A Patient Is Going To Have A Repair Of A Heart Valve. What Type Of Anesthesia Would Be Used?

Indian J Anaesth. 2022 Sep; 61(ix): 721–727.

Valvular eye disease and anaesthesia

Abhijit Paul

Section of Cardiac Anaesthesiology, Narayana Found of Cardiac Sciences, Bengaluru, Karnataka, India

Sucharita Das

Section of Cardiac Anaesthesiology, Narayana Institute of Cardiac Sciences, Bengaluru, Karnataka, India

Abstract

Valvular eye disease presents as mixed spectrum lesion in healthcare settings in the third-world and developing countries. Rheumatic middle affliction still forms the majority of the aetiopathology of valve lesions. Mitral and aortic valve lesions top the listing of valvular pathology. A thorough understanding of the pathophysiology of valvular heart disease is essential while planning anaesthesia and perioperative care for such patients. Meticulous use of optimal fluids, close monitoring of the changing haemodynamics and avoidance of situations that can cause major reduction of cardiac output and fluid shifts are mandatory to achieve good clinical outcome. We searched MEDLINE using combinations of the following: anaesthesia, aortic, mitral, regurgitation, stenosis and valvular heart affliction. Nosotros likewise hand searched textbooks and articles on valvular heart illness and anaesthesia. This article mainly focuses on the agreement the pathophysiology of valvular eye illness in patients presenting for non-cardiac surgeries in secondary and tertiary care setting.

Fundamental words: Anaesthesia, aortic, mitral, regurgitation, stenosis, valvular heart illness

INTRODUCTION

The incidence of middle disease ranges from 0.7% in 18–44 years age group up to xiii.iii% in individuals who are 75 years or older.[1] In industrialised countries, the prevalence of valvular heart disease is estimated at ii.5%.[two] A patient with a diseased heart valve can have associated heart failure or cardiac dysrhythmias such as atrial fibrillation which increase the risk of perioperative adverse events. Proficient perioperative optimisation and adequate monitoring aid overcome haemodynamic disturbance which may occur during anaesthesia and surgery. A thorough understanding of the pathophysiology of valvular heart disease is mandatory for meticulous planning to achieve a favourable clinical result. Perioperative assessment includes a recent evaluation within 6 months along with echocardiography (ECHO) and detailed assessment of the progress of the symptoms. Single or multiple heart valves may be affected with isolated or mixed lesions.

Classification of valvular heart disease can be categorised based upon the aetiology:

Congenital valvular heart disease (atresia, stenosis, malposition, abnormalities of valve structure-bicuspid valves)
Acquired center valve disease
1. Endocarditis (regurgitation more mutual)
2. Rheumatic heart affliction: Mitral stenosis (MS), mitral regurgitation (MR), aortic stenosis (AS), aortic regurgitation (AR)
3. Senile calcific AS
4. Myxomatous mitral valve prolapse leading to regurgitation.

The virtually common valvular lesions in clinical settings are MS and AS.[iii]

AORTIC STENOSIS

Every bit can be congenital or acquired. Idiopathic senile degeneration with sclerosis and calcification of the valve due to chronic inflammation accounts for the bulk of acquired segment of Every bit. There is a articulate clan betwixt the clinical risk factors for atherosclerotic affliction and the development of As, including the process of chronic inflammation.[four] Greater mechanical stress with age and adventure factors such as hypertension, smoking, diabetes and hypercholesterolaemia contribute to 2%–four% of adults >65 years of age suffering from caused AS.[iv] Bicuspid congenital aortic valve may exist noted in 1%–2% of the population built-in with an autosomal dominant blueprint, and a variable penetrance and can develop scarring and calcification of the abnormal folding of the bicuspid leaflets, leading to Equally in the later decades of life.[5,6]

Clinical features and diagnosis

A detailed history and concrete exam, supplemented by Repeat, can arm-twist the diagnosis of Every bit. Symptoms such equally decreased exercise tolerance, exertional dyspnoea, angina, congestive eye failure and syncope should raise suspicion of AS. Ejection systolic murmur with radiation to the carotids is ofttimes found on auscultation. Repeat is used to confirm the diagnosis and too to make up one's mind the multiple aspects of the pathophysiology of the aortic lesion. Normal aortic valve area (AVA) is 2.5–4 cm². The severity of the aortic valve stenosis is adamant past the AVA [Table one].

