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https://directory.hsc.wvu.edu/Individual/Index/31914

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The stroke volume is further determined changes (eg, left-ventricular hypertrophy) or functional by the preload (the volume that enters the left ventricle), changes (eg, ischemia) impairs ventricular filling (preload). A previous myocardial infarction may result in nonfunctioning myocardium that will impair contractility. A recent concept is that ischemic myocardial tissue can be nonfunctioning (hibernating) but revitalized by surgical or medical therapy directed at ischemic heart disease. In basic terms, afterload is the load that the pump has to work against, which is usually clinically estimated by the mean arterial pressure. The Frank-Starling law of the heart states that as the ven also the wall tension and intrathoracic pressure that the tricular volume increases and stretches the myocardial muscle myocardium must work against. Together, these 3 vari fibers, the stroke volume increases, up to its maximum capacity. If stroke volume cannot be main tained, then heart rate must increase to maintain cardiac which elevates left-atrial pressure and pulmonary venous output. Initially, this response will suffice, but pro Based on autonomic input, the heart will respond to the longed activation results in loss of myocytes and maladap same preload with different stroke volumes, depending on tive changes in the surviving myocytes and the extracel inherent characteristics of the heart. The stressed myocardium undergoes remodeling and dilation in response to the insult. Remodeling also results in additional cardiac decompensation from complications, including mitral re gurgitation from valvular annulus stretching, and cardiac arrhythmias from atrial remodeling. Patients presen tation can greatly differ, depending on the chronicity of the disease. For instance, most patients experience dyspnea when pulmonary-artery occlusion pressure exceeds 25 mm Hg. This series of Frank-Starling curves demonstrates that at any given preload (end-diastolic volume), increases in contractility capillaries are recruited and increase capacitance to deal with the added volume. At this point, by action of pressure gradients, fluid will form in the interlobular septae and the perihilar region. As noted above, chronic heart failure is associated with increased venous capacitance and lymphatic drainage of the lung. As a result, crackles are often absent, even in the setting of elevated pulmonary capillary pressure. Con tinued sodium retention preferentially results in peripheral edema and, ultimately, in the development of pleural ef fusions. The long-term response to elevated pulmonary venous pressure includes interstitial fibrosis with thicken ing of the alveolar membrane. Evaluation of the Patient With Congestive Heart Failure patients with dyspnea, a chest radiograph is a useful first test for differentiating patients with heart failure from pa the approach to the patient with suspected heart failure tients with primary pulmonary disease (Fig. Radio includes a history and physical examination, chest radio graphic findings suggestive of heart failure include car graph, and a series of diagnostic tests to assess both the diomegaly (cardiac-to-thoracic ratio above 50%), acuity and severity. History alone is insufficient to make cephalization of blood vessels, increased interstitial mark the diagnosis of heart failure, but often provides clues to ings, and pleural effusions. Patients with previous evi failure can be related to either the reduction of cardiac dence of heart disease, diabetes mellitus, hypertension, or output (fatigue, weakness) or to excess fluid retention (dys documented coronary-artery disease are at increased risk pnea, orthopnea, and cardiac wheezing). Fluid retention also ments of cardiac contractility, there were no laboratory results in peripheral edema and occasionally in increasing tests to assist in the diagnosis of heart failure. Absence of dyspnea triuretic peptide is one of a family of neurohormones that on exertion essentially rules out heart failure due to left is produced by the ventricles in response to increased pres ventricular dysfunction. It works to counteract the effect of crackles and wheezing) is predominant in acute or sub the renin-angiotensin system by providing vasodilation, acute disease. A 45), which correlates with elevated pulmonary-artery oc cut-off value of 100 pg/mL diagnoses heart failure with clusion pressure 80% of the time. Pleural effusion blockers protect the heart from the harmful effects of Tachycardia (120 beats/min) norepinephrine and epinephrine. Intolerance to blockers is uncommon and is usually due to bradycardia or dizziness. Diuretics are essential in the relief of dyspnea and signs Therapy for Congestive Heart Failure of sodium and water retention (peripheral edema or pleural effusion). They are best used in the minimum dose needed Understanding the pathophysiology of heart failure al to maintain the dry weight in patients with symptomatic lows one to achieve the goals of treatment, which are to heart failure. Much litera ventricular synchronization, in the hope of improving car ture and research has been published on medical manage diac output. The basic theories include termination of the brillators reduce the risk of death in patients who have renin-angiotensin system to prevent the long-term compli moderate-to-severe symptomatic heart failure and a re cations of the cascade.

