This document provides an outline and overview of ischemic heart disease and acute myocardial infarction (AMI). It discusses the epidemiology, risk factors, pathophysiology, clinical presentation, diagnosis, and treatment of AMI. The key points are: AMI occurs when cardiac myocytes die due to myocardial ischemia and can be diagnosed based on clinical history, ECG changes, and elevated biomarkers. Treatment involves initial pain relief, reperfusion via PCI or thrombolysis within 12 hours, anticoagulation, and long-term therapies like antiplatelet drugs, ACE inhibitors, beta blockers, and statins to prevent future events. Complications can include arrhythmias, heart failure, or cardiac rupture. Prognosis depends on the extent

1. State Specialist Hospital, Gombe (SSHG)
Department of Internal Medicine
Dr. Ibrahim Adamu
14 March, 2023

2. Outline
• Introduction
• Epidemiology
• Risk factors
• Pathophysiology
• Clinical features
• Diagnosis
• Treatment

3. Introduction
• Ischemic heart disease is a common cause of mortality in the
world
• It is a progressive disease due to build up and rupture
atherosclerotic plaque in the coronary arteries
• Acute coronary syndrome refers to the occlusion of one or
more of the coronary arteries with spectrum of manifestation
• It is a term that encompasses both unstable angina and
myocardial infarction
• Incidence is rising world wide due to urbanization and lifestyle
change

4. Introduction
• Acute MI : A clinical condition that results from complete
thrombotic occlusion of coronary artery(ies) with necrosis of
significant portion of the myocardium (generally >1cm)
• The term “acute” denotes infarction less than 3-5 days old,
when the inflammatory infiltrates is primarily neutrophilic
• Myocardial infarction (MI) occurs when cardiac myocytes die
due to myocardial ischemia, and can be diagnosed on the basis
of appropriate clinical history, 12-lead ECG, elevated
biochemical markers and autopsy

5. Epidemiology
• Incidence of IHD is commoner in Western world ? Sedentary
lifestyle
• Prevalence increase with age
• M:F 3:1
• 3x higher amongst postmenopausal women
• In the U.S 15.4 million people live with IHD and about 1 million
people have MI each year
• M.I accounts for 1 in every 6 death; 400,000 death annually
• 785,000 persons experience first attack of M.I while about
450,000 present as sudden cardiac death

6. • Sudden cardiac death is a prominent feature of CAD. 1in 6 in of
coronary attacks present with sudden death as the first, last
and only symptom
• In 2009, 1 in 5 male and 1 in 8 female deaths were from
coronary artery disease in the U.K
• According to WHO, M.I is the 8th leading cause of death in
Africa and 3.76% death in Nigeria
• ACS was once assumed to be “rare” in African blacks.
• Epidemiological transition in Africa and adoption of western
lifestyle leading to increase in number of cases.
Epidemiology

7. Epidemiology
• Falase, Oladapo, Kanu (2001) - incidence of 1 in 5,000 in UCH
Ibadan
• Another study in Lagos by Oke and Talabi found an incidence
of 1 in 13,500 admission
• In ABUTH, Danbauchi reported 10 cases of MI over period of 10
years (1985-1994)
• In JUTH, from Jan-December 2020 recorded atleast at least 6
confirmed cases of A.M.I
• In a study by Henry, Ayoola, Adamu and Ejegba revealed a rare
prevalence of IHD 0.7% in a 5 year study at FTHG

8. Risk factors
• Modifiable
Cigarette smoking
Hypertension
Diabetes mellitus
Hyperlipidaemia
Sedentary lifestyle
Obesity
Heavy alcohol consumption
Type A personality
Gout

9. Risk factors
• Non-modifiable
Advancing age
Male gender
Race
Family history

10. Risk factors
• Novel/Emerging risk factors
CRP
LP(a)
Small dense LDL- Cholesterol particle
Fibrinogen
Hyperhomocysteinemia
tPA
Cystatin – C
Chronic inflammatory state
HIV

11. Classification
1. Killip Classification Of M.I
Class Features
Class I No evidence of heart failure
Class II Findings of S3 gallop, lung rales,
raised JVP
Class III Overt pulmonary edema
Class IV Cardiogenic shock
2. ECG Findings: STEMI/NSTEMI

12. Etiology
a) Coronary atherosclerosis (95%)
b) Non-atherogenic form (5%)
Arteritis (vasculitis)
Coronary mural thickening
Coronary trauma
Coronary vasospasm
Coronary embolism
Polycythaemia

13. Pathophysiology
• Myocardial ischaemia
occurs when there is an
imbalance between the
supply of oxygen and
demand
• Atherosclerosis is the
underlying mechanism –
atheromas, fibro-fatty
plaques
• Mechanical shear stresses
serve as the trigger for

15. • Ultimately these changes leads to coronary thrombosis and
vasoconstriction
• Area of infarct occurs in the distribution of the occluded vessel
• I: About 25% occlusion: Asymptomatic or mild chest discomfort
• II: 25%-50% occlusion: Stable angina
• III: 50%-75% occlusion: Unstable angina
• IV: 75%-100% occlusion : Myocardial infarction (MI) although
the presence of collateral circulation may prevent an AMI.
Pathophysiology

