Journal of the Practice of Cardiovascular Sciences

: 2019  |  Volume : 5  |  Issue : 3  |  Page : 146--153

Acute Myocardial Infarction: Bedside Case Discussion

Bharath Raj Kidambi, Sai Krishna Reddy, Vijay Surampalli 
 Department of Cardiology, Cardiothoracic and Neurosciences Centre, All Institute of Medical Sciences, New Delhi, India

Correspondence Address:
Dr. Bharath Raj Kidambi
AIIMS, New Delhi


This is a bedside case discussion of a patient presenting with acute myocardial infarction. The symptoms and signs are discussed. The choices at each stage, the electrocardiogram (ECG), the angiogram, and the therapeutic findings are discussed in detail. The context with reference to India is also discussed. The differential diagnosis of the history of presentation is also discussed. ECG localization of myocardial infarction, management of acute coronary occlusion, and medical management of myocardial infarction are discussed.

How to cite this article:
Kidambi BR, Reddy SK, Surampalli V. Acute Myocardial Infarction: Bedside Case Discussion.J Pract Cardiovasc Sci 2019;5:146-153

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Kidambi BR, Reddy SK, Surampalli V. Acute Myocardial Infarction: Bedside Case Discussion. J Pract Cardiovasc Sci [serial online] 2019 [cited 2023 Jun 4 ];5:146-153
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 Case Discussion

A 50-year-old male who hails from Bihar, studied up to 8th standard, presently working as a car driver, presented with chief complaints of:

Chief complaints Duration

Chest pain × 3 h duration

History of Presenting Illness

The patient was apparently alright till 3 h back, when he suddenly felt a vague chest pain present at the center of the chest. Pain was located in the substernal location and was radiating to the right side of the shoulder. The quality of the pain was dull aching, which was increasing in severity rapidly over few hours. Chest pain was aggravated by exertion. Pain was not relieved even during rest. There was profuse sweating associated with the chest pain, and also a sense of doom or impending death. There were mild dyspnea and palpitation associated with the chest pain.

There was no history of pedal edema, abdominal distension and facial puffiness, loss of appetite/fullness, right hypochondriac pain, or increased neck pulsations.

Chest pain was diffuse in nature and not localized. There is no relation of the chest pain to food intake. There were no associated vomiting and hematemesis. There was no history of trauma and no history of any psychological disorders in the past. There was no history of any giddiness or syncope or seizure. There was no history of any preceding fever, cough, or sputum production. There was no history of decreased urine output now or in the past. Review of other systems was normal.

Past history

The patient is not a known diabetic, or hypertensive. He has had no similar history in the past. There was no history of any angina on exertion or dyspnea previously. There was no history of fever, joint pains, involuntary movements, rash, or nodules. There was no history of tuberculosis and bronchial asthma in the past. There was no past surgical history.

Treatment history

The patient is not on any medications. There was no history of any intake of any cardiotoxic drugs (cancer chemotherapy or prolonged steroids).

Birth history/antenatal history

Birth history/antenatal history was normal. The patient was born of a nonconsanguineous marriage, to an uncomplicated full-term normal vaginal delivery. He cried immediately after birth and achieved normal milestones during development. There was no history of any recurrent lower respiratory tract infection, feeding difficulties, inappropriate sweating during feeding, and dyspnea on lying down. There was no history of bluish discoloration or squatting episodes.

Personal history

The patient takes mixed diet and smokes 1 packet cigarette/day for the last 15 years. There was no alleged history of any alcohol or illicit drug abuse.

Socioeconomic history

The patient lives along with the owner in a single room provided near the outhouse. He lives alone, with good sanitary surroundings.


A 50-year-old male patient with significant chronic smoking history presented with acute-onset retrosternal chest pain of 3-h duration, suggestive of typical anginal pain most likely due to acute coronary syndrome.

 Differential Diagnosis

Acute coronary syndromeAortic dissectionMild pulmonary embolismNoncardiac less likely.

