coronary artery disease and Acute coronary syndrome

placement of coronary artery stent

- Make sure on ANTICOAGULANT for period of time so nothing sticks to stent A stent is an expandable meshlike structure designed to keep the vessel open after balloon angioplasty. Because stents are thrombogenic, many different types of drugs are used to prevent platelet aggregation within the stent. Drugs commonly used during PCI are unfractionated heparin (UH) or low-molecular-weight heparin (LMWH), a direct thrombin inhibitor (e.g., bivalirudin [Angiomax]), and/or a glycoprotein IIb/IIIa inhibitor (e.g., eptifibatide [Integrilin]). After PCI, the patient is treated with dual antiplatelet drugs (e.g., aspirin [indefinitely] and clopidogrel) up to 12 months or longer, until the intimal lining grows over the stent and provides a smooth vascular surface. There are two types of stents: bare metal stents (BMS) and drug-eluting stents (DES). DESs are coated with a drug (e.g., paclitaxel, sirolimus) to reduce the risk of overgrowth of the intimal lining (neointimal hyperplasia) within the stent. This is the primary cause of in-stent restenosis (ISR). Following DES placement, dual antiplatelet drugs are taken to prevent thrombus formation within the stent (stent thrombosis) for a minimum of 12 months or longer. The duration of dual antiplatelet drugs for patients with BMS is a minimum of 1 month but ideally one full year after PCI. The most serious complications from stent placement are abrupt closure from coronary artery dissection and vascular injury at the artery access site (femoral or radial), acute MI, stent embolization, coronary spasm, dye allergy, renal compromise, bleeding (e.g., retroperitoneal), infection, stroke and emergent coronary artery bypass graft (CABG) surgery. The possibility of dysrhythmias during and after the procedure is always present.

types of saturated dietary fat

- animal fat (bacon, lard, egg yolk, dairy fat) - Oils (coconut, palm oil) - butter - cream cheese - sour cream

types of monounsaturated

- fish oil - oils (Canola, peanut, olive) - Avocado - Nuts (almonds, peanuts, pecans) - olives (green, black)

Polyunsaturated fats

- vegetable oils (safflower, corn, soybean, flaxseed, cottonseed) - Some fish oil, shellfish - Nuts (walnuts) - seeds (pumpkin, sunflower) - Margarine

stages of atherosclerosis

A. The endothelium (the inner lining the vessel wall) is normally nonreactive to platelets and leukocytes, as well as coagulation, fibrinolytic, and complement factors. However, the endothelial lining can be injured as a result of tobacco use, hyperlipidemia, hypertension, toxins, diabetes, hyperhomocysteinemia, and infection causing a local inflammatory response. CAD is a progressive disease that develops over many years. When it becomes symptomatic, the disease process is usually well advanced. The stages of development in atherosclerosis are (1) fatty streak, (2) fibrous plaque, and (3) complicated lesion. B. Fatty Streak Fatty streaks, the earliest lesions of atherosclerosis, are characterized by lipid-filled smooth muscle cells. As streaks of fat develop within the smooth muscle cells, a yellow tinge appears. Fatty streaks can be seen in the coronary arteries by age 15 and involve an increasing amount of surface area as one ages. C. Fibrous Plaque The fibrous plaque stage is the beginning of progressive changes in the endothelium of the arterial wall. These changes can appear in the coronary arteries by age 30 and increase with age. Once endothelial injury has taken place, lipoproteins (carrier proteins within the bloodstream) transport cholesterol and other lipids into the arterial intima. Collagen covers the fatty streak and forms a fibrous plaque with a grayish or whitish appearance. These plaques can form on one portion of the artery or in a circular fashion involving the entire lumen. The result is a narrowing of the vessel lumen and a reduction in blood flow to the distal tissues. D. Complicated Lesion The final stage in the development of the atherosclerotic lesion is the most dangerous. As the fibrous plaque grows, continued inflammation can result in plaque instability, ulceration, and rupture. Once the integrity of the artery's inner wall is compromised, platelets accumulate in large numbers, leading to a thrombus. The thrombus may adhere to the wall of the artery, leading to further narrowing or total occlusion of the artery. At this stage, the plaque is referred to as a complicated lesion. Injury means I smoke and the toxins get into bloodstream and injure intima; hyperlipidemia; diabetes (lots of glucose in blood stream and extra insulin actually cause damage to intimal layers), infections, toxins Endothelium is usually not permeable to lipids, cholesterol, platelets, etc. When blood vessel is damage that is when this can happen Lipids tend to sneak in and collect there; picked up by body and blood stream as not normal or foreign body; get platelets to gather there and even more endothelial cells; as it grows it causes stretching and narrow slumen of artery; macrophage start to eat up some; in the mean time we have some narrowing Chronic disease ocures that occurs over time Eventually lesions can rupture ; plaque is mae available to entire system; all clotting factors go there to plaque and now thrombis formation; if it breaks then forms emboli and it can travel wherever Acute coronary syndrome occurs when block in left coronary artery causing MI

Coronary artery disease etiology and pathophysiology - C- reactive protein

C-reactive protein (CRP) - Nonspecific marker of inflammation - Increased in many patients with CAD - Chronic exposure to CRP linked with unstable plaques and oxidation of LDL cholesterol C-reactive protein (CRP), a protein produced by the liver, is a nonspecific marker of inflammation. It is increased in many patients with CAD. The level of CRP rises when there is systemic inflammation. Chronic elevations of CRP are linked with unstable plaques and the oxidation of low-density lipoprotein (LDL) cholesterol, further contributing to atherosclerosis. Linked with unstable plaques and oxidation of LDL cholesterol Unstable plaques rupture and cause thrombis formation to emboli

chronic stable angina nursing/interprofessional care - alternative therapies for refractory chronic stable angina

Alternative therapies for refractory chronic stable angina - Enhanced external counterpulsation (EECP) Inflatable cuffs are placed around legs Increase venous return Augment DBP - Spinal cord stimulation For patients with refractory stable angina, enhanced external counterpulsation (EECP) may be used. EECP consists of placing inflatable BP cuffs around the legs. The cuffs sequentially inflate during diastole and deflate during systole from the calves to the thighs. This action is thought to increase venous return and augment diastolic BP in order to increase coronary perfusion, improve LV diastolic filling, and help with collateral circulation. Patients get treatments 5 days a week for a total of 35 treatments. EECP is contraindicated in patients with decompensated HF, severe peripheral arterial disease, and severe aortic insufficiency. Spinal cord stimulation may also help relieve symptoms in patients who are refractory to drugs or revascularization. The stimulation lead is placed in the epidural space between T1 and T2 and is connected to an implanted subcutaneous pulse generator. The mechanism by which angina is reduced is not well understood.