16. • Changes in myocardium is time-based and may often be
reversed with early intervention
Ischemic changes (3-5 mins)
Myocardial death (20 mins)
Myocardial necrosis (2 hrs)
Irreversible after (4-6 hrs)
Pathophysiology

17. Gross findings:
• Early changes are myocardial
pallor
• Myocardial necrosis can be
detected as early as 2-3 hrs of
infarction
• In non-reperfused M.I, it
appears yellow areas
surrounding hyperaemic area
• In reperfused M.I, the infarcted
region appears red because of
Pathophysiology

18. Clinical presentation
• Prodromal symptoms e.g. stable angina or a risk factor – HTN,
DM, Cigarette smoking, Obesity, Drug abuse.
• Chest pain: variable, typically central severe constricting,
crushing, squeezing, tightening retrosternal pain that spreads
to the precordial area. It lasts > 30 mins and is not relieved by
nitrates. It radiates to the jaws & neck, left upper limb or
abdomen.
• There may be sweating, vomiting, restlessness and feeling of
impending doom
• +/- Classical Levin sign
• Patient may be a known HTN/DM

20. • Atypical MI presentation: acute LVF, unusual weakness,
excessive sweating, intractable hiccups, dyspepsia &
indigestion, overwhelming sense of apprehension, unexplained
dyspnoea, arrhythmia, stroke, peripheral embolism, acute
worsening HF, excessive vagal tone with increased urge to
evacuate bowel.
• Silent MI: No chest pain or other symptoms. It is common in the
elderly >70 yrs, diabetics, post transplant hearts and in post op
patients on strong opiates
Clinical presentation

21. Physical examination
Physical examination
• May be unrevealing and is only supportive. Patient will have
findings of the underlying cause e.g HHDx
• There may features of abnormal lipid metabolism e.g xanthoma
• Usually is a middle aged or elderly person
• May be obesed, apprehensive, restless, diaphoretic, confused
and/or pale
Respiratory
• Tachypnea
• Rales

22. Cardiovascular
• Pulse may be irregular (arrhythmia), normal, high
(catecholamines surge), low (cardiogenic shock)
• BP may be high (sympathetic respose), low (cardiogenic shock)
• JVP raised
• 4th heart sound
• Mumur may be present
There may be signs of complications of MI e.g. MR, Pericarditis,
extrasystoles
Physical examination

23. Diagnosis
W.H.O Criteria (1979)
• Clinical features
• 12 Lead ECG
• Cardiac biomarkers
ESC and ACC Modified Criteria
• Typical rise and gradual fall (troponin) or more rapid rise and fall
(CK-MB) with at least one of the following:
a) Ischemic symptoms
b) Development of pathologic Q waves on the ECG
c) ECG changes indicative of ischemia (ST segment elevation or
depression)
d) Coronary artery intervention (e.g angioplasty)

24. Investigation
NON-INVASIVE
• ECG
• ECHO
• Cardiac biomarkers
• CXR
• Others: FBC – leukocytosis and ESR, EUCr, Lipid profile, RBG,
Clotting profile
INVASIVE
• Coronary angiography

25. ECG
• This should be obtained within 5-10 minutes of patients arrival
• It allows categorization of a patients with suspected MI into
STEMI, NSTEMI and UA.
• ST segment elevation greater or equal to 1mm in 2 or more
contiguous leads confirms the diagnosis of STEMI.
• Q wave >1mm broad
• LBBB that is new in a patient with characteristic symptoms
should be regarded as indicative of MI.
• NSTEMI/UA may have T wave inversion

26. ECG

27. ECG

28. Cardiac biomarkers
Enzyme Onset Peak Duration
CKMB 3-12 hr 18-24 hr 36-48 hr
Troponins 3-12 hr 18-24 hr Upto 10 days
Myoglobin 1-4 hr 6-7 hr 24 hr
LDH 6-12 hr 24-48 hr 6-8 days
AST 6-12 hr 24-48 hr 48-72 hr
A rising titre is more important than isolated rise and therefore serial
assays of those enzymes are done

29. ECHO
• ECHO should be considered in all patients with suspected MI
especially those with continuing chest pain and non diagnostic
ECGs.
• Regional hypokinesia implies critical ischaemia or infarction,
which may be old or new.
• Myocardial thinning suggest an old infarct (remodelling).
• May reveal complications, e.g LV aneurysm, PE, thrombi or
myocardial rupture

31. Differential diagnosis
Differentials of chest pain
• Cardiac: Angina, Pericarditis, Myocarditis
• Vascular: Aortic dissection, Pulmonary embolism, PHTN
• Respiratory: Asthma, Pneumothorax, Pleurisy, Pneumonia
• Gastro-intestinal: GERD, Esophagitis, Acute pancreatitis
• Musculoskeletal: Costrochondritis, Tietze syndrome, Blunt
Trauma
Differentials of troponin rise
• HTN Crises, Arrhythmias, Myocarditis, Takotsubo
cardiomyopathy, Stroke, P.E
Differentials of ST elevation
• Takotsubo cardiomyopathy, Persistent LV aneurysm

