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| Diltiazem |
Diltiazem
Diltiazem is a member of the group of drugs known as calcium channel blockers, used in the treatment of hypertension or angina. It is marketed under several brand names, including Cardizem, Cartia XT, and Tiazac.it is a class 3 anti anginal drug.it incites very minimal reflex sympathetic changes.
Category:Calcium channel blockers
Calcium channel blockerCalcium channel blockers are a class of drugs with effects on the muscle of the heart and the muscles of the rest of the body. The main action of calcium channel blockers is to lower the blood pressure. It is for this action that it is used in individuals with hypertension.
Most calcium channel blockers decrease the force of contraction of the myocardium (muscle of the heart). This is known as the negative inotropic effect of calcium channel blockers. It is because of the negative inotropic effects of most calcium channel blockers that they are avoided (or used with caution) in individuals with cardiomyopathy (weak muscle of the heart).
Many calcium channel blockers also slow down the conduction of electrical activity within the heart, by blocking the calcium channel during the plateau phase of the action potential of the heart (see: cardiac action potential). This causes a lowering of the heart rate and may cause heart blocks. This is known as the negative chronotropic effect of calcium channel blockers. The negative chronotropic effects of calcium channel blockers make them a commonly used class of agents in individuals with atrial fibrillation or flutter in whom control of the heart rate is an issue.
Mechanism of action
Calcium channel blockers work by blocking voltage-sensitive calcium channels in the heart and in the blood vessels. This prevents calcium levels from increasing as much in the cells when stimulated, leading to less contraction.
This decreases total peripheral resistance by dilating the blood vessels, and decreases cardiac output by lowering the force of contraction. Because resistance and output drop, so does blood pressure.
With low blood pressure, the heart does not have to work as hard, this can ease problems with cardiomyopathy and coronary disease.
Unlike with beta-blockers, the heart is still responsive to sympathetic nervous system stimulation, so blood pressure can be maintained more effectively.
List of calcium channel blockers
Dihydropyridine calcium channel blockers
- Amlodipine besylate (Norvasc)
- Felodipine (Plendil)
- Nicardipine (Cardene, Carden SR)
- Nifedipine (Procardia, Adalat)
- Nimodipine (Nimotop)
- Nisoldipine (Sular)
- Nitrendipine (Cardif, Nitrepin)
- Lercanidipine (Zanidip)
Phenylalkylamine calcium channel blockers
- Gallopamil (D600)
- Verapamil hydrochloride (Calan, Isoptin)
Benzothiazepine calcium channel blockers
- Diltiazem hydrochloride (Cardizem)
Other
- Menthol (mint oil)
Other drugs with similar uses
Other classes of pharmaceutical agents that have overlapping effects as calcium channel blockers include ACE inhibitors, beta-blockers, and nitrates.
Related topics
- Action potential
- Cardiac action potential
- Angina
- Antiarrhythmic agents
- Hypertension
- Tachycardia
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th:แคลเซียมแชนเนลบล๊อคเกอร์
Hypertension
Hypertension or high blood pressure is a medical condition where the blood pressure is chronically elevated. While it is formally called arterial hypertension, the word "hypertension" without a qualifier usually refers to arterial hypertension.
Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm, and is a leading cause of chronic renal failure.
Definition
Blood pressure is a continuous variable, and risks of various adverse outcomes rise with it. A blood pressure of less than 120/80 mmHg is defined as "normal" in adults. Hypertension is usually diagnosed on finding blood pressure of 140/90 mmHg or above, measured on both arms on three occasions over a few weeks. Recently, the JNC VII (The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure) has defined blood pressure 120/80 mmHg to 140/90 mmHg as "prehypertension". Prehypertension is not a disease category. Rather, it is a designation chosen to identify individuals at high risk of developing hypertension (JNC VII).
In patients with diabetes mellitus or kidney disease studies have shown that blood pressure over 130/80 mmHg should be considered a risk factor and may warrant treatment.
Etiology
Essential hypertension
- Age. Over time, the number of collagen fibres in artery and arteriole walls increases, making blood vessels stiffer. With the reduced elasticity comes a smaller cross-sectional area in systole, and so a raised mean arterial blood pressure.