chronic stable angina interprofessional care - ACE inhibitors and ARB's - B-blockers - calcium channel blockers

Angiotensin-converting enzyme inhibitors (ACE) and angiotensin receptor blockers (ARBs) Captopril, venelopril, lisinopril (-pril are ACE; vasodilates; decreases BP; blocks converstion; those that cannot tolerate can get ARB's) Losartan, valsartan ( block receptors; ARB's = -sartan; also cause vasodilaition β-Blockers Block beta1 ; some do have impact on lungs so have to be careful; Atenolol, metroproprolol -lol is beta blocker Decrease heart rate, afterload, want to decrease ischemia ; vasodilate Calcium channel blockers Decrease HR, can cause major problems with arrhythmias; may also treat arrhythmias Diltazem, amlodipine, dephetapine, dicardapine, Verapamil -pine are calcium channel blockers Patients with chronic stable angina who have an ejection fraction [EF] of 40% or less, diabetes, hypertension, or chronic kidney disease should take an ACE inhibitor (e.g., lisinopril [Zestril]) indefinitely, unless contraindicated. Patients with chronic stable angina and a normal EF, diabetes, and one other CAD risk factor should also take an ACE inhibitor to decrease the risk of MI, stroke and death. These drugs result in vasodilation and reduced blood volume. Most important, they can prevent or reverse ventricular remodeling in patients who have had an MI. For patients who are intolerant of ACE inhibitors (e.g. cough, angioedema), ARBs (e.g., losartan [Cozaar]) are used. β-Blockers are ordered for relief of angina symptoms in patients with chronic stable angina. Patients who have LV dysfunction, elevated BP, or have had an MI should start and continue β-blockers indefinitely, unless contraindicated. These drugs decrease myocardial contractility, HR, SVR, and BP, all of which reduce the myocardial oxygen demand. β-Blockers that have been shown to reduce the risk of death in patients with LV dysfunction, heart failure (HF) or MI are carvedilol (Coreg), metoprolol (Lopressor, Toprol XL), and bisoprolol (Zebeta). β-Blockers have many side effects and can be poorly tolerated. Side effects may include bradycardia, hypotension, wheezing from bronchospasm, and GI complaints. Many patients also complain of weight gain, depression, fatigue, and sexual dysfunction. Absolute contraindications to using β-blockers include severe bradycardia and acute HF. Patients with asthma should avoid β-blockers. They are used cautiously in patients with diabetes, since they mask signs of hypoglycemia. β-blockers should not be stopped abruptly without medical supervision as this may result in an increase in the number and intensity of angina attacks. If β-Blockers are contraindicated, are poorly tolerated, or do not control anginal symptoms, calcium channel blockers are used. The primary effects of calcium channel blockers are (1) systemic vasodilation with decreased SVR, (2) decreased myocardial contractility, (3) coronary vasodilation, and (4) decreased HR. There are 2 groups of calcium channel blockers - those which have more vasodilatory effects and those which have more rate and contractility effects. Teach patients that they increase serum digoxin levels and therefore levels should be closely monitored.

Nursing and interprofessional care: CAD - antiplatelet therapy

Antiplatelet therapy (don't want to form a clot; so use Plavix or aspirin which decreases prostaglandins [antiinflammtory/pain]; 81 mg of aspirin!!; if on 81 mg of aspirin it is NEVER FOR PAIN) ASA Clopidogrel (Plavix) Unless contraindicated (e.g., history of GI bleeding), low-dose aspirin (81 mg) is recommended for most people at risk for CAD. Current recommendations include low-dose aspirin for men over 45 years and high-risk women (i.e., those with a calculated 10-year CAD risk of >20%) unless contraindicated. For high-risk women who are intolerant of aspirin, clopidogrel (Plavix) can be substituted. In healthy women 65 years or older, aspirin therapy may be considered if BP is controlled and the benefit for MI prevention outweighs the risk of GI bleed or hemorrhagic stroke.

coronary artery disease etiology and pathophysiology - atherosclerosis is major cause of ______

Atherosclerosis is major cause of CAD - Characterized by lipid deposits within intima of artery - Endothelial injury and inflammation play a major role in development Atherosclerosis is the major cause of CAD. It is characterized by deposits of lipids within the intima of the artery. Endothelial injury and inflammation play a central role in the development of atherosclerosis. Major cause of CAD Endothelial injury and inflammation play a major role in this development

Coronary Artery disease - Atheroscloerosis

Begins as soft deposits of fat that harden with age Referred to as "hardening of arteries" Atheromas (fatty deposits) prefer coronary arteries Also known as ASHD, CVHD, IHD, CHD Coronary artery disease is a type of blood vessel disorder that is included in the general category of atherosclerosis. The term atherosclerosis comes from two Greek words: athere, meaning "fatty mush," and skleros, meaning "hard." This combination means that atherosclerosis begins as soft deposits of fat that harden with age. Consequently, it is common to refer to atherosclerosis as "hardening of the arteries." Although this disease can occur in any artery in the body, the atheromas (fatty deposits) prefer the coronary arteries. The terms arteriosclerotic heart disease, cardiovascular heart disease, ischemic heart disease, coronary heart disease, and CAD all describe this disease process. Heart disease is number one killer of men and women period Heart disease starts with your arteries CHD- cardiovascular heart disease CAD- coronary artery disease Both talks about atherosclerosis Starts with soft fatty deposits in artery walls themselves Have to have some fat to function throughout life Over time those soft fatty deposits harden; you lose elastin and less responsive to pressure I got fat that is getting hard and arteries that are getting stiff anyway as we get older

chronic stable angina nursing/interprofessional care - cardiac cath/ coronary angiography

Cardiac catheterization/coronary angiography(antiography uses dye and x ray to look at where your going) Visualize blockages (diagnostic) Open blockages (interventional) Percutaneous coronary intervention (PCI) Balloon angioplasty Stent For patients with increasing angina a cardiac catheterization is ordered. Cardiac catheterization and coronary angiography use radiation and IV contrast dye to provide images of the coronary circulation and identify the location and severity of any blockage. If a patient is allergic to IV contrast dye, they must be premedicated with corticosteroids. Patients with chronic kidney disease need hydration pre- and post-procedure. A baseline serum creatinine level is obtained because the IV contrast dye can worsen renal function. Monitor renal function closely after the procedure. This procedure should only be done if the patient is a candidate for percutaneous or surgical coronary revascularization. If a coronary blockage is amenable to treatment, coronary revascularization with an elective percutaneous coronary intervention (PCI) may be recommended. During PCI, a catheter with a deflated balloon tip is inserted into the appropriate coronary artery. The deflated balloon is positioned in the blockage and inflated. This compresses the plaque against the artery wall, resulting in vessel dilation and a larger vessel diameter. This procedure is called balloon angioplasty. Intracoronary stents are usually placed along with balloon angioplasty.