Tabular array 1

Classification of severity of aortic stenosis

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There is increased peak systolic wall stress of the left ventricle (LV) in the presence of an LV outflow tract obstacle, leading to chronic pressure level overload with consequent development of concentric hypertrophy. This leads to diastolic dysfunction with an increase in LV end-diastolic pressure level (LVEDP) and sub-endocardial ischaemia over fourth dimension. The ejection fraction may be decreased over time, indicating reduced left ventricular contractility. In such cases, evaluation of the severity of AS can be complicated as the period across the LV outflow tract and aortic valve is decreased due to poor contractility of the LV.[7] The pressure level–volume correlation of AS is shown in Figure 1 which shows that due to increase in aortic resistance, the LV pressures are increased during ejection with increase in finish-systolic volume and right shift of the loop.

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Left ventricular pressure–book loop in aortic stenosis

ANAESTHETIC CONCERNS IN PATIENTS WITH AORTIC STENOSIS

Pre-operative Repeat generally reveals LV hypertrophy. Breast X-ray may show prominent ascending aorta due to mail service-stenotic dilation. ECHO may reveal the post-obit pressure gradients and aortic velocities which are the virtually reproducible and the strongest predictors of clinical upshot every bit shown in Table one.

Patients with Every bit take a low fixed cardiac output. If there is sudden subtract in cardiac contractility or cardiac abort, breast compressions will not maintain sufficient cardiac output. Thus, induction should focus on stable haemodynamics while achieving adequate anaesthetic depth. Due to diastolic dysfunction and impaired relaxation of the LV, the atrial contribution which accounts for nearly 40% of the total cardiac output should be preserved. Additionally, all efforts should be made to maintain normal sinus rhythm to become the 'atrial kick'.[8] Any possible arrhythmia should be avoided. Information technology is wise to utilize external defibrillator pads before induction of anaesthesia in case any shockable rhythm precipitates during induction of anaesthesia. Both tachycardia and bradycardia should be avoided. Bradycardia is undesirable because cardiac output may become unacceptably depression in the presence of fixed aortic orifice. Whatsoever tachycardia can further jeopardise whatsoever pre-existing compromised coronary supply/demand human relationship in the presence of ventricular hypertrophy and concomitant coronary disease.[9,10] Preload should be maintained adequately to fill the non-compliant LV. Afterload should be maintained or increased. Any systemic hypotension can cause reduced coronary perfusion force per unit area and should be rapidly managed with the early use of boluses of α-adrenergic agonists. Adequate contractility should exist maintained. Good premedication helps prevent perioperative tachycardia in anxious patients. Perioperative monitoring should include electrocardiography (ECG) showing the anterior, lateral and junior leads. There should be monitoring of invasive arterial blood pressure level, central venous pressures (CVP), pulse oximetry (SpO₂) and end-tidal carbon dioxide (EtCO₂). Transoesophageal ECHO (TOE) if bachelor may be used to monitor the haemodynamics intraoperatively. Hypnosis could be achieved using low-dose benzodiazepines, fentanyl, etomidate and sevoflurane. Tracheal intubation may exist achieved using vecuronium or rocuronium bromide with pancuronium pinnacle-ups to counter whatsoever slower heart rates with the combination of the sometime.

AORTIC REGURGITATION

In AR, the claret flows backwards into the LV during diastole. Chronic AR is more common than astute AR and has better long-term outcome. Common causes of AR include built lesions, connective tissue disorders, chronic inflammation, rheumatic affliction and annular dilation from ageing and chronic hypertension. There is coaptation failure of the aortic valve (AV) leaflets due to chronic stress in the leaflets themselves or dilation of the AV annulus and the aortic root.[11] At that place is progressive volume overloading in chronic AR, leading to increase in end-diastolic wall tension. The LV undergoes a process of remodelling with the development of eccentric ventricular hypertrophy and chamber enlargement.[12] The LVEDP may be relatively normal because LV stop-diastolic book (LVEDV) increases slowly. In AR, frontwards flow is improved by peripheral vasodilation and ejection fraction is maintained by a big stroke volume.

