إليكم هذا الموقع الذي يمكتك من الربح من خلال ملفات حاسوبك
موقع يمكنك من تخزين كل ما يوجد على جهاز حاسوب من صور وملفات و فيديو وأغاني وغيرها بلمسات بسيطة كما يمكنك من إرسالها عبر البريد الإلكتروني بسعة تصل إلى أكثر من 200 م.ب في شكل وصلة تحميل مباشرة. كما يمكنك من إنشاء مكتبة للصور (ألبوم) أو للأغاني و الفيديو بجودة و دقة عالية. هذا و أكثر :
مفاجأة : أنت تربح كلما تم تحميل ملفاتك من قبل مستخدمي الأنترنت. لزيارة الموقع و التسجيل: الضغط
29/7/2009
اكتشف كيف استطاع أخي الذي لم يبلغ الثامنة عشر من عمره أن يحقق 800 $ في شهر واحد دون أن يكتب حرفا واحداً..."
5 مواقع جوجل ادسنس مجاناً بتقنية الويب 2.0 فقط لزورا ادسنس سكاي
اشترك في قوائمنا البريديه واحصل على 5 مواقع جوجل ادسنس جاهزه للعمل والربح من اليوم مواقع تعمل على مدار الساعه بطريقه ديناميكيه 100 % لا تحتاج الى اي تدخل منك على الاطلاق هذه المواقع يقدر الموقع منها بقيمة 20 دولار للموقع هديه لزورا موقع ادسنس سكاي
كتاب جميل جدا جدا والأحسن انه سهل في طريقه شرحه وعلشان كده كان من السهل انى افهمه واتبع خطواته خطوه خطوه
لما اشتريت الكتاب ماكنتش اعرف اى حاجه عن الموضوع ده وماكنش معاى غير 7 دولار وماكنش معاى حتى دومين.
بعد كده اتبعت الكتاب خطوه خطوه فى شراء الدومين والاستضفه لانى اكتشفت انه فى حاجات لازم تراعيها وانت بتشترى الدومين والاستضافه لشبكة المواقع الخاصه بك.
بعد كده مشيت مع الكتاب خطوه خطوه لحد ماعملت الموقع بتاعى وبدأت اجيبله ترافيك وفعلا كانت طرق الترافيك كويسه جدا وجابت نتايج جميله جدا.
انا ماكنتش مصدق ان الموضوع ده هايجيب فلوس الا لما جيت فى يوم وعملت 12 دولار.
بعد كده الكتاب بيعرفك ازاى تتابع الشبكة بتاعتك كمان وازاى تتحكم فى الترافيك بتاعك علشان تختار بس الترافيك الاجنبى الى بيجيب فلوس
يعنى الكتاب بمشى معاك من اول خطوه لاخر خطوه.
اشترك في قوائمنا البريديه واحصل على 5 مواقع جوجل ادسنس جاهزه للعمل والربح من اليوم مواقع تعمل على مدار الساعه بطريقه ديناميكيه 100 % لا تحتاج الى اي تدخل منك على الاطلاق هذه المواقع يقدر الموقع منها بقيمة 20 دولار للموقع هديه لزورا موقع ادسنس سكاي
كتاب جميل جدا جدا والأحسن انه سهل في طريقه شرحه وعلشان كده كان من السهل انى افهمه واتبع خطواته خطوه خطوه
لما اشتريت الكتاب ماكنتش اعرف اى حاجه عن الموضوع ده وماكنش معاى غير 7 دولار وماكنش معاى حتى دومين.
بعد كده اتبعت الكتاب خطوه خطوه فى شراء الدومين والاستضفه لانى اكتشفت انه فى حاجات لازم تراعيها وانت بتشترى الدومين والاستضافه لشبكة المواقع الخاصه بك.
بعد كده مشيت مع الكتاب خطوه خطوه لحد ماعملت الموقع بتاعى وبدأت اجيبله ترافيك وفعلا كانت طرق الترافيك كويسه جدا وجابت نتايج جميله جدا.
انا ماكنتش مصدق ان الموضوع ده هايجيب فلوس الا لما جيت فى يوم وعملت 12 دولار.
بعد كده الكتاب بيعرفك ازاى تتابع الشبكة بتاعتك كمان وازاى تتحكم فى الترافيك بتاعك علشان تختار بس الترافيك الاجنبى الى بيجيب فلوس
يعنى الكتاب بمشى معاك من اول خطوه لاخر خطوه.
