31 yr old female/have variant angina/having attacks everyday/meds not working should i go to er?
I have had many doctors say I,m to young to be having a heart attack so I am leery of going to the hospital but my mother just died at the age of 45 from an heart attack and started having them when she was in her 20s so i am worried what should I do
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Absolutely!! get to an ER!! If your results are negative, they will certainly give you cardiology referrals. If any results are positive, that's where you need to be to get medical treatment. I've taken care of many patients in their 20-30's with cardiac conditions. Your young age makes it less likely, but not impossible! You do have a strong family history, symptoms, and perhaps other risk factors that you may be unaware of. Cardiac disease is becoming the number 1 killer of woman, often our symptoms are dismissed as "anxiety", when in fact we truly have heart disease. Women now are under extreme stress with "superwoman" responsibilities, we don't always eat right, we don't always get enough exercise, and we often ignore our bodies cause we just don't have time to see a doctor. Be safe and have yourself checked out-if you're already seeing a cardiologist (not internist), then perhaps a second opinion is what you need. Take care and best of luck!! (
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I'm stationed in Korea and just diagnosed with variant angina need help?
i am a 40 yr old SGt in the ARMY and have been diagnosed with variant angina with a 3x4x1 cm cyst on right coronary artery since no military cardiologist on the peninsula i have been in the care of Korean doctors who speak little english im on meds inc isosorbide, diltiazem, nitroglyceren and zocor the docs want to control with meds but dos not help with the cyst need info on wether i should ask to be transfered to the states for treatment and medical retirement and benefits arrising from this situation iwould like to be under the care of us board certified cardiologist asking for advice and opinions please esp from medical professionals
also i have 70 percent constriction in r coronary artery
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If I was you go home,I looked it up here gos,,,call Prinzmetal's Angina,cause ,...coronary artery spasm in which the artery walls briefly narrows(constricts)which cause temp.reduses or obstracts bloob flow to the muscle,thus chest pain,can be associate with(atherosclerosis)if this be the under line,calcium channel blockers may be needed,RISK,heart attacks,abnormal heart rhythma(arrhythma),....Pearl g..found in yahoo search.com (
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angina vs. angina pectoris?
Some sources define "angina" as a "disease of the throat" while others say it is a "chest pain". Do you always have to specify "angina pectoris" when referring to the heart pain or can you say simply "angina" (some places just say "angina").
Definitions of angina on the Web:
any disease of the throat or fauces marked by spasmodic attacks of intense suffocative pain
angina pectoris: a heart condition marked by paroxysms of chest pain due to reduced oxygen to the heart
wordnetweb.princeton.edu/perl/webwn
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angina (Latin: angere = to strangle) Sense of suffocation or constriction.
Angina pectoris means severe but temporary attack of cardiac pain which may radiate to the arms. Results from myocardial ischæmia. Often the attack is induced by exercise (angina of effort) (
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Myocardial Ischemia and Angina Pectoris are same?
Essentially, yes. Ischemia is when the tissue does not get enough blood and oxygen due to a narrowing or blockage of the coronary arteries. Angina is the pain you feel when you are experiencing ischemia.
Some health care professionals may use the terms interchangeably, leading to some confusion.
Hope this helps! (
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How many types of angina are there?
I know about Stable, Printzmetal's (also know as Variant), Unstable, Vincent's. I've just watched a TV programme which referred to Ludwig's angina (which I had never heard of ) and I wondered if there were any more.
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Angina Pectoris is the name given to the heart condition associated with decreased coronary blood flow.
Its various presentation has given rise to various names eg. Stable, Printzmetal, unstable, etc.. There is also another type in this group which describes chest pain on lying down i.e. Angina decubitus.
The name Angina has also been used to describe non-cardiac condition eg Ludwig's angina for a throat infection
Angina Cruris is pain in the buttocks regions on walking and is a manifestation of Le Riche syndrome.
I hope this answers your question. (
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Home Daycare And Angina Pectoris?