Clinical features and diagnosis

The patients with chronic AR may remain asymptomatic for many years; however, they may eventually nowadays with symptoms of left center failure with increasing practice intolerance, dyspnoea, paroxysmal nocturnal dyspnoea or orthopnoea. Repeat is the best diagnostic tool to note the severity of AR. The width of the AR jet at its origin provides the most reliable color menstruation estimate of regurgitant severity.[8] A crude guideline for approximating severity is the width of the AR jet compared to the width of the LV outflow tract. If this ratio is <1/3, regurgitation is normally mild, 1/3–2/3 moderate and >two/three is astringent. Figure 2 shows the pressure–volume loop correlation in AR, where the loop has shifted to the right in patients with chronic AR. LVEDP remains relatively normal because LVEDV increases slowly over time.

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Left ventricular force per unit area–book loop in aortic regurgitation

Anaesthesia technique should aim at keeping a faster heart rate and avoiding bradycardia. Tachycardia limits the diastolic fourth dimension and so that the time for regurgitation is decreased leading to better forrard menstruation. Sinus rhythm should be preserved. Reduced systemic vascular resistance (SVR) will promote forward menstruation. Skillful contractility needs to be maintained. In case inotropes are needed, inodilators such as milrinone or dobutamine are preferred.

MITRAL STENOSIS

Rheumatic heart affliction is still the master cause of MS in most developing countries. Other causes of MS are attributed to master age-related degenerative valves and congenital mitral valvular abnormalities.

Clinical features and diagnosis

The severity classification as per the 2022 American Heart Association Guidelines for the Management of Patients with Valvular Heart Disease has been tabulated in Table ii.

Table ii

Classification of severity of mitral stenosis

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The diagnosis is confirmed by Echo. As the MS progresses, there could be LV dysfunction due to LV muscle mass atrophy from the chronically nether-filled state, leftward shift of interventricular septum due to RV hypertrophy and dysfunction, sub-valvular calcification, atrial fibrillation due left atrial dilation and enlargement. Thrombus can form in the atrium or left atrial bagginess due to low-velocity claret period. Patients with MS may be on treatment with anticoagulation with intravenous heparin, oral warfarin and drugs for charge per unit command. Pulmonary venous and arterial pressures are elevated, secondary to long-standing elevated LA pressures. The pulmonary vasculature develops reactive pulmonary vasoconstriction secondary to chronic elevation in pulmonary artery pressure.[13] This leads to compensatory right ventricular (RV) hypertrophy. As the RV does not have enough muscle mass, chronic pulmonary hypertension can pb to progressive RV dilation and failure.[14,15] In MS, the LV e'er remains under filled. Although LV role or contractility is presumed to be normal in most patients with MS, it has been shown that LV dysfunction is common in patients with MS.[xvi] A slower heart rate is needed to transfer enough blood from the LA to fill the LV. Whatsoever fast atrial rate or arrhythmias such equally atrial fibrillation diminishes the LV filling and thus the cardiac output. Transvalvular force per unit area gradient beyond the mitral valve is given by the Gorlin'due south formula: F = AVCc, where F = period rate, A = area of the orifice, Five = velocity of claret menses and Cc = Coefficient of orifice wrinkle. For mitral valve, the equation is modified into:

ΔP = (CO/[HR][DFP]/[MVA](44.3)[0.85])² × 10.6

Where ΔP is the transmitral pressure gradient, CO = cardiac output, Hour = center rate, DFP = diastolic filling menses and MVA = mitral valve area. Thus, when the heart rate is increased in a fixed small mitral orifice area, the gradient across the valve increases. Figure iii shows the force per unit area–volume loops in MS patients. The loop is shifted to the left so that LVEDP and LVEDV are lower. The stroke volume is reduced in elevated heart rate and shortened diastolic filling intervals. In that location tin be right-to-left ventricular septal shift due to the result of pulmonary hypertension on the RV.[sixteen]