أربح الدولارات عبر الانترنت مجانا طريقة رائعة ومضمونة
لامن خلص الذهب وانت في لعبة الترافيان فهذا الموقع مجرب و يعد افضل موقع من حيث المصداقيه
وانت عارفين طبعاً أن 99.9% منهم نصابين
أنا جبتلكم الحل الأسهل والأضمن والمجرب
ويمكن الشراء عبر الأنترنت مجااااااااااااااانا يعني راح يكون في حسابك بالباي بال وتشتري فيه أي حاجة عاوزها
مجانا مجانا مجانا
طريقة مضمونة وأنا مجربها بنفسي
وانت عارفين طبعاً أن 99.9% منهم نصابين
أنا جبتلكم الحل الأسهل والأضمن والمجرب
ويمكن الشراء عبر الأنترنت مجااااااااااااااانا يعني راح يكون في حسابك بالباي بال وتشتري فيه أي حاجة عاوزها
مجانا مجانا مجانا
طريقة مضمونة وأنا مجربها بنفسي
6/7/2009
ANTIOXIDANT VITAMINS AND CARDIOVASCULAR DISEASE
Over The past several years, there has been an increasing interest in the role of free radical scavengers, particularly antioxidant vitamins in cardiovascular disease prevention. Free radicals are common by products of many oxidative biochemical reactions in the body. They can damage or destroy biological molecules and have the potential for causing serious tissue and organ damage. They have been implicated in aging and chronic disease processes, including atherosclerotic coronary heart disease. Substantial laboratory, animal, and human data suggest that oxidation of low density lipoprotein (LDL) cholesterol is an important step in the pathogenesis of atherosclerotic lesions1.
Antioxidants vitamins presumably exert their effects through the protection of oxidation. However, some studies have shown that these vitamins may also preserve endothelial function 2, affect hemostasis3, and lower LDL cholesterol level4.
The predominant antioxidants protecting the LDL molecule are a tocopherol, retinyl stearate, gamma tocopherol , and beta carotene. Being lipid soluble, these agents are incorporated into the LDL molecule. a Tocopherol, the most active isomer of the vitamin E family, is the principal lipid soluble antioxidant in tissues and plasma57. Ascorbic acid, on the other hand, is the first line of defense against oxygen free radicals in the water soluble compartment 6,7.
Vitamin E supplementation was found to reduce the risk of coronary heart disease in a study in which 39,910 male health professionals with no history of cardiovascular disease were followed for 4 years9, About 17% of the men took vitamin E supplements. The adjusted relative risk reduction (RRR) of coronary heart disease in men taking at least 100 IU of vitamin E supplements for at least 2 years compared with the men not taking vitamin E supplements was 44% (CI, 19% to 56%).
In a study of 34,486 postmenopausal women10 with no cardiovascular disease followed up for 7 years, the intake of vitamin E from food was inversely associated with the risk of death from coronary heart disease and that such women can lower their risk without using vitamin supplements. By contrast, the intake of vitamins A and C was not associated with lower risks of dying from coronary disease11.
Vitamin C clearly reduced risk in only one large cohort study (in which vitamin E intake was not ascertained) and in none of the small cohort studies. In a prospective study of 11,348 American adults, researchers found a 34% lower standardized mortality ratc (CI, 18% to 47%) among participants who received 50 mg of vitamin C/day or more (by dietor supplements) compared with persons who received less vitamin C12. In another cohort study, Galc and colleagues13 examined the 20year survival of 730 elderly persons who had no initial history of vascular disease. The incidence of stroke in subjects in the highest tertile of vitamin C intake (mean,> 45 mg/day) was significantly reduced (RRR of 50%). However, no such reduction was seen in mortality from coronary heart disease.
Experimental data suggest that vitamin C lowers blood pressure by a small amount, that 2 g daily lowers serum cholesterol concentration and prevents oxidation of LDL and that a similar dose may increase fibrinolytic activity in those with coronary heart disease14,15. However, evidence is required to show more benefit than harm from treatment16.
Reliable estimates of efficacy of antioxidant vitamins can only be obtained from large scale randomized trials. None of the completed randomized trials showed any clear reduction in cardiovascular disease with vitamin E, vitamin C, or beta carotenc supplementation. The trials were not specifically designed to address cardiovascular disease, did not provide data on nonfatal cardiovascular end points, may have had insufficient treatment duration, and used suboptimal vitamin E doses12.
More recently, however, the Cambridge Heart Antioxidant Study (CHAOS) looked at the effects of vitamin E in the secondary prevention of coronary heart disease17, 2002 patients with angiographically confirmed coronary artery disease were randomly assigned to take vitamin E or placebo. Half the patients who had vitamin E were randomized to receive 800 IU daily for 2 years while the other half had 400 IU for 1 year. The primary end points were a combination of cardiovascular death plus nonfatal myocardial infarction. Vitamin E reduced these two end points significantly by 36%;and 66% respectively. There is still much uncertainty about the dose of vitamin E in primary and secondary coronary heart disease prevention. The follow-up of patients receiving 800 IU daily dose was twice as long, yet the number of nonfatal myocardial infarction in the 400 IU daily group seems to have been reduced more18.
