusion of one or more of these blood vessels (coronary occlusion) is one of the major causes of myocardial infarction.
The occlusion may result from the formation of a clot that develops suddenly when an athermanous plaque ruptures through the sub layers of a blood vessel, or when the narrow, roughened inner lining of a scleroses artery leads to complete thrombosis.
The acute MI process takes time. Cardiac cells can withstand in ischemic conditions for approximately 20 minutes before cellular death begins.
The earliest tissue to become ischemic is the sub endocardium (the innermost layer of tissue in the cardiac muscle)
If ischemia persists, it takes approximately 4 to 6 hours for the entire thickness if the heart muscle to become necrosis.
Etiopathogenesis and pharmacotherapy of CONGESTIVE CARDIAC FAILURE
a. the pathophysiology of selected disease states and the rationale for drug therapy;
b. the therapeutic approach to management of these diseases;
c. the controversies in drug therapy;
d. the importance of preparation of individualised therapeutic plans based on diagnosis;
e. needs to identify the patient-specific parameters relevant in initiating drug therapy,
and monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects);
f. describe the pathophysiology of selected disease states and explain the rationale for
drug therapy;
g. summarise the therapeutic approach to management of these diseases including
reference to the latest available evidence;
h. discuss the controversies in drug therapy;
i. discuss the preparation of individualised therapeutic plans based on diagnosis; and
j. identify the patient-specific parameters relevant in initiating drug therapy, and monitoring therapy (including alternatives, time-course of clinical and laboratory indices of therapeutic response and adverse effects).
will help you in understanding myocardial infarction in more detail with its management and therapy with complications and with graphical knowledge you can understand it better and some laboratry test are also included in it .
this is a slide on myocardial infraction to figure you out what exactly it is !
though i have not mentioned the diet based causes ............etc.
so enjoy
A DETAILED STUDY ON SHOCK, MYOCARDIAL INFRACTION & STROKEmartinshaji
This is a detailed study about shock , myocardial infraction , & stroke . also contain descriptions about types of shock, further management ,recognition of shock , treatment, first aid options are also mentioned along with cardiac arrest and stroke & emergency management of stroke etc
please comment if you visited this
thank u
Coronary thrombosis is formation of a blood clot inside a blood vessel of heart. Thrombosis in the heart can pave to a myocardial infarction. Coronary Thrombosis is general in high blood pressure patient, diabetic, and victims of atherosclerosis. The treatment is decreasing pain, improving blood flow to the heart muscle, and preventing irreversible damage to the heart muscle.
Coronary Thrombosis in the heart can pave to a myocardial infarction. Coronary thrombosis and myocardial infarction are sometimes availed as synonyms, although this is technically much inaccurate as the thrombosis refers to the blocking of blood vessels, while the infarction refers to the tissue death due to the consequent loss of blood flow to the heart tissue. The heart comprises many connecting blood vessels, and depending upon the location of the thrombosis, the infarction may cause no symptoms [1, 2] (Fig: 1 &2).
Fig: 1. Coronary Thrombosis
Fig: 2. Heart with blood clot
Facts of Coronary Thrombosis
Studies in Thrombosis and Hemostasis, Thrombosis and Haemostasis, Arteriosclerosis, Thrombosis, and Vascular Biology, Clinical and Applied Thrombosis/Hemostasis were a key investigation topics and research are carried out to encounter problems in these fields
CAD AND MI (CORONARY ARTERY DISEASE AND MYOCARDIAL INFARCTION)kalyan kumar
Coronary artery disease (CAD) causes impaired blood flow in the arteries that supply blood to the heart. Also called coronary heart disease (CHD), CAD is the most common form of heart disease and affects approximately 16.5 million Americans over the age of 20.
It’s also the leading cause of death for both men and women in the United States. It’s estimated that every 40 seconds, someone in the United States has a heart attack.
The most common cause of CAD is vascular injury with cholesterol plaque buildup in the arteries, known as atherosclerosis. Reduced blood flow occurs when one or more of these arteries becomes partially or completely blocked.
The four primary coronary arteries are located on the surface of the heart:
Right main coronary artery
Left main coronary artery
Left circumflex artery
Left anterior descending artery.
When your heart doesn’t get enough arterial blood, you may experience a variety of symptoms. Angina (chest discomfort) is the most common symptom of CAD.
