Dalam hidup ada begitu banyak pilihan, ini berlaku juga dalam urusan diet. Nah, bila Anda sedang diet dan bingung mencari pengganti makanan sehat dan langsing, Berikut ini tips Hidup Lebih Sehat Dengan Alternatif Makanan Pengganti:

1. Ganti Nasi Putih Dengan Kentang Rebus. Nasi sebagai sumber karbohidrat memang bagus sebagai energi. Namun, sesekali ada baiknya Anda mengganti dengan kentang. Kentang mempunyai jenis kerbohidrat komplek, yang sangat baik untuk melancarkan metebolisme tubuh. Kentang juga mengandung zat gula lebih sedikir disbanding nasi.

2. Ganti Beras Putih Dengan Beras Merah. Kandugan gizi beras merah, lebih tinggi dibandingkan dengan beras putih. Zat gizi pada beras, termasuk serta banyak diperoleh dari kulit ari. Sayangnya, dengan proses penggilingan, menyebabkan banyak zat gizi yang hilang.

3. Ganti Roti Putih Dengan Roti Whole Grain. Bila Anda menggantikan tepung terigu biasa dengan gandum utuh misalnya pada roti, cereal atau pun pasta, pasti ada banyak manfaat bagi kesehatan. Ada soluble fiber (serta yang dapat laru dalam air) yang ditemukan dalam gandum, dapat menurunan kadar insulin dan kolesterol jahat.

4. Ganti Seperempat Daging Dengan Ikan. Ikan amat ideal sebagai sumber protein bagi tubuh karena mengandung lemak yang bagus. Dipastikan beberapa jenis ikan seperti salmon, mengandung asam lemak omega 3, yang amat penting bagi kesehatan jantung dan otak Anda.

5. Ganti Seperempat gula dalam resep kue, dengan jumlah yang sama nonfat powdered milk. Kurangi pemakaian gula saat membuat kue, cake atau roti. Ini akan membuat lidah terbiasa dengan pemakaian gula yang sedikit, dan membantu seluruh diet Anda. Pengurangan gula ini juga sebagai bagian program awet muda. Selain itu, gula dapat membuat Anda gemuk dan risiko diabetes. Secara perlahan pemakaian gula yang tinggi dapat menyebabkan glycosylation. Ini merupakan prose molekul-molekul gula dapat mendukung menjadi molekul protein, yang menyebabkan kerusakan sel-sel, dan dapat meningkantkan peradangan, dan menybarkan penyumbatan pembuluh darah.

6. Ganti Sekantong Keripik dengan Irisan Apel. Sepotong apel tidak mengandung lemak, hanya mengandung beberapa kalori, serta tinggi dan antioksidan. Lalu, apa yang ditawarkan keripik kentang? Faktanya, mengandung zero nutrisi alias nihil, dank arena digoreng sudah pasti banyak mengandung minyak, kalori dan garam.

7. Ganti Mil Chocolate dengan Dark Choolate. Dark Chocolate mengandung sedikitnya 60% cocoa, yang merupakan sumber antioksidan yang sangat baik, dengan melindungi sel-sel dari kerusakan. Bandingkan dengan milk chocolate yang hanya mempunyai kandungan coca lebih sedikt. Kabar baikya, lemak dalam dark chocolate tidak meningkatkan kolesterol.

8. Soda dengan Teh. Teh ini juga mengandung antioksidan dibandingkan buruknya gula dalam sekaemng soda. Teh, baik yang hijau atau hitam, dinikmati pasa atau dingin, mempunyai banyak manfaat nutrisi yang baik. Manfaat teh juga banyak untuk merendahkan kolesterol, dan juga termasukmelangsingkan tubuh.

9. Ganti Soda Dengan Air Putih. Hingga kini, terbukti tidak ada minuman yang lebih baik untuk tetap menjaga kadar air yang cukup dalam tubuh, selain air putih. Air putih juga mempunyai peran amat penting, agar istem metabolism di tubuh Anda berjalan mulus. Bila Anda minum soda diet, umumnya mmang dapat mengatsi rasa haus. Namun perlu diingat, banyak ahli yang mengkhawatirkan pemakaian gula buatan, -meskipun sudah dinyatakan aman –dapat menyebabkan kanker.