The Alpha Tocopherol, Beta Carotene and Cancer Prevention Study (ATBC) of 29,133 middle aged heavy smokers in Finland were followed for 6.1 years20. The participants were treated with vitamin E (50 mg/day), beta carotene (20 mg/day), both, or neither. There was no reduction in the incidence of lung cancer nor was there any significant reduction in the incidence of coronary heart disease. The dose of vitamin E was probably too low but the dose of beta carotene was adequate. The participants were heavy smokers and therefore at high risk of both lung cancer and coronary heart disease. It is conceivable that this was a group of men with advanced atherosclerosis. A legitimate question is whether their disease was so far advanced which limits the validity of the trial19.
Recently, the data of two large placebo controlled studies have been published. In the Physicians Health Study, 22,071 American male doctors treated with 50 mg of beta carotene or placebo every other day were followed for an average of 12years20. There were virtually no early or late differences in the overall incidence of malignant neoplasm or cardiovascular disease, deaths from cardiovascular disease, or in the overall mortality.
The Beta Carotene and Retinol Efficacy Trial (CARET) studied 18,314 persons at high risk for lung cancer because of exposure to asbestos or cigarette smoking. They were treated daily with a combination of 30mg of beta carotenc and 25,000 IU of retinol (vitamin A) or with placebo for an average of 4 years20. The trial was stopped 21 months earlier than planned when researchers recognized an elevated risk of death from lung cancer in the group receiving the supplements.
The study showed that the combination of beta carotene and vitamin A had no benefits and may have had an adverse effect on the incidence of lung cancer and on the risk of death from lung cancer, cardiovascular disease, and any cause in smokers and workers exposed to asbestos20.
The results of these last two trials send a clear message to the public , the tens of millions of dollars spent annually on beta carotene supplements should now be diverted to more useful purposes21.
Randomized trials of sufficient power to establish the effectiveness of higher dose antioxidant supplementation in preventing coronary heart disease are currently unerway.
In all trials of vitamin E, doses greater than 3IU/day are being used; such doses should be sufficient to increase serum levels at least two to threefold. A future metaanalysis or a systematic overview of the cumulative numbers from these trials should, by the end of the decade, provide clear answers about the efficacy and safety of the various antioxidant vitamins12.
The combined evidence currently does not support the routuse of antioxidavitamins apreventive measure against cardiovascular disease.
References:
Antioxidants vitamins presumably exert their effects through the protection of oxidation. However, some studies have shown that these vitamins may also preserve endothelial function 2, affect hemostasis3, and lower LDL cholesterol level4.
The predominant antioxidants protecting the LDL molecule are a tocopherol, retinyl stearate, gamma tocopherol , and beta carotene. Being lipid soluble, these agents are incorporated into the LDL molecule. a Tocopherol, the most active isomer of the vitamin E family, is the principal lipid soluble antioxidant in tissues and plasma57. Ascorbic acid, on the other hand, is the first line of defense against oxygen free radicals in the water soluble compartment 6,7.
Vitamin E supplementation was found to reduce the risk of coronary heart disease in a study in which 39,910 male health professionals with no history of cardiovascular disease were followed for 4 years9, About 17% of the men took vitamin E supplements. The adjusted relative risk reduction (RRR) of coronary heart disease in men taking at least 100 IU of vitamin E supplements for at least 2 years compared with the men not taking vitamin E supplements was 44% (CI, 19% to 56%).
In a study of 34,486 postmenopausal women10 with no cardiovascular disease followed up for 7 years, the intake of vitamin E from food was inversely associated with the risk of death from coronary heart disease and that such women can lower their risk without using vitamin supplements. By contrast, the intake of vitamins A and C was not associated with lower risks of dying from coronary disease11.
Vitamin C clearly reduced risk in only one large cohort study (in which vitamin E intake was not ascertained) and in none of the small cohort studies. In a prospective study of 11,348 American adults, researchers found a 34% lower standardized mortality ratc (CI, 18% to 47%) among participants who received 50 mg of vitamin C/day or more (by dietor supplements) compared with persons who received less vitamin C12. In another cohort study, Galc and colleagues13 examined the 20year survival of 730 elderly persons who had no initial history of vascular disease. The incidence of stroke in subjects in the highest tertile of vitamin C intake (mean,> 45 mg/day) was significantly reduced (RRR of 50%). However, no such reduction was seen in mortality from coronary heart disease.
Experimental data suggest that vitamin C lowers blood pressure by a small amount, that 2 g daily lowers serum cholesterol concentration and prevents oxidation of LDL and that a similar dose may increase fibrinolytic activity in those with coronary heart disease14,15. However, evidence is required to show more benefit than harm from treatment16.
