Sterling College, Sterling Kansas. H. Phil, MD: "Purchase cheap Enalapril online - Safe online Enalapril".
Concomitant surgical procedures cheap 5 mg enalapril with visa arteria magna, renal and hepatic dysfunction cheap enalapril 10mg on line prehypertension erectile dysfunction, and preoperative symptomatic status are the principal 8 10 mg enalapril overnight delivery blood pressure essentials reviews,19 order genuine enalapril blood pressure young age,28 determinants of surgical risk. Transcatheter approaches to tricuspid valve repair and replacement using various methods 31,32 and devices are feasible and currently being studied in clinical trials (see Chapter 72). The risk of thrombosis of mechanical prostheses is greater in the tricuspid than in the mitral or the aortic position, presumably because pressure and flow rates are lower in the right side of the heart. For this reason, a bioprosthesis is the valve of choice for the tricuspid position in adults. However, management decisions should be made by a heart valve team, including cardiology, cardiac surgery, and infectious disease specialists. Diseased valvular tissue should be excised to eradicate the endocarditis, and antibiotic treatment can then be continued. A bioprosthetic valve may therefore be inserted several months after valve excision and control of the infection. Rheumatic inflammation of the pulmonic valve is very uncommon, usually is associated with involvement of other valves, and rarely leads to serious deformity. Carcinoid heart disease often involves the pulmonic valve, and plaques, similar to those involving the tricuspid valve, are often present in the outflow tract of the right ventricle of patients with malignant carcinoid. A, Zoomed two-dimensional parasternal short-axis image at the level of the aortic valve shows the pulmonic valve in long axis in mid-diastole, demonstrating a marked thickening with retraction of the pulmonic valve leaflets (arrow) and resulting in failure of leaflet closure. Pulmonic Regurgitation Causes and Pathology Pulmonic regurgitation can result from dilation of the valve ring secondary to pulmonary hypertension (of any cause) or from dilation of the pulmonary artery. These include congenital malformations, such as absent, malformed, fenestrated, or supernumerary leaflets. Less common causes include trauma; carcinoid syndrome, in which leaflet thickening and retraction result in mixed stenosis and regurgitation (see Fig. B, Doppler tracing shows a dense signal in diastole with a steep deceleration slope that reaches the baseline before the end of diastole (arrow). D, Graph of the pulmonary artery flow within the region of interest indicated in C demonstrates both antegrade and retrograde flow. The right ventricle is hyperdynamic and produces palpable systolic pulsations in the left parasternal area, and an enlarged pulmonary artery often produces systolic pulsations in the second left intercostal space. An S and S originating from the right ventricle often are audible, most readily in the3 4 fourth intercostal space at the left parasternal area, and are augmented by inspiration. This murmur is high-pitched, blowing, and decrescendo, beginning immediately after P , and is most prominent in the2 left parasternal region in the second to fourth intercostal spaces. Both the pulmonary artery and right ventricle are usually enlarged, but these signs are nonspecific. Abnormal motion of the septum characteristic of volume overload of the right ventricle in diastole and septal flutter may be evident. Additionally, the density of the Doppler profile of the jet is increased, and reversal of flow in the pulmonary artery by color flow imaging can be detected a distance from the valve. Multivalvular Disease Various clinical and hemodynamic syndromes can be produced by different combinations of valvular abnormalities. It frequently is caused by rheumatic fever but is also seen with congenital heart disease, carcinoid heart disease, radiation heart disease, and connective tissue disorders. Marfan syndrome and other connective tissue disorders may cause multivalve prolapse and dilation, resulting in multivalvular regurgitation. Congenital heart disease may predispose to infective endocarditis or degenerative disease. In patients with multivalvular disease, the clinical manifestations depend on the relative severity of each of the lesions. When the valvular abnormalities are of approximately equal severity, clinical manifestations produced by the more proximal (upstream) of the two valvular lesions (i. It is important to recognize multivalvular involvement preoperatively because failure to correct