10. Ganti Regular Yogurt Dengan Low Fat atau Fat Free Yogurt. Produk makanan atau minuman dari susu sapi (dairy food) memang merupakan sumber dari kalsium dan vitamin D, untuk mencegah kerpos tulang. Namun, hadirnya saturated fat dalam whotel milk, cheese dan yogurt dapat juga menjadi penyebab penyumbatan arteri. Beralih ke yogurt yang rendah atau tanpa lemak, Anda dapat mereguk seluruh manfaat susu bagi tubuh tanpa khawatir.

11. Ganti Anggut Putih Dengan Anggur Merah. Dibandingkan dengan Anggur Putih, Anggur Merah seperti halnya dark chocolate befungsi sebagi anti oksidan. Hal ini diperoleh dari kulit anggut merah yang dihancurkan. Dan kandungan alcohol yang terdapat pada anggur merah dapat mencegah penyumbatan darah. Namun mengingat manfaatnya, mesti dibarengi dengan jumlah yang wajar. Kuncinya, segelas anggur sehari, menurut sebuah penelitian, tampaknya mempunyai manfaat baik bagi kebanyakan wanita. Ingat, jangan berlebihan.

12. Ganti Apel Hijau Dengan Apel Merah. Sebenarnya apa pun pilihannya, mengonsumsi apel tetap yang terbaik. Namun, perlu juga diketahui, apel merah terbukti memiliki 2 kali lebih banyak aktivitas antioksidan disbanding yang hijau. Kadar antioksidan juga 5 kali lebih banyak daripada apel hijau.

What is PAH?

Pulmonary arterial hypertension (PAH) is a syndrome characterised by a progressive increase in pulmonary vascular resistance leading to right ventricular overload and eventually to right ventricular failure and premature death.¹

The increase in pulmonary vascular resistance is related to a number of progressive changes in the pulmonary arterioles, including:

Vasoconstriction
obstructive Remodelling of the pulmonary vessel wall through proliferation in the various layers of the blood vessel wall (smooth muscle cell and endothelial cell proliferation)

Inflammation

in-situ thrombosis.

The main histological features include medial Hypertrophy, intimal thickening, adventitial thickening, plexiform lesions and in-situ thrombosis (Figure 1). The plexifom lesion represents a focal proliferation of endothelial and smooth muscle cells and is pathognomonic of Pulmonary Arterial Hypertension (PAH).

Figure 1: Click to enlarge

Pulmonary Arterial Hypertension (PAH) is defined as a sustained elevation of mean pulmonary arterial pressure to more than 25 mmHg at rest or to more than 30 mmHg while exercising, with a normal pulmonary wedge pressure (< 15 mmHg).²

In most cases the earliest symptom is Dyspnoea on physical exertion. Other symptoms include syncope or near syncope, fatigue and peripheral oedema.^3,4 Chest tightness and pain similar to angina may occur, particularly on physical exertion.

References
1. Sitbon O et al. Long-term response to calcium channel blockers in idiopathic pulmonary arterial hypertension. Circulation 2005; 111: 3105-3111
2. Galiè N, Torbicki A, Barst RJ, et al. Guidelines on diagnosis and treatment of pulmonary arterial hypertension. Eur Heart J 2004;25:2243-2278.
3. Gaine SP, Rubin LJ. Primary Pulmonary Hypertension. Lancet 1998; 352: 719−25.
4. Barst RJ et al. Diagnosis and differential assessment of pulmonary arterial hypertension. J Am Coll Cardiol 2004; 43(Suppl S): 40S-47S

What is PAH in Systemic Sclerosis (SSc)?

The connection between PAH and Systemic Sclerosis

Pulmonary arterial hypertension (PAH) occurs in approximately one in seven scleroderma patients.¹ Pulmonary complications, namely PAH and pulmonary fibrosis, are a common cause of death in SSc patients.² Unfortunately, with such symptoms as breathlessness, fatigue on exercise and syncope, it can masquerade as other respiratory or cardiac complaints with devastating consequences.^{3, 4} Furthermore, some patients may have already reduced daily activities (i.e. mobility problems) and breathlessness may not be the first symptom. Therefore, PAH needs to be considered in the daily management of SSc patients and screening is the key to establishing early diagnosis. International guidelines recommend screening by Doppler echocardiography annually and/or in the presence of unexplained breathlessness.^{1,
4, 5} Effective treatments are now available which may improve quality of life and exercise capacity, slow disease progression and improve long-term outcome.⁶

If you suspect PAH, consider referring the patient to a centre with expertise in PAH.

