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Coronary Artery Disease Diagnosis Criteria: A Comprehensive Guide

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Coronary artery disease (CAD) remains a leading cause of morbidity and mortality worldwide. Characterized by the buildup of atherosclerotic plaque in the coronary arteries, CAD restricts blood flow to the heart muscle, leading to myocardial ischemia. Timely and accurate diagnosis is crucial for effective management and improved patient outcomes. This article provides an in-depth review of the diagnostic criteria for coronary artery disease, emphasizing evidence-based strategies for healthcare professionals.

Understanding Coronary Artery Disease

Coronary artery disease (CAD), often used interchangeably with coronary heart disease (CHD) and ischemic heart disease (IHD), encompasses a spectrum of conditions from stable angina to acute coronary syndromes (ACS). While CHD mortality is largely attributed to CAD, ACS represents a symptomatic and urgent subset, including unstable angina and myocardial infarction. For clarity, we will primarily use “CAD” throughout this discussion.

CAD is a global health crisis, responsible for a significant proportion of deaths and disability-adjusted life years (DALYs) lost, particularly in low- and middle-income countries. Despite advancements in treatment, individuals post-myocardial infarction still face a considerably elevated risk of recurrent events and mortality compared to the general population.[1]

The fundamental issue in CAD is an imbalance between myocardial oxygen supply and demand. This is primarily caused by the progressive narrowing of coronary arteries due to atherosclerotic plaque formation, hindering adequate blood and oxygen delivery to the heart muscle.

Etiological Factors in CAD Diagnosis

CAD etiology is complex and multifactorial, involving both nonmodifiable and modifiable risk factors. Recognizing these factors is vital for risk stratification and guiding diagnostic strategies.

Nonmodifiable Risk Factors:

  • Age: The risk of CAD increases significantly with advancing age.
  • Gender: Men are generally more predisposed to CAD than women, although this gap narrows with age, particularly post-menopause in women.
  • Family History: A positive family history of early-onset CAD significantly elevates individual risk.
  • Genetics: Genetic predispositions play a role in CAD susceptibility.

Modifiable Risk Factors:

  • Hypertension: Elevated blood pressure is a major contributor to CAD development and progression.
  • Smoking: Smoking remains the leading modifiable risk factor for cardiovascular disease, significantly increasing CAD risk.
  • Dyslipidemia: Elevated LDL cholesterol and low HDL cholesterol levels are critical modifiable risk factors.
  • Obesity: Obesity, particularly central obesity (increased waist circumference), is strongly linked to increased CAD risk.
  • Diabetes Mellitus: Diabetes significantly increases the risk and severity of CAD.
  • Psychosocial Factors: Stress, depression, and social isolation can contribute to CAD risk.
  • Inflammation: Elevated markers of inflammation, such as high-sensitivity C-reactive protein (hs-CRP), are associated with increased CAD risk.

Identifying and managing modifiable risk factors is a cornerstone of both primary and secondary prevention of CAD and informs the necessity and urgency of diagnostic evaluations.

Diagnostic Evaluation of Coronary Artery Disease

Diagnosing CAD requires a comprehensive approach, integrating clinical assessment with a range of diagnostic tests. The choice of diagnostic modality depends on the patient’s clinical presentation, risk factors, and pretest probability of CAD.

Clinical Assessment

A thorough clinical evaluation is the first step in CAD diagnosis. This includes:

  • History: Detailed history taking focusing on chest pain characteristics (location, radiation, provoking and relieving factors), associated symptoms (shortness of breath, nausea, diaphoresis), risk factors, and past medical history. Angina pectoris, the hallmark symptom of CAD, is typically described as chest discomfort, pressure, tightness, or pain, often exacerbated by exertion or emotional stress and relieved by rest or nitroglycerin. However, atypical presentations, particularly in women, elderly, and diabetic patients, are not uncommon and may include fatigue, shortness of breath, or back pain.
  • Physical Examination: General physical exam, including vital signs (blood pressure, heart rate), auscultation of heart and lungs, and assessment for signs of heart failure (jugular venous distention, peripheral edema). While physical exam findings are often non-specific in CAD, they are essential to assess overall cardiovascular status and identify potential comorbidities.