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Left ventricular pressure–volume loop in mitral stenosis

Anaesthetic management in MS should focus on command of heart charge per unit, ventricular preload, macerated RV and LV contractile part and coexisting pulmonary hypertension. Tachycardia is poorly tolerated because of the decreased fourth dimension for diastolic filling of LV and should be avoided. Critical MS is like a low-fixed CO state and precautions demand to be taken to avoid any increase in centre rate during induction of amazement or in the perioperative period. Sinus rhythm should be preserved. Any precipitation of atrial fibrillation will lose the 'atrial kick'. Elevated flow beyond the valve can occur during increased sympathetic activity from any stimulus and can all of a sudden increase the pressure level gradient across the valve. This volition elevate the LA pressures and subsequently the PA pressures. If the patient is on digoxin, information technology should be continued pre-operatively. Short-acting β-blockers tin can also be used perioperatively for eye charge per unit control. Fluid should be judiciously administered so as to keep the right middle pressures and PA pressures depression, as over transfusion can precipitate sudden pulmonary oedema in an already elevated chronic pulmonary hypertensive vasculature.[10] In MS, afterload reduction does non aid in augmenting forrard flow because stroke volume is adamant by the mitral valve orifice expanse and the diastolic filling interval. LV contractility and SVR are normally preserved in MS although global systolic dysfunction develops in some MS patients.[xiv]

RV dysfunction is of major business organisation in patients of MS. All measures to avoid increases in pulmonary arterial (PA) pressures (e.chiliad., avoid hypoxia, hypercarbia, acidosis, lung hyperexpansion and nitrous oxide) should exist practiced. Oversedation in the preoperative period should exist avoided to prevent hypoventilation and hypercarbia. Patients may exist on anticoagulation for atrial fibrillation and jell formation. Coagulation contour may need to be checked (prothrombin fourth dimension, activated fractional thromboplastin time [APTT] and international normalised ratio [INR]). About not-cardiac surgeries of short duration may only need ECG, non-invasive blood pressure, SpO₂, EtCO₂ every bit standard monitoring modalities. In long surgeries with anticipated big fluid shifts and major tissue resection, invasive arterial claret pressures and CVP monitoring volition prove useful. Inotropic support may be needed to augment the RV dysfunction.

MITRAL REGURGITATION

MR tin either involve abnormalities in the valve or in sub-valvular components or functional abnormalities due to annular or LV dilation, leading to malcoaptation of the mitral valve leaflets.[17] Structural abnormalities in mitral regurgitant valve may include mitral valve prolapse, rheumatic mitral insufficiency, myxomatous degeneration, cleft valve associated with an AV septal defect and/or any infiltrative/fibrotic processes. Chronic ischaemic heart disease tin cause a functional MR in patients with dilated cardiomyopathy or/and coronary artery disease. The valve morphology is usually normal in such patients. The incompetent mitral valve allows passage of claret from the LV into the left atrium during systole. The regurgitant volume is a function of the size of the mitral orifice, the force per unit area differential betwixt the left atrium and the LV and the elapsing of the regurgitant wheel.[xiv] The MR could be acute or chronic, acute beingness more severe in terms of patient's clinical condition with sudden congestive eye failure needing immediate intubation, inotropes, diuresis and/or dialysis. In chronic MR, patient may mutter of easy fatigability, palpitations and features of congestive heart failure. ECHO is used to quantitatively estimate the regurgitant fraction (the fraction of regurgitant volume in relation to total stroke volume).[xviii] ECHO also stratifies the MR depending on the width of the vena contracta, defined every bit the narrowest cross-sectional expanse of a jet [Table 3]. Note that even with like Repeat features, clinical manifestations of a disease may differ e.chiliad., mixed lesions or due to any sudden demand leading to worsening of haemodynamics.