Reliable estimates of efficacy of antioxidant vitamins can only be obtained from large scale randomized trials. None of the completed randomized trials showed any clear reduction in cardiovascular disease with vitamin E, vitamin C, or beta carotenc supplementation. The trials were not specifically designed to address cardiovascular disease, did not provide data on nonfatal cardiovascular end points, may have had insufficient treatment duration, and used suboptimal vitamin E doses12.
More recently, however, the Cambridge Heart Antioxidant Study (CHAOS) looked at the effects of vitamin E in the secondary prevention of coronary heart disease17, 2002 patients with angiographically confirmed coronary artery disease were randomly assigned to take vitamin E or placebo. Half the patients who had vitamin E were randomized to receive 800 IU daily for 2 years while the other half had 400 IU for 1 year. The primary end points were a combination of cardiovascular death plus nonfatal myocardial infarction. Vitamin E reduced these two end points significantly by 36%;and 66% respectively. There is still much uncertainty about the dose of vitamin E in primary and secondary coronary heart disease prevention. The follow-up of patients receiving 800 IU daily dose was twice as long, yet the number of nonfatal myocardial infarction in the 400 IU daily group seems to have been reduced more18.
The Alpha Tocopherol, Beta Carotene and Cancer Prevention Study (ATBC) of 29,133 middle aged heavy smokers in Finland were followed for 6.1 years20. The participants were treated with vitamin E (50 mg/day), beta carotene (20 mg/day), both, or neither. There was no reduction in the incidence of lung cancer nor was there any significant reduction in the incidence of coronary heart disease. The dose of vitamin E was probably too low but the dose of beta carotene was adequate. The participants were heavy smokers and therefore at high risk of both lung cancer and coronary heart disease. It is conceivable that this was a group of men with advanced atherosclerosis. A legitimate question is whether their disease was so far advanced which limits the validity of the trial19.
Recently, the data of two large placebo controlled studies have been published. In the Physicians Health Study, 22,071 American male doctors treated with 50 mg of beta carotene or placebo every other day were followed for an average of 12years20. There were virtually no early or late differences in the overall incidence of malignant neoplasm or cardiovascular disease, deaths from cardiovascular disease, or in the overall mortality.
The Beta Carotene and Retinol Efficacy Trial (CARET) studied 18,314 persons at high risk for lung cancer because of exposure to asbestos or cigarette smoking. They were treated daily with a combination of 30mg of beta carotenc and 25,000 IU of retinol (vitamin A) or with placebo for an average of 4 years20. The trial was stopped 21 months earlier than planned when researchers recognized an elevated risk of death from lung cancer in the group receiving the supplements.
The study showed that the combination of beta carotene and vitamin A had no benefits and may have had an adverse effect on the incidence of lung cancer and on the risk of death from lung cancer, cardiovascular disease, and any cause in smokers and workers exposed to asbestos20.
The results of these last two trials send a clear message to the public , the tens of millions of dollars spent annually on beta carotene supplements should now be diverted to more useful purposes21.
Randomized trials of sufficient power to establish the effectiveness of higher dose antioxidant supplementation in preventing coronary heart disease are currently unerway.
In all trials of vitamin E, doses greater than 3IU/day are being used; such doses should be sufficient to increase serum levels at least two to threefold. A future metaanalysis or a systematic overview of the cumulative numbers from these trials should, by the end of the decade, provide clear answers about the efficacy and safety of the various antioxidant vitamins12.
The combined evidence currently does not support the routuse of antioxidavitamins apreventive measure against cardiovascular disease.