32. • A.M.I is a medical emergency and treated as such
• Management is multidisciplinary
• Goal of treatment
1. Relief of ischemic pain
2. Assessment of the hemodynamic state and correction of
abnormalities that are present
3. Initiation of reperfusion therapy with PCI or thrombolysis
4. Antithrombotic therapy to prevent re-thrombosis or subtotal
stenosis at the site of an ulcerated plaque
Treatment

33. Treatment
Steps in management of A.M.I
• Acute triage
• Initial therapy
• Reperfusion
• Anticoagulation
• Long term therapy

34. Acute triage
• Respiratory or cardiorespiratory arrest: A.B.C of resuscitation
then appropriate resuscitation algorithms should be followed
• Cardiogenic shock complicating acute MI requires aggressive
evaluation and management
• Left heart failure with hypoxia: Patients who present with
dyspnea, hypoxia, pulmonary edema, and/or impending
respiratory compromise require aggressive oxygenation, airway
stabilization, diuretic therapy, and afterload reduction in
addition to the standard treatments
• Fatal arrhythmias: May require urgent defibrillation

35. Initial therapy
• Supplemental oxygen should be initiated to maintain oxygen
saturation above 90%
• IV access secured and blood work obtained
• Bedrest
• Aspirin at a dose of 162 to 325 mg to chew and swallow
• Sublingual nitroglycerin at a dose of 0.4 mg every 5 min for a
total of three doses. Avoid nitrates in hypotension
• I.V morphine sulfate at an initial dose of 2-4 mg, with
increments of 2mg, repeated at 5 to 15 minute intervals,
should be given for the relief of chest pain and anxiety.
Alternatives include Pethidine and tramadol. Avoid Pentazocine

36. Reperfusion
This is achieved by PCI, Thrombolysis or CABG.
• Primary PCI recommended for any patient with an acute STEMI
or those with new LBBB who presents within 12 hours of
symptom onset. Done within 90 mins
• Fibrinolysis recommended for any patient with an NSTEMI, new
LBBB, or a true posterior MI who presents within 12 hours of
symptom onset, has no contraindications for fibrinolysis,
including high risk for intracranial hemorrhage and done within
30 mins
• IV streptokinase (readily available) 1.5 MU in 100 ml N/S saline
given as infusion over 30-60 mins. Others are alteplase,

37. Anticoagulation
• LMWH could be used only in patients under 75 years of age
who are without significant renal dysfunction at a dose 60U/Kg
or alternatively double anticoagulation with Clopidogrel 300mg
and Aspirin upto 300mg
• Warfarin reduces reinfarction and cerebrovascular accidents
and may reduce mortality following acute MI given for atleast 3
months with INR (2-3) monitoring

38. Long term therapy
• Antiplatelet therapy to reduce the risk of recurrent coronary
artery thrombosis
• Prevention of left ventricular remodeling with an ACE inhibitor
e.g Losartan
• Prevention of recurrent ischemia and life-threatening
ventricular arrhythmias with beta blockers e.g Metoprolol
• Cholesterol lowering with a statin to prevent or slow disease
progression and help in plague maturation e.g Rosuvastatin
• Lifestyle modification

39. Treatment
Other medical therapy
• Tight blood sugar control in new and old DM patients – insulin
therapy (target RBS 5-10mmol/l)
• Maintain K level at 4 mmol/L and Mg at 2 mmol
• Stool softners e.g Lactulose

40. Rehabilitation
• Occupational rehabilitation
• Graded exercise tolerance

41. Complications
• Pericarditis
• Ventricular arrhythmia
• Cardiogenic shock
• Mitral regurgitation
• Recurrent angina
• Acute heart failure
• Myocardial rupture
• Embolism

42. Prognosis
• The prognosis of patients who have survived an acute coronary
syndrome is related to the
Presence of residual myocardial ischemia
Degree of myocardial damage
Presence of ventricular arrhythmias, cardiac rupture
etc
• In almost one-quarter of all cases of M.I, death occurs within a
few minutes without medical care.
• Half the deaths occur within 24 hours of the onset of
symptoms

43. Conclusion
• IHD results commonly from coronary atherosclerosis and has
spectrum of manifestation culminating in myocardial
ischemia/infarction
• Sudden cardiac death is a common presentation
• Risk factors associated with IHD are modifiable or non –
modifiable
• Increase coronary blood flow as early as feasible is overall
objective to avoid muscle necrosis during treatment in acute
stage

44. References
 Lecture notes on IHD by Dr. Adamu Adamu delivered on 24th
January, 2022
 Robert M. Kliegman, Bonita F. Stanton, Joseph W. St. Geme III, Nina
F. Schor, & Richard E. Behrman ‘Outcomes of MI in cormorbid states’
The New England Journal of Medicine. Article No.
10.1056/NEJMoa223456
 Professor Parveen Kumar, Dr. Micheal Clark MD Textbook of Clinical
Medicine 8th edition
 Website:
http://www.emedicine/medscape.com/acutemyocardialinfarction76
3. Accessed on Friday, 12th March 2023, 3:36pm

45. Thank you for listening!