- High salt intake
- Sedentary lifestyle
- Tobacco smoking
- Alcohol abuse
- High levels of saturated fat in the diet
- Obesity. In obese subjects, losing a kilogram of mass generally reduces blood pressure by 2mmHg.
- Stress
- Low birth-weight
- Diabetes mellitus
- Various genetic causes
Inessential hypertension
While most forms of hypertension have no known underlying cause (and are thus known as "essential hypertension" or "primary hypertension", in about 10% of the cases, there is a known cause, and thus the hypertension is secondary hypertension.
Pathophysiology
The mechanisms behind the factors associated with inessential hypertension are generally fully understood, and are outlined at secondary hypertension. However, those associated with essential hypertension are far less understood. What is known is that cardiac output is raised early in the disease course, with total peripheral resistance normal; over time cardiac output drops to normal levels but TPR is increased. Three theories have been proposed to explain this:
- Inability of the kidneys to excrete sodium, resulting in natriuretic factor (note: the existence of this substance is theoretical) being secreted to promote salt excretion with the side-effect of raising total peripheral resistance.
- An overactive renin / angiotension system leads to vasoconstriction and retention of sodium and water. The increase in blood volume leads to hypertension.
- An overactive sympathetic nervous system, leading to increased stress responses.
Signs and symptoms
Hypertension is usually found incidentally - "case finding" by healthcare professionals. It normally produces no symptoms.
Malignant hypertension (or accelerated hypertension) is distinct as a late phase in the condition, and may present with headaches, blurred vision and end-organ damage.
It is recognised that stressful situations can increase the blood pressure; if a normally normotensive patient has a high blood pressure only when being reviewed by a health care professional, this is colloquially termed white coat effect. Since most of what we know of hypertension and its outcome with or without modification is based on large series of readings in doctors' offices and clinics (eg Framingham) it is difficult to be sure of the significance of white-coat hypertension. Ambulatory monitoring may help determine whether traffic and ticket inspectors produce similar sustained rises.
Hypertension is often confused with mental tension, stress and anxiety. While chronic anxiety is associated with poor outcomes in people with hypertension, it alone does not cause it.
Hypertensive urgencies and emergencies
Hypertension is rarely severe enough to cause symptoms. These only surface with a systolic blood pressure over 240 mmHg and/or a diastolic blood pressure over 120 mmHg. These pressures without signs of end-organ damage (such as renal failure) are termed accelerated hypertension. When end-organ damage is possible or already ongoing, but in absence of raised intracranial pressure, it is called hypertensive emergency. Hypertension under this circumstance needs to be controlled, but prolonged hospitalization is not necessarily required. When hypertension causes increased intracranial pressure, it is called malignant hypertension. Increased intracranial pressure causes papilledema, which is visible on ophthalmoscopic examination of the retina.
Complications
While elevated blood pressure alone is not an illness, it often requires treatment due to its short- and long-term effects on many organs. The risk is increased for:
- Cerebrovascular accident (CVAs or strokes)
- Myocardial infarction (heart attack)
- Hypertensive cardiomyopathy (heart failure due to chronically high blood pressure)
- Hypertensive retinopathy - damage to the retina
- Hypertensive nephropathy - chronic renal failure due to chronically high blood pressure
Pregnancy
See the main article: hypertension of pregnancy
Although few women of childbearing age have high blood pressure, up to 10% develop hypertension of pregnancy. While generally benign, it may herald three complications of pregnancy: pre-eclampsia, HELLP syndrome and eclampsia. Follow-up and control with medication is therefore often necessary.
Diagnosis
Measuring blood pressure
Diagnosis of hypertension is generally on the basis of a persistently signficantly raised blood pressure. Usually this requires three separate measurements at least one week apart. Exceptionally, if the elevation is extreme, or end organ damage is present then the diagnosis may be applied and treatment commenced immediately.
Obtaining reliable blood pressure measurements relies on following several rules and being cognizant of the many factors that influence blood pressure reading.
For instance, measurements should be at least 1 hour after caffeine, 30 minutes after smoking and without any stress. Cuff size is also important. The bladder should encircle and cover two-thirds of the length of the arm. The patient should be sitting for a minimum of five minutes. The patient should not be on any adrenergic stimulants, such as those found in many cold medications.