 General Examination

The Patient was average built, is conscious, is oriented, and is anxious at restHe was afebrileThere was no pallor, icterus, cyanosis, clubbing, edema, or lymphadenopathyThere were no markers of atherosclerosis (xanthoma, xanthelasma, Arcus juvenilis, and franks sign)There were no markers of congenital heart disease (low set ears, hypertelorism, epicanthal folds, and limb deformities)There were no markers of rheumatic fever, (IE) Infective endocarditisHeight – 154 cmWeight – 70 kgBMI – 29.2Upper segment – 80 cmLower segment – 74Arm span – 150 cm.


Pulse rate was 120/min (tachycardia) with regular rhythm; there was normal volume with no special character and felt equally in all peripheral accessible vessels, with no radioradial or radiofemoral delay. There was no carotid bruit.

Blood pressure:

Upper left – Sitting left – 138/94 mmHgLower left – Sitting left – 144/90 mmHgJugular venous pressure (JVP) – was not raisedRespiratory rate – 34/min, shallow rapid breathing, abdominothoracic in natureTemperature – Afebrile.

 Cardiovascular Examination


Chest wall is bilaterally symmetrical, and there is no kyphoscoliosis. Trachea is slightly shifted to right. Apex is not visible due to mild obesity. There are no dilated veins or scars.


Inspection findings are confirmed. Apex is located in the 5th intercostal space ½ inch medial to mid clavicular line. There is no parasternal heave or any epigastric pulsations, no palpable sounds or thrills.


Right heart border corresponds to the right border of sternum. Left heart border corresponds to apex. Pulmonary area is resonant on percussion. Liver dullness is present on right and gastric tympany on left.


1st heart sound is loud in intensity (tachycardia) and 2nd heart sound is normal in intensity had a normal split) there is tachycardia. There are no added sounds, or murmurs.

Respiratory system

There was bilateral air entry equally. Normal vesicular breath sounds heard at bases of lung. There were no added sounds like crepitation's or wheeze.


Soft, nontender. No organomegaly noted.

Central nervous system

The patient was conscious, well oriented to time, place person and had no focal neurological deficit.

Provisional diagnosis

Acute coronary syndrome most likely due to thrombotic occlusion of coronary artery, Killip Class 1, with no immediate mechanical complications.

 Bedside Case Discussion

Q) What is the difference between typical chest pain and atypical chest pain and noncardiac chest pain?

Typical angina is defined as substernal chest pain with characteristic quality and duration, which is provoked by exertion or emotion and relieved by rest or nitrates. Atypical chest pain is when only two of these criteria's are fulfilled. Non cardiac pain is when one or none of the characteristics are met.[1]

Q) What is the predictive ability of anginal relief to nitrates in diagnosis of myocardial infarction (MI)?

Previously, chest pain response to nitrates was considered to be of good diagnostic value. But, it can be misleading. In case of symptom relief after nitrates, a repeat electrocardiogram (ECG) is to be performed. A complete normalization of ST segment elevation, with complete relief of symptoms is considered to be suggestive of coronary spasm with or without associated MI. An angiography is recommended then.[2]

Q) What is the differential diagnosis of ST-elevation MI (STEMI)?

Conditions which can have concomitant angina pectoris:

Aortic dissection, stress cardiomyopathy, systemic arterial embolism, hypertensive crisis, aortic stenosis, Cocaine use, NSAAConditions with ST elevation but no ischemia – Early repolarization, left ventricular hypertrophy (LVH), left bundle branch block (LBBB), hyperkalemia, Brugada syndromeConditions with chest pain but no ischemia – Uncomplicated pericarditis, pleuritis, costochondritis, gastroesophageal reflux disease (GERD).

Q) What was the ECG finding in this patient?

There is ST elevation >2 mm in v2–v6, and >1 mm ST-elevation in lead 1 and aVL with some minimal reciprocal changes seen in lead 3 suggestive of anterior wall + lateral wall MI due to complete left anterior descending (LAD) occlusion. Likely in the proximal LAD [Figure 1].{Figure 1}

Q) How to localize within LAD (culprit artery) with ECG? What is the sensitivity and specificity of ECG to localize culprit artery?