clinical manifestations of CAD

Chronic and progressive disease O2 demand > O2 supply → myocardial ischemia (pain I feel is because of ischemia but when I stop and rest the demand goes down so supply gets better and ischemia goes away) (treatment is aimed at increase supply of oxygen; maybe vasodilation or increase contractility and decrease heart rate or BP) Angina = clinical manifestation Occurs when arteries are blocked 70% or more (when you start to see the symptoms this is what is happening; it's a slow complication) 50% or more for left main coronary artery CAD is a chronic and progressive disease. Patients may be asymptomatic for many years or they may develop chronic stable chest pain. When the demand for myocardial oxygen exceeds the ability of the coronary arteries to supply the heart with oxygen, myocardial ischemia occurs. Angina, or chest pain, is the clinical manifestation of myocardial ischemia. It is caused by either an increased demand for oxygen or a decreased supply of oxygen. The most common reason for angina to develop is narrowing of one or more coronary arteries by atherosclerosis. This leads to insufficient blood flow to the heart muscle. For ischemia secondary to atherosclerotic plaque to occur, the artery is usually blocked (stenosed) 70% or more (50% or more for the left main coronary artery).

Coronary artery disease etiology and pathophysiology - collateral circulation

Collateral circulation - Arterial anastomoses (or connections) within coronary circulation - Increased with chronic ischemia - May be inadequate with rapid-onset CAD Normally some arterial anastomoses or connections, called collateral circulation, exist within the coronary circulation. Two factors contribute to the growth and extent of collateral circulation: (1) inherited predisposition to develop new blood vessels (angiogenesis) and (2) presence of chronic ischemia. When plaque blocks the normal flow of blood through a coronary artery and the resulting ischemia is chronic, increased collateral circulation develops. When occlusion of the coronary arteries occurs slowly over a long period, there is a greater chance of collateral circulation developing, and the heart muscle may still receive an adequate amount of blood and oxygen. However, with rapid-onset CAD (e.g., familial hypercholesterolemia) or coronary spasm, time is inadequate for collateral development. Consequently, a reduced blood flow results in a more severe ischemia or infarction. If these happen over time, collateral circulation happens where arteries or connections will be created so signs and symptoms may not be noted Chronic coronary artery disease- may have tons of blockages but may not have any signs and symptosm because of chronic angina; it is because of this and the formation of blood flow

Risk factors for CAD - contributing modifiable risk factors

Contributing modifiable risk factors - Diabetes Diabetes is a big deal because glucose and insulin resistance; glucose constantly being in blood stream is an irritant to intimal layer; irritant to nerve endings [why they lose ability to feel] - Metabolic syndrome Cluster of risk factors; central obesity meaning trunk [big abdomen and little legs] ; HTN [not well controlled]; abnoral lipids and elevated fasting glucose [may or may not mean diabetic or prediabetic ] Diabetes Mellitus The incidence of CAD is 2 to 4 times greater among persons who have diabetes, even those with well-controlled blood glucose levels, than the general population. The patient with diabetes manifests CAD not only more often but also at an earlier age. The person with diabetes has an increased tendency toward endothelial dysfunction. This may account for the development of fatty streaks seen in these patients. Patients with diabetes also have changes in lipid metabolism and tend to have high cholesterol and triglyceride levels. Management of diabetes should include lifestyle changes and drug therapy to achieve a hemoglobin A1c (Hb A1c) level <7%. Metabolic Syndrome Metabolic syndrome refers to a cluster of risk factors for CAD whose underlying pathophysiology may be related to insulin resistance. These risk factors include central obesity, hypertension, abnormal serum lipids, and an elevated fasting blood glucose.

Risk factors for CAD - contributing modifiable risk factors continued...

Contributing modifiable risk factors - Psychologic states Link between someone who has depression and CAD; chronic high stress [type A personalities] - Homocysteine level - Substance abuse Link between cocaine use and methamphetamine use and heart disease Psychologic States Certain behaviors and lifestyles may contribute to the development of CAD. One type of behavior, referred to as type A, includes perfectionism and a hardworking, driving personality. The type A person often suppresses anger and hostility, has a sense of time urgency, is impatient, and often creates stress and tension. This person may be more prone to MIs than a type B person, who is more easygoing, takes upsets in stride, knows personal limitations, takes time to relax, and is not an overachiever. However, the relationship between behaviors and the risk for CAD/MI remains controversial and complex. Psychologic risk factors thought to increase the risk of CAD include depression, acute and chronic stress (e.g., poverty, serving as a caregiver), anxiety, hostility and anger, and lack of social support. In particular, depression is a risk factor for both the development and worsening of CAD. Depressed patients have elevated levels of circulating catecholamines. This may contribute to endothelial injury and inflammation and platelet activation. Higher levels of depression are also associated with an increased number of adverse heart events. Stressful states can contribute to the development of CAD. Sympathetic nervous system (SNS) stimulation and its effect on the heart are the physiologic mechanisms by which stress predisposes a person to the development of CAD. SNS stimulation causes an increased release of catecholamines (i.e., epinephrine, norepinephrine). This stimulation increases HR and the force of myocardial contraction. Both results increase myocardial oxygen demand. Also, stress-induced mechanisms can cause elevated lipid and glucose levels and changes in blood coagulation, which can lead to increased atherosclerosis. Homocysteine High blood levels of homocysteine have been linked to an increased risk for CAD and other CVDs. Homocysteine is produced by the breakdown of the essential amino acid methionine, which is found in dietary protein. High homocysteine levels may contribute to atherosclerosis by (1) damaging the inner lining of blood vessels, (2) promoting plaque buildup, and (3) altering the clotting mechanism to make clots more likely to occur. B-complex vitamins (B6, B12, folic acid) have been shown to lower blood levels of homocysteine. Generally, a screening test for homocysteine is limited to those suspected of having elevated levels. Theses include older patients with pernicious anemia or people who develop CAD at an early age. Substance Abuse The use of illicit drugs, such as cocaine and methamphetamine, can produce coronary spasm resulting in myocardial ischemia and chest pain. Most people who are seen in the emergency department (ED) with drug-induced chest pain are initially indistinguishable from those with CAD. Although MI can occur, these patients often have sinus tachycardia, high BP, angina, and anxiety.

