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This type of athero-occlusive disease commonly produces chronic stable angina pectoris or intermittent claudication on increased demand allergy relief best promethazine 25 mg. Thus the symptomatic phase of atherosclerosis usually begins many decades after lesion initiation allergy medicine you can give dogs buy 25mg promethazine with amex. Acute coronary syndromes may result from thrombi that form as a consequence of disruption 39 of plaques that do not produce a critical stenosis allergy shots edmonton purchase cheap promethazine line. Thrombosis and Atheroma Complication 39,40 Several major modes of plaque disruption provoke most coronary thrombi. Left, Thrombosis caused by erosion, associated with a sessile, “white” thrombus superimposed on a lesion with abundant extracellular matrix and limited expansive remodeling. Endothelial cell desquamation or death can uncover collagen within the plaque that can trigger such platelet-rich thrombi. Right, Thrombosis resulting from rupture, usually associated with lesions with a thin fibrous cap. Tissue factor produced by the numerous macrophages in ruptured plaques promote thrombosis. Advanced atherosclerotic plaques can promote thrombosis by superficial erosion of the endothelial layer, exposing the blood and platelets to the subendothelial basement membrane containing collagen platelet activation and thrombosis. Leukocytes (arrows) have adhered to the subendothelium, which is beginning to be covered with a carpet of platelets. B, High-power view is a field selected from the center of A that shows the leukocytes and platelets adherent to the subendothelium. C, Low-power histologic section through a coronary artery, thrombosed as a result of superficial erosion. D, High-power histologic section through a coronary artery, also thrombosed as a result of superficial erosion. Coronary plaque erosion without rupture into a lipid core: a frequent cause of coronary thrombosis in sudden coronary death. Interstitial forms of collagen provide most of the biomechanical resistance to disruption of the fibrous cap. Thus the metabolism of collagen probably participates in regulating the propensity of a plaque to rupture (Fig. On the other hand, as already noted, certain mediators released from platelet granules during activation (e. In this way, inflammation can threaten the stability of atherosclerotic plaques and increase their tendency to rupture, thereby causing thromboses, which trigger most acute coronary syndromes. The same matrix-degrading enzymes thought to contribute to 39 smooth muscle migration and arterial remodeling also may contribute to weakening of the fibrous cap (see Fig. Thin fibrous caps are associated with plaque rupture, probably from reduced collagen synthesis and increased degradation. Plaques that have fatally ruptured exhibit another microanatomic feature: prominent accumulation of macrophages with a large lipid pool. From a strictly biomechanical viewpoint, a large lipid pool can serve to concentrate biomechanical forces on the shoulder regions of plaques, where they frequently fracture. Animal studies and accumulated data from monitoring peripheral markers of 39,41,42 inflammation in humans support this concept. Thrombosis Caused by Superficial Erosion of Plaques The underlying molecular and cellular mechanisms of superficial erosion have received much less 43 attention than those involved in plaque rupture (Fig. In experimental atherosclerosis in the nonhuman primate, areas of endothelial loss and platelet deposition occur in more advanced plaques (see Fig. The lesions that provoke superficial erosion appear quite distinct from those that cause plaque rupture (see Fig. Lesions associated with superficial erosion contain abundant proteoglycan and glycosaminoglycan, as opposed to the collagen-depleted fibrous cap characteristic of ruptured plaques. Eroded lesions have few macrophages, whereas these chronic inflammatory cells abound in ruptured plaques. In contrast, plaques complicated by superficial erosion have thrombi that contain many granulocytes, acute inflammatory cells. Thrombosis and Healing in Progression of Atheroma Most plaque disruptions do not give rise to clinically apparent coronary events. Careful pathoanatomic examination of hearts obtained from patients who have succumbed to noncardiac death has shown a surprisingly high incidence of focal plaque disruptions with limited mural thrombi. Moreover, hearts fixed immediately after explantation from persons with severe but chronic stable coronary atherosclerosis who had undergone transplantation for ischemic cardiomyopathy show similar evidence for ongoing but asymptomatic plaque disruption.

