History

Fact Explanation
Chest pain Post infarct angina occurs in up to 50% of patients. Most have residual stenosis even after successful thrombolysis.[1]
Syncopal attacks Almost all patients get arrhythmias, such as ventricular fibrillation, ventricular tachycardia, atrial fibrillation and heart block.[2]
Dyspnoea Patients may present with shortness of breath due to the heart failure, pericarditis or embolism. [3],[4],[5]
History of pericarditis (Dressler's Syndrome) Patient experience chest pain which relieved when leaning forward. In Dressler's syndrome is characterized by persisting fever, pericarditis, and pleurisy, may be due to autoimmunity. [6]
Peripheral edema Acute myocardial infarction often followed by thinning and stretching of that segment which leads to the increase in wall stress with progressive dilatation and hypertrophy of remaining ventricle(ventricular remodeling). As the ventricle dilates, it becomes less efficient and heart failure occurs. [7]
References
  1. SCHUSTER E. H., BULKLEY B. H.. Ischemia at a distance after acute myocardial infarction: a cause of early postinfarction angina. Circulation [online] 1980 September, 62(3):509-515 [viewed 12 July 2014] Available from: doi:10.1161/​01.CIR.62.3.509
  2. MCMURRAY JOHN, KøBER LARS, ROBERTSON MICHELE, DARGIE HENRY, COLUCCI WILSON, LOPEZ-SENDON JOSE, REMME WILLEM, SHARPE D. NORMAN, FORD IAN. Antiarrhythmic effect of carvedilol after acute myocardial infarction. Journal of the American College of Cardiology [online] 2005 February, 45(4):525-530 [viewed 12 July 2014] Available from: doi:10.1016/j.jacc.2004.09.076
  3. PFEFFER MARC A., MCMURRAY JOHN J.V., VELAZQUEZ ERIC J., ROULEAU JEAN-LUCIEN, KøBER LARS, MAGGIONI ALDO P., SOLOMON SCOTT D., SWEDBERG KARL, VAN DE WERF FRANS, WHITE HARVEY, LEIMBERGER JEFFREY D., HENIS MARC, EDWARDS SUSAN, ZELENKOFSKE STEVEN, SELLERS MARY ANN, CALIFF ROBERT M.. Valsartan, Captopril, or Both in Myocardial Infarction Complicated by Heart Failure, Left Ventricular Dysfunction, or Both. N Engl J Med [online] 2003 November, 349(20):1893-1906 [viewed 12 July 2014] Available from: doi:10.1056/NEJMoa032292
  4. ABBATE ANTONIO, BIONDI-ZOCCAI GIUSEPPE G.L, BUSSANI ROSSANA, DOBRINA ALDO, CAMILOT DEBORA, FEROCE FLORINDA, ROSSIELLO RAFFAELE, BALDI FELICIANO, SILVESTRI FURIO, BIASUCCI LUIGI M, BALDI ALFONSO. Increased myocardial apoptosis in patients with unfavorable left ventricular remodeling and early symptomatic post-infarction heart failure. Journal of the American College of Cardiology [online] 2003 March, 41(5):753-760 [viewed 12 July 2014] Available from: doi:10.1016/S0735-1097(02)02959-5
  5. ITO H., MARUYAMA A., IWAKURA K., TAKIUCHI S., MASUYAMA T., HORI M., HIGASHINO Y., FUJII K., MINAMINO T.. Clinical Implications of the `No Reflow' Phenomenon : A Predictor of Complications and Left Ventricular Remodeling inReperfused Anterior Wall Myocardial Infarction. Circulation [online] 1996 January, 93(2):223-228 [viewed 12 July 2014] Available from: doi:10.1161/​01.CIR.93.2.223
  6. LAWRENCE MS, WRIGHT R. Tamponade in Dressler's syndrome with immunological studies. Br Med J [online] 1972 Mar 11, 1(5801):665-666 [viewed 12 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1787775
  7. ATHANASULEAS CONSTANTINE L., BUCKBERG GERALD D., STANLEY ALFRED W.H., SILER WILLIAM, DOR VINCENT, DI DONATO MARISA, MENICANTI LORENZO, ALMEIDA DE OLIVEIRA SERGIO, BEYERSDORF FRIEDHELM, KRON IRVING L., SUMA HISAYOSHI, KOUCHOUKOS NICHOLAS T., MOORE WISTAR, MCCARTHY PATRICK M., OZ MEHMET C., FONTAN FRANCIS, SCOTT MEREDITH L., ACCOLA KEVIN A.. Surgical ventricular restoration in the treatment of congestive heart failure due to post-infarction ventricular dilation. Journal of the American College of Cardiology [online] 2004 October, 44(7):1439-1445 [viewed 12 July 2014] Available from: doi:10.1016/j.jacc.2004.07.017

