Coronary heart disease

CORONARY ARTERY DISEASE
By- Dr Bhavishya desai
Moderator – Dr Nagappa

CONTENTS
1) Introduction
2) Biology and pathology of atherosclerosis
3) Epidemiology and prevention of IHD
4) Stable Angina
5) Acute coronary syndrome
6) Percutaneous interventional cardiac procedures vs coronary artery
bypass and valve surgery

PREVIOUSLY ASKED QUESTIONS
1) Discuss acute coronary syndromes and management of acute ST
elevation MI. Add note in fibrinolysis versus PTCA(2008)
2) Discuss the etiology ,clinical features, evaluation and management of
unstable angina (2009)
3) Atherosclerosis and plaque progression .(2009)
4) Discuss the recent concepts of etiopathogenesis ,complication and
prevention of atherosclerosis (2009R)
5) Management of nstemi

INTRODUCTION
• Coronary heart disease is a group of disease characterized by insufficient circulation in coronary
arteries potentially leading to angina pectoris, myocardial infarction ,heart failure and sudden
coronary death.
• It typically occurs when there is an imbalance between myocardial oxygen supply and demand .
• The most common cause of myocardial ischemia is atherosclerotic disease of an epicardial
coronary artery.
• Other less and non atherosclerotic variants of CHD are be due to vasoconstriction ,paradoxical
embolism ,chest trauma , spontaneous coronary dissection and cardiac syndrome X.
• The World Health Organization (WHO) has estimated that 3.8 million men and 3.4 million women
die from cardiovascular disease (CVD) each year, and since 1990, more people have died from
CVD than any other cause.

CORONARY ATHEROSCLEROSIS
• Atherosclerosis is a progressive inflammatory disorder of the arterial wall that is
characterized by focal lipid-rich deposits of atheroma that remain clinically
silent until they become large enough to impair tissue perfusion, or until
ulceration and disruption of the lesion result in thrombotic occlusion or distal
embolization of the vessel.
• Epicardial coronary arteries are the major site of atherosclerotic disease.

RISK FACTORS FOR ATHEROSCLEROSIS
MODIFIABLE NON MODIFIABLE
Smoking Age and sex
Hypertension Family history
Hypercholestrolemia
Physical inactivity
Obesity
alcohol
Dietary factors

• Vulnerable plaques are characterized by a lipid-rich core, a thin fibro cellular cap,
speckled calcification and an increase in inflammatory cells that release specific
enzymes to degrade matrix proteins.
• Stable plaques are typified by a small lipid pool, a thick fibrous cap, heavy
calcification and plentiful collagenous cross-links.

• Primary prevention – along with diet and lifestyle modification ,In patients
without evidence of coronary disease but with high serum cholesterol
concertation .
• Cholesterol lowering with statins will prevent coronary event but not lower
mortality.
• Secondary prevention –In patients with established coronary disease statin
therapy can be safely reduce the 5 year incidence of all cause of death ,as well as
major coronary coronary events
• In established coronary artery disease , aspirin is effective in reducing morbidity
and mortality

ANGINA PECTORIS
• Angina pectoris is a symptom complex caused by transient myocardial
ischemia and constitutes a clinical syndrome rather than a disease.
• Atherosclerosis is by far the most common cause of angina pectoris.
• Other causes like aortic stenosis and hypertrophic cardiomyopathy can
also cause angina pectoris

• Clinical features:
• Stable angina is characterized by central chest pain, discomfort or
breathlessness that is precipitated by exertion or other forms of
stress and is promptly relieved by rest
• Physical examination is usually unremarkable but should include
careful search for evidence of valve disease ,hypertension , left
ventricular dysfunction, carotid bruit

• LABORATORY EXAMINATION
• ELECTROCARDIOGRAM
• ■ A 12-lead ECG recorded at rest may be normal in patients with typical angina pectoris,
but there may also be signs of an old myocardial infarction.
• STRESS TESTING
• ■ Electrocardiographic
• Sensitivity of 68% and specificity
Of 77%

• DUKE TREADMILL SCORE
• It provides a quantitative prognostic assessment and a useful basis for determine the
urgency of urgency of coronary arteriography

• Exercise echo study
• Stress (exercise or dobutamine) echocardiography may cause the emergence of regions of akinesis or
dyskinesis that are not present at rest.
• More sensitive than exercise electrocardiography in the diagnosis of IHD.
• The left ventricular chamber dilated with exercise, and the septal and apical portions became akinetic to
dyskinetic (red arrow). These findings are strongly suggestive of a significant low-limiting stenosis in the
proximal left anterior descending artery.