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For example, dipyridamole, quinidine, imipramine, propranolol, and chlorpromazine are known to have strong affinity for alpha-1-acid glycoprotein; for overdoses of these agents, plasma may be a more appropriate choice. Some venoms also cause coagulopathy, in which case the use of plasma should be considered. References of the identified articles were searched for additional cases and trials. Major syndromes are classified according to the affected central nervous system anatomy but an international workshop consensus statement called for a combination of immunohistochemistry and Western immunoblot ting for proper diagnosis. Autoantibodies reactive against Purkinje cell cytoplasm react on Western blot analysis with 34-kDa and 62-kDa Purkinje cell proteins and are referred to as anti-Yo antibodies. The onset of symptoms, including truncal and limb ataxia, dysarthria (which may be severe), and downbeating nystagmus may precede the diagnosis of cancer by months to years. A serum anti-Hu antibody and rapidly developing symptoms of encephalomyelitis will likely lead to a diagnosis of small cell lung cancer within several months. The onset is often abrupt in adults and may beaccompanied by nausea and vomiting, and then progress to truncal ataxia, generalized myoclonus, altered mental status, and sometimes to stupor and coma. Paraneoplastic Stiff-Person Syndrome, associated with antibodies to the 128 kDa synaptic vesicle-associated protein amphiphysin. It is associated with small cell lung cancer, cervix carcinoma and malignant melanoma. Most patients have serum autoantibodies to the retinal pho toreceptor protein recoverin. A large number of additional antibodies associated with paraneoplastic syndromes of the central and peripheral nervous systems and the neu romuscular junction have been described and extensively reviewed. Neurological improvement or worsening may correlate with tumor response or relapse. Aggressive immunosuppression early in the course is recommended in patients who are identi fied prior to a tumor diagnosis or whose tumors do not yet require specific anti-cancer therapy. References of the identified articles were searched for additional cases and trials. Description of the disease Polyneuropathy can present as acute, subacute, or chronic process with initial sensory symptoms of tingling, prickling, burning or bandlike dysesthesias in the balls of the feet or tips of the toes. Nerve fibers are affected according to axon length, without regard to root or nerve trunk distribution. The polyneuropathies are diverse in timing, severity, mix of sensory and motor features, and pres ence or absence of positive symptoms. The diagnosis can be established based on electrophysiological studies and the presence of monoclonal proteins. Corticosteroids alone tend to be more effective in IgG and IgA polyneuropathies with a response rate of 40 to 60%. Combination therapy with low dose cyclophosphamide and prednisone given monthly over 6 months improves clinical outcome irrespective of antibody specificity or class. Polyneuropathies with IgG monoclonal protein resistant to this treatment have been successfully treated with cyclosporine A and carmus tine. However, this was not confirmed in a small randomized trial and when compared to interferon alpha. These new therapies are likelyto change the therapeutic approach if the benefits are confirmed in larger trials. While some measures did not reach statistical significance, the observed differences were clinically significant. The het erogeneity of the IgG group, which included patients with more treatment refractory axonal neuropathy, may have adversely affected the observed results. The patient may continue to improve over weeks following cessation of plasma exchange. If the level of paraprotein is correlative to the polyneuropathy then it can be monitoredto evaluate the frequency of treatment. However, the titer of the paraprotein may not correlate with the clinical disease state.

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There are special issues in designing and standardizing epidemiological studies for general risk assessment that also apply for chemical-induced autoimmune dis ease. A goal of this research is to be able to estimate the attributable risk that is, the proportion or number of new cases of a disease that could be prevented if a given exposure is reduced or eliminated. Randomized trials of environmental exposures are generally not feasible or ethical. Epidemiological studies use methodologies developed for observational research to reduce the potential role of confounding, selection bias, and misclassification of exposure and of disease that may bias the estimates of disease association, increase the imprecision or uncertainty of the estimates, or limit the ability to apply the results to the general population. Prospective studies in which exposure assessment is determined prior to disease onset avoid the potential problem of a differential misclassification of exposure based on disease status. For both prospective and retrospective designs, however, the adequacy of exposure assessment, in terms of both sensitivity and specificity, is extremely important and has been demonstrated to affect not just the precision, but the magnitude and direction of observed associations between exposures and autoimmune diseases (Parks et al. In addition, there are some unique challenges in epidemiological studies for risk assessment in chemical-induced autoimmunity. For example, although the estimated prevalence of all autoimmune diseases is not rare (3?5% of the population), the incidence of specific autoimmune diseases (more than 60 are suspected) is relatively low, and extremely large populations are needed to have sufficient power to identify significant increased risk. Furthermore, there are no population-based disease registries for most auto immune diagnoses, and the diagnosis can be difficult to ascertain accurately. For example, most cases of a lupus-like illness caused by procainamide or hydralazine usually resolve when the drug is discontinued. Several forms of autoimmune disease, such as Hashimoto thyroiditis and Graves disease, may arise several weeks after delivery. Characteristically, these forms of postpartum auto immune diseases clear spontaneously after several months and, thus, may be difficult to capture in retrospective studies. As described in detail elsewhere in this document, a variety of intrinsic factors. While there is varia bility in the extent of female predominance and no strong association between degree of female predominance and type of disease or age at onset, sex and/or hormonal status clearly play a role in disease susceptibility. Although a majority of autoimmune diseases are less common in children and adolescents, the relative influence of early-life exposures to environmental chemicals or infectious agents on