all significant valvular disease at the time of operation increases mortality. Specific guideline 13,40 recommendations exist for concomitant valve surgery in patients undergoing surgery on another valve. In patients with multivalvular disease, the relative severity of each lesion may be difficult to estimate by clinical examination because one lesion may mask the manifestations of the other. Therefore, patients with suspected multivalvular involvement being considered for surgical treatment should undergo careful clinical evaluation and full Doppler echocardiographic evaluation. Mixed stenotic and regurgitant lesions can be assessed with a combination of two- and three-dimensional imaging, including planimetry of stenotic orifices, color flow imaging, and Doppler. Multiple valves can be systematically assessed during 41 exercise; this is particularly helpful in assessing the patient with exertional symptoms, especially when these seem disproportionate to findings on imaging at rest. Rheumatic aortic valve disease may result in primary regurgitation, stenosis, or mixed stenosis and regurgitation. Echocardiography is of decisive value in the evaluation of patients with rheumatic disease and allows accurate diagnosis of the presence and severity of multivalve involvement, taking into consideration the altered flow conditions with serial lesions. It is vital to recognize the presence of hemodynamically significant aortic valvular disease (i. Physical findings may be confusing because it may be difficult to recognize two distinct systolic murmurs. When both valvular leaks are severe, this combination of lesions is poorly tolerated. With severe combined regurgitant lesions, regardless of the cause of the mitral lesion, blood may reflux from the aorta through both chambers of the left side of the heart into the pulmonary veins. An intrinsically normal mitral valve that is regurgitant because of a dilated annulus should not be replaced. Surgical Treatment of Multivalvular Disease Replacement or repair of multiple valves presently comprises 12% of valve procedures and usually is 43 associated with a higher risk and poorer survival than replacement of either of the valves alone. The operative risk of double-valve replacement is approximately 70% higher than for single-valve replacement. In view of the higher risks, a higher threshold is required for multivalvular versus single-valve surgery. Diagnosis and treatment of tricuspid valve disease: current and future perspectives. Evaluation of tricuspid valve morphology and function by transthoracic three-dimensional echocardiography. Trends and outcomes of tricuspid valve surgery in North America: an analysis of more than 50,000 patients from the Society of Thoracic Surgeons database. Right ventricular systolic function in organic mitral regurgitation: impact of biventricular impairment. Significant lead-induced tricuspid regurgitation is associated with poor prognosis at long-term follow-up. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.
These risk factors include can be intraluminal (distal foreign objects buy enalapril with mastercard arteria supraorbitalis, asthma); age of greater than 60 years purchase enalapril in united states online blood pressure machine name, pulmonary hypertension purchase enalapril 5 mg visa pulse pressure 24, intramural (edema order enalapril 10mg free shipping exo heart attack, bronchomalacia, bronchiolitis); congestive heart failure, chronic lung disease, isch- or extramural (compression from tumor, lymph emic heart disease, stroke, and cancer. The narrowing increases both airway resis- factors that can contribute to thrombus formation in- tance and turbulence of airfow. The imbalance be- clude (1) venous stasis, (2) hypercoagulability, and tween pulmonary ventilation and perfusion affects (3) endothelial injury with infammation to the vessel oxygen exchange. Trauma, muscle spasm, or clot dissolution can harder to maintain adequate ventilation, resulting in cause the thrombus to dislodge, creating an embolus. Emboli circulate in the blood to the right side of the heart and enter the lungs via the pulmonary History of Asthma artery. If the clot is not dissolved within the lungs, it Both adults and children can experience airway ob- occludes the pulmonary artery and obstructs blood struction caused by reactive airways disease or asthma. Hypoxemia and hypercapnia lead to symptoms of dyspnea in individuals with or without prior history dyspnea. Careful questioning regarding associated panied by fever, chest pain, and restlessness. It is isolated disorder or as a part of systemic lupus erythe- often associated