Chronic stable angina interprofessional care - diagnostic studies

Diagnostic studies (expect all of this) Chest x-ray 12-lead ECG (first thing is vitals and 12 lead) Laboratory studies ( may start heparin drip since anticoagulant; may start nitroglycerin drip) Echocardiogram (wont do it right away; if having chest pain may go right to cath lab; if it goes away do echo at bed side) Exercise stress test EBCT Look at troponin levels!! Could indicate MI CCTA When CAD is suspected in a patient or when a patient with chronic stable angina has a change in the anginal pattern, a variety of studies are completed. After a detailed health history and physical examination, a chest x-ray is done to look for cardiac enlargement, aortic calcifications, and pulmonary congestion. A 12-lead ECG is done and compared with a previous ECG whenever possible to look for any changes. Laboratory tests (e.g., lipid profile, C-reactive protein) are done to identify specific risk factors for CAD. An echocardiogram may be done to look for resting LV wall motion abnormalities, which may suggest evidence of CAD. An exercise stress test with or without echocardiography or nuclear imaging may be ordered. For patients with physical limitations in walking, a pharmacologic (adenosine [Adenocard] or dipyridamole [Persantine]) stress test with nuclear imaging, or a pharmacologic (dobutamine [Dobutrex]) stress echocardiogram may be ordered. Coronary blockages less than 70% are not usually detected with stress testing. The electron beam computed tomography (EBCT) scan locates and measures coronary calcification. However, additional testing (e.g., stress testing or cardiac catheterization) is needed to further assess the impact of the lesion on coronary blood flow. Further studies are needed to determine the accuracy of the EBCT scan to diagnose high-grade blockages because many atherosclerotic plaques are not calcified. Coronary computed tomography angiography (CCTA) may be considered. Using IV contrast and radiation, CCTA can detect calcified and noncalcified plaques in the artery, as well as other heart conditions. Limitations of using CCTA include patients with rapid HRs (greater than 90 beats per minute), extensive coronary artery calcifications, obesity, and a history of prior coronary artery stent. Patients allergic to IV contrast dye must be premedicated with corticosteroids. Patients with chronic kidney disease need hydration pre- and post-procedure. A baseline serum creatinine level should be obtained as the IV contrast dye can worsen renal function.

chronic stable angina interprofessional care

Goal: ↓ O2 demand and/or ↑ O2 supply Short-acting nitrates - Dilate peripheral and coronary blood vessels - Give sublingually or by spray - If no relief in 5 minutes, call EMS; if some relief ,repeat every 5 minutes for maximum 3 doses - Patient teaching - Can use prophylactically The treatment of chronic stable angina aims to decrease oxygen demand and/or increase oxygen supply. Short-acting nitrates are first-line therapy for the treatment of angina. Nitrates produce their principal effects by: 1. Dilating peripheral blood vessels. This results in decreased SVR, venous pooling, and decreased venous blood return to the heart (preload). Therefore myocardial oxygen demand is decreased because of the reduced cardiac workload. 2. Dilating coronary arteries and collateral vessels. This may increase blood flow to the ischemic areas of the heart. However, when the coronary arteries are severely atherosclerotic, coronary dilation is difficult to achieve SL NTG or translingual spray (Nitrolingual) will usually relieve pain in about 5 minutes and has a duration of approximately 30 to 40 minutes. The recommended dose of NTG is one tablet taken sublingually (SL) or one metered spray on the tongue for symptoms of angina. If symptoms are unchanged or worse after 5 minutes, the patient should contact the emergency medical services (EMS) system before taking additional NTG. If symptoms are significantly improved by one dose of NTG, instruct the patient or caregiver to repeat NTG every 5 minutes for a maximum of three doses and contact EMS if symptoms have not resolved completely. Instruct the patient in the proper use of NTG. It should be easily accessible to the patient at all times. The patient should store the tablets away from light and heat sources, including body heat, to protect from degradation. Tablets are packaged in dark, airtight containers to maintain potency. Once opened, the tablets tend to lose potency and should be replaced every 6 months. Tell the patient to sit down and place a NTG tablet under the tongue and allow it to dissolve. If using the spray, it should be directed on or under the tongue, not inhaled. SL NTG should cause a tingling sensation when administered; otherwise it may be outdated. Warn the patient that a headache, dizziness, or flushing may occur. Caution the patient to change positions slowly after NTG use because orthostatic hypotension may occur. Patients can use NTG prophylactically before undertaking an activity that is known to cause an angina. In these cases, the patient can take a tablet 5 to 10 minutes before beginning the activity. Tell the patient to report to the HCP any changes in the usual pattern of pain, especially increasing frequency or nighttime angina, or angina at rest. First thing to use is nitrate- antianginal (one sublingual every 5 minutes x3 and if doesn't go away call ambulance; don't chew tablet; put under tongue and let dissolve; should tingle or burn a little bit or tablet is no good

Nursing and interprofessional care: CAD - health promotion identification of people at high risk

Health Promotion - Identification of people at high risk Health history, including family history Presence of cardiovascular symptoms Environmental patterns: diet, activity Psychosocial history Values and beliefs about health and illness The appropriate management of risk factors in CAD may prevent, modify, or slow the progression of the disease. In the United States, there has been a gradual decline in CVD-related deaths over the past 35 years. This relates to the efforts of people to become generally healthier, as well as advances in the treatment of CAD. Prevention and early treatment of heart disease must involve a multifaceted approach and needs to be ongoing throughout the life span. Identification of High-Risk Person Clinical manifestations of CAD will not be apparent in the early stages of the disease. Therefore, it is extremely important to identify people at risk for CAD. Risk screening involves obtaining a thorough health history. Question the patient about a family history of heart disease in parents and siblings. Note the presence of any cardiovascular symptoms. Assess environmental factors, such as eating habits, type of diet, and level of exercise to elicit lifestyle patterns. Include a psychosocial history to determine tobacco use, alcohol intake, recent stressful events (e.g., loss of a spouse), and the presence of any negative psychologic states (e.g., anxiety, depression, anger). The place of work and the type of work provides important information on the kind of activity performed, exposure to pollutants or toxins, and the degree of stress associated with work. Identify the patient's attitudes and beliefs about health and illness. This information can give you insight to how disease and lifestyle changes may affect the patient. It also can reveal possible misconceptions about heart disease.