• ISOTOPE PERFUSION IMAGING
• Stress myocardial radionuclide perfusion imaging after the intravenous administration of thallium 201
or 99m-technetium sestamibi during exercise stress.
• The images demonstrate a medium-size and severe stress perfusion defect involving the inferolateral
and basal inferior walls, showing nearly complete reversibility, consistent with moderate ischemia in the
right coronary artery territory

• Cardiac magnetic resonance (CMR) perfusion imaging ;can be used to assess wall motion
abnormality accompanying ischemia , as well a myocardial perfusion ,ventricular volumes
and ejection fraction.
• Multidetector CT –provide noninvasive coronary arteriograms that are useful in exclusion
of coronary artery disease in low probability of coronary disease (diagnostic sensitivity of
95%)

CORONARY ARTERIOGRAPHY
• This diagnostic method outlines the lumina of the coronary arteries and can be used to detect or
exclude serious coronary obstruction.
• Indications Coronary arteriography is indicated in
• (1) patients with chronic stable angina pectoris who are severely symptomatic despite medical
therapy and are being considered for revascularization, i.e., a percutaneous coronary intervention
(PCI) or coronary artery bypass grafting (CABG)
• (2) patients with troublesome symptoms that present diagnostic difficulties in whom there is a need
to confirm or rule out the diagnosis of IHD
• (3) patients with known or possible angina pectoris who have survived cardiac arrest.
• (4) patients with angina or evidence of ischemia on noninvasive testing with clinical or laboratory
evidence of ventricular dysfunction
• (5) patients judged to be at high risk of sustaining coronary events based on signs of severe ischemia
on noninvasive testing, regardless of the presence or severity of symptoms

TREATMENT OF STABLE ANGINA PECTORIS
• A careful assessment of the extent and severity of arterial disease
• Identification and control of risk factors such as smoking, hypertension and hyperlipidemia
• Control symptoms
• And identification of high risk patients
• ANTI-PLATELETS
Aspirin is an irreversible inhibitor of platelet cyclooxygenase and thereby interferes with platelet
activation.
Chronic administration of 75–325 mg orally per day has been shown to reduce coronary events in
asymptomatic adult men over age 50,
Patients with chronic stable angina, and patients who have or have survived unstable angina and
myocardial infarction.
Clopidogrel (75mg) is equally effective antiplatelet can be given if patient not tolerating aspirin.

ANTI ANGINAL DRUG THERAPY
• NITRATES
Their major mechanisms of action include systemic venodilation with concomitant reduction in LV
end-diastolic volume and pressure, thereby reducing myocardial wall tension and oxygen
requirements; dilation of epicardial coronary vessels; and increased blood flow in collateral vessels.
.They also exert antithrombotic activity by NO-dependent activation of platelet guanylyl cyclase
,causing impairment of intraplatelet calcium flux, and platelet activation.

• They are absorbed rapid and
completely through mucous
membranes.
• Therefore given sublingually in
tablets of 0.4 or 0.6 mg.
• Patients with angina should be
instructed to take the medication
both to relieve angina and also ~5
min before activities that are likely to
induce an episode.
• To minimize the effects of nitrate
tolerance, the minimum effective
dose should be used and a minimum
of 8 h each day kept free of the drug
to restore any useful response

Beta -Adrenergic Blockers
These drugs reduce myocardial oxygen demand by inhibiting the increases in heart rate, arterial pressure,
and myocardial contractability caused by adrenergic activation
Beta blockers with relative β1-receptor specificity such as metoprolol and atenolol may be preferable in
patients with mild bronchial obstruction and insulin requiring diabetes mellitus.
Calcium Channel Blockers
CCB are coronary vasodilators that produce variable and dose dependent reductions in myocardial oxygen
demand, contractility and arterial pressure.
They exert negative inotropic actions and are more likely to aggravate LV failure, particularly when used in
patients with LV dysfunction, especially if the patients are also receiving beta blockers
Verapamil ordinarily should not be combined with beta blockers .
Diltiazem can be combined with beta blockers in patients with normal ventricular function and no
conduction disturbances.

• CCB should be preferred over beta blockers only in following condition for initial therapy.
• (1) inadequate responsiveness to the combination of beta blockers and nitrates; many of
these patients do well with a combination of a beta blocker and a dihydropyridine calcium
channel blocker;
• (2) adverse reactions to beta blockers such as depression, sexual disturbances, and fatigue;
• (3) angina and a history of asthma or chronic obstructive pulmonary disease;
• (4) sick-sinus syndrome or significant atrioventricular conduction disturbances;
• (5) Prinzmetal’s angina
• (6) symptomatic peripheral arterial disease.