As LAD supplies mainly the septum and the anterior wall of the left ventricle, we can divide the area it supplies into 3. The basal septal area is mainly supplied by Septal 1 (S1) branch. The part of LAD prior to S1 is considered as proximal LAD. The Anterolateral area is mainly supplied by the diagonal branch (D1). This part is considered as mid-LAD usually. The part of the left ventricle supplied distal to D1 is ECG wise distal part of the ventricle.

Usually, most ECG signs have poor sensitivity and specificity. Very few signs have a good specificity [Table 1].{Table 1}

The most commonly seen ECG signs with good specificity for proximal LAD (proximal to S1) are:

ST elevation in V1 > aVR, especially if V1 elevation is more than 2.5 mm. If aVR lead ST elevation is more than V1. It is prudent to think of Left main occlusion or severe TVDComplete RBBB new onset (qRBB pattern)ST depression in inferior lead (L3 >2) and v5.

ECG features of lesion distal to S1 and D1 are:

Absence of ST depression in inferior leads (L2, 3, avf)ST depression in aVL (100% specific).

ECG features of lesion between S1 and D1.

When lesion is proximal to D1 – ST depression in inferior leads >1.0 mm (only 50% sensitive and 60% specific).[3]

Q) What are the classical ECG criteria for diagnosing STEMI?

There should be two contiguous leads with ST elevation (measured at J point).


And/or >1 mm in other leads in absence of LVH, LBBB.

For posterior MI, in leads v7–v9, 0.5 mm is itself enough to diagnose posterior wall MI in inferior MI.[1]

Q) What are the conditions where MI can present without any of the mentioned ST-elevation criteria's?

Occlusion of a small branch like diagonal, small septal.

Circumflex obstruction may present as isolated PWMI and ST depressions in V1-V3Left main occlusion or insufficiency (>1 mm ST depression in 8 or more leads)Acute vein graft occlusion.[1]

Q) What are the common mimics of MI in ECG?

Early repolarizationWPW syndromeHyperkalemiaPericarditisMyocarditisChronic obstructive pulmonary diseasePrecordial ECG leads misplacement.

Q) What is the latest definition of STEMI?

The fourth universal definition of MI (UDMI) was released in 2018. According to the UDMI, MI is defined as myocardial injury in the clinical setting of myocardial Ischemia. There are two components:

Myocardial injury which is defined as raise of troponins above the 99th percentileClinical Setting of myocardial ischemia-symptoms and signs of myocardial ischemia, ECG changes with new ischemic changes or pathological Q waves, imaging evidence like loss of viability, regional wall motion abnormality (RWMA), thrombus in angiography, evidence of thrombus in autopsy, sudden cardiac death.[4]

Q) What are the other causes of rise in troponins?

Other causes of myocardial injury and the distinction from MI are elaborated in [Figure 2].{Figure 2}

Conditions such as unstable angina where there is no detectable troponin elevationConditions such as anemia, VT, VF, CHF, CKD, hypotension, shock, and hypoxia which causes a sustained pattern of troponin elevation depending on the causative conditionMI – Acute rise and fall of troponin above the 99th percentile of URL.[4]

Q) What are the different types of MI?

UDMI classifies MI in five types:

Type 1 MI due to thrombosis of an atherosclerotic plaqueType 2 MI due to myocardial oxygen supply demand imbalance in the context of another acute illnessType 3 MI presenting as sudden deathType 4 postpercutaneous coronary intervention (PCI)Type 5 postcoronary artery bypass grafting.[1],[4]

Q) What are the angiographic findings in this patient?

The angiography findings are shown in [Figure 3].{Figure 3}

Q) How is LAD artery classified as ostial, proximal, mid, and distal?