Table 3

Classification of severity of mitral regurgitation

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The left atrium is subjected to both volume and pressure overload; nonetheless, the LA pressures exercise not increase as much as in MS due to gradual modify of chamber dilatation. Atrial fibrillation may exist nowadays. Chronic astringent MR will eventually lead to elevated PA pressures with RV dysfunction. Chronic MR can lead to eccentric hypertrophy of the LV, causing chamber enlargement without significant increases in wall thickness. Large stroke book is ejected past the LV which comprises normal venous return into the left atrium plus the regurgitant volume from the previous cardiac cycle. Over a period, the LV systolic function deteriorates and the LV failure sets in. Effigy iv shows the effect on force per unit area–volume loops in MR. The area of the loop and the end-diastolic volume is grossly increased (shaded), there is the absence of isovolumic contraction phase and the LV volume starts decreasing as soon as the LV starts to contract.

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Left ventricular force per unit area–volume loop in mitral regurgitation

The primary anaesthetic goal in patients with chronic MR is maintaining forrard systemic menstruation.[19] Higher heart rate should be maintained to subtract the regurgitant volume by shortening systole. Dull heart rate will increase the systolic period and prolong regurgitation, and also increment the diastolic filling interval, which would lead to LV distention. Maintaining sinus rhythm is useful to get the atrial contribution to cardiac output. Target should be to achieve afterload reduction to raise frontwards cardiac output and claret pressure. Reduction of SVR with good anaesthetic depth, vasodilators and inodilators volition promote forward period. Higher SVR equally in hypertension and hypervolemia volition increase the regurgitant volume and worsen the MR. Hypotension in patients with significant MR can often be managed with inotropic support. Temporary use of pocket-size doses of ephedrine may be a ameliorate choice. Dobutamine, low-dose epinephrine, and milrinone are all acceptable inotropic choices for continuous infusion. Hypoxia, hypercarbia and acidosis are best avoided to prevent PA hypertension.

MIXED VALVULAR LESIONS

Often mixed valvular lesions such as MS and AR or Every bit and AR could be encountered in clinical settings. In such a case, an anaesthesiologist needs to empathise which pathology is contributing mainly to the adverse haemodynamic challenge in perioperative setting and program the anaesthetic management appropriately. However, the secondary lesion should also exist kept in mind since it could modify the haemodynamics adversely.

Patients of valvular heart disease may frequently be establish on the following medications

Antibiotic Prophylaxis

Prophylactic antibiotics may exist needed in patients with valvular middle disease having increased risk of infective endocarditis (IE)[xx,21] Recent guidelines for the prevention of IE recommend the maintenance of proficient oral health and hygiene rather than prescribing prophylactic antibiotic. Prophylaxis is recommended for patients with prosthetic cardiac valves, previous episode of IE, certain types of congenital heart illness and cardiac transplantation.[22]

Anticoagulation

Patients with valvular heart illness often require anticoagulation for associated finding such equally atrial fibrillation. Non-cardiac surgery in prosthetic valve patients poses risk of IE, haemorrhage and astute and subacute valve thrombosis with interrupted anticoagulation. The electric current guidelines recommend withdrawal of oral anticoagulation 72 h before surgery to lower the INR to <1.five and maintain anticoagulation with unfractionated heparin. The APTT is maintained twice the control value.[23]

Beta-blockade

The use of beta-blocker in patients with stenotic valvular lesions has to exist made on example-to-instance basis and correlated with haemodynamic variables. Generally, once indication of beta-blocker is established, practitioners have to titrate medications co-ordinate to heart rates, which may differ betwixt valvular lesions.[24]

Statins

Statins exert their effect by plaque stabilisation, anti-atherosclerotic, anti-thrombotic, vasodilative and anti-inflammatory backdrop.[25,26] Although there are no conclusive data to propose the benefit of statin therapy in valvular heart illness, discontinuation of statin therapy is associated with worsened outcome.[26,27]

Recombinant BNP

Nesiritide is a recombinant brain-blazon natriuretic peptide (BNP), which decreases PA pressures and myocardial oxygen consumption while increasing coronary flow and urine output. In patients with severe MR, impaired LV role, and pulmonary hypertension, with a loftier operative mortality, the perioperative use of nesiritide has improved early outcomes in these high-risk patients. This may be due to improved ventricular loading atmospheric condition (decreased PA pressures, more than constructive diuresis) and/or a direct myocardial event of BNP.[28]

This article did not specifically talk over the telescopic of regional anaesthesia. This could be used judiciously every bit site-specific regional anaesthesia, following proper screening for bleeding and haemodynamic profile of the patients and adhering to the haemodynamic goals for that patient.