the incidence and severity of disease later in life is largely unexplored. When insufficent evidence exists pertaining to susceptibility, the assumption of equality is generally used. Studies have shown that genetic predisposition plays an impor tant role in susceptibility in the development of autoimmune diseases. The genetic basis for these differences is likely due to functional polymorphisms contained within multiple genes, each of which, by modulating corresponding protein expression, influences disease susceptibility. With the advent of genetic screening assays and their applica tion in population-based epidemiological studies, it may be possible in the near future to establish quantitatively the increased risk associated with these factors that can be applied to the risk assessment. Our lack of understanding regarding the contribution of these individual exposures to the risk of autoimmune disease in genetically suscep tible individuals and the potential for cumulative interactions of many of these components is a significant challenge for the risk assessment process. Thus, in addition to the prevalence of disease, considera tion of the burden of autoimmune disease should include mortality risk and the impact of morbidity (direct costs of health-care utiliza tion and indirect costs from effects of employment, overall quality of life, and burden on non-paid caregivers). The annual per patient direct costs of hospitalization, outpatient services, and medications in rheumatoid arthritis have been estimated as approx imately 2000 euros, with a range of approximately 5 to 10-fold. Substantial variability is seen across studies and countries (Rat & Boissier, 2004; Rosery et al. In a Canadian study of multiple sclerosis, the average cost associated with remission. There are few studies pertaining to costs of many of the other autoimmune diseases. The development of new therapeutic agents has led to a substantial increase in medication costs for rheu matoid arthritis and other diseases (Rubio-Terres & Dominguez-Gil Hurle, 2005; Sorensen & Andersen, 2005). Because of the chronic nature of these diseases, and because these diseases are currently not cured but rather treated, the indirect costs associated with long-term disability are substantial. Studies on several diseases have reported that a large percentage (30% or more) of patients are unable to work, and this figure increases with disease duration (Woolf & Pfleger, 2003; Lacaille, 2005; Alarcon et al. Furthermore, the indirect costs associated with job or produc tivity loss may be greater than the direct costs associated with health-care utilization (Phillips, 2004; Rat & Boissier, 2004; Hulsemann et al. In conclusion, much of the information needed to address the risk of chemical-induced autoimmune diseases is not available. Autoimmune diseases include a wide variety of illnesses tar geting many sites in the body. Furthermore, autoimmune mechanisms play a role in many other diseases; hence, more than these 5% will encounter autoimmune-associ ated health effects.

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Consider discontinuation or use of shorter acting anticoagulant as delivery approaches [see Warnings and Precautions (5. Data Animal Data Dabigatran has been shown to decrease the number of implantations when male and female rats were treated at a dosage of 70 mg/kg (about 2. Treatment of pregnant rats after implantation with dabigatran at the same dose increased the number of dead offspring and caused excess vaginal/uterine bleeding close to parturition. Death of offspring and mother rats during labor in association with uterine bleeding occurred during treatment of pregnant rats from implantation (gestation Day 7) to weaning (lactation Day 21) with dabigatran at a dose of 70 mg/kg (about 2. The risk of stroke and bleeding increases with age, but the risk-benefit profile is favorable in all age groups [see Warnings and Precautions (5), Adverse Reactions (6. Dosing recommendations for patients with CrCl <15 mL/min or on dialysis cannot be provided. Adjust dose appropriately in patients with renal impairment receiving concomitant P-gp inhibitors [see Warnings and Precautions (5. Dosing recommendations for patients with CrCl <30 mL/min or on dialysis cannot be provided. Dabigatran is primarily eliminated by the kidneys with a low plasma protein binding of approximately 35%. Hemodialysis can remove dabigatran; however, data supporting this approach are limited. Using a high-flux dialyzer, blood flow rate of 200 mL/min, and dialysate flow rate of 700 mL/min, approximately 49% of total dabigatran can be cleared from plasma over 4 hours. At the same dialysate flow rate, approximately 57% can be cleared using a dialyzer blood flow rate of 300 mL/min, with no appreciable increase in clearance observed at higher blood flow rates. Upon cessation of hemodialysis, a redistribution effect of approximately 7% to 15% is seen. It is freely soluble in methanol, slightly soluble in ethanol, and sparingly soluble in isopropanol. Each capsule contains dabigatran etexilate mesylate as the active ingredient: 150 mg dabigatran etexilate (equivalent to 172. Because thrombin (serine protease) enables the conversion of fibrinogen into fibrin during the coagulation cascade, its inhibition prevents the development of a thrombus. Both free and clot-bound thrombin, and thrombin-induced platelet aggregation are inhibited by the active moieties. Dabigatran is metabolized to four different acyl glucuronides and both the glucuronides and dabigatran have similar pharmacological activity. Pharmacokinetics described here refer to the sum of dabigatran and its glucuronides. Dabigatran displays dose-proportional pharmacokinetics in healthy subjects and patients in the range of doses from 10 to 400 mg. Absorption the absolute bioavailability of dabigatran following oral administration of dabigatran etexilate is approximately 3 to 7%. After oral administration of dabigatran etexilate in healthy volunteers, Cmax occurs at 1 hour post-administration in the fasted state. The oral bioavailability of dabigatran etexilate increases by 75% when the pellets are taken without the capsule shell compared to the intact capsule formulation. The red blood cell to plasma partitioning of dabigatran measured as total radioactivity is less than 0. Dabigatran pharmacokinetics are dose proportional after single doses of 10 to 400 mg. Renal clearance of dabigatran is 80% of total clearance after intravenous administration. After oral administration of radiolabeled dabigatran, 7% of radioactivity is recovered in urine and 86% in feces. Metabolism After oral administration, dabigatran etexilate is converted to dabigatran. The cleavage of the dabigatran etexilate by esterase-catalyzed hydrolysis to the active principal dabigatran is the predominant metabolic reaction. Dabigatran is subject to conjugation forming pharmacologically active acyl glucuronides.