I am due to see a heart specialist tomorrow to test for angina pectoris. I am only 31 years old and my family doctor thinks I am to young to have this. But I assure you I am 99.9 percent sure I do have this. I have had every symptom for 7 years. In fact I was seen 7 years ago by another doctor who ran blood work and did a chest x-ray and found nothing. But my current doctor says if I have Angina then it wouldn't have show up in my blood or a chest x-ray unless I have congestive heart failure. Which he is positive I don't have that. I think what makes me so mad is that because of my age which would have been 25 then he totally ruled out that it might have been angina. I think he thought it was all in my head In fact he put me on paxil, he called it a mood stabilizer. He said are you stressed out I said always and he slapped a label on it. In which the paxil was awful and made me so sleepy that I could barely care for my own children. Which brings me to my question. I have a home daycare and care for 9 children including my own 2. Will they still allow me to do home daycare? Anyone with knowledge on angina should answer this question?
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Angina, also called angina pectoris (pectoris means chest), may be stable or unstable:
Stable angina (also called chronic stable angina). Unstable angina (signals an impending heart attack) .A third, a rare type of angina called variant angina (also called Prinzmetal's angina) is caused by a coronary artery spasm.
Angina is relatively common. More than 6 million people in North America have angina. Angina can be hard to distinguish from other types of chest pain, such as the pain or discomfort of indigestion.
If your angina is mild, lifestyle changes may be all you need to do. Lifestyle changes and medications are frequently used to treat stable angina. But invasive techniques such as angioplasty and stenting also have been used to reopen narrowed heart arteries. However, recent research suggests it may be appropriate to try lifestyle changes and medications before having angioplasty and stenting. A medical study called the Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) evaluated treatments for chronic, stable angina. The study found angioplasty and stenting was no better than medication and lifestyle changes over the long term when treating stable angina.
Angioplasty and stenting is a good treatment option if you have unstable angina or if lifestyle changes and medications don't effectively treat your chronic, stable angina.
Will they still allow me to do home daycare?
Lifestyle changes and medications are the most common ways to treat and control angina. For many people, lifestyle changes can control or eliminate angina. If you follow all the recommendations from your doctor you should be allowed and able to do home daycare.
Tomorrow you are going to do the test for angina pectoris, be patient and see what happen.
I am not a doctor and I cannot give you the right answer; your cardiologist can give you more accurate information and details. I suffer from chronic stable angina, I understand your concerns.
Take care as always! (
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what should i do when i have a variant angina?
How is Variant Angina Treated?
Variant agnina is treated with drugs called calcium channel blockers. These drugs can decrease variant angina attacks, and are often used in combination with nitrates. Variant angina tends to be cyclic, meaning that it appears for a while and then goes away. This means that after six to 12 months of treatment, your doctor may be able to gradually reduce your medications. If, however, your angina is being caused by a severe blockage, your doctor may schedule a procedure called an angioplasty to treat it.
The goal of treating variant angina is to stop the symptoms. Your doctor will work with you to come up with a plan that includes:
* Stopping the use of any drugs that cause coronary artery spasm
* Taking medication to help prevent coronary spasm
* Reviewing your lifestyle and habits to reduce your risk for heart disease
* Having frequent follow-up appointments to check your progress
* Quitting smoking (
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Patient after under going CABG gets angina pectoris.With the help of tabs how long he can survive?
Angina Pectoris
A clinical syndrome due to myocardial ischemia characterized by precordial discomfort or pressure, typically precipitated by exertion and relieved by rest or sublingual nitroglycerin.
Etiology
The cause is usually critical coronary artery obstruction due to atherosclerosis. Spasm (idiopathic or due to cocaine) or, rarely, a coronary embolism may be causative (see Myocardial Infarction, below). Disease other than atherosclerosis (eg, calcific aortic stenosis, aortic regurgitation, hypertrophic subaortic stenosis) can cause angina directly (by increasing cardiac work) or in combination with CAD.
Pathology and Pathogenesis
Usually, patients with long-standing angina are found at autopsy to have extensive coronary atherosclerosis and patchy myocardial fibrosis. There may be gross or microscopic evidence of old MI.
Angina pectoris occurs when cardiac work and myocardial O2 demand exceed the ability of the coronary arteries to supply oxygenated blood. Heart rate, systolic tension or arterial pressure, and contractility are the major determinants of myocardial O2 demand. An increase in any of these factors in a setting of reduced coronary blood flow may induce angina. Thus, exercise in the patient with a critical degree of coronary stenosis induces angina relieved by rest.
As the myocardium becomes ischemic, coronary sinus blood pH falls, cellular K loss occurs, lactate production replaces lactate use, ECG abnormalities appear, and ventricular performance deteriorates. Left ventricular (LV) diastolic pressure frequently rises during angina, at times to levels inducing pulmonary congestion and dyspnea. The discomfort of angina pectoris is believed to be a direct manifestation of myocardial ischemia and the resultant accumulation of hypoxic metabolites.