Determination

Valvular middle disease is non uncommon in patients coming to the infirmary for various interventions and surgeries. Most of the patients would need some forms of anaesthesia to undergo an uneventful surgical see. Stenotic lesions do well with tight fluid control under general anaesthesia with advisable monitoring and adhering to the haemodynamic goals. Smooth extubation of these patients with a pain-free post-operative period, judicious book titration and cardiac back up volition go a long fashion for ameliorate clinical outcomes and uneventful recovery.

Financial support and sponsorship

Nil.

Conflicts of involvement

There are no conflicts of involvement.

REFERENCES

1. Iung B, Vahanian A. Epidemiology of acquired valvular heart disease. Can J Cardiol. 2014;30:962–70. [PubMed] [Google Scholar]

2. Nkomo VT, Gardin JM, Skelton TN, Gottdiener JS, Scott CG, Enriquez-Sarano M, et al. Burden of valvular eye diseases: A population-based study. Lancet. 2006;368:1005–11. [PubMed] [Google Scholar]

3. Herrera A. Steolting's Anesthesia and Co-Existing Disease. 7th ed. Philadelphia PA: Elsevier; 2022. Valvular center disease; p. 128. [Google Scholar]

iv. Freeman RV, Otto CM. Spectrum of calcific aortic valve affliction: Pathogenesis, affliction progression, and treatment strategies. Circulation. 2005;111:3316–26. [PubMed] [Google Scholar]

5. Aboulhosn J, Child JS. Left ventricular outflow obstruction: Subaortic stenosis, bicuspid aortic valve, supravalvar aortic stenosis, and coarctation of the aorta. Circulation. 2006;114:2412–22. [PubMed] [Google Scholar]

6. Saha S, Bastiaenen R, Hayward M, McEwan JR. An undiagnosed bicuspid aortic valve tin result in severe left ventricular failure. BMJ. 2007;334:420–2. [PMC free commodity] [PubMed] [Google Scholar]

7. Mochizuki Y, Pandian NG. Role of echocardiography in the diagnosis and treatment of patients with aortic stenosis. Curr Opin Cardiol. 2003;eighteen:327–33. [PubMed] [Google Scholar]

8. Labovitz AJ, Ferrara RP, Kern MJ, Bryg RJ, Mrosek DG, Williams GA, et al. Quantitative evaluation of aortic insufficiency by continuous wave doppler echocardiography. J Am Coll Cardiol. 1986;viii:1341–seven. [PubMed] [Google Scholar]

nine. Kertai MD, Bountioukos M, Boersma Due east, Bax JJ, Thomson IR, Sozzi F, et al. Aortic stenosis: An underestimated risk gene for perioperative complications in patients undergoing noncardiac surgery. Am J Med. 2004;116:8–xiii. [PubMed] [Google Scholar]

x. Christ M, Sharkova Y, Geldner G, Maisch B. Preoperative and perioperative care for patients with suspected or established aortic stenosis facing noncardiac surgery. Breast. 2005;128:2944–53. [PubMed] [Google Scholar]

eleven. Bekeredjian R, Grayburn PA. Valvular heart affliction: Aortic regurgitation. Circulation. 2005;112:125–34. [PubMed] [Google Scholar]

12. Scheuble A, Vahanian A. Aortic insufficiency: Defining the role of pharmacotherapy. Am J Cardiovasc Drugs. 2005;five:113–20. [PubMed] [Google Scholar]

13. Otto CM. Valvular Heart Disease. 2nd ed. Philadelphia: Saunders; 2004. Valvular heart disease: Prevalence and clinical outcomes; pp. one–17. [Google Scholar]