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Manning Feinleib of the National Heart, Lung, and Blood Institute and his coworkers who studied the coronary vessels of those who had died, only examined 281 of the 914 dead individuals. Then from the 281, they selected just 127 (14 percent of all dead) who became the subjects of their autopsy study! What I get from this is that with only 14 percent of the Framingham deceased chosen for autopsy, study biases must have been huge because of a condition that is known to cause heart attack death at an early age called familial hypercholesterolemia, this rare disease must have been present in the study subjects, given that they were all located in the same vicinity. Do you see how this could greatly pad their results to get the relation they were looking for if they used a subgroup with this condition in it? The point is that ever since the Framingham study results, the statin companies have been able to keep this belief going that we must have a pill to lower our cholesterol in order to lower our atherosclerosis and heart attack rate. What I have found is that behind it all, there really is little to substantiate that cholesterol is the cause of athero sclerosis! This deserves the quote from Mark Twain: There is something fascinating about science. One gets such a wholesale return of conjecture for such a trifling investment of fact. Ravnskov points out, about 165 healthy people would also have to be treated for five years in order to extend one life by five years. And by using statins to do it, the cost for that one life totals between $750,000 and $1. Blood Pressure-Lowering Drugs Your heart beats more than 100,000 times each day and pumps 2,000 gallons of blood through your blood vessels to feed every tissue and organ in your body. You would think that the force of blood against the vessel wall over time would wear it down. Atherosclerosis is the mechanism to toughen up the vessel?but it also causes a narrowing of the tiny arteries over time so that less blood can feed the tissue with nutrients and oxygen. By the time we are elderly the death rate increases linearly as systolic blood pressure increases. Pills to lower blood pressure make up the largest category of prescribed medications in the U. High blood pressure is a direct cause of heart attack, stroke, congestive heart failure, kidney failure, peripheral blood vessel disease, dementia, blindness, and just about every illness involving soft tissues in the body. Treating this condition is immensely important because it is estimated that for each 20mmHg increase in your systolic pressure you double your risk of a heart attack, beginning at 120mmHg! Indeed, keeping blood pressure in normal range is a valuable treatment, yet the use of these medications are not as profound as you would think given the tremendous cost and attention given to them. Let me explain this further after I first give some details about these prescription medications that are used to lower blood pressure. These are the medications such as Lisinopril, Enalapril, Cozaar, and Atacand. Adverse side effects are fewer with these two classes of medications than the other anti-hypertensive meds. If you have suffered a heart attack or stroke the safest and most effective prescription medications for preventing a recurrent event are the beta-blockers like metoprolol or atenolol. These prescription medications act primarily to slow the heart and lower the power of each heart beat, thereby lowering pressure throughout the blood vessels. They often make patients fatigued, depressed, or dizzy when they stand up too quickly. As any excess water retention is reduced, then that translates into less fluid inside the blood vessels, too. Another useful class of medications used to lower blood pressure are calcium channel blockers, the classics being nifedipine, diltiazem, and verapamil. They relax the smooth muscle of the blood vessel wall so that pressure inside the vessel drops. As I alluded to earlier, keeping blood pressure in normal range with prescription medications is not really very impressive given the tremendous cost and attention we give to them.