References
1. Hachulla E, Coghlan JG. A new era in the management of pulmonary arterial hypertension related to scleroderma: endothelin receptor antagonism. Ann Rheum Dis 2004; 63:1009-14.
2. Steen V et al. Changes in causes of death in systemic sclerosis, 1972-2002. Ann Rheum Dis 2007; 940-944
3. Runo JR, Loyd JE. Primary pulmonary hypertension. Lancet 2003; 361:1533-44.
4. McGoon M, Gutterman D, Steen V et al. Screening, early detection, and diagnosis of pulmonary arterial hypertension: ACCP evidence-based clinical practice guidelines. Chest 2004; 126:14S−34S.
5.Galie N, Torbicki A, Barst R et al. Guidelines on diagnosis and treatment of pulmonary arterial hypertension. The Task Force on Diagnosis and Treatment of Pulmonary Arterial Hypertension of the European Society of Cardiology. Eur Heart J. 2004; 25:2243-78.
6.Badesch DB, Abman SH, Ahearn GS et al. Medical therapy for pulmonary arterial hypertension. ACCP evidence-based clinical practice guidelines. Chest 2004; 126:35S-62S.

What is PAH in Systemic Sclerosis (SSc)?

The connection between PAH and Systemic Sclerosis

How is PAH diagnosed?

The early symptoms of Pulmonary arterial hypertension (PAH) -such as Dyspnoea, dizziness and fatigue - are often mild and are common to many other conditions. At rest there are often no symptoms and no apparent signs of illness. As a result, diagnosis can be delayed for months or even years meaning that Pulmonary Arterial Hypertension (PAH) is frequently not recognised until the disease is relatively advanced.¹ Pulmonary Arterial Hypertension (PAH) is often diagnosed only once other conditions have been investigated and ruled out.

The non-specific nature of symptoms associated with Pulmonary Arterial Hypertension (PAH) means that the diagnosis cannot be made on symptoms alone. A series of investigations is required to make an initial diagnosis, to refine that diagnosis in terms of clinical class of pulmonary hypertension (please click here for classification of pulmonary hypertension) and to evaluate the degree of functional and haemodynamic impairment (Figure 2). Consequently, it can be useful to adopt a four stage approach:

Clinical suspicion of pulmonary hypertension

Breathlessness (dyspnoea) without overt signs of specific heart or lung disease
Screening of patients with associated conditions (Connective Tissue Disease, Congenital heart disease, HIV, Sickle Cell Disease)
Incidental findings on examination for other clinical reasons

Detection of pulmonary hypertension

ECG
Chest radiograph, may show evidence of cardiomegaly and enlarged pulmonary arteries (Figure 3)
Doppler echocardiogram (Figure 2)

Identify other causes of Pulmonary hypertension

pulmonary function tests (PFTs) and arterial blood gas samples
ventilation and perfusion lung scan
high resolution computed tomography (HRCT)
pulmonary angiography

4.	Pulmonary Arterial Hypertension (PAH) evaluation and classification (type, functional capacity, haemodynamics)
	blood tests and immunology, HIV test, abdominal ultrasound scan 6 minute walk test (6-MWT) and peak VO2 Right heart catheterisation and vasoreactivity testing.

Figure 2: Click to enlarge

Figure 3: Click to enlarge

Echocardiography - value as a screening tool
Transthoracic Doppler-echocardiography (TTE) is a non-invasive screening test for pulmonary hypertension. TTE is able to estimate pulmonary arterial systolic pressure, which is equivalent to right ventricular systolic pressure in the absence of pulmonary outflow obstruction, and can provide additional information about the cause and consequences of PH, including right and left ventricular dimensions and function, heart valve abnormalities, right ventricular ejection and left ventricular filling characteristics and presence of a pericardial effusion. In the initial investigation of patients with Pulmonary Arterial Hypertension (PAH) it is important to obtain adequate images of the right heart. Pulmonary arterial pressure can be estimated from the tricuspid regurgitant (TR) jet (Figure 4).