References:
hEART VALVES IN PREGNANCY
DR. HASSAN CHAMSI-PASHA
Published in Journal of Saudi Heart Association
Pregnancy causes dramatic, usually reversible, changes in a woman’s cardiovascular system. Maternal heart disease (present in 2%) of all pregnancies is the most important non-obstetric cause of death in pregnant women. Valvular heart disease may have a significant impact on fetal and maternal health during pregnancy, labor, and delivery. Pregnant women with valvular heart disease should be managed by a high-risk obstetric service that can provide cardiology consultation, close obstetric supervision and provisions for delivery with hemodynamic monitoring when required.(1)
Valvular heart lesions associated with high maternal and/or fetal risk during pregnancy include severe aortic stenosis, aortic and mitral regurgitation with functional class III-IV symptoms, mitral stenosis with class II-IV symptoms, aortic and/or mitral valve disease resulting in severe pulmonary hypertension or associated with severe LV dysfunction and mechanical prosthetic valve requiring anticoagulation. On the other hand, valvular heart lesions associated with low maternal and fetal risk include asymptomatic mild to moderate aortic stenosis with normal LV systolic function, aortic or mitral regurgitation with NYHA functional class I or II with normal LV systolic function, mitral valve prolapse with mild to moderate MR, and mild to moderate mitral stenosis without severe pulmonary hypertension.(2)
Young pregnant women with a previous history of acute rheumatic fever and carditis should continue to receive penicillin prophylaxis as indicated in the non-pregnant state. The most common rheumatic lesion in this age group remains mitral stenosis (MS). Patients with mild to moderate MS can almost always be managed with judicious use of diuretics and B-blockade. Diuretics are given to relieve pulmonary and excess systemic venous congestion. Patients with severe MS who are symptomatic before conception should be considered for percutaneous balloon mitral valvotomy before conception. Patients with severe MS who develop NYHA functional Class III-IV symptoms during pregnancy should undergo percutaneous balloon valvotomy.(2) The reported results with mitral balloon valvotomy have been excellent.(3) In developing countries, there is a long history of successful surgical closed commissurotomy for pregnant women.
Patients with mitral regurgitation (MR) usually tolerate pregnancy and can be managed medically. Medical management includes diuretics for patients with pulmonary congestion. Vasodilator therapy is indicated only in the presence of concomitant systemic hypertension and should not be advised in the setting of normal or low systemic blood pressure. ACE inhibitors are considered unsafe in pregnancy while hydralazine and nitrates are known to be safe.
Patients with mild to moderate aortic stenosis (AS) and normal LV systolic function can usually be managed conservatively through the entire pregnancy. Patients with pressure gradient >50 mm Hg or symptoms should be advised to delay conception until relief of AS can be obtained. For those with severe AS whose disease is first appreciated during pregnancy, consideration may have to be given to either percutaneous aortic balloon valvotomy (4) or surgery before labor if heart failure has developed or syncope has occurred. These procedures are fraught with danger to both the mother and fetus.
Isolated aortic regurgitation (AR), like MR, can usually be managed medically with a combination of diuretics and, if necessary, vasodilator therapy. Women with symptoms and/or signs of LV failure should be carefully monitored throughout labor and delivery with strict attention to volume status and blood pressure.
The approach to the patient with tricuspid valve involvement as part of a more complex congenital or acquired heart disease is predicated on the features of the associated lesions. Isolated TR should not pose a significant problem, although greater care may be necessary to protect against diuretic-induced hypoperfusion.(2) Vasodilators and digoxin are unlikely to be beneficial.(5)
The management of women with prosthetic heart valves during pregnancy poses a particular challenge as there are no available guidelines for effective antithrombotic therapy.(6)
Warfarin crosses the placenta and has been associated with an increased incidence of spontaneous abortion, prematurity, and stillbirth. Warfarin embryopathy occurs in 4% to 10% of patients.(7) The risk may be dose-related and appears to be highest if exposure occurs during the 6th to 12th weeks of gestation.
Heparin does not cross the placenta and is generally considered safer. Its long-term use, however, is complicated by sterile abscesses, osteoporosis, thrombocytopenia, and bleeding. Subcutaneous administration of heparin has been reported to be ineffective in preventing thromboembolic complications.(6) Thromboembolic complications, including fatal valve thrombosis, in high-risk pregnant women managed with subcutaneous heparin was reported in 12-24% of patients.(8) Thromboembolism, however, has been reported mostly in patients with older-generation mechanical valves (Starr-Edwards, Bjork-Shiley and so forth) in the mitral portion.(5) These findings led to recommendations included in the American College of Cardiology/American Heart Association Guidelines for the use of Warfarin as an anticoagulant of choice for the first 35 weeks of pregnancy in patients with a mechanical prosthetic valve. These guidelines state that “the decision whether to use heparin during the first trimester or to continue oral anticoagulation throughout pregnancy should be made after full discussion with the patient and her partner; if she chooses to change to heparin for the first trimester, she should be made aware that heparin is less safe for her, with a higher risk of both thrombosis and bleeding. High-risk women who choose not take warfarin during the first trimester should receive continuous heparin intravenously. Transition to warfarin can occur thereafter”(2).
These recommendations have been problematic and have not been adopted by both patients and physicians, especially in United States. Women in general are not willing to take warfarin during the first trimester of pregnancy.(5) The attitude of physicians is reflected by the fact that 96% of 438 members of the Society of Perinatal Obstetricians surveyed on their preferred management of a pregnant patient with a mechanical prosthesis in the mitral position selected discontinuation of warfarin and use of full-dose heparin for the duration of pregnancy.(9)
Vitale et al recently made an important contribution demonstrating a close dependency between warfarin dosage and fetal complications. In his study, 22 of 25 pregnant women (88%) whose warfarin dose was >5 mg/day had fetal complications with a 9% incidence of warfarin embryopathy. In contrast, only 5 of 33 cases (15%) treated with a small dose warfarin (< 5 mg/day) had fetal complications and non of them had warfarin embryopathy.(10) These findings may suggest the feasibility of risk free use of warfarin during pregnancy in patients with prosthetic heart valves who can be well anticoagulated with < 5 mg of warfarin per day.