Occasionally allergy symptoms for eyes buy promethazine 25 mg with visa, women may consider preimplantation genetic screening allergy medicine 029 purchase promethazine online, and this requires input from genetics and fertility specialists allergy forecast ft lauderdale purchase 25mg promethazine amex. A careful discussion of the maternal and fetal risks, and of whether or not these risks might change with time or treatment, is indicated. The possibility that pregnancy might cause irreversible hemodynamic deterioration should be considered; this is specifically relevant to women with ventricular dysfunction. The long-term outlook for the mother is a difficult, but important, aspect of counseling. If the woman is going to pursue a pregnancy, a strategy should be outlined regarding the frequency of follow-up evaluation by the cardiologist, and a plan should be put in place for obstetric and cardiovascular management during the pregnancy. An assessment of maternal cardiac risk incorporates general risk predictors, lesion-specific risks, and individual factors. General predictors of adverse maternal cardiac events in women with heart disease include (1) a prior cardiac event (e. Risk scores based on these predictors 9-11 have been developed and can be used as a starting point in risk stratification. Some series, for example, include only patients with congenital heart disease; others include patients with acquired heart disease. In all series there are high-risk patient populations, such as those with clinically significant 9-11 pulmonary hypertension or dilated aortas, who are underrepresented. A British working group created a risk stratification tool using a World Health Organization classification that incorporates general and 12,13 lesion-specific diagnoses. All of these risk prediction tools should be used as a guide, along with known lesion-specific risks, other clinical information, and, of course, clinical judgment. There is a growing population of women conceiving with fertility therapy, including women with heart 14 disease. When fertility therapy is being considered in the cardiac patient, in addition to the cardiac- related risks described earlier, it is important to consider the risks associated with the underlying cause of infertility (i. Contraindications to Pregnancy In some situations, the maternal risk from pregnancy is prohibitively high, and women should be counseled to avoid pregnancy and sometimes even to consider termination of pregnancy if it occurs (Table 90. No data exist regarding the precise level of pulmonary hypertension that poses a major threat to the mother, but systolic pulmonary artery pressures higher than 60% to 70% of the systemic pressure are likely to be associated with maternal compromise; in these circumstances, pregnancy is best avoided. Women who have a left ventricular ejection fraction of less than 30% from any cause are not likely to withstand the volume load that pregnancy imposes and should be advised not to become pregnant. Patients with Marfan syndrome and a dilated aortic root more than 45 mm in diameter are vulnerable to progressive aortic dilation, dissection, and rupture during pregnancy. A number of other high-risk cardiac conditions, such as complex congenital heart disease, mechanical valves, and severe 14a,14b asymptomatic aortic stenosis, require careful preconception risk stratification. Because of the altered hemodynamics during pregnancy, the physical examination findings in a healthy pregnant woman reflect such changes and may mimic those in cardiac disease. By the middle of the second trimester, the jugular venous pressure may be slightly elevated, with brisk descents, because of the volume overload and reduced peripheral resistance. The second sound also may appear accentuated, and these combined auscultatory features may suggest an atrial septal defect or pulmonary hypertension. An ejection systolic murmur is commonly heard at the left sternal edge, never more than grade 3/6 in intensity, which relates to increased flow through the left or right ventricular outflow tract. Continuous murmurs also may be heard, as either a cervical venous hum or a mammary souffle, and are caused by the hyperdynamic circulation. The mammary souffle (continuous or systolic) is due to increased flow in the mammary arteries and is heard over the breast late in pregnancy or during lactation. Laboratory Evaluation Despite the hemodynamic volume load of pregnancy, most healthy pregnant women have low levels of B- type natriuretic peptide throughout pregnancy and after delivery. By comparison, women with heart disease have higher B-type natriuretic peptide levels throughout pregnancy compared with nonpregnant women, and normal B-type natriuretic peptide levels have a good negative predictive value for predicting 15 adverse cardiac events. Imaging Chest Radiography A chest radiograph is not obtained routinely in any pregnant patient because of concern about radiation exposure to the fetus, but it should not be withheld when the history and clinical findings raise concerns about maternal cardiac status. The chest radiograph in a normal healthy patient may show slight prominence of the pulmonary artery, and as pregnancy advances, elevation of the diaphragm may suggest an increase in the cardiothoracic ratio. Echocardiography Transthoracic echocardiography is the cornerstone of cardiac evaluation in pregnancy. In a normal pregnancy, the left ventricular end-diastolic measurement is slightly increased, and there may be similar increases in right ventricular size and the volumes of both atria. There can also be a small increase in the left ventricular wall thickness during pregnancy.