Chest radiograph in PAH - Click this image to enlarge.

Figure 4: Click to enlarge

Right heart catheterisation - the diagnostic gold standard
Right heart catheterisation is required for a definitive diagnosis of Pulmonary Arterial Hypertension (PAH) (Figure 5 and 6),^1,2 to assess the severity of haemodynamic impairment and to test the vasoreactivity of the pulmonary circulation. The following parameters should always be assessed: right atrial pressure (RAP), pulmonary arterial pressure (PAP [systolic, diastolic and mean]), pulmonary capillary wedge pressure (PCWP), cardiac output / index, pulmonary (PVR) and systemic vascular resistance, blood pressure and arterial and mixed venous oxygen saturation.
Pulmonary Arterial Hypertension (PAH) is defined as a sustained elevation of mean pulmonary arterial pressure to > 25 mmHg at rest or to > 30 mmHg while exercising, with a mean pulmonary wedge pressure or left ventricular end-diastolic pressure of < 15 mmHg and pulmonary vascular resistance of ≥3 woods units.³ A positive vasoreactive response is defined as a reduction in mean Pulmonary artery pressure (mPAP) ≥ 10 mmHg to reach an absolute value of mPAP ≤ 40 mmHg with an increase or unchanged cardiac output. A positive response is shown in only 10-15% of patients, and sustained response is shown in even fewer (less than 7%).⁴

Figure 5.

Figure 6: Click to enlarge

6-minute walk test - evaluation of exercise capacity
In patients with Pulmonary Arterial Hypertension (PAH), the 6-MWT is reflective of a patients' ability to exercise; the distance a Pulmonary Arterial Hypertension (PAH) patient can walk in 6 minutes is a critical endpoint in studies evaluating the benefit of different therapeutic options.

To allow meaningful comparisons, it is important that the 6-MWT be performed under supervision according to a standardised protocol.⁵

A 30 m corridor should be available, marked at 3 m intervals
The patient should rest for at least 10 minutes prior to the test and should not have performed any rigorous exercise within the previous 2 hours
The patient should be asked to rate their baseline dyspnoea
The patient should be instructed to walk to their maximum capacity but not to run or jog; they should be permitted to rest as necessary
The supervisor should count each lap as the patient finishes it
The patient should be asked to rate their dyspnoea at the end of the test
The test should be repeated at approximately the same time of day on each occasion

References
1. Gaine SP, Rubin LJ. Primary Pulmonary Hypertension. Lancet 1998; 352: 719-25-
2. Barst RJ, McGoon M, Torbicki A et al. Diagnosis and differential assessment of pulmonary arterial hypertension. J Am Coll Cardiol 2004;43 (Suppl S): 40S-47S
3. Galiè N, Torbicki A, Barst RJ, et al. Guidelines on diagnosis and treatment of pulmonary arterial hypertension. Eur Heart J 2004;25:2243-2278.
4. Sitbon O, Humbert M, Jaïs X et al. Long-term response to Calcium channel blockers in idiopathic pulmonary arterial hypertension. Circulation 2005; 11:3105-11
5. ATS. ATS statement: guidelines for the 6-minute walk test. Am J Crit Care 2002; 166: 111-7.

How is PAH treated?

There is currently no cure for Pulmonary arterial hypertension (PAH) but advances in understanding how the disease develops (see section: Why does PAH develop?

) means that there are now treatments available which have helped to improve prognosis for patients with this disease.