The definition of coronary artery segments is defined in the syntax score. LAD is divided into proximal, mid and apical as follows [Figure 4].{Figure 4}

LAD proximal – Proximal to and including first major septal branchLAD mid – LAD immediately distal to origin of first septal branch and extending to the point where LAD forms an angle (RAO view). If this angle is not identifiable this segment ends at one half the distance from the first septal to the apex of the heartLAD apical – Terminal portion of LAD, beginning at the end of previous segment and extending to or beyond the apex.

A tutorial with all definition of segments is available in the syntax website: (

Q) What is the angiographic characteristic of thrombus?

Thrombus is identified in angiography by reduced contrast density, haziness, irregular lesion contour. Smooth convex meniscus at sight of total occlusion is suggestive but not diagnostic of thrombus.[5]

Q) What is the angiographic grading of thrombus?

Thrombus grading in angiography is given by TIMI grading.

Grade 0 - No angiographic evidence of thrombus presentGrade 1 - Possible thrombusrade 2 - There is definite thrombus with greatest dimension Grade 3 – Definite thrombus with greatest linear dimension >½ but <2 times vessel diametersGrade 4 – Definite thrombus with greatest linear dimension >2 vessel diametersGrade 5 – Total occlusion.[5]

Q) What is the role of thrombus aspiration in primary PCI?

Routine manual aspiration of thrombus in primary PCI is not recommended as of now as it has not shown any substantial clinical benefit. This is based on the meta-analysis data with three large trials TAPAS, TASTE and TOTAL. However it is still a valuable tool if performed carefully in selected patients with huge thrombus burden.[1],[5]

Q) What is the preferred route for PCI?

The ESC STEMI guidelines in 2017 favored a trans-radial approach based on the results of the MATRIX trial. Subsequent trials like RIVAL and RIFLE– STEACS also showed similar benefit of reduced vascular access complications. However a recent trial SAFARI STEMI presented in March 2019 in ACC, showed that a good transfemoral approach under experienced operators was equal to trans-radial approach in terms of efficacy and vascular complication outcomes. The trial was, however, underpowered and was not statistically significant.[1],[6]

Q) What are the evidences for the medical management given for this patient?

Patient has been treated with:


Evidences of the above treatment in ACS are:

Aspirin – ISIS 2 was the landmark trial in 1988 after which aspirin was considered as mainstay in ACS patientsDAPT – benefit of DAPT in ACS setting and post-PCI setting were shown in CURE and PCI CURE trials, where they used Clopidogrel as the p2y12 inhibitor of choice. There was a significant reduction in composite primary endpoint of cardiovascular (CVS) mortality, non-fatal MI and stroke (9.3 vs. 11.4%) with number needed to treat (NNT = 48)Ticagrelor was compared to clopidogrel in PLATO trial. Addition of ticagrelor to aspirin was able to further reduce composite primary endpoint of cardiovascular mortality, non-fatal MI, and stroke from 11.7% to 9.8% (P < 0.001) with an insignificant increase in major bleeding (11.6% vs. 11.2%)Statins have a huge body of evidence both for early initiation and intensive treatment strategy mainly from meta-analysis data by cholesterol treatment trialist. Most of the trials utilized atorvastatin in the STEMI setting. With high intensity statin defined as the atorvastatin 40-80 mg with an ability to decrease LDL cholesterol by >50%Beta-blocker also has huge robust evidence in patients with ACS. Largest trial with metoprolol was with COMMIT collaborative groupACE inhibitor trials are the SAVE, AIRE and TRACE trials which demonstrated mortality benefit of starting ACE inhibitors within first 24 h. AIRE trial used the drug ramiprilMineralocorticoid receptor antagonist used in patients with LV systolic dysfunction with ejection fraction <40%, diabetic and with symptoms of heart failure. The trial supporting their use was EPHASUS which used eplerenone. However we generally use spironolactone in our country due to cost issues.[1]

Q) How do you determine the duration of DAPT in your patient?