Non-invasive Diagnostic Tests

Non-invasive tests play a crucial role in the initial evaluation and risk stratification of patients with suspected CAD.

Electrocardiogram (ECG)

ECG is a readily available and fundamental tool in CAD diagnosis. It assesses the heart’s electrical activity and can detect:

  • Acute Ischemia: ST-segment elevation or depression, T-wave inversions in ACS.
  • Arrhythmias: CAD-related arrhythmias.
  • Prior Myocardial Infarction: Pathological Q waves.
  • Other Abnormalities: Left ventricular hypertrophy, bundle branch blocks.

While ECG is highly valuable, a normal resting ECG does not exclude CAD, especially in stable angina. Pre-hospital ECGs performed by EMS personnel can expedite diagnosis and treatment initiation in ACS, particularly STEMI.

Exercise Stress Testing

Exercise stress testing is used to evaluate for myocardial ischemia during physical exertion. It is indicated in patients with suspected stable angina or angina equivalents. Diagnostic criteria for a positive stress test include:

  • ECG Changes: ST-segment depression (horizontal or downsloping ≥1mm) is the most common ECG criterion for ischemia.
  • Anginal Symptoms: Development of typical angina during exercise.
  • Hemodynamic Response: Exertional hypotension or excessive hypertensive response.

Stress testing can be performed using a treadmill or bicycle. Various modalities can be combined with stress testing to enhance diagnostic accuracy, including:

  • Stress Echocardiography: Evaluates wall motion abnormalities during stress, indicating ischemia.
  • Nuclear Stress Testing (SPECT or PET): Uses radioactive tracers to assess myocardial perfusion during stress and rest, identifying areas of ischemia and infarction.

Echocardiography

Echocardiography, or cardiac ultrasound, is a non-invasive imaging technique that provides valuable information about cardiac structure and function. In CAD diagnosis, echocardiography can assess:

  • Wall Motion Abnormalities: Regional wall motion abnormalities at rest or during stress are suggestive of ischemia or prior infarction.
  • Left Ventricular Function: Ejection fraction, diastolic function, which are important prognostic indicators in CAD.
  • Valvular Function: Assess for valvular heart disease that can mimic or coexist with CAD.
  • Other Cardiac Pathology: Hypertrophic cardiomyopathy, pericardial disease.

Stress echocardiography, combining exercise or pharmacological stress with echocardiography, enhances the detection of ischemia-induced wall motion abnormalities.

Chest Radiography

Chest X-ray is not a primary diagnostic tool for CAD but is useful in evaluating:

  • Cardiomegaly: Enlarged heart size, suggestive of heart failure.
  • Pulmonary Congestion: Signs of heart failure.
  • Other Pulmonary Conditions: To rule out alternative causes of chest pain.

Coronary Artery Calcium (CAC) Scoring

CAC scoring using non-contrast computed tomography (CT) quantifies the amount of calcium in the coronary arteries. A CAC score of zero effectively excludes obstructive CAD in symptomatic patients with low to intermediate risk. However, a high CAC score indicates the presence of atherosclerosis but does not directly quantify the severity of stenosis. CAC scoring is primarily used for risk stratification and guiding further diagnostic testing.

Computed Tomography Angiography (CTA)

Coronary CTA is a non-invasive imaging technique that uses contrast dye to visualize the coronary arteries. CTA can accurately detect:

  • Coronary Artery Stenosis: Identifies and quantifies the degree of luminal narrowing.
  • Plaque Morphology: Characterizes plaque composition (calcified vs. non-calcified).
  • Anatomical Variations: Coronary artery anomalies.

CTA is particularly useful in patients with intermediate risk of CAD and can be an alternative to invasive angiography in selected patients. However, it involves radiation exposure and contrast dye, which may be contraindicated in some individuals.