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Peaked P waves in V and V not meeting voltage criteria for right2 3 atrial overload allergy meter 25mg promethazine with mastercard. Left atrial isomerism means that there is no sinus node in either atrium; thus the abnormal P wave axis allergy treatment for cats promethazine 25 mg fast delivery. Atrial flutter (often in an atypical form allergy treatment vancouver buy discount promethazine 25mg, or so-called intraatrial reentrant tachycardia) is much more common in young patients than is atrial fibrillation. Deep Q waves in the left chest leads can be caused by left ventricular volume overload in a young person with aortic or mitral regurgitation. Pathologic Q waves can be evidence of the anomalous origin of the left coronary artery from the pulmonary artery. The Chest Radiograph The chest radiograph is another valuable tool for the discerning physician caring for patients with congenital heart defects (see Chapter 15). Although more recent technologies have rightly attracted much attention, there is value in learning how to interpret the chest radiograph. The following sections provide a number of clinical and radiographic differential diagnoses. Criteria for Shunt Vascularity The criteria for shunt vascularity include (1) uniformly distributed vascular markings with absence of the normal lower lobe vascular predominance; (2) a right descending pulmonary artery diameter that exceeds 17 mm; and (3) a pulmonary artery branch that is larger than its accompanying bronchus (best noted in the right parahilar area). Prominent vascularity is apparent only if the pulmonary-to-systemic flow ratio is greater than 1. The group of cyanotic patients with shunt vascularity include those with a single ventricle with transposition, persistent truncus arteriosus, tricuspid atresia without significant pulmonary outflow obstruction, total anomalous pulmonary venous connection, double-outlet right ventricle, and a common atrium. Causes of large central pulmonary arteries include increased pulmonary flow (main pulmonary artery and branches), increased pulmonary pressure (main pulmonary artery and branches), valvular pulmonary stenosis (main and left pulmonary arteries), and idiopathic dilation of the pulmonary artery (main pulmonary artery). This technique can generate information never previously available and do so more easily or more accurately than any other means. Major advances in hardware design, new pulse sequences, and faster image reconstruction techniques now permit rapid high-resolution imaging of the complex cardiovascular anatomy. Echocardiography Fetal Echocardiography Fetal echocardiography has “graduated” from being a special area of interest for some pediatric cardiologists to one of standard care. This is in part because of the limited number of views that are possible with the relatively fixed position of the transducer. Impact of Fetal Echocardiography Most major structural congenital heart defects are now accurately categorized through fetal echocardiography. Once the abnormalities are identified, families and obstetric caregivers can be counseled as to the impact of the abnormality both on the fetus and the family. Although termination of pregnancy is one of the consequences of prenatal diagnosis, it is not the main objective. In fact, data are starting to appear in the literature indicating that prenatal diagnosis of some major cardiac malformations has a direct impact on the outcome, from the vantage points of survival rates, morbidity rates, and costs. This is in part due to the fact that when a prenatal diagnosis is made, subsequent caregivers are prepared for the immediate postnatal effects of the defect. For example, in hypoplastic left heart syndrome and other duct-dependent lesions, prostaglandin E can be started immediately after birth, hopefully in a hospital within or attached1 to a pediatric cardiology facility. Fetal echocardiography has also permitted an improved understanding of the evolution of certain congenital cardiac malformations. For example, although the fetal heart is fully formed by the time a prenatal scan is performed, tremendous growth of the cardiac structures still must occur. Direct Fetal Intervention The next step is direct intervention for specific cardiac lesions. Intervention has initially involved obstructive lesions, thus far mainly being limited to the left ventricle. The rationale behind this therapy is based on the notion that the relief of obstructive outflow tract lesions will permit growth of the affected ventricle, potentially changing a neonatal pathway from univentricular to biventricular. Cardiac surgery for the fetus is also a future option, and indeed there is already a considerable amount of research on the impact of this in fetal animal models. A morphologic right atrium has a broad right atrial appendage, whereas a morphologic left atrium has a narrow left atrial appendage. Right and left atrial appendages, however, are difficult to visualize by transthoracic echocardiography, and one often has to rely on the abdominal situs to determine the atrial situs.