Symptoms and Signs
The discomfort of angina pectoris is not usually perceived as pain. It may be a vague, barely troublesome ache, or it may rapidly become a severe, intense precordial crushing sensation. It has a variable location but is most commonly felt beneath the sternum. It may radiate to the left shoulder and down the inside of the left arm, even to the fingers; straight through to the back, into the throat, jaws, and teeth; and occasionally down the inside of the right arm. It may also be felt in the upper abdomen. Because discomfort seldom occurs in the region of the cardiac apex, the patient who points to this precise area or describes fleeting, sharp, or hot sensations usually does not have angina.
Between and even during attacks of angina, signs of heart disease may be absent. However, during the attack, heart rate may increase modestly, BP is often elevated, heart sounds become more distant, and the apical impulse is more diffuse. Palpation of the precordium may reveal localized systolic bulging or paradoxical movement, reflecting segmental myocardial ischemia and regional dyskinesia. The second heart sound may become paradoxical because of more prolonged LV ejection during the ischemic episode. A fourth heart sound is common. A midsystolic or late-systolic apical murmur--shrill but not especially loud due to localized papillary muscle dysfunction secondary to ischemia--may occur.
Angina pectoris is typically triggered by physical activity and usually persists no more than a few minutes, subsiding with rest. Response to exertion is usually predictable, but in some persons a given exercise that is tolerated one day may precipitate angina the next. Angina is worsened when exertion follows a meal. Also, symptoms are exaggerated in cold weather: walking into the wind or first contact with cold air on leaving a warm room may precipitate an attack.
Angina may occur at night (nocturnal angina) preceded by a dream that is accompanied by striking changes in respiration, pulse rate, and BP. Nocturnal angina may also be a sign of recurrent LV failure, an equivalent of nocturnal dyspnea. Attacks may vary from several/day to occasional episodes with symptom-free intervals of weeks, months, or years. They may increase in frequency (crescendo angina) to a fatal outcome or may gradually decrease or disappear if adequate collateral coronary circulation develops, if the ischemic area becomes infarcted, or if heart failure or intermittent claudication supervenes and limits activity.
Angina may occur spontaneously at rest (angina decubitus), usually accompanied by modest increases in heart rate and a rise in BP that may be marked. If the angina is not relieved, the higher BP and fast heart rate increase unmet myocardial O2 need and make MI more likely.
Because the characteristics of angina are usually constant for a given patient, any deterioration in the pattern of symptoms-- increased intensity, decreased threshold of stimulus, longer duration, occurrence when the patient is sedentary or waking from sleep--should be considered serious. Such changes are termed unstable angina (see below).
Syndrome X: In a few patients with typical symptoms of angina relieved by rest or nitroglycerin, the exercise test is abnormal and myocardial lactate production during ischemia occurs, yet the coronary arteriogram is normal. Reflex intramyocardial coronary constriction can be demonstrated in some patients, and coronary flow reserve is reduced. Available data suggest a benign prognosis, although symptoms of ischemia may recur for years. The symptoms in many patients improve with beta-blockers. This condition should not be confused with variant angina due to epicardial coronary spasm (see Variant Angina, below).
Diagnosis
Diagnosis is based on a characteristic complaint of chest discomfort brought on by exertion and relieved by rest. Diagnosis may be confirmed if reversible ischemic ECG changes are seen during a spontaneous attack. A wide variety of changes may appear: ST segment depression (typically), ST segment elevation, decreased R-wave height, intraventricular or bundle branch conduction disturbances, and arrhythmia (usually ventricular extrasystoles). Between attacks, the ECG (and usually LV function) at rest is normal in about 30% of patients with a typical history of angina pectoris, even with extensive three-vessel CAD (an abnormal resting ECG alone does not establish or refute the diagnosis). Alternatively, diagnosis can be confirmed by a test dose of sublingual nitroglycerin, which characteristically should relieve the discomfort in 1.5 to 3 min.
Exercise stress ECG testing: Because the diagnosis of angina is usually primarily based on the patient's history, exercise testing in a patient with typical symptoms is generally used to determine functional and ECG response to graded stress (for exercise stress testing using radionuclide imaging, see Ch. 198; for exercise testing in asymptomatic persons to determine fitness for exercise programs, see below).
