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![ Sleep-disordered breathing
◦ Treatment with nocturnal positive airway pressure improves
oxygenation ， L VEF ， and 6-minute walk distance.
Anemia
◦ Anemia in heart failure is more common in the elderly ， in
those with advanced stages of HFrEF ， in the presence
of renal insufficiency ， and in women and African
Americans.
◦ The mechanisms include iron deficiency ， dysregulation
of iron metabolism ， and occult gastrointestinal bleeding.
Intravenous iron using either iron sucrose or
carboxymaltose (Ferric Carboxymaltose)
◦ Assessment in Patients with Iron Deficiency and Chronic
Heart Failure [FAIR-HF] trial) has been shown to correct
anemia and improve functional capacity. Erythropoiesis-
regulating agents such as erythropoietin analogues have
been studied with disappointing results.](https://image.slidesharecdn.com/heartfailure-180406170811/75/Heart-failure-68-2048.jpg)
More Related Content
Heart failure
- 1. PRESENTER: DR. JITHINGEORGE
- 4. Low-output HFoccurs secondary to ischemic heart disease, hypertension, dilated cardiomyopathy, and valvular and pericardial disease. high-output HF occurs in patients with reduced systemic vascular resistance, i.e., hyperthyroidism, anemia, pregnancy, arteriovenous fistulas, beriberi, and Paget’s disease.
- 5. in manypatients with low-output HF, the cardiac output may actually be just above the lower limit of normal range at rest (although lower than it had been previously), but fails to rise normally during exertion in patients with so-called high-output HF, the output may not exceed the upper limits of normal (although it would have been abnormally elevated had it been measured before HF supervened); instead, it may have fallen to within normal limits with HF.
- 17. In mildor moderately severe HF, the patient appears in no distress at rest except feeling uncomfortable when lying flat for more than a few minutes. In severe HF, the pulse pressure may be diminished, reflecting a reduction in stroke volume, and the diastolic arterial pressure may be elevated as a consequence of generalized vasoconstriction. In severe acute HF, systolic hypotension may be present, with cool, diaphoretic extremities, and Cheyne- Stokes respiration.
- 21. Electrocardiogram (ECG) presenceof LV hypertrophy or a prior MI (presence or absence of Q waves) as well as to determine QRS width to ascertain whether the patient may benefit from resynchronization therapy.
- 22. two-dimensional (2-D)echocardiogram/ Doppler provide a semiquantitative assessment of LV size and function as well as the presence or absence of valvular and or regional wall motion abnormalities (indicative of a prior MI). The presence of left atrial dilation and LV hypertrophy together with abnormalities of LV diastolic filling provided by pulse-wave and tissue Doppler, is useful for the assessment of HF with a preserved EF. The 2-D echocardiogram/Doppler is also invaluable in assessing RV size and pulmonary pressures ， which are critical in the evaluation and management of cor pulmonale
- 23. The mostuseful index of L V function is the EF (stroke volume divided by end-diastolic volume). EF has a number of limitations as a true measure of contractility ， since it is influenced by alterations in afterload and/or preload
- 24. Both B-typenatriuretic peptide (BNP) and N -terminal pro- BNP (NT-proBNP), which are released from the failing heart:sensitive markers for the presence of HF with depressed EF; they also are elevated in HF patients with a preserved EF. Natriuretic peptide levels ◦ increase with age and renal impairment, ◦ are more elevated in women ◦ can be elevated in right HF from any cause. Levels can be falsely low in obese patients. Other biomarkers, such as soluble ST -2 and galectin-3,are newer biomarkers that can be used for determining the prognosis of HF patients.
- 25. Treadmill orbicycle exercise testing is not routinely advocated for patients with HF useful for assessing the need for cardiac transplantation in patients with advanced HF A peak oxygen uptake (vo) < 14 mL/kg per min is associated with a relatively poor prognosis.