• Ranolazine, a piperazine derivative, may be useful for patients with chronic angina
despite standard medical therapy .
• Its antianginal action is believed to occur via inhibition of the late inward sodium current
(I Na).
• The benefits of INa inhibition include limitation of the Na overload of ischemic myocytes
and prevention of Ca2+ overload via the Na+–Ca2+ exchanger.
• A dose of 500–1000 mg orally twice daily is usually well tolerated.
• Ranolazine is contraindicated in patients with hepatic impairment or with conditions or
drugs associated with QTc prolongation and when drugs that inhibit the CYP3A
metabolic system.

ACUTE CORONARY SYNDROME
• The term ‘acute coronary syndrome ’ encompasses both unstable angina and
myocardial infarction.
• It is characterized by new onset or rapidly worsening angina ,angina on minimal
exertion or angina at rest in the absence of myocardial damage.
• There are three component to the clinical diagnosis of ACS
1. The symptom description
2. ECG
3. Biomarker evidence of myocyte necrosis

• Unstable angina : typical ischemia symptoms without ST elevation on ECG and without elevated
biomarkers of necrosis
• Non – STEMI :typical ischemic symptoms without ST elevation on ECG but with biomarkers of
necrosis above the diagnostic threshold
• STEMI: typical ischemic symptoms with ST-elevation on ECG and with biomarkers of necrosis
above the diagnostic threshold.

Stable angina – Ischemia due to fixed atheromatous stenosis of one or more
coronary arteries
Unstable angina – Ischemia caused by dynamic obstruction of coronary artery due
to plaque rupture or erosion with superimposed thrombosis
Myocardial infarction – Myocardial necrosis caused by acute occlusion of any
coronary artery due to plaque rupture or erosion with superimposed thrombosis

ST-ELEVATION MYOCARDIAL INFARCTION
• The universal definition of myocardial infarction classifies MI into five
types, depending on the circumstances in which the MI occurs
• Type 1: Spontaneous Myocardial Infarction
• Spontaneous MI related to atherosclerotic plaque rupture, ulceration, fissuring,
erosion, or dissection with resulting intraluminal thrombus in one or more of the
coronary arteries that leads to decreased myocardial blood flow or distal platelet
emboli with ensuing myocyte necrosis.

• Type 2: Myocardial Infarction Secondary to Ischemic Imbalance
• imbalance between myocardial oxygen supply and/or demand (e.g., coronary
endothelial dysfunction, coronary artery spasm, coronaryembolism,
tachy/bradyarrhythmia, anemia, respiratory failure, hypotension, hypertension, ± left
ventricular hypertrophy).
• Type 3: Myocardial Infarction Resultingin Death When Biomarker Values Are
Unavailable
• New ischemic changes on the ECG or new LBBB, but death occurring before blood
samples could be obtained, before cardiac biomarkers could rise, or in rare
cases, when cardiac biomarkers were not collected.

• Type 4a: Myocardial Infarction Related to Percutaneous Coronary
Intervention
• Type 4b: Myocardial Infarction Related to Stent Thrombosis
• Type 5: Myocardial Infarction Related to Coronary Artery Bypass Grafting

CAUSES OF MYOCARDIAL INJURY
a) Injury Related to Primary Myocardial Ischemia
Plaque rupture ,Intraluminal coronary artery thrombus formation
b) Injury Related to the Supply-Demand Imbalance of Myocardial Ischemia
Tachyarrhythmias/bradyarrhythmia
Aortic dissection
severe aortic valve disease ,
Hypertrophic cardiomyopathy
Severe respiratory failure ,
Severe anemia

c) Injury Not Related to Myocardial Ischemia
• Cardiac contusion, pacing, or defibrillator shocks
• Rhabdomyolysis with cardiac involvement
• Myocarditis
• Cardiotoxic agents
d) Multifactorial or Indeterminate Myocardial Injury
• Heart failure
• Stress (takotsubo) cardiomyopathy
• Severe pulmonary embolism
• Pulmonary hypertension
• Severe acute neurologic diseases (e.g., stroke, subarachnoid hemorrhage)
• Infiltrative diseases (e.g., amyloidosis, sarcoidosis)

PATHOPHYSIOLOGY OF STEMI
• STEMI usually occurs when coronary blood flow decreases abruptly after a
thrombotic occlusion of a coronary artery previously affected by atherosclerosis.
• Initial platelet monolayer forms at the site of the disrupted plaque, various agonists
(collagen, ADP, epinephrine, serotonin) promote platelet activation. After agonist
stimulation of platelets, thromboxane A2 is released, further platelet activation
occurs, and potential resistance to fibrinolysis develops.
• Activation of platelets by agonists promotes a conformational change in the
glycoprotein 9IIb/IIIa receptor.