The patient exercises to a predetermined goal (eg, 80 to 90% of maximal heart rate, which can be approximated as 220 less the age in years), unless distressing cardiovascular symptoms (dyspnea, reduced endurance, fatigue, hypotension, or chest pain) supervene.
The ischemic ECG response during or after exercise is characterized by a flat or downward-sloping ST segment depression >= 0.1 millivolts (1 mm on the ECG when properly calibrated) lasting >= 0.08 sec. J junction depression with an upward-sloping ST segment is difficult to interpret, and many such patients do not have CAD. Interpretation of exercise testing is further complicated by the increased incidence of CAD with age; tests are falsely positive in >= 20% patients under age 40 but in < 10% over age 60. The frequency of true-positive tests increases with the number of coronary arteries obstructed, and greater degrees of ST segment depression generally correlate with more extensive disease.
Exercise testing is most predictive of CAD in men with chest discomfort suggestive of angina (specificity, 70%; sensitivity, 90%). Exercise tests are more difficult to interpret in women aged < 55; a high incidence of false-positive responses, probably related in part to a lower pretest incidence of the disease in the younger population, reduces the specificity. However, women are more likely than men to have an abnormal ECG in the presence of disease (32 vs. 23%). The false-negative rate in women is comparable to that in men, suggesting that a negative test is a reliable indicator of absence of disease.
In patients with atypical symptoms, a negative exercise test generally rules out angina pectoris and CAD. A positive test may indicate exercise-induced ischemia but may not explain atypical symptoms, suggesting the need for further investigation.
Patients with unstable angina or those in whom recent MI is suspected should not undergo exercise testing. However, with proper indications and close monitoring, an exercise test in an ischemic patient carries a low risk. The patient's response provides valuable prognostic information and helps to evaluate the need for angiography and possible bypass surgery in those on maximal medical therapy. A complete life support system, including emergency drugs, airway, and defibrillator, should be immediately available for any patient undergoing exercise testing.
Coronary angiography documents the extent of anatomic coronary artery obstruction (see also under Cardiac Catheterization in Ch. 198). Coronary angiography findings parallel postmortem findings, but the extent and severity of disease are usually underestimated. Vessels as small as 1 mm may be visualized with high-quality imaging. CAD is recognized by narrowing, beading, or occlusion of the vessels. Obstruction is assumed to be physiologically significant when the luminal diameter is reduced > 70%, which correlates well with the presence of angina pectoris; lesser degrees of obstruction are unlikely to result in ischemia, unless spasm or thrombosis is superimposed. Evaluation of wall motion by LV angiography is important if not contraindicated by potential adverse effects of contrast agent on renal or ventricular function.
Echocardiography (see also in Ch. 198) can be used for anatomic and functional myocardial analysis. Valve anatomy is well depicted, and PA pressure can be reliably estimated. Patients with poor ventricular function, evidence of reduced contractility, have a decreased life expectancy. Yet, if poor function is due to CAD, these patients benefit most from coronary artery bypass grafting, if they survive the operation.
Radionuclide images provide information about cardiac anatomy, cardiac function, myocardial perfusion, and metabolism. Radionuclide ventriculography depicts systolic and diastolic left ventricular volumes (hence ejection fraction) and with first-pass techniques right ventricular ejection fraction. Relative myocardial perfusion is imaged with single-photon emission computed tomography (SPECT) after injection of thallium-201 and technetium-99m-sestamibi. Images showing areas of reduced intensity after exercise or pharmacologic stimulation of coronary flow are compared with images obtained at rest to evaluate the presence of local ischemia or infarction. Positron emission tomography (PET) images depict absolute regional myocardial blood flow or myocardial metabolism after administration of the appropriate tracer and pharmacologic stimulation. The physician must choose which technique is best suited to the individual patient.
Differential Diagnosis
Many conditions must be considered in the differential diagnosis (eg, abnormalities of the cervicothoracic spine, costochondral separation, nonspecific chest wall pain). However, few truly mimic angina, which is generally so characteristic that errors in diagnosis usually result from careless history taking.
GI disorders: Diagnostic difficulties arise when the patient has atypical anginal symptoms, especially GI symptoms (eg, bloating; belching, which may give relief; abdominal distress) that are often ascribed to indigestion. Peptic ulcer, hiatus hernia, and gallbladder disease may cause symptoms similar to angina pectoris or may precipitate attacks in persons with preexisting CAD. Nonspecific changes in the T waves and ST segments have been reported in esophagitis, peptic ulcer disease, and cholecystitis, which can further complicate diagnosis.