- 28. The severityof RV enlargement in cor pulmonale is a function of the increase in afterload. When the pulmonary vascular resistance is elevated and relatively fixed, as in pulmonary vascular or severe parenchymal lung disease, an elevation in cardiac output, as occurs with physical exertion, can elevate pulmonary artery pressure markedly. RV afterload may be augmented when the lungs are hyperinflated, as in chronic obstructive lung disease (COLD), due to the compression of the alveolar capillaries and the lengthening of the pulmonary vessels. RV afterload can also increase when lung volume is reduced following extensive pulmonary resection, as well as in restrictive lung diseases in which pulmonary vessels are compressed and Distorted. RV afterload rises with hypoxic pulmonary vasoconstriction caused by hypoxia or acidosis, which are important causes of pulmonary hypertension
- 29. symptoms ofchronic cor pulmonale generally are related to the underlying pulmonary disorder. Dyspnea Abdominal pain and ascites that occur with cor pulmonale are similar to the right HF that ensues in chronic HF. Lower-extremity edema may occur secondary to neurohormonal activation,elevated RV filling pressures,or increased levels of carbon dioxide and hypoxemia ， which can lead to peripheral vasodilation and edema formation
- 30. ECG insevere pulmonary hypertension shows P pulmonale, right axis deviation, and RV hypertrophy.
- 32. Therapeutic targetsin HFpEF include control of congestion: stabilization of heart rate and blood pressure, and improving exercise tolerance.
- 33. Candesartan inHeart Failure- ◦ Assessment of Mortality and Morbidity (CHARM) Preserved study: statistically significant reduction in hospitalizations but no difference in all-cause mortality in patients with HFpEF. Group (DIG) trial found no role for digoxin in the treatment of HFpEF. In the Study of the Effects of Nebivolol Intervention on Outcomes and Rehospitalization in Seniors with Heart Failure (SENIORS) trial of nebivolol HFpEF did not appear to benefit in terms of all-cause or cardiovascular mortality studies in the elderly with the angiotensin-ιonverting enzyme inhibitor (ACEI) enalapril showed no effect on peak exercise oxygen consumption,6-minute walk distance, aortic distensibility, left ventricular mass ， or peripheral neurohormone expression
- 35. Among whoreceived sildenafil at 20 mg three times daily for 3 months, followed by 60 mg three times daily for another 3 months ， compared with a placebo. There was no improvement in functional capacity ， quality of life ， or other clinical and surrogate parameters. Spironolactone improved echocardiographic indices of diastolic dysfunction but failed to improve exercise capacity ， symptoms ， or quality-of-life measures.
- 36. A uniquemolecule that hybridizes an ARB with an endopeptidase inhibitor ， LCZ696 ， increases the generation of myocardial cyclic guanosine 3’5' -monophosphate ， enhances myocardial relaxation ， and reduces ventricular hypertrophy. This dual blocker has been shown to reduce circulating natriuretic peptides and reduce left atrial size to a significantly greater extent than valsartan alone in patients with HFpEF.
- 38. tackle knownprecipitants of decompensation. Identification and management of medication nonadherence and use of prescribed medicines such as nonsteroidal anti-inf1ammatory drugs ， cold and f1u preparations with cardiac stimulants ， and herbal preparations ， including licorice ， ginseng ， and ma huang (an herbal form of ephedrine now banned in most places) ， are required. Aιtive infection and overt or ιovert pul monary thromboembolism should be sought ， identified ， and treated when clinical clues suggest such direction.
- 39. When possible， arrhythmias should be corrected by controlling heart rate or restoring sinus rhythm in patients with poorly tolerated rapid atrial fibrillation and by correcting ongoing ischemia with coronary revascularization or by correcting offenders such as ongoing bleeding in demand-related ischemia. A parallel step in management involves stabilization of hemodynamics in those with instability. The routine use of a pulmonary artery catheter is not recommended and should be restricted to those who respond poorly to diuresis or experience hypotension or signs and symptoms suggestive of a low cardiac output
- 41. Intravenous DiureticAgents ◦ thiazide diuretic agent such as metolazone in combination provides a synergistic effect and is often required in patients receiving long-term therapy with loop diuretiι agents.