Invasive Diagnostic Tests

Cardiac Catheterization and Coronary Angiography

Coronary angiography, performed during cardiac catheterization, remains the gold standard for diagnosing and assessing the severity of CAD. This invasive procedure involves:

  • Catheter Insertion: Insertion of a catheter into a peripheral artery (femoral or radial) and advancing it to the coronary arteries.
  • Contrast Injection: Injection of contrast dye into the coronary arteries to visualize their anatomy and identify stenoses under fluoroscopy.
  • Assessment of Stenosis: Quantification of stenosis severity, typically expressed as percent diameter stenosis. Stenosis greater than 70% is generally considered hemodynamically significant, while stenosis between 50% and 70% may be functionally significant and require further evaluation (e.g., fractional flow reserve – FFR).

Cardiac catheterization and angiography are indicated for:

  • Patients with ACS: STEMI and high-risk NSTEMI/unstable angina.
  • Patients with high-risk stable angina: Despite optimal medical therapy.
  • Patients with equivocal non-invasive testing: When non-invasive tests are inconclusive or discordant with clinical suspicion.

While highly accurate, cardiac catheterization is an invasive procedure with potential complications, including bleeding, infection, stroke, and contrast-induced nephropathy.

Intravascular Ultrasound (IVUS) and Optical Coherence Tomography (OCT)

IVUS and OCT are catheter-based imaging modalities used during cardiac catheterization to provide detailed images of the coronary artery wall and plaque characteristics. They offer higher resolution imaging compared to angiography and can:

  • Assess Plaque Morphology: Identify plaque composition, plaque burden, and vulnerable plaque features.
  • Guide PCI: Optimize stent deployment during percutaneous coronary intervention (PCI).
  • Evaluate Stent Failure: Assess for stent restenosis or thrombosis.

Serum Biomarkers

Serum biomarkers play a limited role in the diagnosis of chronic CAD but are crucial in the diagnosis and risk stratification of acute coronary syndromes (ACS).

  • Cardiac Troponins: Highly sensitive and specific markers of myocardial necrosis. Elevated troponin levels are essential for diagnosing myocardial infarction (NSTEMI and STEMI).
  • Creatine Kinase-MB (CK-MB): Another marker of myocardial injury, less specific than troponin and less commonly used now.
  • B-type Natriuretic Peptide (BNP) and NT-proBNP: Markers of cardiac stress and heart failure. Elevated levels are associated with adverse outcomes in CAD and ACS but are not specific for CAD diagnosis.
  • Lipid Panel: Fasting lipid profile (total cholesterol, LDL-C, HDL-C, triglycerides) is essential for risk assessment and management of CAD but not for acute diagnosis.
  • High-sensitivity C-reactive protein (hs-CRP): An inflammatory marker associated with increased CAD risk, but not a diagnostic criterion for acute CAD.

Diagnostic Criteria Summary

The diagnosis of coronary artery disease is based on a combination of clinical presentation, risk factors, and results from diagnostic tests. There are no single, definitive “Coronary Artery Disease Diagnosis Criteria” in the sense of a checklist, but rather a constellation of findings that, when taken together, establish the diagnosis and guide management.

Key Diagnostic Considerations:

  • Clinical Presentation: Typical angina, atypical symptoms, or ACS presentation.
  • Risk Factors: Presence of modifiable and nonmodifiable CAD risk factors.
  • ECG Findings: Evidence of ischemia or prior infarction.
  • Stress Test Results: ECG changes, symptoms, or imaging evidence of ischemia during stress.
  • Echocardiography Findings: Wall motion abnormalities, LV dysfunction.
  • Coronary Imaging: CAC score, CTA findings, or angiographic evidence of coronary artery stenosis.
  • Biomarkers (ACS): Elevated cardiac troponins in ACS.