• The coagulation cascade is activated on exposure of tissue factor in damaged
endothelial cells at the site of the disrupted plaque. Factors VII and X are activated,
ultimately leading to the conversion of prothrombin to thrombin, which then converts
fibrinogen to fibrin.
• The culprit coronary artery eventually becomes occluded by a thrombus containing
platelet aggregates and fibrin strands

DIAGNOSIS OF STEMI
• The laboratory tests of value in confirming the diagnosis may be divided into four
groups:
• (1) ECG,
• (2) serum cardiac biomarkers,
• (3) cardiac imaging, and
• (4) nonspecific indices of tissue necrosis and inflammation.

ECG
• The ECG is central to the diagnosis of acute and chronic ischemic heart disease.
• Ischemia exerts complex time-dependent effects on the electrical properties of
myocardial cells. Severe, acute ischemia lowers the resting membrane potential
and shortens the duration of the action potential.
• Such changes cause a voltage gradient between normal and ischemic zones. As
a consequence, current flows between those regions. These currents of injury
are represented on the surface ECG by deviation of the ST segment
• Multiple factors affect the amplitude of acute ischemic ST deviations. Profound
ST elevation or depression in multiple leads usually indicates very severe
ischemia.

• Abnormal Q waves were once considered markers of transmural
myocardial infarction, whereas subendocardial infarcts were thought not
to produce Q waves.
• However, careful ECG-pathology correlative studies have indicated that
transmural infarcts may occur without Q waves and that subendocardial
(nontransmural) infarcts sometimes may be associated with Q waves.
• Q waves not related to ischemic heart disease (pseudoinfarct patterns).

• The ECG has important limitations in both sensitivity and specificity in the
diagnosis of ischemic heart disease.
• Although a single normal ECG does not exclude ischemia or even acute infarction,
a normal ECG throughout the course of an acute infarct is distinctly uncommon.
• the diagnostic changes of acute or evolving ischemia are often masked by the
presence of left bundle branch block, electronic ventricular pacemaker patterns,
and Wolff- Parkinson-White preexcitation.

CARDIAC BIOMARKERS IN ACS
• An ideal biomarker should be sensitive to detect small degree of
damage to the heart ,should be specific to the heart muscle and should
guide us to the severity of injury and prognosis .
• Most importantly it should detect early
• Troponins do fulfil a lot of these criteria but they are not detect till 4-6
hours have passed after myocardial injury causing a delay in detection
and diagnosis .

SERUM CARDIAC BIOMARKER
• Cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI) have amino-acid
sequences different from those of the skeletal muscle forms of these proteins.
• These differences permitted the development of quantitative assays for cTnT and cTnI with
highly specific monoclonal antibodies.
• cTnT and cTnI may increase after STEMI to levels many times higher than the upper
reference limit (the highest value seen in 99% of a reference population not suffering from
MI),
• The measurement of cTnT or cTnI is of considerable diagnostic usefulness, and they are
now the preferred biochemical markers for MI

• CK rises within 4–8 h and generally returns to normal by 48–72 h.
• An important drawback of total CK measurement is its lack of specificity for STEMI,
as CK may be elevated with skeletal muscle disease or trauma, including
intramuscular injection.
• The MB isoenzyme of CK has the advantage over total CK that it is not present in
significant concentrations in extracardiac tissue and, therefore, is considerably more
specific.

• MYOGLOBIN
• Myoglobin assists in oxygen transport in all muscle tissues. It is released within one hour
and rises more rapidly than cTn or CK-MB, peaks at 8-10 hours and returns to normal within
24 hours.
• It is sensitive early indicator of cardiac damage
• However it is nonspecific to the myocardium.
• It has a negative predictive value .