- 42. Cardiorenal syndome ◦interplay of neurohormonal factors, potentially exacerbated by "backward failure" resulting from increased intra-abdominal pressure and impairment in return of renal venous blood flow ◦ diuretic therapy may be associated with a reduction in glomerular filtration rate and a worsening of cardiorenal syndrome when right-sided filling pressures remain elevated.
- 43. Ultrafiltration ◦ controlledrates of fluid removal,neutral effects on serum electrolytes,and decreased neurohormonal activity Current UF systems function with two large- bore, peripherally inserted venous lines. The primary end point is a change in serum creatinine and change in weight (reflecting fluid removal) at 96 hours.
- 44. VASCULAR THERAPY ◦Nitrates,nitroprusside, and nesiritide (a recombinant brain-type natriuretic peptide) ◦ Nesiritide was not associated with an increase or a decrease in the rates of death and rehospitalization and had a clinically insignificant benefit on dyspnea. Recombinant human relaxin 2 or serelaxin signs and symptoms of congestion ， and was associated with less early worsening of HF. Exploratory endpoints of hard outcomes at 6 months suggested positive signals in favor of mortality reduction
- 45. INOTROPIC THERAPY ◦increase intracellular concentration of cyclic adenosine monophosphate via direct or indirect pathways ， such as sympathomimetic amines (dobutamine) and phosphodiesterase-3 inhibitors (milrinone) respectively. ◦ activity leads to an increase in cytoplasmic calcium milrinone is slower acting and is renally excreted and thus requires dose adustments in the setting of kidney dysfunction. milrinone acts downstream from the ßl -adrenergic receptor, it may provide an advantage in patients receiving beta blockers when admitted to the hospital
- 46. Levosimendan isa calcium sensitizer that provides inotropic activity, but also possesses phosphodiesterase-3 inhibition properties that are vasodilators in action. This makes the drug unsuitable in states of low output in the setting of hypotension. Omecamtiv mecarbil, selective myosin activator, prolongs ejective period and increased fractional shortening.
- 47. NEUROHORMONAL ANTAGONISTS ◦Selective A l Adenosine Receptor Antagonist Rolofylline ◦ Tolvaptan - vasopressin 2 antagonist
- 52. ACEIs exerttheir beneficial effects in HFrEF as a class; however ， the beneficial effects of betablockers are thought to be limited to specific drugs. beta blocker use in HFrEF should be restricted to carvedilol ， bisoprolol, and metoprolol succinate it matters little which agent is initiated first; what does matter is that optimally titrated dose
- 53. Aldosterone antagonismis associated with a reduction in mortality in all stages of symptomatic NYHA class 1 to IV HFrEF. Elevated aldosterone levels in HFrEF promote sodium retention ， electrolyte imbalance ， and endothelial dysfunction and may directly contribute to myocardial fibrosis. The selective agent eplerenone (tested in NYHA Class 2 and post- myocardial infarction heart failure) and the nonselective antagonist spironolactone (tested in NYHA class III and IV heart failure) reduce mortality and hospitalizations ， with significant reductions in sudden cardiac death (SCD).
- 54. The ValsartanHeart Failure Trial (Val-HeFT) suggested that addition of valsartan in patients already receivingbtreatment with ACEIs and beta blockers was associated with a trend toward worse outcomes. Similarly, adding valsartan to captopril in patients with heart failure after myocardial infarction who were receiving background beta blocker therapy was associated with an increase in adverse events without any added benefit compared with monotherapy for either group. Thus ， the initial clinical strategy should be to use a two-drug combination first (ACEI and beta blocker; if beta blocker intolerant ， then ACEI and ARB; if ACEI intolerant ， then ARB and beta blocker). In symptomatic patients (NYHA class 11 一 IV) ， an aldosterone antagonist should be strongly considered ， but four-drug therapy should be avoided.