When taking manual measurements, the person taking the measurement should be careful to inflate the cuff at least 30 mmHg greater than systolic pressure. A stethoscope should be placed lightly over the brachial artery. The arm should be at the level of the heart and the cuff should be deflated at a rate of 2 to 3 mmHg/s. Systolic pressure is the pressure reading at the onset of the sounds described by Korotkoff (Phase one). Diastolic pressure is then defined as the pressure at which the sounds disappear (K5) or sometimes the K4 point, where the sound is abruptly muffled. Two measurements should be made at least 5 minutes apart and if there is a discrepancy of more than 5 mmHg, a third reading should be done. The readings should then be averaged. An initial measurement should include both arms. Also, in elderly patients, it is recommended to measure pressures in multiple postures as they are at risk for orthostatic hypotension.
Distinguishing primary vs. secondary hypertension
Once the diagnosis of hypertension has been made it is important to attempt to exclude or identify reversible (secondary) causes.
- Over 90% of adult hypertension has no clear cause and is therefore called essential/primary hypertension. Often, it is part of the metabolic "syndrome X" in patients with insulin resistance: it occurs in combination with diabetes mellitus (type 2), combined hyperlipidemia and central obesity.
- In hypertensive children most cases are secondary hypertension, and the cause should be pursued diligently.
Blood tests commonly performed in a newly diagnosed hypertension patient
- Creatinine (renal function)
- Electrolytes (sodium, potassium)
- Glucose (to identify diabetes mellitus)
- Cholesterol
Epidemiology
The level of blood pressure regarded as deleterious has been revised down during years of epidemiological studies. A widely quoted and important series of such studies is the Framingham Heart Study carried out in an American town: Framingham, Massachusetts. The results from Framingham and of similar work in Busselton, Western Australia have been widely applied. To the extent that people are similar this seems reasonable, but there are known to be genetic variations in the most effective drugs for particular sub-populations. Recently (2004) the Framingham figures have been found to overestimate risks for the UK population considerably. The reasons are unclear. Nevertheless the Framingham work has been an important element of UK health policy.
Treatment
Lifestyle modification
Doctors recommend weight loss and regular exercise, as well as discontinuing smoking, as the first steps in treating mild to moderate hypertension. These steps are highly effective in reducing blood pressure. Unfortunately these actions are easier to suggest than to achieve and most patients with moderate or severe hypertension end up requiring indefinite drug therapy to bring their blood pressure down to a safe level.
Mild hypertension is usually treated by diet, exercise and improved physical fitness. A diet rich in fruits and vegetables and fat-free dairy foods and low in fat and sodium lowers blood pressure in people with hypertension. Dietary sodium (salt) causes hypertension in some people and reducing salt intake decreases blood pressure in a third of people. Regular mild exercise improves blood flow, and helps to lower blood pressure.
Medications
There are many classes of medications for treating hypertension, together called antihypertensives, which—by varying means—act by lowering blood pressure. Evidence suggests that reduction of the blood pressure by 5-6 mmHg can decrease the risk of stroke by 40%, of coronary heart disease by 15-20%, and reduces the likelihood of dementia, heart failure, and mortality from vascular disease.
Which type of medication to use initially for hypertension has been the subject of several large studies. The JNC7 (The Seventh Report of the Joint National Committee on Prevention of Detection, Evaluation and Treatment of High Blood Pressure) recommends starting with a thiazide diuretic if single therapy is being initiated and a another medication is not indicated. This is based on a slightly better outcome for chlorothiazide in the ALLHAT study versus other anti-hypertensives and because thiazide diuretics are relatively cheap. Another large study (ANBP2) published after the JNC7 did not show this small difference in outcome and actually showed a slightly better outcome for ACE-inhibitors. The bottom line is this - the fundamental goal of treatment should be blood pressure control and in reality all three classes of medications are very effective.
There is also anecdotal evidence that consumption of cinnamon is very effective in lowering blood pressure. The USDA has three ongoing studies that are monitoring this effect.