Etiopathogenesis and pharmacotherapy of CONGESTIVE CARDIAC FAILURE
a. the pathophysiology of selected disease states and the rationale for drug therapy;
b. the therapeutic approach to management of these diseases;
c. the controversies in drug therapy;
d. the importance of preparation of individualised therapeutic plans based on diagnosis;
e. needs to identify the patient-specific parameters relevant in initiating drug therapy,
and monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects);
f. describe the pathophysiology of selected disease states and explain the rationale for
drug therapy;
g. summarise the therapeutic approach to management of these diseases including
reference to the latest available evidence;
h. discuss the controversies in drug therapy;
i. discuss the preparation of individualised therapeutic plans based on diagnosis; and
j. identify the patient-specific parameters relevant in initiating drug therapy, and monitoring therapy (including alternatives, time-course of clinical and laboratory indices of therapeutic response and adverse effects).
will help you in understanding myocardial infarction in more detail with its management and therapy with complications and with graphical knowledge you can understand it better and some laboratry test are also included in it .
this is a slide on myocardial infraction to figure you out what exactly it is !
though i have not mentioned the diet based causes ............etc.
so enjoy
A DETAILED STUDY ON SHOCK, MYOCARDIAL INFRACTION & STROKEmartinshaji
This is a detailed study about shock , myocardial infraction , & stroke . also contain descriptions about types of shock, further management ,recognition of shock , treatment, first aid options are also mentioned along with cardiac arrest and stroke & emergency management of stroke etc
please comment if you visited this
thank u
Coronary thrombosis is formation of a blood clot inside a blood vessel of heart. Thrombosis in the heart can pave to a myocardial infarction. Coronary Thrombosis is general in high blood pressure patient, diabetic, and victims of atherosclerosis. The treatment is decreasing pain, improving blood flow to the heart muscle, and preventing irreversible damage to the heart muscle.
Coronary Thrombosis in the heart can pave to a myocardial infarction. Coronary thrombosis and myocardial infarction are sometimes availed as synonyms, although this is technically much inaccurate as the thrombosis refers to the blocking of blood vessels, while the infarction refers to the tissue death due to the consequent loss of blood flow to the heart tissue. The heart comprises many connecting blood vessels, and depending upon the location of the thrombosis, the infarction may cause no symptoms [1, 2] (Fig: 1 &2).
Fig: 1. Coronary Thrombosis
Fig: 2. Heart with blood clot
Facts of Coronary Thrombosis
Studies in Thrombosis and Hemostasis, Thrombosis and Haemostasis, Arteriosclerosis, Thrombosis, and Vascular Biology, Clinical and Applied Thrombosis/Hemostasis were a key investigation topics and research are carried out to encounter problems in these fields
CAD AND MI (CORONARY ARTERY DISEASE AND MYOCARDIAL INFARCTION)kalyan kumar
Coronary artery disease (CAD) causes impaired blood flow in the arteries that supply blood to the heart. Also called coronary heart disease (CHD), CAD is the most common form of heart disease and affects approximately 16.5 million Americans over the age of 20.
It’s also the leading cause of death for both men and women in the United States. It’s estimated that every 40 seconds, someone in the United States has a heart attack.
The most common cause of CAD is vascular injury with cholesterol plaque buildup in the arteries, known as atherosclerosis. Reduced blood flow occurs when one or more of these arteries becomes partially or completely blocked.
The four primary coronary arteries are located on the surface of the heart:
Right main coronary artery
Left main coronary artery
Left circumflex artery
Left anterior descending artery.
When your heart doesn’t get enough arterial blood, you may experience a variety of symptoms. Angina (chest discomfort) is the most common symptom of CAD.
Characteristics of high maturity organisations - how CMMI & LSS integration can improve product quality, processes, bottom line and customer satisfaction
Left Ventricular Apical Ballooning, Catecholamine Toxicity, and Cardiomyopathyasclepiuspdfs
Case reports and clinical experiences have implicated catecholamine. Excess likely contributes to the pathophysiologic process as a cause of cardiac dysfunction, impaired hemodynamic function, and poor outcomes. Cardiac dysfunction has also been described in many other diseases; there is likely a common underlying pathophysiology. In this review, we will examine the pathophysiology of cardiac dysfunction after catecholamine surge and discuss the evidence surrounding cardiac dysfunction.
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1. Angina Pectoris http://emedicine.medscape.com/article/150215-overview
Author: Jamshid Alaeddini, MD, FACC; Chief Editor: Eric H Yang, MD more...
Updated: Aug 10, 2011
Background
Angina pectoris is the result of myocardial ischemia caused by an imbalance between myocardial blood supply and
oxygen demand. Angina is a common presenting symptom (typically, chest pain) among patients with coronary artery
disease. A comprehensive approach to diagnosis and to medical management of angina pectoris is an integral part of
the daily responsibilities of health care professionals.
Pathophysiology
Myocardial ischemia develops when coronary blood flow becomes inadequate to meet myocardial oxygen demand.