Our patient has had an acute coronary event (STEMI) who has undergone primary PCI with DES stenting. He is a 56-year-old male, with only smoking as risk factor. He does not have any features of high bleeding risk which are shown in the table below. He is a candidate with a Low Bleeding risk with a moderate ischemic risk. PRECISE DAPT SCORE in this patient is <25. Hence, my strategy for DAPT duration will be till 12 months with Aspirin 75 mg dose and ticagrelor 90 mg BD dose. I would like to reassess the patient at the end of 12 months, with DAPT score. If the patient is found to have high ischemic risk features, I would prefer continuing the patient on ticagrelor 60 mg BD till 3 years' duration if cost is not an issue for greater benefit [Figure 5].{Figure 5}

One major or two minor criteria if met, then the patient is considered to be under high bleeding risk. HBR is defined as a BARC 3 or 5 bleeding risk of ≥4% at 1 year or a risk of an intracranial hemorrhage (ICH) of ≥1% at 1 year. Thus, a major criterion for ARC-HBR is defined as any criterion that, in isolation, is considered to confer a BARC 3 or 5 bleeding risk of ≥4% at 1 year or any criterion considered to be associated with a risk of ICH of ≥1% at 1 year. A minor criterion for ARC-HBR is defined as any criterion that, in isolation, is considered to confer increased bleeding risk, with a BARC 3 or 5 bleeding rate of <4% at 1 year [Table 2].[7],[8]{Table 2}

Q) How are smokers classified according to recent NHIS CDC classification?

According to latest definitions from the NHIS glossary (CDC).

Current smoker: An adult who has smoked 100 cigarettes in his or her lifetime and who currently smokes cigarettesEvery day smoker: An adult who has smoked at least 100 cigarettes in his or her lifetime, and who now smokes every day. Previously called a “regular smoker”Former smoker: An adult who has smoked at least 100 cigarettes in his or her lifetime but who had quit smoking at the time of interviewNever smoker: An adult who has never smoked, or who has smoked <100 cigarettes in his or her lifetimeSomeday smoker: An adult who has smoked at least 100 cigarettes in his or her lifetime, who smokes now, but does not smoke every day. Previously called an “occasional smoker.”[9]

Q) What is the data on myocardial infarction in the young from India?

There are limited data specifically for young MI from IndiaData from ACS registries in India follow different age cut off for young MI. Kerala ACS had 22.4% of patients <50 years coming with STEMIOne study from Kanpur AMIYA study and other study from Andhra Pradesh had more than 1100 patients of Young MI had taken an age cut off of <40 years. However, these were retrospective hospital-based observational studies.

Standard definition for young CAD includes patients who get myocardial infarction <40 years. Several studies were done analyzing the risk factors of CAD in young such as Multinational monitoring of trends and determinants in cardiovascular disease study, INTERHEART, and EURO HEART ACS epidemiologic studies, along with randomized controlled trials (RCTs), have shown that certain risk factors such as family history, obesity, dyslipidemia, and use of tobacco products, are more potent predictors of outcomes in the young than in their older counterparts. ACS in young, based on angiographic characteristics, can be due to atherosclerotic and non-atherosclerotic CAD which includes arteritis, thrombosis, embolization, and spasm (cocaine abuse). Coronary artery thrombus can be seen in hypercoagulable states such as protein C and S deficiency, antiphospholipid antigen, and nephrotic syndromeMales are more commonly affectedFamily history is present in 39%–64%Tobacco smoking is an important independent risk factor for CAD in young adults. Current smoking of >10 cigarettes or beedi a day is associated with a 6.7-fold increase in the risk of MI. Prevalence of smoking is more in age <40 than in age >40 yearsIndians are more prone to diabetes and hyperinsulinemiaHigher incidence of having atherogenic dyslipidemia (with higher TG levels and low HDL levels) compared to older individuals who are usually on statin therapy.