Examination

Fact Explanation
Pulse As patient can get arrhythmias by examining pulse can help in identification of arrhythmia, eg:- tachycardia, bradycardia, slow rising pulse [1]
murmur Pansystolic murmur can occur due to the rupture of the papillary muscle which cause mitral regurgitation or due to the rupture of interventricular septum which lead to the ventricular septal defect. [2],[3]
s3 As a result of ventricular remodeling left ventricular failure may occur in some patients. They get s3 ,best heard at the apex, which occurs due to the left ventricular dysfunction [4]
crackles Fine bi-basal crackles occur in heart failure. [5]
elevated jugular venous pressure jugular vein may be useful in the assessment of mean venous pressure and pulse contour. In heart failure due to the volume overload jugular venous pressure gets elevated.[6]
pitting edema Acute myocardial infarction often followed by thinnning and stretching of that segment which leads to the increase in wall stress with progressive dilatation and hypertrophy of remaining ventricle(ventricular remodeling). As the ventricle dilates, it becomes less efficient and heart failure occurs. [7]
References
  1. PARKINSON J, PAPP C. REPETITIVE PAROXYSMAL TACHYCARDIA Br Heart J [online] 1947 Oct, 9(4):241-262 [viewed 13 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC503591
  2. GIULIANI E. R., DANIELSON G. K., PLUTH J. R., ODYNIEC N. A., WALLACE R. B.. Postinfarction Ventricular Septal Rupture: Surgical Considerations and Results. Circulation [online] 1974 March, 49(3):455-459 [viewed 13 July 2014] Available from: doi:10.1161/​01.CIR.49.3.455
  3. LAMAS G. A., MITCHELL G. F., FLAKER G. C., SMITH S. C., GERSH B. J., BASTA L., MOYE L., BRAUNWALD E., PFEFFER M. A.. Clinical Significance of Mitral Regurgitation After Acute Myocardial Infarction. Circulation [online] 1997 August, 96(3):827-833 [viewed 13 July 2014] Available from: doi:10.1161/​01.CIR.96.3.827
  4. PITT BERTRAM, WHITE HARVEY, NICOLAU JOSE, MARTINEZ FELIPE, GHEORGHIADE MIHAI, ASCHERMANN MICHAEL, VAN VELDHUISEN DIRK J., ZANNAD FAIEZ, KRUM HENRY, MUKHERJEE ROBIN, VINCENT JOHN. Eplerenone Reduces Mortality 30 Days After Randomization Following Acute Myocardial Infarction in Patients With Left Ventricular Systolic Dysfunction and Heart Failure. Journal of the American College of Cardiology [online] 2005 August, 46(3):425-431 [viewed 13 July 2014] Available from: doi:10.1016/j.jacc.2005.04.038
  5. PASTERKAMP HANS, KRAMAN STEVE S., WODICKA GEORGE R.. Respiratory Sounds. Am J Respir Crit Care Med [online] 1997 September, 156(3):974-987 [viewed 13 July 2014] Available from: doi:10.1164/ajrccm.156.3.9701115
  6. Applefeld MM. The Jugular Venous Pressure and Pulse Contour. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 19. Available from: http://www.ncbi.nlm.nih.gov/books/NBK300/
  7. ATHANASULEAS CONSTANTINE L., BUCKBERG GERALD D., STANLEY ALFRED W.H., SILER WILLIAM, DOR VINCENT, DI DONATO MARISA, MENICANTI LORENZO, ALMEIDA DE OLIVEIRA SERGIO, BEYERSDORF FRIEDHELM, KRON IRVING L., SUMA HISAYOSHI, KOUCHOUKOS NICHOLAS T., MOORE WISTAR, MCCARTHY PATRICK M., OZ MEHMET C., FONTAN FRANCIS, SCOTT MEREDITH L., ACCOLA KEVIN A.. Surgical ventricular restoration in the treatment of congestive heart failure due to post-infarction ventricular dilation. Journal of the American College of Cardiology [online] 2004 October, 44(7):1439-1445 [viewed 12 July 2014] Available from: doi:10.1016/j.jacc.2004.07.017