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It is becoming evident that inflammatory processes play an important role in the atherosclerotic process. Most patients with severe cardiac symptoms will require coronary angiography to determine the appropriate means for revascularization. All patients should be given appropriate medical therapy to treat symptoms and atherosclerotic risk factors (see section B1). Cardiac assessment scores may be useful in the context of patients being considered for peripheral revascularization (76). In patients with a high cardiac risk assessment score, current guidelines recommend further evaluation of the patient for possible coronary revascularization (76). In addition, patients who underwent coronary revascularization had a significantly longer time to vascular surgery compared with patients who did not. Therefore, this strategy of a pre-emptive coronary revascularization prior to peripheral vascular surgery should not normally be pursued. In most patients, perioperative use of beta-adrenergic-blocking agents is associated with reduced cardiovascular risks of surgery. Recent studies have shown that beta-adrenergic blockade with bisoprolol significantly decreased the risk for cardiovascular events during vascular surgery and afterwards (78, 79). Besides controlling symptoms of myocardial ischemia, treatment with beta-blocking agents also has the benefit of favorably influencing prognosis in these patients (80). When there are no contraindications, beta-adrenergic blockers should be given perioperatively to patients with peripheral arterial disease undergoing vascular surgery in order to decrease cardiac morbidity and mortality [A]. Evaluation of the carotid circulation should be based on a history of transient ischemic attack or stroke. Further evaluation and consideration for revascularization should be based on current guidelines (81, 82). In such cases, evaluation and treatment should be based on current guidelines (5, 83, 84). Patients may describe muscle fatigue, aching or cramping on exertion that is relieved by rest. The symptoms are most commonly localized to the calf, but may also affect the thigh or buttocks. Importantly, patients without classical claudication also have walking limitations that may be associated with atypical or no limb symptoms (85). Typical claudication symptoms may not occur in patients who have co-morbidities that prevent sufficient activity to produce limb symptoms. Patients with intermittent claudication have normal blood flow at rest (and, therefore, have no limb symptoms at rest). With exercise, occlusive lesions in the arterial supply of the leg muscles limits the increase in blood flow, resulting in a mismatch between oxygen supply and muscle metabolic demand that is associated with the symptom of claudication. Key components of the general examination include measurement of blood pressure in 62 both arms, assessment of cardiac murmurs, gallops or arrhythmias, and palpation for an abdominal aortic aneurysm (does not include the presence of an aneurysm). The presence of a bruit in the region of the carotid, aorta or femoral arteries may arise from turbulence and suggest significant arterial disease. The specific peripheral vascular examination requires palpation of the radial, ulnar, brachial, carotid, femoral, popliteal, dorsalis pedis and posterior tibial artery pulses. In a small number of healthy adults, the dorsalis pedis pulse on the dorsum of the foot may be absent due to branching of the anterior tibial artery at the level of the ankle. In this situation, the distal aspect of the anterior tibial artery may be detected and assessed at the ankle. Also, a terminal branch of the peroneal artery may be palpated at the lateral malleolus. For simplicity, pulses may be graded from 0 (absent), 1 (diminished) and 2 (normal). An especially prominent pulse at the femoral and/or popliteal location should raise the suspicion of an aneurysm.

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Although knowledge of the factors governing circulatory readjustments and their mechanism of action is incomplete, it appears that partial pressures of oxygen and carbon dioxide play a role, presumably through their action on chemoreceptors. This mechanism allows preferential delivery of nutrients and oxygen to vital organs, thereby compensating for diminished placental resources. Consequently, arterial vessels are unsuitable for longitudinal monitoring of growth-restricted fetuses. Cardiac and venous velocity waveforms give more information regarding fetal well-being or compromise. Flow velocity waveforms from the middle cerebral artery in a normal fetus with low diastolic velocities (right, top) and in a growth-restricted fetus with high diastolic velocities (right, bottom). This suggests that the maximum degree of vascular adaptation to hypoxemia precedes the critical degree of impairment of fetal oxygenation. Moreover, in fetal sheep, chronic hypoxemia was found to alter cerebral vascular contractility through changes in vascular smooth muscle and endothelial cells, with the net result of a relative decrease in cerebral blood flow 57. Table 1 Hemodynamic changes occurring in fetal arterial vessels during hypoxemia and acidemia induced by uteroplacental insufficiency. Vessel Impedance to flow Descending aorta increased Renal artery increased Femoral artery increased Peripheral pulmonary artery increased Mesenteric arteries increased Cerebral arteries decreased Adrenal arteries decreased Splenic arteries decreased Coronary arteries decreased Fetal arterial Doppler studies are useful in the differential diagnosis of small-forgestation fetuses. However, the cerebroplacental ratio did not appear to correlate significantly with outcome after 34 weeks. There is no evidence that the use of other peripheral arterial fetal vessels, such as renal artery 51, splenic artery 64 or peripheral pulmonary arteries 63provides any advantage in the identification of intrauterine growth-restricted fetuses. Figure 4: Color Doppler examination of the descending thoracic aorta (left) with normal flow velocity waveforms showing positive flow velocities during diastole (right, top) and in a growth-restricted fetus with reversed end-diastolic velocities (right, bottom). Fetal cardiac Doppler Cardiac flow is greatly influenced by the modifications of arterial impedance to flow. Cerebral vasodilatation produces a decrease