Nursing and interprofessional care - increase lipoprotein removal - decrease cholesterol absorption

Increase lipoprotein removal - Bile acid sequestrants (make you secrete lipids; if elevated LDL can use statins or bie acid sequestrants; doesn't make BM pleasant) (prevalite, cholestyramine) [same drug] Increase conversion of cholesterol to bile acids GI side effects; bind with other drugs - Decrease cholesterol absorption Ezetimibe (Zetia) Decrease absorption of dietary and biliary cholesterol Drugs That Increase Lipoprotein Removal Bile-acid sequestrants increase conversion of cholesterol to bile acids and decrease hepatic cholesterol. The primary effect is a decrease in total cholesterol and LDL levels. These drugs have been associated with complaints related to taste and a variety of upper and lower GI symptoms. These include belching, heartburn, nausea, abdominal pain, and constipation. The bile-acid sequestrants interfere with absorption of many other drugs (e.g., warfarin, thiazides, thyroid hormones, β-adrenergic blockers). Separating the time of administration of these drugs from other drugs decreases this adverse effect. Drugs that Decrease Cholesterol Absorption Ezetimibe (Zetia) selectively inhibits the absorption of dietary and biliary cholesterol across the intestinal wall. It serves as an adjunct to dietary changes, especially in patients with primary hypercholesterolemia. Drug therapy for hyperlipidemia often continues for a lifetime. Concurrent diet modification is essential to reduce the need for drug therapy. The patient must fully understand the rationale and goals of treatment, as well as the safety and side effects of lipid-lowering drugs.

Gerontologic considerations CAD

Increased incidence and mortality associated with CAD in older adults Strategies to reduce risk and treat CAD are effective Treat hypertension, ↑ lipids Smoking cessation Necessary to modify guidelines for physical activity Longer warm-up Longer periods of low-level activity Longer rest periods Avoid extremes of temperature 30 minutes most days minimum Most likely to change when hospitalized or symptomatic The incidence of heart disease is greatly increased in older adults and is the leading cause of death in older persons. In the older adult, CAD is often a result of the complex interaction of nonmodifiable risk factors (e.g., age) and lifelong modifiable risk behaviors (e.g., inactivity, tobacco use). Strategies to reduce CAD risk and to treat CAD are effective in this age-group. Aggressive treatment of hypertension and hyperlipidemia will stabilize plaques in the coronary arteries of older adults, and cessation of tobacco use helps decrease the risk for CAD at any age. Similarly, you should encourage the older patient to consider a planned program of physical activity. Activity performance, endurance, and ability to tolerate stress are improved in the older adult with physical training. Positive psychologic benefits can be derived from physical activity and can include increased self-esteem and emotional well-being and improved body image. For the older adult who is obese, making modest dietary changes and slowly increasing physical activity (e.g., walking) will result in more positive benefits than aiming for a significant weight loss. When planning a physical activity program for the older adult, recommend the following: (1) longer warm-up periods, (2) longer periods of low-level activity, or (3) longer rest periods between sessions. Heat intolerance in the older adult results from a decreased ability to sweat efficiently. Teach the patient to avoid physical activity in extremes of temperature and to maintain a moderate pace. The older adult should exercise a minimum of 30 minutes on most days of the week as able. Encouraging the older patient to adopt a healthy lifestyle may increase the quality of life and reduce the risk of CAD and fatal heart events. The older adult faces many of the same challenges when it comes to making lifestyle changes. There are two points in time when the older adult is more likely to consider change: (1) when hospitalized and (2) when symptoms (e.g., chest pain) are the result of CAD and not normal aging. First, assess the older adult for readiness to change and health literacy. Then help the patient to select the lifestyle changes most likely to produce the greatest reduction in risk for CAD.

Clinical manifestations of CAD Chronic stable angina

Intermittent chest pain that occurs over a long period with same pattern of onset, duration, and intensity of symptoms - Never changes and when I rest it goes away Few minutes in duration ST segment depression and/or T-wave inversion - Elevation is a sign of ACUTE INJURY PATTERN - ST segment depression is ischemia Control with drugs Chronic stable angina refers to chest pain that occurs intermittently over a long period of time with a similar pattern of onset, duration, and intensity of symptoms. It is often provoked by physical exertion, stress, or emotional upset. When asked, some patients may deny feeling pain but describe a pressure, heaviness, or discomfort in the chest. This discomfort is often described as a squeezing, heavy, tight, or suffocating sensation. It may be associated with other symptoms such as dyspnea or fatigue. Chronic angina pain usually does not change with position or breathing and is rarely described as sharp or stabbing. The pain of chronic stable angina usually lasts for only a few minutes and commonly subsides when the precipitating factor is resolved (resting, calming down, using sublingual NTG). Pain at rest is unusual and is often a symptom of UA. A 12-lead electrocardiogram (ECG) often shows ST segment depression and/or T-wave inversion indicating ischemia. The ECG will return to baseline when the pain is relieved. Chronic stable angina is controlled with drugs on an outpatient basis. Because chronic stable angina is often predictable, drugs are timed to provide peak effects during the time of day when angina is likely to occur. For example, if angina occurs when rising, the patient can take the drug as soon as awakening and wait 30 minutes to 1 hour before engaging in activity.

chronic stable angina interprofessional care - lipid lowering drugs

Lipid lowering drugs Sodium current inhibitor Ranolazine (Ranexa) Although patients with chronic stable angina are encouraged to follow a diet low in saturated fat and cholesterol, a moderate or high dose of a lipid lowering drug should be ordered, unless contraindicated. Ranolazine (Ranexa), a sodium current inhibitor, is used to treat chronic angina in patients who have not had an adequate response with other antianginals. It is not a first-line drug for chronic stable angina. Because ranolazine prolongs the QT interval, patients with a long QT interval or who are taking QT-prolonging drugs (e.g., fluoxetine [Prozac]) should not use it. Common side effects of ranolazine include dizziness, nausea, constipation, and headache.

Nursing and interprofessional care: CAD - lipid lowering drug therapy continued the other drug besides statins and what are side effects of this drug

Lipid-lowering drug therapy - Niacin (if homocysteine levels are increased can also combine drugs with niacin; vitamin B12, 6; can make you nauseated, give you indigestion; someone who has genetic predisposition or male in family who had MI young) Lowers LDL and triglyceride by inhibiting synthesis Increases HDL Flushing, pruritus, GI side effects, orthostatic hypotension - Fibric acid derivatives (Lopid) Decrease triglycerides and increase HDL GI side effects Drugs that Restrict Lipoprotein Production Niacin (Niaspan), a water-soluble B vitamin, is highly effective in lowering LDL and triglyceride levels by interfering with their synthesis. Niacin also increases HDL levels better than many other lipid-lowering drugs. Unfortunately, side effects of this drug are common and may include severe flushing, pruritus, gastrointestinal (GI) symptoms, and orthostatic hypotension. The fibric acid derivatives work by aiding the removal of VLDLs and increasing the production of apolipoproteins A-I and A-II. They are the most effective drugs for lowering triglycerides and increasing HDL levels. They have no effect on LDLs. Although most patients tolerate the drugs well, complaints may include GI irritability.