CARDIAC IMAGING
• Abnormalities of wall motion on two-dimensional echocardiography are
almost universally present. Although acute STEMI cannot be distinguished
from an old myocardial scar or from acute severe ischemia by
echocardiography.
• When the ECG is not diagnostic of STEMI, early detection of the presence or
absence of wall motion abnormalities by echocardiography can aid in
management decisions, such as whether the patient should receive
reperfusion therapy.
• The presence of right ventricular (RV) infarction, ventricular aneurysm,
pericardial effusion, and LV thrombus can be identified

MANAGEMENT OF STEMI
• INITIAL MANAGEMENT
• MANAGEMENT IN THE EMERGENCY DEPARTMENT
• HOSPITAL PHASE MANAGEMENT

PREHOSPITAL CARE
The major elements of prehospital care of patients with suspected STEMI include
1. Recognition of symptoms by the patient and prompt seeking of medical
attention
2. Rapid deployment of an emergency medical team capable of performing
resuscitative maneuvers, including defibrillation
3. Transportation of the patient to a hospital facility that is continuously staffed by
physicians and nurses skilled in managing arrhythmias and providing advanced
cardiac life support
4. Expeditious implementation of reperfusion therapy

E M E R G E N C Y
M E D I C A L
S E R V I C E
S Y S T E M S

GENERAL TREATMENT MEASURES
• Aspirin –Initial management strategy for patients with suspected STEMI.
• Rapid inhibition of cyclooxygenase-1 in platelets followed by a reduction of
thromboxane A2 levels is achieved by buccal absorption of a chewed 160–
325-mg tablet
• To achieve therapeutic blood levels rapidly, the patient should chew a
non–enteric-coated tablet to promote buccal absorption by passing the
gastric mucosa.
• 300mg -600mg of clopidogrel followed by 75mg/day
• 80 mg of atorvastatin should be given.

CONTROL OF CARDIAC PAIN
• Sublingual nitroglycerin can be given safely to most patients with
STEMI.
• Up to three doses of 0.4 mg should be administered at about 5-min
intervals.
• In addition to diminishing or abolishing chest discomfort, nitroglycerin
may be capable of both decreasing myocardial oxygen demand (by
lowering preload) and increasing myocardial oxygen supply

• Morphine is a very effective analgesic for the pain associated with STEMI.
• Morphine is routinely administered by repetitive (every 5 min) intravenous injection
of small doses (2–4 mg),
• Intravenous beta blockers are also useful in the control of the pain of STEMI.
• These drugs control pain effectively in some patients, by diminishing myocardial O2
demand

PERCUTANEOUS CORONARY INTERVENTION
Primary PCI –
• Primary angioplasty is defined as PCI without concomitant fibrinolytic therapy.
• Randomized clinical trials of primary PCI vs thrombolysis have shown Primary PCI has superior outcomes.
• Primary PCI requires a highly experienced interventional team and an integrated approach
• Candidates for primary PCI
1. Reperfusion of choice ,if FMC to balloon time is <120min
2. Patients presenting at 12-24 hour with ongoing pain or ECG showing evidence of ongoing ischemia
3. All STEMI patient with cardiogenic shock
4. STEMI with presence of acute heart failure
5. When diagnosis of STEMI is in doubt

•RESCUE PCI
Thrombolytic therapy may fail to achieve effective reperfusion in 30% or more in those
treated for STEMI
Patients experience continuing symptoms of ischemia and failure of resolution of ST
elevation on ECG (<50% resolution of the ST elevation within 1 h of administration )
Rescue PCI is more effective than repeat thrombolysis or conservative treatment
(REACT trial )

•FACILITATED PCI –
• The combination of full dose or reduced dose fibrinolysis followed by
emergency PCI has been tested in large scale trials and shown worse
outcomes and greater bleeding risks (ASSENT 4 trail ).
• Hence planned emergency PCI after thrombolysis is not recommended,
although later PCI after thrombolysis impact is resolved may be of
benefit (GRACIA 2 study )

CORONARY ARTERY BYPASS SURGERY
• Patients with STEMI referred for CABG are those with persistent or recurrent ischemia despite
fibrinolysis or primary PCI with residual coronary disease not amenable to PCI, high-risk
Coronary anatomy (e.g., left main stenosis) discovered at initial catheterization,
• a complication of STEMI such as ventricular septal rupture or severe mitral regurgitation
caused by papillary muscle dysfunction.
• STEMIpatients with continued severe ischemic and hemodynamic instability will probably
benefit from emergency revascularization.
• Unless such mechanical complications are present ,the hazards of acute bypass surgery are
significantly increased compared to delayed revascularization in a stabilized patient .

THROMBOLYTIC TREATMENT
• Thrombolytic treatment refers to combination of antiplatelets therapy
( aspirin and clopidogrel ) with fibrinolytic treatment .
• The fibrinolytic agents direct or indirectly converts plasminogen to
plasmin and plasmin lyses fibrin in the clot .
• Twotrials, LATE (Late Assessment of Thrombolytic Efficacy) and
EMERAS (Estudio Multicéntrico Estreptoquinasa Repúblicas de
América del Sur), when viewed together, provide evidence that a
reduction in mortality may still be observed in patients treated with
thrombolytic agents between 6 and 12 hours after the onset of
ischemic symptoms.