The main treatment options for patients with Pulmonary Arterial Hypertension (PAH) are:¹

Treatments that are routinely used but with little evidence of an impact on the disease:

Anticoagulants, such as warfarin, to address the observed thrombotic changes and potential predisposition in the pulmonary microcirculation for in-situ thrombosis
Diuretics, for treatment of right heart failure
oxygen therapy, to maintain oxygen saturation at > 90% at all times.
calcium-channel blockers (CCBs). Less than 10% of IPAH patients benefit from CCBs therapy. This figure is even lower in other forms of Pulmonary Arterial Hypertension (PAH). If not used in appropriate candidates (patients with demonstrated vasoreactivity during Right heart catheterisation), CCBs can decrease cardiac output and systemic vascular resistance without any improvement in PAP and PVR and therefore may be deleterious.²

Treatments that have been specifically studied in Pulmonary Arterial Hypertension (PAH)

endothelin receptor antagonists - endothelin is implicated in the pathogenesis of Pulmonary Arterial Hypertension (PAH) through actions on the pulmonary vasculature. Endothelin is found to be elevated in patients with Pulmonary Arterial Hypertension (PAH) and levels of endothelin are directly related to disease severity and prognosis. Endothelin receptor antagonists (ERAs) are oral treatments that either block the ET_A receptor alone or both the ET_A and ET_B receptors.^3,4
Prostacyclin analogues - may be delivered by continuous intravenous or subcutaneous infusion or via an intermittent nebuliser.¹ To date, oral agents have shown limited effectiveness
phosphodiesterase 5 inhibitors - oral agents which induce relaxation and antiproliferative effects on vascular smooth muscle cells by preventing the reduction in levels of cGMP.⁵

In very severe cases surgical options may be considered:

balloon atrial septostomy
heart and lung transplantation - the use of transplantation is constrained by the limited number of donor organs.

References
1. Humbert H et al. Treatment of pulmonary arterial hypertension. N Engl J Med 2004; 351: 1425-36
2. Sitbon O, Humbert M, Jaïs X et al. Long-term response to Calcium channel blockers in idiopathic pulmonary arterial hypertension. Circulation 2005; 11:3105-11
3. Channick RN, Simonneau G, Sitbon O et al. Effects of the dual endothelin-receptor antagonist bosentan in patients with pulmonary hypertension: a randomised placebo-controlled study. Lancet 2001;358:1119-23
4. ESC Guidelines. Guidelines to diagnosis and treatment of pulmonary arterial hypertension. European Heart Journal 2004; 25:2243-78
5. Galiè N et al. Sildenafil citrate treatment for pulmonary arterial hypertension. N Engl J Med 2005; 353: 2148-57

Assessing the severity of PAH

The severity of symptoms and the degree of physical limitation in patients with Pulmonary Arterial Hypertension (PAH) may be assessed by World Health Organization functional class, WHO FC (see Table 1 below). Such assessment provides useful information on the current level of physical function, correlates to prognosis and can help guide decisions on therapy. There are four WHO functional classes for Pulmonary Arterial Hypertension (PAH), with class I being the least severe and class IV being the most advanced.¹

Pulmonary Arterial Hypertension (PAH) is a devastating disease, which can progress rapidly, even in mildly symptomatic patients. Without treatment, patients in WHO FC II can rapidly deteriorate within 6 months to more advanced Pulmonary Arterial Hypertension (PAH) as evidenced by progression of symptoms.²

Table 1. NYHA/WHO Classification of Functional Status of Patients With Pulmonary Hypertension¹

Class	Symptomatic profile
Class I	Patients with pulmonary hypertension but without resulting limitation of physical activity. Ordinary physical activity does not cause Dyspnoea or fatigue, chest pain or near syncope
Class II	Patients with pulmonary hypertension resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity causes undue dyspnoea or fatigue, chest pain or near syncope
Class III	Patients with pulmonary hypertension resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary activity causes undue dyspnoea or fatigue, chest pain or near syncope
Class IV	Patients with pulmonary hypertension with inability to carry out any physical activity without symptoms. These patients manifest signs of right heart failure. Dyspnoea and/or fatigue may even be present at rest. Discomfort is increased by any physical activity.