This causes myocardial cells to switch from aerobic to anaerobic metabolism, with a progressive impairment of
metabolic, mechanical, and electrical functions. Angina pectoris is the most common clinical manifestation of
myocardial ischemia. It is caused by chemical and mechanical stimulation of sensory afferent nerve endings in the
coronary vessels and myocardium. These nerve fibers extend from the first to fourth thoracic spinal nerves, ascending
via the spinal cord to the thalamus, and from there to the cerebral cortex.
Studies have shown that adenosine may be the main chemical mediator of anginal pain. During ischemia, ATP is
degraded to adenosine, which, after diffusion to the extracellular space, causes arteriolar dilation and anginal pain.
Adenosine induces angina mainly by stimulating the A1 receptors in cardiac afferent nerve endings.[1]
Heart rate, myocardial inotropic state, and myocardial wall tension are the major determinants of myocardial metabolic
activity and myocardial oxygen demand. Increases in the heart rate and myocardial contractile state result in increased
myocardial oxygen demand. Increases in both afterload (ie, aortic pressure) and preload (ie, ventricular end-diastolic
volume) result in a proportional elevation of myocardial wall tension and, therefore, increased myocardial oxygen
demand. Oxygen supply to any organ system is determined by blood flow and oxygen extraction. Because the resting
coronary venous oxygen saturation is already at a relatively low level (approximately 30%), the myocardium has a
limited ability to increase its oxygen extraction during episodes of increased demand. Thus, an increase in myocardial
oxygen demand (eg, during exercise) must be met by a proportional increase in coronary blood flow.
The ability of the coronary arteries to increase blood flow in response to increased cardiac metabolic demand is
referred to as coronary flow reserve (CFR). In healthy people, the maximal coronary blood flow after full dilation of the
coronary arteries is roughly 4-6 times the resting coronary blood flow. CFR depends on at least 3 factors: large and
small coronary artery resistance, extravascular (ie, myocardial and interstitial) resistance, and blood composition.
Myocardial ischemia can result from (1) a reduction of coronary blood flow caused by fixed and/or dynamic epicardial
coronary artery (ie, conductive vessel) stenosis, (2) abnormal constriction or deficient relaxation of coronary
microcirculation (ie, resistance vessels), or (3) reduced oxygen-carrying capacity of the blood.
Atherosclerosis is the most common cause of epicardial coronary artery stenosis and, hence, angina pectoris.
Patients with a fixed coronary atherosclerotic lesion of at least 50% show myocardial ischemia during increased
myocardial metabolic demand as the result of a significant reduction in CFR. These patients are not able to increase
their coronary blood flow during stress to match the increased myocardial metabolic demand, thus they experience
angina. Fixed atherosclerotic lesions of at least 90% almost completely abolish the flow reserve; patients with these
lesions may experience angina at rest.
Coronary spasm can also reduce CFR significantly by causing dynamic stenosis of coronary arteries. Prinzmetal
angina is defined as resting angina associated with ST-segment elevation caused by focal coronary artery spasm.
Although most patients with Prinzmetal angina have underlying fixed coronary lesions, some have angiographically
normal coronary arteries. Several mechanisms have been proposed for Prinzmetal angina: focal deficiency of nitric
oxide production,[2] hyperinsulinemia, low intracellular magnesium levels, smoking cigarettes, and using cocaine.
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2. Angina Pectoris http://emedicine.medscape.com/article/150215-overview
Approximately 30% of patients with chest pain referred for cardiac catheterization have normal or minimal
atherosclerosis of coronary arteries. A subset of these patients demonstrates reduced CFR that is believed to be
caused by functional and structural alterations of small coronary arteries and arterioles (ie, resistance vessels). Under
normal conditions, resistance vessels are responsible for as much as 95% of coronary artery resistance, with the
remaining 5% being from epicardial coronary arteries (ie, conductive vessels). The former is not visualized during
regular coronary catheterization. Angina due to dysfunction of small coronary arteries and arterioles is called
microvascular angina. Several diseases, such as diabetes mellitus, hypertension, and systemic collagen vascular
diseases (eg, systemic lupus erythematosus, polyarteritis nodosa), are believed to cause microvascular abnormalities
with subsequent reduction in CFR.
The syndrome that includes angina pectoris, ischemialike ST-segment changes and/or myocardial perfusion defects
during stress testing, and angiographically normal coronary arteries is referred to as syndrome X. Most patients with
this syndrome are postmenopausal women, and they usually have an excellent prognosis.[3] Syndrome X is believed to
be caused by microvascular angina. Multiple mechanisms may be responsible for this syndrome, including (1)
impaired endothelial dysfunction,[4] (2) increased release of local vasoconstrictors, (3) fibrosis and medial hypertrophy
of the microcirculation, (4) abnormal cardiac adrenergic nerve function, and/or (5) estrogen deficiency.[5]
A number of extravascular forces produced by contraction of adjacent myocardium and intraventricular pressures can
influence coronary microcirculation resistance and thus reduce CFR. Extravascular compressive forces are highest in
the subendocardium and decrease toward the subepicardium. Left ventricular (LV) hypertrophy together with a higher
myocardial oxygen demand (eg, during tachycardia) cause greater susceptibility to ischemia in subendocardial layers.