in left ventricle afterload, whereas increased placental and systemic resistance produce increased right ventricle afterload. Hypoxemia may also impair cardiac contractility directly, while changes in blood viscosity due to polycythemia may alter preload 5. Consequently, growth-restricted fetuses show, at the level of the atrioventricular valves, impaired ventricular filling (lower ratio of early passive to late active ventricular filling phase E/A ratio) 67, lower peak velocities in the aorta and pulmonary arteries. These hemodynamic intracardiac changes are compatible with a preferential shift of cardiac output in favor of the left ventricle, leading to improved cerebral perfusion. Thus, in the first stages of the disease, the supply of substrates and oxygen can be maintained at near normal levels despite any absolute reduction of placental transfer 71. Longitudinal studies of deteriorating growth-restricted fetuses have shown that peak velocity and cardiac output gradually decline, suggesting a progressive worsening in cardiac function 71. Similarly, there is a symmetrical decrease in ventricular ejection force at the level of both ventricles, despite the dramatically different hemodynamic conditions present in the vascular district of ejection of the two ventricles. This supports a pivotal role of the intrinsic myocardial function in the compensatory mechanism of the growth-restricted fetus following the establishment of the brain-sparing effect. Ventricular ejection force dramatically decreases in a short time interval (about 1 week), showing an impairment of ventricular force close to fetal distress. Fetal venous Doppler Animal studies have shown that, in severe hypoxemia, there is redistribution in the umbilical venous blood towards the ductus venosus at the expense of hepatic blood flow. Consequently, the proportion of umbilical venous blood contributing to the fetal cardiac output is increased. There is a doubling of umbilical venous-derived oxygen delivery to the myocardium and an increase in oxygen delivery to the fetal brain 73,74. In vitro perfusion studies have shown that, at reduced umbilical venous pressures, a proportionally greater fraction of umbilical venous flow is directed through the ductus venosus in comparison to blood flow through the liver 75. Mechanical forces seem to play a key role in the regulation of umbilical venous flow distribution between the liver and the ductus venosus. Under unfavorable conditions, the ductus venosus seems to ensure blood flow directly to the fetal heart and, in extreme conditions, umbilical blood may pass exclusively through the ductus venosus. This may lead to an impaired perfusion of the liver with potential impact on its metabolic properties.

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As well as thrombosis of placental vessels, non-thrombotic mechanisms are also thought to be important. Complement activation and enhanced apoptosis of embryonic and placental cells may also play a role in the pathways that lead to recurrent early miscarriage, fetal loss, pre-eclampsia and placental insuf? This has been discussed in detail by the Antiphospholipid Antibody Task Force who reported their? One cohort study demonstrated an association with intrauterine growth restriction. These include variation in isotypes tested by different centres, variability in the sensitivity and speci? The Antiphospholipid Antibodies Task Force recently reported that further validation studies were being performed and it is hoped that this will help to address issues regarding standardisation of assays and reduce inter-laboratory and inter-assay variability [33]. Coordination of prospective, longitudinal studies is vital to improve our understanding of this fascinating group of autoantibodies. Acknowledgments: the author would like to thank Jack Bourke for review of the manuscript. Thrombus formation induced by antibodies to beta2-glycoprotein I is complement dependent and requires a priming factor. Solution structure of human and bovine beta(2)-glycoprotein I revealed by small-angle X-ray scattering. Beta2-glycoprotein I can exist in 2 conformations: Implications for our understanding of the antiphospholipid syndrome. The antibacterial activity of peptides derived from human beta-2 glycoprotein I is inhibited by protein h and m1 protein from streptococcus pyogenes. Beta(2)-glycoprotein I, the major target in antiphospholipid syndrome, is a special human complement regulator. Complement C3 activation is required for antiphospholipid antibody-induced fetal loss. A novel inhibitor of the alternative complement pathway prevents antiphospholipid antibody-induced pregnancy loss in mice. Anti-beta2-glycoprotein I: Prevalence, clinical correlations, and importance of persistent positivity in patients with antiphospholipid syndrome and systemic lupus erythematosus. Anti-beta 2 glycoprotein I antibodies in a general obstetric population: Preliminary results on the prevalence and correlation with pregnancy outcome. Anti-beta2 glycoprotein I antibodies are associated with some obstetrical complications, mainly preeclampsia-eclampsia. Risk of venous and arterial thrombosis according to type of antiphospholipid antibodies in adults without systemic lupus erythematosus: A systematic review and meta-analysis. International consensus guidelines on anticardiolipin and anti-beta2-glycoprotein I testing: Report from the 13th international congress on antiphospholipid antibodies. The presence of IgG antibodies against beta2-glycoprotein I predicts the risk of thrombosis in patients with the lupus anticoagulant. Immunoglobulin G is the only anti-beta-2-glycoprotein I isotype that associates with unprovoked thrombotic events among hospital patients. IgM anti-beta2 glycoprotein I is protective against lupus nephritis and renal damage in systemic lupus erythematosus. Catastrophic antiphospholipid syndrome associated with anti-beta-2-glycoprotein I IgA. High frequency of abnormal levels of IgA anti-beta2-glycoprotein I antibodies in patients with systemic lupus erythematosus: Relationship with antiphospholipid syndrome. IgA-class anti-beta2-glycoprotein I in women with unexplained recurrent spontaneous abortion. The clinical relevance of IgA anticardiolipin and IgA anti-beta2 glycoprotein I antiphospholipid antibodies: A systematic review. Value of isolated IgA anti-beta2 -glycoprotein I positivity in the diagnosis of the antiphospholipid syndrome.