Nursing and interprofessional care: CAD - lipid lowering drug therapy first line therapy and what complications/side effects to look out for

Lipid-lowering drug therapy - If diet and exercise ineffective - Statins (any drug ending in -statin; designed to lower lipids in the body; some may increase HDL and lower LDL; some may be combination drugs) Inhibit cholesterol synthesis, decrease LDL, increase HDL Monitor for liver damage and myopathy (muscle pain) A- antiplatelets, anticoagulation, antianginals, ACE, ARB's B- Beta blockers C- cholesterol management; smoking cessation; calcium channel blockers D- Diet, Diabetes management; depression screening E- education (yourself and patients); exercise [be role model] F- Flu vaccine [ increased risk of MI in first two months after you had the flu] An estimated 31.9 million American adults have cholesterol levels greater than or equal to 240 mg/dL (6.2 mmol/L). Guidelines for treatment of high cholesterol focus on LDL cholesterol. A complete lipid profile is recommended every 5 years beginning at age 20. Guidelines recommend the following groups of people receive statin therapy: (1) patients with known CVD, (2) patients with primary elevations of LDL cholesterol levels greater than or equal to 190 mg/dL (e.g., familial hypercholesterolemia), (3) patients between 40 and 75 years old with diabetes and LDL cholesterol levels between 70 and 189 mg/dL, and (4) patients between 40 and 75 years old with LDL cholesterol levels between 70 and 189 mg/dL and a 10-year risk for CVD of at least 7.5%. Treatment also includes weight loss (if overweight), decreased dietary fat and cholesterol intake, and increased physical activity. Serum lipid levels should be reassessed after 6 weeks of therapy. If they remain elevated, additional dietary options and drug therapy may be considered. Several classifications of drugs are used to decrease serum lipids. Drugs that Restrict Lipoprotein Production The statin drugs are the most widely used lipid-lowering drugs. These drugs inhibit the synthesis of cholesterol in the liver. An unexplained result of the inhibition of cholesterol synthesis is an increase in hepatic LDL receptors. Consequently, the liver is able to remove more LDLs from the blood. In addition, statins produce a small increase in HDLs and lower CRP levels. Serious adverse effects of these drugs are rare and include liver damage and myopathy that can progress to rhabdomyolysis (breakdown of skeletal muscle). Liver enzymes (e.g., aspartate aminotransferase, alanine aminotransferase) are initially monitored and rechecked with any increase in dosage.

chronic stable angina interprofessional care - long acting nitrates

Long-acting nitrates - To reduce angina incidence - Main side effects: headache, orthostatic hypotension - Methods of administration Oral Nitroglycerin (NTG) ointment Transdermal controlled-release NTG Long-acting nitrates are used to reduce the frequency of anginal attacks. The main side effect of all nitrates is headache from the dilation of cerebral blood vessels. Advise patients to take acetaminophen (Tylenol) to relieve the headache. Over time, the headaches may decrease but the antianginal effects are still present. Orthostatic hypotension is a complication of all nitrates. You should monitor BP after the initial dose as the venous dilation that occurs may cause a drop in BP, especially in volume-depleted patients. Tolerance to long-acting NTG can develop. To limit this, patients are often scheduled a 10-14 hour nitrate-free period every day. Remind patients that taking a long-acting NTG preparation should not keep them from using transligual or SL NTG if angina develops. Can be given orally, such as isosorbide dinitrate (Isordil) and isosorbide mononitrate (Imdur), Nitropaste is a 2% NTG topical ointment dosed by the inch. It is placed on the upper body or arm, over a flat muscular area that is free of hair and scars. Once absorbed, it produces anginal prophylaxis for 3 to 6 hours. It is especially useful for nighttime and UA. The ointment should be wiped off to allow for a 10-14 hour nitrate free interval in order to prevent nitrate tolerance. Currently two systems are available for transdermal NTG drug delivery: silicone gel and polymer matrix. These systems allow timed release of NTG over a 24-hour period. These preparations should also be removed in the evening to allow for a 10-14 hour nitrate free interval. Nitroglycerin ointment; nitroglycerin patches; nitroglycerin spray Must be careful when they put this on; SEVERE HEADACHE will happen if it comes in contact with those that don't need it since blood vessels dilate with this remind them to GIVE THEMSELVES A MINUTE

Risk factors for CAD - major modifiable risk factors continued

Major modifiable risk factors - Hypertension (the silent killer) >140/90 mm Hg Goal for > age 60 is <150/90 mm Hg Lower risk of atherosclerosis Begin lifestyle changes for prehypertension Treat stage 1 or 2 hypertension with drugs Hypertension The second major risk factor in CAD is hypertension, which is defined as a BP >140/90 mm Hg. For people older than 60 years, a goal BP of less than 150/90 mmHg is recommended (JNC8 recommendations) to prevent stroke, CVD, and heart failure. Hypertension increases the risk of death from CAD 10-fold in all persons. The stress of an elevated BP increases the rate of atherosclerosis. This relates to the shearing stress that causes endothelial injury. Therapeutic lifestyle changes should begin in people with prehypertension (BP of 120 to 139 mm Hg/80 to 89 mm Hg). Normal BP is <120/80 mm Hg. Stage 1 hypertension is 140 to 159/90 to 99 mm Hg. Stage 2 hypertension is BP > 160/100 mm Hg. Those with stage 1 or 2 hypertension often require more than one drug to reach therapeutic goals.

Risk factors for CAD - major modifiable risk factors continued....

Major modifiable risk factors - Physical inactivity 30 minutes a day of moderate exercise; I can do 10 minute intervals three times a day; idea Is get off your ass. - Obesity Women's weight changes throughout our life Defined by the BMI currently Physical Inactivity Physical inactivity is the fourth major modifiable risk factor. Physical inactivity implies a lack of adequate physical exercise on a regular basis. An example of health-promoting regular physical activity is brisk walking (3 to 4 miles per hour) for at least 30 minutes 5 or more times a week. Physically active people have increased HDL levels. Exercise improves thrombolytic activity, thus reducing the risk of clot formation. Exercise may also encourage the development of collateral circulation in the heart. Obesity The death rate from CAD is higher in obese persons. Obesity is defined as a body mass index (BMI) of >30 kg/m2 and a waist circumference ≥40 inches for men and ≥35 inches for women. The increased risk for CAD is proportional to the degree of obesity. People who tend to store fat in the abdomen (an "apple" figure) rather than in the hips and buttocks (a "pear" figure) have a higher incidence of CAD. Obesity is often linked with hypertension and insulin resistance.