Myocardial ischemia can also be the result of factors affecting blood composition, such as reduced oxygen-carrying
capacity of blood, as is observed with severe anemia (hemoglobin, < 8 g/dL), or elevated levels of
carboxyhemoglobin. The latter may be the result of inhalation of carbon monoxide in a closed area or of long-term
smoking.
Ambulatory ECG monitoring has shown that silent ischemia is a common phenomenon among patients with
established coronary artery disease. In one study, as many as 75% of episodes of ischemia (defined as transient ST
depression of ≥ 1 mm persisting for at least 1 min) occurring in patients with stable angina were clinically silent. Silent
ischemia occurs most frequently in early morning hours and may result in transient myocardial contractile dysfunction
(ie, stunning). The exact mechanism(s) for silent ischemia is not known. However, autonomic dysfunction (especially in
patients with diabetes), a higher pain threshold in some individuals, and the production of excessive quantities of
endorphins are among the more popular hypotheses.[6]
Epidemiology
Frequency
United States
Approximately 9.8 million Americans are estimated to experience angina annually, with 500,000 new cases of angina
occurring every year. In 2009, an estimated 785 000 Americans will have a new coronary attack, and about 470 000
will have a recurrent attack. Only 18% of coronary attacks are preceded by angina. An additional 195,000 silent first
myocardial infarctions are estimated to occur each year.[7]
Mortality/Morbidity
About every 25 seconds, an American will have a coronary event, and about every minute someone will die from one.
Coronary heart disease (CHD) caused about 1 of every 5 deaths in the United States in 2005. Final 2005 coronary
heart disease mortality in 2005 was 445,687 (232,115 males and 213,572 females). On the basis of 2005 mortality
rate data, nearly 2,400 Americans die of cardiovascular disease (CVD) each day—an average of 1 death every 37
seconds. The 2006 overall preliminary death rate from cardiovascular disease was 262.9.[7]
Race
The annual rates per 1000 population of new episodes of angina are as follows:[7]
Age 45-54 years
8.5 for nonblack men
10.6 for nonblack women
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3. Angina Pectoris http://emedicine.medscape.com/article/150215-overview
11.8 for black men
20.8 for black women
Age 55-64 years
11.9 for nonblack men
11.2 for nonblack women
10.6 for black men
19.3 for black women
Age 65-74 years
13.7 for nonblack men
13.1 for nonblack women
8.8 for black men
10.0 for black women
Sex
Angina pectoris is more often the presenting symptom of coronary artery disease in women than in men, with a
female-to-male ratio of 1.7:1. It has an estimated prevalence of 4.6 million in women and 3.3 million in men. In one
analysis, this female excess was found across countries and was particularly high in the American studies and higher
among nonwhite ethnic groups than among whites.[8] The frequency of atypical presentations is also more common
among women compared with men. Women have a slightly higher rate of mortality from coronary artery disease
compared with men, in part because of an older age at presentation and a frequent lack of classic anginal symptoms.
The estimated age-adjusted prevalence of angina is greater in women than in men.
Age
The prevalence of angina pectoris increases with age. Age is a strong independent risk factor for mortality. More than
150,000 Americans killed by CVD in 2005 were younger than 65 years. However, in 2005, 32% of deaths from
cardiovascular disease occurred before the age of 75 years, which is well before the average life expectancy of 77.9
years.[7]
Contributor Information and Disclosures
Author
Jamshid Alaeddini, MD, FACC Clinical Cardiac Electrophysiologist, Inland Cardiology Associates
Jamshid Alaeddini, MD, FACC is a member of the following medical societies: American College of Cardiology and
American Heart Association
Disclosure: Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; St.
Jude Honoraria Speaking and teaching; Reliant Honoraria Speaking and teaching
Coauthor(s)
Jamshid Shirani, MD Director of Cardiology Fellowship Program, Director of Echocardiography Laboratory, St
Luke's Hospital and Health Network
Jamshid Shirani, MD is a member of the following medical societies: American Association for the Advancement of
Science, American College of Cardiology, American College of Physicians, American Federation for Medical
Research, American Heart Association, American Society of Echocardiography, and Association of Subspecialty
Professors
Disclosure: Nothing to disclose.