Diagnostic Approach:

  1. Risk Stratification: Assess pretest probability of CAD based on clinical presentation and risk factors.
  2. Initial Non-invasive Testing: ECG, stress testing (exercise ECG, stress echo, or nuclear stress test), or CTA, depending on risk level and clinical scenario.
  3. Selective Invasive Angiography: Consider cardiac catheterization and angiography for high-risk patients, those with positive or equivocal non-invasive tests, or those with ACS.
  4. Integration of Findings: Synthesize clinical information and test results to establish the diagnosis, assess disease severity, and guide treatment strategies.

Differential Diagnosis

Chest pain, the primary symptom of CAD, has a broad differential diagnosis, including:

  • Non-cardiac Chest Pain: Gastroesophageal reflux disease (GERD), musculoskeletal pain (costochondritis), pulmonary embolism, pleuritis, anxiety disorders.
  • Other Cardiac Conditions: Pericarditis, myocarditis, hypertrophic cardiomyopathy, valvular heart disease, aortic dissection.

A careful history, physical examination, and appropriate diagnostic testing are crucial to differentiate CAD from other conditions presenting with similar symptoms.

Conclusion

Accurate and timely diagnosis of coronary artery disease is paramount for effective management and improving patient outcomes. The diagnostic approach involves a comprehensive evaluation integrating clinical assessment, non-invasive and invasive testing modalities, and serum biomarkers (particularly in ACS). Understanding the diagnostic criteria for CAD, including the strengths and limitations of each diagnostic test, empowers healthcare professionals to develop clinically guided strategies for evaluating and managing this prevalent and life-threatening condition. A tailored diagnostic approach, considering individual patient risk profiles and clinical presentations, is essential to optimize diagnostic accuracy and ensure appropriate and timely interventions.

Figure: Classification of Coronary Artery Disease. Illustrating the spectrum of CAD presentations from stable ischemic heart disease to acute coronary syndromes.

Figure: Atherosclerotic Plaque Formation. Depicting the key stages of plaque development, from initiation and progression to stability and calcification.