- 56. Hydralazine reducessystemic vascular resistance and induces arterial vasodilatation by affecting intracellular calcium kinetics; nitrates are transformed in smooth muscle cells into nitric oxide ， which stimulates cyclic guanosine monophosphate production and consequent arterial-venous vasodilation. This combination improves survival ， but not to the magnitude evidenced by ACEIs or ARBs.
- 57. Ivabradine, theheart rate without a negative inotropic effect. In the 2012 European Society of Cardiology guidelines for the treatment of heart failure ， ivabradine was suggested as second-line therapy before digoxin is considered in patients who remain symptomatic after guideline-based ACEIs, beta blockers, and mineralocorticoid receptor antagonists and with residual heart rate >70 beats/min. Another group in whom potential benefit may be expected includes those unable to tolerate beta blockers
- 59. ◦ diuretic agentsshould ideally ◦ be used in tailored dosing schedules to avoid excessive exposure CALCIUM CHANNEL ANTAGONISTS ◦ Amlodipine and felodipine ， second-generation calcium channel blocking agents. ◦ The firstgeneration agents ， including verapamil and diltiazem ， may exert negative inotropic effects and destabilize previously asymptomatic patients.
- 63. long-chain omega3polyunsaturated fatty acid(ω3 PUFAs) enriched circulating eicosapentaenoic acid (EP A) and docosahexaenoic acid (DHA) .
- 64. Thiamine deficiencyhave to be corrected.
- 65. Peripheral lowerextremity therapy using graded external pneumatic compression at high pressure is administered in 1 -hour sessions for 35 treatments (7 weeks) and has been proposed to reduce angina symptoms and extend time to exercise-induced ischemia in patients with coronary artery disease
- 66. The HeartFailure: A Controlled Trial Investigating Outcomes of Exercise Training (HF-ACTION) study investigated short-term (3-month) and long-term ( 1 2- month) effects of a supervised exercise. Maximal changes in 6-minute walk distance were evident at 3 months with significant improvements in cardiopulmonary exercise time and peak oxygen consumption persisting at 12 months. Therefore, exercise training is recommended as an adjunctive treatment in patients with heart failure.
- 68. Sleep-disordered breathing ◦Treatment with nocturnal positive airway pressure improves oxygenation ， L VEF ， and 6-minute walk distance. Anemia ◦ Anemia in heart failure is more common in the elderly ， in those with advanced stages of HFrEF ， in the presence of renal insufficiency ， and in women and African Americans. ◦ The mechanisms include iron deficiency ， dysregulation of iron metabolism ， and occult gastrointestinal bleeding. Intravenous iron using either iron sucrose or carboxymaltose (Ferric Carboxymaltose) ◦ Assessment in Patients with Iron Deficiency and Chronic Heart Failure [FAIR-HF] trial) has been shown to correct anemia and improve functional capacity. Erythropoiesis- regulating agents such as erythropoietin analogues have been studied with disappointing results.
- 69. Depression ◦ iscommon in HFrEF ◦ Antidepressants may improve depression ， promote vascular health ， and decrease systemic inflammation in HFrEF the Sertraline Against Depression and Heart Disease in Chronic Heart Failure (SADHART -CHF) trial, showed that sertraline was safe ， but did not provide greater reduction in depression or improve cardiovascular status among patients with heart failure and depression compared with nurse-driven multidisιiplinary management
- 70. Rhythm controlmay be achieved via pharmacotherapy or by percutaneous or surgiιal techniques. Antiarrhythmic drug therapy should be restricted to amiodarone and dofetilide ， both of which have been shown to be safe and effective but do not alter the natural history of the underlying disease
- 71. The singlemost important association of extent of dyssynchrony is a widened QRS interval on the surface electrocardiogram ， particularly in the presence of a left bundle branch block pattern. With placement of a pacing lead via the coronary sinus to the lateral wall of the ventricle ， cardiac resynchronization therapy (CRT) enables a more synchronous ventricular contraction by aligning the timing of activation of the opposing walls. Early studies showed improved exercise capacity, reduction in symptoms, and evidence of reverse remodeling.
