Consecutive studies have revealed that plasminogen activator inhibitor type 1 (PAL-1) is a risk factor for cardiovascular disease (CVD) and other related ailments such as myocardial infarction and angina pectoris (Crainich et al, 2003, p. 1799). PAL-1 in conjunction with tissue-type plasminogen activator (t-PA) has also been identified as risk factors for hypertension, diabetes and thromboembolic disease (Asselbergs et al, 2007, p. 313).
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Indeed, elevated circulating PAL-1 has been implicated as a risk factor for stroke in patients with end-stage renal disease (Petrie et al, 2004, p.2267). To date, data seeking to explain the association between cardiovascular diseases and enhanced levels of PAL-1 has not been described and documented comprehensively (Asselbergs et al, 2007, p. 313). This paper attempts to critically evaluate how PAL-1 increases the risk of cardiovascular diseases between genders.
PAL-1 is vitally important in the proper functioning of many body processes. By description, PAL-1 is the primary inhibitor of the vital activators of plasminogen in the body, namely the tissue plasminogen activator (t-PA) and by extension, Urokinase (Bosnyak et al, 2003, p. 148). According to Kellerman (n.d.), PAL-1 is secreted by the adipose tissue. Elevated levels of PAL-1 are widely believed to trigger a partial or complete malfunction of fibrinolysis; a process that oversees the physiological breakdown of potentially fatal blood clots in blood vessels. Crainich et al (2003) argues that “during fibrinolysis, plasminogen is converted to plasmin, which in turn lyses fibrin clots.” (p. 1799).
According to Bosnyak (2003, p. 148) fibrinolysis is an intricate process that thwarts excess fibrin accumulation in the blood vessels. The serene protease inhibitor PAL-1 is largely viewed as the controlling agent of these conversions which occurs in the presence of Urokinase plasminogen activator (u-PA). The conversions are also known to occur in the presence of tissue plasminogen activator (t-PA).
According to Asselbergs et al (2007, p. 314), both males and females are affected by cardiovascular diseases in diverse ways. Great variations have been noted between the genders in terms of the onset of the cardiovascular ailment, diagnosis, treatment procedures and treatment responses. Research has revealed that males develop cardiovascular disease at an early age than females. According to Asselbergs et al (2007), “…variability in traditional and novel risk factors between genders may account for the different risk profiles and might provide a framework for gender-specific diagnosis and treatment of cardiovascular disease” (p. 314). In addition to these factors, consecutive studies have correlated PAL-1 to a number of cardiovascular complications affecting humans across gender.
Available literature reveals that enhanced levels of PAL-1 are indirectly to blame for an increase in cholesterol and triglycerides by the very nature of inhibiting the fibrinolysis process (Asselbergs et al, 2007, p. 313). According to the researchers, increased levels of PAL-1 are also known to trigger conditions that jeopardize the proper functioning of cardiovascular activities such as increasing the systolic and diastolic blood pressure in the vessels, and inhibiting urinary albumin excretion. It should be noted that these conditions are triggered by the partial or complete failure of the fibrinolysis process. As such, numerous heart conditions such as coronary artery disease (CAD) and heart failure have been linked to the augmented levels of PAL-1 in the blood system (Bosnyak et al, 2003, p. 148).
Indeed, contemporary treatment procedures for some heart conditions centres around coming up with effective strategies and procedures that can be effectively used to limit PAL-1 to the required levels. A study conducted by Petrie (2004, p. 2267) revealed that targeting PAL-1 in treatment procedures can assist medical professionals in the management and treatment of cardiovascular-related conditions. In the study conducted by Petrie and others, patients treated with calcitriol and paricalcitol exhibited considerable reductions of PAL-1 in their endothelial cells.
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According to Sobel et al (1998, p. 2214) and Bosnyak et al (2003, p. 148), inhibition of the fibrinolysis process caused by elevated concentrations of PAL-1 in the blood is also associated with reported instances of insulin resistance, type 1 and type 2 diabetes and hyperinsulinemia. According to available statistics, diabetic patients are two to four times more likely to suffer from cardiovascular artery disease (CAD) than individuals with no known incidences of diabetes (Bosnyak et al, 2003, p. 148).
Such a revelation clearly points to the intricate relationship that exists between PAL-1, fibrinolysis, diabetic conditions and cardiovascular-related ailments. According to the researchers, insulin resistance only serves to worsen the situation. Consequently, a multiplicity of haemostatic abnormalities in diabetic patients occasioned by acute failure in the fibrinolytic system is known to cause unpronounced cases of CAD. It should be noted that the starting point of this interplay of factors and influences is the enhanced level of PAL-1 in the blood triggered by a wide array of factors. In diabetic patients, elevated concentrations of PAL-1 can be triggered by insulin resistance (Sober et al, p. 2216).
Patients suffering from end-stage renal disease (ESRD) have also been found with an impaired fibrinolysis. Indeed, patients undergoing the process of haemodialysis for ESRD have exhibited a high mortality rate arising from cardiovascular-related ailments (Petrie et al, 2004, p. 2266). According to Bergstein, Riley & Bang (1992, p. 756), kidney failure affects its capacity to remove some of the harmful impurities found in the blood. Some of the impurities are known to elevate the concentrations of PAL-1 in the blood, triggering a scenario that inhibits the proper functioning of fibrinolysis.