References

  1. Ralapanawa U, Sivakanesan R. Epidemiology and the Magnitude of Coronary Artery Disease and Acute Coronary Syndrome: A Narrative Review. J Epidemiol Glob Health. 2021 Jun;11(2):169-177.
  2. Dalen JE, Alpert JS, Goldberg RJ, Weinstein RS. The epidemic of the 20(th) century: coronary heart disease. Am J Med. 2014 Sep;127(9):807-12.
  3. Mensah GA, Roth GA, Fuster V. The Global Burden of Cardiovascular Diseases and Risk Factors: 2020 and Beyond. J Am Coll Cardiol. 2019 Nov 19;74(20):2529-2532.
  4. Bauersachs R, Zeymer U, Brière JB, Marre C, Bowrin K, Huelsebeck M. Burden of Coronary Artery Disease and Peripheral Artery Disease: A Literature Review. Cardiovasc Ther. 2019;2019:8295054.
  5. Jamal A, Phillips E, Gentzke AS, Homa DM, Babb SD, King BA, Neff LJ. Current Cigarette Smoking Among Adults – United States, 2016. MMWR Morb Mortal Wkly Rep. 2018 Jan 19;67(2):53-59.
  6. Petrazzini BO, Chaudhary K, Márquez-Luna C, Forrest IS, Rocheleau G, Cho J, Narula J, Nadkarni G, Do R. Coronary Risk Estimation Based on Clinical Data in Electronic Health Records. J Am Coll Cardiol. 2022 Mar 29;79(12):1155-1166.
  7. Nasir K, DeFilippis A. Big Data and ASCVD Risk Prediction: Building a Better Mouse Trap? J Am Coll Cardiol. 2022 Mar 29;79(12):1167-1169.
  8. Koenig W. High-sensitivity C-reactive protein and atherosclerotic disease: from improved risk prediction to risk-guided therapy. Int J Cardiol. 2013 Oct 15;168(6):5126-34.
  9. Klein S, Allison DB, Heymsfield SB, Kelley DE, Leibel RL, Nonas C, Kahn R., Association for Weight Management and Obesity Prevention. NAASO, The Obesity Society. American Society for Nutrition. American Diabetes Association. Waist circumference and cardiometabolic risk: a consensus statement from Shaping America’s Health: Association for Weight Management and Obesity Prevention; NAASO, The Obesity Society; the American Society for Nutrition; and the American Diabetes Association. Am J Clin Nutr. 2007 May;85(5):1197-202.
  10. Ross R, Neeland IJ, Yamashita S, Shai I, Seidell J, Magni P, Santos RD, Arsenault B, Cuevas A, Hu FB, Griffin BA, Zambon A, Barter P, Fruchart JC, Eckel RH, Matsuzawa Y, Després JP. Waist circumference as a vital sign in clinical practice: a Consensus Statement from the IAS and ICCR Working Group on Visceral Obesity. Nat Rev Endocrinol. 2020 Mar;16(3):177-189.
  11. Sharma S, Batsis JA, Coutinho T, Somers VK, Hodge DO, Carter RE, Sochor O, Kragelund C, Kanaya AM, Zeller M, Park JS, Køber L, Torp-Pedersen C, Lopez-Jimenez F. Normal-Weight Central Obesity and Mortality Risk in Older Adults With Coronary Artery Disease. Mayo Clin Proc. 2016 Mar;91(3):343-51.
  12. Ferreira-González I. The epidemiology of coronary heart disease. Rev Esp Cardiol (Engl Ed). 2014 Feb;67(2):139-44.
  13. Brown JC, Gerhardt TE, Kwon E. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jan 23, 2023. Risk Factors for Coronary Artery Disease.
  14. Tsao CW, Aday AW, Almarzooq ZI, Anderson CAM, Arora P, Avery CL, Baker-Smith CM, Beaton AZ, Boehme AK, Buxton AE, Commodore-Mensah Y, Elkind MSV, Evenson KR, Eze-Nliam C, Fugar S, Generoso G, Heard DG, Hiremath S, Ho JE, Kalani R, Kazi DS, Ko D, Levine DA, Liu J, Ma J, Magnani JW, Michos ED, Mussolino ME, Navaneethan SD, Parikh NI, Poudel R, Rezk-Hanna M, Roth GA, Shah NS, St-Onge MP, Thacker EL, Virani SS, Voeks JH, Wang NY, Wong ND, Wong SS, Yaffe K, Martin SS., American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart Disease and Stroke Statistics-2023 Update: A Report From the American Heart Association. Circulation. 2023 Feb 21;147(8):e93-e621.