Differential Diagnoses

Fact Explanation
Acute myocardial infarction Occurs with central/retrosternal tightening chest pain/discomfort with radiation to jaw/ left arm. [1]
Left ventricular failure Patient may present with dyspnoea, orthopnea, pitting edema [2]
Chronic heart failure These patients may present with dyspnoea, orthopnea, pitting edema. Patient may have history of hypertension, cardiomyopathies, alcohol intake and endocrine disorders.[3]
References
  1. THYGESEN KRISTIAN, ALPERT JOSEPH S., WHITE HARVEY D.. Universal Definition of Myocardial Infarction. Journal of the American College of Cardiology [online] 2007 November, 50(22):2173-2195 [viewed 13 July 2014] Available from: doi:10.1016/j.jacc.2007.09.011
  2. Rector TS, Taylor BC, Greer N, et al. Use of Left Ventricular Assist Devices as Destination Therapy in End-Stage Congestive Heart Failure: A Systematic Review [Internet]. Washington (DC): Department of Veterans Affairs; 2012 May. Available from: http://www.ncbi.nlm.nih.gov/books/NBK99059/
  3. DICKSTEIN KENNETH, COHEN-SOLAL ALAIN, FILIPPATOS GERASIMOS, MCMURRAY JOHN J.V., PONIKOWSKI PIOTR, POOLE-WILSON PHILIP ALEXANDER, STRöMBERG ANNA, VAN VELDHUISEN DIRK J., ATAR DAN, HOES ARNO W., KEREN ANDRE, MEBAZAA ALEXANDRE, NIEMINEN MARKKU, PRIORI SILVIA GIULIANA, SWEDBERG KARL, VAHANIAN ALEC, CAMM JOHN, DE CATERINA RAFFAELE, DEAN VERONICA, DICKSTEIN KENNETH, FILIPPATOS GERASIMOS, FUNCK-BRENTANO CHRISTIAN, HELLEMANS IRENE, KRISTENSEN STEEN DALBY, MCGREGOR KEITH, SECHTEM UDO, SILBER SIGMUND, TENDERA MICHAL, WIDIMSKY PETR, ZAMORANO JOSE LUIS, TENDERA MICHAL, AURICCHIO ANGELO, BAX JEROEN, BöHM MICHAEL, CORRà UGO, DELLA BELLA PAOLO, ELLIOTT PERRY M., FOLLATH FERENC, GHEORGHIADE MIHAI, HASIN YONATHAN, HERNBORG ANDERS, JAARSMA TINY, KOMAJDA MICHEL, KORNOWSKI RAN, PIEPOLI MASSIMO, PRENDERGAST BERNARD, TAVAZZI LUIGI, VACHIERY JEAN-LUC, VERHEUGT FREEK W. A., ZAMORANO JOSE LUIS, ZANNAD FAIEZ. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008‡. European Journal of Heart Failure [online] December, 10(10):933-989 [viewed 14 July 2014] Available from: doi:10.1016/j.ejheart.2008.08.005

Investigations - for Diagnosis

Fact Explanation
Electrocardiography The presence of pathological Q waves on the 12-lead ECG signifies a prior transmural myocardial infarction. Q wave may regress or even disappear over time in as many as 25% to 63% of patients with a history of a Q-wave MI by ECG. The overall sensitivity of a Q wave for prior MI is limited by the ECG and is as low as 25% for a lateral MI. [1] Also done to identify arrhythmias, pericarditis
Echocardiography Important in identification of pericarditis, ventricular remodeling, heart failure(left ventricular function) and murmurs due to mitral regurgitation or ventricular septal defect.[2]
Chest radiography CXR is done to assess for the presence of Enlarged cardiac silhouette, Cephalization of pulmonary vessels, pleural effusion, interstitial edema, Alveolar edema, hyperinflated lungs.[3]
References
  1. DAS M. K.. Significance of a Fragmented QRS Complex Versus a Q Wave in Patients With Coronary Artery Disease. Circulation [online] 2006 May, 113(21):2495-2501 [viewed 13 July 2014] Available from: doi:10.1161/​CIRCULATIONAHA.105.595892
  2. KERBER R. E., ABBOUD F. M.. Echocardiographic Detection of Regional Myocardial Infarction: An Experimental Study. Circulation [online] 1973 May, 47(5):997-1005 [viewed 13 July 2014] Available from: doi:10.1161/​01.CIR.47.5.997
  3. MCCULLOUGH P. A.. B-Type Natriuretic Peptide and Clinical Judgment in Emergency Diagnosis of Heart Failure: Analysis From Breathing Not Properly (BNP) Multinational Study. [online] December, 106(4):416-422 [viewed 13 July 2014] Available from: doi:10.1161/​01.CIR.0000025242.79963.4C