More robust studies and RCT including this cohort in the future are required to assess the differences in the etiology and management of this subset of patients.[10],[11],[12],[13],[14],[15],[16],[17],[18],[19],[20]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


1Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2018;39:119-77.
2Henrikson CA, Howell EE, Bush DE, Miles JS, Meininger GR, Friedlander T, et al. Chest pain relief by nitroglycerin does not predict active coronary artery disease. Ann Intern Med 2003;139:979-86.
3Engelen DJ, Gorgels AP, Cheriex EC, De Muinck ED, Ophuis AJ, Dassen WR, et al. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol 1999;34:389-95.
4Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, et al. Fourth Universal Definition of Myocardial Infarction (2018). J Am Coll Cardiol 2018;72:2231-64.
5Mangiacapra F, Sticchi A, Barbato E. Thrombus aspiration in primary percutaneous coronary intervention: Still a valid option with improved technique in selected patients! Cardiovasc Diagn Ther 2017;7:S110-4.
6Komócsi A, Aradi D, Kehl D, Ungi I, Thury A, Pintér T, et al. Meta-analysis of randomized trials on access site selection for percutaneous coronary intervention in ST-segment elevation myocardial infarction. Arch Med Sci 2014;10:203-12.
7Urban P, Mehran R, Colleran R, Angiolillo DJ, Byrne RA, Capodanno D, et al. Defining High Bleeding Risk in Patients Undergoing Percutaneous Coronary Intervention. Circulation 2019;140:240-61.
8Valgimigli M, Bueno H, Byrne RA, Collet JP, Costa F, Jeppsson A, et al. 2017 ESC focused update on dual antiplatelet therapy in coronary artery disease developed in collaboration with EACTS: The Task Force for dual antiplatelet therapy in coronary artery disease of the European Society of Cardiology (ESC) and of the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J 2018;39:213-60.
9NHIS – Adult Tobacco Use-Glossary. Available from: [Last accessed on 2019 Nov 03].
10Iragavarapu T, Radhakrishna T, Babu Kj, Sanghamitra R. Acute coronary syndrome in young – A tertiary care centre experience with reference to coronary angiogram. Pract Cardiovasc Sci 2019;5:18. Available from: [Last accessed on 2019 Nov 03].
11Gupta R, Guptha S, Sharma KK, Gupta A, Deedwania P. Regional variations in cardiovascular risk factors in India: India heart watch. World J Cardiol 2012;4:112-20.
12World Health Organization. Global Status Report on Noncommunicable Diseases 2014. Geneva: World Health Organization; 2014.
13Sharma M, Ganguly NK. Premature coronary artery disease in Indians and its associated risk factors. Vasc Health Risk Manag 2005;1:217-25.
14Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): Case-control study. Lancet 2004;364:937-52.
15Hoit BD, Gilpin EA, Henning H, Maisel AA, Dittrich H, Carlisle J, et al. Myocardial infarction in young patients: An analysis by age subsets. Circulation 1986;74:712-21.
16Prajapati J, Jain S, Virpariya K, Rawal J, Joshi H, Sharma K, et al. Novel atherosclerotic risk factors and angiographic profile of young Gujarati patients with acute coronary syndrome. J Assoc Physicians India 2014;62:584-8.
17Siddique MA, Shrestha MP, Salman M. Age related differences of risk profile and angiographic findings in patients with coronary heart disease. BSMMU J 2010;3:13-7.
18Mammi MV, Pavithran K, Abdu Rahiman P, Pisharody R, Sugathan K. Acute myocardial infarction in north Kerala-a 20 year hospital based study. Indian Heart J 1991;43:93-6.
19Mähönen MS, McElduff P, Dobson AJ, Kuulasmaa KA, Evans AE, WHO MONICA Project. Current smoking and the risk of non-fatal myocardial infarction in the WHO MONICA Project populations. Tob Control 2004;13:244-50.
20Rosengren A, Wallentin L, Simoons M, Gitt AK, Behar S, Battler A, et al. Age, clinical presentation, and outcome of acute coronary syndromes in the Euroheart acute coronary syndrome survey. Eur Heart J 2006;27:789-95.