References
- Chobanian AV et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003;289:2560-72. [http://jama.ama-assn.org/cgi/content/full/289.19.2560v1 Fulltext]. PMID 12748199.
See also
- Hypertensive emergency
- Hypertensive urgency
- Malignant hypertension
- Exercise hypertension
External links
- [http://www.nhlbi.nih.gov/about/framingham/ The Framingham Heart Study]
- [http://allhat.sph.uth.tmc.edu/default.htm#study Information on ALLHAT]
- [http://www.nhlbi.nih.gov/hbp/ A guide to lowering high blood pressure] from the National Heart, Lung, and Blood Institute
- [http://www.nhlbi.nih.gov/hbp/prevent/h_eating/h_eating.htm The DASH diet] from the National Heart, Lung, and Blood Institute
- [http://www.americanheart.org/presenter.jhtml?identifier=2114 High Blood Pressure] (from the American Heart Association)
- [http://kidney.niddk.nih.gov/kudiseases/pubs/hypertension/index.htm High Blood Pressure and Kidney Disease] from The National Kidney and Urologic Diseases Information Clearinghouse
- [http://medlineplus.nlm.nih.gov/medlineplus/highbloodpressure.html High Blood Pressure] from MedlinePlus
Category:Cardiology
Category:Nephrology
Category:General practice
Category:Medical_conditions_related_to_obesity
ms:Penyakit Darah Tinggi
ja:高血圧
Angina
Angina pectoris is chest pain due to ischemia (a lack of blood and hence oxygen supply) to the heart muscle, generally due to obstruction or spasm of the coronary arteries (the heart's blood vessels). Coronary artery disease, the main cause of angina, is due to atherosclerosis of the cardiac arteries. The term derives from the Greek ankhon ("strangling") and the Latin pectus ("chest"), and can therefore be translated as "a strangling feeling in the chest".
Worsening ("crescendo") angina attacks, sudden-onset angina at rest, and angina lasting more than 15 minutes are symptoms of unstable angina or acute coronary syndrome. As these may herald myocardial infarction (a heart attack), they require urgent medical attention and are generally treated quite similarly.
Symptoms
Most patients with angina complain of chest discomfort rather than actual pain, the discomfort is usually described as a pressure, heaviness, squeezing, burning, or choking sensation. Anginal pain may be localized primarily in the epigastrium (upper central abdomen), back, neck, jaw, or shoulders. Typical locations for radiation of pain are arms, shoulders, and neck. Angina typically is precipitated by exertion or emotional stress, and exacerbated by having a full stomach or cold temperatures (the "4 Es": exertion, emotion, eating and extreme temperature). Pain may be accompanied by sweating and nausea in some cases. It usually lasts for about 1 to 5 minutes, and is relieved by rest or specific anti-angina medication. Chest pain lasting only a few seconds is normally not angina.
Some experience "autonomic symptoms" (related to increased activity of the autonomic nervous system) such as nausea, vomiting and pallor.
Major risk factors for angina include family history of premature heart disease, cigarette smoking, diabetes, high cholesterol, and high blood pressure.
A variant form of angina (Prinzmetal's angina) occurs in patients with normal coronary arteries or insignificant atherosclerosis. It is thought to be caused by spasms of the artery. It occurs more in younger women.
Diagnosis
In patients with occasional angina who are not having chest pain, an electrocardiogram (ECG) is typically normal, unless there have been other cardiac problems in the past. During pain, depression of the ST segment may be observed. To elicit these changes, an exercise ECG test ("treadmill test") may be performed, during which the patient exercises to the point that the pain occurs; if the ECG changes are documented, the test is considered diagnostic for angina. Other alternatives include a thallium scintigram (in patients that cannot exert enough for the purposes of the treadmill tests, e.g., due to asthma or arthritis).
In patients in whom noninvasive testing is diagnostic, a coronary angiogram is typically performed to identify the nature of the coronary lesion, and whether this would be a candidate for angioplasty, coronary artery bypass graft (CABG) or other treatments.
Pathophysiology
Increases in heart rate result in increased oxygen demand by the heart. The heart has a limited ability to increase its oxygen intake during episodes of increased demand. Therefore, an increase in oxygen demand by the heart (e.g., during exercise) has to be met by a proportional increase in blood flow to the heart.