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However, in conditions of particularly high velocities (such as the ductus arteriosus), continuous Doppler may be useful because it avoids the aliasing effect. These measurements are particularly prone to errors, mainly due to inaccuracies in valve area. Area is derived from the valve diameter, which is near the limits of ultrasound resolution, and is then halved and squared in its calculation, thus amplifying potential errors. However, they can be used properly in longitudinal studies over a short period of time during which the valve dimensions are assumed to remain constant. This index estimates the energy transferred from right and left ventricular myocardial shortening to work done by accelerating blood into the pulmonary and systemic circulations, respectively 28. This index appears to be less influenced by changes in preload and afterload than other Doppler indices 28 and may be more accurate than other Doppler variables, such as peak velocities, for the assessment of ventricular function in adults with chronic congestive heart failure. The force developed by ventricular contraction, to accelerate a column of blood into the aorta or pulmonary artery, represents transfer of energy of myocardial shortening to work done on the pulmonary and systemic circulation. The mass component in this model is the mass of blood accelerated into the outflow tract over a time interval, and may be calculated as the product of the density of blood (1. Doppler depiction of fetal cardiac circulation In the human fetus, blood flow velocity waveforms can be recorded at all cardiac levels, including venous return, foramen ovale, atrioventricular valves, outflow tracts, pulmonary arteries and ductus arteriosus. The factors affecting the shape of the velocity waveforms include preload 29,30, afterload 30,31, myocardial contractility 32, ventricular compliance 33 and fetal heart rate 34. These factors differ in their effect on waveforms recorded from different sites and parts of the cardiac cycle. Atrioventricular valves Flow velocity waveforms at the level of the mitral and tricuspid valves are recorded from the apical four-chamber view of the fetal heart and are characterized by two diastolic peaks, corresponding to early ventricular filling (E-wave) and to active ventricular filling during atrial contraction (A-wave) (Figure 14). The ratio between the E and A waves (E/A) is a widely accepted index of ventricular diastolic function and is an expression of both the cardiac compliance and preload conditions 24,29,35. Outflow tracts Flow velocity waveforms from the aorta and pulmonary arteries are recorded respectively from the five-chamber and short-axis views of the fetal heart (Figure 13). The former is influenced by several factors, including valve size, myocardial contractility and afterload 24,30,31, while the latter is believed to be secondary to the mean arterial pressure 36. Coronary blood flow Coronary blood flow may be visualized with the use of high-resolution ultrasound equipment and color Doppler echocardiography. In normal fetuses, both right and left coronary arteries may be identified after 31 weeks of gestation under optimal conditions of fetal imaging 37. In compromised fetuses, these vessels may be identified at an earlier gestational age, probably due to an increased coronary blood flow 37. Pulmonary vessels Velocity waveforms may be recorded from the right and left pulmonary arteries or from peripheral vessels within the lung 38?41. The morphology of the waveforms is different according to the site of sampling and there is a progressive increase in the diastolic component in the more distal vessels 40,41 (Figure 17). Ductus arteriosus Ductal velocity waveforms are recorded from a short-axis view showing the ductal arch and are characterized by a continuous forward flow through the entire cardiac cycle 42. Figure 16: Five-chamber view of the fetal heart with superimposed color Doppler showing the aorta (blue) originating from the left ventricle (top). Short-axis view of the fetal heart with superimposed color Doppler showing the pulmonary artery originating from the right ventricle (bottom). Errors in Doppler blood flow velocity waveforms A major concern in obtaining absolute measurements of velocities or flow is their reproducibility. To obtain reliable recordings, it is particularly important to minimize the angle of insonation, to verify in real-time and color flow imaging the correct position of the sample volume before and after each Doppler recording, and to limit the recordings to periods of fetal rest and apnea, as behavioral states greatly influence the recordings44,45. In these conditions, it is necessary to select a series of at least five consecutive velocity waveforms characterized by uniform morphology and high signal to noise ratio before performing the measurements. Using this technique of recording and analysis, it is possible to achieve a coefficient of variation below 10% for all the echocardiographic indices with the exception of those needing the valve dimensions 46?48. Figure 17a: Flow velocity waveform from the pulmonary artery at 32 weeks of gestation. Figure 17b: Flow velocity waveform from the pulmonary vein at 32 weeks of gestation.