Dyspnea: Angina may be confused with dyspnea, partly because of the sharp and reversible rise in LV filling pressure that often accompanies the ischemic attack. The patient's description may be imprecise, and whether the problem is angina, dyspnea, or both may be difficult to determine. Recurrent breathlessness on mild exertion may reflect increased LV filling pressure secondary to ischemia, with or without pain.
Silent ischemia: Twenty-four hour Holter monitoring has revealed a surprising incidence (up to 70% of episodes) of T-wave and ST segment abnormalities in the absence of pain in patients with CAD. Such changes are rare in persons without CAD. Radionuclide studies have documented myocardial ischemia in some persons during mental stress (eg, mental arithmetic) and during spontaneous ECG change. Silent ischemia and angina pectoris may coexist. In silent ischemia, the prognosis is defined by the severity of CAD. Revascularization may improve prognosis by reducing the incidence of subsequent MI or sudden death.
Prognosis
The major adverse outcomes are unstable angina, MI, recurrent MI, and sudden death due to arrhythmias. Annual mortality is about 1.4% in men with angina and no history of MI, a normal resting ECG, and normal BP. The rate rises to about 7.5% if systolic hypertension is present, to 8.4% when the ECG is abnormal, and to 12% if both risk factors are present.
Lesions of the left main coronary artery or in the proximal anterior descending vessel indicate particularly high risk. Although outcome correlates with number and severity of coronary vessels involved, in stable patients the prognosis is surprisingly good, even with three-vessel disease, if ventricular function is normal.
Reduced ventricular function, often measured by analysis of ejection fraction, adversely influences prognosis, especially in patients with three-vessel disease.
Prognosis also correlates with symptoms; it is better in patients with mild or moderate angina (class I or II) than in those with severe exercise-induced angina (class III).
Age is a major risk factor in the elderly.
Treatment
The major tenet of treatment is to prevent or reduce ischemia and minimize symptoms. The underlying disease, usually atherosclerosis, must be delineated and the primary risk factors reduced as much as possible (see Ch. 201). Smokers should quit: Discontinuing smoking for >= 2 yr reduces the risk of MI to the level of those who never smoked. Hypertension should be treated diligently because even mild hypertension increases cardiac work. Angina sometimes improves markedly with treatment of mild LV failure. Paradoxically, digitalis occasionally intensifies angina, presumably because increased myocardial contractility raises O2 demand in the presence of fixed coronary blood flow. Aggressive reduction of total and LDL cholesterol (with dietary treatment supplemented by drugs as necessary--see Ch. 15) in patients at risk retards progression of CAD and may cause some lesions to regress. An exercise program emphasizing walking often improves the sense of well-being, reduces risk, and improves exercise tolerance.
Three classes of drugs are usually effective, alone or in combination, in relieving symptoms: nitrates, beta-blockers, and Ca blockers.
Nitroglycerin is a potent smooth-muscle relaxer and vasodilator. Its major sites of action are in the peripheral vascular tree, especially in the venous or capacitance system and on the coronary blood vessels. Even severely atherosclerotic vessels may dilate in areas without atheroma. Nitroglycerin lowers systolic BP and dilates systemic veins, thus reducing myocardial wall tension, a major determinant of myocardial O2 need. Overall, the drug helps balance myocardial O2 supply and demand.
Sublingual nitroglycerin 0.3 to 0.6 mg is the most effective drug for the acute episode or for prophylaxis before exertion. Dramatic relief is usual within 1.5 to 3 min, is complete by about 5 min, and lasts up to 30 min. The dose may be repeated after 4 to 5 min three times if initial relief is incomplete. Patients should carry nitroglycerin tablets or aerosol spray with them at all times to use promptly at the onset of an angina attack. The drug loses potency unless stored in a tightly sealed, light-resistant glass container; small amounts should be obtained frequently.
Long-acting nitrates are available in oral and cutaneous preparations. They improve exercise tolerance for several hours in patients with angina.
Isosorbide dinitrate 10 to 20 mg po qid is effective within 1 to 2 h, and its effects persist 4 to 6 h. The initial dosage may be increased, depending on response, to 40 mg qid. Sustained-release preparations are also available.