Most affected patients allergy medicine holistic buy promethazine mastercard, however allergy forecast irvine ca cheap promethazine 25 mg with visa, have normal valve function until late in life allergy shots better than pills cheap promethazine 25mg visa, when superimposed calcific changes result in valve obstruction (see later, Bicuspid Aortic Valve Disease). Differences in the biology driving the initiation and progression phases of calcific aortic valve disease could have important implications for medical therapies aimed at preventing, slowing, or reversing the path from aortic sclerosis to severe stenosis, both in terms of which pathways are relevant to target and when along the disease spectrum drugs targeting them are most likely to be effective. Endothelial disruption with inflammation (dashed line) and lipid infiltration are key elements in the initiation of disease. There are few data on the prevalence of disease initiation in at-risk patients, and progressive disease develops in only a subgroup of these patients. With end-stage disease, tissue calcification (red line) is the predominant tissue change, resulting in valve obstruction. Current imaging approaches are reliable only when substantial leaflet changes are present (in patients with progressive disease or valve obstruction), which limits clinical studies of interventions to prevent or slow the progression of early disease. Through a complex interplay of molecular events, the pliable, flexible valve becomes stiff and immobile, characterized grossly by fibrosis and calcification. The process is initiated by lipid infiltration and oxidative stress, which attract and activate inflammatory cells and promote the elaboration of cytokines 4 (Fig. Endothelial injury can be triggered by several factors, including lipid-derived species, cytokines, mechanical stress, and radiation injury. Osteoblast-like cells subsequently coordinate calcification of the aortic valve as part of a highly regulated process analogous to skeletal bone formation. In turn, neovascularization increases the recruitment of inflammatory cells and bone marrow–derived osteoprogenitor cells. Calcific nodules develop on both surfaces, and the orifice is reduced to a small, round or triangular opening (Fig. However, once even mild obstruction is present, hemodynamic progression occurs in almost all patients, with the interval from mild to severe obstruction ranging from less than 5 to more than 10 years (Fig. Decreased diastolic time and coronary perfusion pressure decrease myocardial O supply. In some cases, additional measures of hemodynamic severity, such as the energy loss index, valvular impedance, or evaluation with changing loading conditions (e. In response, the ventricle typically undergoes hypertrophic remodeling characterized by myocyte hypertrophy and increased wall thickness (Fig. Cardiac hypertrophy in response to pressure overload involves both adaptive and maladaptive 30 processes. Left Ventricular Diastolic Function 33,34 Hypertrophic remodeling also impairs diastolic myocardial relaxation and increases stiffness, as 35 modulated by cardiovascular and metabolic comorbidities. Higher cardiomyocyte stiffness, increased myocardial fibrosis, advanced-glycation end products, and metabolic abnormalities each contribute to 33 increased chamber stiffness and higher end-diastolic pressures. The development and severity of systolic dysfunction is the result of a complex interplay of factors, including the severity of valve obstruction, metabolic abnormalities, vascular load, inadequate hypertrophy (given the inverse correlation between wall stress and systolic performance), maladaptive hypertrophy (resulting 4,32,38 in impaired contractility), ischemia, and fibrosis. While patients may initially manifest pulmonary venous hypertension alone, some will go on to develop increased pulmonary vascular resistance, perhaps influenced by specific comorbidities and 46-48 chronicity of pulmonary venous hypertension. Among asymptomatic patients, exercise induced 49 pulmonary hypertension is associated with decreased event-free survival. Together, this creates an imbalance between myocardial O supply and demand, with the ischemia most pronounced in the subendocardium (2 see Fig. As valve obstruction becomes more severe, coronary flow reserve progressively decreases. Exercise or other states of increased O demand may exacerbate this imbalance and cause angina2 indistinguishable from that caused by epicardial coronary obstruction. Most patients now are diagnosed before symptom onset on the basis of the finding of a systolic murmur on physical examination, with confirmation of the diagnosis by echocardiography. Alternatively, exertional symptoms may be a result of the limited ability to increase cardiac output with exercise. More severe exertional dyspnea, with orthopnea, paroxysmal nocturnal dyspnea, and pulmonary edema, reflects various degrees of pulmonary venous hypertension. Syncope most often is caused by the reduced cerebral perfusion that occurs during exertion when arterial pressure declines because of systemic vasodilation and an inadequate increase in cardiac output related to valvular stenosis. Exertional hypotension also may be manifested as “graying-out spells” or dizziness on effort. This complication arises from shear stress–induced platelet aggregation with a reduction in high-molecular-weight 57 multimers of von Willebrand factor and increases in proteolytic subunit fragments.