- 75. Coronary arterybypass grafting (CABG) is considered in patients with ischemic cardiomyopathy with multivessel coronary artery disease. Revascularization is most robustly supported in individuals with ongoing angina and left ventricular failure. Revascularizing those with left ventricular failure in the absence of angina remains controversial
- 76. remodel theleft ventricle by reshaping it surgically in patients with ischemic cardiomyopathy and dominant anterior left ventricular dysfunction. in a 1000-patient trial in patients with HFrEF who underwent CABG alone or CABG plus SVR ， the addition of SVR to CABG had no diseae modifying effect. left ventricular aneurysm surgery is still advocated in those with refractory heart failure ， ventricular arrhythmias ， or thromboembolism arising from an akinetic aneurysmal segment of the ventricle
- 77. with varyingdegrees in patients with HFrEF and dilated ventricles. Ischemic MR (or infarct-related MR) is typically associated with leaflet tethering and displacement related to abnormal left ventricular wall motion and geometry. No evidence to support the use of surgical or percutaneous valve correction for functional MR exists as disease modifying therapy even though MR can be corrected.
- 78. Two preliminarypilot trials delivering cells via an intracoronary approach have been reported. In one ， autologous c-kit-positive cells isolated from the atria obtained from patients undergoing CABG were cultured and reinfused. In another ， cardiosphere-derived cells grown from endomyocardial biopsy specimens were used. These small trials demonstrated improvements in left ventricular function but require far more work to usher in a clinical therapeutic success
- 79. Targeting molecularaberrations using gene transfer therapy ， mostly with an adenoviral vector ， is emerging in HFrEF. Cellular targets under consideration include ß2- adrenergic receptors and calcium cycling proteins such as inhibitors of phospholamban. SERCA2a is deficient in patients with HFrEF and is primarily responsible for reincorporating calcium into the sarcoplasmic reticulum during diastole.
- 80. CUPID trialused coronary arterial infusion of adeno- associated virus type 1 carring the gene for SERCA2a and demonstrated that natriuretic peptides were decreased ， reverse remodeling was noted ， and symptomatic improvements were forthcoming. Stromal-derived factor 1 enhances myocardial repair and facilitates "homing" of stem cells to the site of tissue injury. Strategies using intramyocardial injections to deploy this gene at sites of injury are being studied.
- 83. Both methodsof implantation leave the recipient with a surgically denervated heart that does not respond to any direct sympathetic or parasympathetic stimuli but does respond to circulating catecholamines. The physiologic responses of the denervated heart to the demands of exercise are atypical but quite adequate for continuation of normal physical activity.
- 84. Allocation ofdonor hearts within a region is decided according to a system of priority that takes into account (1) the severity of illness, (2) the geographic distance from the donor ， and (3) the patient's time on the waiting list. A physiologic limit of -3 h of "ischemic" (out-of- body) time for hearts precludes a national sharing of hearts.