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Therefore, if a genetic variant or a drug leads to higher or lower concentrations of a lipoprotein and this further leads to higher or lower risk of cardiovascular disease, then it is quite likely that it is the lipoprotein that causes the effect on cardiovascular disease. In contrast, results from observational epidemiology can mislead through confounding and reverse causation. Confounding is if a third factor influences both lipoprotein concentrations and cardiovascular disease risk, while reverse causation implies that cardiovascular disease leads to changes in lipoprotein concentrations, rather than vise versa. There are several early examples of studies that suggest the idea that if a risk factor is elevated or reduced due to genetic variation, and if such genetic variation is or is not associated with a disease of interest, then it would be possible to infer or exclude causality of the risk factor(98-100). This idea involving the causal genetic influence of high Lp(a) concentrations on risk of coronary heart disease was already presented in 1992 by Gerd Utermann and colleagues(101;102). Growing out of the awareness of the limitations of observational epidemiology, it was suggested that Mendelian randomization, that is, the random assortment of genes from 9 parents to offspring that occurs during gamete formation and conception, would provide a method for assessing the causal nature of risk factors on disease. The clear formulation of these ideas has substantially influenced thinking on how to understand disease causality, especially in cardiovascular medicine and most importantly for the role of Lp(a) as a cause of cardiovascular disease. Epidemiology alone cannot determine causality, due to potential problems with confounding and reverse causation (Figure 4, double-pointed arrow #1). Thus, potential confounders including life-style factors may be unevenly distributed between those with high and low Lp(a) concentrations, and such confounders may be the real explanation for the high risk of cardiovascular disease in those with high Lp(a) (Figure 5, left panel). In contrast, in the Mendelian randomization study design such confounders are always evenly distributed between those with high and low Lp(a), and therefore, cannot explain the high cardiovascular risk in those with genetically high Lp(a) concentrations (Figure 5, middle and left panels). The other major potential limitation of observational studies is reverse causation, that is, the possibility that cardiovascular disease leads to high Lp(a) concentrations, rather than vice versa (Figure 5, left panel). In the Mendelian randomization study design, reverse causation is simply not possible, as cardiovascular disease cannot change your genes (Figure 5, middle and left panels). In other words, the Mendelian randomization study design can be used to infer causality just like a randomized, double-blind, placebo-controlled Lp(a) reducing trial and these two types of studies share many advantages and have similar limitations (see Figure 5 in reference(65)). Unfortunately however, so far no randomized, double-blind, placebo-controlled Lp(a) reducing trials to prevent cardiovascular disease have been published or even initiated. Therefore, for now the human evidence to suggest that high Lp(a) causes cardiovascular disease has to depend on genetics and the Mendelian randomization approach. While these approaches are powerful, it is naturally the totality of evidence that counts in understanding causality. Another limitation of observational studies is the problem of regression dilution bias(109;110) because risk factors typically are only measured once, and therefore the association observed will only represent a single point estimate (Figure 5, left panel). Regression dilution bias means that the effect size of the risk estimate is 10 underestimated, although this bias does not influence statistical significance. Mendelian randomization studies using human genetics have many similarities with randomized, double-blind, placebo-controlled trials, and thus advantages over traditional observational studies (Figure 5). Mendelian randomization studies have the additional advantage over conventional epidemiology that genetics typically capture a life-long effect (Figure 5, middle and right panels), while observational studies only include the time between risk factor assessment and end of follow-up. Also, population admixture can be a major problem if both genotype and the disease studied are found preferentially in certain subpopulations; however, this potential problem can be largely circumvented by studying ethnically homogeneous populations or by adjusting for different ethnicity using genetic information. Technically, what is done in a complete Mendelian randomization study is depicted in Figure 4. Published examples of this complete design that are easy to follow for the non-specialist include that low concentrations of vitamin D are causally associated with high all-cause mortality(114), and that low concentrations of nonfasting triglycerides are causally associated with low all-cause mortality(115). First, the well-known observational association is shown in the study population (Figure 4, double-pointed arrow #1). This allows assessment of the value of the genotype as an instrument in the Mendelian randomization study design (Figure 4, single-pointed arrow #2). At this stage, it is also important to exclude pleiotropic effects, that is, genotype should not be associated with any other factor that might cause cardiovascular disease (Table 1). Third, genotype is then directly associated with cardiovascular disease, using a study with sufficient statistical power to document or reject the causal association (Figure 4, single-pointed arrow #3). Fourth, the formal test of causality involves running an instrumental variable analyses (Figure 4, single-pointed arrows #4) that integrates the effect of genotype on Lp(a) concentrations (arrow #2) with the effect of genotype on cardiovascular disease risk (arrow #3). Observational and genetic, causal risk estimates can then be compared directly, as arrows #1 and #4 will be on the same scale, that is, for Lp(a) per. For research on Lp(a) as a cause of cardiovascular disease, it can be argued that even conventional epidemiology will suffice in understanding causality of Lp(a), as the concentrations of this lipoprotein are largely genetically determined(14;39) and minimally confounded by environmental variables (Table 1). Although this seems to be a valid statement, experience has shown that it was mainly the large-scale genetic Mendelian randomization 12 studies published from 2009 and onwards that have paved the path for a general understanding that high concentrations of Lp(a) are a direct cause of myocardial infarction, atherosclerotic stenosis, and aortic valve stenosis (Figure 1).

References:

  • http://www.marshall.edu/forensics/files/Kennedy_Seminar_4-18-14.pdf
  • https://www.yakimamemorial.org/pdf/about/community-hna-2016.pdf
  • https://www.epa.gov/sites/production/files/2016-10/documents/asbestos.pdf