  15. Puymirat É. [Epidemiology of coronary artery disease]. Rev Prat. 2015 Mar;65(3):317-20.
  16. Al Thani H, El-Menyar A, Alhabib KF, Al-Motarreb A, Hersi A, Alfaleh H, Asaad N, Saif SA, Almahmeed W, Sulaiman K, Amin H, Alsheikh-Ali AA, Alnemer K, Suwaidi JA. Polyvascular disease in patients presenting with acute coronary syndrome: its predictors and outcomes. ScientificWorldJournal. 2012;2012:284851.
  17. Ferreira-González I, Permanyer Miralda G, Heras M, Ribera A, Marsal JR, Cascant P, Arós F, Bueno H, Sánchez PL, Cuñat J, Civeira E, Marrugat J., Investigadores del Estudio MASCARA. Prognosis and management of patients with acute coronary syndrome and polyvascular disease. Rev Esp Cardiol. 2009 Sep;62(9):1012-21.
  18. Cotter G, Cannon CP, McCabe CH, Michowitz Y, Kaluski E, Charlesworth A, Milo O, Bentley J, Blatt A, Krakover R, Zimlichman R, Reisin L, Marmor A, Lewis B, Vered Z, Caspi A, Braunwald E., OPUS-TIMI 16 Investigators. Prior peripheral arterial disease and cerebrovascular disease are independent predictors of adverse outcome in patients with acute coronary syndromes: are we doing enough? Results from the Orbofiban in Patients with Unstable Coronary Syndromes-Thrombolysis In Myocardial Infarction (OPUS-TIMI) 16 study. Am Heart J. 2003 Apr;145(4):622-7.
  19. Calais F, Eriksson Östman M, Hedberg P, Rosenblad A, Leppert J, Fröbert O. Incremental prognostic value of coronary and systemic atherosclerosis after myocardial infarction. Int J Cardiol. 2018 Jun 15;261:6-11.
  20. Weight N, Moledina S, Zoccai GB, Zaman S, Smith T, Siller-Matula J, Dafaalla M, Rashid M, Nolan J, Mamas MA. Impact of pre-existing vascular disease on clinical outcomes. Eur Heart J Qual Care Clin Outcomes. 2022 Dec 13;9(1):64-75.
  21. Nakahara T, Dweck MR, Narula N, Pisapia D, Narula J, Strauss HW. Coronary Artery Calcification: From Mechanism to Molecular Imaging. JACC Cardiovasc Imaging. 2017 May;10(5):582-593.
  22. Hashmi S, Shah PW, Aherrahrou Z, Aikawa E, Aherrahrou R. Beyond the Basics: Unraveling the Complexity of Coronary Artery Calcification. Cells. 2023 Dec 12;12(24)
  23. DeVon HA, Mirzaei S, Zègre-Hemsey J. Typical and Atypical Symptoms of Acute Coronary Syndrome: Time to Retire the Terms? J Am Heart Assoc. 2020 Apr 07;9(7):e015539.
  24. Abdullatef M, Omran M, Bitar A, Alsaid B. Prevalence of classic and non-classic pain sites of coronary artery disease: a cross-sectional study. BMC Cardiovasc Disord. 2024 Aug 24;24(1):445.
  25. Mirzaei S, Steffen A, Vuckovic K, Ryan C, Bronas UG, Zegre-Hemsey J, DeVon HA. The association between symptom onset characteristics and prehospital delay in women and men with acute coronary syndrome. Eur J Cardiovasc Nurs. 2020 Feb;19(2):142-154.
  26. Zègre-Hemsey JK, Patel MD, Fernandez AR, Pelter MM, Brice J, Rosamond W. A Statewide Assessment of Prehospital Electrocardiography Approaches of Acquisition and Interpretation for ST-Elevation Myocardial Infarction Based on Emergency Medical Services Characteristics. Prehosp Emerg Care. 2020 Jul-Aug;24(4):550-556.
  27. Sicari R, Cortigiani L. The clinical use of stress echocardiography in ischemic heart disease. Cardiovasc Ultrasound. 2017 Mar 21;15(1):7.