Risk factors for CAD - major modifiable risk factors cont...

Major modifiable risk factors - Tobacco use (vasoconstriction!!! [already small from fatty plaque]; oxygen free radiacals which is an irritant that causes more damage; more lipids in and more fatty plaques) Increased catecholamine release ↑ LDL, ↓ HDL, ↑oxygen radicals ↑ Carbon monoxide - Second-hand smoke (exposed to it because around people that smoke all the time) - Third hand smoke (when it gets into furniture, bedding, pillows, etc.) Tobacco Use A third major risk factor in CAD is tobacco use. The risk of developing CAD is two to six times higher in those who smoke tobacco or use smokeless tobacco than in those who do not. Further, tobacco smoking decreases estrogen levels, placing premenopausal women at greater risk for CAD. Risk is proportional to the number of cigarettes smoked. Nicotine in tobacco smoke causes catecholamine (i.e., epinephrine, norepinephrine) release. These neurohormones cause an increased heart rate (HR), peripheral vasoconstriction, and increased BP. These changes increase the heart's workload. Tobacco smoke is also related to an increase in LDL level, a decrease in HDL level, and release of toxic oxygen radicals. All of these add to vessel inflammation and thrombosis. Carbon monoxide, found in tobacco smoke, affects the oxygen-carrying capacity of hemoglobin by reducing the sites available for oxygen transport. Thus the effects of an increased cardiac workload, combined with the oxygen-depleting effect of carbon monoxide, significantly decrease the oxygen available to the heart muscle. There is also some indication that carbon monoxide is a chemical irritant, and causes injury to the endothelium. The benefits of smoking cessation are dramatic and almost immediate. CAD mortality rates drop to those of nonsmokers within 12 months. However, nicotine is highly addictive and often calls for intensive intervention to assist people to quit. Chronic exposure to environmental tobacco (secondhand) smoke also increases the risk of CAD. People who live in the same house as the patient should be encouraged to stop smoking. This reinforces the person's effort and decreases the risk of ongoing exposure to environmental smoke. Pipe and cigar smokers, who often do not inhale, have an increased risk of CAD similar to those exposed to secondhand smoke.

Risk factors for CAD - Major modifiable risk factors

Major modifiable risk factors - Elevated serum lipids Cholesterol >200 mg/dL (5.2 mmol/L) We have a problem Triglycerides >150 mg/dL (3.7 mmol/L) High-density lipoproteins (HDL) Higher the number the better; the good fats; don't have a tendency to go into intima Low-density lipoproteins (LDL) Bad fats; keep it as low as possible Try and get it down to 50 Treatment according to guidelines based on 10-year and life time risk score Modifiable risk factors include elevated serum lipids, elevated BP, tobacco use, physical inactivity, obesity, diabetes, metabolic syndrome, psychologic states, and elevated homocysteine level. Elevated Serum Lipids An elevated serum lipid level is one of the four most firmly established risk factors for CAD. The risk of CAD is associated with a serum cholesterol level of more than 200 mg/dL (5.2 mmol/L) or a fasting triglyceride level of more than 150 mg/dL (3.7 mmol/L). For lipids to be used and transported by the body, they must become soluble in blood by combining with proteins. Lipids combine with proteins to form lipoproteins. Lipoproteins are vehicles for fat mobilization and transport, and vary in composition. Three major lipoproteins are high-density lipoproteins (HDLs), LDLs, and very-low-density lipoproteins (VLDLs). HDLs carry lipids away from arteries and to the liver for metabolism. Therefore, high serum HDL levels are desirable and lower the risk of CAD. In general, HDL levels are higher in women, decrease with age, and are low in persons with CAD. Physical activity and moderate alcohol intake increase HDL levels. LDLs contain more cholesterol than any of the lipoproteins and have an attraction for arterial walls. Elevated LDL levels correlate most closely with an increased incidence of atherosclerosis and CAD. Therefore, low serum LDL levels are desirable. Guidelines for treating elevated LDL cholesterol are based on a person's 10-year and life time risk for having heart disease or stroke. The following data generate a risk score: (1) age, (2) gender, (3) race, (4) use of tobacco, (5) diabetes, (6) systolic BP (7) diastolic BP, (8) use of BP drugs, (9) total cholesterol level, and (10) HDL cholesterol level. A 10-year risk calculator is available at http://www.cvriskcalculator.com/ as well as for smartphones (e.g., ASCVD Risk Estimator app). In general, persons with no or only one risk factor are considered at low risk for the development of CAD, and their LDL goal is <160 mg/dL (4.14 mmol/L). Those at very high risk for developing CAD have multiple risk factors. They have an LDL goal of <70 mg/dL (1.8 mmol/L).

chronic stable angina types of angina - silent ischemia

Silent ischemia (causes damage and they don' t feel pain; come in complaining of extreme tiredness) Ischemia that occurs in absence of any subjective symptoms Associated with diabetic neuropathy Confirmed by ECG changes Silent ischemia refers to ischemia that occurs in the absence of any subjective symptoms. Patients with diabetes have an increased prevalence of silent ischemia. This is most likely due to diabetic neuropathy affecting the nerves that innervate the cardiovascular system. Silent ischemia is documented by ECG changes.

Nursing and Interprofessional care: CAD

Manage high-risk persons by controlling modifiable risk factors Encourage lifestyle changes (stop adding salt; get up and walk around) - Education - Clarify personal values - Set realistic goals Management of High-Risk Persons Recommend preventive measures for all persons at risk for CAD. Risk factors such as age, gender, ethnicity, and genetic inheritance cannot be modified. However, the person with any of these risk factors can still reduce the risk of CAD by controlling the additive effects of modifiable risk factors. For example, a young man with a family history of heart disease can decrease the risk of CAD by maintaining an ideal body weight, getting adequate physical exercise, reducing intake of saturated fats, and avoiding tobacco and illicit drug use. People who have modifiable risk factors should be encouraged to make lifestyle changes to reduce their risk of CAD. You can play a major role in teaching health-promoting behaviors. For highly motivated persons, knowing how to reduce this risk may be the information that they need to get started. For persons who are less motivated to take charge of their health, the idea of reducing risk factors may be so remote that they are unable to perceive a threat of CAD. Few people desire to make lifestyle changes, especially in the absence of symptoms. First help these patients to clarify their personal values. Then, discuss risk factors and have them identify their individual risks. This can help patients set realistic goals and choose which risk factor(s) to change first. Some persons are reluctant to change until they begin to have symptoms or actually suffer an MI. Others, having suffered an MI, may find the idea of changing lifelong habits still unacceptable. You must be able to identify their choices and respect them.