Specialty Editor Board
Alan D Forker, MD Professor of Medicine, University of Missouri at Kansas City School of Medicine; Director,
Outpatient Lipid Diabetes Research, MidAmerica Heart Institute of St Luke's Hospital
Alan D Forker, MD is a member of the following medical societies: Alpha Omega Alpha, American College of
Cardiology, American College of Physicians, American Heart Association, American Medical Association, American
Society of Hypertension, and Phi Beta Kappa
Disclosure: Research Grant Grant/research funds Hospital contracts to do research; I am a hospital employee with
no personal profit; Speakers Bureau Honoraria Speaking and teaching
3 of 8 9/3/2011 8:16 AM
4. Angina Pectoris http://emedicine.medscape.com/article/150215-overview
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College
of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Steven J Compton, MD, FACC, FACP Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence
and Alaska Regional Hospitals
Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical
Association, American College of Cardiology, American College of Physicians, American Heart Association,
American Medical Association, and Heart Rhythm Society
Disclosure: Nothing to disclose.
Amer Suleman, MD Private Practice
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American
Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American
Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and
Interventions
Disclosure: Nothing to disclose.
Chief Editor
Eric H Yang, MD Associate Professor of Medicine, Director of Interventional Cardiology Fellowship Program,
Henry Ford Hospital
Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha
Disclosure: Nothing to disclose.
References
1. Crea F, Pupita G, Galassi AR, et al. Role of adenosine in pathogenesis of anginal pain. Circulation. Jan
1990;81(1):164-72. [Medline].
2. Kugiyama K, Yasue H, Okumura K, et al. Nitric oxide activity is deficient in spasm arteries of patients with
coronary spastic angina. Circulation. Aug 1 1996;94(3):266-71. [Medline].
3. Rosano GM, Collins P, Kaski JC, et al. Syndrome X in women is associated with oestrogen deficiency. Eur
Heart J. May 1995;16(5):610-4. [Medline].
4. Kaski JC, Elliott PM, Salomone O, et al. Concentration of circulating plasma endothelin in patients with angina
and normal coronary angiograms. Br Heart J. Dec 1995;74(6):620-4. [Medline].
5. Lanza GA, Giordano A, Pristipino C, et al. Abnormal cardiac adrenergic nerve function in patients with
syndrome X detected by [123I]metaiodobenzylguanidine myocardial scintigraphy. Circulation. Aug 5
1997;96(3):821-6. [Medline].
6. Deedwania PC, Carbajal EV. Silent ischemia during daily life is an independent predictor of mortality in stable
angina. Circulation. Mar 1990;81(3):748-56. [Medline].
7. Lloyd-Jones D, Adams R, Carnethon M, De Simone G, Ferguson TB, Flegal K, et al. Heart disease and
stroke statistics--2009 update: a report from the American Heart Association Statistics Committee and Stroke
Statistics Subcommittee. Circulation. Jan 27 2009;119(3):e21-181. [Medline].
8. Hemingway H, Langenberg C, Damant J, Frost C, Pyorala K, Barrett-Connor E. Prevalence of angina in
women versus men: a systematic review and meta-analysis of international variations across 31 countries.
Circulation. Mar 25 2008;117(12):1526-36. [Medline].
9. Kuo L, Davis MJ, Chilian WM. Longitudinal gradients for endothelium-dependent and -independent vascular
responses in the coronary microcirculation. Circulation. Aug 1 1995;92(3):518-25. [Medline].
10. Grundy SM, Cleeman JI, Merz CN, et al. Implications of recent clinical trials for the National Cholesterol
4 of 8 9/3/2011 8:16 AM
5. Angina Pectoris http://emedicine.medscape.com/article/150215-overview
Education Program Adult Treatment Panel III Guidelines. J Am Coll Cardiol. Aug 4 2004;44(3):720-32.
[Medline].
11. O'Keefe JH Jr, Barnhart CS, Bateman TM. Comparison of stress echocardiography and stress myocardial
perfusion scintigraphy for diagnosing coronary artery disease and assessing its severity. Am J Cardiol. Apr
13 1995;75(11):25D-34D. [Medline].
12. [Guideline] Greenland P, Bonow RO, Brundage BH, Budoff MJ, Eisenberg MJ, Grundy SM. ACCF/AHA 2007
clinical expert consensus document on coronary artery calcium scoring by computed tomography in global
cardiovascular risk assessment and in evaluation of patients with chest pain: a report of the American College
of Cardiology Foundation Clinical Expert Consensus Task Force (ACCF/AHA Writing Committee to Update
the 2000 Expert Consensus Document on Electron Beam Computed Tomography) developed in
collaboration with the Society of Atherosclerosis Imaging and Prevention and the Society of Cardiovascular
Computed Tomography. J Am Coll Cardiol. Jan 23 2007;49(3):378-402. [Medline].