with cough that is worse in the morn- matosus, can lead to abnormal clotting. This has a he- ing, clear to yellow color sputum, exercise intolerance, reditary component and can occur as a spontaneous and fatigue. In children with heart disease, dyspnea occurs be- cause of insuffcient blood being pumped to the lungs Oral Contraceptives/Estrogen as a result of congenital structural anomaly or pump The estrogen in oral contraceptives causes increased failure or secondary to pulmonary hypertension. A complete medication history can provide clues to a Chronic progressive dyspnea because of lung involve- possible hypercoagulability state. Periodic recurrent dyspnea is most often the result of Key Questions bronchospasm and infamed bronchi caused by asthma. The patient or parent may report audible wheezes, decreased exercise Past History of Disease tolerance, and frequent cough. All of these factors lead to turbulent expi- related to activity and is relieved with rest or use of ratory fow and audible wheeze. Hematological diseases can affect the oxygen- carrying capacity of the blood, resulting in tissue hy- Medication Use poxia and a decrease in arterial pH, which stimulates The dyspnea related to asthma may be relieved by use the central nervous system to produce the symptom of of bronchodilator agents and steroids. Dyspnea can occur whenever the oxygen- Allergies carrying capacity of the blood is decreased because of Exposure to cold and/or allergens, exercise, and viral the inability of hemoglobin to bind oxygen. Carbon respiratory tract infections frequently precipitate chronic monoxide poisoning, cyanide poisoning, and methe- recurrent dyspnea associated with asthma. Recumbence, missed medications, high sodium in- The progressive dyspnea of anemia is usually asso- take, and exertion often precipitate chronic dyspnea ciated with fatigue, palpitations, light-headedness, or associated with heart failure. Hyperventilation Alleviating Factors Hyperventilation syndrome, a nonemergent but fright- Alleviating factors for dyspnea include sitting upright, ening experience, is usually accompanied by paresthe- taking diuretic medications, using bronchodilators, and sias around the mouth and of the distal extremities. Anxiety-related dyspnea should not be diagnosed until more serious causes have been ruled out. When dyspnea is caused by pulmonary or cardiac conditions, the shortness of breath worsens with in- Key Questions creasing activity and improves with rest. Key Questions l What activities are associated with shortness of Immunizations breath? Nausea, vomiting, and diarrhea result, Chronic dyspnea of pulmonary origin is most fre- followed by cranial nerve involvement, diplopia, weak quently precipitated and aggravated by exposure to suck, facial weakness, and absent gag refex. This is true for both progressive and recurrent ized hypotonia and weakness then develop and can dyspnea. As the disease progresses, less and Farm Residence less intense exercise, even talking, and respiratory Organophosphate chemicals that are commonly used tract infection can result in increased shortness of as insecticides can cause a myasthenia-like syndrome Chapter 14 • Dyspnea 163 in children exposed to these toxins. This is caused by an increase in the metabolic requirement for Neuromuscular Effects a given amount of work. In addition, the diaphragm Abnormalities of neural or neuromuscular transmission moves against increased abdominal pressure and the to the respiratory muscles can result in paresis or paraly- chest wall is heavier, resulting in more energy required sis, leading to alveolar hypoventilation. Note General Appearance and Observe Posture In children, some causes that affect the primary re- Patients who appear in acute distress with manifesta- spiratory center are myopathies, insecticide poisoning, tions of severe oxygen deprivation require emergent and lead poisoning. Tachypnea and hypopnea are critical clues to Secondary Causes impending respiratory failure. Use of accessory mus- Diseases that affect the central nervous system and cles to breathe, posturing, and chest retraction all produce respiratory distress include meningoencepha- point to severe dyspnea. In such situations consider pulmonary em- bolism, anaphylaxis, foreign body aspiration, pneu- Does the patient have any pertinent risk factors that will mothorax, status asthmaticus, and severe heart fail- point me in the right direction? Determine if the patient has to lean forward or sit l What type of work do you do? Individuals at risk for developing dyspnea are those A child who is in acute respiratory distress, sitting with a history