Myocardial ischemia can result from:
# a reduction of blood flow to the heart caused by the stenosis or spasm of the heart's arteries
# resistance of the blood vessels
# reduced oxygen-carrying capacity of the blood.
Atherosclerosis (narrowing of the blood vessels) is the most common cause of stenosis of the heart's arteries and, hence, angina pectoris.
Many people with chest pain have normal or minimal narrowing of heart arteries. This has shown that resistance of the blood vessels (abnormal constriction or deficient relaxation of heart vessels) can be responsible for as much as 95% of coronary artery resistance.
Myocardial ischemia also can be the result of factors affecting blood composition, such as reduced oxygen-carrying capacity of blood, as seen with severe anemia (low number of red blood cells), or long-term smoking.
Epidemiology
Roughly 6.3 million Americans are estimated to experience angina. Angina is more often the presenting symptom of coronary artery disease in women than in men. The prevalence of angina rises with an increase in age. Similar figures apply in the remainder of the Western world. All forms of coronary heart disease are much less-common in the Third World, as its risk factors are much more-common in Western and Westernized countries; it could therefore be termed a disease of affluence. The increase of smoking, obesity and other risk factors has already led to an increase in angina and related diseases in countries such as China.
Treatment
The main goals of treatment in angina pectoris are relief of symptoms, slowing progression of the disease, and reduction of future events, especially heart attacks. An aspirin (75 mg to 100 mg) per day has been shown to be beneficial for all patients with stable angina that have no problems with its use. Beta-blockers and nitroglycerin medication are used for symptomatic relief of angina and prevention of ischemic events, and calcium channel blockers (such as verapamil).
Identifying and treating risk factors of coronary heart disease is a priority in patients with angina. This means testing for elevated cholesterol, diabetes, hypertension (high blood pressure), stopping smoking and losing weight.
Unstable angina
Physicians distinguish between stable angina, which occurs during exercise or stress, and is relieved with a nitrate spray or tablet (e.g., amyl nitrite), and unstable angina, which occurs at rest, or is unrelieved by the usual medication. A patient with angina that is increasing in frequency or severity is also said to have unstable angina.
Unstable angina is very predictive of a heart attack, and requires immediate medical attention. As it is only one of the many potential causes of chest pain, the patient usually has a number of tests in the emergency department, such as a chest X-ray, blood tests (including myocardial markers such as troponin I or T, and a D-dimer if a pulmonary embolism is suspected) and telemetry (monitoring of the heart rhythm).
If the ECG does not show the changes (ST elevation) typical of myocardial infarction (heart attack), the patient may still have suffered a "non-ST elevation MI" (NSTEMI). The accepted management of unstable angina and acute coronary syndrome is therefore empirical treatment with aspirin, heparin (usually a low molecular weight heparin such as enoxaparin), clopidogrel, and intravenous glyceryl trinitrate if the pain persists. A blood test is generally performed for cardiac troponins twelve hours after onset of the pain. If this is positive, coronary angiography is typically performed on an urgent basis, as this is highly predictive of a heart attack in the near-future. If the troponin is negative, a treatmill exercise test or a thallium scintigram may be requested.
See also
- Ludwig's angina
- Prinzmetal's angina
Category:Ischemic heart disease
ja:狭心症
City Beautiful movementThe City Beautiful movement was a Progressive reform movement in North American architecture and urban planning that flourished in the 1890s and 1900s with the intent of using beautification and monumental grandeur in cities to counteract the perceived moral decay of poverty-stricken urban environments. The movement, which was originally most closely associated with Chicago and Washington, D.C., did not seek beauty for its own sake, but rather as a social control device for creating moral and civic virtue among urban populations. Advocates of the movement believed that such beautification could thus provide a harmonious social order that would improve the lives of the inner-city poor.
virtue]]
History
Origins and impact
The movement arose in the United States in response the perceived wretched conditions of inner-city poverty in crowded tenement districts, itself a product of increased immigration and consolidation of rural populations into cities. The movement flourished for several decades, but it also achieved great influence in urban planning that extended throughout the 20th century, in particular in regard to the later creation of housing projects in the United States. The "Garden City" movement in Britain influenced the contemporary planning of some newer suburbs of London, and there was cross-fertilization between the two esthetics, one based in formal garden plans and urbanization schemes of the Baroque the other, with its "semi-detached villas" evoking a more rural atmosphere. Critics of the movement asserted that the uniformity and high-mindedness of the style created dullness and sterility in urban environments, ironically contributing to an increase in the urban blight that the original advocates of the movement were seeking to ameliorate.