14. Rahimtoola SH, Dell'Italia LJ. Mitral valve disease. In: Fuster V, Wayne AR, O'Rourke RA, editors. Hurst'southward the Heart. 11th ed. New York: McGraw-Loma Medical Publishing Division; 2004. pp. 1669–89. [Google Scholar]

15. Mentum KM, Kim NH, Rubin LJ. The right ventricle in pulmonary hypertension. Coron Artery Dis. 2005;16:13–8. [PubMed] [Google Scholar]

16. Klein AJ, Carroll JD. Left ventricular dysfunction and mitral stenosis. Heart Fail Clin. 2006;two:443–52. [PubMed] [Google Scholar]

17. Borger MA, Alam A, Murphy PM, Doenst T, David TE. Chronic ischemic mitral regurgitation: Repair, replace or rethink? Ann Thorac Surg. 2006;81:1153–61. [PubMed] [Google Scholar]

18. Zoghbi WA, Enriquez-Sarano M, Foster E, Grayburn PA, Kraft CD, Levine RA, et al. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003;sixteen:777–802. [PubMed] [Google Scholar]

19. Nussmeier NA, Hauser M, Sarwar M, Grigore A, Searles B. Anesthesia for Cardiac Surgery. In: Miller RD, editor. Miller'southward Anesthesia. 7th ed. Philadelphia, PA: Elsevier; 2010. pp. 1889–976. [Google Scholar]

xx. Steckelberg JM, Wilson WR. Gamble factors for infective endocarditis. Infect Dis Clin Northward Am. 1993;7:nine–nineteen. [PubMed] [Google Scholar]

21. Mylonakis E, Calderwood SB. Infective endocarditis in adults. N Engl J Med. 2001;345:1318–thirty. [PubMed] [Google Scholar]

22. Allen U. Infective endocarditis: Updated guidelines. Can J Infect Dis Med Microbiol. 2010;21:74–7. [PMC gratis article] [PubMed] [Google Scholar]

23. Ortel TL. Perioperative direction of patients on chronic antithrombotic therapy. Blood. 2012;120:4699–705. [PMC gratuitous article] [PubMed] [Google Scholar]

24. Fleisher LA, Beckman JA, Dark-brown KA, Calkins H, Chaikof East, Fleischmann KE, et al. ACC/AHA 2006 guideline update on perioperative cardiovascular evaluation for noncardiac surgery: Focused update on perioperative beta-blocker therapy: A written report of the American higher of cardiology/American heart association job force on practise guidelines (Writing commission to update the 2002 guidelines on perioperative cardiovascular evaluation for noncardiac surgery): Developed in collaboration with the American society of echocardiography, American society of nuclear cardiology, centre rhythm society, society of cardiovascular anesthesiologists, society for cardiovascular angiography and interventions, and society for vascular medicine and biology. Circulation. 2006;113:2662–74. [PubMed] [Google Scholar]

25. Folkeringa RJ, Van Kraaij DJ, Tieleman RG, Nieman FH, Pinto YM, Crijns HJ, et al. Statins associated with reduced mortality in patients admitted for congestive centre failure. J Bill of fare Fail. 2006;12:134–8. [PubMed] [Google Scholar]

26. Fukuta H, Sane DC, Brucks S, Little WC. Statin therapy may be associated with lower mortality in patients with diastolic heart failure: A preliminary report. Circulation. 2005;112:357–63. [PubMed] [Google Scholar]

27. Le Manach Y, Godet G, Coriat P, Martinon C, Bertrand One thousand, Fléron MH, et al. The impact of postoperative discontinuation or continuation of chronic statin therapy on cardiac outcome afterward major vascular surgery. Anesth Analg. 2007;104:1326–33. [PubMed] [Google Scholar]

28. Salzberg SP, Filsoufi F, Anyanwu A, von Harbou M, Gass A, Pinney SP, et al. Loftier-take a chance mitral valve surgery: Perioperative hemodynamic optimization with nesiritide (BNP) Ann Thorac Surg. 2005;80:502–half-dozen. [PubMed] [Google Scholar]

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