of pulmonary and/or heart disease, ciga- forward, and perhaps speaking with a muffed voice or rette smokers and those subjected to passive exposure drooling may have epiglottitis and immediate assis- or second-hand smoke, people exposed to noxious tance should be secured. Do not attempt to lay the child environmental pollutants, and individuals with a pre- down or inspect the throat because this can occlude the disposition to allergies or asthma. Work Assess Level of Consciousness Occupational exposure to asbestos, silicon, paint and Diminished level of consciousness, confusion, and chemical fumes, and coal dust place the patient at risk restlessness are manifestations of hypoxia in a patient for lung disease with resultant dyspnea. Obesity An acutely ill child can have an alteration in level of Physically deconditioned and obese people report dys- consciousness, restlessness, mouth breathing, and far- pnea on exertion more frequently than their physically ing of the nostrils. The chest cannot be adequately to overcome the elastic forces of the lung, the tissue viewed through clothing. Many respiratory abnormali- viscosity of the lung and chest wall, and airway resis- ties are unilateral or localized. When there is a problem with any of these, the one side of the body with those on the other. Also com- accessory muscles (sternocleidomastoid, serratus ante- pare front to back. Retractions begin in lower intercostal spaces and deformities of the chest wall and reduction in lung vol- then move up to the higher spaces. In an infant, head ume and pulmonary compliance secondary to pathologi- bobbing in time with respiration refects use of the cal changes in the lung parenchyma or pleura. Decreased vol- Observe the Rate, Rhythm, and Depth ume necessitates an increase in respiratory rate to main- of Respiration for 1 Full Minute tain a normal volume. The work of breathing must be In children, the respiratory rate should be counted increased to overcome the reduced compliance. Kyphoscoliosis is associated with marked structural Tachypnea is an early sign of most pulmonary, pa- abnormality of the thoracic cage, leading to abnormal renchymal, cardiac, or systemic causes of respiratory positioning and functioning of the respiratory muscles. Hyperventilation can occur secondary to aci- The lungs are compressed by the thoracic deformity, dosis or central nervous system disease. Breathing entails a vous system depression can lead to hypoxemia and high work and energy cost, and dyspnea can appear. Shallow respirations, which are rapid, indicate chest infection and respiratory failure because of de- that restrictive forces must be overcome. Pectus carinatum is associated with chronic lung disease such Box 14-1 Abnormal Breathing Patterns as asthma or with cystic fbrosis, heart disease such as mitral valve prolapse, Marfan syndrome, and idio- Cheyne-Stokes respirations are manifested by rhythmic pathic scoliosis.
Purchase enalapril 10mg with mastercard. Good Practice for Blood Pressure Monitors.
Overall discount enalapril online visa pre hypertension natural cure, new or worsened ventricular tachyarrhythmias occur in approximately 4% of patients taking sotalol; this response is the result of TdP in approximately 2 discount 5 mg enalapril free shipping blood pressure medication od. Other adverse effects typically seen with other beta blockers also apply to sotalol purchase enalapril 10mg without a prescription heart attack japanese. Ibutilide is administered intravenously and has a large volume of distribution (see Table 36 cheap 10mg enalapril with mastercard blood pressure how low is too low. Clearance is predominantly renal, with a drug half-life averaging 6 hours, but with considerable interpatient variability. A second 1-mg dose may be given after the first dose is finished if the arrhythmia persists. Patients must have continuous electrocardiographic monitoring throughout the dosing period and for 6 to 8 hours thereafter because of the risk for ventricular arrhythmias. Ibutilide has been used safely and effectively in patients who were already taking amiodarone or propafenone but should be used with caution in these cases. In one study, all 50 patients given ibutilide before attempted electrical cardioversion achieved sinus rhythm, whereas only 34 of 50 who did not receive the drug converted to sinus rhythm. Of note, all 16 patients who did not respond to electrical cardioversion without ibutilide were successfully electrically cardioverted to sinus rhythm when a second attempt was made after ibutilide pretreatment. This effect develops within the first 4 to 6 hours of dosing, after which the