Investigations - Fitness for Management

Fact Explanation
plasma potassium level Maintaining adequate potassium level is important to prevent any hyper or hypokalemia.[1]
References
  1. STEWART D E, IKRAM H, ESPINER E A, NICHOLLS M G. Arrhythmogenic potential of diuretic induced hypokalaemia in patients with mild hypertension and ischaemic heart disease.. Heart [online] 1985 September, 54(3):290-297 [viewed 13 July 2014] Available from: doi:10.1136/hrt.54.3.290

Investigations - Followup

Fact Explanation
ambulatory electrocardiography Done to evaluate conduction impairment. For patients with nonsustained episodes of palpitations/ arrhythmias, an ambulatory electrocardiogram or an event monitor can be useful in capturing an ECG during an episode. [1]
Lipid profile Patient's lipid levels should be assessed as hyperlipidaemia increase the risk of subsequent infarction and the benefit of lipid(LDL) reduction has now been strongly supported by the significant decrease in cardiovascular events, including cardiovascular mortality. [2]
Blood glucose levels People with impaired glucose tolerance have a cardiovascular mortality rate twice that of their counterparts with normal glucose tolerance. Therefore assess and maintain normal blood glucose level is important[3]
References
  1. DAS M. K.. Significance of a Fragmented QRS Complex Versus a Q Wave in Patients With Coronary Artery Disease. Circulation [online] 2006 May, 113(21):2495-2501 [viewed 13 July 2014] Available from: doi:10.1161/​CIRCULATIONAHA.105.595892
  2. Secondary Prevention by Raising HDL Cholesterol and Reducing Triglycerides in Patients With Coronary Artery Disease : The Bezafibrate Infarction Prevention (BIP) Study. Circulation [online] 2000 July, 102(1):21-27 [viewed 13 July 2014] Available from: doi:10.1161/​01.CIR.102.1.21
  3. BARTNIK M, MALMBERG K, NORHAMMAR A, TENERZ A, OHRVIK J, RYDEN L. Newly detected abnormal glucose tolerance: an important predictor of long-term outcome after myocardial infarction. European Heart Journal [online] 2004 November, 25(22):1990-1997 [viewed 13 July 2014] Available from: doi:10.1016/j.ehj.2004.09.021