Meschengieser et al recently studied 92 pregnancies in 59 women with mechanical heart valve prosthesis. In 31 pregnancies, subcutaneous heparin was started when pregnancy was diagnosed and in the second trimester oral anticoagulants were resumed. In 61 pregnancies oral anticoagulants were continued during the first trimester. Abortion or fetal losses were similar in the two groups while embolic episodes were more common (p=.0029) in women who received heparin (4.92%) compared with those on oral anticoagulants (0.33%).(11)
Recently Chan et al(6) made a systematic review of the literature and found that the use of oral anticoagulants throughout pregnancy was associated with warfarin embryopathy in 6.4% of live births. The substitution of heparin at or prior to 6 weeks, and continued until 12 weeks, eliminated this risk. The regimen associated with the lowest risk of valve thrombosis (3.9%) was the use of oral anticoagulants throughout; using heparin only between 6 and 12 weeks’ gestation was associated with increased risk of valve thrombosis (9.2%).(6)
The additional use of low-dose aspirin should be considered, particularly in women with high-risk valves, women with previous transient ischemic attacks and/or strokes, and women with atrial fibrillation.(12)
A more recent and theoretically more promising approach consists of therapy with low-molecular-weight heparins (LMWH), which do not cross the placenta, do not require frequent partial thromboplastin time monitoring and have a longer half-life than sodium heparin.(1) There is a great deal of interest in the use of LMWH as a substitute for unfractionated heparin in patients with prosthetic heart valves during pregnancy. The data to support the use of LMWH, however, is not yet available. A successful use of LMWH was reported in small number of patients and more information is required before LMWH can be recommended for anticoagulation in a patient with a prosthetic valve during pregnancy.(5) Recently, two cases of LMWH treatment failure resulting in thrombosed prosthetic heart valves were reported.(13)
Another important issue related to pregnancy is whether pregnancy affects the durability of valvular bioprostheses or not. Anecdotal reports of early failure of biological heart valves in pregnant patients tend to raise concerns. (14) Recently Salazar et al(15) reported data from 48 women who became pregnant after bovine pericardial valve replacement. Their data confirm recent reports that pregnancy does not significantly affect durability of bioprosthesis. In their study, the actuarial freedom from dysfunction was 90.4% at 5 years and 77% at 8 years for the pregnancy group and 86.3% and 73.4% respectively, for the control group (p = not significant). This study, however, has more than one limitation. First, the number of patients is relatively small, and secondly, the study is limited to the hard end points of death and reoperation. Conceivably, pregnancy could cause more subtle valvular dysfunction not detected by analysis of death and reoperation. The primary implication of this study is that bioprostheses remain the devices of choice for young women willing to trade earlier operation for the opportunity of pregnancy.(16)
References:
1) Teerlink JR, Foster E. Valvular Heart Disease in Pregnancy. Cardiol Clin 1998,16:573-95.
2) Bonow RO, Carabello B, de Leon AC Jr, Edmunds LH Jr, Fedderly BJ, Freed MD, Gaasch WH, McKay CR, Nishimura RA, O’Gara PT, O’Rourke RA, Rahimtoola SH. ACC/AHA guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients With Valvular Heart Disease). J Am Coll Cardiol. 1998;32:1486-588.
3) Martinez-rios MA, Tovar S, Luna J, Eid-Lidt G. Percutaneous Mitral Commissurotomy. Cardiol Review 1999,7:108-16.
4) Banning AP, Pearson JF, Hall RJ. Role of balloon dilatation of the aortic valve in pregnant patients with severe aortic stenosis. Br Heart J 1993;70:544-45.
5) Elkayam U. Pregnancy through a prosthetic heart valve. J Am Coll Cardiol 1999;33:1642-5.