According to Crainich (2003, p. 1799), the process of fibrinolysis is charged with the responsibility of overseeing physiological breakdown of potentially deadly blood clots in blood vessels. Cardiovascular-related ailments such as CAD are bound to occur if the process of fibrinolysis fails to act on the blood clots. A study conducted by Bergstein, Riley & Bang (1992, p. 758) revealed that treatment procedures that revolved around stabilizing PAL-1 levels in patients with kidney problems had a positive impact on renal function. Normalization of PAL-1 levels in such patients can be achieved through peritoneal dialysis.
The significance of clearly understanding the implications of PAL-1 in the containment of cardiovascular-related diseases can never be underestimated. Indeed, statistics reveal that instances of fatalities arising from cardiovascular-related conditions have been on the increase worldwide (Crainich et al, 2003, p.1800). According to the above discussion, the fact that PAL-1 is largely to blame for the rising numbers of patients exhibiting cardiovascular-related conditions is undeniable.
However, data relating to the inhibitor and its effects on the proper functioning of the body system, especially the blood vessels, has never been collated or documented to levels that may positively assist all stakeholders to manage the problem. From the discussion, it is possible for health professionals to sketch the interplay of factors and influences that exist between PAL-1, fibrinolysis and a wide array of cardiovascular ailments that continue to affect populations around the world.
Although there exist some challenges about the collation and documentation of available data and statistics relating to PAL-1, the fact that elevated levels of the hormone has been constantly accused of causing cardiovascular-related complications cannot be viewed as controversial. This particular discussion has intensively relied on a number of studies done by credible researchers who have posted resoundingly similar results in terms of PAL-1 and cardiovascular diseases.
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Until now, it may not be clear how elevated levels of PAL-1 in the blood affects different individuals according to race, age-category or gender (Sobel et al, 1998, p. 2217). But according to the selected study readings for this particular discussion, the fact that an elevated concentration of PAL-1 is to blame for cardiovascular ailments is not contested. In this perspective, this topic cannot be termed as controversial.
In conclusion, it is important to note that an elevated level of PAL-1 is not sorely responsible for causing the discussed ailments. In retrospect, increases of PAL-1 in the blood stream triggers a dysfunction of the body’s natural ability to deal with blood clots in the vessels (Crainich, 2003, p. 1781). This dysfunction is believed to cause many heart-related conditions such as CAD and heart failure. This study has also revealed the correlation that exists between PAL-1, other medical conditions such as diabetes and renal failure, and, ultimately, fatalities arising from cardiovascular-related complications. Above all, the study has touched on some treatment procedures that can be used to stabilize PaL-1 levels with the aim of reversing medical conditions attributable to high concentrations of PAL-1.
Asselbergs, F.W., Williams, S.M., Herbert, P.R., Coffey, C.S., Hillege, H.L, Navis, G., Vaughan, D.E., Van Gilst, W.H., & Moore, J.H. (2007). “Gender specific correlations of plasminogen activator-1 and tissue plasminogen activator levels with cardiovascular disease-related traits. “Journal of Thrombosis and Haemostasis, 5:313-320.
Bergstein, J.M., Riley, M., & Bang, N.U. (1992). “Role of plasminogen-activator inhibitor type 1 in the pathogenesis and outcome of the haemolytic uremic syndrome.” The New England Journal of Medicine, 327(11): 755-759.
Bosnyak, Z., Forrest, K.Y.Z., Marsert, R.E., Becker, D., & Orchard, T.J. (2002). “Do plasminogen activator inhibitor (PAL-1) or tissue plasminogen activator PAL-1 complexes predict complications in type 1 diabetes: The Pittsburgh epidemiology of diabetes complications study.” Diabetic Medicine, 20: 147-151.
Crainich, P., Jenney, N.S., Tang, Z., Arnold, A.M., Kuller, L.H., Manolio, T., Sharrett, A.R., & Tracey, R.P. (2003). “Lack of association of the plasminogen activator inhibitor-1 4G/5G promotion polymorphism with cardiovascular disease in the elderly.” Journal of Thrombosis and Haemostasis, 1:1799-1804.
Kellerman, G.M. (n.d.). Adipose tissue as an endocrine organ. Web.
Petrie, M.S., Hariel, T.E., Schwartz, G.G., & Sane, D.C. (2004). “Production of plasminogen activator inhibitor-1 (PAL-1) by endothelial cells: differential responses to calcitriol and paricalcitol, Journal of Thrombosis and Haemostasis, 2:2266-7.
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Sobel, B.E., Woodcock-Mitchell, J., Schneider, D.J., Holt, R.E., Marutsuka, K., & Gold, H. (1998). Increased plasminogen activator inhibitor type 1 in coronary arteryathierectonomy specimens from type 2 diabetic compared with nondiabetic patients.” American Heart Association, 97: 2213-2221.