Isosorbide mononitrate, the active metabolite of the dinitrate, is administered 20 mg po bid, waiting 7 h between first and second doses. Extended-release tablets (30 or 60 mg/day, increased to 120 mg/day or, rarely, 240 mg/day if needed) appear to be effective throughout the day without evidence of tolerance.
Nitroglycerin ointment provides good skin absorption, especially in a moist environment. Dispensed as a 2% preparation (15 mg/2.5 cm [1 inch]), 1.25 cm (0.5 inches) is spread evenly over the skin of the upper torso or arms every 6 to 8 h and covered with plastic. The dose is increased to 7.5 cm (3 inches) as tolerated. Ointment should be removed for several hours each day to avoid tolerance (see below) because of continuous absorption.
Cutaneous nitroglycerin patches provide a prolonged therapeutic effect by slow release of drug. Response is related to size of the patch and concentration of the drug. Exercise capacity is improved 4 h after patch application, but most studies fail to show sustained improvement at 18 to 24 h. The patch should be removed after 14 to 18 h because tolerance may develop (see below).
Nitrate tolerance may occur, usually within 24 h when plasma concentrations are constant. Tolerance appears to be due in part to sulfhydryl depletion in smooth muscles, reducing activation in cyclic GMP. Because of diurnal variation in MI risk (highest in early morning), an afternoon or early evening rest period from nitrates is reasonable if clinical circumstances permit. For nitroglycerin, 8 h appears to be sufficient. Isosorbide may require a 12-h rest period.
beta-Blockers completely block sympathetic stimulation of the heart and reduce systolic pressure, heart rate, contractility, and cardiac output, thus decreasing myocardial O2 demand and increasing exercise tolerance. Additionally, they increase the threshold for ventricular fibrillation. Because tissue O2 requirements are met by greater O2 extraction from capillary blood, systemic arteriovenous O2 difference is widened. These drugs are extremely useful in reducing symptoms and are well tolerated by most patients.
Ca blockers are the important third arm in the approach to angina pectoris and CAD. These vasodilators are useful in the treatment of angina with hypertension and counter coronary spasm if present. They are often highly effective in variant angina (see below), but their effectiveness may be limited by negative chronotropic and inotropic effects (diltiazem, verapamil).
Antiplatelet drugs are important in opposing platelet aggregation, which is pivotal in the genesis of MI and unstable angina. Aspirin, which binds irreversibly to platelets and inhibits cyclooxygenase and platelet aggregation in vitro, has been shown in epidemiologic studies to reduce coronary events (MI, sudden death) in CAD patients. Thus, many authorities recommend that aspirin 80 to 325 mg/day be given prophylactically to these patients. For patients unable to take aspirin, ticlopidine 250 mg bid and clopidogrel 75 mg/day are available. These drugs block adenosine diphosphate-induced platelet aggregation. Ticlopidine appears to be more effective than aspirin in patients at high risk for transient ischemic attack, stroke, ischemic heart disease, and peripheral artery occlusion but carries a risk of bone marrow suppression.
Angioplasty involves insertion of a balloon-tipped catheter into an artery at the site of a partially obstructive atherosclerotic lesion. Inflation of the balloon can rupture the intima and media and dramatically dilate the obstruction. About 20 to 30% of obstructions reocclude in a few days or weeks, but most can be redilated successfully. Use of stents significantly reduces the reocclusion rate, which continues to decline with application of newer techniques. Repeat angiography 1 yr later reveals an apparently normal lumen in about 30% of vessels undergoing the procedure. Angioplasty is an alternative to bypass surgery in a patient with suitable anatomic lesions. The risk is comparable with that of surgery: Mortality is 1 to 3%; MI rate is 3 to 5%; emergency bypass for intimal dissection with recurrent obstruction is required in < 3%; and the initial success rate is 85 to 93% in experienced hands. Results continue to improve with advances in technique, catheter and balloon mechanics, and pharmacotherapy to maintain postangioplasty patency.
Coronary arterial bypass surgery is highly effective in selected patients with angina. The ideal candidate has severe angina pectoris, a normal-sized heart, no history of MI, localized disease suitable for bypass, good ventricular function, and no additional risk factors. In such patients, elective surgery carries a < 5% risk of perioperative MI and a mortality of <= 1%. About 85% of patients have complete or dramatic relief of symptoms. At 1 yr, about 85% of the bypass grafts remain patent. Exercise testing shows positive correlation between graft patency and improved exercise tolerance, but some patients improve significantly despite closure of the bypass. Operative risk is higher in patients with poor LV function or associated mitral or aortic valve abnormality. Operative mortality for a second bypass procedure is three to five times higher than for the first bypass, so that optimal timing of the first bypass is important.