- 85. the highestpriority according to severity of illness is assigned to patients requiring hospitalization at the transplantation center for IV inotropic support ， with a pulmonary artery catheter in place for hemodynamic monitoring ， or to patients requiring mechanical circulatory support The second highest priority is given to patients requiring ongoing inotropic support ， but without a pulmonary artery catheter in place. All other patients are assigned a priority according to time accrued on the waiting list ， matching generally is based only on compatibility in terms of ABO blood group and gross body size
- 86. Most patientswho reach stage D ， or refractory end-stage heart failure ， are appropriately treated with compassionate end-Of life care. A subset of such patients who are younger and without significant comorbidities can be considered as candidates for heart transplantation. Exact criteria vary in different centers but generally take into consideration the patient' s physiologic age and the existence of comorbidities such as peripheral or cerebrovascular disease ， obesity ， diabetes ， cancer ， or chronic infection
- 87. Most cardiactransplantation programs currently use a three-drug regimen that includes a calcineurin inhibitor (cyclosporine or tacrolimus ， an inhibitor of T cell proliferation or differentiation (azathioprine ， mycophenolate mofetil ， or sirolimus) ， and at least a short initial course of glucocorticoids. Many programs also include an initial "induction" course of polyclonal or monoclonal antibodies to T cells in the perioperative period to decrease the frequency or severity of early posttransplantation rejection. Most recently introduced have been monoclonal antibodies (daclizumab and basiliximab) that block the interleukin 2 receptor
- 88. Cardiac allograftrejection is usually diagnosed by endomyocardial biopsy conducted either on a surveillance basis or in response to clinical deterioration. Biopsy surveillance is performed on a regular basis in most programs for the first year postoperatively (or the first 5 years in many programs).
- 90. generally adiffuse ， concentric ， and longitudinal process that is quite different from "ordinary" atherosclerotic CAD ， which is more focal and often eccentric. The underlying etiology most likely is primarily immunologic injury of the vascular endothelium ， but a variety of risk factors influence the existence and progression of CAD ， including nonimmunologic factors such as dyslipidemia ， diabetes mellitus ， and cytomegalovirus (CMV) infection.
- 91. the immunosuppressiveagents mycophenolate mofetil and the mammalian target of the rapamycin (mTOR) inhibitors sirolimus and everolimus have been shown to be associated with short-term lower incidence and extent of coronary intimal thickening. The use of statins also is associated with a reduced incidence of this vasculopathy ， and these drugs are now used almost universally in transplant recipients unless contraindicated. Palliation of CAD with percutaneous interventions is probably safe and effective in the short term ， although the disease often advances relentlessly Because of the denervated status of the organ ， patients rarely experience angina, pectoris ， even in advanced stages of disease. Retransplantation is the only definitive form of therapy for advanced allograft CAD
- 92. Lymphoproliferativen disordersare among the most frequent posttransplantation. Mostly EBV. Most recently ， specific antilymphocyte (CD20) therapy. Cutaneous malignancies (both basal cell and squamous cel1 carcinomas) also occur.
- 93. since theintroduction of cyclosporine ， infections with unusual and opportunistic organisms are still the major cause of death during the first postoperative year and remain a threat to the chronically immunosuppressed patient throughout life. CMV ， Aspergillus ， and other opportunistic agents
- 94. as temporary"bridges" to heart transplantation in candidates in whom medical therapy begins to fail before a donor heart becomes available.
- 95. patients atrisk of imminent death from cardiogenic shock are eligible for mechanical support. if patients have a left ventricular ejection fraction <25% or a peak VO ， < 14 mL/kg per min or are dependent on inotropic therapy or support with intra-aortic balloon counterpulsation ， they may be eligible for mechanical support.
- 97. Pulsatile devicesare ventricular assist devices whose mechanism of action mandates the alternating filling and emptying of a volume chamber within the device that mimics the mechanism of action of the natural heart. Nonpulsatile devices have a mechanism of action that results in continuous blood flow through the device,eliminating the need for pulsatility. The pulsatile devices are larger ， bulkier ， and associated with greater energy requirements and higher rates of complications than the nonpulsatile devices.
- 98. The olderdesigns have tended to be axial-flow pumps ， which operate on the Archimedes screw principle. Continuous-flow devices have been dependent on the presence of blood-washed bearings within the pump housing and may be associated with an increased risk of blood and platelet activation. The newer devices are centrifugal in design; the blood flow takes a 90 degree turn between the inlet section of the pump and the outlet section Another major difference in the newer devices is the absence of blood washed bearings (with most devices having magnetical1y levitated impel1ers) .