Architectural idioms
The particular architectural style of the movement borrowed heavily from the contemporary Beaux-Arts movement, which emphasized the necessity of order, dignity, and harmony. The movement also borrowed from classical monumental planning but differed from the true neoclassical style in that in the City Beautiful movement, the classical idiom was adopted only partially, mixed with Beaux-Arts elements, and subjugated as means to the end of creating uniformity and harmony in style.
World Columbian Exposition
The first large-scale elaboration of the City Beautiful is considered to have been the "White City", as it came to be called, at the World Columbian Exposition of 1893 in Chicago. The planning of the exposition was headed by architect Daniel Burnham, who brought in architects from the eastern United States, as well as the sculptor Augustus Saint-Gaudens, to build large-scale Beaux-Arts monuments that were vaguely classical with uniform cornice height. The exposition displayed a model city of grand scale, with clean state-of-the-art transport systems and no visible poverty. The exposition is credited with leading to the wide-scale embrace of the monumental idiom in American architecture for the next 15 years. Richmond, Virginia's Monument Avenue is one expression of this initial movement.
1901 Washington, D.C. Plan
Monument Avenue extend the central axis]]
The first attempt to use City Beautiful ideal for a city plan with intent of creating social order through beautification was the 1901 Plan for Washington, D.C., which arose from the Senate Park Commission's redesign of the monumental core of the city to commemorate the city's centennial and to fulfill unrealized aspects of the city plan of Pierre Charles L'Enfant a century earlier.
The Washington planners, who included Burnham, Saint-Gaudens, Charles McKim, and Frederick Law Olmsted, Jr., visited many of the great cities of Europe with the intent of putting Washington on par with the European capitals of the era and creating a sense of the legitimacy of government in a time of social upheaval in the United States. The essence of the plan surrounded the U.S. Capitol with monumental government buildings to replace "notorious slum communities". At the heart of the design was the creation of the National Mall and eventually included Burnham's Union Station. The implementation of the plan was interrupted by World War I but resumed after the war, culminating the construction of the Lincoln Memorial in 1922.
The movement's success in Washington is credited with influencing subsequent plans for beautification in many other cities, including Chicago, Cleveland, Montreal, Denver and San Francisco. In New Haven, John Russell Pope drew up a plan for Yale University that swept away substandard housing, but banished the urban poor to the peripheries.
:Main article: Civic Center, Denver
In Denver the energy behind extensive City Beautiful planning came from Mayor Robert Speer, whose plan centered round a Civic Center, disposed along agrand esplanade that led to the Colorado State Capitol. The plan was partly realized, on a reduced scale, with the Greek amphitheater, Voorhies Memorial and the Colonnade of Civic Benefactors, completed in 1919. The Andrew Carnegie Foundation funded the Denver Public Library (1910), which was designed as a three-story Greek Revival temple with a colossal Ionic colonnade across it front; inside it featured open shelves, an art gallery and a children's room. Monuments capping vistas were an essential feature of City Beautiful urban planning: in Denver Paris-trained American sculptor Frederick MacMonnies was commissioned to design a monument marking the end of the Smoky Hill Trail. The bronze Indian guide he envisaged was vetoed by the committee and replaced with an equestrian Kit Carson.
Decline
The movement waned after 1909 when it came under assault from planners and critics who disliked its expensive, impractical, and allegedly elitist and superficial characteristics.
External links
- [http://xroads.virginia.edu/~CAP/CITYBEAUTIFUL/city.html University of Virginia: The City Beautiful movement]
- http://www.historicrichmond.com/monument.html
- [http://photoswest.org/exhib/gallery2/dcb.htm Denver Public Library: Denver, The City Beautiful]
Category:Architectural styles
Category:Urban studies and planning
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