risk is negligible. Thus, patients must undergo electrocardiographic monitoring for up to 8 hours after dosing. This requirement makes using ibutilide in emergency departments or private offices problematic. The safety of ibutilide during pregnancy has not been well studied, and its use in pregnant women should be restricted to those in whom no safer alternative exists. This effect is more prominent in the atria than in the ventricles—30% increase in the atrial refractory period versus 20% in the ventricle. Its mean elimination half-life is 7 to 13 hours, with 50% to 60% excreted unchanged in urine (see Table 36. Significant drug-drug interactions have been reported in patients taking dofetilide; cimetidine, verapamil, ketoconazole, and trimethoprim, alone or in combination with sulfamethoxazole, cause a significant elevation in the dofetilide serum concentration and should not be used with this drug. Oral dofetilide is indicated for prevention of episodes of supraventricular tachyarrhythmias, particularly atrial flutter and fibrillation. Because the risk for TdP is highest at drug initiation, it should be used continuously and not as intermittent outpatient dosing. Its use in pregnancy has not been studied extensively, and it should probably be avoided in pregnant women if possible. Nifedipine and other dihydropyridine agents exhibit minimal electrophysiologic effects at clinically used doses; these drugs are not discussed here. L in all cardiac fibers, verapamil reduces the plateau height of the action potential, slightly shortens muscle action potential at pharmacologic concentrations, and slightly prolongs Purkinje fiber action potential (see Tables 36. Verapamil suppresses slow responses elicited by various experimental methods, as well as sustained triggered activity and early and late afterdepolarizations. Verapamil slows activation of the slow channel and delays its recovery from inactivation. The l-isomer blocks the slow inward current carried by calcium, as well as other ions, traveling through the slow channel. Verapamil can also cause other effects that indirectly alter cardiac electrophysiology, such as decreasing platelet adhesiveness or reducing the extent of myocardial ischemia. The spontaneous sinus rate may decrease slightly, an effect only partially reversed by atropine. More often, the sinus rate does not change significantly because verapamil causes peripheral vasodilation, transient hypotension, and reflex sympathetic stimulation, which mitigates any direct slowing effect that verapamil exerts on the sinus node. If verapamil is given to a patient who is also receiving a beta blocker, the sinus node discharge rate may slow because reflex sympathetic stimulation is blocked. Verapamil does not exert a significant direct effect on atrial or ventricular refractoriness or on the anterograde or retrograde properties of accessory pathways. Because verapamil interferes with excitation-contraction coupling, it inhibits vascular smooth muscle contraction and causes marked vasodilation in coronary and other peripheral vascular beds. The reflex sympathetic effects of verapamil may reduce its marked negative inotropic action on isolated cardiac muscle, but the direct myocardial depressant effects of verapamil may predominate when the drug is given in high doses. In patients with well-preserved left ventricular function, combined therapy with propranolol and verapamil appears to be well tolerated, but beta blockade can accentuate the hemodynamic depressant effects produced by oral verapamil. Patients with reduced left ventricular function may not tolerate the combined blockade of beta receptors and calcium channels; thus, in these patients, verapamil and a beta blocker should be used in combination either cautiously or not at all. Verapamil reduces myocardial oxygen demand while decreasing coronary vascular resistance. Peak alterations in hemodynamic variables occur 3 to 5 minutes after completion of a verapamil injection, with the major effects dissipating within 10 minutes. Systemic resistance and mean arterial pressure decrease, as does left ventricular dP/dtmax, and left ventricular end-diastolic pressure increases. Heart rate, cardiac index, and mean pulmonary artery pressure do not change significantly in individuals with normal resting left ventricular systolic function. Thus the afterload reduction produced by verapamil significantly counterbalances its negative inotropic action, so the cardiac index may not be reduced. In addition, when verapamil slows the ventricular rate in a patient with tachycardia, hemodynamics may also improve. Nevertheless, caution should be