13. Kannel WB, Feinleib M. Natural history of angina pectoris in the Framingham study. Prognosis and survival.
Am J Cardiol. Feb 1972;29(2):154-63. [Medline].
14. Meijboom WB, Van Mieghem CA, van Pelt N, Weustink A, Pugliese F, Mollet NR. Comprehensive
assessment of coronary artery stenoses: computed tomography coronary angiography versus conventional
coronary angiography and correlation with fractional flow reserve in patients with stable angina. J Am Coll
Cardiol. Aug 19 2008;52(8):636-43. [Medline].
15. [Best Evidence] Bamberg F, Truong QA, Blankstein R, Nasir K, Lee H, Rogers IS, et al. Usefulness of age
and gender in the early triage of patients with acute chest pain having cardiac computed tomographic
angiography. Am J Cardiol. Nov 1 2009;104(9):1165-70. [Medline].
16. den Uil CA, Valk SD, Cheng JM, Kappetein AP, Bogers AJ, van Domburg RT, et al. Prognosis of patients
undergoing cardiac surgery and treated with intra-aortic balloon pump counterpulsation prior to surgery: a
long-term follow-up study. Interact Cardiovasc Thorac Surg. May 15 2009;[Medline].
17. Campbell AR, Satran D, Zenovich AG, Campbell KM, Espel JC, Arndt TL. Enhanced external
counterpulsation improves systolic blood pressure in patients with refractory angina. Am Heart J. Dec
2008;156(6):1217-22. [Medline].
18. Arora RR, Chou TM, Jain D, et al. The multicenter study of enhanced external counterpulsation (MUST-
EECP): effect of EECP on exercise-induced myocardial ischemia and anginal episodes. J Am Coll Cardiol.
Jun 1999;33(7):1833-40. [Medline].
19. Kumar A, Aronow WS, Vadnerkar A, Sidhu P, Mittal S, Kasliwal RR, et al. Effect of enhanced external
counterpulsation on clinical symptoms, quality of life, 6-minute walking distance, and echocardiographic
measurements of left ventricular systolic and diastolic function after 35 days of treatment and at 1-year follow
up in 47 patients with chronic refractory angina pectoris. Am J Ther. Mar-Apr 2009;16(2):116-8. [Medline].
20. Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients
with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. Nov 19
1994;344(8934):1383-9. [Medline].
21. Schwartz GG, Olsson AG, Ezekowitz MD, et al. Effects of atorvastatin on early recurrent ischemic events in
acute coronary syndromes: the MIRACL study: a randomized controlled trial. JAMA. Apr 4
2001;285(13):1711-8. [Medline].
22. Sever PS, Dahlof B, Poulter NR, et al. Prevention of coronary and stroke events with atorvastatin in
hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-
Scandinavian Cardiac Outcomes Trial--Lipid Lowering Arm (ASCOT-LLA): a multicentre randomi. Lancet. Apr
5 2003;361(9364):1149-58. [Medline].
23. Shepherd J, Blauw GJ, Murphy MB, et al. Pravastatin in elderly individuals at risk of vascular disease
(PROSPER): a randomised controlled trial. Lancet. Nov 23 2002;360(9346):1623-30. [Medline].
24. LaRosa JC, Grundy SM, Waters DD, et al. Intensive lipid lowering with atorvastatin in patients with stable
coronary disease. N Engl J Med. Apr 7 2005;352(14):1425-35. [Medline].
25. National Cholesterol Education Program. Executive Summary of The Third Report of The National
Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood
5 of 8 9/3/2011 8:16 AM
6. Angina Pectoris http://emedicine.medscape.com/article/150215-overview
Cholesterol In Adults (Adult Treatment Panel III). JAMA. May 16 2001;285(19):2486-97. [Medline].
26. Nissen SE, Tardif JC, Nicholls SJ, Revkin JH, Shear CL, Duggan WT. Effect of torcetrapib on the progression
of coronary atherosclerosis. N Engl J Med. Mar 29 2007;356(13):1304-16. [Medline].
27. Bots ML, Visseren FL, Evans GW, Riley WA, Revkin JH, Tegeler CH. Torcetrapib and carotid intima-media
thickness in mixed dyslipidaemia (RADIANCE 2 study): a randomised, double-blind trial. Lancet. Jul 14
2007;370(9582):153-60. [Medline].
28. Ridker PM, Manson JE, Gaziano JM, et al. Low-dose aspirin therapy for chronic stable angina. A randomized,
placebo-controlled clinical trial. Ann Intern Med. May 15 1991;114(10):835-9. [Medline].