chronic stable angina types of angina - microvascular angina

Microvascular angina - Typical of women - Women have smaller blood vessels and not usually in same place; they don't have same symptoms; always tired and need to rest; get short of breath; maybe they can't sleep Because of microvascular or smaller vessel sizes Syndrome X Chest pain occurs in the absence of significant CAD or coronary spasm of a major coronary artery Prevention and treatment follows CAD recommendations In microvascular angina, chest pain occurs in the absence of significant CAD or coronary spasm of a major coronary artery. In these patients, chest pain is related to myocardial ischemia associated with atherosclerosis or spasm of the small distal branch vessels of the coronary microcirculation. This is known as coronary microvascular disease (MVD). It is also referred to as Syndrome X. It is more common in postmenopausal women. Often the angina is prolonged and brought on by physical exertion. These patients usually have positive stress test results and have an inconsistent response to nitrates. Prevention and treatment of coronary MVD follows the same recommendations as for CAD.

Risk factors for CAD - nonmodifiable risk factors

Nonmodifiable risk factors - Age - Gender (gender you are BORN with) - Ethnicity (whites, African americans tend to have more of a problem) - Family history (is it male or female and when did they have their first heart attack) - Genetic predisposition Risk factors are characteristics or conditions that are linked with a high incidence of a disease. Many risk factors have been associated with CAD. They are grouped as nonmodifiable and modifiable Nonmodifiable risk factors are age, gender, ethnicity, family history, and genetic inheritance. The incidence of CAD is highest among middle-aged men. After age 75, the incidence of serious heart events in men and women equalizes, although CVD causes more deaths in women than men. On average, women with CAD are older than men who have CAD, and are more likely to have co-morbidities (e.g., hypertension, diabetes). Most women have atypical symptoms of angina rather than symptoms of MI when presenting with their initial heart event. African Americans have an earlier onset and more severe CAD than there CAD counterparts. Additionally, CAD incidence and mortality rates are greater in African American women than their white counterparts. Family history is a risk factor for CAD and MI. Often, patients with angina or MI can name a parent or sibling who has died of CAD. The genetic basis of CAD/MI is complex and poorly understood. It is estimated that the genetic contribution to CAD/MI is as high as 40% to 60%. This proportion relates mainly to genes that control known risk factors (e.g., lipid metabolism).

Nursing and Interprofessional care: CAD - nutritional therapy

Nutritional therapy (eat fish; ↓ Saturated fats and cholesterol ↑ Complex carbohydrates and fiber ↓ Red meat, egg yolks, whole milk ↑ Omega-3 fatty acids The National Heart, Lung, and Blood Institute recommends therapeutic lifestyle changes for all people to reduce the risk of CAD by lowering LDL cholesterol. These recommendations emphasize a decrease in saturated fat and cholesterol and an increase in complex carbohydrates (e.g., whole grains, fruit, vegetables) and fiber. Red meat, egg yolks, and whole milk products are major sources of saturated fat and cholesterol and should be reduced or eliminated from diets. If the serum triglyceride level is elevated, alcohol and simple sugars should be reduced or eliminated. Patients with CAD are encouraged to take EPA and DHA supplements with their diet. The AHA also recommends eating tofu and other forms of soybean, canola, walnut, and flaxseed because these products contain alpha-linolenic acid, which becomes omega-3 fatty acid in the body. Lifestyle changes, including a low-saturated-fat, high-fiber diet; avoidance of tobacco; and increase in physical activity, can promote the reversal of CAD and reduce coronary events.

Nursing and interprofessional care: CAD - physical fitness

Physical fitness - FITT formula: 30 minutes most days plus weight training 2 days a week - Regular physical activity contributes to Weight reduction Reduction of >10% in systolic BP In some men more than women, increase in HDL cholesterol Physical Activity A physical activity program should be designed to improve physical fitness by following the FITT formula: Frequency (how often) Intensity (how hard) Type (isotonic) Time (how long) Everyone should aim for at least 30 minutes of moderate physical activity on most days of the week. In addition, adding weight training to an exercise program 2 days a week can help treat metabolic syndrome and improve muscle strength. Examples of moderate physical activity include brisk walking, hiking, biking, and swimming. Regular physical activity helps with weight reduction, reduces systolic BP, and, in some men more than women, increases in HDL cholesterol.

chronic stabel angina types of angina - prinzmetal's (variant) angina what meds could be used associated with what diagnoses/lifestyle choices

Prinzmetal's (variant) angina Associated with those with Raynaud's (overactive blood vessel) Nitroglycerin Rare Occurs at rest Can be seen in patients with a history of migraine headaches, Raynaud's phenomenon and heavy smoking Spasm of a major coronary artery CAD may or may not be present Prinzmetal's angina (variant angina) is a rare form of angina that often occurs at rest and not with increased physical demand. Strong contraction (spasm) of smooth muscle in the coronary artery results from increased intracellular calcium. Factors causing coronary artery spasm include increased myocardial oxygen demand and increased levels of certain substances (e.g., tobacco smoke, alcohol, amphetamines). When spasm occurs, the patient experiences angina and transient ST-segment elevation. The pain may occur during rapid-eye-movement (REM) sleep when myocardial oxygen consumption increases or when exposed to cold temperatures. The pain may be relieved by moderate exercise, with SL NTG, or it may disappear spontaneously. Cyclic, short bursts of pain at a usual time each day may also occur with this type of angina. Calcium channel blockers and/or nitrates are used to control the pain, as well as stopping any offending substances.

Serum lipids

Serum lipids and their role in cholesterol metabolism. Injure intima and lipds go into the intima; into vessel walls

Locations and patterns of angina and MI

mid sternum left shoulder and down both arms neck and veins substernal radiating to neck and jaw substernal radiating down left arm epigastric epigastric radiating to neck, jaw and arms intrascapular Although most angina pain occurs substernally, it may radiate to other locations, including the jaw, neck, shoulders, and/or arms. Many people with angina complain of indigestion or a burning sensation in the epigastric region. The sensation may also be felt between the shoulder blades. Often people who complain of pain between the shoulder blades or indigestion type pain dismiss it as not being heart related. Some patients, especially women and older adults, report atypical symptoms of angina including dyspnea, nausea, and/or fatigue. This is referred to as angina equivalent. Same place and intensity every single time