exercised in giving verapamil to patients with severe myocardial depression or those receiving beta blockers or disopyramide because hemodynamic deterioration may progress in some patients. After oral administration, absorption is almost complete, but its overall bioavailability of 20% to 35% suggests substantial first-pass metabolism in the liver, particularly of the l-isomer. Norverapamil is a major metabolite that may contribute to the electrophysiologic actions of verapamil. Significant hypotension resulting from intravenous diltiazem can be countered by volume expansion or the judicious use of a pure vasoconstrictor agent such as phenylephrine. Various long-acting preparations (once daily) are available for verapamil and diltiazem. Verapamil must be used cautiously in patients with significant hemodynamic impairment or in those receiving beta blockers, as noted earlier. Hemodynamic collapse has been noted in infants, and verapamil should be used cautiously in children younger than 1 year. Verapamil should also be used with caution in patients with sinus node abnormalities because marked depression of sinus node function or asystole can result in some of these patients. Isoproterenol may be more effective for the treatment of bradyarrhythmias, and calcium may be used for the treatment of hemodynamic dysfunction secondary to verapamil. Although these drugs should probably not be used in patients with overt heart failure, if it is caused by one of the supraventricular tachyarrhythmias noted earlier, verapamil or diltiazem may restore sinus rhythm or significantly decrease the ventricular rate and thereby lead to hemodynamic improvement.
This is believed to be secondary to alterations in doxorubicin metabolism when they are given with taxanes cheap enalapril 5mg overnight delivery blood pressure 7860. Alkylating and Alkylating-Like Agents Cyclophosphamide cheap enalapril 10mg visa blood pressure medication on empty stomach, used in the treatment of breast cancer and hematologic malignancies buy discount enalapril 5 mg on line arrhythmia in dogs, is typically well tolerated enalapril 5mg arterial line. Platinum-based agents, often considered alkylating-like agents, are commonly used in germ-cell testicular cancer, as well as ovarian, lung, and breast cancers and other solid tumors. Platinum cardiotoxicity has been perhaps most well studied in the testicular cancer population. Some studies have also suggested that platinum is associated with endothelial damage, because plasma platinum levels remain detectable in patients up to 20 years after therapeutic exposure. These symptoms, often treatable with nitrates and calcium channel blockers, have historically been attributed to vasospasm, although the mechanism and pathophysiology remain poorly defined. The oral agent capecitabine (Xeloda), which is metabolized to fluorouracil, has also been associated with a 6. Additional Cancer Therapies Proteasome Inhibitors Proteasome inhibitors, such as bortezomib and carfilzomib, are used in the treatment of relapsed or refractory and newly diagnosed cases of multiple myeloma, a disorder characterized by an excess of bone marrow cells and monoclonal protein. Cancer cells generally have higher levels of proteasome activity compared with normal cells, and are thus believed to be particularly susceptible to the proapoptotic effects of proteasome inhibitors. Protein homeostasis, 11 however, is also hypothesized to play a role in the maintenance of cardiac function. Immune-Modulating Agents Immune modulatory agents such as thalidomide and lenalidomide are used in the treatment of multiple 12 myeloma. Reportedly, this incidence increases significantly when the agents are used in combination with other agents such as dexamethasone or anthracyclines. To mitigate the risk of thromboembolism, the International Myeloma Working Group recommends the use of aspirin, low-molecular-weight heparin, or warfarin with combination therapy, with the exact agent dependent upon the risk factor profile and the individual patient. Immune check-point inhibitors are a newer class of agents used in a variety of solid tumors. These agents have been associated with a very low, but clinically significant, risk of myocarditis. Targeted Therapies The treatment of a number of malignant neoplasms has changed radically during the past few years with the advent of so-called targeted therapies. As opposed to traditional chemotherapeutics, which target basic cellular processes present in most cells, these therapies target factors that are specifically dysregulated in cancerous cells. It was hoped that this approach would reduce toxicities