29. Juul-Moller S, Edvardsson N, Jahnmatz B, et al. Double-blind trial of aspirin in primary prevention of
myocardial infarction in patients with stable chronic angina pectoris. The Swedish Angina Pectoris Aspirin
Trial (SAPAT) Group. Lancet. Dec 12 1992;340(8833):1421-5. [Medline].
30. Yusuf S, Zhao F, Mehta SR, et al. Effects of clopidogrel in addition to aspirin in patients with acute coronary
syndromes without ST-segment elevation. N Engl J Med. Aug 16 2001;345(7):494-502. [Medline].
31. Rossouw JE, Anderson GL, Prentice RL, et al. Risks and benefits of estrogen plus progestin in healthy
postmenopausal women: principal results From the Women's Health Initiative randomized controlled trial.
JAMA. Jul 17 2002;288(3):321-33. [Medline].
32. Lacoste LL, Theroux P, Lidon RM, et al. Antithrombotic properties of transdermal nitroglycerin in stable angina
pectoris. Am J Cardiol. Jun 1 1994;73(15):1058-62. [Medline].
33. Norwegian Multicenter Study Group. Timolol-induced reduction in mortality and reinfarction in patients
surviving acute myocardial infarction. N Engl J Med. Apr 2 1981;304(14):801-7. [Medline].
34. Miwa K, Miyagi Y, Igawa A, et al. Vitamin E deficiency in variant angina. Circulation. Jul 1 1996;94(1):14-8.
[Medline].
35. Kaski JC, Rosano G, Gavrielides S, Chen L. Effects of angiotensin-converting enzyme inhibition on exercise-
induced angina and ST segment depression in patients with microvascular angina. J Am Coll Cardiol. Mar 1
1994;23(3):652-7. [Medline].
36. Losordo DW, Henry TD, Davidson C, et al. Intramyocardial, Autologous CD34+ Cell Therapy for Refractory
Angina. Circ Res. Aug 5 2011;109(4):428-436. [Medline].
37. Morice MC, Serruys PW, Sousa JE, et al. A randomized comparison of a sirolimus-eluting stent with a
standard stent for coronary revascularization. N Engl J Med. Jun 6 2002;346(23):1773-80. [Medline].
38. Kastrati A, Mehilli J, Pache J, Kaiser C, Valgimigli M, Kelbaek H. Analysis of 14 trials comparing sirolimus-
eluting stents with bare-metal stents. N Engl J Med. Mar 8 2007;356(10):1030-9. [Medline].
39. Boden WE, O'Rourke RA, Teo KK, Hartigan PM, Maron DJ, Kostuk WJ. Optimal medical therapy with or
without PCI for stable coronary disease. N Engl J Med. Apr 12 2007;356(15):1503-16. [Medline].
40. Oesterle SN, Sanborn TA, Ali N, et al. Percutaneous transmyocardial laser revascularisation for severe
angina: the PACIFIC randomised trial. Potential Class Improvement From Intramyocardial Channels. Lancet.
Nov 18 2000;356(9243):1705-10. [Medline].
41. Allen KB, Dowling RD, Fudge TL, et al. Comparison of transmyocardial revascularization with medical therapy
in patients with refractory angina. N Engl J Med. Sep 30 1999;341(14):1029-36. [Medline].
42. Losordo DW, Schatz RA, White CJ, Udelson JE, Veereshwarayya V, Durgin M. Intramyocardial
transplantation of autologous CD34+ stem cells for intractable angina: a phase I/IIa double-blind, randomized
controlled trial. Circulation. Jun 26 2007;115(25):3165-72. [Medline].
43. Banai S, Ben Muvhar S, Parikh KH, Medina A, Sievert H, Seth A. Coronary sinus reducer stent for the
treatment of chronic refractory angina pectoris: a prospective, open-label, multicenter, safety feasibility first-
in-man study. J Am Coll Cardiol. May 1 2007;49(17):1783-9. [Medline].
44. Anderson HV. Angiotensin-converting enzyme inhibitors: ischemia is not the correct measure of benefit. J Am
Coll Cardiol. Dec 17 2003;42(12):2060-2. [Medline].
6 of 8 9/3/2011 8:16 AM
7. Angina Pectoris http://emedicine.medscape.com/article/150215-overview
45. Khan NA, Hemmelgarn B, Herman RJ, Bell CM, Mahon JL, Leiter LA, et al. The 2009 Canadian Hypertension
Education Program recommendations for the management of hypertension: Part 2--therapy. Can J Cardiol.
May 2009;25(5):287-98. [Medline].
46. Ambrosio G, Betocchi S, Pace L, et al. Prolonged impairment of regional contractile function after resolution
of exercise-induced angina. Evidence of myocardial stunning in patients with coronary artery disease.