CAD may progress despite bypass surgery. Postoperatively, the rate of proximal occlusion of bypassed vessels is increased. Vein graft obstruction proceeds as early thrombus formation and later (several years) as slow atherosclerotic degeneration of the intima and media. Aspirin prolongs vein graft patency. Patency rates for internal mammary artery bypass grafts are much higher than for venous grafts; after 10 yr, as many as 97% remain functioning, and the artery hypertrophies to accommodate increased flow to the myocardium.
Patients with left main obstruction, those with three-vessel disease and poor LV function, and some patients with two-vessel disease have improved survival after bypass. However, in patients with mild or moderate angina (class I or II), three-vessel disease, and good ventricular function, survival appears to be only marginally improved with surgery. In patients with one-vessel disease, outcomes are similar with medical therapy, percutaneous transluminal coronary angioplasty, and coronary artery bypass grafting, except in left main or proviral left anterior descending disease, in which revascularization appears to be advantageous.
UNSTABLE ANGINA
(Acute Coronary Insufficiency; Preinfarction Angina; Crescendo Angina; Intermediate Syndrome)
Angina characterized by a progressive increase in anginal symptoms, new onset of rest or nocturnal angina, or onset of prolonged angina.
Unstable angina is precipitated by an acute increase in coronary obstruction due to rupture of the fibrous plaque covering an atheroma with consequent platelet adhesion. In unstable angina, >= 1/3 of patients studied angiographically have partially occluding thrombi in the vessel subtending the recurrent ischemic area. Because recognition of a thrombus on angiography may be difficult, the incidence is probably underreported.
Compared with stable angina, the pain of unstable angina is generally more intense, lasts longer, is brought on by less effort, occurs spontaneously at rest (angina decubitus), is progressive (crescendo) in nature, or involves any combination of these changes.
About 30% of patients with unstable angina will probably suffer an MI within 3 months of onset; sudden death is less common. Presence of marked ECG changes with chest pain is an important marker for subsequent MI or death.
Unstable angina is a medical emergency to be treated in a cardiac care unit (CCU). Both heparin and aspirin reduce the incidence of subsequent MI. To reduce intracoronary clotting, aspirin 325 mg po and IV heparin should be instituted immediately. If aspirin cannot be tolerated or is contraindicated, ticlopidine 250 mg bid or clopidogrel 75 mg/day is a possible alternative. Ticlopidine requires monitoring of WBC at regular intervals because of the risk of neutropenia.
Cardiac work should be reduced by slowing heart rate and lowering BP with beta-blockers and IV nitroglycerin, thus restoring the balance between cardiac O2 demand and coronary blood flow. Contributing disorders (eg, hypertension, anemia) should be vigorously treated. Bed rest, nasal O2, and nitrates are useful. Ca blockers may be useful for patients with hypertension and possible coronary artery spasm. Thrombolytic drugs are not useful and may be harmful. Use of the antiplatelet glycoprotein IIb/IIIa receptor antagonist, the humanized chimeric Fab fragment abciximab, has been shown to improve outcome in a randomized trial in patients with refractory unstable angina. Tirofiban has been shown to prevent cardiac ischemic events in unstable angina and non-Q-wave infarction. Other IIb/IIIa receptor antagonists are being evaluated in acute ischemic syndromes.
The patient's symptoms should be brought under control within a few hours of intensive treatment. After 24 to 48 h, if therapy is not effective, more aggressive treatment may be required. The intra-aortic counterpulsating balloon reduces systolic afterload and increases diastolic pressure, the driving force for coronary blood flow. It frequently relieves continuous anginal pain and may be used to support the circulation during diagnostic cardiac catheterization prior to revascularization with coronary bypass surgery or angioplasty. Angiography may be indicated in a patient poorly responsive to medical therapy in order to identify the culprit lesion and evaluate the extent of CAD and LV function, with a plan for percutaneous transluminal coronary angioplasty or coronary artery bypass grafting if technically feasible.
VARIANT ANGINA
(Prinzmetal's Angina)
Angina pectoris that is usually secondary to large vessel spasm and is characterized by discomfort at rest and by ST segment elevation during the attack.