typical of standard chemotherapeutics (e. In some situations, this has been the case, but concerns about cardiotoxicity have surfaced for several agents. Studies suggest that adherence to cardiac monitoring may be low, and some clinicians favor the notion that monitoring be 16 performed only in high-risk individuals. This classification has largely fallen out of favor because of its oversimplification of the situation and because of the lack of strong evidence that the biologic underpinnings and clinical manifestations of anthracycline and trastuzumab cardiotoxicity are fundamentally distinct and do not overlap. Dose delays and interruptions have also been shown to be associated with worse overall survival rates, emphasizing the importance of the delivery of cancer therapy. It is widely speculated that the cardiac dysfunction observed with trastuzumab is a direct consequence of 6,7 ErbB2 inhibition in cardiomyocytes, but this remains to be definitively proven (Fig. Basic studies have been limited, in part, by the lack of robust systems to study the in vitro and in vivo effects of trastuzumab, a humanized antibody. All of these pathways are fundamental for cardiac homeostasis, cell survival, mitochondrial function, cell growth, and focal adhesion formation. ErbB2 and ErbB4 expression is preserved during compensated hypertrophy, but it declines in the early stages of systolic dysfunction in mice subjected to pressure overload. Overall, these findings suggest that perturbations in ErbB receptor signaling are important in the maintenance of cardiac function. More recent data suggest that disruption of ErbB2 signaling results in endothelial dysfunction and an altered vascular phenotype, potentially contributing to the cardiomyopathic phenotype. There are a number of newer ErbB antagonists, including pertuzumab and ado-trastuzumab emtansine. As with trastuzumab, clinical guidelines for pertuzumab suggest monitoring of cardiac function every 3 months. The maytansine-derived cytotoxic agent, which is able to inhibit cell division and induce tumor cell death, is attached to trastuzumab by a stable thioether linker. To date, no major signal for dose-limiting cardiotoxicity has been observed, although long-term data with larger numbers of patients are needed to define the risk of cardiotoxicity with greater certainty. Tyrosine Kinase Inhibitors and Monoclonal Antibodies Many of the targeted cancer therapeutics inhibit the activity of tyrosine kinases. Both bevacizumab and sorafenib have less pronounced cardiotoxic effects than sunitinib. Recent studies have suggested its potential effectiveness in the adjuvant renal cell carcinoma setting. Of these agents, we focus on describing the epidemiology and basic mechanisms of sunitinib, because it is the most well studied agent to date and is used widely in clinical practice. The majority of these events occur early after the initiation of therapy, primarily within the first 3 months, with a low risk of late cardiotoxicity. Additional content on the mechanisms of sunitinib toxicity are presented in the online supplement titled Sunitinib Cardiotoxicity. Nilotinib and ponatinib have both been associated with peripheral vascular disease and ischemic heart disease. Retrospective studies suggest the incidence of peripheral arterial disease is on the order of 1. Comprehensively deciphering the mechanisms of these kinase inhibitors remains challenging given their nonselectivity; they typically affect more than 30 different kinases. These therapies have adverse metabolic effects, and observational studies suggest that they result in increased body weight, decreased insulin sensitivity, and dyslipidemia. Selective Estrogen Receptor Modulators and Aromatase Inhibitors Tamoxifen is a selective estrogen receptor modulator widely used in adjuvant therapy for estrogen receptor–positive breast cancer. Some studies demonstrate a potential effect on decreasing the ischemic heart disease 24 incidence, with a relative risk of 0. An increased risk of thromboembolic events, however, is well established; they occur largely during the first 2 years of exposure and in older women. The two major classes that are currently in use differ according to their ability to bind reversibly versus irreversibly to aromatase. Retrospective analyses of 4456 women treated between 1954 and 1984 who had survived at least 5 years after breast cancer treatment were evaluated an average of 28 years after cancer therapy. In a single-center, retrospective analysis of 1279 Hodgkin lymphoma survivors treated with mediastinal radiation, the cumulative incidence of cardiac 30 disease increased from 2.