While there may be one or more causes of Primary Pulmonary Hypertension, recent studies have found certain anti-depressant medications and weight loss suppressants are the known culprits. Most people who are diagnosed with this disease are sensitive to certain internal or external factors which constrict the blood vessels when exposed to these factors.
Case in point: Raynaud’s disease is a condition in which the fingers and toes turn blue when cold because the blood vessels in the fingers and toes are particularly sensitive to cold. Individuals with Raynaud’s disease are more likely to develop Primary Pulmonary Hypertension.
Moreover, diet suppressants such as Fen-Phen, has been the leading agent which has ultimately caused PPH and for which PPH lawsuits are on-going. Other factors contributing to Primary Pulmonary Hypertension include pregnant women who take anti-depressants, specifically Paxil or any of the other more common prescribed anti-depressant medications. Further, this has caused increased litigation among those women whose babies have been born with serious defects or, in some cases, died.
It is important to point out how PPH begins. It starts with injury to the layer of cells that line the small blood vessels of the lungs. As a result, the smooth muscle contracts more than normal and thereby narrows the vessel. The process eventually results in the development of extra amounts of tissue in the walls of the pulmonary arteries.
The amount of muscle increases in some arteries, and muscle appears in the walls of arteries that normally have no muscle. With time, scarring, or fibrosis, of the arteries takes place, and they become stiff as well as thickened. Some vessels may become completely blocked. There is also a tendency for blood clots to form within the smaller arteries.
Due to the demands placed on it by PPH, the heart muscle gets bigger, and the right ventricle expands in size. Becoming overworked and enlarged, the right ventricle gradually becomes weak and loses its ability to pump enough blood to the lungs. Eventually, the right side of the heart may fail completely, resulting in death.
This brings us to the treatment of Primary Pulmonary Hypertension and the drug Fen-Phen. Studies have revealed that treatment with this weight loss supplement increased the risk of PPH by 28 times. Therefore, individuals with Primary Pulmonary Hypertension developed this disease as a direct result of the drug Fen-Phen. Law firms who specialize in pharmaceutical litigation have been deeply involved in PPH lawsuits, and those who have been diagnosed with this disease by a PPH specialist, have sought a PPH attorney to handle such litigation.
Fen-Phen is a combination drug that was introduced for weight loss treatment in the 1990’s. It was recalled from the market by the FDA in 1997 because of data showing that this drug caused heart valve damage and PPH. Studies showed that patients who took these appetite suppressants, particularly those whose treatment lasted for more than three months, were much more likely to develop Primary Pulmonary Hypertension.
As mentioned earlier, the anti-depressant Paxil is just one of the known causes of Primary Pulmonary Hypertension in babies. This, too, has resulted in women retaining the services of a PPH attorney for the express purpose of filing PPH lawsuits on the newborn mom’s behalf.
Pregnant women and those who plan to become pregnant should avoid taking the anti-depressant Paxil if possible because of the risk of birth defects. Two studies of pregnant women who were taking Paxil during their first trimester have shown that their babies have heart defects at a rate that is as much as twice the norm.
However, a conundrum exists. The American College of Obstetricians and Gynecologists said the decision whether to treat pregnant women with SSRIs, a class of anti-depressants that includes Prozac, Zoloft and Lexapro as well as Paxil, should be considered on an individual basis.
However, it is clear that exposure to SSRIs late in pregnancy has been associated with short-term complications in newborns. A caveat, however, was also mentioned in that reproductive-age women have the highest prevalence of major depressive disorders. The benefit to the mother of treatment with any of the drugs may outweigh the risk to the fetus.
It is worth reiterating that Paxil, taken when pregnant, does pose a risk to the unborn.
In addition, if you or anyone you know has ever taken Fen-Phen, and are experiencing symptoms, it is vital that you seek a PPH attorney so that he or she can litigate this matter via a PPH lawsuit on your behalf. Moreover, it is important that you consult a PPH specialist immediately. PPH treatments, while they may be unable to stop the progression of the disease, can help to improve your quality of life.
Nick Johnson
http://www.articlesbase.com/health-articles/causes-of-primary-pulmonary-hypertension-135730.html
Pulmonary Hypertension?
Hi, I have recently been diagnosed with pulmonary hypertension. I had a follow up with my cardiologist. So far it is not known if I have PRIMARY, or SECONDARY pulmonary hypertension. I am going tomorrow to have a transesophageal echocardiogram test performed to see if there might be a clot, or a hole in my heart that is causing the PH. My Question is, other than a hole in the heart, or a blood clot somewhere, does anyone know of any other causes that could be considered primary pulmonary hypertension, that could be ruled out/ possibly treated, before I would be Diagnoses as having Secondary PH??? I know I can find out most of this at my appointment. tomorrow, but I am just really nervous and curious as well (not about the procedure, but the outcome). I also wanted to know before-hand so that I can ask the doc questions before I am under sedation for the procedure.