Most patients have significant fixed proximal obstruction of at least one major coronary vessel. Spasm usually occurs within 1 cm of the obstruction (often accompanied by ventricular arrhythmia). Between anginal attacks, which tend to occur with regularity at certain times of day, the ECG may be normal or may present a stable abnormal pattern. Ergonovine IV has been used as a provocative test to induce spasm, but this should be done only by experienced personnel in an angiographic laboratory. Although the average survival at 5 yr is 89 to 97%, patients with variant angina and severe coronary artery obstruction are at greater risk. Relief of variant angina is usually prompt after sublingual nitroglycerin; Ca blockers appear to be highly effective. (
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Could This Be Angina Pectoris?
I haven't done anything active since I broke my arm in October of 2008. I mean i've ran a little bit, and played some soccer, but nothing major. I have always been athletic though. I weight 165 lbs. I'm only 19 years old. A couple days ago, I went to go play some soccer. It was about 85 degrees outside, wasn't very humid. I played for about 15-20 minutes and had chest pains, trouble breathing, and my heart was racing. I would also experience dizziness every few minutes. I looked up this problem and my symptoms looked like Angina Pectoris. I'm really worried, I'd say my heart rate was about 140-150 bpm. I had never felt like this before and could usually workout and run without running short of breath. Could i just be really out of shape, or is this something serious?
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I would guess you are out of shape and a temperature of 85 degrees wouldn't help.
There is great danger in the phrase 'I looked up this problem'.
See your doctor for a proper diagnosis. We can only guess, scare you with all that could be wrong (and probably isn't).
Book that appointment, relax and stay away from medical sites for a bit. (
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Coronary Artery Disease(Angina Pectoris) Case Study?
Mrs. Smith, 57, is complaining of chest pain for the last couple of months. Prior to the current pain she used to complain of tightness in her chest. She smokes 20 cigarettes a day, drinks one glass of wine in the evening, exercises every day for 1 hour.
She is under a lot of pressure at work, because her boss is rushing her to finish an office project before the deadline.
Her family history indicates that her mother had a “bad cholesterol”, and died at 65y/o of a “heart problem”.
Physical examination: the patient is slightly pale;
BP = 140/80 mm Hg, Heart Rate = 80/min, irregular.
Her blood test results are:
-CBC with the differential WBC count: within the reference range
-Electrolytes: very mild hypernatremia
-Low HDL/LDL ratio
Her other blood test parameters are within normal limits.
After a panel of other test and studies Mrs. Smith was diagnosed with Coronary Artery Disease (Angina Pectoris).
1.Discuss the predisposing factors that could contribute to Mrs. Smith’s condition.
2.Discuss the protective factors that would prevent Mrs. Smith from developing Coronary artery disease.
3.Discuss the etiological factors that lead to Mrs. Smith’s condition.
4.Explain possible findings in Mrs. Smith’s EKG.
5.Describe pathogenesis of CAD.
6.What are the possible complications of Mrs. Smith’s condition?
7.How do you explain irregularity of Mrs. Smith’s heart rate?
8.What treatment would you expect to be prescribed to the Patient?
9.What other diseases would you be “looking for” in this patient, and why?
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bubblegal- Your questions are good, but would require an extraordinarily long answer. Here are some comments on your numbered questions:
1- Predisposing factors include cigarette smoking, job pressure, family history, mild hypertension, irregular heart beat, and low HDL.
2- Protective factors = daily one glass of wine, and daily exercise.
3- Etiologic factors include predisposing factors of both genetic (hereditary and familial), and chemistries, as well as smoking.
4- EKG findings may include irregular beats (intervals prolonged), and other variations in irregular beats.
5- Pathogenesis involves factors relating to genetics, and arteriosclerosis with several possible complicating diseases, such as diabetes.
6- Complications may include sudden heart attack (M.I.) with death, stroke, peripheral artery disease, blindness, kidney failure, aortic aneurysm...
7- "Electrical" conductive system in the heart is interfered with my heart enlargement and scarring due to lack of oxygen and narrowing of coronary arteries.
8- Stop smoking. Reduce sodium (normal salt) in the diet. Take water pills (diuretics). Take heart meds such as beta-blockers. Take cholesterol lowering drugs such as Lipitor.
9- Check for diabetes, vision, peripheral artery disease, increasing hypertension... (
+ info)
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