6) Chan WS, Anand S, Ginsberg JS. Anticoagulation
Published in Journal of Saudi Heart Association
Pregnancy causes dramatic, usually reversible, changes in a woman’s cardiovascular system. Maternal heart disease (present in 2%) of all pregnancies is the most important non-obstetric cause of death in pregnant women. Valvular heart disease may have a significant impact on fetal and maternal health during pregnancy, labor, and delivery. Pregnant women with valvular heart disease should be managed by a high-risk obstetric service that can provide cardiology consultation, close obstetric supervision and provisions for delivery with hemodynamic monitoring when required.(1)
Valvular heart lesions associated with high maternal and/or fetal risk during pregnancy include severe aortic stenosis, aortic and mitral regurgitation with functional class III-IV symptoms, mitral stenosis with class II-IV symptoms, aortic and/or mitral valve disease resulting in severe pulmonary hypertension or associated with severe LV dysfunction and mechanical prosthetic valve requiring anticoagulation. On the other hand, valvular heart lesions associated with low maternal and fetal risk include asymptomatic mild to moderate aortic stenosis with normal LV systolic function, aortic or mitral regurgitation with NYHA functional class I or II with normal LV systolic function, mitral valve prolapse with mild to moderate MR, and mild to moderate mitral stenosis without severe pulmonary hypertension.(2)
Young pregnant women with a previous history of acute rheumatic fever and carditis should continue to receive penicillin prophylaxis as indicated in the non-pregnant state. The most common rheumatic lesion in this age group remains mitral stenosis (MS). Patients with mild to moderate MS can almost always be managed with judicious use of diuretics and B-blockade. Diuretics are given to relieve pulmonary and excess systemic venous congestion. Patients with severe MS who are symptomatic before conception should be considered for percutaneous balloon mitral valvotomy before conception. Patients with severe MS who develop NYHA functional Class III-IV symptoms during pregnancy should undergo percutaneous balloon valvotomy.(2) The reported results with mitral balloon valvotomy have been excellent.(3) In developing countries, there is a long history of successful surgical closed commissurotomy for pregnant women.
Patients with mitral regurgitation (MR) usually tolerate pregnancy and can be managed medically. Medical management includes diuretics for patients with pulmonary congestion. Vasodilator therapy is indicated only in the presence of concomitant systemic hypertension and should not be advised in the setting of normal or low systemic blood pressure. ACE inhibitors are considered unsafe in pregnancy while hydralazine and nitrates are known to be safe.
Patients with mild to moderate aortic stenosis (AS) and normal LV systolic function can usually be managed conservatively through the entire pregnancy. Patients with pressure gradient >50 mm Hg or symptoms should be advised to delay conception until relief of AS can be obtained. For those with severe AS whose disease is first appreciated during pregnancy, consideration may have to be given to either percutaneous aortic balloon valvotomy (4) or surgery before labor if heart failure has developed or syncope has occurred. These procedures are fraught with danger to both the mother and fetus.
Isolated aortic regurgitation (AR), like MR, can usually be managed medically with a combination of diuretics and, if necessary, vasodilator therapy. Women with symptoms and/or signs of LV failure should be carefully monitored throughout labor and delivery with strict attention to volume status and blood pressure.
The approach to the patient with tricuspid valve involvement as part of a more complex congenital or acquired heart disease is predicated on the features of the associated lesions. Isolated TR should not pose a significant problem, although greater care may be necessary to protect against diuretic-induced hypoperfusion.(2) Vasodilators and digoxin are unlikely to be beneficial.(5)
The management of women with prosthetic heart valves during pregnancy poses a particular challenge as there are no available guidelines for effective antithrombotic therapy.(6)
Warfarin crosses the placenta and has been associated with an increased incidence of spontaneous abortion, prematurity, and stillbirth. Warfarin embryopathy occurs in 4% to 10% of patients.(7) The risk may be dose-related and appears to be highest if exposure occurs during the 6th to 12th weeks of gestation.
Heparin does not cross the placenta and is generally considered safer. Its long-term use, however, is complicated by sterile abscesses, osteoporosis, thrombocytopenia, and bleeding. Subcutaneous administration of heparin has been reported to be ineffective in preventing thromboembolic complications.(6) Thromboembolic complications, including fatal valve thrombosis, in high-risk pregnant women managed with subcutaneous heparin was reported in 12-24% of patients.(8) Thromboembolism, however, has been reported mostly in patients with older-generation mechanical valves (Starr-Edwards, Bjork-Shiley and so forth) in the mitral portion.(5) These findings led to recommendations included in the American College of Cardiology/American Heart Association Guidelines for the use of Warfarin as an anticoagulant of choice for the first 35 weeks of pregnancy in patients with a mechanical prosthetic valve. These guidelines state that “the decision whether to use heparin during the first trimester or to continue oral anticoagulation throughout pregnancy should be made after full discussion with the patient and her partner; if she chooses to change to heparin for the first trimester, she should be made aware that heparin is less safe for her, with a higher risk of both thrombosis and bleeding. High-risk women who choose not take warfarin during the first trimester should receive continuous heparin intravenously. Transition to warfarin can occur thereafter”(2).