• The current recommended regimen of tPA consists of a 15-mg
bolus followed by 50 mg intravenously over the first 30 min,
followed by 35 mg over the next 60 min.
• Streptokinase is administered as 1.5 million units (MU)
intravenously over 1 h.
• rPA is administered in a double-bolus regimen consisting of a 10-
MU bolus given over 2–3 min, followed by a second 10-MU bolus
30 min later.
• TNK is given as a single weight-based intravenous bolus of 0.53
mg/kg over 10 s.

ASSESSMENT OF
REPERFUSION
• TIMI Flow Grad
• When assessed angiographically, flow in the culprit coronary artery is described by
a simple qualitative scale called the Thrombolysis in Myocardial Infarction (TIMI)
grading system:
• grade 0 indicates complete occlusion of the infarct-related artery;
• grade 1 indicates some penetration of the contrast material beyond the point of
obstruction, but without perfusion of the distal coronary bed;
• grade 2 indicates perfusion of the entire infarct vessel into the distal bed, but with
flow that is delayed compared with that of a normal artery
• grade 3 indicates full perfusion of the infarct vessel with normal flow.
• the goal of reperfusion therapy is to attain full perfusion of the infarct .

• TIMI frame count a simple count of the number of angiographic frames elapsed
until the contrast material arrives in the distal bed of the vessel of interest.
• This objective and quantitative index of coronary bloodflow independently predicts
in-hospital mortality from STEMI and also separates patients with TIMI grade 3 flow into
low-risk and high-risk groups.
• The TIMI frame count can also be used to quantitate coronary blood flow (mL/sec),
as calculated by:
• 21/(observed TIMI frame count ) x1.7

ANTITHROMBOTIC AGENTS
• Goal of treatment with antiplatelet and anticoagulant agents is to maintain patency of the infarct-
related artery, in conjunction with reperfusion strategies.
• A secondary goal is to reduce the patient’s tendency to thrombosis and, thus, the likelihood of
mural thrombus formation or deep-venous thrombosis, either of which could result in pulmonary
embolization.
• The standard anticoagulant agent used in clinical practice is unfractionated heparin (UFH).
• The available data suggest that when UFH is added to a regimen of aspirin and a non-fibrin-
specific thrombolytic agent such as streptokinase, additional mortality benefit occurs
• The recommended dose of UFH is an initial bolus of 60 U/kg (maximum 4000 U) followed by an
initial infusion of 12 U/kg per h (maximum 1000 U/h). The activated partial thromboplastin time
during maintenance therapy should be 1.5–2 times the control value.

• Enoxaparin has been shown to reduce significantly the risk of death/nonfatal
reinfarction and death/nonfatal reinfarction/urgent revascularization compared with
UFH in STEMI patients who receive fibrinolysis.
• Treatment with enoxaparin is associated with higher rates of serious bleeding, but net
clinical benefit—a composite endpoint that combines efficacy and safety—still favors
enoxaparin over UFH.

BETA-ADRENOCEPTOR BLOCKERS
• Acute intravenous beta blockade improves the myocardial O2 supply-demand
relationship, decreases pain, reduces infarct size, and decreases the incidence of
serious ventricular arrhythmias.
• In patients who undergo fibrinolysis soon after the onset of chest pain,recurrent
ischemia and reinfarction are reduced.

INHIBITION OF THE RENIN-ANGIOTENSIN-
ALDOSTERONE SYSTEM
• ACE inhibitors reduce the mortality rate after STEMI,
• The maximum benefit is seen in high-risk patients those who are elderly or who have an anterior infarction, a
prior infarction, and/or globally depressed LV function, but evidence suggests that a short- term benefit
occurs when ACE inhibitors are prescribed unselectively to all hemodynamically stable patients with STEMI
• Before hospital discharge, LV function should be assessed with an imaging study. ACE inhibitors should be
continued indefinitely in patients who have clinically evident CHF, in patients in whom an imaging study shows
a reduction in global LV function or a large regional wall motion abnormality, or in those who are
hypertensive.
• Long-term aldosterone blockade should be prescribed for STEMI patients without significant renal dysfunction
(creatinine ≥2.5 mg/dL in men and ≥2.0 mg/dL in women) or hyperkalemia (potassium ≥5.0 mEq/L) who are
already receiving therapeutic doses of an ACE inhibitor, have an LV ejection fraction ≤40%, and have either
symptomatic heart failure or diabetes mellitus.