  28. Picano E, Pierard L, Peteiro J, Djordjevic-Dikic A, Sade LE, Cortigiani L, Van De Heyning CM, Celutkiene J, Gaibazzi N, Ciampi Q, Senior R, Neskovic AN, Henein M. The clinical use of stress echocardiography in chronic coronary syndromes and beyond coronary artery disease: a clinical consensus statement from the European Association of Cardiovascular Imaging of the ESC. Eur Heart J Cardiovasc Imaging. 2024 Jan 29;25(2):e65-e90.
  29. Bamouni J, Naibe DT, Yameogo RA, Mandi DG, Millogo GRC, Yameogo NV, Kologo JK, Thiam-Tall A, Nébié LAV, Zabsonré P. [Contribution of stress test to the treatment of ischemic heart disease]. Pan Afr Med J. 2018;31:229.
  30. Meda JR, Kusima HL, Magitta NF. Angiographic characteristics of coronary artery disease in patients undergoing diagnostic coronary angiography at a tertiary hospital in Tanzania. BMC Cardiovasc Disord. 2024 Feb 26;24(1):125.
  31. Gould KL, Lipscomb K. Effects of coronary stenoses on coronary flow reserve and resistance. Am J Cardiol. 1974 Jul;34(1):48-55.
  32. Pedersen ER, Hovland S, Karaji I, Berge C, Mohamed Ali A, Lekven OC, Kuiper KJ, Rotevatn S, Larsen TH. Coronary calcium score in the initial evaluation of suspected coronary artery disease. Heart. 2023 Apr 12;109(9):695-701.
  33. Bahit MC, Kochar A, Granger CB. Post-Myocardial Infarction Heart Failure. JACC Heart Fail. 2018 Mar;6(3):179-186.
  34. Katz D, Gavin MC. Stable Ischemic Heart Disease. Ann Intern Med. 2019 Aug 06;171(3):ITC17-ITC32.
  35. Makki N, Brennan TM, Girotra S. Acute coronary syndrome. J Intensive Care Med. 2015 May;30(4):186-200.
  36. Smith JN, Negrelli JM, Manek MB, Hawes EM, Viera AJ. Diagnosis and management of acute coronary syndrome: an evidence-based update. J Am Board Fam Med. 2015 Mar-Apr;28(2):283-93.
  37. Virani SS, Newby LK, Arnold SV, Bittner V, Brewer LC, Demeter SH, Dixon DL, Fearon WF, Hess B, Johnson HM, Kazi DS, Kolte D, Kumbhani DJ, LoFaso J, Mahtta D, Mark DB, Minissian M, Navar AM, Patel AR, Piano MR, Rodriguez F, Talbot AW, Taqueti VR, Thomas RJ, van Diepen S, Wiggins B, Williams MS., Peer Review Committee Members. 2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With Chronic Coronary Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation. 2023 Aug 29;148(9):e9-e119.
  38. Arnett DK, Blumenthal RS, Albert MA, Buroker AB, Goldberger ZD, Hahn EJ, Himmelfarb CD, Khera A, Lloyd-Jones D, McEvoy JW, Michos ED, Miedema MD, Muñoz D, Smith SC, Virani SS, Williams KA, Yeboah J, Ziaeian B. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019 Sep 10;140(11):e596-e646.
  39. Koo BK, Kang J, Park KW, Rhee TM, Yang HM, Won KB, Rha SW, Bae JW, Lee NH, Hur SH, Yoon J, Park TH, Kim BS, Lim SW, Cho YH, Jeon DW, Kim SH, Han JK, Shin ES, Kim HS., HOST-EXAM investigators. Aspirin versus clopidogrel for chronic maintenance monotherapy after percutaneous coronary intervention (HOST-EXAM): an investigator-initiated, prospective, randomised, open-label, multicentre trial. Lancet. 2021 Jun 26;397(10293):2487-2496.
  40. García Rodríguez LA, Martín-Pérez M, Hennekens CH, Rothwell PM, Lanas A. Bleeding Risk with Long-Term Low-Dose Aspirin: A Systematic Review of Observational Studies. PLoS One. 2016;11(8):e0160046.
  41. Elam MB, Majumdar G, Mozhui K, Gerling IC, Vera SR, Fish-Trotter H, Williams RW, Childress RD, Raghow R. Patients experiencing statin-induced myalgia exhibit a unique program of skeletal muscle gene expression following statin re-challenge. PLoS One. 2017;12(8):e0181308.
  42. Straka BT, Ramirez CE, Byrd JB, Stone E, Woodard-Grice A, Nian H, Yu C, Banerji A, Brown NJ. Effect of bradykinin receptor antagonism on ACE inhibitor-associated angioedema. J Allergy Clin Immunol. 2017 Jul;140(1):242-248.e2.