These recommendations have been problematic and have not been adopted by both patients and physicians, especially in United States. Women in general are not willing to take warfarin during the first trimester of pregnancy.(5) The attitude of physicians is reflected by the fact that 96% of 438 members of the Society of Perinatal Obstetricians surveyed on their preferred management of a pregnant patient with a mechanical prosthesis in the mitral position selected discontinuation of warfarin and use of full-dose heparin for the duration of pregnancy.(9)
Vitale et al recently made an important contribution demonstrating a close dependency between warfarin dosage and fetal complications. In his study, 22 of 25 pregnant women (88%) whose warfarin dose was >5 mg/day had fetal complications with a 9% incidence of warfarin embryopathy. In contrast, only 5 of 33 cases (15%) treated with a small dose warfarin (< 5 mg/day) had fetal complications and non of them had warfarin embryopathy.(10) These findings may suggest the feasibility of risk free use of warfarin during pregnancy in patients with prosthetic heart valves who can be well anticoagulated with < 5 mg of warfarin per day.
Meschengieser et al recently studied 92 pregnancies in 59 women with mechanical heart valve prosthesis. In 31 pregnancies, subcutaneous heparin was started when pregnancy was diagnosed and in the second trimester oral anticoagulants were resumed. In 61 pregnancies oral anticoagulants were continued during the first trimester. Abortion or fetal losses were similar in the two groups while embolic episodes were more common (p=.0029) in women who received heparin (4.92%) compared with those on oral anticoagulants (0.33%).(11)
Recently Chan et al(6) made a systematic review of the literature and found that the use of oral anticoagulants throughout pregnancy was associated with warfarin embryopathy in 6.4% of live births. The substitution of heparin at or prior to 6 weeks, and continued until 12 weeks, eliminated this risk. The regimen associated with the lowest risk of valve thrombosis (3.9%) was the use of oral anticoagulants throughout; using heparin only between 6 and 12 weeks’ gestation was associated with increased risk of valve thrombosis (9.2%).(6)
The additional use of low-dose aspirin should be considered, particularly in women with high-risk valves, women with previous transient ischemic attacks and/or strokes, and women with atrial fibrillation.(12)
A more recent and theoretically more promising approach consists of therapy with low-molecular-weight heparins (LMWH), which do not cross the placenta, do not require frequent partial thromboplastin time monitoring and have a longer half-life than sodium heparin.(1) There is a great deal of interest in the use of LMWH as a substitute for unfractionated heparin in patients with prosthetic heart valves during pregnancy. The data to support the use of LMWH, however, is not yet available. A successful use of LMWH was reported in small number of patients and more information is required before LMWH can be recommended for anticoagulation in a patient with a prosthetic valve during pregnancy.(5) Recently, two cases of LMWH treatment failure resulting in thrombosed prosthetic heart valves were reported.(13)
Another important issue related to pregnancy is whether pregnancy affects the durability of valvular bioprostheses or not. Anecdotal reports of early failure of biological heart valves in pregnant patients tend to raise concerns. (14) Recently Salazar et al(15) reported data from 48 women who became pregnant after bovine pericardial valve replacement. Their data confirm recent reports that pregnancy does not significantly affect durability of bioprosthesis. In their study, the actuarial freedom from dysfunction was 90.4% at 5 years and 77% at 8 years for the pregnancy group and 86.3% and 73.4% respectively, for the control group (p = not significant). This study, however, has more than one limitation. First, the number of patients is relatively small, and secondly, the study is limited to the hard end points of death and reoperation. Conceivably, pregnancy could cause more subtle valvular dysfunction not detected by analysis of death and reoperation. The primary implication of this study is that bioprostheses remain the devices of choice for young women willing to trade earlier operation for the opportunity of pregnancy.(16)
References:
1) Teerlink JR, Foster E. Valvular Heart Disease in Pregnancy. Cardiol Clin 1998,16:573-95.
2) Bonow RO, Carabello B, de Leon AC Jr, Edmunds LH Jr, Fedderly BJ, Freed MD, Gaasch WH, McKay CR, Nishimura RA, O’Gara PT, O’Rourke RA, Rahimtoola SH. ACC/AHA guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients With Valvular Heart Disease). J Am Coll Cardiol. 1998;32:1486-588.
3) Martinez-rios MA, Tovar S, Luna J, Eid-Lidt G. Percutaneous Mitral Commissurotomy. Cardiol Review 1999,7:108-16.
4) Banning AP, Pearson JF, Hall RJ. Role of balloon dilatation of the aortic valve in pregnant patients with severe aortic stenosis. Br Heart J 1993;70:544-45.
5) Elkayam U. Pregnancy through a prosthetic heart valve. J Am Coll Cardiol 1999;33:1642-5.
6) Chan WS, Anand S, Ginsberg JS. Anticoagulation
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