COMPLICATIONS AND THEIR MANAGEMENT
• VENTRICULAR DYSFUNCTION
• HEMODYNAMIC ASSESSMENT
• HYPOVOLEMIA
• CARDIOGENIC SHOCK
• RIGHT VENTRICULAR INFARCTION
• ARRHYTHMIAS
• PERICARDITIS

SECONDARY PREVENTION
• Dietary and lifestyle modification
• Smoking cessation
• Exercise
• Management of obesity
• Lipid lowering therapy
• Antianginal therapy if revascularization is incomplete
• Low dose aspirin
• DAPT for at least one month in STEMI and a year for non-
STEMI as determined by the type of stents implanted

NSTEMI
• Diagnosis of NSTEMI is established if a patient has typical ischemic symptoms without
ST elevation on ECG but with biomarkers of necrosis above the diagnostic threshold

NSTE–ACS PATHOPHYSIOLOGY
• NSTE-ACS is caused by an imbalance between myocardial oxygen supply
and demand resulting to formation of thrombus by one or more of the
following process
a) Disruption of and unstable coronary plaque due to plaque rupture
,erosion or calcified protruding nodule that leads to intracoronary
thrombus formation and an inflammatory response.
b) Coronary arterial vasoconstriction
c) Gradual intramural narrowing
d) Increased myocardial oxygen demand produced by conditions such as
fever ,tachycardia and thyrotoxicosis in the presence of fixed epicardial
coronary obstruction .

CLINICAL PRESENTATION
Typical chest discomfort which is severe and has features like
• Occurrence at rest (or with minimum exertion )
• Lasting >10 mins
• recent onset
• crescendo pattern
• Anginal equivalents such as dyspnea ,epigastric discomfort ,nausea can also
be present and are more common in type 2 diabetics and women.

• ECG – new ST depression occurs in about one –third of patients with NSTE-ACS . ST-segment depressions
as little as 0.05mV are sensitive (but not specific) marker for NSTE-ACS. Greater degrees of ST-segment
depression predict poorer outcomes.
• T-wave changes are more common but are less specific signs of ischemia ,unless they are new and deep T-
wave inversions (>0.3 mV).
• More than half of NSTEMI may have normal or
nondiagnostic ECGs. Because ischemia may occur in a territory that is not well represented on the
standard 12-lead ECG or because the patient may have episodic ischemia that is missed on the
initial ECG, tracings should be repeated every 20 to 30 minutes until the symptoms resolve, or the
diagnosis of MI is established or excluded

• Cardiac biomarkers –
• Patients with NSTEMI have elevated biomarkers of necrosis, such as cardiac troponin (cTn) I or T,
which are specific, sensitive, and the preferred markers of myocardial necrosis.
• Since the sensitivities of different troponin assays vary in clinical practice, consensus
recommendation is to define MI by an elevation in cTnI or cTnT >99thpercentile of
the normal range of the specific assay used, with a typical temporal rise and fall occurring in a
patient with a clinical presentation consistent with ACS.
• The MB isoform of creatine kinase (CK-MB) is a less sensitive alter- native.
• Elevated levels of any of these markers distinguish patients with NSTEMI from those with UA.

• Newer hsTn assays it is possible with a single measurement at presentation less
than 5ng/L to classify almost 2/3 of patients presenting to the ED with suspected
ACS as “very low risk ’’ for MI or cardiac death in the next 30 days possible.
• Absolute changes in hsTn greater than 9.2ng/L are even more predictive of
acute MI

RISK ASSESSMENT SCORES
• Several risk scores that integrate clinical variables and findings on the ECG and from
serum biomarkers have been developed for patients with NSTE-ACS.
• The TIMI (Thrombolysis in Myocardial Ischemia) risk score for UA/NSTEMI identifies
seven independent risk factors;
• Their sum correlates directly with death or recurrent ischemic events
• This simple, rapid assessment at the initial evaluation identifies high-risk patients who
can derive benefit from an early invasive strategy and more intensive
antithrombotic therapy.

MANAGEMENT
• Consists of an acute phase focused on the clinical symptoms and
stabilization of the culprit lesion and
• a longer-term phase that involves therapies directed at the prevention
of disease progression and future plaque rupture/erosion.

ANTI-ISCHEMIC THERAPY
• Guidelines emphasize the early useof anti-ischemic therapies to
improve the balance between oxygen supply and demand.
• The goals of anti-ischemic therapy include relief of symptoms and
prevention of early sequelae of ACS, including recurrent MI, HF,
arrhythmias, and death.