Management - General Measures

Fact Explanation
Smoking cessation Cessation rapidly reduces the risk of cardiovascular events including fatal events. The risk of recurrent coronary events decreases 50% at 1to 2 years after smoking cessation. 5 year mortality doubled in patients who continue to smoke than who quit smoking. If cessation last for 15 years, the risk of coronary heart disease becomes that of a nonsmoker's[1], [2]
Lowering hyperlipidaemia The plasma levels of total cholesterol and low-density lipoprotein (LDL) cholesterol are important risk factors for coronary heart disease. lowering cholesterol levels slows the progression and promotes the regression of coronary atherosclerosis. Lowering hyperlipidaemia done by statins as dietary modifications are ineffective. Irrespective of serum cholesterol concentration all patients should receive statin therapy. [4]
Maintain blood glucose levels Mortality among diabetic patients myocardial infarction remains high. Many factors, such as severe coronary artery disease, diabetic cardiomyopathy, disturbed autonomic balance, and decreased fibrinolytic function, may contribute to the unfavorable outcome. Therefore dietary measurement and correct medication as oral hypoglycemics and/or insulin should be taken. Intensive glucose control, lowering glycated hemoglobin levels (A1C) values to ≤7% in both type 1 and type 2 diabetes, provides strong benefits for microvascular complications and, if achieved early in the disease, might also provide a significant macrovascular benefit, especially as part of a multifactorial treatment approach. More intensive glucose control, A1C ≤6.5%, may be sought in patients with a shorter duration of diabetes, no evidence of significant cardiovascular disease and longer life expectancy, provided this does not result in a significant increase in hypoglycemia. An A1C target ≤8.5% may be more appropriate in type 1 and type 2 patients with limited life expectancy, higher level of functional dependency, a history of severe hypoglycemia, advanced comorbidities, and a failure to attain established glucose targets despite treatment intensification[3],[6]
Diet Patients should take a Mediterranean‐style diet—more bread, fruit, vegetables and fish; less meat; and replace butter and cheese with products based on vegetable and plant oils. this will reduces total mortality and the risk of myocardial infarction. They have to consume at least 7 g of omega‐3 fatty acids per week from 2–4 portions of oily fish per week. If within 3 months of a myocardial infarction and patients are not achieving this, they should be considered for providing at least 1 g daily of omega‐3‐acid ethyl esters treatment licensed for secondary prevention after myocardial infarction for up to 4 years. Initiation of omega‐3‐acid ethyl esters supplement treatment is not routinely recommended in patients that have had a myocardial infarction more than 3 months earlier. Achieve and maintain a healthy weight is also important. Therefore patients who are overweight or obese should be offered appropriate advice and support. [5] Patients should be advised against taking: Supplements containing beta‐carotene as they may increase risk of cardiovascular death; Antioxidant supplements and folic acid supplements as no evidence of benefit.
Alcohol intake Patients have to restrict their alcohol intake to within recommended safe limits of 14 units per week for women and 21 units per week for men, and avoid binge drinking.[5]
Cardiac rehabilitiation With an exercise component (reduces mortality) should be offered to all patients, and made accessible regardless of the patient's age, gender, ethnicity, socioeconomic status or comorbidities. Should include the following components: exercise (reduces mortality), health education, and stress management (reduces anxiety, depression and the risk of non‐fatal myocardial infarction); however complex psychological interventions such as cognitive behavioural therapy should not be routinely offered. Patients should take regular physical activity sufficient to increase exercise capacity (reduces total mortality), and building up physical activity to 20–30 min/day to the point of slight breathlessness. [5]
References
  1. MCKENNA W J, CHEW C Y, OAKLEY C M. Myocardial infarction with normal coronary angiogram. Possible mechanism of smoking risk in coronary artery disease.. Heart [online] 1980 May, 43(5):493-498 [viewed 13 July 2014] Available from: doi:10.1136/hrt.43.5.493
  2. SARGENT R. P. Reduced incidence of admissions for myocardial infarction associated with public smoking ban: before and after study. BMJ [online] 2004 April, 328(7446):977-980 [viewed 13 July 2014] Available from: doi:10.1136/bmj.38055.715683.55
  3. MALMBERG K., NORHAMMAR A., WEDEL H., RYDEN L.. Glycometabolic State at Admission: Important Risk Marker of Mortality in Conventionally Treated Patients With Diabetes Mellitus and Acute Myocardial Infarction : Long-Term Results From the Diabetes and Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) Study. Circulation [online] 1999 May, 99(20):2626-2632 [viewed 13 July 2014] Available from: doi:10.1161/​01.CIR.99.20.2626
  4. SACKS FRANK M., PFEFFER MARC A., MOYE LEMUEL A., ROULEAU JEAN L., RUTHERFORD JOHN D., COLE THOMAS G., BROWN LISA, WARNICA J. WAYNE, ARNOLD J. MALCOLM O., WUN CHUAN-CHUAN, DAVIS BARRY R., BRAUNWALD EUGENE. The Effect of Pravastatin on Coronary Events after Myocardial Infarction in Patients with Average Cholesterol Levels. N Engl J Med [online] 1996 October, 335(14):1001-1009 [viewed 14 July 2014] Available from: doi:10.1056/NEJM199610033351401
  5. SKINNER JS, COOPER A, FEDER GS. Secondary prevention for patients following a myocardial infarction: summary of NICE guidance Heart [online] 2007 Jul, 93(7):862-864 [viewed 14 July 2014] Available from: doi:10.1136/hrt.2007.124321
  6. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. Canadian Diabetes Association 2013 Clinical Practice Guidelines for the Prevention and Management of Diabetes in Canada. Can J Diabetes 2013;37(suppl 1):S1-S212.[viewed 14 July 2014] Available from: http://guidelines.diabetes.ca/Browse/Chapter8