  43. Reejhsinghani R, Lotfi AS. Prevention of stent thrombosis: challenges and solutions. Vasc Health Risk Manag. 2015;11:93-106.
  44. Tabei SM, Senemar S, Saffari B, Ahmadi Z, Haqparast S. Non-modifiable Factors of Coronary Artery Stenosis in Late Onset Patients with Coronary Artery Disease in Southern Iranian Population. J Cardiovasc Thorac Res. 2014;6(1):51-5.
  45. Michniewicz E, Mlodawska E, Lopatowska P, Tomaszuk-Kazberuk A, Malyszko J. Patients with atrial fibrillation and coronary artery disease – Double trouble. Adv Med Sci. 2018 Mar;63(1):30-35.
  46. Nesković AN, Marinković J, Bojić M, Popović AD. Early mitral regurgitation after acute myocardial infarction does not contribute to subsequent left ventricular remodeling. Clin Cardiol. 1999 Feb;22(2):91-4.
  47. Frampton J, Ortengren AR, Zeitler EP. Arrhythmias After Acute Myocardial Infarction. Yale J Biol Med. 2023 Mar;96(1):83-94.
  48. Oleynikov VE, Averyanova EV, Oreshkina AA, Burko NV, Barmenkova YA, Golubeva AV, Galimskaya VA. A Multivariate Model to Predict Chronic Heart Failure after Acute ST-Segment Elevation Myocardial Infarction: Preliminary Study. Diagnostics (Basel). 2021 Oct 18;11(10)
  49. Sharma H, Radhakrishnan A, Nightingale P, Brown S, May J, O’Connor K, Shakeel I, Zia N, Doshi SN, Townend JN, Myerson SG, Kirchhof P, Ludman PF, Adnan Nadir M, Steeds RP. Mitral Regurgitation Following Acute Myocardial Infarction Treated by Percutaneous Coronary Intervention-Prevalence, Risk factors, and Predictors of Outcome. Am J Cardiol. 2021 Oct 15;157:22-32.
  50. Elbadawi A, Elgendy IY, Mahmoud K, Barakat AF, Mentias A, Mohamed AH, Ogunbayo GO, Megaly M, Saad M, Omer MA, Paniagua D, Abbott JD, Jneid H. Temporal Trends and Outcomes of Mechanical Complications in Patients With Acute Myocardial Infarction. JACC Cardiovasc Interv. 2019 Sep 23;12(18):1825-1836.
  51. Lador A, Hasdai D, Mager A, Porter A, Goldenberg I, Shlomo N, Vorobeichik D, Beigel R, Kornowski R, Iakobishvili Z. Incidence and Prognosis of Pericarditis After ST-Elevation Myocardial Infarction (from the Acute Coronary Syndrome Israeli Survey 2000 to 2013 Registry Database). Am J Cardiol. 2018 Mar 15;121(6):690-694.
  52. Vallabhajosyula S, Kanwar S, Aung H, Cheungpasitporn W, Raphael CE, Gulati R, Singh M. Temporal Trends and Outcomes of Left Ventricular Aneurysm After Acute Myocardial Infarction. Am J Cardiol. 2020 Oct 15;133:32-38.
  53. Mansencal N, Nasr IA, Pillière R, Farcot JC, Joseph T, Lacombe P, Dubourg O. Usefulness of contrast echocardiography for assessment of left ventricular thrombus after acute myocardial infarction. Am J Cardiol. 2007 Jun 15;99(12):1667-70.
  54. James S, Akerblom A, Cannon CP, Emanuelsson H, Husted S, Katus H, Skene A, Steg PG, Storey RF, Harrington R, Becker R, Wallentin L. Comparison of ticagrelor, the first reversible oral P2Y(12) receptor antagonist, with clopidogrel in patients with acute coronary syndromes: Rationale, design, and baseline characteristics of the PLATelet inhibition and patient Outcomes (PLATO) trial. Am Heart J. 2009 Apr;157(4):599-605.
  55. Schwartz GG, Olsson AG, Szarek M, Sasiela WJ. Relation of characteristics of metabolic syndrome to short-term prognosis and effects of intensive statin therapy after acute coronary syndrome: an analysis of the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) trial. Diabetes Care. 2005 Oct;28(10):2508-13.

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