INVASIVE VERSUS CONSERVATIVE
MANAGEMENT
• Two general approaches to cardiac catheterization and revascularization can be used to
manage patients with NSTE-ACS
1) An early invasive (within 48 hours of initial evaluation) cardiac catheterization, followed
by PCI, CABG, or continuing medical therapy, depending on the coronary anatomy.
2) An ischemia-guided (or selective invasive) approach, with initial medical management
and catheterization being reserved for patients with hemodynamic instability or
recurrent ischemia, either at rest or on a noninvasive stress test, followed by
revascularization if the anatomy is suitable

• An early invasive strategy is not recommended in patients with
extensive comorbidities in whom the risks of revascularization
outweigh the potential benefits, or in patients with acute chest
pain with low clinical likelihood of ACS and a negative troponin assay.
• A meta-analysis of seven trials confirmed an overall significant 25%
reduction in mortality and a 17% reduction in nonfatal MI
after 2 years of follow-up in patients managed with an early invasive
strategy.
• Thus, an early invasive strategy, in the absence of contraindication, is
recommended in patients with NSTE-ACS who have ST-segment changes
and/or positive troponin assay on admission, or in whom these
high-risk features develop over the subsequent 24hours. Other high-risk
indicators, such as recurrent ischemia or evidence of congestive heart
failure, also indicate an early invasive strategy.

• An early invasive strategy is also advised in patients with
NSTE-ACS previously treated with CABG and in patients
who have had NSTE-ACS within 6 months of a previous PCI
and in whom restenosis may be the cause.
• Indications for an initial conservative strategy include patients with
life-threatening comorbid conditions or in whom the risks outweigh
the potential benefits, and in low-risk patients without recurrent
symptoms.

TIMING OF AN INVASIVE APPROACH
• A meta-analysis of four trials involving 4013 patients with NSTE-ACS compared an early
invasive strategy (time to angiography, 1.2 to 14 hours following hospital presentation) with a
delayed invasive strategy (time to angiography, 21 to 86 hours).
• Mortality and MI rates in the two strategies did not differ, but the early invasive approach was
associated with significant reductions in recurrent ischemia (41%) and duration of hospital stay
(28%) and with favorable trends with respect to bleeding and the composite of CV death, MI,
or stroke.

PRINZMETAL VARIANT ANGINA
• In 1959, Prinzmetal and colleagues described a syndrome of
ischemic pain that occurred at rest, accompanied by ST-segment
elevation.
• Prinzmetal variant angina (PVA) may be associated with
acute MI, VT or VF, and sudden cardiac death (SCD). Spasm of a
proximal coronary artery with resultant transmural ischemia and
abnormalities in LV function are the diagnostic hallmarks of PVA.
• Patients with PVA tend to be younger than those with NSTE-ACS
attributable to coronary atherosclerosis, and many do not
exhibit the classic coronary risk factors, except they are frequently
heavy cigarette smokers

• Angina is often extremely severe, tends to cluster between midnight and
8 AM, and may be accompanied by syncope related to AV block,
asystole, or ventricular tachyarrhythmia. Increased QT dispersion appears to be a
risk marker for SCD in these patients.
• The key to diagnosis of PVA lies in the detection of episodic ST-segment
elevation, often accompanied by severe chest pain, usually occurring at rest.
• Multiple asymptomatic episodes of (silent) ST-segment elevation occur in many
patients. ST- segment deviations may be present in any leads, depending on the
artery involved.

MANAGEMENT
• Discontinue smoking
• Calcium antagonist or combination with a long-acting nitrate.
• PCI and occasionally CABG may be indicated in patients with PVA
associated with discrete, proximal, fixed obstructive lesions, but revascularization is
contraindicatedin patients with isolated coronary artery spasm without
accompanying fixed obstructive disease.
• Patients who have experienced ischemia-associated VF and continue to manifest
ischemic episodes despite maximal medical treatment should receive an implantable
cardioverter-defibrillator (ICD).

MYOCARDIAL INFARCTION WITH NONOBSTRUCTIVE
CORONARY ARTERIES (MINOCA)
• Defined as evidence of MI (positive cardiac biomarker and corroborative clinical evidence of infarction)
with angiographically normal or near-normal coronary arteries (the absence of obstructive CAD on
angiography,i.e. no coronary artery stenosis ≥50%], in any potential infarct-related artery), and no other
explanation for the resentation.

SYNDROME X
• The constellation of typical angina on effort, objective evidence of
myocardial ischemia on stress testing, and normal coronary arteries on
angiography is sometimes known as syndrome X.

Coronary heart disease

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