References
1. Barst RJ, McGoon M, Torbicki A, et al. Diagnosis and differential assessment of pulmonary arterial hypertension. J Am Coll Cardiol 2004;43:40S-47S.
2. Galiè N, Rubin LJ, Hoeper MM et al. Treatment of patients with mildly symptomatic pulmonary arterial hypertension with bosentan (EARLY study): a double-blind, randomised controlled trial. Lancet 2008; 371: 2093-2100

Early identification and intervention of PAH

Early diagnosis and therapeutic intervention may offer improved outlook for patients. Prognosis and response to treatment have both been shown to be better for patients in less severe WHO functional class (WHO FC) compared with those who do not begin targeted therapy until their Pulmonary Arterial Hypertension (PAH) is in a more severe stage (ie, WHO FC III/IV)¹ (see section, ‘Assessing the severity of PAH'

By recognising and treating patients as early as possible, disease progression may be delayed. However, this poses a challenge to healthcare professionals because many of the initial symptoms of Pulmonary Arterial Hypertension (PAH) - breathlessness, chest tightness and fatigue - are mild and non-specific and so many patients are diagnosed when their disease is already quite severe.² Although the mean time from onset to diagnosis is estimated to be approximately two years,² different patients will progress at different rates, which depend on various factors (see section, ‘How is PAH diagnosed?'

) . This makes it even more important to diagnose early.

References
1. Sitbon O, Humbert M, Nunes H, et al. Long-term intravenous epoprostenol infusion in primary pulmonary hypertension: prognostic factors and survival. J Am Coll Cardiol 2002;40:780-788.
2. Humbert M, Sitbon O, Chaouat A, et al. Pulmonary arterial hypertension in France: results from a national registry. Am.J.Respir.Crit Care Med. 2006;173:1023-1030.

Screening for PAH

The key to early diagnosis is introducing screening for high risk patient populations if they are asymptomatic.

High risk patient populations include:
• Family members of a patient with familial Pulmonary Arterial Hypertension (PAH)
• Patients with systemic sclerosis (SSc)
• Patients with HIV
• Patients with portopulmonary hypertension (PoPH)

The results of a disease registry in France indicated that without screening, the majority of patients were diagnosed in FC III or FC IV, and only 24% of patients were in FC II at diagnosis.¹ (See Fig. 1, left panel.) Furthermore, the results of a national screening programme in a high-risk population indicated that it is possible to detect Pulmonary Arterial Hypertension (PAH) in an earlier stage in a high-risk population (see Fig. 1, right panel).²

Figure 1. WHO FC at diagnosis, with or without screening
Humbert et al 2006 Am.J.Respir.Crit Care Med. 173, Hachulla et al 2005 Arthritis Rheum. 52

International guidelines now recommend annual screening high-risk groups with Doppler echocardiography.^3-5 Doppler echocardiography is currently the most effective method for screening, however, for a definitive diagnosis right heart catheterisation has to be performed (see ‘How is PAH diagnosed?'

References
1. Humbert M, Sitbon O, Chaouat A, et al. Pulmonary arterial hypertension in France: results from a national registry. Am.J.Respir.Crit Care Med. 2006;173:1023-1030.
2. Hachulla E, Gressin V, Guillevin L, et al. Early detection of pulmonary arterial hypertension in systemic sclerosis: a French nationwide prospective multicenter study. Arthritis Rheum. 2005;52:3792-3800.
3. Hachulla E and Coghlan JG. A new era in the management of pulmonary arterial hypertension related to scleroderma: endothelin receptor antagonism. Ann.Rheum.Dis. 2004;63:1009-1014.
4. Galiè N, Torbicki A, Barst RJ, et al. Guidelines on diagnosis and treatment of pulmonary arterial hypertension: The Task Force on Diagnosis and Treatment of Pulmonary Arterial Hypertension of the European Society of Cardiology. Eur Heart J 2004;25:2243-2278.
5. McGoon M, Gutterman D, Steen V, et al. Screening, early detection, and diagnosis of pulmonary arterial hypertension: ACCP evidence-based clinical practice guidelines. Chest 2004;126:14S-34S.

MAGENTA

Minggu, 25 Desember 2011

Merawat Perhiasan

Meanings and history of the name Magenta:

Jumat, 16 Desember 2011

Makanan Penganti

What Is Pulmonary Arterial Hypertension ??

What is PAH?

What is PAH in Systemic Sclerosis (SSc)?

The connection between PAH and Systemic Sclerosis

What is PAH in Systemic Sclerosis (SSc)?

The connection between PAH and Systemic Sclerosis

How is PAH diagnosed?

How is PAH treated?

Assessing the severity of PAH

Early identification and intervention of PAH

Screening for PAH