If anyone can help, I would greatly appreciate it.
This may help:
Diagnostic evaluation of pulmonary hypertension
Authors
Lewis J Rubin, MD
William Hopkins, MD
Section Editor
Jess Mandel, MD
Deputy Editor
Kevin C Wilson, MD
Last literature review version 17.1: January 2009 | This topic last updated: February 10, 2009 (More)
INTRODUCTION — Patients suspected of having pulmonary hypertension (PH) undergo extensive diagnostic testing. The goal of diagnostic testing is to confirm that PH exists and to identify its underlying cause. The diagnostic tests used to evaluate a patient with suspected PH will be reviewed here. The definition, classification, epidemiology, etiologies, pathogenesis, clinical manifestations, treatment, and prognosis of PH are discussed separately. (See "Overview of pulmonary hypertension" and see "Pathogenesis of pulmonary hypertension" and see "Treatment of pulmonary hypertension").
NOMENCLATURE — The World Health Organization (WHO) classifies patients with PH into five groups based upon etiology. Patients in the first group are considered to have pulmonary arterial hypertension (PAH), whereas patients in the remaining four groups are considered to have pulmonary hypertension (PH) (show table 1). When all five groups are discussed collectively, the designation PH is generally used. We adhere to this nomenclature in the discussion that follows. The WHO classification system is described in detail elsewhere. (See "Overview of pulmonary hypertension", section on Classification).
DIAGNOSTIC TESTS — Numerous diagnostic tests may be used to evaluate a patient with suspected PH. The sequence in which the tests are performed is determined by the patient’s clinical history and physical exam. (See "Recommended diagnostic approach" below).
Chest radiograph — The characteristic chest radiograph shows enlargement of the central pulmonary arteries with attenuation of the peripheral vessels, resulting in oligemic lung fields (show radiograph 1) (show radiograph 2). Right ventricular enlargement (diminished retrosternal space) and right atrial dilatation (prominent right heart border) may also be seen. Occasionally, the underlying cause of the PH is apparent on the chest radiograph (eg, interstitial lung disease).
Electrocardiography — The electrocardiogram (ECG) may demonstrate signs of right ventricular hypertrophy or strain (show ECG 1). In addition, findings suggestive of chronic right ventricular overload may exist, including right axis deviation, an R wave/S wave ratio greater than one in lead V1, incomplete or complete right bundle branch block, or increased P wave amplitude in lead II (P pulmonale) due to right atrial enlargement (show figure 1 and show ECG 2). Most ECG signs are specific but not sensitive for the detection of right ventricular disease. ECG changes cannot determine disease severity or prognosis [1,2].
Echocardiography — Echocardiography is performed to estimate the pulmonary artery systolic pressure and to assess right ventricular size, thickness, and function (show echocardiogram 1). In addition, echocardiography can evaluate right atrial size, left ventricular systolic and diastolic function, and valve function, while detecting pericardial effusions and intracardiac shunts Atrial septal defect color Doppler 2 Ventricular septal defect small four chamber color Doppler echocardiogram [3,4].
Echocardiography uses Doppler ultrasound to estimate the pulmonary artery systolic pressure. This technique takes advantage of the tricuspid regurgitation that usually exists. The maximum tricuspid regurgitant jet velocity is recorded and the pulmonary artery systolic pressure (PASP) is then calculated:
PAP systolic = (4 x tricuspid jet velocity squared) + RAP
where RAP is the right atrial pressure estimated from the size and respiratory variation of flow in the inferior vena cava. A systolic pulmonary artery pressure greater than 40 mmHg, which corresponds to a tricuspid regurgitant velocity on Doppler echocardiography of 3.0 to 3.5 m/sec, is suggestive of PH [5]. (See "Principles of Doppler echocardiography").
Doppler echocardiography is limited when an adequate tricuspid regurgitant jet can not be identified, or underlying cardiopulmonary disease alters cardiac function. Despite this, it is more accurate than clinical history and physical examination in detecting PH [6,7].
Patients with PH may have echocardiographic signs of right ventricular pressure overload, including paradoxical bulging of the septum into the left ventricle during systole and hypertrophy of the right ventricular free wall and trabeculae (show echocardiogram 4) Pulmonary hypertension short axis echocardiogram. As the right ventricle fails, there is dilation and hypokinesis, septal flattening, right atrial dilation, and tricuspid regurgitation (show echocardiogram 6) Pulmonary hypertension four chamber echocardiogram. Tricuspid regurgitation is not due to an intrinsic abnormality of the tricu
References :
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