Management - Specific Treatments

Fact Explanation
Drug therapy - Aspirin and clopidogrel Platelet activation and aggregation play a key role in initiating and propagating coronary-artery thrombosis. Aspirin imparts its primary antithrombotic effects through the inhibition of PGH-synthase/COX by the irreversible acetylation. Clopidogrel is an adenosine diphosphate–receptor antagonist, a class of oral antiplatelet agents that block the P2Y12 component of the adenosine diphosphate receptor and thus inhibit the activation and aggregation of platelets.Low dose aspirin (75 mg/ day) therapy reduce future risk of infarction by 25%. [1][2]
Drug therapy - Beta blockers Continuous treatment with oral Beta blockers reduce the mortality by 25%. But some patients (patients with bradycardia, asthma, hypotension) do not tolerate beta blockers. Beta-blockers bind to beta-adrenoceptors located in cardiac nodal tissue, the conducting system, and contracting myocytes. Because there is generally some level of sympathetic tone on the heart, beta-blockers are able to reduce sympathetic influences that normally stimulate chronotropy , inotropy , dromotropy and lusitropy. Therefore, beta-blockers cause decreases in heart rate, contractility, conduction velocity, and relaxation rate.[3]
Drug therapy - Angiotensin converting enzyme inhibitors (ACEI) long term treatment can counteract ventricular remodeling and prevent heart failure. This can be achieved by enalapril 10mg 12 hourly or ramipril 2.5 - 5 mg 12 hourly.[4]
Management of Dressler's syndrome Medical management consist of the use of nonsteroidal anti-inflammatory drugs such as aspirin, given for 4-6 weeks and is tapered as fluid decreases. For patients who does not respond to aspirin, acorticosteroid (prednisone) may be administered for 1 week, with a 4-week tapering period followed. Immediate pericardiocentesis is necessary to relieve life-threatening cardiac tamponade. [5]
References
  1. AWTRY E. H., LOSCALZO J.. Aspirin. Circulation [online] 2000 March, 101(10):1206-1218 [viewed 14 July 2014] Available from: doi:10.1161/​01.CIR.101.10.1206
  2. SABATINE MARC S., CANNON CHRISTOPHER P., GIBSON C. MICHAEL, LóPEZ-SENDóN JOSE L., MONTALESCOT GILLES, THEROUX PIERRE, CLAEYS MARC J., COOLS FRANK, HILL KAREN A., SKENE ALLAN M., MCCABE CAROLYN H., BRAUNWALD EUGENE. Addition of Clopidogrel to Aspirin and Fibrinolytic Therapy for Myocardial Infarction with ST-Segment Elevation. N Engl J Med [online] 2005 March, 352(12):1179-1189 [viewed 14 July 2014] Available from: doi:10.1056/NEJMoa050522
  3. LUBBE WILHELM F., PODZUWEIT THOMAS, OPIE LIONEL H.. Potential arrhythmogenic role of cyclic adenosine monophosphate (AMP) and cytosolic calcium overload: Implications for prophylactic effects of beta-blockers in myocardial infarction and proarrhythmic effects of phosphodiesterase inhibitors. Journal of the American College of Cardiology [online] 1992 June, 19(7):1622-1633 [viewed 14 July 2014] Available from: doi:10.1016/0735-1097(92)90629-2
  4. FLATHER MARCUS D, YUSUF SALIM, KøBER LARS, PFEFFER MARC, HALL ALISTAIR, MURRAY GORDON, TORP-PEDERSEN CHRISTIAN, BALL STEPHEN, POGUE JANICE, MOYé LEMUEL, BRAUNWALD EUGENE. Long-term ACE-inhibitor therapy in patients with heart failure or left-ventricular dysfunction: a systematic overview of data from individual patients. The Lancet [online] 2000 May, 355(9215):1575-1581 [viewed 14 July 2014] Available from: http://vtcardsfellows.com/pdf/Guidelines/Reviewarticles/ACEi_in_Heart_Failure.pdf
  5. ENGLE M. A., MCCABE J. C., EBERT P. A., ZABRISKIE J.. The Postpericardiotomy Syndrome and Antiheart Antibodies. Circulation [online] 1974 March, 49(3):401-406 [viewed 14 July 2014] Available from: doi:10.1161/​01.CIR.49.3.401