Circulation. Nov 15 1996;94(10):2455-64. [Medline].
47. Brown G, Albers JJ, Fisher LD, et al. Regression of coronary artery disease as a result of intensive lipid-
lowering therapy in men with high levels of apolipoprotein B. N Engl J Med. Nov 8 1990;323(19):1289-98.
[Medline].
48. Califf RM, Armstrong PW, Carver JR, et al. 27th Bethesda Conference: matching the intensity of risk factor
management with the hazard for coronary disease events. Task Force 5. Stratification of patients into high,
medium and low risk subgroups for purposes of risk factor management. J Am Coll Cardiol. Apr
1996;27(5):1007-19. [Medline].
49. Cannon CP, Braunwald E, McCabe CH, et al. Intensive versus moderate lipid lowering with statins after acute
coronary syndromes. N Engl J Med. Apr 8 2004;350(15):1495-504. [Medline].
50. Chauhan A, Mullins PA, Taylor G, et al. Both endothelium-dependent and endothelium-independent function is
impaired in patients with angina pectoris and normal coronary angiograms. Eur Heart J. Jan 1997;18(1):60-8.
[Medline].
51. Connolly DC, Elveback LR, Oxman HA. Coronary heart disease in residents of Rochester, Minnesota. IV.
Prognostic value of the resting electrocardiogram at the time of initial diagnosis of angina pectoris. Mayo Clin
Proc. Apr 1984;59(4):247-50. [Medline].
52. Frileux S, Munoz Sastre MT, Mullet E, Sorum PC. The impact of the preventive medical message on intention
to change behavior. Patient Educ Couns. Jan 2004;52(1):79-88. [Medline].
53. [Guideline] Gibbons RJ, Abrams J, Chatterjee K, Daley J, Deedwania PC, Douglas JS, et al. ACC/AHA 2002
guideline update for the management of patients with chronic stable angina--summary article: a report of the
American College of Cardiology/American Heart Association Task Force on practice guidelines (Committee
on the Management of Patients With Chronic Stable Angina). J Am Coll Cardiol. Jan 1 2003;41(1):159-68.
[Medline].
54. [Guideline] Gibbons RJ, Balady GJ, Bricker JT, et al. ACC/AHA 2002 guideline update for exercise testing:
summary article: a report of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines (Committee to Update the 1997 Exercise Testing Guidelines). Circulation. Oct 1
2002;106(14):1883-92. [Medline].
55. Khan NE, De Souza A, Mister R, et al. A randomized comparison of off-pump and on-pump multivessel
coronary-artery bypass surgery. N Engl J Med. Jan 1 2004;350(1):21-8. [Medline].
56. Margolis JR, Chen JT, Kong Y, et al. The diagnostic and prognostic significance of coronary artery
calcification. A report of 800 cases. Radiology. Dec 1980;137(3):609-16. [Medline].
57. Mark DB, Califf RM, Morris KG, et al. Clinical characteristics and long-term survival of patients with variant
angina. Circulation. May 1984;69(5):880-8. [Medline].
58. Maseri A, Crea F, Kaski JC, Davies G. Mechanisms and significance of cardiac ischemic pain. Prog
Cardiovasc Dis. Jul-Aug 1992;35(1):1-18. [Medline].
59. Piatti P, Fragasso G, Monti LD, et al. Endothelial and metabolic characteristics of patients with angina and
angiographically normal coronary arteries: comparison with subjects with insulin resistance syndrome and
normal controls. J Am Coll Cardiol. Nov 1 1999;34(5):1452-60. [Medline].
60. Rocco MB, Nabel EG, Campbell S, et al. Prognostic importance of myocardial ischemia detected by
ambulatory monitoring in patients with stable coronary artery disease. Circulation. Oct 1988;78(4):877-84.
[Medline].
61. Rubins HB, Robins SJ, Collins D, et al. Gemfibrozil for the secondary prevention of coronary heart disease in
men with low levels of high-density lipoprotein cholesterol. Veterans Affairs High-Density Lipoprotein
Cholesterol Intervention Trial Study Group. N Engl J Med. Aug 5 1999;341(6):410-8. [Medline].
7 of 8 9/3/2011 8:16 AM
8. Angina Pectoris http://emedicine.medscape.com/article/150215-overview
62. Wenger NK, Speroff L, Packard B. Cardiovascular health and disease in women. N Engl J Med. Jul 22
1993;329(4):247-56. [Medline].
63. Yusuf S, Sleight P, Pogue J, et al. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on
cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N
Engl J Med. Jan 20 2000;342(3):145-53. [Medline].
8 of 8 9/3/2011 8:16 AM